Coronary perfusion pressure is a combination of proximal perfusion pressure and distal coronary artery pressure resulting from contraction and relaxation of the myocardium and the consequences on the microcirculation. Wave intensity analysis (WIA) defines dominant waves causing coronary filling during the cardiac cycle and allows separation of proximally and distally originating waves.Reduced myocardial perfusion has been shown to predict mortality in hypertrophic cardiomyopathy (HCM), however no study has assessed the relationship between coronary filling patterns and downstream absolute myocardial perfusion.To obtain data for WIA, simultaneous pressure and coronary flow velocity in the proximal coronary arteries was obtained in 20 patients with HCM at rest and with adenosine. Patients then underwent cardiovascular magnetic resonance (CMR) perfusion imaging at rest and with adenosine. Myocardial blood flow (MBF) was quantified from CMR perfusion images using a pixel-wise model-constrained deconvolution algorithm.All patients completed the study successfully. No patients had significant epicardial coronary artery disease. On WIA, distally originating waves predominated compared to proximally occurring waves. The backward expansion wave, which occurs due to myocardial relaxation, correlated with MBFat rest . On CMR, myocardial perfusion reserve was reduced (mean 1.52±0.42) withan endocardial to epicardial ratio that worsened with adenosine .Patients with HCM had predominantly distal waves governing coronary filling, emphasisingthe importance of the microcirculation in this disease. There was an increased backward compression wave during systole in keeping with compression of the microcirculation with a relative reduction in the size of the backward expansion wave. CMR demonstrated the downstream effects of these abnormalities, with reduced myocardial perfusion and an abnormal endocardial to epicardial ratio. Patients with a smaller backward expansion wave had a lower MBF, suggesting that impaired myocardial relaxation results in poorer myocardial perfusion.This work was funded by the British Heart Foundation and the NIHR Cardiovascular BRU.


In addition, the diagnostic accuracy of the proposed method was further confirmed by the coronary angiography. The results of this study provide a new way to promote the development of the 3D visualization of the standard 12-lead ECG, which has a great help for inexperienced doctors or ordinary family members in their diagnosis of patients with myocardial ischemia.A novel method was proposed for transforming the ischemic information in the 12-lead electrocardiogram (ECG) into the pseudo-color pattern displayed on a 3D heart model based on the projection of a ST injury vector in this study. The projection of the ST injury vector at a point on the heart surface was used for identifying the presence of myocardial ischemia by the difference between the projection value and the detection threshold. Supposing that myocardial ischemia was uniform and continuous, the location and range of myocardial ischemia could be accurately calculated and visually displayed in a color-encoding way. The diagnoses of the same patient were highly consistent (kappa coefficient  It is an important prerequisite for patients with myocardial ischemia to get timely and effective treatment that their information of myocardial ischemia can be obtained accurately and reliably –4. The 1The visualization methods of the 12-lead ECG can be divided into two kinds, two-dimensional methods and three-dimensional methods. The ST compass is a method of two-dimensional display , 11, whiIn order to realize the visualization of the 12-lead ECG, we developed a novel method for displaying information relating to myocardial ischemia on a 3D heart model created by scanning a physical model of the heart. The central point of the region under ischemia is accurately located by the orientation of ST injury vector. Meanwhile, the equivalent region of myocardial ischemia is obtained by the magnitude of the ST injury vector under the hypothesis of uniformity and continuity of ischemic distribution in the circular region. The proposed method is generally applicable, as it does not theoretically and technically need any special restriction on patients to be detected. The experimental results of the proposed method will be compared to the diagnostic results of experienced cardiologists and the detection results of coronary arteriography to check the feasibility and validity of the method in this paper. Using this new method, experienced professionals can more quickly and accurately diagnose the degree and range of myocardial ischemia; inexperienced novices can decrease their misdiagnosis and missed diagnosis; ordinary people can perform self-diagnosis so as to see a doctor in time.A good 3D heart model is essential for the correct 3D display of the information of myocardial ischemia in the 12-lead ECG –16. To axc, yc, and zc are the three-dimensional coordinates of the center point, respectively. The surface finite elements can be replaced as the micro triangles, as the surface obtained by scanning is composed of a large number of micro triangles. As a result,  and the proASIC3  were used as the core chips of the amplification-acquisition unit. A conversion module for RS-232 to USB was used as a communication interface, which was responsible for transmitting the ECG data to a personal computer.The ST injury vector was calculated by the ST deviation of each lead of the 12-lead ECG. Therefore, it is very important to accurately get the ST deviation. The ST segment measurement point is at the 108 ms after the R wave crest and the isopotential reference point at the 80 ms before the R wave crest. The potential difference between two points is defined as the ST segment deviation Δst –19.V1, V2,…, V6) distributed on the horizontal plane [XYZ coordinate system, the x-y plane is the frontal plane and the x-z plane is the horizontal plane. It is worth noting that all vectors and subvectors are starting from the center point of the left ventricle. Respectively , 90° (V2), 65° (V3), 40° (V4), 15° (V5), and −10° (V6) on the x-z plane.A ST injury vector could be decomposed into two orthogonal subvectors, al plane –23. In tvely see , the limXYZ coordinate system was located at the center point of the left ventricle; however, our follow-up study found that it was in conflict with the axis positions identified by the panel of experts. The three coordinate axes of the XYZ coordinate system were not perpendicular to each other. Therefore, the origin needed to be adjusted to calibrate the XYZ coordinate system to ensure that its three-axes are in the right direction. It should be noted that such a calibration of the XYZ coordinate system is only in line with the definition of the XYZ orthogonal coordinate system, and it is easy to get the recognition of most medical experts but may not be consistent with the laws of cardiac electrophysiology. For the ST injury vector, this kind of artificial inconsistency is equivalent to the transformations of translation and rotation. In addition, the human heart and body are not spherical, so those electrodes are different in the distance to the heart, which will change the size and direction of the ST injury vector. This means that the theoretical calculation of the ST injury vector also needs to be calibrated with a PET or other “gold standard” equipment. We choose the PET image and use it to calibrate the ST injury vector. In this paper, the weighting coefficient ei  for the ST segment deviation Δsti is expressed asli  is the projection length of i = 1, 2,…, 6) while li  is the projection length of i = 7, 8,…, 12). The coordinates of a unit vector calculated as i = 1, 2,…, 6) in x-y plane are  while those of xp, yp, 0). The least square method was used for minimizing the error induced by the static indeterminateness of the inverse projection equationsAs mentioned previously, the origin of the r as the radius to make a circular cylinder; then the intersection line of the cylindrical outer circle and the surface of the heart is the boundary line of the regional myocardial ischemia. It is needed to point out that the myocardial ischemia is assumed to be uniformly distributed within this equivalent region. The radius r is specifically calibrated by PET images. We chose the scheme for pseudo-color display as follows: normal myocardium was in red and the ischemic myocardium in blue purple.In our method, the myocardial ischemic region cannot be truly reproduced as a PET image due to the limited information provided by the 12-lead ECG. The central point of the myocardial ischemic region is relatively easy to be determined, that is, the intersection point of the ST injury vector with the heart surface. The regional distribution of myocardial ischemia is complicated. We have to simplify the calculation of the regional distribution because there is only one parameter, the magnitude of the ST injury vector, available. We use the ST injury vector as the axis and The purpose of clinical validation is to explore the feasibility of the diagnosis of myocardial ischemia by ordinary people without medical knowledge based on the method of 3D heart model display. The specific contents validated were the comparisons with the experienced cardiologists' diagnoses according to the standard 12-lead ECG and coronary angiography images. Both patients with coronary heart disease and healthy people were selected as subjects and mixed into a few groups. The control clinical trials were designed with double blind method and the results were statistically analyzed by Kappa. The equipment used for the clinical trials was a FX-7500 ECG machine  and a digital subtraction angiography . The clinical trials were carried out at the 105th hospital of the People's Liberation Army. The study protocol was approved by the institutional review board of the University of Science and Technology of China, Hefei, China, and all patients provided written informed consent.P0 = 0.9583; the opportunity consistency Pe = 0.5703; Kappa coefficient k = 0.9030. Considering the sampling error, u-test was carried out for the assumption of k = 0. There is a strong consistency (k > 0.81) between the two methods due to the result of u = 13.47 larger than the standard normal quantile of 1.96. The inconsistent diagnostic results mainly occurred in the ST deviation near the threshold value of 0.1 mV. In this case, the repeatability of the 12-lead ECG detection is very poor, so it needs to be combined with clinical data detected by other equipment to make the diagnosis. In fact, many experienced cardiologists were also full of praise for the patterns displayed on the 3D heart model because of the obvious advantages in the determination of the region of myocardial ischemia. The results of a 69-year-old female patient are shown in 48 patients randomly selected from the total subjects, 25 males and 23 females, age from 46 to 93 years, were diagnosed by ordinary people without medical knowledge and experienced cardiologists, respectively. Although the total positive and negative numbers of the two diagnostic results were the same, their common positive or negative numbers are different. The fourfold table is shown in Coronary angiography is the gold standard for the diagnosis of coronary artery stenosis. The left anterior descending, left circumflex, and right coronary artery supply blood to their respective regional myocardium. The corresponding myocardial region will be ischemic when a coronary artery stenosis occurs. It can be said that coronary angiography is one of the most reliable solutions to verify the display of myocardial ischemia on the 3D heart model. We conducted a total of 72 cases of comparative clinical trials, and the correct rate of display of myocardial ischemia on the 3D heart model was 98.4%. The myocardial ischemic region on the 3D heart model of a 60-year-old male patient is shown in Coronary stent implantation is another scheme reliable to verify the display of myocardial ischemia on the 3D heart model. The myocardial tissue in ischemia due to coronary artery stenosis will restore the normal blood supply after stent implantation. It should be noted that the complete recovery of the normal blood supply to the cardiomyocytes is about two weeks after the stent is placed. We have established a new method for the 3D visualization of the information of myocardial ischemia in the 12-lead ECG, which displays a realistic pattern of myocardial ischemia and does not require any restriction on the patient to be detected. Unlike earlier methods with many constraints, our method is based on the ST injury vector, which can accurately get the distribution range and the location of the myocardial ischemia in uniform and continuous distribution. The clinical validation protocol adopted was the comparison of the results obtained by our method with the diagnoses of experienced cardiologists and the results of coronary angiography. The experimental results indicate that our new method is successful, which can not only reduce the rate of misdiagnosis and missed diagnosis of medical professionals, but also make ordinary people diagnose their own myocardial ischemia like an experienced cardiologist. Our work and results have very good application prospect in medical clinical practice and health care field and are possible to make the 12-lead ECG into thousands of households.There is a drawback to be further improved. At present, our method can only display a single continuous distribution of myocardial ischemia, but its actual distribution may be scattered in multiple regions.


