During the last 20 years, the management of heart failure has significantly improved by means of new pharmacotherapies, more timely invasive treatments and device assisted therapies. Indeed, advances in mechanical support, namely with the development of more efficient left ventricular assist devices (LVAD), and the total artificial heart have reduced mortality and morbidity in patients with end-stage heart failure awaiting for transplantation. However, the transplant cannot be the only solution, due to an insufficient number of available donors, but also because of the high number of patients who are not candidates for severe comorbidities or advanced age. New perspectives are emerging in which the VAD is no longer conceived only as a “Bridge to Transplant”, but is now seen as a destination therapy. In this review, the main VAD classification, current basic indications, functioning modalities, main limitations of surgical VAD and the total artificial heart development are described. Heart failure (HF) is one of the main causes of death in Western Countries. Its prevalence  increases exponentially with age. Over the next 3 decades, the population of individuals aged ≥65 years with HF is expected to be more than double, so we can assume that the number of individuals at risk of HF will increase dramatically in the near future .Because of the impossibility of carrying out a conventional surgical procedure in refractory HF, the only therapeutical solution in this case is that of a cardiac transplantation or, if the patient is hemodynamically unstable, the implantation of a ventricular assist device (VAD) as a bridge to transplant support . This teNowadays, the main objectives of a mechanical circulatory support program is to hemodynamically stabilize patients with acute or chronic HF and to preserve the organ function in order not to preclude subsequent therapeutical options. Patients with end stage HF usually have symptoms at rest and a significant impairment of quality of life and are encumbered by a 1-year mortality of approximately 50% . These pThe term VAD means a mechanical circulatory support that is temporarily or permanently able to replace cardiac function in response to the needs of the organism. In other words it substitutes or supports a heart that is not able to perform its pump function. VADs are designed to assist either the right (RVAD) or left (LVAD) ventricle, or both at once (BiVAD); VADs need to be clearly distinguished from artificial hearts, which are designed to take over cardiac function completely.The pumps used in VADs can be divided into two main categories: pulsatile pumps, that mimic the natural pulsing action of the heart, and continuous flow pumps. On the basis of the implant location, VADs can be distinguished in extracorporeal, paracorporeal and intracorporeal devices.In these devices, the inflow and outflow cannulas are equipped with artificial valves to allow unidirectional flow; the artificial ventricular pump receives blood from the cardiac chambers through the inflow cannula, that can be placed in the left or right atrium or in the ventricular apex; the outflow cannula returns blood to either the aorta  or pulmonary artery . The pump is connected to a pneumatic driver: the driver provides alternating pneumatic pressure and vacuum in a pulse-like fashion for ejection and filling. In general, the filling of the artificial ventricle depends on the atrial filling pressure and on the entity of the suction. Output of the pump depends on intravascular volume status and downstream vascular resistances.The first generation devices were extracorporeal: they were located externally to the patient and mounted on a pole. They were designed for short-term use and burdened with a high rate of complications; in addition, the patient was compelled to stay in bed. An example is the system Abiomed BVS 5000.Subsequently, paracorporeal VADs (PVADs) have been developed. There are several advantages in the design of PVADs: the paracorporeal location allows for right, left or biventricular support and ease of exchange in the event of device malfunction, thrombosis or infection; what is more, a portable driver is available so that the patient can be discharged from hospital. These systems, still in use today, can act as a “bridge to transplant” or “bridge to recovery” support. The most used devices of this category are Berlin Heart Excor and Thoratec.A significant advance is represented by intracorporeal systems (IVADs): these are implantable pulsatile pumps, pneumatically or electrically driven. These devices can support only the left ventricle and are equipped with unidirectional valves. Because of their dimensions, the implant is abdominal, intra- or extraperitoneal. The pump is connected to the cardiac chambers through inflow and outflow cannulas. A percutaneous line connects the device to an external driver. Nowadays, the most used models of this category are Heartmate I XVE and Novacor. The main disadvantages are represented by their size , the presence of longer lines of connection (which may be a source of infections) and the high rate of thromboembolic events .There has been a trend in the evolution in the VADs from extracorporeal pulsatile to implantable pulsatile to implantable continuous flow. Newer generation LVADs have been developed with continuous flow, rotary pump technology and are smaller and quieter than older pulsatile volume displacement LVADs. Continuous flow VADs normally use either centrifugal pumps or an axial flow pump: unlike the other pumps, which completely unload the ventricle, many patients with an axial flow pump maintain a pulsatile pattern of blood flow. The partial dependence of these devices from gradients of pump (pressure difference between inflow and outflow) in terms of induced flows, suggests using them when a minimum residual left ventricular function is guaranteed, stressing that they are only LVAD.Obviously, the higher the residue pressure produced from the ventricle, the lower the gradients of pump.Their small size allows implantation into smaller patients (with possible developments as pediatric assist device in the near future), makes placement easier and makes them extremely interesting as a destination therapy. This category of devices can be classified on the basis of the implant position: on one side the Impella  system and the extracorporeal and paracorporeal centrifugal pumps, on the other the most used intracorporeal axial pumps such as Berlin Heart Incor, De Bakey, Jarvik 2000, Heartmate II.On April 4, 1969, Liotta and Cooley replaced a dying man's heart with a mechanical heart inside the chest at The Texas Heart Institute in Houston as a bridge for a transplantation. The patient woke up and recovered well. After 64 hours, the pneumatic-powered artificial heart was removed and replaced by a donor heart. The TAH is the most developed implantable pump. It replaces the patient's heart and the ventricular function. It is used as a bridge for a transplantation. The patient woke up and recovered well. After 64 hours, the pneumatic-powered artificial heart was removed and replaced by a donor heart. The TAH is the most developed implantable pump. It replaces the patient's heart and the ventricular function. It is used as a bridge to transplantation support. It's important to ensure a balance between the stroke volume of both ventricles and adjust the flow to the physiological needs of the organism. Among TAH, two models are currently FDA approved: AbiomedAbioCor Total Artificial Heart and Jarvik 7-CardioWest. Their clinical use is far from being widespread, but important developments are expected in the future. The only situations in which their application is indicated are represented by patients waiting for cardiac transplantation in which no other kind of assistance is possible.Depending on the use, the mechanical circulatory support can be distinguished in temporary, mid-term and long-term .To date, there are no consensus guidelines for VAD implantation . HoweverCurrently, VADs seem to be significantly underused because of their elevated costs, not considering their therapeutical and economic advantages . Strong The improvement in results related to the use of latest generation VADs leads to reconsider the clinical care pathways of patients in order to find better solutions. The relatively young patients waiting for transplantation should be subjected to mechanical assistance because otherwise they have a poor prognosis . Older pThe most important factor for improving patient outcomes after LVAD is careful patient selection. In literature, people most likely to develop complications are those with: age > 60-70 years old; previous cardiosurgical interventions; liver disease; kidney failure with oliguria; infections; tumors; need for other mechanical support such as ventilation or ultrafiltration; cachexia as an index of chronic HF . The evaMost of the complications related to the VAD are due to the therapies and to the technical aspects. The postoperative bleeding rate is rather high after VAD implantation, because of the aggressive anticoagulation regimen . PatientThe most used classification for HF, the NYHA and the ACC/AHA , use to The fourth annual report  summarizThe fifth annual report  summarizRecent technological advances improved outcomes and led to a greater utilization of VADs in the vast number of patients impaired with advanced HF and who are not candidates for transplants. In the future, thanks to the development of innovative solutions that enable the miniaturization of power systems and the total deliverability of the VAD, it is conceivable that, given the small number of donations , the VAD


Background: Participation in triathlon competitions has increased in recent years. Many studies have described left or right ventricular injury in endurance athletes. The goal of this study was to examine the right and left ventricular cardiac structures and function and dynamic cardio-pulmonary performance in a large cohort of middle- and long-distance triathletes. Methods: 87 triathletes  were examined using spiroergometry and echocardiography. The inclusion criterion was participation in at least one middle- or long distance triathlon. Results: Male triathletes showed a maximum oxygen absorption of 58.1 ± 8.6 mL/min/kg , maximum ergometer performance of 347.8 ± 49.9 W . Left ventricular ejection fraction (EF) was normal  and systolic right ventricular area change fraction (RV AFC%) showed normal values . Doppler indices of diastolic function were normal in both groups. With respect to the echocardiographic readings the left ventricular mass for males and females were 217.7 ± 41.6 g and 145.9 ± 31.3 g, respectively. The relative wall thickness for males was 0.50 ± 0.07, whereas it was 0.47 ± 0.09 for females. The probability of left ventricular mass >220 g increased with higher blood pressure during exercise  or with higher training volume . Conclusions: Right or left ventricular dysfunction could not be found, although the maximal participation in triathlon competitions was 29 years. A left ventricular mass >220 g is more likely to occur with higher arterial pressure during exercise and with a higher training volume. The possibility of myocardial damage due to physical activity has been known since ancient times. According to legend, a soldier named Pheidippides (more likely Philippides) dropped dead after running to Athens from the battle at Marathon with the news of victory . A soldiSome papers have reported on common deaths in triathlon competitions  and exer-Are there signs of cardiac “fatigue” when triathletes have trained hard over a period of years? Are there risks for right ventricular or left ventricular dysfunction for amateur athletes?