Angiotensin converting enzyme-2 (ACE2) is an analogue of the ACE that cleaves Angiotensin II to Angiotensin 1-7, a peptide with vasodilatory properties. Previous studies showed increased ACE2 activity among patients with chronic heart failure. ACE2 activity has been shown to correlate with the NYHA functional class in this setting, suggesting a compensatory role in advanced heart failure. The relationship between ACE2 activity and myocardial function in patients with ST-elevation acute myocardial infarction (STEMI) remains unknown.We sought to explore the relationship between ACE2 activity, infarct size and acute left ventricular (LV) systolic function following STEMI.We prospectively included 44 patients with their first STEMI reperfused by primary percutaneous intervention. Baseline blood samples were drawn between 12 and 24 hs from admission and at 7 days. A standard cine and contrast enhanced-cardiac magnetic resonance study was performed during admission. LV end-diastolic (LVED) and end-systolic (LVES) indexes, ejection fraction (EF) and infarct size (expressed as % of the LV mass), were computed by manual plannimetry on sequential short axis cine and delayed enhanced images, respectively. Serum ACE2 activity was measured by fluorometric assay using a specific substrate.Baseline ACE2 activity did not correlate with LV volume indexes, EF, infarct size and BNP. By paired analysis, ACE2 activity significantly increased from baseline to 7 days in STEMI patients . Furthermore, at 7 days a significant direct correlation was observed between ACE2 activity and all, LVES index , infarct size  and baseline BNP levels . Additionally, a significant inverse correlation between ACE2 activity and EF was observed . See figure.ACE2 serum activity rises during the first week following STEMI and the increase is related to infarct size and underlying indicators of LV systolic dysfunction. As suggested in chronic heart failure stages, ACE2 activation may reflect a compensatory mechanism to limit left ventricular dysfunction and could potentially indicate a new target for therapy following STEMI reperfusion.


Surgical management of tetralogy of Fallot (TOF) results in anatomic and functional abnormalities in the majority of patients. Although right ventricular volume load due to severe pulmonary regurgitation can be tolerated for many years, there is now evidence that the compensatory mechanisms of the right ventricular myocardium ultimately fail and that if the volume load is not eliminated or reduced by pulmonary valve replacement the dysfunction might be irreversible. Cardiovascular magnetic resonance (CMR) has evolved during the last 2 decades as the reference standard imaging modality to assess the anatomic and functional sequelae in patients with repaired TOF. This article reviews the pathophysiology of chronic right ventricular volume load after TOF repair and the risks and benefits of pulmonary valve replacement. The CMR techniques used to comprehensively evaluate the patient with repaired TOF are reviewed and the role of CMR in supporting clinical decisions regarding pulmonary valve replacement is discussed. Although the management of tetralogy of Fallot (TOF) has evolved considerably since Blalock and Taussig described the first systemic artery-to-pulmonary artery shunt in 1945 and Lillehei and Varco reported the first repair by an open-heart procedure in 1954 , optimalRight ventricular (RV) dilation from pulmonary regurgitation (PR), residual atrial and/or ventricular septal defect, tricuspid regurgitation, right ventricular outflow tract (RVOT) aneurysm, pulmonary artery stenosis, and tachyarrhythmias are some of the abnormalities frequently encountered in patients with repaired TOF. Although the hemodynamic burden associated with these anomalies is often tolerated well during childhood and adolescence, the incidences of arrhythmias, exercise intolerance, heart failure, and death nearly triple during the third postoperative decade and afterward -13. SeveThis article comprises two parts. The first part reviews the pathophysiology, natural history, and clinical challenges late after TOF repair. The second part discusses the role of CMR in clinical decision making with an emphasis on its role in supporting patient selection for PVR.Relief of RVOT obstruction in TOF often involves disruption of pulmonary valve integrity, which leads to PR in the majority patients. Both experimental evidence and clinical data have shown that the severity of PR can increase over time -20. The 2 - P1) = mean diastolic pressure difference between the MPA and RV. Unlike aortic regurgitation, the diastolic pressure difference between the MPA and the RV is small. Therefore, the PR volume is largely determined by other factors, namely the size of the regurgitation orifice , the capacitance of the pulmonary arteries [Where ROA = regurgitation orifice area; C = constant (empiric number); DT = diastolic time; , these procedures often lead to akinesis or dyskinesis of the RVOT, outflow patch aneurysm Figure , fibrosimax) were significantly reduced 3 months after induction of PR.Studies in animal models of RV volume load similar to conditions seen after TOF repair provide insight into myocardial adaptation. Kiriazis et al. studied an in-vitro preparation of RV papillary muscle subjected to volume load . They shHuman studies in repaired TOF patients using CMR provide insights regarding ventricular mechanics and clinical outcomes in this population ,44-47. SThe right and left ventricles function in series and, in the absence of shunts, have similar net outputs. In 1910 the French physiologist Bernheim first recognized interdependence between LV and RV function. He postulated that alterations in the size and function of the LV adversely impact the geometry and function of the RV, a phenomenon termed 'Bernheim effect' . Many suThe adverse impact of RV dilatation and dysfunction on LV geometry and function (both diastolic and systolic) has been demonstrated in patients with congenital  and acquired heart disease . Through a complex interplay involving the shared myofibers, septum, pericardium, and coronary flow, RV volume load leads to septal shift towards the LV, leftward shift of the LV pressure-volume loop, and reduction in LV operant volumes. Initially, LV function is preserved but with progressive RV dysfunction, LV function deteriorates. Ventricular dyssynchrony, both intra- and inter-ventricular, likely contribute to adverse RV-LV interaction ,67. In tEarly survival of patients with TOF is excellent with 1-2% operative mortality ,69. Two The common theme that has emerged from the literature on risk stratification of major adverse events  late after TOF repair is that there are 3 major categories of outcome predictors: 1) history ; 2) electrophysiological markers ; and 3) hemodynamic sequelae of severe PR .Multiple studies have addressed risk factors for sudden death and for tachyarrhythmias late after TOF repair. Gatzoulis et al. studied 793 patients from 6 centers . They foIn a study that used CMR to measure PR and biventricular dimensions and function in 100 late survivors of TOF repair, RV and LV dysfunction were strongly associated with impaired clinical status, but the degree of PR was not ,82. KnauRecommendation for PVR in patients with repaired TOF and severe PR are based on risk/benefit analysis that takes into account the natural history and pathophysiology of the disease, procedural risks, and its potential benefits.The operative mortality for surgical PVR is low Table . There iWhen considering the risks associated with PVR, the risk of valve failure should also be considered. All valves inserted in the pulmonary position have a limited life expectancy, with wide variations in rates of freedom from valve failure and reoperation, depending of the type of valve and patient age. Calderone et al. reported freedom from reoperation in 81% of patients at 5 years, 58% at 10 years, and 41% at 15 years . These aThe advent of transcatheter pulmonary valve implantation ,91, howeThere is strong evidence that PVR is highly effective in eliminating or greatly reducing PR -95. MultThe data regarding the effects of PVR on QRS duration, arrhythmia propensity, and objective exercise parameters is inconsistent. Some investigators have reported modest improvements in one or more of these categories whereas others have shown no significant change from pre- to post-PVR. Therrien et al. reported that the incidence of ventricular tachycardia was lower after PVR (9% post operatively versus 23% preoperatively) and that the rate of increase in QRS duration had stabilized after the procedure . In cont2 in one study [2, whereas RV size normalized in 9 of 10 patients with pre-operative end-diastolic volume ≤170 ml/m2 [2 and end-systolic volume <82 ml/m2 as associated with normal postoperative RV size [2 as the threshold value below which RV size returns to the normal range after PVR [2, RV end-systolic volume of 91 ± 18 ml/m2, and RV ejection fraction 47 ± 8%, RV size and function was, on average, within normal limits one year after PVR. The authors, therefore, recommend PVR before RV end-diastolic volume exceeds 150 ml/m2. We analyzed pre-PVR predictors of normal post-PVR RV size (end-diastolic volume index ≤114 ml/m2) and function (ejection fraction ≥48%) in 64 patients with severe chronic PR [2 and QRS duration <140 ms.Although conclusive confirmation that PVR improves survival late after TOF repair is still lacking, a growing body of evidence has emerged during the last decade supporting the rationale for the procedure. There is strong evidence that without intervention severe PR in repaired TOF leads to severe RV dilatation and dysfunction, tricuspid valve regurgitation, LV dysfunction, tachyarrhythmias, diminished exercise tolerance, heart failure symptoms, and death , and RV70 ml/m2 . Oosterh RV size . Buechelfter PVR . Frigiolfter PVR . With anronic PR . IndepenThus, the timing and indications for PVR after TOF repair must balance the benefits of elimination of RV volume load before irreversible dysfunction occurs and the disadvantages of a premature surgical or transcatheter procedure. As with any other medical procedure, the risks and benefits of the procedure must be weighed on a case-by-case basis, taking into account not only cardiac risk factors but also the risks associated with non-cardiac morbidities. With the above considerations in mind, the following summarizes the author's current recommendations for PVR in patients with repaired TOF or similar physiology. These recommendations will undoubtedly continue to evolve as new information becomes available and as valve technology and implantation methods continue to improve.Indications for PVR in patients with repaired TOF or similar physiology with moderate or severe pulmonary regurgitation (regurgitation fraction ≥25%):2 or Z-score >4. In patients whose body surface area falls outside published normal data: RV/LV end-diastolic volume ratio >2a. RV end-diastolic volume index >150 ml/m2b. RV end-systolic volume index >80 ml/mc. RV ejection fraction <47%d. LV ejection fraction <55%e. Large RVOT aneurysmf. QRS duration >140 msg. Sustained tachyarrhythmia related to right heart volume loadh. Other hemodynamically significant abnormalities:○ RVOT obstruction with RV systolic pressure ≥2/3 systemic○ Severe branch pulmonary artery stenosis (<30% flow to affected lung) not amenable to transcatheter therapy○ ≥ Moderate tricuspid regurgitation○ Left-to-right shunt from residual atrial or ventricular septal defects with pulmonary-to-systemic flow ratio ≥ 1.5○ Severe aortic regurgitation○ Severe aortic dilatation (diameter ≥5 cm)Symptoms and signs attributable to severe RV volume load documented by CMR or alternative imaging modality, fulfilling ≥1 of the quantitative criteria detailed above. Examples of symptoms and signs include2 for age and gender not explained by chronotropic incompetence)a. Exercise intolerance not explained by extra-cardiac causes , with documentation by exercise testing with metabolic cart c. Syncope attributable to arrhythmiaa. Due to higher risk of adverse clinical outcomes in patients who underwent TOF repair at age ≥3 years , PVR mayb. Women with severe PR and RV dilatation and/or dysfunction may be at risk for pregnancy-related complications . AlthougBecause it is not limited by acoustic window, not associated with exposure to ionizing radiation, and is noninvasive, CMR is ideally suited for longitudinal follow-up in patients with repaired TOF . Since iThe goals of CMR in patients with repaired TOF include:• Quantitative assessment of left and right ventricular volumes, mass, stroke volumes, and ejection fraction.• Evaluation of regional wall motion abnormalities.• Imaging the anatomy of the right ventricular outflow tract, pulmonary arteries, aorta, and aorto-pulmonary collaterals.• Quantification of PR, tricuspid regurgitation, cardiac output, and pulmonary-to-systemic flow ratio.• Assessment of myocardial viability with particular attention to scar tissue in the ventricular myocardium aside from sites of previous surgery .