The cardiovascular consequences related to amyotrophic lateral sclerosis are relatively underappreciated. The disease invokes a systematic degeneration of autonomic neurons leading to autonomic dysfunction. We therefore hypothesized that patients with amyotrophic lateral sclerosis may have a predilection to the development of cardiac conduction disorders.A 65-year-old Caucasian man with advanced amyotrophic lateral sclerosis presented with progressive dyspnea and palpitations. A previous evaluation attributed his dyspnea to neuromuscular weakness and he underwent a pulmonary evaluation. Pulmonary function tests did not indicate a worsening from baseline. An electrocardiogram was obtained which demonstrated new third degree atrioventricular block. A previously obtained electrocardiogram indicated normal sinus rhythm. On echocardiogram, a structurally normal heart was observed without significant valvular disease. He was offered a permanent dual chamber pacemaker for definitive treatment, however, he declined.We believe that his symptoms were probably attributable to atrioventricular block. Patients with advanced amyotrophic lateral sclerosis experience loss of heart rate variability and enhanced vasomotor responses. As patients progress later in the disease, sympathetic denervation and vagal predominance contribute to the development of atrioventricular block. We conducted a query using the Explorys database of patients with amyotrophic lateral sclerosis and heart block. The prevalence of heart block was estimated to be 25% higher in patients with the disease as compared to the general population. This is the first reported case that attempts to describe the relationship of atrioventricular block with amyotrophic lateral sclerosis. The cardiovascular consequences related to amyotrophic lateral sclerosis (ALS) are relatively underappreciated. Well-characterized consequences of the illness are derangements related to the autonomic nervous system which include critical mechanisms involved in regulating blood pressure, heart rate, and other homeostatic functions such as digestion and temperature regulation. ALS affects the autonomic nervous system initially by invoking degeneration of neurons that lead to sympathetic predominance and vagal withdrawal. In ALS there are losses of the baroreflex response and perturbations of preganglionic sympathetic ganglia. We therefore hypothesized that patients with ALS may have a predilection to the development of cardiac conduction disorders. We then examined the prevalence of heart block via a national database and conducted a literature search to explain the pathogenesis of heart block in a patient with ALS.Our patient was a 65-year-old Caucasian man with an 18-month history of ALS, who presents with progressive dyspnea and palpitations. A previous evaluation of his dyspnea attributed the cause to neuromuscular weakness and he underwent a pulmonary evaluation. A chest X-ray demonstrated clear lung fields. His arterial blood gas revealed a pH 7.4, carbon dioxide partial pressure 62, oxygen partial pressure 117, on fraction of inspired oxygen 40% and concomitant blood chemistry demonstrated elevated serum bicarbonate, both consistent with chronic carbon dioxide retention. Pulmonary function testing indicated a forced expiratory volume in 1 second (FEV1) of 79% and FEV1/forced vital capacity of >80%. These pulmonary function tests did not represent a significant decrement from baseline.An electrocardiogram (ECG ) was obtained which demonstrated hemodynamically stable new third degree atrioventricular (AV) block with a junctional escape rate of 50 beats per minute  using International Classification of Diseases, Ninth Revision, diagnosis codes for both conditions . We sought to determine the difference between the prevalence of heart block in the general population and in those with ALS.In Explorys, there was a base of 14,092,470 patients of which 3470 had ALS. Heart block was present in 73,801 patients without ALS and in 30 patients with ALS. The prevalence in the diagnosis of heart block in the general population was 0.52%. In ALS the prevalence of the diagnosis of heart block was 0.86%. The difference in prevalence of heart block was therefore estimated to be 25% higher in patients with ALS .ALS is a neurodegenerative disorder affecting both upper and lower motor neurons. Patients eventually succumb to total paralysis and respiratory failure. Research efforts have focused on the improvement and prevention of further neuromuscular deterioration and the management of respiratory failure.Cardiovascular consequences related to ALS are relatively underappreciated. In fact, it is believed that concomitant heart diseases are rare in ALS . Like PaAutonomic dysfunction in ALS is common. Autonomic aberrations were first reported in small series that showed reductions in blood pressure during sustained hand grip . Later oThe impact of ALS upon the autonomic nervous system is sympathetic predominance and vagal withdrawal ,6. CardiIn addition, in ALS there is a loss of baroreflex response and perturbations of preganglionic sympathetic ganglia ,11. StudCardiovascular autonomic dysfunction contributes to the morbidity of the disease. Perhaps the progression of autonomic dysfunction in ALS is under-reported. As previously described, sympathetic predominance with vagal withdrawal tends to occur early on in disease. However, in advanced ALS, the spinal cord sympathetic ganglia known as the intermediolateral nucleus also undergoes degeneration ,13,14. IArrhythmias associated with ALS may occur as a result of autonomic dysfunction. The most common arrhythmic manifestations are sinus tachycardia resulting from vagal withdrawal, interval prolongations of the QT interval, and bradycardia due to sympathetic denervation . DisruptIn drug treatment studies, abnormal augmentation of sympathetic tone in ALS make directed treatments for hypertension and tachycardia difficult. In infusion experiments with low doses of phentolamine, an alpha-antagonist, abrupt drops in blood pressure occurred and only modest increases in heart rate were observed. Likewise beta-antagonism with propranolol leads to considerable decreases in both blood pressure and heart rate with prolonged bradycardia . As repoBradycardia likewise can be explained in ALS by sympathetic denervation followed by the predominance of vagal function. Autonomic dysfunction begins with vagal release with enhanced sympathetic tone causing tachycardia. As patients later progress in ALS, sympathetic denervation occurs, followed by vagal predominance, leading to the development of bradycardia ,13. In aThe cardiovascular manifestations of ALS are often an understated problem encountered through the course of the disease. Concomitant autonomic dysfunction in ALS seems to play a large role in the pathogenesis and the natural history for both vasomotor instability and cardiac arrhythmias. While ALS is a progressive illness that leads to eventual respiratory failure from neuromuscular weakness, the autonomic dysfunction is similarly progressive. It begins with vagal disruption, followed by enhanced sympathetic activity and eventually sympathetic denervation with vagal predominance.The degree of autonomic dysfunction may offer insight into the natural course of the disease. As in the patient presented, AV nodal block argues that sympathetic denervation had occurred and suggests advanced ALS. Cardiac arrhythmias are often untreated and symptoms are often attributed to a pulmonary or psychiatric cause. This is the first reported case of complete heart block occurring in ALS.While the findings are not well documented in the literature, the findings are well supported by previous physiological studies in ALS as well as a survey from a reputable database. Utilizing the data from the Explorys platform, there was a higher prevalence of heart block in patients with ALS. While the small number of affected individuals confers some statistical uncertainty, it suggests that a degree of AV block occurs more frequently in patients with ALS. Autonomic dysfunction occurs in other neurodegenerative illnesses and may shed light into their disease progression as well as potential treatment.Written informed consent for publication could not be obtained despite all reasonable attempts at contacting our deceased patient's next of kin. Every effort has been made to protect the identity of our patient and there is no reason to believe that our patient would have objected to publication.The authors declare that they have no competing interests.KS, SP and JM helped with the contribution to the conception and design. DK and KS conducted the data acquisition analysis and interpretation of data. All authors assisted in drafting and revising the article. All authors were critically important for the intellectual content of the article. All authors read and approved the final manuscript.


Systemic amyloidosis related to mutation of TTR gene can be complicated with Familial Amyloid Cardiomyopathy (TTR-FAC), a severe and life threatening form of heart failure with preserved ejection fraction, with a poor prognosis. To date there is no proven effective specific treatment against TTR-FAC, and the usual treatments of chronic heart failure are either ineffective or contra indicated, except for diuretics. Progression of the disease results in reduction of physical capacity, repeated hospitalizations, increase in diuretics dose, and ultimately in refractory heart failure.Cardiac transplantation has been performed in TTR-FAC since 2003, and reported in 40 patients in the literature with acceptable results in highly selected patients. The results of combined heart and liver transplantation appear to be similar or even better than for isolated heart transplantation, due to a “tolerance” phenomenon, with less cardiac rejection and less graft coronary artery disease.We performed heart transplantation for TTR-FAC in 10 pts , NYHA class II to IV, isolated in 6 and combined with a liver transplantation in 4. Patients had received a pacemaker (n=3) or a defibrillator (n=3) during their preoperative course. Mutations of patients were TYR77 in 5, SER24 in 1, GLU62 in 1, MET30 in 1. In hospital mortality was 40%.Patients can be considered as good candidates to heart transplantation for TTR-FAC if they have symptomatic heart failure persisting under optimal medical therapy, disregarding their ejection fraction, normal pulmonary resistance, no major comorbidities, an acceptable physical and psychological condition, and limited neurologic involvement (ability to engage in a post-operative rehabilitation program is mandatory).In the future, indications of combined heart and liver transplantations will have to be weighed against isolated heart transplantation in association with specific medical treatments .


