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This clinical image vignette describes the inadvertent placement of a balloon pump in the vena cava during a "code blue" scenario, and the lessons to be learned from that experience. The hemodynamic benefits of intra-aortic balloon pump during experimental cardiac arrest include shorter circulation time and increases in end-tidal CO2 and coronary perfusion pressure. However, the hemodynamic effects of venous diastolic augmentation during experimental cardiogenic shock vary, being detrimental in cases of low preload, and possibly beneficial in a high preload state. When performed emergently at the bedside, inadvertent intra-caval placement of a balloon pump can occur due to elevated venous pressures, in the presence of severe tricuspid regurgitation, or through an arteriovenous fistula. A similar radiographic appearance can also be seen in the presence of a right-sided aortic arch. Clues to improper position include an abnormal pressure waveform and the absence of hemodynamic changes or blood pressure augmentation.

Background: In ≈25% of patients with heart failure and reduced left-ventricular ejection fraction, right-ventricular (RV), and left-ventricular (LV) filling pressures are discordant (ie, one is elevated while the other is not). Whether clinical assessment allows detection of this discordance is unknown. We sought to determine the agreement of clinically versus invasively determined patterns of ventricular congestion. Methods: In 156 heart failure and reduced LV ejection fraction subjects undergoing invasive hemodynamic assessment, we categorized patterns of ventricular congestion (no congestion, RV only, LV only, or both) based on clinical findings of RV (jugular venous distention) or LV (hepatojugular reflux, orthopnea, or bendopnea) congestion. Agreement between clinically and invasively determined (RV congestion if right atrial pressure [RAP] ≥10 mm Hg and LV congestion if pulmonary capillary wedge pressure [PCWP] ≥22 mm Hg) categorizations was the primary end point. Results: The frequency of clinical patterns of congestion was: 51% no congestion, 24% both RV and LV, 21% LV only, and 4% RV only. Jugular venous distention had excellent discrimination for elevated RAP (C=0.88). However, agreement between clinical and invasive congestion patterns was poor, к=0.44 (95% CI, 0.34–0.55). While those with no clinical congestion usually had low RAP and PCWP (67/79, 85%), over one-half (24/38, 64%) with isolated LV clinical congestion had PCWP Conclusions: While clinical examination allows accurate detection of elevated RAP, it does not allow accurate detection of discordant RV and LV filling pressures.

IVC stenosis is a rare complication of bicaval orthotopic heart transplant. IVC stenosis can occur at either the cavo-atrial anastomosis, or the caval cannulation site, with presentations ranging from acute shock early post transplant to a more indolent course. Causes include extensive hemostatic suturing, fibrous contraction, and donor-recipient size mismatch. Treatment strategies include percutaneous balloon angioplasty, stenting, and surgical revision. Evaluating for IVC stenosis is recommended for unexplained lower-extremity edema, new-onset ascites, or liver abnormalities after bicaval heart transplant.

Varicella zoster virus (VZV) infection commonly presents as varicella during childhood, and zoster, later in life. Here, we present a rare and interesting case of VZV infection that manifested with both cerebral and spinal infarctions and cutaneous vasculitis in the absence of a classic vesicular rash in an immunocompromised patient.

Intracardiac thrombi are associated with an increased morbidity and mortality due to their unpredictability and embolic potential. Right heart thrombus is infrequently encountered in clinical practice outside the scenario of acute pulmonary embolism with hemodynamic compromise, and even more uncommon is the presence of a massive right heart thrombus. Embolic potential is high, and historically, management has revolved around open surgical removal or systemic thrombolysis. We hereby present a case of a massive right heart thrombus in a high surgical risk patient, which was successfully removed using a percutaneous aspiration device.

Reliable identification of patients at high risk for right ventricular failure is very important. We identify 4 parameters as hemodynamic red flags to left ventricular assist device implantation.