• The importance of careful attention to details of patient preparation and placement in the scanner cannot be overemphasized. Optimal placement of ECG leads is paramount to quality gating. A peripheral intravenous cannula for injection of gadolinium-based contrast is placed in the following circumstances:1. First CMR examination2. >3 years since last late gadolinium enhancement (LGE) evaluation3. Deterioration in clinical status4. Regional or global ventricular function has worsenedExceptions are made in young patients when placement of an intravenous cannula might result in loss of patient cooperation.Localizing images: ECG-gated steady-state free precession (SSFP) localizing imaging in the axial, coronal, and sagittal planes followed by real-time interactive sequences for identification of key imaging planes and structures targeted for additional sequences .• ECG-triggered, breath-hold cine SSFP in the following planes:• LV 2-chamber   Figure Ventricular short-axis .▪ Parallel to the Axial plane for imaging of the outflow tracts and branch pulmonary arteries .▪ Representative imaging parameters: echo time 1.7 ms; repetition time 3.3 ms; flip angle 60°; sensitivity encoding (SENSE) acceleration factor 2; field of view 260 mm; matrix 160 × 160 reconstructed to 256 × 256; voxel size 1.6 × 1.8 × 6-8 mm reconstructed to 1.0 × 1.0 × 6-8 mm; 30 reconstructed images per cardiac cycle.Magnetic resonance angiogram (MRA): Non-gated, breath-hold gadolinium-enhanced (0.2 mmol/kg gadopentetate dimeglumine) 3-dimensional MRA   Figure . RepreseFlow measurements: ECG-triggered, breathe-through cine phase contrast flow measurements in the MPA : ECG-triggered, breath-hold, phase sensitive LGE imaging performed 10-20 minutes after contrast administration in the following planes: ventricular short-axis .• ECG-triggered, breath-hold cine SSFP in the outflow tracts and branch pulmonary arteries in patients with image artifacts from metallic implants.• ECG-triggered, breath-hold turbo (fast) spin echo sequence with blood suppression for imaging of the branch pulmonary arteries (when branch pulmonary artery stenosis is identified).• ECG-triggered, breathe-through cine phase contrast flow measurements in the coronary arteries or as a substitute for contrast magnetic resonance angiography.• ECG-triggered, respiratory navigated, free breathing 3-dimensional isotropic SSFP for evaluation of the In a cooperative patient the above protocol is typically completed in 65-70 minutes.The importance of a structured report with an organized, comprehensive structure that addresses all key elements pertinent to clinical decision-making cannot be overemphasized. Key data reporting elements include:• Anatomy of the RVOT and main and branch pulmonary arteries with emphasis on obstruction and/or dilatation or aneurysm formation.• Biventricular size and function .• Vessel dimensions: aortic root, ascending aorta, MPA, right and left pulmonary arteries; if abnormal , diameters of the atrioventricular valve.• Flow measurements:▪ Ascending aorta, MPA, right and left pulmonary arteries▪ Pulmonary valve regurgitation▪ Other valve regurgitation• Late gadolinium enhancement: presence, location, and extent.• Associated anomalies: systemic and pulmonary veins, aortic arch sidedness and branching order.An example of CMR report in a hypothetical patient with repaired TOF is available in Additional File 3).Quantification of right and left ventricular size and function and blood flow is performed using dedicated software available either from the manufacturers of MRI equipment or from third party vendors. Measurements of biventricular diastolic and systolic volumes and mass are performed on ECG-gated cine SSFP images, which provide a high contrast between the blood pool (T2/T1 = 360/1200 = 0.3) and the myocardium (T2/T1 = 75/880 = 0.085) . AccuratSeveral approaches to measurements of biventricular size and function have been reported. In general, these can be divided into 2 broad categories: 1) methods that rely on summation of discs (Simpson's principle) ; and 2) In the second category either a formula based on a geometrical model or extrapolation from sparse data are used to generate ventricular volumes -120. TheIn our center ventricular volumes and mass are measured from short-axis cine SSFP images . Cross-rThe technique for measuring blood flow is well established . PR fracMost studies on the reproducibility of volumetric measurements by CMR have focused on the LV and those that included RV measurements were based on healthy volunteers or patients with acquired heart disease ,127. FewMooij et al. analyzed the intra- and inter-observer variability of RV and LV size and function in 60 patients--20 with a normal RV, 20 with ASD or partially anomalous pulmonary venous connection, and 20 with repaired TOF . In pati2) will likely lead the clinician to recommend expectant follow-up whereas the same shunt in a patient with moderate PR  and RV dilatation  will prompt a discussion about transcatheter device closure of the atrial septal defect versus PVR and atrial septal defect closure.CMR supports clinical decision making in patients with repaired TOF by providing comprehensive anatomic and functional information on postoperative cardiovascular abnormalities. Especially important in these patients is quantitative information on RV size, global and regional RV function, LV size and function, myocardial scar, RVOT aneurysm or obstruction, valve regurgitation , residual intracardiac shunts, and anatomic abnormalities of the pulmonary arteries and aorta. CMR is increasingly being incorporated into clinical surveillance protocols once patients with repaired TOF reach adolescence . The comPerhaps the most critical role of CMR in supporting clinical decisions in patients with repaired TOF is determining when to replace or insert a pulmonary valve . As indiAlthough CMR has become the reference standard modality for follow-up of patients with repaired TOF, specific patient groups require a multimodality approach . Table 4Research efforts in TOF aim to address the many facets of the anomaly. Examples include elucidating the genetic and developmental etiologies of the anomaly, refining the initial surgical management to minimize late complications, defining markers of late adverse outcomes, refining the criteria for PVR to optimize late outcomes, and developing new tools to address the failing RV before and after PVR. CMR plays an important role in several of these research fronts. For example, CMR is used to evaluate the function of tissue-engineered semilunar valve implanted in the pulmonary position in sheep . This anmax, ventricular-arterial coupling). Other advanced image analysis techniques such as CMR speckle tracking may overcome some of the limitations of RV tissue tagging and provide further insight into RV-LV mechanics in patients with repaired TOF , for many years. In other patients, the pathophysiology is further complicated by abnormalities in the pulmonary arterial tree. Over time, however, the risks of ventricular dysfunction, exercise intolerance, heart failure symptoms, arrhythmias, and death increase substantially. CMR has evolved to become a crucial diagnostic tool in this growing patient population. Key to optimal use of CMR in these patients is a comprehensive imaging protocol and implementation of steps to ensure consistency and reproducibility of measurements. Finally, CMR continues to play a key role in research efforts directed at improving outcomes of patients with tetralogy of Fallot.CMR: cardiovascular magnetic resonance; LGE: late gadolinium enhancement; LV: left ventricle; PR: pulmonary regurgitation; PVR: pulmonary valve replacement; RV: right ventricle; RVOT: right ventricular outflow tract; TOF: tetralogy of Fallot;The author declares that they have no competing interests.Video clip of severe RV dilatation and dysfunction after TOF repair. Cine SSFP imaging in a 37 year-old patient with repaired TOF, severe pulmonary regurgitation, moderate tricuspid regurgitation (arrow), and severe right ventricular dilatation (end-diastolic volume index 386 ml/m2) and dysfunction (ejection fraction 15%). This patient who also exhibited severe heart failure symptoms had only modest decrease in RV size and no improvement in RV function after pulmonary valve replacement.Click here for fileVideo clip of cine imaging of the RV long-axis. Evaluation of the right ventricular outflow tract (RVOT) long-axis by ECG-gated cine SSFP MR. Along with the RV 2-chamber plane , this view demonstrates patency of the RVOT and main pulmonary artery, presence or absence of pulmonary valve tissue, and wall motion abnormalities.Click here for fileVideo clip of pulmonary regurgitation after TOF repair. Evaluation of pulmonary regurgitation (PR) by ECG-gated cine phase contrast MR. Antegrade flow from the RV to the MPA is encoded red and retrograde flow from the MPA to the RV (PR) is encoded blue.Click here for fileCMR report in repaired TOF. Example of CMR report in a hypothetical patient with repaired TOFClick here for fileVideo clip of computer modeling of the RV after TOF repair. Computer model of right ventricular stress map based on CMR data of a patient with repaired TOF.Click here for file


However, the prevalence is likely to be higher than reported, as older patients are less likely to be diagnosed due to absence of classical symptoms of sympathetic overactivity and confounding effects of aging, comorbidities, and medications. We describe a hypertensive elderly patient with incidentally diagnosed pheochromocytoma complicated by recurrent urosepsis, cardiomyopathy, and fatal myocardial infarction. Our case demonstrates that, in older hypertensive patients without classical symptoms, orthostatic hypotension and urinary retention, which are common in the elderly, may indicate catecholamine excess and that the deleterious cardiovascular consequences of catecholamine excess in the elderly are not prevented by pharmacological  Pheochromocytomas are rare catecholamine-producing tumors of chromaffin cells in the adrenal medulla or extra-adrenal paraganglia. They are diagnosed most frequently in the fourth and fifth decades  and are E. coli urinary tract infection (UTI). Urine and blood cultures grew E. coli, sensitive to penicillin and ceftriaxone. Her serum creatinine was elevated at 164 μmol/L, which was attributed to dehydration causing prerenal azotemia (urea 8.4 mmol/L), urosepsis, and obstructive uropathy. Serum sodium, potassium, calcium, and phosphate were within normal ranges. Serum urea and creatinine normalized with hydration.A 77-year-old woman with a history of hypertension on nifedipine LA 30 mg daily, osteoarthritis, and cognitive impairment, who required minimal assistance in activities of daily living, was admitted with fever, postural dizziness, dysuria, and inability to pass urine for one day. Her temperature was 38.9 degrees Celsius, blood pressure (BP) 180/100 mmHg, pulse rate 104/minute, and physical examination revealed a tender distended bladder which drained 2700 mL of turbid urine. She had experienced two episodes of urine retention and incontinence over the previous month, the most recent of which required urethral catheterization and outpatient antibiotic treatment for μg/L/hr (NR 0.66–3.08). The imaging features of the adrenal mass, and elevation of urine metanephrine and normetanephrine 2-fold above the upper limit of normal, were, therefore, suggestive of pheochromocytoma. A 131I-metaiodobenzylguanidine (MIBG) scan demonstrated an MIBG-avid mass in the right suprarenal region, consistent with pheochromocytoma (α-adrenergic blockade. Her left ventricular ejection fraction (LVEF) was 45% with grade 1 diastolic dysfunction and left ventricular hypertrophy, but no wall motion abnormalities. Coronary angiogram showed no significant stenosis. As she refused adrenalectomy, she was continued on pharmacological α- and β-adrenergic blockade. Postural hypotension resolved, and her BP was 130/70 mmHg on POB 10 mg t.d.s. and atenolol 50 mg once daily on discharge.Her BP was persistently elevated above 170/100 mmHg despite increasing nifedipine LA to 60 mg and adding atenolol. She had postural dizziness and one documented episode of postural hypotension (BP supine 158/72 and standing 106/66 mmHg) on the 3rd day of admission despite intravenous rehydration and clinically normal hydration status. Computed tomography scan of the abdomen, performed to exclude renal abscess, showed a heterogeneous vascular right adrenal mass measuring 6.5 × 3.3 cm that enhanced with contrast, reported as being suggestive of pheochromocytoma . 