Pulmonary hypertension has been associated with right ventricular (RV) dyssynchrony. In patients with left side heart failure, treating left ventricular dyssynchrony has been shown to improve patient outcome. Previous studies have demonstrated that RV dyssynchrony was associated with RV dilation, interventricular septum diastolic flatterning and eccentric hypertrophy. We propose simple parameters from cine MRI that can potentially help quantify the complex movements without using special sequences or algorithms.Four healthy subjects  and 11 pulmonary arterial hypertension (PAH) patients  were included in the study. Two patients had QRS duration of >120 ms.The study population underwent cardiac MRI exams on 1.5 T units . Cine short axis data were obtained using steady state free procession imaging with voxel size 1.67x1.67mm, repetition time 29.4ms, echo time 1.19ms for the Siemens unit, and voxel size 1.42x1.42mm, repetition time 2.49ms, echo time 1.25ms for the Phillips unit.Short axis cine and RVOT images were imported into QMass . Endocardial contours were manually traced in all phases for the RV in QMass. Trabeculation was included in the contours, and RV structural information was subsequently calculated.0, ti respectively. We calculated two parameters to describe the levels of dyssynchrony present in different subjects: TDEVslices_MinV, the deviation of {ti} from t0, and TSDslices, the standard deviation of {ti}.For each ventricle, we identified the global min volume phases, the min volume phase for each slice, and converted phase numbers into exact timing. We denoted the two timings as tDEVslices_MinV)  for healthy subjects was 67.0±4.0%, and 60.3±6.5% for PAH patients. The average RVEF for healthy subjects was 54.5±6.7%, and 38.5±12.7% for PAH patients. RV septal wall bounce was observed in majority of our patient population. In the quantitative assessments for LV, RV, and two ventricles combined, PAH patients showed higher variation in the timing of contraction among individual slice positions as well as higher deviation from the minimal RV volume phase (TSDslices and TDEVslices_MinV derived from cine CMR to describe RV dyssynchrony in PAH patients.RV function is an important clinical measurement especially in the prognosis of pulmonary hypertension. We proposed simple parameters TCMREF: cardiovascular medical research and education fund.


Heart failure (HF) is a costly, challenging and highly prevalent medical condition. Hospitalization for acute decompensation is associated with high morbidity and mortality. Despite application of evidence-based medical therapies and technologies, HF remains a formidable challenge for virtually all healthcare systems. Repeat hospitalizations for acute decompensated HF (ADHF) can have major financial impact on institutions and resources. Early and accurate identification of impending ADHF is of paramount importance yet there is limited high quality evidence or infrastructure to guide management in the outpatient setting. Historically, ADHF was identified by physical exam findings or invasive hemodynamic monitoring during a hospital admission; however, advances in medical microelectronics and the advent of device-based diagnostics have enabled long-term ambulatory monitoring of HF patients in the outpatient setting. These monitors have evolved from piggybacking on cardiac implantable electrophysiologic devices to standalone implantable hemodynamic monitors that transduce left atrial or pulmonary artery pressures as surrogate measures of left ventricular filling pressure. As technology evolves, devices will likely continue to miniaturize while their capabilities grow. An important, persistent challenge that remains is developing systems to translate the large volumes of real-time data, particularly data trends, into actionable information that leads to appropriate, safe and timely interventions without overwhelming outpatient cardiology and general medical practices. Future directions for implantable hemodynamic monitors beyond their utility in heart failure may include management of other major chronic diseases such as pulmonary hypertension, end stage renal disease and portal hypertension. Cardiovascular disease remains the leading cause of death in the United States and worldwide To contain costs and standardize management of patients hospitalized for ADHF, the Centers for Medicare and Medicaid Services have recently introduced regulations to withhold or reduce payments for unnecessary hospitalizations for HF  technology which had already established the safety of right ventricular pacing leads and was being used in the target population. Early devices used innovative transvenous lead technology to provide mixed venous oxygen saturation and pressures in the right ventricle (RV)  , and pulmonary artery pressure (PAP) ambulatory heart failure monitoring implantable devices were developed as purely diagnostic devices Figures . LAP monN = 1200) to verify the robustness, safety and usefulness of CardioMEMS in the complex real-world setting, particularly in reducing the rate of HF hospital readmissions and in improving patients' quality of life .Monitoring of PAP has been used for decades by cardiologists to detect early signs of HF in the intensive care setting  consisting of a coil and capacitor encased in silicone, with a nitinol wire loop at each end of the sensor Figure . The CarPatients enrolled in the CHAMPION trial were asked to make daily measurements of their PAPs using their portable electronic unit and a special pillow containing an antenna to take daily sensor readings which are transmitted through a modem or cellphone to a secure patient database  is accessible to healthcare professionals to view the interrogated data. The HeartPOD, CardioMEMS and other non-EP  implantable monitoring systems have built-in, untapped features including cardiac output, heart rate variability, and electrocardiographic monitoring. If officially approved by the FDA, these additional monitoring parameters will likely improve characterization of hemodynamic derangements, and potentially reduce false-positive results, and associated resource utilization.Both the HeartPOD and CardioMEMS systems use a physician-guided self-management model that is intuitive and conceptually sound. However, experts in the field have universally acknowledged the challenges in conducting implantable monitoring trials to demonstrate impacts on clinical outcomes, particularly with how the interrogated physiologic data are handled  between PCWP and LAP in all settings with the PCWP being consistently 35% higher than the LAP. A more contemporary study of lightly sedated dogs reported that the mean PCWP accurately reflected LAP . However, a study of 43 dogs and 30 patients in severe hemorrhagic, traumatic or septic shock noted that a dangerous rise in PAP was not reflected by PCWP or even central venous pressure . The PCWP is often considered to reflect left ventricular preload and pulmonary capillary hydrostatic pressure, however, there is ongoing debate about the validity of this assumption in the setting of various conditions including chronic pulmonary disease, mechanical ventilation and pulmonary venous scarring. In principal, the LAP would be a more accurate measurement as it is physically and physiologically closer to the gold standard, LVEDP, however it is more invasive to measure. A brief literature review did not reveal any studies comparing the three measurements simultaneously, however there are a few studies comparing LAP and PCWP. In 1962, the PAP, PCWP, and LAP measurements of 11 patients with either clinically normal hearts or suspected mitral valve disease were studied with right heart catheterization in a control state, during a norepinephrine infusion, and during positive and negative intraalveolar pressures  Furthermore, in advanced HF patients with known arrhythmias, there can be a role to assess the clinical impact of supraventricular arrhythmias such as atrial fibrillation and ventricular arrhythmias, as well as addressing the question of whether these rhythm disturbances are causal or secondary to ADHF. Additionally, with the pressure to avoid indwelling lines, invasive procedures and overburdening intensive care units, pre-existing internal devices that monitor filling pressures could facilitate the management of these particularly high risk patients when admitted for both cardiac and non-cardiac issues, including perioperative hemodynamic and fluid management.In advanced HF patients with left ventricular assist devices (LVAD) who are recurrently admitted with symptoms of congestion and fluid overload, LAP and PAP monitors may potentially help to discern elevated left sided filling pressures from other causes of dyspnea, and volume overload . However, further clinical review and evaluation still may be necessary to exclude a failing right ventricle in response to LVAD placement and manage other non-cardiac etiologies for recurrent hospitalizations. These devices may also be able to detect low filling pressures in patients with LVADs who urgently need increased intravascular volume in order for optimal device function and cardiac output. It remains to be seen whether regulatory agencies and transplantation societies will endorse the use of implantable LAP or PAP monitors as an alternative to indwelling PA catheters in the pre-heart transplant setting, with the intent to obviate the need for hospitalization in the intensive care unit and periodic replacement of PA catheters that are associated with procedural and other risks including line infection, sepsis, and thromboembolism.N = 16) met criteria based on continuously observed PAP over the first week post-implantation. This implies that an implantable heart monitor may assist with improved diagnosis of pulmonary hypertension and perhaps better guide future trials targeting pulmonary hypertension (Frantz et al., There are also innumerable non-cardiac scenarios in which continuous assessment of cardiac hemodynamics and filling pressures would be invaluable. A recently published substudy of the CHAMPION trial found that of the 217 patients who did not meet criteria for pulmonary hypertension during the implantation right heart catheterization, 48.8% (The review was initially conceived of and manuscript outlined by all authors. DM prepared the first draft in collaboration with EF. RD and DS provided substantial revisions and contributions. DS contributed Figure Rahul N. Doshi has served as a consultant for St. Jude Medical, Inc. David M. Shavelle is a consultant and received research support from St Jude Medical, Inc. Deirdre M. Mooney and Erik Fung declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