Background: Duchenne muscular dystrophy (DMD) is an X-linked neuromuscular disorder characterized by progressive muscle degeneration. The leading cause of death is complications from the development of DMD-associated cardiomyopathy. The majority of DMD patients have skeletal abnormalities that limit the quality of echocardiograms (ECHO). Although cardiac magnetic resonance imaging (cMRI) is the gold standard cardiac imaging tool, the vast majority of DMD patients are evaluated by ECHO rather than cMRI. We hypothesized that when compared to ECHO, cMRI more accurately assesses cardiac function and provides more valuable data for the diagnosis of DMD-associated cardiomyopathy. Methods: We undertook a retrospective study of 20 DMD patients referred to the UT Southwestern Adult Neuromuscular Cardiomyopathy Clinic who had undergone both an ECHO and cMRI within 15 months of each other. We assessed the proportion of studies demonstrating reduced left ventricular (LV) function [cMRI LVEF Results: Amongst these patients, 10% of cMRIs and 85% of ECHOs were technically difficult. By cMRI, 30% of the studies were normal (LVEF 64±2 %), while 70% showed reduced function (LVEF: 44±12%). By ECHO, 75% of the studies were normal (FS 32±5), while 25% showed reduced function (FS: 15±8). Of the patients with truly reduced function by cMRI, 64% were considered normal by ECHO. Finally, 61% of cMRI studies showed LGE (50% with normal LVEF and 67% with reduced LVEF). Conclusions: In summary, cMRI is superior to ECHO in assessing cardiac function in DMD. ECHO underestimates left ventricular dysfunction, likely due to the poor quality of studies obtained in this patient population. In addition, cMRI identifies LGE, a marker associated with increased mortality, irrespective of cardiac function. Earlier utilization of cMRI will expedite the diagnosis of DMD-associated cardiomyopathy and enable the cardiologist to initiate aggressive guideline-directed medical therapy at an earlier age.

Introduction: Duchenne muscular dystrophy (DMD) is an X-linked neuromuscular disorder. DMD-associated cardiomyopathy is the primary mode of premature death in the majority of male DMD patients, but the prevalence of cardiomyopathy and its clinical significance in female DMD carriers is less well characterized. Hypothesis: We hypothesized that a significant proportion of DMD carriers develop maladaptive left ventricular (LV) structural remodeling and cardiomyopathy over time. Methods: A cross-sectional study was undertaken comparing cardiac magnetic resonance imaging (cMRI) and cardiopulmonary stress test (CPX) parameters between DMD carriers and healthy age- and sex-matched controls from the Dallas Heart Study (DHS). Demographic data, cMRI parameters, and CPX parameters were collected retrospectively on 30 consecutive DMD carriers and 26 control DHS subjects. Results: Overall, DMD carriers had a significantly lower LVEF compared to DHS controls (58+8% vs 70+7%, p< 0.0001). The overall prevalence of reduced LVEF in DMD carriers (defined as LVEF 2 vs 58+7, p< 0.0001; 31+10 ml/m 2 vs 17+5, p< 0.0001; respectively). LV concentricity was also significantly lower among all DMD carriers compared to DHS controls (3.10+0.65 g/mL 0.67 vs 3.73+0.79, p =0.002). LV concentricity was significantly lower in DMD carriers with reduced EF compared to controls (3.09+0.51 g/mL 0.67 vs 3.73+0.79, p = 0.012), while DMD carriers with preserved EF also had reduced concentricity compared to controls (3.12+0.86 vs 3.73+0.79, p = 0.054). Finally, peak VO 2 was lower in DMD carriers compared to DHS controls (23+6 ml/kg/min vs 25+4, p =0.076), though this difference did not reach statistical significance. Conclusions: Collectively, the data suggest that middle-aged female DMD carriers are at greater risk of developing left ventricular systolic dysfunction and cardiomyopathy associated with decreased exercise capacity. A possible mechanism driving the development of this cardiomyopathy is progressive, maladaptive left ventricular dilatation and cardiac atrophy.