24-hourmocytoma , with noKlebsiella pneumoniae with extended-spectrum betalactamase. She was found to have an acute myocardial infarction with pulmonary oedema on the 3rd day of admission when she went hypotensive and became increasingly dyspnoeic: an electrocardiogram (ECG) showed ST-segment depression and T inversion in the anterior chest leads, and troponin T level was elevated at 0.94 ng/mL . α- and β-blockade were stopped when her BP decreased to 90/52 mmHg, and intravenous frusemide was given cautiously. Echocardiography revealed impaired left ventricular ejection fraction of 20% with biventricular hypokinesia, multiple global wall motion abnormalities, and dilated atria, consistent with cardiomyopathy. Aspirin and subcutaneous fraxiparine were started. Her serum calcium  was low at 1.92 mmol/L, which was corrected with intravenous calcium gluconate infusion to 2.14 mmol/L. Shock and acute pulmonary oedema remained intractable despite inotropic support with dopamine infusion, and she became asystolic the same night. Cardio-pulmonary resuscitation was unsuccessful.Over the next 5 years, atenolol was increased to 100 mg daily to maintain BP below 140/90 mmHg. POB dose titration was limited by symptomatic postural hypotension despite clinically adequate hydration. Despite several episodes of acute urinary retention requiring outpatient urethral catheterization, she refused to consider intermittent catherization. She was admitted thrice for urosepsis and during her last admission; intravenous imipenem was started as urine and blood cultures were positive for ∼45 years [β-adrenergic blockade may worsen hypertension without α-blockade. Orthostatic hypotension in pheochromocytoma may be due to abnormal sympathetic vascular regulation [Our patient demonstrates that the diagnosis of pheochromocytoma is frequently overlooked in the elderly due to paucity of classical symptoms of sympathetic overactivity, and features of catecholamine excess being confounded by the effects of aging, comorbidities, and medications. In large cohort studies of pheochromocytoma patients, 9–27% were aged 60 or older, but adults in this age group comprised 65–80% of cases diagnosed at autopsy [45 years –7. 60–9045 years . Common gulation  and causThe relatively large size of our patient's tumor may be a cause, as well as a consequence, of the lack of symptoms, which is concordant with observations that pheochromocytomas are more likely to be incidentally diagnosed in older patients , 9. Moreα-adrenergic receptors overstimulation in the bladder neck and urethra, seen on urodynamic studies in patients with pheochromocytoma [α-adrenergic antagonist. Chronic urine retention increases the risk of urosepsis in elderly patients, in whom urinary tract infections are common due to urinary dysfunction from reduced mobility, comorbidities, and effects of medications. In our patient, urinary retention may have occurred due to suboptimal α-adrenergic blockade due to intolerance of postural hypotension. This may have contributed to recurrent urosepsis.Urinary retention in our patient was likely to be due to the mocytoma , who werα- and β-blockade. Poor LVEF was also exacerbated by acute myocardial infarction, which is known to be precipitated by sepsis-induced catecholamine surges [β2-adrenoceptors, triggering protein-kinase-A-mediated phosphorylation of the receptor which initiated a switch from Gs to Gi protein signaling [Elderly patients are highly susceptible to the deleterious effects of chronic catecholamine excess and surges of catecholamine secretion, particularly cardiomyopathy and myocardial injury. Catecholamine-induced cardiomyopathy is associated with left ventricular dilatation, dysfunction, and dyskinesia which may be apical (Takotsubos pattern)  or basale surges , leadinge surges , coronare surges , 18). Pue surges . Cardioge surges , and posignaling  called signaling  which fuIt is important to have a high index of suspicion for pheochromocytoma in hypertensive elderly patients with recurrent urinary retention and orthostatic hypotension. Our patient demonstrates that pharmacological adrenergic blockade does not prevent the potentially fatal cardiovascular complications of pheochromocytoma, supporting the recommendation of adrenalectomy for all patients who are fit for surgery, including the elderly.


The aim of the study was to test the reproducibility and variability of myocardial T2 mapping in relation to sequence type and spatial orientation in a large group of healthy volunteers. For control T2 mapping was also applied in patients with true edema. Cardiovascular magnetic resonance (CMR) T2-mapping has potential for the detection and quantification of myocardial edema. Clinical experience is limited so far. The variability and potential pitfalls in broad application are unknown.Healthy volunteers  and patients with edema  underwent CMR at 1.5 T. Steady state free precession (SSFP) cine loops and T2-weighted spin echo images were obtained. In patients, additionally late gadolinium enhancement images were acquired. We obtained T2 maps in midventricular short axis (SAX) and four-chamber view (4CV) based on images with T2 preparation times of 0, 24, 55 ms and compared fast low angle shot (FLASH) and SSFP readout. 10 volunteers were scanned twice on separate days. Two observers analysed segmental and global T2 per slice.In volunteers global myocardial T2 systematically differed depending on image orientation and sequence . Anteroseptal and apical segments had higher T2 than inferior and basal segments . 14 volunteers had segments with T2 ≥ 70 ms. Mean intraobserver variability was 1.07 ± 1.03 ms (r = 0.94); interobserver variability was 1.6 ± 1.5 ms (r = 0.87). The coefficient of variation for repeated scans was 7.6% for SAX and 6.6% for 4CV. Mapping revealed focally increased T2  in all patients with edema.Myocardial T2 mapping is technically feasible and highly reproducible. It can detect focal edema und differentiate it from normal myocardium. Increased T2 was found in some volunteers most likely due to partial volume and residual motion. In acute myocardial infarction or inflammation T2-weighted cardiovascular magnetic resonance (CMR) can detect myocardial edema in vivo -4. IncreCMR T2-mapping is a promising tool for characterizing myocardial edema -19. WhilThe local ethical committee approved the study. All participants were enrolled after informed consent was obtained.The study complies with the declaration of Helsinki. The ethical committee of Charite Medical University approved the study on January 27th, 2011. The application number was EA1/276/10.We scanned 73 healthy volunteers  without any cardiovascular disease, no symptoms of inflammation and a normal electrocardiogram. All participants were seen by a cardiologist. We discouraged alcohol intake one day before the scan to avoid inflammatory reaction [We investigated a group of consecutive patients  with acute myocardial damage. Edema was defined as a regional area of hyperintense signal on T2-weighted fast spin echo images corresponding to evidence of focal myocardial damage like wall motion abnormality or late gadolinium enhancement (LGE). The group comprises 20 patients with acute myocardial infarction (imaging 3 ± 1 days after admission), 5 patients with acute myocarditis , 2 postmenopausal female patients with Takotsubo cardiomyopathy  and 1 patient with cardiac sarcoidosis .Using a 1.5 T scanner  with a 12-channel chest coil we obtained steady state free precession (SSFP) cine loops  during breathhold in three long and at least one midventricular short axis matching the slice position for mapping. T2-weighted STIR images  were obtained in the same short axis as cine and additionally in long axis, if a focal abnormality was seen. In patients we additionally acquired fast low angle shot (FLASH) inversion recovery gradient echo LGE images in short and long axes  after 0.2 mmol/kg Gadolinium-DTPA.For T2-mapping we applied a prototype sequence based on either FLASH or SSFP gradient echo  in one mWe scanned a spherical phantom of 20 cm diameter filled with manganese chloride doped distilled water. The RR-interval was simulated to be 1000 ms. A 2D multi contrast spin echo sequence  in conjunction with a mono-exponential three-parameter-fit served as T2 reference measurement . We addihttp://www.osirix-viewer.com) and QMASS  in all subjects. The endocardial and epicardial contours were manually drawn on the last corresponding T2-weighted raw image with the echo time of 55 ms. The myocardium was then segmented  into 6 segments according to the AHA segmentation scheme [For signal analysis we used Osirix  were calculated. Bland-Altman-plots were obtained to analyse intra- and interobserver variability. Volunteer and patient data were compared using 95% tolerance intervals with 90% coverage. These tolerance intervals cover 90% of all observations of a normal distribution with 95% confidence when the mean and the standard deviation are known. Influencing factors were identified by sequence using the candidates age, gender, heart rate, body surface area, body mass index and the interaction terms in an analysis of variance with forward selection (criterion for selection p < 5%). We compared the data on healthy volunteers and patients using a mixed linear model with compound symmetry as working correlation matrix to account for the multiple measurements of up to four sequences by subject. Gender and age  were included as covariates. We performed a multivariate analysis including wall thickness, diastolic motion and a combination thereof to assess the impact on myocardial T2.Evaluation of multi contrast spin echo data in the phantom yielded T2 = 62.0 ± 0.5 ms. The T2-mapping variant using FLASH readout resulted in T2 = 55.5 ± 1.0 ms, whereas SSFP readout revealed T2 = 70.9 ± 0.8 ms . The remaining 69 formed the healthy study group..In all subjects maps could be generated in diagnostic quality. Mean heart rate was 73 ± 10 bpm. Global myocardial T2 measurements are summarized in Table With both sequences anteroseptal segments had higher T2-values than inferior segments in SAX , while T2 of remote myocardium was 51 ± 3 ms  and residual diastolic motion were related to higher myocardial T2. Close observation of cine loops and analysis with m-mode-like projection confirm diastolic wall motion in particular in young volunteers with thin walls . The lowInclusion of even small amounts of neighbouring entities like blood (T2 of about 200 ms) and pericardial fat (T2 of about 80 ms) can grossly influence the measurement of myocardial T2. Improving spatial resolution should minimize partial-volume effect, however this also prolongs the acquisition window increasing motion artefacts. We found T2-values of up to 80 ms even in our volunteer group, where as the T2 for edema associated with acute infarction has been reported to be 69 ± 6 ms . TherefoFor the future imaging at individually optimized time points within the cardiac cycle should be considered if cine imaging indicates abundant myocardial motion even in mid-diastole. Depending on individual wall motion across the cardiac cycle in cine loops systole or early diastole may be chosen. However, previous T1 mapping experiments in volunteers indicate that results might slightly differ between systole and diastole .A clinical advantage for myocardial T2 mapping can be expected in particular in patients with pronounced apical wall motion abnormalities where conventional T2-weighted imaging can be challenging. A severe apical wall motion abnormality may result in hyperintense intraluminal blood signal that is difficult to differentiate from bright signal within the wall that truly reflects edema. In these circumstances T2-mapping seems to offer additional options for clinical routine to confirm true edema while conventional T2-weighted spin echo remains inconclusive Figure . In addiWe enrolled patients with focal lesions only. Theoretically mapping offers the potential to quantify diffuse tissue damage that is less obvious on conventional CMR images. Future studies including patients with known diffuse disease might enlighten this phenomenon. We included two cases of typical Takotsubo cardiomyopathy and one case of sarcoidosis with typical late Gadolinium enhancement corresponding to focal edema. Edema has been previously described in both entities including a large multicentre study for Takotsubo cardiomyopathy -35.The power calculation took into account the differentiation of patients and volunteers as a whole group. The study and its sample size were not designed to reveal subtle differences among e.g. women of different decades of age. There is no dedicated gold standard for true edema. We assumed edema in myocardial areas where it made sense clinically based on concomitant late gadolinium enhancement or obvious wall motion abnormalities in patients with evidence of acute myocardial damage in laboratory results and electrocardiogram.Myocardial T2 mapping is technically feasible and highly reproducible in a large number of normal volunteers. Differences in sequences and spatial resolution result in small differences in myocardial T2 values. Quantifying T2 easily detects focal myocardial edema and differentiates it from remote myocardium. T2 mapping may offer a more stable and truly quantitative alternative for edema detection in cases when conventional T2-weighted imaging fails. Mapping in thin and rapidly moving myocardial walls can result in overestimation of myocardial T2 and must not be confused with true edema.CMR: Cardiovascular magnetic resonance; STIR: Short tau triple inversion recovery; SSFP: Steady state free precession; FLASH: Fast low angle shot; SAX: Short axis; 4CV: Four-chamber view; CI: Confidence interval; LGE: Late gadolinium enhancementA Greiser is an employee of Siemens AG, Erlangen, Germany. The authors declare no other competing interests.RW and JSM conceived of and designed the study. RW, MP, WU, MD, AG and FVK acquired, analysed and interpreted the data. RW wrote the manuscript with input from WU, FVK, MD and JSM. All authors read and approved the final manuscript.