Previous work indicates that dilatation of the pulmonary artery (PA) itself or in relation to the ascending aorta (PA:Ao ratio) predicts pulmonary hypertension (PH). Whether these results also apply for heart failure with preserved ejection fraction (HFpEF) is unknown.In the present study we evaluated the diagnostic and prognostic power of PA diameter and PA:Ao ratio on top of right ventricular (RV) size, function, and septomarginal trabeculation (SMT) thickness by cardiovascular magnetic resonance (CMR) in HFpEF.159 consecutive HFpEF patients were prospectively enrolled. Of these, 111 underwent CMR and invasive hemodynamic evaluation.p < 0.001), PA:Ao ratio , and SMT diameter . The strongest correlation with mPAP was found for PA:Ao ratio . By ROC analysis the best cut-off for the detection of moderate/severe PH was found for a PA:Ao ratio of 0.83.By invasive assessment 64 % of patients suffered from moderate/severe PH (mean pulmonary artery pressure (mPAP) ≥30 mmHg). Significant differences between groups with and without moderate/severe PH were observed with respect to PA diameter . By multivariable Cox-regression analysis PA:Ao ratio was independently associated with event-free survival (p = 0.003).Patients were followed for 22.0 ± 14.9 months. By Kaplan Meier analysis event-free survival was significantly worse in patients with a PA:Ao ratio ≥0.83 (log rank, PA:Ao ratio is an easily measureable noninvasive indicator for the presence and severity of PH in HFpEF, and it is related with outcome. About 50 % of patients presenting with symptoms of heart failure are diagnosed with heart failure with preserved ejection fraction (HFpEF). HFpEF is characterized by impaired diastolic function due to abnormal relaxation of the left ventricle (LV) as well as increased chamber stiffness . The patAccurate assessment of PH requires invasive measurement of pulmonary artery (PA) pressure and pulmonary arterial wedge pressure (PAWP) . BecauseCardiovascular magnetic resonance (CMR) is the current gold-standard technique to assess right heart dimensions, function, wall thickness, as well as the dimensions of the great arteries . PreviouThe present study was intended to determine the usefulness and prognostic significance of easily measureable variables such as PA diameter and PA:Ao ratio on top of CMR derived right ventricular (RV) dimension, ejection fraction, SMT dimensions, and RV free wall thickness (RVFW) in a prospective, well defined HFpEF cohort.This was a prospective observational study performed at the Medical University of Vienna. All participants gave written informed consent. The institutional review board approved the study protocol (EK #796/2010).2. All patients underwent ventilation-perfusion scans and lung function testing including diffusing capacity of the lung for carbon monoxide to rule out chronic thromboembolic PH and PH due to significant lung disease.Consecutive patients with suspected HFpEF-PH were invited to participate. HFpEF was diagnosed in the presence of: (1) symptoms or signs of heart failure; (2) normal or mildly reduced left ventricular (LV) systolic function (LV ejection fraction (EF) >50 %); (3) evidence of abnormal LV relaxation or diastolic stiffness  NT-proBNP serum levels ≥220 pg/mL . ReasonsPAWP, mean pulmonary artery pressure (mPAP), and cardiac output (CO) were determined. CO was measured by both thermodilution and Fick method. Simultaneously, all patients underwent direct assessment of LV filling pressures, followed by coronary angiography. Derived hemodynamic parameters were calculated according to standard formulae . PH was All CMR studies were performed on a 1.5-T scanner  within 30 days of RHC (mean 14.8 ± 9.0 days). Studies consisted of functional and Late Gadolinium Enhancement (LGE) imaging, according to standard protocols . For cinPA and Ao diameters were measured from inner-edge to inner-edge in axial half-Fourier single-shot turbo spin-echo (HASTE) black blood images  at the level of the PA bifurcation .Patients were prospectively followed by ambulatory visits and telephone calls at 6-month intervals. The main outcome measure was a combined endpoint consisting of hospitalization for heart failure or death from cardiac causes. Endpoints were ascertained by follow-up visits and phone calls.Categorical data are presented as total numbers or percent, and continuous variables as mean ± standard deviation. Chi square test or Fisher´s exact test were applied for categorical variables and the Wilcoxon two-sample test for continuous variables. Kaplan-Meier estimates were used to calculate cardiac event rates. Differences between Kaplan-Meier curves were analyzed using the log rank test.p-value <0.05 in the univariable model were entered into a multivariable model using a stepwise approach. Hazard and odds ratios for the PA:Ao ratio were reported as PA diameter divided by Ao diameter times 100. Receiver Operating Characteristic (ROC) curves were used to determine cut-off values for the detection of moderate/severe PH. Interobserver variability was described by using Intra Class Correlation Coefficients (ICCs). Statistical analyses were performed with SPSS Statistics version 18 . Results were considered statistically significant if p-values were <0.05.Binary logistic regression analysis was used to identify variables associated with moderate/severe PH (mPAP ≥30 mmHg). In addition, a univariable Cox regression analysis was used to identify parameters  associated with event-free survival. In a second step these parameters were adjusted for potential cofounding clinical variables such as age, sex, atrial fibrillation, arterial hypertension, diabetes, chronic obstructive pulmonary disease, and coronary artery disease. All variables with a 2, or claustrophobia. Of the remaining 111 patients  who underwent CMR, 64 % suffered from moderate or severe PH (mPAP ≥ 30 mmHg by RHC). Clinical characteristics, hemodynamic measurements, and CMR parameters of registered patients are summarized in Table Between 2010 and 2013 159 consecutive patients were enrolled. Of these, 48 had to be excluded from the study because CMR was not possible due to pacemakers, GFR <30 mL/min/ 1.73 mp = 0.006), non-significant coronary artery disease/previous revascularization ; shorter 6-min walk distances  and had more dilated left atria .With respect to baseline clinical parameters, patients with moderate/severe PH more frequently presented with diabetes .Invasive assessment showed significant differences between patients with and without moderate/severe PH with respect to all measured variables except for CO, which was similar in both groups  patients had a TPG >12 mmHg (formerly classified as “out-of-proportion PH”) and 13 (12 %) had a DPG ≥7 mmHg, indicating combined pre- and postcapillary pulmonary hypertension .p = 0.001) whereas PA:Ao ratios did not differ between patients with a DPG of ≥ and <7 mmHg . However, this lack in statistical significance may be due to the small proportion of patients with DPGs ≥7 mmHg (12 % of the study cohort).Patients with a TPG >12 mmHg had a significantly higher PA:Ao ratio as compared to patients with a TPG ≤12 mmHg  of our patients and involved 8.8 ± 4.3 % of left ventricular myocardial mass. In the majority (n = 22), LGE was present at the insertion point of the right ventricle; 8 patients had midmyocardial and 4 subendocardial enhancement. There were no significant differences in LGE pattern or degree between groups with and without moderate/severe PH.LGE was present in 31 % (p < 0.001) and also had significantly higher PA:Ao ratios . SMT diameters  were larger in patients with moderate/severe PH, while areas did not differ between groups (p = 0.136). RVFW showed a wide range from 2.0 to 7.2 mm (4.2 ± 1.1 mm) and did also not differ between patients with and without moderate/severe PH (p = 0.183). PA:Ao ratio, PA diameter and SMT diameter were significantly correlated with mPAP . Fig. Dimensions of the great arteries and indices of RV hypertrophy by CMR are displayed in Table p = 0.010), PA diameter (p < 0.001), and PA:Ao ratio (p < 0.001) were associated with moderate/severe PH. However, by multivariable analysis only PA:Ao ratio remained independently associated with the presence of moderate/severe PH.Table By ROC analysis, a PA:Ao ratio of 0.83 was found to best detect mPAP ≥30 mmHg with a sensitivity of 73.2 % and a specificity of 67.5 %, and an area under the curve (AUC) of 0.759 Fig. .Fig. 4ReMeasurements of PA:Ao ratio and PA diameter showed excellent inter-observer agreement with an Intra Class Correlation Coefficient (ICC) of 0.815 and 0.905 while ICCs for SMT diameters were only 0.563, and for RVFW 0.581.Patients were followed for 22.0 ± 14.9 months. During follow-up 40 cardiac events  occurred.p = 0.023), RVFW (p = 0.034), PA diameter (p = 0.002), and PA:Ao ratio (p = 0.003) were significantly associated with cardiovascular events. After adjustment for age, sex, atrial fibrillation, diabetes, chronic obstructive pulmonary disease and coronary artery disease, PA diameter (p = 0.003), and PA:Ao ratio (p = 0.002) remained significant predictors of outcome. However, after multivariable adjustment, only PA:Ao ratio remained independently associated with event-free survival.Table p = 0.004).By Kaplan Meier analysis Fig. , event-fThe present study demonstrates that the PA:Ao ratio can be used as a simple and straight-forward indicator of PH associated with HFpEF. Moreover, the PA:Ao ratio is of prognostic value with respect to cardiac events.In patients suffering from HFpEF right heart variables are of particular interest as they play an important role in terms of prognosis , 22–27. RV mass and RV mass to LV mass ratio (VMI) have been shown to correlate reasonably well with mPAP in previous studies , 34, butRVFW thickness is much more easy to assess than RV mass or VMI. In a historical series this parameter appeared useful as surrogate marker of PH  and was n = 49) found that SMT mass could be a useful marker for the identification of PH [The SMT is a prominent muscle band that originates from the basal ventricular septum and runs apical-laterally towards the RV free wall . A recenon of PH . HoweverIn contrast to the aforementioned parameters , the size of PA and Ao are easy to measure. Such measurements do not require dedicated software or advanced expertise. In the present study PA:Ao ratio was identified as the most potent predictor for the presence of moderate/severe PH. It correlated better with mPAP than PA diameter or indices of RV hypertrophy and showed excellent reproducibility. In addition, PA:Ao ratio was independently associated with event-free survival. From a clinical perspective the differentiation between isolated post-capillary PH and combined forms is crucial, in particular with regard to prognosis  and therSeveral previous studies have evaluated the usefulness of the PA:Ao ratio for the detection of PH –15. HoweOther studies have used a PA:Ao ratio cut-off of >1.0 for the suspicion of PH. These included 60 patients with chronic obstructive pulmonary disease , 81 patiPresented data have been collected in a single center setting. Therefore, a center-specific bias cannot be excluded. However, the major advantages of limiting data collection to a single center are 1. inclusion of a homogenous patient population, 2. adherence to a constant clinical routine, 3. constant quality of echocardiographic and CMR work-up and 4. constant follow-up.PA and Ao diameters were acquired from axial HASTE black blood images and were not planned exactly in line with the vessel orientation. This may have led to some over- or underestimation of the vessel size.The majority of patients included in this study were suffering from PH (83.8 % had mPAP ≥25 mmHg). Sixty four percent had at least moderate PH (mPAP ≥30 mmHg). Due to the small number of patients in the group without PH, patients were dichotomized in groups with mPAPs above and below 30 mmHg, defined as groups with no/mild PH versus moderate/severe PH. However, previous work shows that a PA:Ao ratio of 0.84 also discriminates between patients with mPAPs above and below 25 mmHg . In addiPA:Ao ratio is an easily assessable, straight-forward marker of PH in HFpEF patients. Moreover, it is strongly associated with outcome. Other CMR derived indices of RV pressure overload such as RVFW or SMT thickness are less accurate and reproducible.