Background: Muscular dystrophies (MD) are genetic disorders that cause progressive peripheral skeletal myopathies. The majority of MD patients will develop atrial and ventricular arrhythmias and/or an associated cardiomyopathy with a high degree of morbidity and mortality. However, it remains unknown the degree of atrial remodeling that may also occur in MD patients. We hypothesize maladaptive atrial remodeling occurs in MD patients. Methods: Utilizing the UT Southwestern Cardiomyopathy Clinic, MD [total: 79 patients (34 females, 45 males)] and non-ischemic cardiomyopathy (NICM) [total: 81 patients (29 females, 52 males)] patients were identified who underwent a cardiac MRI (cMRI) between 2011 and 2015. A matched, healthy control cohort from the Dallas Heart Study (DHS) [total: 101 patients (40 females, 61 males)] were identified. Most MD patients had Duchenne/Becker MD, Limb-Girdle MD or myotonic MD. Two blinded, independent readers made volumetric measurements from cMRIs to assess right atrial (RA) and left atrial (LA) dimensions with low inter-reader variability. A third independent investigator analyzed the RA and LA data with aggregate data presented in the Table. The statistical significance of the data (p Results: Analysis of the cMRI data revealed significant differences in both the structure and function of the RA and the LA between MD and NICM patients. In addition, the data revealed significant differences in the LA but not the RA emptying fraction in MD patients as compared to the DHS patients. Conclusion: Collectively, the data suggests MD patients develop significant maladaptive remodeling of the LA but not the RA, predisposing these patients to atrial arrhythmias. Investigation into differences in atrial remodeling as a function of gender and the type of MD need to be explored.

Background Duchenne muscular dystrophy (DMD) is a neuromuscular disorder caused by mutations within the dystrophin gene. DMD is characterized by progressive skeletal muscle degeneration and atrophy and progressive cardiomyopathy. It has been observed the severity of cardiomyopathy varies in patients with DMD. Methods and Results A cohort of male patients with DMD and female DMD carriers underwent whole exome sequencing. Potential risk factor variants were identified according to their functional annotations and frequencies. Cardiac function of 15 male patients with DMD was assessed by cardiac magnetic resonance imaging, and various cardiac magnetic resonance imaging parameters and circulating biomarkers were compared between genotype groups. Five subjects carrying potential risk factor variants in the cystic fibrosis transmembrane regulator gene demonstrated lower left ventricular ejection fraction, larger left ventricular end‐diastolic volume, and higher NT‐proBNP (N‐terminal pro‐B‐type natriuretic peptide) levels compared with 10 subjects who did not carry the potential risk factor variants ( P =0.023, 0.019 and 0.028, respectively). Conclusions This study revealed heterozygous cystic fibrosis transmembrane regulator gene missense variants were associated with worse cardiac function in patients with DMD. The cystic fibrosis transmembrane regulator gene may serve as a genetic modifier that accounts for more severe cardiomyopathy in patients with DMD, who would require more aggressive management of the cardiomyopathy.

Described herein is a 42-year-old woman who suddenly developed a spontaneous isolated coronary arterial dissection which led to massive acute myocardial infarction with shock, unsuccessful coronary artery bypass grafting, transiently successful extracorporeal life support, and finally successful heart transplant. Such a sequence of events is exceedingly rare for patients with coronary dissection and prompted this report.

A young man with Duchenne muscular dystrophy presented to the UT Southwestern Neuromuscular Cardiomyopathy Clinic with advanced heart failure. Despite maximal medical therapy, his cardiac function continued to decline requiring initiation of inotrope therapy. Given the patient's clinical deterioration, a left ventricular assist device (LVAD) was implanted as destination therapy after undergoing a multidisciplinary assessment. The patient tolerated the surgical implantation of the LVAD without any significant complications, and he has had a relatively unremarkable course 38 months post-LVAD implantation. A critical factor contributing to the long-term success of this patient was the decision to select an LVAD that would not disrupt the diaphragm and thus preserve the respiratory muscle strength. This case demonstrates that permanent mechanical LVADs should be considered for appropriately selected Duchenne muscular dystrophy patients with medically refractory end-stage cardiomyopathy.