Heart failure affects millions of patients all over the world, and its treatment is a major clinical challenge. Cardiac dyssynchrony is common among patients with advanced heart failure. Resynchronization therapy is a major advancement in heart failure management, but unfortunately not all patients respond to this therapy. Hence, many diagnostic tests have been used to predict the response and prognosis after cardiac resynchronization therapy. In this paper we summarize the usefulness of different diagnostic modalities with special emphasis on the role of surface electrocardiogram as a major predictor of response to cardiac resynchronization therapy. Heart failure is estimated to affect more than 23 million people worldwide with an approximately 2 million new cases diagnosed annually . In the Correction of left ventricular (LV) dyssynchrony is thought to be the main therapeutic effect of CRT. In the past decade several imaging techniques were used to quantify mechanical dyssynchrony and predict CRT response; these imaging techniques include M-mode echocardiography, Tissue Doppler imaging (TDI), Strain imaging, 3-dimensional echocardiography, magnetic resonance imaging, and nuclear cardiology. In addition to the technical difficulty and increased cost associated with the use of these imaging techniques, the accuracy of such modalities in predicting CRT is questionable.Multiple echocardiographic parameters had been shown to correlate with the response to CRT in several trials; however, the PROSPECT, large, multicenter, and prospective study, of 498 patients demonstrated that the tested 12 different echocardiographic dyssynchrony measures were unable to distinguish responders from nonresponders to a degree that may influence clinical decision –16. Real-time 3-dimensional echocardiography (RT3DE) is an emerging technique for left ventricular (LV) dyssynchrony assessment. The advantage of RT3DE is its ability to provide simultaneous information of the global LV contractility . In a seNuclear imaging with single photon emission computed tomography (SPECT) and magnetic resonance imaging (MRI) are another modalities, which have been used in the assessment of LV mechanical dyssynchrony. Additional advantage of both techniques is their ability to assess the presence and location of LV transmural scar, which may influence LV lead positioning Despite the wide availability of clinical and investigational imaging modalities to evaluate the patient response to CRT with variable accuracy, a simple 12-lead remains the standard test for patient selection. Several ECG parameters used to predict the response to CRT, including baseline rhythm, QRS duration, QRS morphology, LV activation sequence, and the PR interval.Prolonged QRS duration (≥120 ms) as measured on the standard 12-lead ECG is the most commonly used parameter in clinical practice to identify eligible candidates for CRT –28. DespMore than 27% of heart failure patients with reduced left ventricular systolic function and QRS duration <120 ms have evidence of mechanical dyssynchrony by TDI, and the presence of which seems to be associated with increased mortality –32. Few The degree of QRS duration prolongation is an indicator of severity of electrical dyssynchrony . QRS durBaseline QRS morphology is probably equally important as QRS duration to predict response to CRT. Patients with a prolonged QRS duration may have a left bundle-branch block (LBBB), right bundle-branch Block (RBBB), nonspecific intraventricular conduction delay (IVCD), or paced rhythm. The presence of typical LBBB morphology is a strong predictor of response compared with right bundle branch block (RBBB) morphology and non-specific intraventricular conduction delay (IVCD) that has a much lower probability of CRT response , 40. In LBBB significant depolarization delay between the anteroseptal and posterolateral walls occurs which thought to explains the efficacy of CRT in this patients population. Careful evaluation of the QRS morphology in patients with apparent LBBB may yield important further information. An early report by Grant and Doge suggested that reversal of the intraventricular septal activation pattern should occur with the onset of LBBB, which is reflected in the initial 40 ms of the QRS complex; however, these expected changes were absent in 40% of the study patients who developed new LBBB . Similarmax) on baseline ECG are associated with higher probability of reverse remodeling. LVATmax is the difference between the total QRS duration and the right ventricular activation time (RVAT), where the RVAT represents the interval between the beginning of QRS and the early QRS notch P = 0.49) or nonspecific IVCD  [P = 0.0001 [Unlike LBBB, ventricular activation is not largely affected in RBBB, therefore from theoretical perspective CRT is not expected to be effective in this subgroup of patients . Less th = 0.28) . Further= 0.0001 .Patient rhythm, interatrial conduction delay and the magnitude of atrioventricular delay, as represented by the native PR interval are additional valuable information that may influence CRT response and can be easily obtained from the baseline 12-lead ECG. The role of CRT in patients with atrial fibrillation is not well established: major clinical trials of resynchronization included mainly patients in sinus rhythm. However, other studies suggested a positive outcome in AF patients –51. A meInteratrial conduction delay is characterized by a wide and notched P wave in lead II with a wide terminal negative deflection in lead V1. Significant interatrial delay may results in left atrial contraction during LV systole, which may negatively affect CRT outcome. In such cases simultaneous activation of both atria could be achieved by implantation of the atrial lead in the interatrial septum . P < 0.01) versus normal PR  intervals [To ensure near 100% biventricular pacing in CRT, the programmed AV delay should be shorter than the native PR interval, this programming may truncate the left ventricular filling resulting in a suboptimal response to CRT; however, the presence of a long native PR interval may permit a more physiological AV delay programming. Subgroup analysis of patients in the COMPANION trial demonstrated that randomization to CRT was associated with a reduction in the endpoint, but the strength of the association was greater for those with prolonged PR (hazard ratio = 0.54; Prediction of CRT response is a complex and subject of extensive research over the past decade. Despite all we know about CRT, a significant proportion of heart failure patient dose not respond to CRT. However, careful analysis of simple 12-lead ECG can yield impressive data difficult to replace by any of the available more sophisticated clinical tools.


Post-gadolinium bolus T1 mapping was used to assess interstitial myocardial fibrosis in a group of patients with severe aortic stenosis. The changes identified were correlated with regional contractile perfomance as assessed by CSPAMM tagging. T1 mapping proved to be a practical feasible approach for assessing diffuse fibrosis.Aortic stenosis (AS) is associated with increased interstitial myocardial fibrosis (IMF). This is detectable by cardiovascular magnetic resonance (CMR) after gadolinium infusion. T1-mapping-derived partition coefficients (λ) and extracellular volume fractions (Ve) have also been shown to correlate with IMF after a simple bolus administration of gadolinium. We hypothesized that the λ and Ve would also detect interstitial expansion in severe AS patients compared to healthy controls and that these measures would correlate with abnormal myocardial strain using a high temporal-resolution tagging sequence.A Modified Look-Locker Inversion Recovery (MOLLI) sequence was used to generate eleven T1-weighted images. Myocardial and blood pool T1 values were derived by fitting a signal intensity-time curve using CMR42®. The λ was determined by plotting (1/T1myo vs. 1/T1blood pool) at various time points once contrast equilibrium was reached. Ve was derived accounting for the hematocrit. Ventricular long-axis and short-axis T1 maps  were acquired using a 1.5T scanner (Siemens) before and 1,2,5,8,15,20,25 and 30 minutes after contrast. Myocardial tagging images were acquired using both single- and multiple-breath-hold Complementary Spatial Modulation of Magnetization (CSPAMM) sequences in multiple planes and analysed with inTag® .Subjects with severe AS displayed higher λ and Ve (p=0.02). The λ and Ve correlated with indices of reduced myocardial function including reduced strain (p<0.05) and increased left atrial dilatation (p=0.001). In this presentation, the tips and pitfalls of T1 mapping using MOLLI will be discussed, including detailed discussion of imaging planes, arrhythmia management, breath-hold times, gadolinium administration and artefact reduction.T1-mapping-derived λ and Ve are significantly elevated in patients with AS compared to healthy controls and correlate well with indices of reduced myocardial performance. This difference was quantifiable after a simple bolus administration of gadolinium. T1-mapping λ and Ve derivation after bolus gadolinium administration is clinically practical and holds promise for the detection of IMF in severe AS.This project was supported by the NIHR Royal Brompton Cardiovascular Biomedical Research Unit.