The use of ventricular assist devices has expanded significantly since their approval by the Food and Drug Administration in the United States in 1994. In addition to this, the prevalence of heart failure continues to increase. We aim to provide an overview of perioperative considerations and management of these patients for non-cardiac surgery. We performed a Medline search for the words “ventricular assist device,” “Heartmate” and “HeartWare” to gain an overview of the literature surrounding these devices, and chose studies with relevance to the stated aims of this review. Patients with ventricular assist devices are presenting more frequently for surgery not related to their cardiac pathology. As the mechanically supported population grows, general anesthesiologists will be faced with managing these patients, possibly outside of the tertiary care setting. The unique challenges of this patient population can best be addressed by a thorough understanding of ventricular assist device physiology and a multidisciplinary approach to care. Since the approval of ventricular assist devices (VADs) by the Food and Drug Administration (FDA) in the United States in 1994, their indications and prevalence have continued to expand , 3. InitSince their first use in the early 1990s, VADs have developed and undergone multiple evolutions resulting in the devices currently in use. First-generation devices attempted to assist the failing ventricle by assuming its pump function. These pumps were either pneumatically or electrically driven and operated in a fill-to-empty mechanism, which produced pulsatile flow in an asynchronous fashion with the native ventricle . These cSecond generation devices abandoned efforts to replace the function of the ventricle and instead unload volume from the failing ventricle in a continuous, nonpulsatile fashion. An inflow cannula is placed in either the left atrium or, more commonly, the apex of the left ventricle (LV) and blood is pumped via a rotating impeller in an axial or centrifugal fashion to the ascending aorta , 12. Themax – Qmin)/Qavg. These values can be monitored on an external display, which can be useful clinically  [The HeartMate II®  Figs. , 2, 3 is output) , 16.Fig.The HVAD™  Figs.  and 5 isThe physiologic changes associated with heart failure are complex and systemic. These patients clearly have reduced stroke volume and cardiac output associated with slow circulation times and decreased end-organ hypoperfusion. Compensation occurs via neurohormonal activation—high circulating catechol amines, natriuretic peptides, endothelin, and activation of the renin-angiotensin-aldosterone system—which results in ventricular remodeling. Hence, the mainstay of treatment is neurohormonal blockade . The lonThe device itself also depends upon several physiologic variables. The output of second- and third-generation devices is directly related to pump speed and inversely related to the pressure gradient across the pump , 16, 20.Another important physiologic consideration after LVAD implantation is the coagulopathy associated with shear stress and nonpulsatile flow. Evidence suggests an acquired von-Willebrand Syndrome exists where a decreased amount of circulating high-molecular-weight von-Willebrand multimers are found, similar to that of severe aortic stenosis , 21, 22.In addition to the standard components of a preoperative assessment, evaluation of a patient with an LVAD should include a few additional components. When possible, all LVAD patients undergoing non-cardiac surgery should have a multidisciplinary team of subspecialists coordinating their care. This should include not only the primary surgical and anesthesia teams, but also cardiac surgery, heart failure cardiologists, and dedicated VAD personnel , 24, 25.Next, baseline physical exam findings should be noted, with special concern to organ systems which may be affected by the baseline heart failure  or those which may be affected by LVAD complications, such as a neurologic deficit secondary to a thromboembolic event. Assessment of laboratory values with attention to the same organ systems should be included , 26. ManAll modern LVAD patients will generally be maintained on anticoagulation, which will have to be managed preoperatively. Patients, therefore, will generally not be candidates for neuraxial anesthesia , 16, 26.Intraoperative monitoring of LVAD patients presents unique challenges due to their nonpulsatile nature. Standard ASA monitors, such as pulse oximetry and noninvasive blood pressure monitoring, rely on pulsatility and oscillations, respectively. Cerebral tissue oxygenation (SctO2) measurements have been used successfully as a surrogate for pulse oximetry in these patients , 16, 26.After preoperative optimization and coordination of a multidisciplinary team, when patient condition permits, the patient can be taken to the operating room. Patients should be transported to the operating room in coordination with VAD personnel who have knowledge of VAD intricacies, such as connecting the portable power supply, control console and changing VAD settings if necessary. Once in the operating room, the device should be attached to a secure power supply for the duration of the procedure , 20, 30.The presence of an LVAD does not preclude the use of anesthetic drugs or techniques that would otherwise be acceptable for these patients. Standard induction agents and balanced anesthetic techniques have been used safely , 20, 30.Goals of care for LVAD patients undergoing non-cardiac surgery should be directed at maintaining forward flow and adequate perfusion. Three main factors that affect LVAD flow are preload, RV function, and afterload. First, optimizing preload includes ensuring adequate volume status without overloading the right ventricle , 9, 11. The right ventricle is the primary means of LVAD filling; therefore, maintaining RV function is imperative . NegativKeeping in mind the LVAD’s preload dependence and afterload sensitivity is key to managing changes in hemodynamics , 20, 34.Managing arrhythmia may present a unique challenge in LVAD-dependent patients. Many patients may have implanted defibrillators or pacemakers which may require reprogramming prior to the procedure , 27. ExtIntraoperative events that affect preload and afterload should be completed cautiously. Position changes should be performed gradually and extremes in position should be avoided. Preoperative volume loading has been shown to stabilize hemodynamics when positions are required that decrease preload, such as lateral decubitus or reverse Trendelenburg , 26, 30.Managing device complications may present a challenge that requires a multidisciplinary team to diagnose and treat . Motor fIn general, the postoperative care of LVAD-dependent patients undergoing non-cardiac surgery is largely uneventful. Patients should be extubated when they meet standard criteria , 24, 30.There is an increasing frequency of LVAD-dependent patients presenting for non-cardiac surgery. These trends will likely increase due to advances in cardiac care and the consequent increase in life expectancy and prevalence of end-stage cardiac disease. The general anesthesiologist needs to be prepared to evaluate these patients and mitigate cardiac risk in the perioperative period. The unique challenges of this patient population can best be addressed by a thorough understanding of LVAD physiology and a multidisciplinary approach to care.


The Transvalvular Impedance (TVI) is derived between atrial and ventricular pacing electrodes. A sharp TVI increase in systole is an ejection marker, allowing the hemodynamic surveillance of ventricular stimulation effectiveness in pacemaker patients. At routine follow-up checks, the ventricular threshold test was managed by the stimulator with the supervision of a physician, who monitored the surface ECG. When the energy scan resulted in capture loss, the TVI system must detect the failure and increase the output voltage. A TVI signal suitable to this purpose was present in 85% of the tested patients. A total of 230 capture failures, induced in 115 patients in both supine and sitting upright positions, were all promptly recognized by real-time TVI analysis (100% sensitivity). The procedure was never interrupted by the physician, as the automatic energy regulation ensured full patient's safety. The pulse energy was then set at 4 times the threshold to test the alarm specificity during daily activity . The median prevalence of false alarms was 0.336%. The study shows that TVI-based ejection assessment is a valuable approach to the verification of pacing reliability and the autoregulation of ventricular stimulation energy. The automatic adaptation of ventricular pacing energy to the individual capture threshold has been available in the cardiac stimulation practice for the last two decades. Different systems have been proposed by the industry to prevent unnecessary high pacing output, based either on periodic threshold assessment performed by the implanted device , 2 or onIn beat-by-beat capture check as well as periodic threshold measurement, the confirmation of capture relies on the detection of pacing-induced active myocardial depolarization, that is, the action potential generated by excited myocardial fibers in the surrounding of the stimulating electrode, generally referred to as evoked potential. The evoked electrical response must be discriminated from the electrode polarization produced by the spike itself –8, whichIn spite of the good performance of capture recognition systems based on the evoked potential detection, alternative strategies can be considered. In particular, the presence of cardiac activity could be assessed at the mechanical level, rather than from the electrical response . In thisThe ejection surveillance at every beat must rely on an effective haemodynamic sensor, suited to drive the pacing device in almost real time. In this aim, the measurement of cardiac impedance in transvalvular configuration (TVI) has been proposed as a tool for timely ejection recognition after either ventricular sensing or pacing . TVI is The study was performed during routine follow-up checks in 4 cardiac stimulation centers in Sicily, involving 142 patients implanted with the DDDR pacemaker Sophòs 455  for sick sinus syndrome and/or AV block. This pacemaker is endowed with the TVI sensor and the related functions of ejection surveillance after ventricular pacing and sensing and can display the telemetric TVI waveform during a threshold test controlled by TVI. The standard implantation procedure was followed, leaving the implanting physician totally free to choose the preferred pacing leads. The atrial lead was placed in right appendage and the ventricular lead in right apex. The final location was set based on threshold and intrinsic electrogram measurement, while no effort was devoted to the optimization of the TVI signal, which was not recorded at implantation.