-What type of athletes’ hearts or what type of hypertrophy, concentric or eccentric, is found most often in triathletes?-Are there signs of reduced physiological performance?Triathlon is an endurance sport, especially when performed in middle- and long-distance formats , mainly under aerobic conditions. It is particularly important for triathletes to perform at sub-maximal levels over a long period to avoid reaching a state of exhaustion ,11. AmatEighty-seven triathletes were examined, including 54 males and 33 females. All triathletes were examined by echocardiography  and spiroergometry. Triathletes underwent their annual medical check-up or examination for training preparation in 2011/2012, which would have been performed as part of the normal clinical routine. All examinations were performed by Dr. Roman Leischik or Dr. Norman Spelsberg. The participants were invited to participate in the study during their routine check-up or routine training preparation, and announcements in social media and triathlon clubs were also made. Dr. Roman Leischik is the medical supervisor of the Triathlon Club PV-Witten since 2007. This study was prospective in design.A Vivid 7 echocardiograph, produced by General Electric  was used for the examinations. The Ergobike 8I, produced by Daum , and the Metalizer 3B, produced by Cortex , were used for the spiroergometric examination.2/min/kg at the aerobic threshold). The 20 males and 15 females with the highest values were designated as elite.To compare the data from elite triathletes with those of non-elite triathletes, both males and females were divided into two groups according to their aerobic capacity  were classified as elite.The spiroergometric analyses were conducted according to the literature. VAT was determined as the first non-linear increase in the ventilatory equivalent for oxygen without a simultaneous increase of the ventilatory equivalent for COndations ,22. VO2mAll athletes gave verbal and written consent to voluntary performance testing and for use of their data in this study. All data were anonymized. Triathletes underwent their annual medical check-up or examination for training preparation in 2011/2012, which would have been performed in any case as it is clinical routine. The study was approved as a doctoral dissertation by the Dissertation Audit Committee of the University Witten/Herdecke. All examinations (echocardiography and spiroergometry) were a part of the routine clinical and diagnostic care for the triathletes. All examinations were performed by two experienced investigators (see chapter methods). This study did not introduce any pharmaceutical interventions or changes in the clinical course of the triathletes.The entire statistical analysis was designed as follows. Stata/IC 11.2 for Windows was used for data preparation and statistical analysis. The Mann-Whitney U-Test was used to compare the groups. The Kaplan-Meier product limit method and the Cox proportional hazards model were used to estimate the odds ratios for analysis of the relationship between arterial pressure and the probability of a left ventricular muscle mass (LVM) >220 g. All statistical tests were two-sided, with a significance level of 0.05.Anthropometric data and the general cardiac parameters of the participants are listed in vs. 22.8%). Heart cavities and stroke volume are significant larger, without differences in systolic function (EF) or diastolic function (Doppler parameters).Male triathletes have significant greater weight, BMI, and BSA than female triathletes, but lower body fat  were measured at the maximal watts level (Wmax). The odds ratios showed a significant relationship between the arterial pressure values during exercise (at the aerobic and anaerobic threshold). There was an additional relationship between the overall training time and a LVM >220 g  at the peak capacity (maximum wattage), but this difference was not significant. This difference was found only in males; the average arterial pressure values for females were not different and did not increase. Indicators of an increase in wall thickness additional other than dilatation have been confirmed in a study of female athletes [et al. [In the present study, odds ratio analysis showed a relationship between myocardial thickening and exercise arterial pressure. Intense, long-term training with exercise-induced blood pressure elevation can lead to hypertrophy that mimics the conditions of pathological arterial pressure changes. The male triathletes with a wall thickness >1.2 cm had higher arterial pressure  averageathletes  was at V2max for males 64 ± 6.7 vs. 54.9 ± 6.7 mL/kg−1·min−1 and VO2 for VAT 53.1 ± vs. 39.8 ± 5.5 mL/kg−1·min−1). A similar difference in the range of VO2max was observed for female athletes  or 35 mL/kg−1·min−1 . In terms of the echocardiographic measurement, we can expect concentric remodeling/concentric hypertrophy. Valve dysfunctions are possible but rare. Accordingly, the blood pressure values should be thoroughly examined during routine or pre-event check-up. We conclude that the relationship between myocardial thickening and arterial blood pressure during exercise remains an open issue. With respect to echocardiography, we did not observe cardiac dysfunction in our athletes.The data of the present study on German triathletes participating in the middle- and long-distance events allow for the practical use of this information as a routine part of sports medicine in classifying the efficiency of performance diagnostic centers. In males, the training goals aim for an aerobic capacity of VAT = 45 mL/kgca. 11 h).The idea of exercise-induced cardiac disease was suggested by Heidbüchel  and LaGeChlamydia pneumoniae [et al. [There is no doubt that athletes have a higher incidence of atrial fibrillation  and bradeumoniae  or othereumoniae . Abnormaeumoniae . Furthereumoniae ,74 is ad [et al.  reportedGiven the value of competitive sporting activities to hobby-athletes, the media, and other industries, physical activity in the general population is of fundamental importance . Further


Type 2 diabetes (T2D) and obesity are associated with nonalcoholic fatty liver disease, cardiomyopathy, and cardiovascular mortality. Both show stronger links between ectopic and visceral fat deposition, and an increased cardiometabolic risk compared with subcutaneous fat.This study investigated whether lean patients (Ln) with T2D exhibit increased ectopic and visceral fat deposition and whether these are linked to cardiac and hepatic changes.1- and T2*-mapping yielding “iron-corrected T1” [cT1].Twenty-seven obese patients (Ob) with T2D, 15 Ln-T2D, and 12 normal-weight control subjects were studied. Subjects underwent cardiac computed tomography, cardiac magnetic resonance imaging (MRI), proton and phosphorus MR spectroscopy, and multiparametric liver MR, including hepatic proton MRS, T1) was only evident in Ob-T2D patients. cT1 correlated with hepatic and epicardial fat .Diabetes, with or without obesity, was associated with increased myocardial triglyceride content (p = 0.01), increased hepatic triglyceride content (p = 0.04), and impaired myocardial energetics (p = 0.04). Although cardiac structural changes, steatosis, and energetics were similar between the T2D groups, epicardial fat (p = 0.04), hepatic triglyceride (p = 0.01), and insulin resistance (p = 0.03) were higher in Ob-T2D. Epicardial fat, hepatic triglyceride, and insulin resistance correlated negatively with systolic strain and diastolic strain rates, which were only significantly impaired in Ob-T2D . Fibroinflammatory liver disease (elevated cTIrrespective of body mass index, diabetes is related to significant abnormalities in cardiac structure, energetics, and cardiac and hepatic steatosis. Obese patients with T2D show a greater propensity for ectopic and visceral fat deposition. Type 2 diabetes (T2D) and obesity are both associated with nonalcoholic fatty liver disease (NAFLD), cardiomyopathy Ectopic and visceral fat storage may be linked to insulin resistance, and it is widely known that insulin resistance is the strongest predictor of development of diabetes 1H-MRS) allows quantification of lipid content in the liver and the heart. Multiparametric magnetic resonance (MR) of the liver, including 1H-MRS for assessment of steatosis and T1 and T2* mapping (yielding iron corrected T1 [cT1]) Epicardial adipose tissue, a form of visceral fat, may affect the underlying myocardium by secreting a wide range of adipokines 31P-MRS) allows noninvasive assessment of the PCr/ATP.Myocardial energetic compromise is an important feature of both the diabetic 1H-MRS, and 31P-MRS to assess and compare epicardial, hepatic, and myocardial fat deposition; hepatic fibroinflammatory changes; and cardiac structure, function, and energetics in lean and obese patients (Ob) with T2D and in control subjects without diabetes.Our primary aim was to test the hypothesis that lean patients (Ln) with T2D exhibit increased ectopic and visceral fat deposition. Our secondary aim was to test whether or not ectopic and visceral adiposity in diabetes is associated with insulin resistance and cardiac and hepatic changes. We used cardiac CT, multiparametric liver magnetic resonance imaging (MRI), cardiac MRI, The study was approved by the National Research Ethics Committee (Ref 13/SW/0257), and informed written consent was obtained from each participant. Patients were recruited from general practice surgeries in Oxfordshire, United Kingdom. A total of 27 Ob-T2D, 15 Ln-T2D, and 12 healthy normal weight control subjects were recruited to the study. We have previously reported changes in myocardial energetics, triglyceride content, and left ventricular (LV) structure and function in patients with diabetes compared with healthy volunteers 2); if they were tobacco smokers; if their alcohol intake was above 21 units in a week for men or 14 units for women; or if they were insulin dependent.Subjects were excluded if they had a previous diagnosis of cardiovascular or liver disease, hypertension (resting systolic blood pressure >140 mm Hg and diastolic blood pressure >90 mm Hg), contraindications to MRI, ischemic changes on 12-lead electrocardiography, or renal impairment , or hypertension and were not taking any medications. Study assessments were carried out on a single visit for the healthy control subjects and over 2 or 3 visits for patients with T2D, depending on individuals’ consent for attending cardiac CT assessments .