Previous studies using positron emission tomography demonstrated that decrease in global coronary flow reserve (CFR) predisposes to major cardiac events in patients with coronary artery disease. However, the value of MR assessment of CFR has not been clarified for predicting future cardiac events in hypertrophic cardiomyopathy (HCM). The purpose of this study was to evaluate a prognostic significance of CFR measurement in the coronary sinus in patients with HCM.Fifty-three patients with HCM underwent MR flow measurements in the coronary sinus during adenosine stress and in the resting state, cine MRI and late gadolinium enhanced (LGE) MRI between 2005 and 2008. CFR was calculated as the ratio of hyperemic blood flow divided by resting blood flow. After exclusion of 13 patients who had impaired LV systolic function on cine MRI  or congestive heart failure , 40 patients with a mean age of 62.6±10.7 years were followed for a mean duration of 4.8±1.9 years. Unfavorable outcomes were defined as cardiovascular death, unplanned cardiovascular hospital stay, and sustained ventricular arrhythmias requiring the implantation of cardioverter-defibrillator.Thirteen (33%) of 40 patients had unfavorable outcomes . Reduced CFR in response to adenosine was strongly associated with unfavorable outcomes (Figure Reduced CFR assessed by MR flow measurement in the coronary sinus is a strong, independent predictor of unfavorable cardiac outcomes in HCM patients with preserved LV systolic function.Departmental research funding.


We sought to determine the prevalence of echocardiographically determined left ventricular systolic dysfunction in asymptomatic hypertensive subjects seen in Abeokuta, Nigeria.Echocardiography was performed in 832 consecutive hypertensive subjects referred for cardiac evaluation over a three-year period.Data were obtained in 832 subjects (50.1% women) aged 56.0 ± 12.7 years . The prevalence of left ventricular systolic dysfunction (LVSD) was 18.1% in the study population . In a multivariate analysis, male gender, body mass index and LV mass were the predictors of LVSD.Significant numbers of hypertensive subjects in this study had varying degrees of left ventricular systolic dysfunction. Early introduction of disease-modifying drugs in these patients, such as angiotensin converting enzyme inhibitors or angiotensin receptor blockers may retard or prevent the progression to overt heart failure. High blood pressure affects about a billion people worldwide.5Hypertension and its complications are responsible for about 25% of urban hospital medical admissions in Nigeria,8High blood pressure is also by far the commonest cause of chronic renal failure, stroke, heart failure and sudden unexpected death in Nigeria.9In Nigeria, the prevalence of asymptomatic left ventricular systolic dysfunction (LVSD) among people with hypertension is unknown. The aim of the study was therefore to determine the prevalence of asymptomatic LVSD in hypertensive subjects in Abeokuta, Nigeria.2. SHH is one of the oldest hospitals in Nigeria, established in 1897 by the German Catholic Mission.The study was conducted at the Federal Medical Centre (FMC), Idi-Aba and the Sacred Heart Hospital (SHH), Lantoro, both in Abeokuta, the capital city of Ogun State in south-western Nigeria. FMC was established in 1993 by the federal government of Nigeria to cater for the health needs of the people of Ogun State and its environs in south-western Nigeria. The state has a population of about 3.2 million and a surface area of about 16 409.26 kmCardiological services commenced in the city in September 2005 and since then a registry of patients and services rendered has been kept. A cardiologist (OSO) covers the two cardiac units, which are about 5 km apart, assisted by senior medical officers and postgraduate resident doctors and well as nurses. Facilities available for cardiac evaluation include chest radiography, 12-lead electrocardiography (ECG), exercise ECG, Holter ECG, ambulatory blood pressure-monitoring devices, spirometry and echocardiography (ECHO).This was a cross-sectional study, conducted within a three-year period. Hypertensive patients were eligible for the study if they fulfilled the following criteria: (1) no evidence of valvular abnormality. This was based on clinical examination and absence of features of valvular heart disease at echocardiography; (2) absence of congestive heart failure based on previous history of admission for heart failure or symptoms and signs of heart failure in the past or at the time of evaluation, using the Framingham criteria; (3) absence of sickle cell disease based on self-reported haemoglobin electrophoretic pattern of the subject and/or absence of stigmata of the disease; (4) absence of self-reported history of renal failure or serum creatinine ≥ 2 mg/dl; (5) absence of ischaemic heart disease based on history, as well as absence of ischaemic ECG changes at the time of the study (other than left ventricular hypertrophy with strain pattern); (6) other exclusion criteria included morbid obesity, pulmonary heart disease , chest abnormality that obscured echo-window and left bundle branch block pattern on the 12-lead ECG.Using a simple questionnaire, a nurse screened the patients for history or symptoms of these and history of previous hospital admissions relating to the exclusion criteria. All the echocardiography request forms were also assessed for evidence of exclusion criteria. 102. Body surface area (BSA) was calculated using the formula of Dubois.12Baseline clinical and demographic characteristics were obtained from the subjects. These included date of birth, age, gender and history of diabetes. Blood pressure measurements were obtained according to standard guidelines,M-mode, two-dimensional (2-D) and Doppler echocardiography were performed using a standard protocol and an ALOKA SSD 4000 echocardiography machine . Two-dimensional guided M-mode measurements were made according to the recommendations of the American Society of Echocardiography (ASE).13One experienced cardiologist performed all the echocardiography. In our laboratory, the intra-observer concordance correlation coefficient and measurement error have been reported.14Left ventricular systolic performance (LVSP) was assessed using the fractional shortening of the left ventricle and the ejection fraction. Left ventricular ejection fraction (LVEF) was calculated using the Teichholz formula.LVIDd – LVIDsLVID×100Fractional shortening = r = 0.90)p = 0.93) in one study.Left ventricular mass (LVM) was calculated using the formula of Devereux and Reichek.2.7) > 51 g/m2.7.2.7 was used since this was the only criterion that demonstrated as the optimal threshold value for left ventricular hypertrophy in blacks, irrespective of gender, in two previous studies. Left ventricular systolic function was categorised as follows:Left ventricular hypertrophy (LVH) was defined by LV mass indexed by allometric signal  with Scheffe’s post hoc test was used for the comparison of multiple groups. A two-tailed p-value of 0.05 was assumed statistically significant.SPSS version 11.0 software  was used in the analysis of the data. Continuous variables were expressed as mean ± SD, while categorical variables were expressed as counts (percentages). Comparison between the two groups was assessed with the Student’s A total of 832 subjects, 415 men (49.9%) and 417 women (50.1%) were eligible for analysis. Fig. 1 shows the criteria for selection of subjects for analysis.The overall mean age of the population was 56.0 ± 12.7 years (range 15–88). Normal LVSF, defined as ejection fraction (EF) ≥ 50% was present in 89.9% of the subjects. The remaining 18.1% had LVSD . p < 0.0001). Compared with individuals with normal LVSF or mild LVSD, those with severe LVSD were older, more likely to be men, had larger left atrial diameter, larger LV dimensions and LV mass, and as expected, lower fractional shortening and ejection fraction. This finding was consistent in both genders and progressed from normal LVSF to severe LVSD  and this was statistically significant . LVEF was used as the dependent variable, while independent variables were taken from clinical variables  and echocardiographic variables  that were significant in the univariate analysis.Although LV dimensions were significantly related to LVEF in the univariate analysis, they were not added in the final model since these parameters were used in the determination of LVM. Categorical variables such as gender and presence or absence of diabetes mellitus were entered as indicator variables. None of the blood pressure variables were significant in the univariate analysis.p = 0.036]; gender ; BMI ; left atrial diameter ; end-diastolic diameter , end-systolic diameter ; LVM ; and RWT .In the univariate analysis, EF was related to age [B (unstandardised regression coefficients) = –0.84, β (standardised regression coefficient) = –0.72, In a multivariate analysis, lower LVEF was independently related to BMI, gender, LV mass, left atrial diameter and relative wall thickness.Hypertension is the commonest cardiovascular disease in Nigeria and sub-Saharan Africa. It is the commonest risk factor for heart failure, stroke and chronic renal impairment. In Nigeria and most African countries, the majority of patients first present with evidence of target-organ damage such as overt heart failure. Most often, overt heart failure is preceded by asymptomatic left ventricular systolic dysfunction. Information on the prevalence and burden of both symptomatic and asymptomatic LVSD is based on population studies as well as studies done in hypertensive subjects in Europe and America.23The burden of LVSD (symptomatic or asymptomatic) in hypertensive subjects is largely unknown in Nigeria and in most African countries, hence the reason for the present study. Echocardiographic methods have been shown to provide a high yield of quantitative measurement of LV function and can be used to assess the determinants of LV function, both in hypertensive and general populations.The main findings of the study are: the majority of our hypertensive patients fell within the middle-aged group with a peak age of 50 years, about 18% of our hypertensive subjects had asymptomatic LVSD, the prevalence of LVSD was higher in men than in women, LVSD increased with age, although LVSD was independent of age, and the main predictors of LVSD were male gender, body mass index, left ventricular mass and LV relative wall thickness.All over sub-Saharan Africa, the peak age of presentation of cardiovascular diseases such as hypertension has been well defined.In a univariate analysis, age was related to LVEF. However, when other factors such as gender, LV mass, relative wall thickness and BMI were factored in, the association with age became insignificant. The plausible reason for this is that the impact of age on LVSF is probably mediated through other factors. Our finding is similar to the report of other workers.28The study shows that the prevalence of impaired LVSF is about twice as common in men as in women. In a multivariate analysis, male gender was found to be an independent predictor of impaired LVSF. This is similar to the findings of authors in studies done in hypertensive subjects or in the general population.Tables 1 and 2 show that diastolic blood pressure and mean arterial blood pressure were higher in the group with severe LVSD compared to other groups. No significant difference was found in the systolic blood pressure and pulse pressure among the groups.et al.,In univariate and multivariate analyses, blood pressure was not found to be related to LVSF. This finding is similar to that of Devereux et al.In this study, BMI was found to decrease from subjects with normal LVSF to those with severe LVSD . The impact of BMI persisted in the multivariate analysis. This relationship between LVSF and BMI was also reported by Devereux In a univariate analysis, we did not find any relationship between LVSD and the presence of diabetes in this study. This is at variance with the report by some workers.The left atrial size was found to be independently related to LVSF. The larger the left atrium, the poorer the LVSF. Similar findings have been reported by other investigators.34We noted the following limitations with this study. It was a hospital-based study and may not reflect the situation in the general population. We did not run metabolic profile functions  in the present study, as was done in studies in industrialised nations, due to lack of funds.Newer measures of assessment of LVSF such as LV mid-wall shortening, circumferential end-systolic measurements as well as measures of arterial wall stiffening (pulse pressure/stroke index) were not assessed in our study. Absence of ischaemic heart disease was only assessed based on clinical history and 12-lead ECG. This may not exclude sub-clinical ischaemic heart disease.LVSD, assessed as ejection fraction < 50%, was detected in 18.1% of our hypertensive population, who did not have symptoms of overt heart failure. Male gender, body mass index, LVM and relative wall thickness were found as independent predictors of LVSF in our study.Significant numbers of hypertensive subjects in this study had varying degrees of left ventricular systolic dysfunction. Early introduction of disease-modifying drugs in these patients, such as angiotensin converting enzyme inhibitors/angiotensin receptor blockers may retard or prevent the progression to overt heart failure.It must be stated that since echocardiography is expensive, it cannot be placed as the first line of systematic screening of hypertensive patients, however, the predictive factors of LVSD are accessible to primary-care physicians. For instance, the combination of male gender and obesity should draw the attention of clinicians to the possible presence of LVSD, a pathogenic precursor of heart failure.