μA. Impedance is defined by the ratio between voltage and current. The TVI detector performs this measurement with 16 ms interval, throughout the cardiac cycle. In each cycle, the voltage samples are processed by the device in order to work out the minimum TVI in the presystolic interval and the maximum TVI during the following systolic interval. All samples are displayed during waveform telemetry, while data analysis by the pacemaker starts 100 ms after the spike emission (a blanking period set to avoid artifact sensing). The difference between maximum and minimum TVI assessed after the blanking period provides the peak-to-peak TVI excursion (TVIpk-pk). To allow the system application in ejection surveillance, the TVI signal must reach or exceed a minimum TVIpk-pk and satisfy the expected time-course, in which the minimum presystolic TVI precedes the systolic maximum. Therefore, as a preliminary step, the basic properties of the TVI signal in the patient group were assessed and compared in the presence of AV sequential pacing  and VVI stimulation at overdrive rate . The significance of differences in TVIpk-pk related to the pacing modality was evaluated by the paired Student's t test. The spread of the data is always expressed as standard deviation.The TVI system was enabled during a follow-up session scheduled at 2 months from the implantation. The signal can be derived between the atrial ring electrode and either the ring or tip ventricular electrode. Once the recording configuration is chosen, the pacemaker automatically sets the current intensity required for optimal impedance resolution, up to a maximum of 45 pk-pk in the current cycle is equal or higher than 50% of the reference value, which corresponds in turn to the latest updating of the average TVIpk-pk derived from 8 positive TVI signals. If this condition is not satisfied during standard operation, the pulse energy is increased and a threshold test is then carried out automatically by the pacemaker. If the condition is not satisfied during a threshold test started by the programmer within a check-up session, the procedure is broken and the permanent pulse parameters are resumed, storing in memory as threshold data the lowest amplitude and width which induced a positive TVI response.In case of ventricular pacing, capture is confirmed if TVITo test TVI reliability in capture surveillance, the ventricular threshold analysis was carried out in VVI mode at overdrive pacing rate in both supine and sitting upright position. The procedure was simultaneously monitored by both the pacemaker through the TVI signal and the physician through the surface ECG. On the occurrence of TVI-indicated pacing failure, the pacemaker automatically restored the programmed pulse energy and quit the test mode. Only in the event of undetected capture loss, the threshold test must be manually aborted by the physician. When the procedure was stopped for any reason, the pacemaker diagnosis of a positive or negative response to stimulation in the last paced beat was cross-checked with the physician's evaluation, assumed as the golden standard. The test was considered successful in each patient only if TVI-based autoregulation of pulse energy scan down to the threshold was consistent with the physician's interpretation of the ECG in both supine and sitting position. The TVI sensitivity to capture failure was expressed by the proportion of patients where a true capture loss was properly recognized by TVI in both conditions, with respect to the number of patients where the threshold was reached. The positive predictive value was given by the proportion of patients where a true capture loss was properly recognized by TVI in both conditions, with respect to the total number of tested patients. Two-tailed 95% confidence limits of these indices were derived from the binomial distribution.In addition, at the end of the check session the pacemaker was set in DDD with AV delay shorter than the intrinsic PR interval by at least 50 ms, and the ventricular pulse energy was transiently programmed at four times the threshold, in order to make virtually nil the likelihood of capture failure. The function of TVI-based ejection surveillance was set in passive mode  and the patients were asked to alternate sitting and standing up positions with periods of walking at their usual speed, for a 10 to 15 min observation interval. During this period, the pacemaker stored in memory the number of cycles where a capture failure was indicated by the TVI sensor, together with the total number of ventricular pacing events and the trend of the alarm frequency as a function of the time. The data were retrieved by telemetry at the end of the test. The prevalence of TVI-indicated capture failures  was considered as a negative indicator of the system specificity. The frequency distribution of the individual alarm prevalence in the patient group was summarized by its quartiles.pk-pk was higher with AV sequential than VVI pacing . The individual ratio of TVIpk-pk in VVI and VDD averaged 0.87 ± 0.22 in this subgroup of patients. When TVI was derived in atrial ring-ventricular ring configuration, TVIpk-pk was remarkably lower and no significant difference related to the pacing mode was noticed . In most cases featuring a lower TVIpk-pk with VVI pacing, the difference resulted from a higher beat-to-beat variability compared with sequential activation , associated with the anticipation of TVI rise. Due to the earlier signal onset, the actual minimum TVI could occur in the blanking period following the ventricular spike and thus could be skipped by the measurement of TVI excursion performed by the pacemaker. A comparison of TVI signals recorded in the same patient in VDD and VVI pacing is shown in pk-pk averaged 45.8 ± 3.3 Ohm with a variation coefficient equal to 0.07. In VVI, in contrast, the TVI rise started within the blanking, so that the measured TVIpk-pk was reduced to 26.8 ± 9.7 Ohm, with a variation coefficient of 0.36.TVI was derived with the tip ventricular electrode in 52% of the patients and with the ring in the remaining 48%. When the atrial ring-ventricular tip configuration was chosen, TVISince the ventricular threshold test was performed in VVI pacing and the quality of the TVI signal was worsened in such conditions, the system enabled the procedure under TVI control in 120 out of 142 patients (85% of the cases). The energy scan was broken by TVI for a real capture loss confirmed by the surface ECG in both supine and sitting position in 115 patients, while in 5 cases the procedure was incorrectly stopped by TVI for a false alarm of capture failure occurring in either supine or sitting position. In no case the procedure was manually closed by the physician in the event of capture failure undetected by TVI, as all 230 episodes of missing capture  were promptly recognized by the system. TVI sensitivity to capture loss thus resulted 100% in the tested group, with 95% confidence limits ranging from 96.8 to 100% in the population. The positive predictive value was 95.8% in the sample, with 95% confidence limits from 92.3 to 99.4%.An example of the system operation is illustrated in Although TVI proved very sensitive to the absence of mechanical activity following ventricular pacing, the system could not discriminate between different activation patterns. Therefore, the only feature suitable to distinguish intrinsic and evoked ventricular contraction was the time-relationship with the pacing spike. In few cases where the TVI signal was so deteriorated in VVI to be unacceptable to the control system, a threshold test was attempted in the presence of sequential pacing. Unless the intrinsic AV conduction was absent or very slow, a TVI fluctuation due to natural conduction was detected anyway within the expected systolic interval triggered by the pacing pulse, even with a short AV delay. As a result, properly timed ejection was confirmed by TVI and no capture-loss alarm was raised when the QRS shifted from an evoked wide complex to a narrow signal, indicating the occurrence of intrinsic conduction instead of effective stimulation. An example is provided in The prevalence of false alarms of capture loss during daily life activity did not exceed 0.25% of paced ventricular beats in 47% of the patients. The frequency distribution of the individual prevalence featured a 1st quartile equal to 0.047%, a median of 0.336%, and a 3rd quartile corresponding to 1.110%. This means that, on the average, 1 false alarm was produced in more than 2128 paced beats in 25% of the patients, in more than 298 beats in 50% of the patients, and in more than 90 beats in 75% of the patients.To calculate the energy cost of this error rate, it must be pointed out that the pacing pulse parameters in Sophòs pacemakers are specified by the minimum and maximum amplitude and width, which are all programmable. As long as ventricular capture is confirmed by TVI, the minimum pulse amplitude and width are applied. Following an alarm of capture failure, the maximum amplitude and width are enabled for 8 beats; then width and amplitude are decreased in sequence down to the programmed minimum values, with a reduction speed of 1 programming step per cardiac cycle. Therefore, the increase in pacing energy induced by a single alarm depends on the programmed pacing configuration. Assuming that the maximum amplitude is twice the minimum with 12 programming steps in between and with constant pulse width, the 1st quartile alarm prevalence would imply a 1.8% increase in the current drain due to ventricular pacing. The median and 3rd quartile prevalence would result, respectively, in 12.6 and 41.6% rise in the consumption required for ventricular stimulation with respect to the minimum predicted in case of no alarms. To restrict the extraconsumption below 25% in this simulation, the alarm rate must not exceed an upper limit of 1 in 150 paced cycles, corresponding to a prevalence of 0.67%.Checking the regular occurrence of ventricular ejection at every beat might substantially increase the patient's safety and improve the quality of the pacing therapy. Our experience has shown that the absence of ventricular contraction after ineffective stimulation was promptly detected by the TVI system and that all the episodes of asystole were recognized and properly managed . The higIn conditions of ventricular pacing as well, TVI looks best suited to a function of ejection confirmation aimed at increasing the reliability of the pacing system, rather than to the continuous measurement of the pacing threshold required for the fine regulation of pulse energy , 12. IndAs the TVI system has been designed to detect the ejection, no matter if it is produced by ventricular stimulation or intrinsic activity, it could be difficult to assess the pacing threshold in the presence of intrinsic AV conduction . HoweverThe high signal-to-noise ratio generally exhibited by TVI allowed a strict definition of the positive response, which must feature a sufficiently large TVI rise taking place within a specified time interval. This strategy intentionally optimized the sensitivity to capture loss to the prejudice of specificity and general system applicability. In addition, the present experience shows that the quality of the TVI signal worsened in VVI with respect to AV sequential pacing, even if the QRS complex was very similar, indicating a fully evoked ventricular activation in both cases . HoweverA less demanding identification of a positive TVI response to ventricular stimulation is also expected to reduce the prevalence of capture failure alarms in daily life, with consequent decrease of the total energy used to pace the ventricle. Although the alarm rate was lower with the TVI system than in the early experience with electrical evoked potentials, where a back-up pulse was delivered in 1.1% of paced cycles mostly due to undersensing of fusion beats , the curAt present, TVI is the only hemodynamic sensor proposed as a tool for ejection surveillance at every beat. While capture recognition based on evoked potential detection still requires the use of low polarization electrodes for full reliability –26, TVI TVI-based ejection surveillance can be applied in the presence of ventricular pacing and sensing as well, and might substantially increase the safety of bradyarrhythmic patients treated with cardiac stimulation.The reported experience was limited to the acute evaluation of TVI performance in the detection of a capture failure and the autoregulation of the pacing energy. Chronic clinical studies are required to establish the reliability of the system and its energy cost in long-term follow-up.