−1])/22.5 Height and weight were recorded and BMI was calculated. Brachial blood pressure was recorded as an average of 3 supine measures taken over 10 min . Fasting venous blood was drawn for glucose, insulin, hemoglobin A1c (HbA1c), triglycerides, renal function, liver function, and free fatty acids. Insulin levels and HbA1c were checked in the patients with diabetes, but not in control subjects. Homeostasis model assessment of insulin resistance (HOMA-IR) was used to evaluate insulin resistance using the following equation:  was offered to patients with diabetes to exclude obstructive coronary artery disease  and for assessment of epicardial fat volumes. CCTA was performed with a GE VCT 64 slice scanner  and a Snapshot Pulse protocol with prospective electrocardiographic triggering. Participants received beta-blockade (intravenous metoprolol) and sublingual glyceryl trinitrate prior to the scan to achieve a heart rate of <65 beats/min. During the CCTA acquisition, 70 ml of iodinated contrast  was injected at a rate of 6 ml/s followed by a 50-ml saline flush. The scan covered a region from 1 to 2 cm above the left main coronary artery to 1 to 2 cm below the myocardial apex in a single breath hold.CT images were reconstructed using medium-soft kernel (standard) with slice thickness of 0.625 mm and then transferred to a dedicated workstation for image processing . The adipose tissue volume was quantified using contrast-enhanced CT images. The layer of the epicardium was manually traced, and a 3-dimensional image was constructed using a semiautomated method. The volume was then calculated by a blinded operator (S.T.) and defined as the tissue with attenuation of −190 to −30 HU.All LV imaging was performed on a 3.0-T MR system . Images for LV volumes and diastolic function were acquired using a steady-state free precession sequence and analyzed using cmr42 . To determine midventricular systolic circumferential strain and diastolic strain rate, myocardial tagging was performed 31P-MRS was performed to obtain the rest PCr/ATP from a voxel placed in the midventricular septum, with the subjects lying prone with their heart over the center of the 31P heart/liver coil in the isocenter of the magnet. 31P-MRS post-processing analysis was performed using in-house software within Matlab version R2012a . A more detailed description of the cardiac 31P-MRS acquisition parameters is included in the 1H-MRS was obtained from the midinterventricular septum. Liver triglyceride content was measured using 1H-MRS, avoiding vascular and biliary structures. Spectroscopic acquisitions were performed using electrocardiographic trigger. Water-suppressed spectra were acquired to measure myocardial and liver triglyceride content, and spectra without water suppression were acquired and used as an internal standard. Spectra were analyzed using Matlab and the AMARES algorithm in the Java-based Magnetic Resonance User Interface. Myocardial and liver triglyceride contents were calculated as a percentage relative to water:  × 100. A more detailed description of the 1H-MRS acquisition parameters is included in the Myocardial 1 and T2* MR maps were acquired for the estimation of extracellular fluid and liver iron, respectively. Patients fasted overnight prior to their MRI scans.The liver multiparametric MR protocol has been previously described 1 relaxation time increases with increases in extracellular fluid, such as in fibrosis and inflammation. However, the presence of iron, which can be accurately measured from T2* maps, has an opposing effect on the T1. An algorithm has been created that allows for the bias introduced by elevated iron to be removed from the T1 measurements, yielding the cT1.T1 from T1 and T2* maps. For this study, the LiverMultiScan was used to analyze anonymized images by investigators blinded to the clinical data . cT1 was measured in a single, operator-defined region of interest away from vascular and biliary structures.LiverMultiScan  is a software product specifically developed to measure cTt test was used for comparison of normally distributed datasets where data were obtained for only 2 T2D groups. Significance was defined as p < 0.05.All statistical analysis was performed with commercially available software packages . All data were checked for normality using the Kolmogorov-Smirnov test and presented as mean ± SD. Comparisons between the 3 groups were performed by 1-way analysis of variance with post hoc Bonferroni corrections. Bivariate correlations were performed using the Pearson or Spearman method as appropriate. The Student 2, mean diabetes duration 6.1 ± 4.7 years, mean HbA1c 7.7 ± 1.4%), 15 Ln-T2D patients , and 12 healthy volunteers  were recruited. Participants in all groups were of similar age and sex, and there were no significant differences in blood pressure, diabetes duration, diabetes treatment, or metabolic profile between the 2 diabetes groups . Epicardial fat volume assessment was carried out in 33 patients (79% of the study patients) who have opted for CCTA. The Ob-T2D group had higher epicardial fat volumes compared with the Ln-T2D group , whereas cT1 in the Ob-T2D group was significantly increased compared with the Ln-T2D group (p = 0.004) and control subjects (p < 0.001), indicating significant fibroinflammatory liver disease in this group. 1 across the study cohorts. There was a positive correlation between the hepatic cT1 and hepatic triglyceride content . Importantly, despite the presence of hepatic steatosis and fibroinflammatory changes in the Ob-T2D group, there was no significant difference in liver enzymes compared with control subjects, and there was no association between liver cT1 and liver enzymes. Alanine aminotransferase levels were only minimally elevated (>45 to <80 IU/l) in 5 Ob-T2D patients and were normal in all other patients. The 1H-MR spectra, and a liver T1 map in a volunteer and in a lean and an obese patient with T2D.Mean cT1 , and there was a negative correlation between HOMA-IR and peak circumferential systolic strain . Furthermore, peak circumferential systolic strain also correlated negatively with the hepatic triglyceride  and epicardial fat volumes . Similarly, diastolic strain rate correlated negatively with hepatic triglyceride  and epicardial fat volumes . Myocardial triglyceride did not correlate with epicardial fat volumes  or with hepatic triglyceride .Insulin resistance, measured by HOMA-IR, was significantly higher in the Ob-T2D compared with the Ln-T2D group (p = 0.03). When investigating all T2D subjects, there was a positive correlation between the HOMA-IR and epicardial fat volumes , hepatic triglyceride , and hepatic cTThis study demonstrates for the first time that diabetes, even in the absence of obesity, is associated with significant cardiac structural and metabolic abnormalities, whereas significant functional changes, such as reductions in peak systolic strain and diastolic strain rates, are only evident in obese patients with diabetes. Furthermore, we show that those patients with diabetes who are also obese have higher epicardial fat volumes, significant NAFLD, and higher insulin resistance. Importantly, we demonstrate here that the degree of hepatic and epicardial fat accumulation is associated with cardiac contractile dysfunction in diabetes. We confirm the findings of previous studies showing the association between epicardial fat deposition and insulin resistance Finally, as is widely known, the spectrum of NAFLD ranges from fatty liver alone to nonalcoholic steatohepatitis Our results suggest that Ln-T2D patients are likely to have less pronounced insulin resistance, lower levels of epicardial and hepatic fat accumulation, and better cardiac function than Ob-T2D patients. It is now widely accepted that adipose tissue is a dominant regulator of lipid and glucose metabolism Epicardial adipose tissue has dichotomous functional characteristics, both adverse and protective, interacting locally with the coronary arteries and the myocardium through paracrine and vasocrine pathways. Under physiological conditions, epicardial fat supplies heat to the myocardium and exerts a protective effect on the coronary arteries 1H-MRS in a large cohort of patients with T2D and were the first to show that hepatic triglyceride was not predictive of myocardial triglyceride In our study, the dissociation of myocardial steatosis from epicardial and liver fat is in keeping with a previous study in patients without diabetes and supports the hypothesis that myocardial lipid accumulation may represent a separate entity that is influenced by factors beyond visceral adiposity 1 compared with Ln-T2D patients and healthy volunteers. This would indicate a greater burden of fibroinflammatory liver disease in this group of patients who should be prioritized for NAFLD screening in clinical practice. Importantly, these differences were present on imaging but not on alanine aminotransferase levels, suggesting that alanine aminotransferase alone is not a sensitive screening test for the presence of NAFLD in these patients. It has previously been shown that liver cT1 is associated with fibrosis Our results suggest that Ln-T2D patients are more likely to have simple steatosis and Ob-T2D patients are more likely to have steatohepatitis. Our study is the first to date to noninvasively assess the severity of liver damage using a multiparametric MRI protocol in Ln- and Ob-T2D patients and to determine the effect of fibroinflammatory liver disease on the cardiac phenotype. We have demonstrated that asymptomatic Ob-T2D patients have significantly higher liver cTNAFLD is defined as excessive fat accumulation in the liver (>5.6%) This study is limited by a relatively small sample size. Of 42 patients with T2D, 9 patients (21%) did not consent to have CCTA performed, and it is possible that occult coronary artery disease could be present in this minority of patients. CCTA was not performed in normal volunteers to avoid unnecessary radiation exposure. Significant coronary artery disease was deemed to be unlikely in this normal cohort, and epicardial fat volumes were therefore only assessed and compared in Ob- and Ln-T2D patients.For assessment of liver disease, we have not used liver biopsy, the current gold standard, because it is invasive and limited by sampling and observer-dependent variability Although the differences in mean peak systolic strain and diastolic strain rates in Ln-T2D compared with control subjects did not reach statistical significance, this may be due to the relatively small sample size. Larger studies of Ln-T2D patients are needed to confirm this. Although the release of adipokines including adiponectin and leptin has been considered among the important actions of adipocytes, we did not assess circulating levels of adiponectin or leptin.There is evidence of a role for the sympathetic nervous system in the relationship between insulin and hypertension in obese patients with hypertension Finally, the observational nature of our findings precludes inferences of causality. Additional research is necessary to further delineate the relationship between ectopic and visceral adiposity with potential systemic effects such as insulin resistance and their role in the development of cardiac dysfunction in patients with T2D.PerspectivesCOMPETENCY IN MEDICAL KNOWLEDGE: Diabetes is associated with abnormalities of cardiac structure, energetics, and steatosis irrespective of BMI. Ob-T2D patients have a greater propensity for ectopic and visceral fat deposition, cardiac dysfunction, fibroinflammatory liver disease, and insulin resistance.TRANSLATIONAL OUTLOOK: Further studies are needed to delineate the mechanistic relationships between ectopic and visceral adiposity, insulin resistance, and cardiac dysfunction in patients with T2D.Ob-T2D patients show a greater propensity than Ln-T2D patients for ectopic and visceral fat deposition that is associated with cardiac contractile dysfunction and fibroinflammatory liver disease.