This study sought to demonstrate the potential for myocardial arterial spin labeling (ASL) to identify the ischemic myocardial segments due to stenosis in coronary arteries as detected by X-ray angiography.stress/MBFrest), which is a common indicator for the severity of coronary artery disease. In healthy myocardium, perfusion reserve is known to be approximately four [Myocardial ASL is a technique for the assessment of myocardial blood flow (MBF) without contrast agents. It can be safely applied to patients with end-stage renal disease who are not candidates for first-pass imaging with contrast agents. Myocardial ASL perfusion imaging performed at rest and during adenosine stress provides perfusion reserve (MBFely four .Twenty nine patients were recruited from those scheduled for routine cardiac MR (CMR) and X-ray angiography. Myocardial ASL measurements were obtained from a single mid short-axis slice at rest and during adenosine infusion (dosage: 0.14 mg/kg/min) on a GE Signa 3T scanner. The ASL sequence was composed of flow-sensitive alternating inversion recovery (FAIR) tagging and balanced steady-state free precession (SSFP) imaging . PerfusiTen of the twenty-nine patients were found to have significant stenosis on X-ray angiography. Table There was visual agreement  and no statistically significant difference between ischemic myocardial segments identified by ASL perfusion reserve maps and by X-ray angiograms. This suggests that myocardial ASL with vasodilation may have a potential to identify ischemic myocardial segments in patients with stenosis.


Cardiac structure and function are well-studied in Western countries. However, epidemiological data is still scarce in China.Our study was conducted in the framework of cardiovascular health examinations for the current and retired employees of a factory and their family members. According to the American Society of Echocardiography recommendations, we performed echocardiography to evaluate cardiac structure and function, including left atrial volume, left ventricular hypertrophy and diastolic dysfunction.P ≤ 0.002) increased with age, except for the moderate-to-severe left ventricular diastolic dysfunction. After adjustment for age, gender, body height and body weight, left atrial enlargement was associated with plasma glucose (P = 0.009), and left ventricular hypertrophy and diastolic dysfunction were significantly associated with systolic and diastolic blood pressure (P ≤ 0.03), respectively.The 843 participants (43.0 years) included 288 (34.2%) women, and 191 (22.7%) hypertensive patients, of whom 82 (42.9%) took antihypertensive drugs. The prevalence of left atrial enlargement, left ventricular hypertrophy and concentric remodeling was 2.4%, 5.0% and 12.7%, respectively. The prevalence of mild and moderate-to-severe left ventricular diastolic dysfunction was 14.2% and 3.3%, respectively. The prevalence of these cardiac abnormalities significantly (The prevalence of cardiac structural and functional abnormalities increased with age in this Chinese population. Current drinking and plasma glucose had an impact on left atrial enlargement, whereas systolic and diastolic blood pressures were major correlates for left ventricular hypertrophy and diastolic dysfunction, respectively. Cardiac structure and function are well-studied in Western populations, such as the Framingham Heart Study,2, the RSeveral clinical studies reported prevalence and correlates of left ventricular hypertrophy in Chinese hypertensive patients,10. HoweThe present study was conducted in the year 2006 in the framework of comprehensive cardiovascular health examinations for all employees (including those retired but still lived in the area of the factory at the time of the study) of a factory located in an isolated coast area, 300 kilometers south of Shanghai. The famOf the 1052 study subjects (participation rate 80.7%), 877 participated in the echocardiographic study. We excluded 34 subjects from the present analysis, because they had poor quality of echocardiogram (n = 9), moderate or severe valvular regurgitation or stenosis (n = 20), congenital heart disease (n = 3), atrial fibrillation (n = 1) or hypertrophic cardiomyopathy (n = 1). Thus, the number of participants included in the present analysis was 843.One experienced physician measured each participant’s blood pressure five times consecutively by conventional sphygmomanometry, after at least 5 minutes rest in the sitting position. These five blood pressure readings were averaged for analyses. The same observer also administered a standardized questionnaire to collect information on medical history, smoking habits, alcohol consumption and the use of medications. Current smoking and drinking were defined as at least smoking one cigarette per day or drinking once per week in the past year, respectively. Daily alcohol consumption was calculated according to the consumption of various types of alcoholic beverages during the past month. In the study area, beer was sold in a bottle of 750 mL, whereas yellow aperitif, rice aperitif and hard liquor were traded in a unit of 500 grams. We estimated that one bottle of beer and a unit of aperitif and liquor contained on average 30, 90 and 200 g of ethanol, respectively. From the type and quantity of the alcoholic beverages used, we computed daily alcohol consumption in grams per day. Drinking subjects were further categorized into tertiles of daily alcohol consumption, with mild, moderate and heavy drinking defined as daily alcohol consumption <18 g/d, 18 to 36 g/d, and > 36 g/d, respectively. Hypertension was defined as a blood pressure of at least 140 mmHg systolic or 90 mmHg diastolic, or the use of antihypertensive drugs. One trained technician measured body height and body weight. Body mass index was calculated as body weight in kg divided by the square of body height in meters. Venous blood samples were taken after overnight fasting for measurements of plasma glucose concentration and concentrations of total, high-density lipoprotein (HDL), and low-density lipoprotein (LDL) cholesterol and triglycerides.One echocardiographer performed all echocardiographic measurements using the portable Mylab 30 CV machine  according to the American Society of Echocardiography (ASE) recommendations. Two-dimensional and color Doppler images were first recorded, and then analyzed offline. Moderate or severe valvular regurgitation or stenosis was diagnosed as valvular heart disease using color Doppler imaging.2 according to ASE recommendations took antihypertensive drugs), 87 (10.4%) patients with hyperlipidemia, 17 (2.0%) patients with diabetes mellitus, and 2 (0.3%) patients with a LVEF less than 50%. TableP < 0.001) and plasma glucose (P = 0.008), LVM with systolic blood pressure (P < 0.001), and E/A ratio with diastolic blood pressure (P < 0.001) and the total-to-HDL cholesterol ratio . Indeed, the prevalence of left ventricular concentric remodeling increased from 8.3% in subjects younger than 40 years (n = 421) to 20.9% in subjects of at least 60 years (n = 134). The corresponding values were from 1.9% to 13.4% for left ventricular hypertrophy, and from 1.5% to 46.6% for left ventricular diastolic dysfunction .In addition to age, male gender, body height and body weight, left atrial enlargement was significantly associated with plasma glucose , left ventricular hypertrophy with systolic blood pressure , and left ventricular diastolic dysfunction with diastolic blood pressure , and remained at low level (1.3%) in subjects with a plasma glucose concentration below 4.70 mmol/L (quartiles 1 to 3) and increased to 7.3% in subjects with plasma glucose concentration above 4.70 mmol/L  and in men for diastolic dysfunction  and left ventricular hypertrophy and diastolic dysfunction in men and women, separately, in relation to their correlates identified from above-mentioned analysis as categorical variables. The prevalence of left atrial enlargement in men increased from 1.29% in non-drinkers n = 309), to 2.25% in mild drinkers (n = 89), to 5.56% in moderate drinkers (n = 54), and to 10.2% in heavy drinkers .It is unexpected to find a significant association of left atrial volume and enlargement with plasma glucose in the present study. In literature, Milutinović S et al. have reported that hypertensive patients with diabetes, compared to those without, had significantly higher left atrial volume. We foun2 (men) or >110 g/m2 (women) in the present study, our major finding remained unaltered. Specifically, the prevalence of left ventricular hypertrophy would be 1.7% (n = 14), and its influential factors would include only systolic blood pressure . Secondly, diastolic dysfunction was solely evaluated by Pulse-wave Doppler Imaging, but not Tissue Doppler Imaging in the present study. This technological limitation might, to some extent, influence the accuracy in the classification of diastolic dysfunction. However, this conventional diagnostic technique has been used in most of pervious population studies, and is more applicable in the screening for asymptomatic disease. Lastly, since the present population was recruited in a factory located in southeast China, our finding probably cannot be extrapolated to the entire Chinese population.One of the major limitations in the present study is its small sample size, especially in women. In addition, since the present study was conducted in a relatively young and healthy Chinese population, we applied a “low” criterion to define left ventricular hypertrophy, which was also recommended by ASE. If we applied the criterion of LVMI >125 g/mIn conclusion, even in a middle-aged and relatively healthy Chinese population, cardiac structural and functional abnormalities, mostly asymptomatic, were prevalent, and had higher prevalence with age advancing and in the presence of several known cardiovascular risk factors, such as heavy drinking of alcohol, hyperglycemia, and high blood pressure. The clinical implications of our finding is that echocardiography probably should be performed for screening subclinical cardiac structural and functional abnormalities, especially in the elderly or in the presence of common cardiovascular risk factors.HDL: High-density lipoprotein; LDL: Low-density lipoprotein; ASE: American Society of Echocardiography; LVM: Left ventricular mass; LVMI: Left ventricular mass index; RWT: Relative wall thickness; E/A ratio: Ratio of early transmitral diastolic peak flow (E) and atrial peak flow (A); DTE: Deceleration time of early transmitral diastolic flow; LVEF: Left ventricular ejection fraction; OR: Odds ratio; CI: Confidential interval.The authors declare that they have no competing interests.YZ has made substantial contributions to the conception and design of the paper and the analysis and interpretation of data, and been involved in drafting the manuscript. YL, ML, CSS and QFH have participated in patient evaluations, data collection, and the analysis of data. JGW has made substantial contributions to the conception and design of the paper, and been involved in revising the manuscript. All the authors have read and approved the final version of the manuscript.The pre-publication history for this paper can be accessed here:http://www.biomedcentral.com/1471-2261/12/86/prepub


In the current study, we prospectively compared the diagnostic value of SW-CG-HYPR and conventional SR-Turbo-FLASH for myocardial perfusion MRI in patients with suspected CAD. Compared with conventional SR-Turbo-FLASH, SW-CG-HYPR allows increased spatial coverage (whole left ventricular coverage), improved temporal and spatial resolution and SNR, reduced motion artifacts and has higher diagnostic accuracy in patients with suspected CAD.A sliding-window (SW) conjugate-gradient (CG) highly constrained back-projection reconstruction (HYPR) (SW-CG-HYPR) technique has been developed for time-resolved myocardial perfusion imaging. Using this method, the acquisition time per cardiac cycle can be reduced dramatically while maintaining the temporal resolution of one frame per heartbeat in myocardial perfusion MRI, allowing increased spatial coverage (whole left ventricular coverage), improved temporal and spatial resolution and SNR, and reduced motion artifacts compared with the conventional SR-Turbo-FLASH sequence. However, the diagnostic accuracy of myocardial perfusion MRI with SW-CG-HYPR for detecting coronary artery disease (CAD) has not been directly compared to that with conventional SR-Turbo-FLASH. The purpose of this study was to prospectively compare the diagnostic value of SW-CG-HYPR and conventional SR-Turbo-FLASH for myocardial perfusion MRI in patients with suspected CAD.Thirty consecutive patients  with suspected CAD who were scheduled for coronary angiography underwent myocardial perfusion MRI with both SW-CG-HYPR and SR-Turbo-FLASH at 3.0T. Perfusion defects were interpreted visually by 2 blinded observers and were correlated to x-ray angiographic stenoses ≥ 50%. Receiver-operating characteristic (ROC) curve analysis was used to compare the diagnostic performance of the two imaging techniques.The prevalence of CAD was 60%. Compared with SR-Turbo-FLASH, SW-CG-HYPR produced better left ventricular (LV) coverage (whole LV vs. only 3 slices). In the per-patient analysis, SW-CG-HYPR provided a higher sensitivity (94% vs. 89%), specificity (83% vs. 75%) and diagnostic accuracy (90% vs. 83%) for the detection of CAD than SR-Turbo-FLASH. In the per-vessel analysis, the diagnostic performance of SW-CG-HYPR was significantly greater than that of SR-Turbo-FLASH for the overall detection of CAD .High-resolution, whole left ventricle myocardial perfusion MRI with SW-CG-HYPR allows higher diagnostic accuracy than conventional SR-Turbo-FLASH in patients with suspected CAD.This work was supported by National Institute of Health (NIBIB EB002623) and National Natural Science Foundation of China (30828009).