This study aimed to compare the efficacy and safety of the classic Morrow septal myectomy with the modified procedure in treating hypertrophic obstructive cardiomyopathy (HOCM).A retrospective study was conducted to compare the outcomes of classic with modified Morrow septal myectomy in 42 patients treated from January 2005 to July 2011. Preoperative and postoperative ventricular septal thickness, left ventricular (LV) outflow tract velocity and gradient were measured echocardiographically.In both groups, the ventricular septal thickness, LV outflow tract velocity, and LV outflow tract gradient were significantly decreased after the operation. The modified Morrow procedure group, however, showed significantly greater reduction in these echocardiographic parameters than the classic procedure group. All patients in the modified procedure group were asymptomatic postoperatively with a postoperative transvalvular pressure gradient <30 mm Hg. In the classic procedure group, only 14 (87.5%) patients, however, were asymptomatic postoperatively with a postoperative transvalvular pressure gradient <30 mm Hg, and 2 patients still had severe LV outflow obstruction postoperatively.The modified Morrow septal myectomy is safe and effective in treating HOCM patients, and is superior to the classic procedure in reducing the LV outflow tract gradient and velocity, restoring normal anatomic atrioventricular size, and alleviating symptoms associated with HOCM. This disease is characterized by concentric and asymmetric cardiac hypertrophy, and increased thickness of cardiac walls, potentially complicated by abnormal left ventricular ejection fraction.3 In the classic Morrow operation, cardiac obstruction is relieved by resecting relatively small (2–5 g) sections of muscle tissue in the proximal ventricular septum, which widens the outflow tract and decrease the flow drag (Venturi).2 Thus, systolic combined contact between the mitral valve and hypertrophied septum allow for an immediate gradient reduction that can relieve symptoms.4 Recently, many different modifications of the classic procedure have been proposed, aiming to reconstruct the left ventricular (LV) outflow with better outcomes by enlarging the resected area.8 The modified Morrow septal myectomy has been used in our hospital since 2005. There, however, is no concluded results in the efficacy comparison of the modified operations with the classic Morrow operation. This has caused more debate about the preferred treatments for HOCM between the alternative methods  and surgical myectomy.The classic Morrow operation  was described for the first time in 1975.The current study was conducted to compare the efficacy and safety of the classic Morrow septal myectomy with the modified procedure in treating HOCM patients.This is a retrospective study including 42 HOCM patients treated with classic or modified Morrow septal myectomy from January 2005 to July 2011 at the Department of Cardiac Surgery of the Beijing Anzhen Hospital, China. There were 27 men and 15 women with a mean age of 45 ± 16 years. The study protocol was approved by the Department of Cardiac Surgery, Beijing Anzhen Hospital Affiliated to Capital Medical University, China.9; age >18 years; exertional or nonexertional symptoms of dyspnea, syncope, or cardiac dysfunction; LV outflow ≥50 mm Hg; the ratio of ventricular septum to LV posterior wall >1.3:1; resting differential pressure of LV outflow >75 mm Hg.Patients were included if then met the following criteria: diagnosed with HOCM10 and categorized as mild reflux (regurgitation jet area <4 cm2), moderate reflux (regurgitation jet area ≥4 and <8 cm2), and severe reflux (regurgitation jet area ≥8 cm2).The clinical data and demographic information were extracted from the medical records of each patient, including age, sex, presence of preoperative systolic anterior motion (SAM), complete atrioventricular block, complete left bundle branch block, Alfieri technique, anterior mitral valve transversally folded shape, mitral valve replacement, coronary artery bypass grafting, and right ventricular outflow tract enlargement. Preoperative mitral insufficiency degree was determined by echocardiographyAll septal myectomy operations were performed under general anesthesia with low temperature extracorporeal circulation. Continuous anterograde cold blood cardioplegia was used for myocardial protection. A proximal incision was made below the aortic valve to dredge the LV outflow. Mitral valves were managed by interatrial groove pathways. Operations were guided by transthoracic echocardiography and transesophageal echocardiography.3 For the modified Morrow septal myectomy procedure, a 5 to 6-cm incision was made by extending the classic incision with a midventricular resection, from the ventricular septum  to the anterior mitral valve contact of the mitral valve  was measured at postoperative 1 week.t-tests. Efficacy was compared between groups using independent samples t-tests. A P-value less than 0.05 were considered statistically significant.Continuous variables are expressed as means ± standard deviations (SD), and categorical variables as frequencies or percentages. SPSS v.17  was used for the statistical analysis. Preoperative and postoperative data were compared using paired Of the 42 HOCM patients, 16 (38.1%) patients were treated with the classic Morrow procedure and 26 (61.9%) with the modified Morrow procedure. There was no significant difference in the clinical characteristics between the 2 groups  patients were asymptomatic postoperatively with a postoperative TPG < 30 mm Hg, and 2 (12.5%) patients showed LV outflow velocity of 411 mm/s with severe LV outflow obstruction (postoperative TPG > 90 mm Hg). One patient in the classic procedure group showed third-degree atrioventricular block. On the contrary, all 26 (100%) patients in the modified Morrow group were asymptomatic postoperatively with a postoperative TPG < 30 mm Hg. Two patients died from low cardiac output in the classic procedure group within 30 days and 1 year postoperatively, respectively. No patients died in the modified procedure group within 1 year postoperatively. No complications, such as heart failure and thromboembolism occurred in the modified procedure group.11 Gao et al7 reported a modified Morrow procedure than could achieve full mitral regurgitation, improve or eliminate SAM in all cases, which is consistent with the findings of our study. In addition, patients treated with the modified Morrow procedure were asymptomatic postoperatively, or only showed mild dyspnea but no syncope.7 Similarly, Dörge et al8 reported good early results in HOCM patients after extended surgical myectomy and reconstruction of the subvalvular mitral apparatus, with significantly decreased mortality and morbidity, and good functional capacity even in high risk patients with severe preoperative symptoms.8 Therefore, modified Morrow procedure demonstrated optimal results compared with the classic surgery, with potential long-term survival benefits and immediate alleviation of symptoms.Classic and modified Morrow procedures have been used since 1961, and many variations of this procedure have been reported with varied efficacies.9 This is because the abnormal blood flow remains, allowing symptoms to progress and raising the risk of interventricular septum perforation.9 Separation of papillary muscle can correct the abnormal connection between the musculi papillares and the front wall, posteriorly displace the mitral valve, and prevent abnormal outflow and blood flow driving force.12 In rare conditions, enlarged sail leaf valves may cause SAM symptoms to remain even after the treatment, which is an indication of folding the anterior mitral valve.13 Furthermore, Cooley et al14 suggested that folding the anterior mitral valve can reduce valve size and abnormal stresses, thus reducing the chordae tendineae and the valve slack. Mitral valve replacement, however, can eliminate symptoms of SAM at the cost of increasing the risk of severe artificial valve related complications.15 Thus, mitral valve replacement is only recommended for patients with mitral valve abnormalities, such as prolapse, calcification, or >18 mm length of anterior ventricular septum.16Based on the current understanding of HOCM mechanisms, SAM cannot be eliminated using incisions that only affect the aortic valve, even when the LV outflow is enlarged.17 Thus, accurate assessment of the anatomic features is essential for selecting the proper and optimal treatment of HOCM patients. Notably, the wider incision area offered by the modified Morrow procedure may be more optimal for treating direct papillary muscle connection and fusion to the interventricular septum, achieving long-term symptom alleviation in a large portion of patients.18 Thus, the papillary muscle fusion zone should be separated, and isolation or incision is required in case of abnormal chordae tendineae or mitral valve fiber attachment to the ventricular septum or free wall.Up to 66% of HOCM patients have structural abnormalities of the mitral valve, including increased leaflet area, leaflet elongation, or anomalous papillary muscle insertion into the anterior mitral leaflets. These conditions that can lead to death or incomplete remission of the obstruction if not recognized and managed.In conclusion, the modified Morrow septal myectomy is safe and effective in treating patients with HOCM, and is superior to the classic Morrow procedure in reducing the LV outflow tract gradient and velocity, restoring normal anatomic atrioventricular size, and alleviating the symptoms associated with HOCM.


FDG-PET/CT is widely used to diagnose cardiac inflammation such as cardiac sarcoidosis. Physiological myocardial FDG uptake often creates a problem when assessing the possible pathological glucose metabolism of the heart. Several factors, such as fasting, blood glucose, and hormone levels, influence normal myocardial glucose metabolism. The effect of outdoor temperature on myocardial FDG uptake has not been reported before. We retrospectively reviewed 29 cancer patients who underwent PET scans in warm summer months and again in cold winter months. We obtained myocardial, liver, and mediastinal standardized uptake values (SUVs) as well as quantitative cardiac heterogeneity and the myocardial FDG uptake pattern. We also compared age and body mass index to other variables. The mean myocardial FDG uptake showed no significant difference between summer and winter months. Average outdoor temperature did not correlate significantly with myocardial SUVmax in either summer or winter. The heterogeneity of myocardial FDG uptake did not differ significantly between seasons. Outdoor temperature seems to have no significant effect on myocardial FDG uptake or heterogeneity. Therefore, warming the patients prior to attending cardiac PET studies in order to reduce physiological myocardial FDG uptake seems to be unnecessary. The outside temperature between summer and winter varies greatly in Finland, exposing people to either very cold or very warm weather. The body adapts to these changes in ambient temperature in various ways; brown adipose tissue (BAT), for example, is known to be activated during the colder months , so commWe found no significant difference in myocardial FDG uptake between warm summer months and cold winter months. Our study population comprised nearly as many subjects with a higher myocardial SUV in summer than in winter as subjects with a higher myocardial SUV in winter. The change in myocardial SUVs between summer and winter throughout the study population was quite dispersed, so we observed no consistent change. Outside temperature or changes in it therefore do not seem to be a significant factor influencing the metabolism of the heart.Standard protocol requires that patients rest at least one hour before scanning, so in each case, they spend time indoors prior to their PET study. If the heart is able to adapt rapidly to warmer conditions, that is, within an hour, it could influence our findings.Because the patients in our study were all cancer patients, their fast lasted only 6 hours before the PET scan, contrary to the longer, 12-hour fast used when assessing cardiac inflammation such as CS. This is a minor limitation, as the purpose of our study was to investigate intraindividual physiological variation in myocardial FDG uptake.We did not control the time each subject spent outdoors before their scans. Our study aimed to compare scans taken in different seasons and the effect of a long time exposure to different ambient temperatures on myocardial FDG uptake. All of the subjects in this study were mobile outpatients and not in-house patients representative of a typical patient for a PET scan at our institution.We could not evaluate the possible effect of blood glucose levels on the seasonal variation in myocardial FDG uptake, since the blood glucose levels were not routinely noted at the time of the first scans. At the time of the second scan, however, we found no significant correlation between the blood glucose levels and the myocardial SUVs.In conclusion, our study shows that outside temperature changes between seasons seem to have no significant effect on myocardial FDG uptake. In addition, seasonal variance in outside temperature does not affect heterogeneity of myocardial FDG uptake. The glucose metabolism of the myocardium does not react to seasonal temperature changes in the same way as brown adipose tissue does, so such temperature changes should not be a confounding factor in myocardial FDG-PET studies, such as when a diagnosis of cardiac sarcoidosis is in question. Warming the patients prior to cardiac FDG-PET studies to lower the physiological myocardial FDG uptake seems to be unnecessary.