Native T1 is increased in acute myocardial infarction. Extracellular volume fraction (ECV) can be calculated using T1 mapping following contrast. The timing of imaging following contrast in acute myocardial infarction is not established. 15 minutes has been proposed for conditions with and ECV < 0.4. 15 minutes may not be applicable in acute myocardial infarction due to infarct characteristics (ie MVO) impacting on contrast pharmacokinetics and the relatively higher ECV. The aim of this study was to determine if ECV is affected by the timing of imaging for post contrast T1 maps in STEMI.30 consecutive patients presenting with ST segment elevation myocardial infarction to the Bristol Heart Institute Primary PCI service were approached for inclusion in the study. Patients had a CMR scan day 2 following STEMI. Native T1 was assessed on T1 mapping . Post contrast T1 mapping was performed at 15 and 25 minutes following contrast administration. ECV was calculated as: Myocardial ECV = (1−hematocrit) × (ΔR1myocardium/Δ R1blood), where R1 = 1/T1. The difference in ECV at both time points was assessed by paired t-test. All patients gave written informed consent. The study was approved by the local ethics committee.2=0.90, r=0.95). However, there is a significant difference between ECV calculated at 15 minutes  and 25 minutes , p<0.0001(Figure There was good correlation of ECV calculated from post contrast T1 mapping at 15 and 25 minutes p<0.0001 (rIn acute myocardial infarction, timing of post contrast T1 mapping affects ECV calculation.This study was funded by the National Institute for Health Research Biomedical Research Unit in Cardiovascular Disease at the University Hospitals Bristol NHS Foundation Trust and the University of Bristol.


Diastolic wall strain (DWS), defined using posterior wall thickness (PWT) measurements from standard echocardiographic images (DWS = [PWT(systole)-PWT(diastole)]/PWT(systole)), has been proposed as a marker of left ventricular (LV) diastolic stiffness. However, the equation for DWS is closely related to systolic radial strain, and whether DWS is associated with abnormal cardiac mechanics (reduced systolic strains and diastolic tissue velocities) is unknown. We sought to determine the relationship between DWS and systolic and diastolic cardiac mechanics.We calculated DWS and performed speckle-tracking analysis in a large population- and family-based study . We measured global longitudinal, circumferential, and radial strain  and early diastolic (e’) tissue velocities, and we determined the independent association of DWS with cardiac mechanics using linear mixed effects models to account for relatedness among study participants. We also prospectively performed receiver-operating characteristic (ROC) analysis of DWS for the detection of abnormal cardiac mechanics in a separate, prospective validation study (N = 35).20, P = 0.97). On prospective speckle-tracking analysis, DWS correlated well with GLS, GCS, and GRS . C-statistics for DWS as a diagnostic test for abnormal GLS, GCS, and GRS were: 0.78, 0.79, and 0.84, respectively.In HyperGEN , mean DWS was 0.38 ± 0.05. DWS decreased with increasing comorbidity burden . DWS was independently associated with GLS, GCS, GRS, and e’ velocity (adjusted P < 0.05) but not LV chamber compliance  tissue velocities but not LV chamber compliance. Left ventricular (LV) diastolic dysfunction is common in the general population, and is associated with incident heart failure and increased mortality, 2. The Recently, a non-invasive, load-independent, and reproducible estimator of LV stiffness using 2-dimensional (2D) echocardiography, namely diastolic wall strain (DWS), has been proposed, 4. DWS,However, DWS, as it name implies, is closely related to systolic strain. DWS, calculated as [(PWTs) – (PWTd)]/(PWTs), can be simplified purely in terms of myocardial  strain, defined as [(PWTs) – (PWTd)]/(PWTd). By rearranging the two equations, DWS can be expressed as [/]. Takeda Though Takeda et al. demonstrated that DWS correlates moderately well  with invasive measurements of myocardial stiffness. DWS canThe evaluation of echocardiograms from the Hypertension Genetic Epidemiology Network (HyperGEN) study permits a robust assessment of the relationship between DWS and cardiac mechanics. HyperGEN, conducted from 1996–2002, originally sought to determine the genetic basis for familial hypertension. Advantages of the HyperGEN study include a bi-racial sample of approximately 3600 participants, comprehensive clinical and laboratory data collection, and 2D/Doppler echocardiographic data. Though Therefore, we sought to determine the association of DWS with LV systolic and diastolic mechanics. We hypothesized that DWS correlates with both systolic and diastolic measures of LV performance. We further hypothesized that reduced DWS is associated with systolic LV mechanics , even when adjusting for LV geometry and echocardiographic indices of filling pressures and myocardial relaxation.HyperGEN, part of the National Institutes of Health Family Blood Pressure Program (FBPP), is a cross sectional-study consisting of five U.S. sites, while four participated in an ancillary echocardiographic study . The goal of HyperGEN was to identify and characterize the genetic basis of familial hypertension; complete details of the HyperGEN study design have been reported previously. Study e2. Chronic kidney disease was defined by an estimated glomerular filtration rate ≤ 60 ml/min/1.73 m2.Demographic, clinical, and laboratory data were collected during the initial HyperGEN visit. Height, weight, blood pressure, and waist circumference were measured by a technician. Histories of myocardial infarction, transient ischemic attack, or stroke were obtained by self-report. Diabetes mellitus was defined by fasting glucose ≥ 126 mg/dl, use of hypoglycemic medication, or a self-reported history. Obesity was defined by a body mass index ≥ 30 kg/m2 in women or > 115 g/m2 in men. DWS was calculated as [(PWTs) – (PWTd)/(PWTs)], 4. Part/(PWTs)], 4.Archived echocardiograms in analog format were converted to digital format using the TIMS 2000 DICOM System . Cine loops of 2–4 cardiac cycles from the parasternal short axis (papillary muscle level) and apical four chamber views were digitized at a frame rate of 30 to 40 frames per second and stored offline in DICOM format. Each study was assessed for image quality by an experienced operator, blinded to all other clinical and echocardiographic data, using a 4-point scale based on the degree of endocardial border visualized , similar to scales used previously, 14.Digitized cine loops were analyzed using 2D wall motion tracking software . After isolating the highest quality cardiac cycle, the endocardial and epicardial borders were traced at end-systole in each view. Computerized speckle-tracking analysis was performed, and endocardial and epicardial border tracings were manually adjusted to optimize tracking.Components of LV strain  and tissue velocities  values were recorded. For ease of display, all strain values were converted to absolute values . Lower absolute strain values, lower e’ tissue velocities, and higher E/e’ ratio were used to indicate worse cardiac function. Speckle-tracking tissue velocities were used instead of tissue Doppler velocities since HyperGEN echocardiograms were acquired at a time prior widespread use of tissue Doppler technology. However, we converted speckle-tracking echocardiography-derived tissue velocities into tissue Doppler velocities using a regression equation constructed from a separate cohort of 100 prospectively studied patients referred to the Bluhm Cardiovascular Institute  for clinically indicated echocardiography with tissue Doppler imaging . All patients gave written, informed consent, and the Northwestern University Institutional Review Board approved the study of these patients. These echocardiograms were analyzed using the same software used in the analysis of HyperGEN participants , and velocities from the 2 methods (speckle-tracking vs. tissue Doppler) were compared. A regression equation was constructed for each tissue velocity . A validation of the digitization and speckle-tracking techniques employed here has been published elsewhere deceleration time).Figures Table To determine the clinical utility of DWS as a predictor of abnormal myocardial strain, we conducted a prospective validation study using digital speckle-tracking echocardiography at high frame rates of 50–70 fps. Scatterplots depicting the relationship between DWS and peak systolic strains in this study are shown in Figure In one of the largest speckle-tracking studies to date, using echocardiograms from 1907 HyperGEN participants, we found that DWS correlated with both systolic and diastolic indices of LV performance and was independently associated with several indices of abnormal cardiac mechanics. These findings were significant after controlling for EF, LV mass index, and even diastolic indices of impaired relation (tissue e’ velocity) and filling pressures (E/e’ ratio). Our study is the first to comprehensively examine the association of DWS with systolic and diastolic echocardiographic parameters as well as the first to show the association of DWS with indices of systolic and diastolic cardiac mechanics. DWS, we conclude, is an overall marker of cardiac performance, including systolic and diastolic mechanics, but it is not a marker of LV diastolic chamber stiffness.20 or mitral inflow deceleration time, both established non-invasive markers of LV stiffness. We do, however, provide here the first evidence of significant correlations and associations between DWS and systolic echocardiographic indices  in humans. Interestingly, significant correlations between DWS and systolic parameters were not observed in an animal study, but this study consisted of only 25 rats and may have been underpowered. Though Our results should be interpreted in the context of a few limitations. First, DWS is measured in the parasternal long axis view, whereas cardiac mechanics were measured in our study in the parasternal short axis and apical four chamber views. Thus, we did not assess myocardial mechanics precisely at the posterior wall in the parasternal long axis view where DWS is derived. Second, because HyperGEN echocardiographic data were collected at a time prior to tissue Doppler imaging, tissue velocities were recorded here using speckle-tracking analysis. However, we demonstrated that correlation between the two approaches is high and were able to convert our measurements into tissue Doppler values. Third, speckle-tracking was performed retrospectively on echocardiograms that were acquired without specific attention to optimizing endocardial border definition, a necessity for speckle-tracking software. This maDWS correlates with both systolic and diastolic echocardiographic parameters. In addition, DWS is independently associated with multiple measures of systolic cardiac mechanics. DWS appears to reflect overall myocardial performance, and caution should be exercised clinically implementing this index to assess LV diastolic stiffness. Nevertheless, given its ease of use and widespread applicability, calculation of DWS could be a powerful new technique for the detection of subclinical cardiac disease.