Recently, the symptom of bendopnea, that is, shortness of breath when bending forwards such as when putting on shoes, has been described in heart failure patients and found to be associated with higher ventricular filling pressures, particularly in the setting of low cardiac index. However, it is not known whether bendopnea is associated with clinical outcomes.In a prospective convenience sample of 179 patients followed in our heart failure disease management clinic, we determined the presence of bendopnea at the time of enrollment and ascertained clinical outcomes through 1 year of follow-up. We performed univariate and stepwise multivariable modeling to test the association of bendopnea with clinical outcomes.Bendopnea was present in 32 of 179 (18%) subjects. At 1 year, those with versus without bendopnea were at increased risk of the composite endpoint of death, heart failure admission, inotrope initiation, left ventricular assist device implantation, or cardiac transplantation in univariate (hazard ratio [HR] 1.9, P.05) but not multivariable (HR 1.9, P = .11) analysis. Bendopnea was more strongly associated with short-term outcomes including heart failure admission at 3 months in both univariate (HR 3.1, P.004) and multivariable (HR 2.5, P = .04) analysis.Bendopnea was associated with an increased risk of adverse outcomes in ambulatory patients with heart failure, particularly heart failure admission at 3 months.

Background The practice of induction therapy with either rabbit anti-thymocyte globulin (r-ATG) or interleukin-2 receptor antagonists (IL-2RA) is common among heart transplant recipients. However, its benefits in the setting of contemporary maintenance immunosuppression with tacrolimus/mycophenolic acid (TAC/MPA) are unknown. Methods We compared post-transplant mortality among three induction therapy strategies (r-ATG vs IL2-RA vs no induction) in a retrospective cohort analysis of heart transplant recipients maintained on TAC/MPA in the Organ Procurement Transplant Network (OPTN) database between the years 2006 and 2015. We used a multivariable model adjusting for clinically important co-morbidities, and a propensity score analysis using the inverse probability weighted (IPW) method in the final analysis. Results In multivariable IPW analysis, r-ATG (HR = 1.23; 95% CI = 1.05-1.46, P = 0.01) remained significantly associated with a higher mortality. There was a trend toward having a higher mortality in the IL2-RA (HR = 1.11; 95% CI = 1.00-1.24, P = 0.06) group. Subgroup analyses failed to show a patient survival benefit in using either r-ATG or IL2-RA among any of the subgroups analyzed. Conclusion In this contemporary cohort of heart transplant recipients receiving TAC/MPA, neither r-ATG nor IL2-RA were associated with a survival benefit. On the contrary, adjusted analyses showed a significantly higher mortality in the r-ATG group and a trend toward higher mortality in the IL2-RA group. While caution is needed in interpreting treatment effects in an observational cohort, these data call into question the benefit of induction therapy as a common practice and highlight the need for more studies.

Agitated saline during central line placement is described for the purpose of identifying the subclavian vein during ultrasound-guided procedures.

There have been over 15,000 continuous flow left ventricular assist devices (LVADs) implanted in the United States1 . As the care of these patients expands into the general community, it is important for providers at all levels to be familiar with the sound of a normal LVAD. The sound generated is normally described as an “LVAD hum”. That non-descriptive term may be misunderstood as all LVADs or “hums” are the same, when in fact the sound produced is unique to each device. Another common misconception held by some providers, is the absence of heart sounds in a normally functioning LVAD. Using apex phonocardiography we were able to better visualize these unique characteristics (Figures 1-4, phonocardiograms of three United States Food and Drug Administration approved durable LVADs), and suggest a refined description of each device sound. The recordings were made on normal functioning LVADs using the EKO Core stethoscope attachment (EKO, Berkeley, CA).