Pulmonary arterial hypertension (PAH) is a devastating disease with significant morbidity and mortality. At the macroscopic level, disease progression is observed as a complex interplay between mean pulmonary artery pressure, pulmonary vascular resistance, pulmonary vascular stiffness, arterial size, and flow. Wall shear stress (WSS) is known to mediate or be dependent on a number of these factors. Given that WSS is known to promote architectural vessel remodeling, it is imperative that the changes of this factor be quantified in the presence of PAH.In this study, we analyzed phase contrast imaging of the right pulmonary artery derived from cardiovascular magnetic resonance to quantify the local, temporal and circumferentially averaged WSS of a PAH population and a pediatric control population. In addition, information about flow and relative area change were derived.2, P = 0.018) and systolic WSS  was significantly depressed in the PAH population as compared to the controls. BSA-indexed PA diameter was significantly larger in the PAH population .Although the normotensive and PAH shear waveform exhibited a WSS profile which is uniform in magnitude and direction along the vessel circumference at systole, time-averaged WSS (2.2 ± 1.6 vs. 6.6 ± 3.4 dynes/cmIn the presence of preserved flow rates through a large PAH pulmonary artery, WSS is significantly decreased. This may have implications for proximal pulmonary artery remodeling and cellular function in the progression of PAH. Pulmonary arterial hypertension (PAH) is a devastating disease with significant morbidity and mortality . ClassifResearch efforts are complicated by the multifactorial nature of the disease -14, invoA key link in these events is the quantification of how wall shear stress (WSS) - the primary mechanical force affecting cell mechanotransduction - changes in disease conditions . The WSSn = 5). For the normotensive group, we included patients who were referred for syncope with normal CMR, vascular rings, and mild left-sided cardiac anomalies that include non-stenotic bicuspid aortic valve and uncomplicated coarctation repair. Demographic data for control versus PAH subjects are shown in Table With the approval of the Institutional Review Board at the Children’s Hospital Colorado, all available CMR studies on patients with PAH at our institution were retrospectively analyzed. Patients with prior history of pulmonary artery surgery, right ventricular surgery, pulmonary arterial stenosis, pulmonary valve insufficiency, and chronic thrombolic pulmonary hypertension were excluded. In cases in which multiple studies were performed on a single patient, we chose to analyze the study with the best delineation of the RPA lumen and a high signal-to-noise ratio phase contrast data. Patients with a poor slice position through the RPA, sternal wire susceptibility artifacts, or poorly defined artery lumen boundaries were excluded (A fast low-angle shot gradient echo sequence was used to obtain retrospectively gated tissue intensity and phase velocity maps encoded in the through-plane direction (1.5 T Siemens Magnetom Avanto). Double oblique imaging slices were positioned between the proximal and the first branch of the RPA, orthogonal to the vessel long axis. A typical sequence used temporal resolution of 14–28 ms, echo times of 2.2-3.5 ms, and a flip angle of 25˚. Depending on patient size and field of view, the cross sectional pixel resolution was 0.82 × 0.82 to 1.56 × 1.56 mm with slice thicknesses of 5 mm. Velocity encoding values were adjusted according to the maximum velocities encountered during scout sequences to optimize the velocity map resolution .Vmax), and the temporal and spatial WSS fields [max-Amin)/Amin], where Amax and Amin represent the maximum and minimum measured cross-sectional areas.The RPAs were carefully segmented Figure  over theS fields ,24. PulmS fields . The relQavg), flow rate at systole (Qsys), and regurgitant fraction (RF) were calculated according to convention. To facilitate the calculation of the shear fields and remove RPA bulk motion, the images were cropped to the RPA size and transformed from Cartesian to polar coordinates using oversampling  and bicubic interpolation to retain image integrity at the region of interest (ROI) edges. As previously described, a linearized axial shear stress approximation was used to obtain the axial RPA shear field over all time-steps   . These rThe results from our study are in concordance with previous efforts. Pelc et al. initially noted that main pulmonary artery flow at peak systole in PAH patients was more spatially heterogeneous and demonstrated a greater percentage of retrograde flow . Buildin2. There was no statistical difference between the vessels for circumferential or radial WSS. Our study extends these previous investigations to determine the axial WSS forces in pediatric PAH patients. Table WSSt_avg and WSSsystole were all found to differ significantly. The difference in the calculated WSS values between these two patient groups appears to be associated with artery dilation, as seen in the artery morphology comparison of matched patients in Figure 2/m2 and 2.7 cm2/m2, respectively. We postulate that as a result of this arterial size difference in the normotensive patient, and thus a change in spatial velocity gradients, the peak WSS magnitude is more than 4.5 times than that of the PAH patient.In addition, Morgan et al. has looked at the WSS forces in healthy pulmonary arteries . As mentGan used area distensibility and relative area change to predict mortality in PAH . BesidesA number of concomitant factors contribute to changes in the pulmonary arterial pressure of PAH patients, including increased PVR, increased blood flow due to shunting, and alterations in pulmonary vascular stiffness. The influence of pathologic pulmonary pressures, PVR, and pulmonary vascular stiffness on proximal morphologic and hemodynamic factors may include pulmonary arterial dilatation, flow waveform alterations, and WSS alterations . Since WLimitations to the study include those inherent to a retrospective study. We recognize that our CMR control population is small as this number is severely restricted by availability of RPA PC-CMR sequences in children without right heart disease. To address this, we included echocardiography results from healthy controls with no known heart disease, which shows significant differences in pulmonary arterial vasculature compared to pediatric PAH population. For the PC-CMR sequences, we included children with mild left-sided heart disease with no evidence of abnormal pulmonary artery pressure. However, we recognize the potential for mild pulmonary arterial flow abnormality caused by upstream anatomic anomalies. Efforts to enroll healthy children with no cardiac structural disease are ongoing.We have demonstrated the use of PC-CMR to quantify hemodynamic WSS in PAH patients. Pulmonary artery dilation occurs at a significantly faster rate in PAH patients, while systolic flow does not vary between populations. Thus, the consequence of maintaining similar net flow through a larger artery is a WSS decrease in PAH patients. This may have implications for proximal pulmonary artery remodeling and cellular function.CMR: Cardiovascular magnetic resonance; PAH: Pulmonary arterial hypertension; PC: Phase-contrast; PVR: Pulmonary vascular resistance; RPA: Right pulmonary artery; RV: Right ventricle; WSS: Wall shear stress.The authors declare that they have no competing interests.UT- writing manuscript, study design, subject scanning, data selection. BF- Study design, subject recruitment, subject scanning. JD- data selection, statistical analysis. SB- statistical analysis. CL-design of analysis program. DI-study design. RS-study design. KH- Study design, statistical analysis, editing and writing manuscript. AB- study design, data analysis, editing and writing manuscript. All authors read and approved the final manuscript.Uyen Truong and Brian Fonseca are co-first authors.Kendall Hunter and Alex J Barker are co-senior authors.