Advances in the imaging techniques of the heart have fueled the interest in understanding of right heart pathology. Recently, speckle tracking echocardiography has shown to aid in understanding various right heart diseases and better management. Its role is well established in diagnosing right heart failure, pulmonary artery hypertension, arrhythmogenic right ventricular dysplasia and congenital heart disease. We review the basic mechanics of speckle tracking and analyze its role in various right heart conditions. For the past three decades, the left ventricular anatomy and function has been extensively researched and studied. The right ventricle (RV) has been ignored probably due to the technical difficulties in imaging as well as the poor understanding of its function and hemodynamics. Recent advances in medicine led to the better understanding of the role of RV in various medical conditions including congenital heart disease, pulmonary hypertension, arrhythmogenic right ventricular dysplasia and right ventricular myocardial infarction. This provided the impetus to focus on the management of various right heart pathologies to prevent unfavorable outcomes, like right heart failure, hemodynamically significant ventricular arrhythmias and pulmonary hypertension. RV is involved in several cardiac conditions and evaluation of the RV anatomy and function is an essential component of clinical management .RV is being recognized as a separate entity with unique anatomy, physiology and function compared to the left ventricle. Multiple imaging modalities are used in imaging the RV to understand its anatomy and function. One of the most common imaging modality is 2D transthoracic echocardiogram, which is readily available. But its utility is limited by technical difficulty in imaging the RV secondary to various factors including patient’s body habitus sonographer’s skills and expertise and the dependency on angle. In this article, the role of speckle tracking in various right ventricular pathologies is reviewed.Strain imaging is a novel method that has been developed to quantify regional myocardial function. Myocardial strain imaging was initially obtained by tissue Doppler imaging (TDI) . More reThe systolic tissue velocities at any given point are described as the sum of the longitudinal shortening (deformation) of the entire myocardial wall from that point to the apex that is the sum of the regional strain rates. In normal or symmetrically diseased myocardium, the strain rate and the tissue velocity obtained by TDI are comparable. In regionally diseased myocardium such as in myocardial infarction and focal scarring, akinesia in one segment will lead to reduced velocities in normally contracting contiguous or other distinct segments due to tethering . Thus, eMyocardial deformation, assessed by strain and strain rate, is more useful than wall motion analysis (velocity and displacement) for detection of regional myocardial abnormalities. Nevertheless, TDI can be used to obtain strain and strain rate.There are multiple disadvantages to TDI imaging. One of the primary limitations of TDI derived strain imaging is angle dependency . FurtherSpeckles are natural acoustic markers that occur naturally in the ultrasound images. They are equally distributed throughout the myocardium. Their size is about 20 - 40 pixels . The geoAcute increase in preload increases cardiac contractility and should theoretically cause deformation of the right ventricular myocardium. Missant et al investigated the relation between RV contractility and regional deformation . They coTransthoracic echocardiography (TTE) provides a standard evaluation of RV function in most cases. There are certain limitations with TTE such as the reproducibility of different measurements and the lack of normal references based on age, BMI and gender. Also, there is poor correlation of the 2D data with 3D echocardiographic data , 11. DueThe role of 3D speckle tracking imaging in assessing the RV function has been studied by Atsumi et al, who noted that in patients with RV dysfunction, 3D STI indicated low peak systolic area change ratio in the damaged area .Multiple studies have shown that RV ejection fraction (EF) is an independent prognostic factor in patients with chronic systolic heart failure , 21. ThePAH is characterized by chronic RV pressure overload due to pulmonary vascular obstruction either by thrombus or smooth-muscle proliferation due to various medical conditions. 2D TTE is the most common initial imaging modality used in assessing the pulmonary hypertension. Speckle tracking has been recently studied in assessing the changes in the right heart due to pulmonary hypertension. Li et al compared 42 patients with pulmonary hypertension to 31 healthy controls by assessing multiple parameters thought to be predictive of RV changes . This inIn summary, speckle tracking echocardiography (STE) has a valid and reproducible role in the assessment of RV changes in pulmonary hypertension when used in conjunction with TTE. Multiple studies studied the prognostic role of speckle tracking in patients with chronic pulmonary hypertension. In a study of 49 patients with chronic thromboembolic pulmonary hypertension, patients were divided into two groups based on their ability to complete 6-minute walk test by walking less or more than 300 m. In patients who walked less than 300 m, RV basal-lateral strain and strain rate were lower compared to patients who were able to walk more than 300 m . The autARVD is a hereditary cardiomyopathy characterized by fibro fatty replacement of the RV myocardium that leads to ventricular arrhythmias and right ventricular failure and sudden death . EchocarThe role of speckle tracking in congenital heart disease is currently in the development stage. Few studies have reviewed its ability in evaluation of complex congenital heart disease. In a recent study, Kempny quantified biventricular myocardial function in repaired TOF by comparing CMR to speckle tracking . In thisIn a study done in fetuses with congenital heart disease, longitudinal left ventricular and right ventricular free wall strain and the strain ratio were measured in 14 fetuses . In simpThe limitations of speckle tracking echocardiography are the dependency on strict frame rate, conceivable inaccuracies in tracing the epicardial/endocardial border in images with poor quality, and the need for sufficient experience using analysis software . Also, tSTE is a promising modality in the evaluation of global and regional cardiac function. The application of speckle tracking in cardiac conditions in which present diagnostic techniques are inadequate is being studied. Also, 3D STE may offer superior spatial resolution than 2D STE. It has great potential, but is yet to gain mainstream clinical application.STE offers a promising imaging modality in various cardiac conditions. Owing to its inherent advantages including angle independency and reproducibility, it is gaining mainstream role in the world of echocardiography. With more research being focused on the clinical application of speckle tracking, it is likely to provide an advantage in better patient selection for current and newer therapies as well as in tracking disease progression, which is important in prognosis.


To evaluate malignant middle cerebral artery (MCA) infarction (defined as space-occupying edema in more than 50% to 75% of the MCA territory) on magnetic resonance imaging (MRI) with susceptibility-weighted imaging (SWI) sequence and assess the usefulness of SWI findings, diffusion-weighted imaging (DWI) findings, and apparent diffusion coefficient (ADC) as predictors of clinical outcome.Data from 16 patients with large MCA infarction previously admitted to our institution between December 2009 and October 2012 were retrospectively collected and analyzed. Within 7 days after stroke onset, 1 neurologist and 1 neuroradiologist estimated the area of infarction on DWI/ADC and extent of prominent vessel sign (PVS) on SWI images using the Stroke Program Early MR Score (SPEMRS). The PVS on SWI was defined as a local prominence of hypointense vessels with either increased vessel number or diameter in the target area, when compared with the number or diameter of the contralateral MCA territory vessels.P < 0.001).Six patients died and 10 survived. Although the DWI/ADC-SPEMRS and clinical profiles were similar between the nonsurvivor and survivor groups, SWI-SPEMRS was significantly lower in the nonsurvivor group (The area of deoxygenation on SWI in patients with malignant MCA infarction can predict mortality. Lower SWI-SPEMRS is a potentially better predictor of poor outcome than lower DWI-SPEMRS. A larger prospective study is needed to clarify the role of SWI as a therapeutic guide in malignant MCA. Identification of early predictors of infarct growth and malignant course can help to improve treatment decision-making. Currently, patients at particular risk of malignant MCA infarction are identified based on the presence of mismatch between the area of abnormality on diffusion-weighted imaging (DWI) and perfusion-weighted imaging, reduced cerebral blood flow on single-photon-emission CT, and decreased cerebral oxygen metabolism on positron emission tomography and microdialysis.4 However, most of these procedures are relatively expensive, time-consuming, and not always feasible.One of the most devastating forms of ischemic stroke, “malignant” middle cerebral artery (MCA) infarction is associated with a fatality rate of up to 80%, if untreated.5 It is highly sensitive in detecting intravascular venous deoxygenated blood and extravascular blood products.6 Cerebral ischemia results in impaired oxygen metabolism due to inadequate perfusion in relation to the high oxygen demands of cerebral tissue. Cerebral infarction is linked to an increase in deoxyhemoglobin concentration due to an imbalance between cerebral oxygen supply and demand in the infarct area. The presence of prominent vessel sign (PVS) on SWI has been reported to reflect an increase in the oxygen extraction fraction compensating for a decrease in arterial cerebral blood flow in acute cerebral infarction, and to be closely related to the amount of deoxyhemoglobin in the veins and capillaries draining the ischemic tissue.7Susceptibility-weighted imaging (SWI) is a noninvasive, fast, high-spatial-resolution, 3-dimensional gradient-echo magnetic resonance imaging (MRI) technique that utilizes postprocessing reconstruction of phase information to accentuate the paramagnetic properties of blood products and thereby contrast.8SWI can predict the extent of impaired perfusion in ischemic brain tissue indirectly by focusing on the venous aspect, while DWI and ADC correlate with the usually irreversibly injured ischemic core. A match between SWI and DWI suggests that the brain tissue at risk is already infarcted.The aim of our study was to determine whether the extent of the PVS evident on SWI could serve as a predictor of clinical outcome in acute malignant MCA infarction.The study protocol was reviewed and approved by the Institutional Review Board of Taipei Medical University. From the stroke registry in our hospital, we retrieved data on consecutive patients