Conduction abnormalities are known to occur after heart transplantation. In some cases, a permanent pacemaker is required. Conventional transvenous pacemakers can result in several complications, mainly related to the leads and device pocket. Leadless pacemaker technology was developed to overcome these issues. We report what we believe is the first US case of a leadless pacemaker implant (specifically in a heart transplant recipient) with the longest reported duration of follow-up.

To the Editor : We read with great interest the article by Mgbokikwe et al about newer and more sophisticated imaging modalities for the evaluation of infective endocarditis.[1][1] As outlined in Table 1 of the article, each imaging method has its advantages and limitations. One further imaging

Bloodstream infections (BSIs) are common in patients with continuous-flow left ventricular assist devices (CF-LVADs). Whether CF-LVADs modulate the febrile response to BSIs is unknown. We retrospectively compared the febrile response to BSIs in patients with heart failure (HF) with CF-LVADs versus a control population of patients with HF receiving inotropic infusions. BSIs were adjudicated using the Centers for Disease Control and Prevention and the National Healthcare Safety Network criteria. Febrile status (temperature ≥38°C, 100.4 °F), temperature at presentation with BSI, and the highest temperature within 72 hours (Tmax) were collected. We observed 59 BSIs in LVAD patients and 45 BSIs in controls. LVAD patients were more likely to be afebrile and to have a lower temperature at presentation than control (88% vs 58%, p=0.002, and 37°C ±0.7 vs 37.7°C ±1.0, p=0.0009, respectively). By 72 hours, the difference in afebrile status diminished (53% vs 44%, p=0.42), and the Tmax was similar between the LVAD and control groups (37.9°C±0.9 vs 38.2°C±0.8, respectively, p=0.10). In conclusion, at presentation with a BSI, the vast majority of CF-LVAD patients were afebrile, an event which occurred at a higher frequency when compared with patients with advanced HF on chronic inotropes via an indwelling venous catheter. These data alert clinicians to have a very low threshold to obtain blood cultures in CF-LVAD patients even in the absence of fever. Further study is needed to determine whether a delayed or diminished febrile response represents another pathophysiological consequence of CF-LVADs.

Background: Basic and advanced cardiac life support guidelines do not address resuscitation of patients with continuous-flow (CF) left ventricular assist devices (LVADs). As the population of LVAD patients increases, it becomes important to understand how to provide emergency care to such patients.We retrospectively reviewed a consecutive series of patients with an implanted CF-LVAD who had an in-hospital cardiopulmonary arrest at our medical center from January 2011 to October 2013. We compared them with a matched cohort of patients without LVADs who had an inhospital cardiopulmonary arrest during the same time period. Code documentation was used to determine arrest characteristics, perfusion assessment techniques, and time to cardiopulmonary resuscitation (CPR) initiation. There were 415 in-hospital arrests during the study period, and 4% (n 5 16) occurred in patients with CF-LVADs. Response teams used various approaches to assess arterial perfusion, including palpation or Doppler of the arterial pulse and measurement of blood pressure by Doppler or arterial line. Nine of the 16 patients required CPR, but only 5 (56%) received CPR in !2 minutes. In the control group (n 5 32) of patients without an LVAD, 22 received CPR, which was initiated within 2 minutes in all (100%) of the patients.Cardiopulmonary arrests in LVAD patients accounted for 4% of all arrests in our center. We identified important time delays in CPR initiation, highlighting the need to develop resuscitation guidelines for this patient population.