Heart failure (HF) is the main cause of mortality and morbidity in Western countries. Although evidence-based treatments have substantially improved outcomes, prognosis remains poor with high costs for health care systems. In patients with HF, poor dietary behaviors are associated with unsatisfactory quality of life and adverse outcome. The HF guidelines have not recommended a specific nutritional strategy. Despite the role of micronutrient deficiency it has been extensively studied, and data about the efficacy of supplementation therapy in HF are not supported by large randomized trials and there is limited evidence regarding the outcomes. The aim of the present review is to analyze the state-of-the-art of nutritional deficiencies in HF, focusing on the physiological role and the prognostic impact of micronutrient supplementation. Heart failure (HF) is the main cause of mortality and morbidity in Western countries . Acute HThe unsatisfactory quality of life emphasizes depression, discontinuation of therapy, and insufficient intake of nutrients ,7,8. In The aim of the present review is to analyze the state-of-the-art of nutritional deficiency in HF, focusing on the evidence regarding the physiological role and the prognostic impact of supplementation therapies in HF patients.The failing heart is an energy-compromised organ, characterized by “metabolic remodeling” . Abnormal-carnitine, thiamine, and taurine are associated with specific cardiomyopathies [Several micronutrients are essential cofactors of metabolic reactions and contribute to the efficiency and the appropriate utilization of energy . The genopathies . It has opathies . ConsequHF is characterized by loss of muscle mass and function (sarcopenia), and/or loss of tissue mass (cachexia) ,27. It hThe effects of supplementation in HF patients are reported in Coenzyme Q10 (CoQ10) is a natural antioxidant synthesized and diet-supplied lipid-soluble cofactor that acts in the mitochondrial membrane . CoQ10 in = 420)) [Observational studies have demonstrated that the serum CoQ10 concentration is an independent predictor of mortality in patients hospitalized for HF, which has not been confirmed in a larger cohort after adjustment for several variables ,31. Thes = 420)) . The pri = 420)) . The aut2+) utilization is impaired and myocardial contractility is negatively affected [In patients with HF, intracellular ionized calcium  in HF patients with vitamin D deficiency. The results did not show an improvement in physical performance, despite a significant increase in plasmatic vitamin D levels and a reduction in aldosterone concentration ,69,70. AIn conclusion, vitamin D supplementation may be a good target to improve frailty, fatigue and functional decline in patients with HF, but more data are necessary to recommend it for HF patients.Iron is a key element in the human metabolism, it is involved as an enzyme in oxygen transport and storage, and it is involved in the oxidative metabolism in the heart and skeletal muscles . Iron deThiamine is one of the first compounds recognized as a vitamin, known as vitamin B1. Thiamine acts as a coenzyme for oxidation-reduction reactions in the glucose metabolism and in the citric acid cycle, and as a coenzyme in the reactions catalyzed by the enzyme pyruvate dehydrogenase . The actA randomized trial conducted in patients with AHF did not show an improvement in dyspnea 4 h after thiamine administration, or on hospitalization rate and duration of hospital stay . Two recNevertheless, no studies to date were considerable enough to prove a prognostic role of thiamine deficiency correction in HF. In conclusion, thiamine supplementation has beneficial effects on cardiac function in HF patients, but larger studies are needed to test its prognostic significance.Creatine is an important energetic molecule in skeletal muscles and the heart; it is able to store and transfer high-energy phosphate. Creatine is synthesized from arginine, glycine, and methionine in the kidneys, liver, and pancreas . In healAmino acids (AAs) are fundamental compounds of proteins and their metabolism represents a complex process involving a large number of fundamental metabolites, which are found in vitamins, dietary proteins and nutritional supplements . AAs’ avTaurine is a semi-essential non-codified AA, resulting from cysteic acid decarboxylation. It is expressed at high levels in the myocytes, but its function has not been completely clarified yet . Taurinel-carnitine is a non-proteic, non-essential AA acting as a cofactor in fatty acid transport into mitochondria, acetyl-CoA production and glucose metabolism [l-carnitine supplementation improves cardiac metabolic and left ventricular (LV) function and also has a protective effect on the ischemic myocardium, preventing fatty acid ester accumulation that occurs during acute ischemic episodes [l-carnitine levels are reduced up to 50% [l-carnitine to such patients has been largely studied, even in a double-blind placebo-controlled study. Overall, they demonstrated an improvement only in exercise capacity and in LV volumes [tabolism ,119. l-cepisodes . In HF p volumes ,123,124. volumes ,126. To  volumes .Arginine is a semi-essential AA involved in creatine synthesis. It is also the substrate of nitric oxide (NO) synthase which produces NO, leading to vasodilation and restoring endothelial function . Some stAA supplementation has been recently encouraged due to the possible beneficial effects on both the myocardium and skeletal muscle . Aquilanl-carnosine is a dipeptide  present at high concentrations in the myocardium, skeletal muscles and brain [l-carnosine, added to conventional therapy, has beneficial effects on exercise performance and quality of life in stable, chronic HF [nd brain . It has nd brain ,136,137.nd brain . Recent nd brain . Our groronic HF . FurtherThe approach of supplementing HF patients with multiple micronutrients is compelling. Theoretically, it may warrant the correction of several deficiencies, thus improving multiple metabolic pathways. Witte et al. analyzed the effect of a combination of 10 different micronutrients on LV function and quality of life in 30 elderly patients with stable systolic HF due to ischemic heart disease compared to controls . This stMicronutrients may act synergistically with traditional therapies in patients with HF, improving energetic metabolism and energy transfer. Despite plenty of small evidence, large clinical trials are still lacking. In addition, to date, only a few small studies have evaluated a multiple micronutrient approach to overcome the limitations with a single-supplement method. Future research is needed to address these important questions.


Anthracyclines and Herceptin are well known amongst chemotherapeutic agents to cause cardiotoxicity. Anthracyclines, particularly in combination with, Herceptin are seen in studies to cause cumulative, dose-related, progressive myocardial damage with decrease in left ventricular(LV) ejection fraction (EF) ultimately leading to clinical heart failure, which can be irreversible. There is lack of appropriate guidelines to monitor cardiac function in these patients. We hypothesized that changes in tissue distribution of gadolinium (Gd) and/or myocardial strain identified using (Gd)-enhanced cardiac magnetic resonance (CMR) could help identify early myocardial damage which can lead to systolic dysfunction.Patients naïve to chemotherapy, with newly diagnosed cancer for which athracycline or Herceptin based regimen was used, and who had normal baseline LV systolic function were recruited in the study. CMR was conducted at three time points: before chemotherapy, 20 days after completion of first round and 1 to 6 months after completion of all chemotherapy treatment. CMR measures of LV systolic and diastolic function, strain (cine dense imaging), T2 mapping, VENC (velocity encoded) imaging, and distribution of gadolinium (Gd) contrast via T1 mapping and late gadolinium enhancement were examined. High sensitive troponins were measured at the time of the CMRs.We present data on our initial 28 patients. The mean age of our patient population is 48 ± 11 years, 86% are females, 24 have breast cancer while 2, 1 and 1 respectively have leukemia, lymphoma and sarcoma. Twenty one were treated with anthracyclines and 7 were on Herceptin. None of the patients had combined therapy. 24 patients have completed their 1st post-chemotherapy CMR, while 13(46%) have completed all three. The mean anthracycline dose was 174 ± 189 mg. LV EF drop of < 50% was noted only in 1 patient (3.5%). However diastolic dysfunction based on mitral E/A ratio(< 1 or > 2) was detected in 33% of the patients. In patients with at least one follow up CMR study, no significant trends in LV volumes, strain values or changes in the volume of distribution of gadolinium were observed  drop in left ventricular ejection fraction was seen in our patients treated with Anthracyclines or Herceptin. Thus, we were unable to show a benefit of CMR in detecting predisposing factors to an EF decline. However with further follow-up, additional patients may demonstrate a decline. The reduced incidence of LV dysfunction compared to historical incidence may be due to a recent shift in oncology practice with regards to the use of these chemotherapeutic agents, including avoiding simultaneous use of Anthracyclines with Herceptin and reduction in the maximum Anthracyclines dosage.AHA (American heart association).