with acute stroke admitted between December 2009 and October 2012. Patients were included if they completed the stroke MRI protocol, and had acute large MCA infarction (infarct area more than 50%) identified as hyperintensities on DWI, a complete DWI sequence, and PVS identified on SWI no later than 7 days after symptom onset and confirmed as hypointensities on an apparent diffusion coefficient (ADC) map. Patients were excluded if they had nonlarge MCA infarcts, parenchymal hemorrhage, or hemicraniectomy, or if image quality was poor.9A total of 16 patients  met the study criteria and provided their written informed consent. Patients were divided into nonsurvivors  and survivors . Risk factors for ischemic stroke, including diabetes mellitus, hypertension, hyperlipidemia, arrhythmia, coronary artery disease, congestive heart failure, smoking, and old cerebrovascular accident were obtained by chart review.2, and matrix 128 × 128 pixels. The trace images and ADC maps were computed. The magnitude and phase images of the 3-dimensional SWI sequence were obtained with the following parameters: TR/TE 49/40, slice thickness 2 mm with 64 slices in a single slab, flip angle 15°, iPAT factor 2, and matrix 224 × 256 pixels. The image-processing sequence was adapted from Haacke et al10 and performed automatically by a Siemens scanner. The picture archiving and communication system was used to upload data and retrieve the phase, minimal intensity projection, and magnitude of SW images. The total scan time for each subject was less than 30 minutes.In the present study, we used a 1.5-T MR system  equipped with a standard 12-channel head coil. The following sequences were run: axial T1 spin echo, T2 fast spin echo, fluid attenuated inversion recovery (FLAIR), DWI, and SWI. A slice thickness of 5 mm, gap of 1 mm, and matrix of 256 × 206 pixels were used in all these sequences. Single-shot echo-planar DWI was performed with the following parameters: repetition time/echo time (TR/TE) 3700/109, slice thickness 5 mm, bmax 1000 second/mm11 In this topographic system, one point is subtracted from the initial score of 10 if there is evidence of infarction in a region. The location of the infarct is recorded as C (caudate nucleus), L (lentiform nucleus), IC , I (insula), M1–3 (lower MCA territory), and M4–6 (higher MCA territory).8 This is a negative ordinal scale in which an infarct involving the entire MCA territory is rated 0 and no hyperintensity on DWI/ADC is rated 10. Compared with ASPECTS, SPEMRS is a more quantitative measure of early ischemic change on brain MRI scans.The images of selected subjects were retrospectively reviewed independently by 1 senior neurologist (C-IC) and 1 senior neuroradiologist (CYC) who were blinded to the clinical data and to each other's findings. Differences in areas of acute large infarcts measured by the 2 observers on DWI within 7 days after stroke onset were resolved by consensus. The definition of an acute infarct was an area with high signal intensity on DWI and low signal intensity on ADC. The infarct extent was estimated using the Alberta Stroke Program Early CT Score (ASPECTS) modified for MRI (SPEMRS). ASPECTS is a validated 10-point quantitative topographic CT scoring system with the reliability and accuracy needed to assess the extent of the infarct area and forecast outcome in patients with acute large MCA stroke.12 Consensus by both observers was reached.The PVS on SWI was defined as a local prominence of hypointense vessels with either increased vessel number or diameter in the target area, when compared with the number or diameter of the contralateral MCA territory vessels.The SPEMRS system was used to estimate the extent of the PVS. The MCA territory was divided into 10 zones, as mentioned previously. Because the thalamostriate vein drains the caudate nucleus, internal capsule, and lentiform nucleus, 3 points were deducted if any PVS was in the thalamostriate vein. Two examples are shown in Figures U test was used to compare the results of DWI/ADC and extents of the PVS on SWI between the nonsurvivor and survivor groups. A threshold of P < 0.001 was used to determine statistical significance.All statistical analyses used SPSS, version 18.0 . DWI/ADC data and PVS on SWI are expressed as mean ± standard deviation. The Fisher exact test was used for statistical comparison of all parameters except age and SPEMRS. The Mann–Whitney The patients’ clinical profiles and stroke risk factors are presented in Table P < 0.001), significantly different between groups for the caudate nucleus, lentiform nucleus, internal capsule, and lower MCA territory (P < 0.001), and correlated with outcome.The extent and distribution of the lesions on the DWI/ADC and SWI scans are summarized in Tables 13 Hyperintensity on T2-weighted imaging (T2WI) is indicative of vasogenic edema or infarction. A previous study showed that similar areas of signal intensity on both DWI and T2-weighted images 24 hours after cerebral infarction indicate the coexistence of secondary cytotoxic edema and vasogenic edema. However, compared to T2-weighted imaging findings, the 80% ADC threshold is a better predictor of final infarct volume,14 and ADC is a more sensitive measure of the extent of ischemia early after the onset of infarction.15 According to Drier et al.16 the ADC-based method is as efficient as perfusion-weighted imaging-based methods for estimating infarct growth during the subacute phase.Acute stroke initially causes cellular swelling (cytotoxic edema) which leads to vasogenic edema and infarction. ADC reduction is related directly to the early phase of cytotoxic edema development during ischemia.17 Because T2∗-weighted images rarely show the presence of asymmetrically hypointense veins, SWI is a much more suitable candidate sequence18 and a better tool to monitor PVS.SWI produces images with very strong T2∗ contrast enhancement and uses both phase and magnitude images to differentiate pial vessels from the background.12 Kao et al19 found that the perfusion information provided by SWI and by mean transit time methods were similar and that SWI–DWI/ADC mismatch can be a indicator of ischemic penumbra and a predictor of stroke evolution. Mucke et al20 identified asymmetric deep medullary veins on SWI as a predictor of stroke severity in patients with acute MCA stroke. Another study also demonstrated that asymmetrical PVS in patients with MCA territory acute ischemic stroke is a strong neuroimaging predictor of 90-day unfavorable prognosis and early neurological deterioration.21 Since it signifies oxygen supply and demand imbalance, PVS on SWI is a useful prognosis predictor and SWI-SPEMRS is a useful predictor of outcome in malignant MCA infarction, with lower SWI-SPEMRS indicative of poor outcome.In our study, SWI-SPEMRS correlated with outcome in patients with large MCA infarction. Previous studies showed an association of asymmetric deoxygenated cortical vessels and/or transcerebral veins with prognosis in acute stroke patients.22 The extent of the deoxygenated area on SWI in malignant MCA infarction can thus predict mortality.The main finding of our study is that the extent of PVS on SWI in patients with large MCA infarction can predict mortality. In our study, 6 of 16 patients with malignant MCA infarction had large areas of prominent blood vessels on SWI, all of whom died. A previous report showed that a match between SWI and DWI indicated the brain tissue at risk was already infarcted.26 The reason for this inconsistency between ours and previous studies may be related to small sample size and differences between patient groups. Further study will therefore be needed to clarify this issue.Af was more frequent in our study's survivor group. However, previous studies demonstrated a higher risk of death during the acute phase of stroke in patients with Af than in patients without Af.Limitations of our study included potential bias from small sample size and patient selection. We defined PVS indirectly by comparing the affected side with the contralateral side rather than directly measuring the diameter of the vessel; therefore bias in PVS assessment on SWI existed. The influence of systemic conditions  is unavoidable. In addition, quantification by the SPEMRS system using SWI is controversial.To the best of our knowledge, this study is the first to show that SWI-SPEMRS is potentially a better parameter than DWI/ADC-SPEMRS for predicting mortality in patients with malignant MCA infarction. The use of the PVS on SWI as a semiquantitative measure in the early stage of large MCA infarction can predict the patient's outcome with a high degree of diagnostic accuracy.


Alkaptonuria is a rare autosomal recessive metabolic disorder with an incidence of 1 case in 250,000 to 1 million live births. This genetic abnormality involves the tyrosine metabolism pathway which results in homogentisic acid accumulation throughout various tissues, including the heart. The purpose of this study is to prospectively determine the prevalence of cardiovascular abnormalities characterized by MRI in patients with alkaptonuria.A group of 57 consecutive adult patients with laboratory confirmed alkaptonuria were referred for evaluation including transthoracic echocardiography and cardiac MRI, which included cine and phase contrast imaging at either 1.5T or 3T. Phase-sensitive inversion-recovery delayed enhancement imaging was performed after gadolinium-DTPA contrast administration. Late gadolinium enhancement patterns were determined by consensus read between two experienced cardiologists using a 17-segment model.Overall, 56 completed cine MRI, 53 received gadolinium contrast and 1 subject experienced claustrophobia precluding any imaging. Of the 56 who had CMR imaging, 77% (41 of 56) were male and the average age was 49 ± 12 years old. The prevalence of atypical delayed enhancement was 70% (37 of 53) and predominately involved the right ventricular insertion point . Other delayed enhancement patterns included midwall , near aortic root , focal nodular , mitral papillary muscle involvement , and patchy/intermediate . Involvement of the right ventricular point has been associated with pulmonary hypertension; however, this group of alkaptonuria patients had normal estimated right ventricular systolic pressures measured on echocardiography performed within 1 day (median). The number of segments with atypical delayed enhancement was 2.7 ± 1.4 per patient. The prevalence of any atypical delayed enhancement trended higher for females vs. males  and was not associated with age. One subject had subendocardial delayed enhancement in a coronary artery distribution consistent with myocardial infarction.Myocardial fibrosis based on late gadolinium enhancement abnormalities, especially involving the right ventricle insertion site, are common in patients with alkaptonuria despite not having pulmonary hypertension or cardiac structural abnormalities and suggests myocardial involvement due to this metabolic disorder. Further study is required to determine the etiology and clinical significance.This work was funded by the Division of Intramural Research, National Heart, Lung, and Blood Institute, National Institutes of Health, USA.