Background Duchenne muscular dystrophy ( DMD ) is frequently complicated by development of a cardiomyopathy. Despite significant medical advances provided to DMD patients over the past 2 decades, there remains a group of DMD patients who die prematurely. The current study sought to identify a set of prognostic factors that portend a worse outcome among adult DMD patients. Methods and Results A retrospective cohort of 43 consecutive patients was followed in the adult UT Southwestern Neuromuscular Cardiomyopathy Clinic. Clinical data were abstracted from the electronic medical record to generate baseline characteristics. The population was stratified by survival to time of analysis and compared with characteristics associated with death. The DMD population was in the early 20s, with median follow‐up times over 2 years. All the patients had developed a cardiomyopathy, with the majority of the patients on angiotensin‐converting enzyme inhibitors (86%) and steroids (56%), but few other guideline‐directed heart failure medications. Comparison between the nonsurviving and surviving cohorts found several poor prognostic factors, including lower body mass index (17.3 [14.8–19.3] versus 25.8 [20.8–29.1] kg/m 2 , P P =0.001), maximum inspiratory pressures (13 [0–30] versus 33 [25–40] cmH 2 O, P =0.03), and elevated cardiac biomarkers (N‐terminal pro‐brain natriuretic peptide: 288 [72–1632] versus 35 [21–135] pg/mL, P =0.03]. Conclusions The findings demonstrate a DMD population with a high burden of cardiomyopathy. The nonsurviving cohort was comparatively underweight, and had worse respiratory profiles and elevated cardiac biomarkers. Collectively, these factors highlight a high‐risk cardiovascular population with a worse prognosis.

Background Induction therapy in simultaneous heart-kidney transplantation (SHKT) is not well studied in the setting of contemporary maintenance immunosuppression consisting of tacrolimus (TAC), mycophenolic acid (MPA), and prednisone (PRED). Methods We analyzed the Organ Procurement and Transplant Network registry from January 1, 2000, to March 3, 2015, for recipients of SHKT ( N = 623) maintained on TAC/MPA/PRED at hospital discharge. The study cohort was further stratified into 3 groups by induction choice: induction ( n = 232), rabbit anti-thymoglobulin (r-ATG; n = 204), and interleukin-2 receptor-α ( n = 187) antagonists. Survival rates were estimated using the Kaplan-Meier estimator . Multivariable inverse probability weighted Cox proportional hazard regression models were used to assess hazard ratios associated with post-transplant mortality as the primary outcome. The study cohort was censored on March 4, 2016, to allow at least 1-year of follow-up. Results During the study period, the number of SHKTs increased nearly 5-fold. The Kaplan-Meier survival curve showed superior outcomes with r-ATG compared with no induction or interleukin-2 receptor-α induction. Compared with the no-induction group, an inverse probability weighted Cox proportional hazard model showed no independent association of induction therapy with the primary outcome. In sub-group analysis, r-ATG appeared to lower mortality in sensitized patients with panel reactive antibody of 10% or higher (hazard ratio, 0.19; 95% confidence interval, 0.05–0.71). Conclusion r-ATG may provide a survival benefit in SHKT, especially in sensitized patients maintained on TAC/MPA/PRED at hospital discharge.

Hypoglycemia in people with diabetes mellitus (DM) has been potentially linked to cardiovascular morbidity and mortality. Pathophysiologically, hypoglycemia triggers activation of the sympathoadrenal system, leading to an increase in counter-regulatory hormones and, consequently, increased myocardial workload and oxygen demand. Additionally, hypoglycemia triggers proinflammatory and hematologic changes that provide the substrate for possible myocardial ischemia in the already-diseased diabetic cardiovascular system. Hypoglycemia creates electrophysiologic alterations causing P-R-interval shortening, ST-segment depression, T-wave flattening, reduction of T-wave area, and QTc-interval prolongation. Patients who experience hypoglycemia are at an increased risk of silent ischemia as well as QTc prolongation and consequent arrhythmias. The Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial showed an increase in all-cause mortality with intensive glycemic control, whereas the Action in Diabetes and Vascular Disease: Preterax and Diamicron Modified Release Controlled Evaluation (ADVANCE) study and Veteran's Affairs Diabetes Trial (VADT) showed no benefit with aggressive glycemic control. Women, elderly patients, and those with renal insufficiency are more vulnerable to hypoglycemic events. In fact, hypoglycemia is the most common metabolic complication experienced by older patients with DM in the United States. The concurrent use of medications like β-blockers warrants caution in DM because they can mask warning signs of hypoglycemia. Here we aim to elucidate the pathophysiology, review the electrocardiographic changes, analyze the current clinical literature, and consider the safety considerations of hypoglycemia as it relates to the cardiovascular system. In conclusion, in the current era of DM and its vascular ramifications, hypoglycemia from a cardiologist's perspective deserves due attention.