It is objective to show the feasibility of volumetric velocity-encoded MRI (3D-TPM) to derive velocity based motion quantification parameters.About 30% of patients treated with cardiac resynchronization therapy (CRT) do not benefit from the procedure. The introduction of quantitative parameters for selection of patients appears mandatory. However, parameters based on 2D imaging techniques may be less reproducible caused by rapid changes of the motion pattern along the cardiac axis.2mm2, isotropic resolution of 3x3x3mm3, FOV in through-plane direction =63mm in healthy volunteers (this FOV was increased in patients due to their enlarged heart corresponding to the distance between basis and apex), acquisition matrix =128x124, TR/TE=7.1ms/4.9ms, flip angle =15°, SENSE =4, nominal scan duration =15:30 minutes, 3 k-lines per segment, phase interval =37.3ms and 25 cardiac phases for 60bpm. The acquisition of the whole heart data was split into 3 chunks to ensure sufficient black blood contrast.12 volunteers (26±7 years) and 2 patients  were investigated at a 3T whole body MR scanner  with a 32 channel cardiac coil. A 3D black blood velocity encoded navigated segmented gradient echo sequence (3D-TPM) was applied for whole heart coverage. The acquisition parameters were: FOV=380l,sys), SD, SD, SD[l = vl,max-vl,min, Δvr = vr,max-vr,min and the new parameter temporal uniformity of velocity (TUV) in radial, longitudinal and circumferential direction, which was defined analogously to the temporal uniformity of strain defined in [From the 3D-TPM data, the following parameters were evaluated: longitudinal and radial standard deviation of time to peak systolic and diastolic velocities SD, the meaTPr,dias), the lonfined in .sys,r) is increased in case of asynchrony.Figure It is feasible to determine motion quantification parameters based on 3D velocity data. Huge differences could be observed between asynchronous patients and volunteers. A study including more patients is necessary to decide whether 3D -TPM data may in future distinguish between responders and non-responders to CRT.AL and VR have a research agreement with Philips Healthcare. PE is employed by Philips Healthcare.


Left ventricular non-compaction (LVNC) is a recently recognized rare disorder. Magnetic resonance imaging (MRI) may help to clarify the uncertainties related to this genetic cardiomyopathy. Despite the fact that many articles have been published concerning the use of MRI in the study of LVNC, there is a lack of data describing the disease in the North African population. The aim of our study is to clarify MRI findings of LVNC in North African patients.In our retrospective cohort, twelve patients  underwent MRI for suspected LVNC. Correlations were investigated between the number of non-compacted segments per patient and left ventricular ejection fraction (LVEF), then between the number of non-compacted segments and left ventricular end diastolic diameter. The presence or absence of late gadolinium enhancement (LGE) was qualitatively determined for each left ventricular myocardial segment.Non-compaction was more commonly observed at the apex, the anterior and the lateral walls, especially on their apical and mid-cavity segments. 83% of patients had impaired LVEF. There was no correlation between the number of non-compacted segments per patient and LVEF , nor between the number of non-compacted segments per patient and left ventricular end diastolic diameter . LGE was observed in 22 left ventricular segments. No association was found between the pattern of fibrosis and non-compaction distribution .The distribution of LVNC in North African patients does not differ from other populations. Ventricular dysfunction is independent from the number of non-compacted segments. Myocardial fibrosis is not limited to non-compacted areas but can extend to compacted segments. Left ventricular non-compaction (LVNC) is a rare form of cardiomyopathy characterized by excessive and prominent trabeculations associated with deep recesses that communicate with the ventricular cavity ,2. SinceMagnetic resonance imaging (MRI) is a non-invasive exploration increasingly being employed in the diagnosis of LVNC. Due to its high quality cardiac imaging, this examination method may help to characterize and understand this disease. Thus, several MRI studies have been published describing LVNC features -14, yet We retrospectively reviewed morphological cine magnetic resonance imaging findings of ventricular non-compaction in twelve patients between 2007 and 2010. Those patients had been referred for MRI examination in order to investigate suspected LVNC or dilated cardiomyopathy. Information regarding presenting symptoms and echocardiographic data were obtained from referring centers. Patients with associated coronary artery disease were ruled out of the study.MRI was performed using a 1.5-Tesla magnetic resonance scanner . An eight-element cardiac phased-array receiver surface coil, with breath- holding in expiration and electrocardiogram (ECG) gating, was used for signal reception. The MRI sequences were conducted as follows: echo planar cine true-fisp imaging; dark-blood turbo spin echo T1-weighted; dark-blood turbo spin echo T2-weighted; and dark-blood half-Fourier single shot turbo spin echo. Images were obtained in two-chamber, four-chamber, and short-axis (from the atrioventricular ring to the apex) planes. After baseline imaging, a bolus injection of gadolinium was administered. Ten minutes later, delayed enhancement MRI was performed using an inversion recovery-prepared gated fast gradient-echo pulse sequence. The late gadolinium enhancement (LGE) images were acquired in end-systole in the same views used for cine images.All examinations were transferred to a dedicated workstation. Cine images were analyzed using Argus post-processing software . The cine loops were reviewed and the end-diastolic and end-systolic frames were identified.Assessment of LVNC was performed on short and long axis slices. All left ventricular (LV) myocardial segments were visually screened for the presence of a two-layer structure, with a thin epicardial compacted layer and a thick non-compacted endocardial one, with excessive trabeculations and deep intertrabecular recesses that communicate with the ventricular cavity. The ratio of non-compacted to compacted (NC/C) myocardium was measured for each involved myocardial segment in diastole, on short axis slices. For each patient, we considered the minimal NC/C ratio for subsequent analysis. Non-compaction was defined as a ratio of NC/C myocardium > 2.3 at end-diastole . The disLV diameters, volumes and ejection fraction (EF) were measured using standard volumetric techniques with dedicated software . Left veFor each patient, correlations were investigated between the number of non-compacted segments and EF, then between the number of non-compacted segments and LV end diastolic diameter.The presence of late gadolinium enhancement (LGE), a surrogate of myocardial fibrosis, was qualitatively determined for each LV myocardial segment using the seventeen-segment cardiac model. All short and long axis contrasted-enhanced images were reviewed, with a particular focus on images with elevated signal intensity. Patterns of LGE were visually classified as sub-endocardial, sub-epicardial, mid-myocardial, or transmural .The data was assembled using the computer software "EXCEL" (Microsoft). All analyses were performed with SPSS (version 18.0), in collaboration with the Faculty of Medicine's Biostatistics Department at the University of Rabat. Continuous variables are expressed as the mean and the standard deviation, and nominal variables as numbers and percentages. Univariate and multivariate analyses were made with the binary logistic regression model. Pearson correlation analyses were used for univariate correlations. A two-tailed p value of < 0.05 was considered statistically significant.Because this study was done retrospectively, no ethics committee approval was required.A total of twelve n = 12) cases of LVNC were included in our study. The mean age was 53 ± 8 years. Seven (58%) patients were male; two 2 (17%) were of sub-Saharan descent. Most patients (92%) were symptomatic. Six patients presented with dyspnea and four with palpitations. One patient had both dyspnea and chest pain. In seven patients, LVNC had been previously suspected on echocardiography. Four cases had been labeled as dilated cardiomyopathy. One case has the diagnosis of LVNC been made by echocardiography.  patients had impaired LVEF (LVEF < 50%). Among the segments analyzed in our study, 120 (59%) were identified as non-compacted segments. The mean number of non-compacted segments per patient was 10 ± 2.7 and the mean NC/C ratio was 2.8 ± 0.5. , nor between the number of non-compacted segments per patient and LV end diastolic diameter  Figures .significant discrepancy between non-compacted and compacted segments concerning fibrosis involvement  [Figure A total of four (33%) patients showed LGE. LGE was mid-myocardial in two cases and sub-endocardial in the remaining patients Figure . OverallThe non-compaction of the LV myocardium is a congenital heart disease caused by an arrest of normal ventricular embryogenesis, which causes an excessive number of endomyocardial trabeculae, spaced out by deep recesses ,18. ReceOur study is one of the first series assessing MRI features of LVNC in the North African population. In only one instance was the diagnosis of LVNC confirmed by transthoracic echocardiography. In the others, the diagnosis has been given by MRI. Our findings are in agreement with prior research which asserts that even though LVNC diagnosis remains difficult , the useThe findings of our study are in agreement with those of previous reports: non-compacted segments are most commonly located at the apex and the lateral wall; the septal segments are rarely affected by LVNC ,25. It iIn our study, we tried to investigate the relationship between the extent of LVNC and LV impairment. Although 83% of patients had impaired LVEF, our analysis of the study group found no correlation between the number of non-compacted segments and LVEF. Previous reports have studied the contribution of non-compacted segments to LV dysfunction. Aras et al found that the number of LV segments affected by non-compaction is a major determinant of LV systolic dysfunction . LofiegoA distinct advantage of MRI is its capability of myocardial tissue characterization and its ability to demonstrate myocardial fibrosis with enhanced delayed imaging. Fibrosis is commonly found in association with LVNC, the diagnosis of which is unattainable with other non-invasive imaging modalities -7. In ouIn our patients, myocardial fibrosis was detected in not only involved segments but also morphologically normal ones, with a similar prevalence in both non-compacted and compacted zones. This result supports the hypothesis that non-compaction may be a diffuse disease process involving both non-compacted and compacted area ,30. The The major limitations of our study are its retrospective design and its small sample size, which can be explained by the high cost of MRI. Moreover, patients included in the study were referred for MRI from other centers. Thus, there was a selection bias in this population representing a group of mainly symptomatic patients, so the true severity of the disease was probably overestimated. In addition, pediatric cases were not included. Furthermore, we did not undertake family screening, nor were clinical data and follow up information available. Finally, we were unable to compare echocardiographic and MRI findings because echocardiographic examinations were not performed in the same institution.LVNC is an enigmatic cardiomyopathy that is still not widely known. Our study supports the hypothesis that LVNC diagnosis is not always clear and that MRI, with its high spatial resolution, seems to be able to improve the detection of this condition. Although our data refers to a small population, it suggests that the distribution of LVNC in North African patients does not differ from other populations. In addition, the extent of non-compaction appears to be unrelated to LV systolic dysfunction in this population. Furthermore, our findings indicate that myocardial scarring, which can be identified non-invasively by MRI, is not limited to the non-compacted myocardium, but can extend to morphologically normal areas. Finally, further studies of larger populations, including long-term follow up, are still needed in order to better clarify different facets of this cardiomyopathy. Accordingly, we propose the creation of a LVNC registry for North Africa.C: Compacted; CMR: Cardiac magnetic resonance; F: Female gender; LGE: Late gadolinium enhancement; LV: Left ventricular; LVD: Left ventricular end diastolic diameter; LVEF: Left ventricular ejection fraction; LVNC: Left ventricular non-compaction; LVSD: Left ventricular systolic dysfunction; M: Male gender; MRI: Magnetic resonance imaging; NC: Non compacted; TTE: Transthoracic echocardiography.The authors declare that they have no competing interests.The contributions of each author to this manuscript are as follows: AL and ND were involved in the design of the study, in cardiovascular magnetic resonance imaging and analyzing images, in acquisition, analysis and interpretation of the data, and in drafting of the manuscript. YE and OT were involved in cardiovascular magnetic resonance imaging. AB, LH, JZ, RC, IF, AA and IA were involved in echocardiography's examination of the patients. FE and AE were involved in analysis and interpretation of the data. MC was involved in the design of the study and in revising the manuscript. All authors have read and approved the final manuscript.