Left dominant arrhythmogenic cardiomyopathy (LDAC) is a rare condition characterised by progressive fibrofatty replacement of the myocardium of the left ventricle (LV) in combination with ventricular arrhythmias of LV origin.A thirty-five-year-old male was referred for evaluation of recurrent sustained monomorphic ventricular tachycardia (VT) of 200 bpm and right bundle branch block (RBBB) morphology. Cardiac magnetic resonance imaging showed late gadolinium enhancement distributed circumferentially in the epicardial layer of the LV free wall myocardium including the rightward portion of the interventricular septum (IVS). The clinical RBBB VT was reproduced during the EP study. Ablation at an LV septum site with absence of abnormal electrograms and a suboptimum pacemap rendered the VT of clinical morphology noninducible. Three other VTs, all of left bundle branch block (LBBB) pattern, were induced by programmed electrical stimulation. The regions corresponding to abnormal electrograms were identified and ablated at the mid-to-apical RV septum and the anteroseptal portion of the right ventricular outflow tract. No abnormalities were found at the RV free wall including the inferolateral peritricuspid annulus region. Histological examination confirmed the presence of abnormal fibrous and adipose tissue with myocyte reduction in endomyocardial samples taken from both the left and right aspects of the IVS.LDAC rarely manifests with sustained monomorphic ventricular tachycardia. In this case, several VTs of both RBBB and LBBB morphology were amenable to endocardial radiofrequency catheter ablation. Left dominant arrhythmogenic cardiomyopathy (LDAC) has been recently introduced as a rare condition characterised by progressive fibrofatty replacement exclusive to the myocardium of the left ventricle (LV) in combination with ventricular arrhythmias of LV origin -9. SustaA thirty-five-year-old male was referred for evaluation of recurrent hemodynamically tolerated sustained monomorphic ventricular tachycardia of 200 bpm, which had right bundle branch block (RBBB) morphology with leftward axis deviation Figure . He suffBecause of recurrent VT despite medical therapy, an electrophysiological study, 3D electroanatomical mapping, and ablation were indicated. The procedure was performed under local anesthesia and mild conscious sedation with midazolam and alfentanyl. At the beginning of the procedure, clinical VT of 191 bpm and RBBB morphology  into affected regions according to electroanatomical mapping. Histological examination confirmed the presence of abnormal fibrous and adipose tissue with myocyte reduction in endomyocardial samples taken from both left and right aspects of the IVS Figure . MutatioA cardioverter-defibrillator (ICD) was implanted and the patient was discharged on the same dosage of bisoprolol and trandolapril medication. No class I or III antiarrhythmic drugs were given. During the 18-month follow-up, the patient experienced only a single episode of monomorphic VT (243 bpm) when bisoprolol medication was discontinued by mistake. LV dilatation and mild dysfunction remained stable at regular check-ups.The phenotypic spectrum of arrhythmogenic cardiomyopathy includes either left dominant, right dominant or bi-ventricular variant. Isolated left and right ventricular abnormalities are at two extremes of the clinical manifestation of the disease . There wThe designation as a purely LV entity might be questioned because a small region of fibrofatty replacement was present at the mid-anterior portion of the RV free wall, as assessed by LGE CMR. An additional region of abnormal electrograms was present at the anterior RVOT by electroanatomical mapping , complemented by the observation that inducible VT #4 exited from this site. This is still compatible with LDAC because LV involvement including IVS clearly dominated and subtle RV regional abnormalities or the presence of additional arrhythmogenic substrate in RV has been observed in the majority of LDAC patients .Although the presence of ventricular arrhythmias is an essential component of the clinical picture of LDAC, sustained monomorphic VT has been reported rarely. Besides the cases diagnosed post-mortem, the predominant arrhythmias were frequent ventricular premature beats or non-sustained VT of LV origin . SustainSimilarly to classic ARVC, catheter ablation therapy in LDAC may be indicated in patients with recurrent VT despite therapy with antiarrhythmic drugs. In this case we preferred non-pharmacological treatment because of the considerable burden of arrhythmia, in order to prevent frequent ICD therapy and to avoid long-term medical therapy, which may be ineffective and/or associated with adverse effects.Because of the non-transmural and rather homogeneous distribution of pathological tissue, electroanatomical mapping (both bipolar and unipolar) showed voltages almost invariably within the normal arbitrary range and thus was of little help. For this reason pre-procedural CMR was extremely valuable for tailoring the ablation strategy. It demonstrated from the very beginning that the clinical VT could only be effectively targeted by endocardial ablation from the RV aspect of IVS - the only site where the potential substrate was localized close to the endocardial surface. Any other LV targets would require an epicardial approach. Fortunately, VT #1 - #3 originated at the IVS. It is likely that the clinical VT (VT #1) originated from the RV subendocardium at the IVS with a preferential leftward exit, which could explain the RBBB morphology. Initial ablation at the LV aspect of the IVS probably modified the route of propagation. This explains why subsequent VT #2 and #3 had LBBB morphology. It is not known whether the initial LV ablation had any other impact besides changing the exit route.Indeed, there was a preponderance of mappable arrhythmogenic substrate at the RV aspect of the IVS, although in sinus rhythm the abnormal electrograms were considerably masked by the fast activation of the septum from both sides via the intact His-Purkinje system conduction. Pacing from the LV would probably be helpful maneuver to reveal pathological electrograms or late potentials at the right side of the IVS, but this was not done in the present case. Ablation at the RV aspect of the IVS was performed rather extensively to target not only the critical zones of inducible VTs but also to homogenize the scar in order to prevent other VTs that did not manifest during the procedure.Although the patient presented with VT of RBBB morphology, this case also suggests that, at least in theory, LDAC may manifest by ventricular arrhythmias of LBBB morphology alone. This might be taken into account when the clinical criteria of LDAC are refined in the future.Endomyocardial biopsy guided by electroanatomical mapping confirmed the presence of fibrous and adipose tissue in samples obtained from both aspects of the IVS. Positive sampling from the right-sided IVS, fully affected by the pathological process, was expected in our case. The biopsy from the LV endomyocardium, without macroscopic signs of pathology by LGE CMR, was taken from the apicoseptal region of LV, which was the only site with borderline abnormal electrograms. Such an approach could possibly increase the diagnostic yield, as already reported .Because of structural heart disease that manifested by malignant ventricular arrhythmia and the existence of large-scale, potentially arrhythmogenic substrate, which could not be safely eliminated by catheter ablation, and because of the progressive nature of disease, the cardioverter-defibrillator was implanted for secondary prevention of sudden cardiac death. Despite the fact that single episode of VT was documented during the follow-up, it is likely that catheter ablation prevented frequent VT recurrences.Left dominant arrhythmogenic cardiomyopathy is an infrequent structural heart disease, which rarely manifests with sustained monomorphic ventricular tachycardia. In this case, extensive circumferential LV involvement by fibrofatty replacement was distributed epicardially at the LV free wall and subendocardially at the RV aspect of the interventricular septum. Several VTs of both RBBB and LBBB morphology were amenable to endocardial radiofrequency catheter ablation.Written informed consent was obtained from the patient to the publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor of this journal.


Systolic myocardial strain is load dependent, but the CMR literature largely disregards effects of myocardial afterload on strain and strain rate. This may reflect well known limitations of conventional myocardial afterload assessment using wall stress analyses, which are based on erroneous assumptions about left ventricular(LV) geometry and/or myocardial material properties. Therefore, we compared the utility of a nongeometric afterload index(NGI) derived from LV pressure(P) volume(V) and mass, which requires no assumptions about material properties, to that of conventional noninvasive end-systolic circumferential stress(CWS) as determinants of CMR LV circumferential strain(CST), ejection fraction(EF) and strain rate(SR) in normals(NL) and patients with nonischemic dilated cardiomyopathy(CM).We obtained breath-hold volumetric short-axis SSFP cines, cuff systolic P, systolic duration, LVV, M and EF, feature-tracking global CST(TomTec Imaging Systems) and mean SR in NLsyrs) and CM  yrs, EF 27.2%(sd10.8%). CWS was calculated using Mirsky's formula(Biophys. J.1969) while NGI was determined as end-systolic PV/M.EF, CST and CSR were markedly reduced in CM compared to NL(EF 27.2%sd10.8)vs 58.4%(4.6), (-53%)p < 0.0001; CST -10.7%(5.3) vs -23.9%(4.3), (-55%), p < 0.0001);(CSR -32.1%/s(14.8) vs -65.7(14.9) p < 0.0001). But CWS was also markedly elevated in CM versus NL(CWS 307.6(9.2) vs 176.2(42.1)x 103 dyn/cm2,(+75%), p < 0.0001). Thus afterload excess due to adverse LV remodeling, may account for most EF, strain and strain rate reduction in CM. However, PV/M was more markedly increased than CWS, (162.6(sd48.9) vs 84.4(18.4)(+93%) p < 0.0001) and correlated more closely and significantly with EF, CST and CSR than CWS in the expected inverse relationship in both NL and CM subgroups(Table 0.8vs 58.Afterload excess due to adverse LV remodeling is an important determinant of reduced myocardial and LV chamber function in CM, making a major contribution to reductions in EF, CST and SR, but PV/M, a simple, nongeometric afterload index, is superior to conventional wall stress calculation as a quantitative afterload index.St. Francis Research Foundation.


We hypothesized that the contrast medium gadobutrol is not inferior compared to Gd-DTPA in identifying and quantifying ischemic late gadolinium enhancement (LGE), even by using a lower dose.We prospectively enrolled 30 patients with chronic myocardial infarction as visualized by LGE during clinical routine scan at 1.5 T with 0.20 mmol/kg Gd-DTPA. Participants were randomized to either 0.15 mmol/kg gadobutrol (group A) or 0.10 mmol/kg gadobutrol (group B). CMR protocol was identical in both exams.LGE was quantified using a semiautomatic approach. Signal intensities of scar, remote myocardium, blood and air were measured. Signal to noise (SNR) and contrast to noise ratios (CNR) were calculated.p = 0.0001) and CNR between injured and remote myocardium  were lower in gadobutrol. Infarct size was lower in both gadobutrol groups compared to Gd-DTPA .Signal intensities were not different between Gd-DTPA and gadobutrol in group A, whereas significant differences were detected in group B. SNR of injured myocardium (53.5+/−21.4 vs. 30.1+/−10.4, Taking application of 0.2 mmol/kg Gd-DTPA as the reference, the delineation of infarct scar was similar with 0.15 mmol/kg gadobutrol, whereas the use 0.10 mmol/kg gadobutrol led to reduced tissue contrast.2010-020775-22. Registration date: 2010.08.10The study had been registered under EudraCT Number:  Myocardial infarction is a leading cause of mortality worldwide. Accurate assessment of infarct size and morphology is important for clinical decision making in a lot of clinical settings , 2. Curr1 relaxivity compared to Gd-DTPA  [Gadobutrol is a macrocyclic nonionic gadolinium chelate with a higher Tt 37 °C) . The bint 37 °C) . TherefoToday, there are only limited data available analyzing the influence of contrast agents with different relaxivities on LGE quantification. In this study, we hypothesized that gadobutrol, which is characterized by a higher relaxivity compared to Gd-DTPA, is not inferior to Gd-DTPA in identifying and quantifying ischemic LGE, even when using a lower dose.Between September 2010 and December 2011, patients with a history of a chronic myocardial infarction and LGE as assessed during a clinical CMR scan using 0.20 mmol/kg Gd-DTPA were screened and asked for participation in a second study-related CMR scan. All included patients gave written informed consent and were scheduled for a second CMR examination afterwards. The study had been registered under EudraCT number: 2010-020775-22 and was accordingly approved by the ethical board of the city of Berlin (LAGESO).The sample size of this randomized prospective trial was calculated based on a power calculation. The assumption was, that for a two-sided alpha of 5 % and a power of 80 % based on a delta of 0.15, 15 patients per dose gadobutrol have to be included.Patients were randomized for either 0.15 mmol/kg (group A) or 0.10 mmol/kg (group B) gadobutrol. All patients were in normofrequent sinus rhythm.between 18 and 80 years of agechronic myocardial infarction (>3 months old) based on coronary artery disease (CAD), detected by invasive angiographysuccessfully performed clinical LGE CMR study within the last 4 weeksevidence of single myocardial infarction on LGE CMR with “hyper-enhancement” involving at least two contiguous short-axis sliceswritten informed consentsevere arrhythmia, atrial fibrillationhistory of moderate or severe impairment of renal function (GFR < 60 ml/min)additional myocardial infarction or acute coronary syndrome during the last 4 weeksgeneral contraindications for CMRCMR was performed on a 1.5Tesla cardiac-dedicated clinical MR system  using a 12-channel coil. Identical CMR protocols were applied for both examinations.LGE was assessed in all patients starting 13 min after contrast administration in a short axis stack by using a 2D inversion recovery gradient echo sequence  with an inversion time (TI) adjusted to null signal from normal myocardium. In case of questionable bright signal in the myocardium during the scan, we changed the read out or acquired a perpendicular slice to exclude artefacts. Slice position was identical as for cine imaging using a single slice single breathold approach.1 quantification was performed with a Modified Look-Locker Inversion-recovery (MOLLI) sequence [Tsequence , acquire42, circle, Calgary, Canada). LV mass was calculated as total myocardial volume multiplied by the specific gravity of the myocardium (1.05 g/ml). LV mass and LV end diastolic volume were indexed to height.For analyzing LV function and volumes, the endocardial and epicardial contours were manually drawn in systole and diastole using dedicated software . For signal-to-noise ratio (SNR) and contrast-to-noise ratio (CNR) the following sequations were used [Signal intensities of scar tissue, remote myocardium, blood and air were measured by drawing free-hand ROIs of approximately 10–20 pixels in each LGE short axis stack. Reproducible locations were achieved by using anatomical landmarks in dedicated software  and SPSS 21.0 for windows . Data are presented as mean ± standard deviation. Statistical tests were performed using non-parametric methods due to the low sample size within each group. Continuous data were compared using the Wilcoxon rank sum tests. Paired data were compared using Wilcoxon signed rank tests. Categorical data were compared using Fisher's exact test. Statistical tests were considered significant with the two-sided p < 0.05. Spearman correlation coefficient’s were used to determine observer-related variability. Boxplots were generated with SPSS and show median (line in the middle), 1st quartile (bottom of box), 3rd quartile (top of box), lowest case within 1.5 times IQR (bottom whisker), highest case within 1.5 times IQR (top whisker) and outliers.We screened 252 patients and identified 51 who met our criteria. 30 patients agreed to participate in the trial and were prospectively enrolled in the study and randomized to either 0.15 mmol/kg gadobutrol (group A) or 0.10 mmol/kg gadobutrol (group B). 21 patients refused participation due to a lack of motivation or fear of repeated contrast administration. There were no significant differences between groups relating age, scar amount and signal intensities for control agent Gd-DTPA .In group A signal intensities showed no differences between Gd-DTPA and gadobutrol Table  and 3. AIn group B signal intensities showed significant differences between Gd-DTPA and gadobutrol. In particular SNR of injured myocardium and CNR between injured and remote myocardium were significantly lower in gadobutrol resulting in a significant smaller scar size as defined by the amount of LGE Table  and 5.TaInterobserver variability was low and without differences between the contrast agents in both groups Table .Table 4S1 times of the different tissues at different time- points after contrast administration  The applied sequence was a first generation one as described in the method section. II) The most frequent limitation was the registration failure of the raw images especially in regions of wall thinning respectively the infarct area.In the present study we compared the depiction of chronic myocardial infarction using two different contrast media and different doses in a prospective randomized setting. The null hypothesis of our study was, that the infarct volume with gadobutrol is not equivalent to the infarct volume with the control agent. This was confirmed by our results. The main results are the following:I) Scar was detectable with each contrast media and dose. II) The use of 0.15 mmol/kg BW (body weight) gadubutrol led to similar results compared to 0.2 mmol/kg BW Gd-DTPA regarding signal intensity and contrast whereas the application of 0.1 mmol/kg gadobutrol led to a significant poorer delineation of scar tissue. III) Both doses gadobutrol led to a smaller infarct size taking 0.2 mmol/kg BW Gd-DTPA as the reference. IV) Observer variability of LGE quantification was independent from type and dose of contrast agent.Although our sample size was small, but defined in a random setting, we could confirm in part the data by Durmus et al., who compared 0.15 mmol/kg BW gadobutrol with 0.2 mmol/kg BW Gd-DTPA in 20 patients with myocardial infarction . They shDeCobelli et al. compared gadobutrol with Gd-DTPA in patients with positive LGE regardless of its etiology . They shOne would assume that parametric mapping techniques will help to overcome that problem. Whereas mapping techniques are already applied in different diseases and also for the quantification of extracellular volumes , 24, no Independent of the quantification method itself, contrast media with higher relaxivity are warranted for potential dose reduction. The concept of dose reduction in contrast agents with higher relaxivity was also analyzed for gadobenate dimeglumine. Recent studies have shown a similar diagnostic performance and delineation of infarct scars using reduced doses of gadobenate dimeglumine compared to standard dose Gd-DTPA (0.2 mmol/kg BW) –28. WhenReduced dose of gadobutrol allows a reproducible detection of myocardial infarction in all patients. In clinical routine visual assessment of scar is accepted and eye balling is accepted . But scaThe present study was conducted at a single center with a relatively small sample size. The study only included men to omit the influence of sex on the results. Further studies in women are necessary to extend the conclusions to both sexes.SNR- and CNR of LGE images are influenced by inversion time. Its adjustment is operator-dependent. T1-mapping was expected to add information on contrast-media timing, but for technical reasons we were only able to complete a pairwise T1 analysis in six patients of group A. Larger studies preferably with mapping techniques are needed to confirm our results.The use of 0.15 mmol/kg BW gadobutrol led to comparable results as 0.20 mmol/kg BW Gd-DTPA in delineation of myocardial infarction and only to a small, clinically non-relevant deviation in quantification of infarct scar and may be an appropriate alternative under consideration of the lower risk for NSF. In contrast, the dose of 0.10 mmol/kg BW gadobutrol was associated with lower signal intensity and higher discrepancy regarding infarct size. Our results underline that accurate scar evaluation during follow-up depends on type of contrast agent and contrast dose and therefore requires constant study conditions.


Invasive right heart catheterization plays a central role in the investigation of patients with cardiac and pulmonary vascular disease. Physiological provocations during invasive heart catheterization augment the diagnostic yield and can provide useful prognostic information. MRI catheterization combines invasive hemodynamic measurements with MRI structural and functional evaluations - thus providing superior diagnostic information than either test alone. An additional benefit to both patient and operator is no ionizing radiation, which is of particular value in pediatric patients.We propose a diagnostic algorithm for MRI catheterization integrating serial physiological provocations designed to unmask latent pathology and aid prognostication. The algorithm allows each MRI catheterization to be tailored to the individual patient. We have developed a concise MRI examination protocol to be performed alongside invasive hemodynamic measurements during each provocation. This protocol provides cardiac chamber volumes, pulmonary and systemic blood flow measurements with each provocation. The MRI examination is performed free breathing, which allows the study to be performed in patients with dyspnea or under moderate sedation.Real-time MRI provides excellent anatomical imaging for catheter navigation. Challenging procedural steps using X-ray guidance, such as navigating into the SVC Figure  or left Provocative MRI catheterization can uncover diagnoses not apparent at rest and can provide incremental structural and functional information compared with invasive heart catheterization or MRI alone.This work is supported by the Division of Intramural Research , National Heart Lung and Blood Institute, National Institutes of Health, USA.