Background We previously reported that after completion of 3 months of prophylactic treatment with valganciclovir in cytomegalovirus (CMV) donor positive, recipient negative (D+/R-) heart transplant patients, there was a high incidence of CMV disease, with six out of seven recipients (86%) developing CMV disease within the next 6 months. A novel, three-tiered CMV prophylactic strategy for D+/R-heart transplant recipients was thus implemented at our center in 2010. The efficacy of this strategy is unknown. Methods We retrospectively reviewed consecutive heart transplants between September 2010 and December 2013. The novel 3-tiered CMV protocol administered to D+/R- patients consisted of: 1) Renally-dosed valganciclovir, starting on post-operative day 5 and continuing for 12 months, if tolerated; 2) CMV Immune Globulin administration through 16 weeks; and 3) Azathioprine rather than mycophenolate mofetil for immunosuppression. The diagnosis of CMV disease, consisting either of the CMV syndrome or tissue-invasive CMV infection, was established according to American Society of Transplantation Guidelines for clinical CMV infection. Results Of seventy-five heart transplant recipients, 17 (23%) were CMV D+/R-. Three of the 17 died of non-CMV causes within the first year. Among the remaining 14 recipients, CMV disease occurred in the first year in 3 (21%) recipients. Following cessation of valganciclovir at one year, another 4 (29%) recipients developed CMV disease within the next 6 months. Conclusion CMV D+/R- heart transplant recipients appear to have a lower incidence of CMV disease in the first year using a novel prophylactic regimen as compared to a historical group at our program. CMV D+/R- patients remain at risk of developing CMV disease with valganciclovir discontinuation, even after a full year of prophylactic treatment. Figure 1

Background: DMD-associated cardiomyopathy is the primary cause of death in DMD, but the mechanism has not been well characterized. In DMD, skeletal muscle degeneration and atrophy occurs. Therefore, we hypothesize that cardiac remodeling occurs secondary to cardiac atrophy rather than pathological

Although risk factors for left ventricular (LV) hypertrophy in the native heart are well known, as is its association with increased risk of adverse outcomes, such information is poorly defined in heart transplant (HTx) recipients. We determined whether increased LV mass and concentricity (mass/volume) were associated with death in patients after HTx.Between May 2003 and May 2006, 140 HTx recipients underwent cardiac magnetic resonance imaging (MRI). Clinical characteristics associated with increased LV mass were determined. Cox proportional hazard models were constructed to assess the relationship of LV mass and concentricity with death.MRIs were acquired a median of 6.0 years after transplant. The top quartile of indexed LV mass and concentricity were 35.8 g/m(2.7) or higher and 1.5 g/ml or higher, respectively. History of rejection (odds ratio [OR], 5.9; 95% confidence interval [CI], 2.1-16.4; p0.01), diabetes (OR, 3.3; 95% CI, 1.3-8.2; p = 0.01), and post-transplant year of MRI acquisition (OR, 1.2; 95% CI, 1.1-1.4; p0.01) were associated with the top quartile of LV mass in multivariable models. LV mass and concentricity were independently associated with cardiovascular death (hazard risk [HR], 1.11 per g/m;(2.7) HR, 10.1 per g/ml, p ≤ 0.01, respectively). LV concentricity was independently associated with all-cause mortality (HR, 4.4 per g/ml, p0.01).A history of rejection and diabetes are associated with increased LV mass. Increased LV mass, particularly of a concentric phenotype, is an independent risk factor for cardiovascular and all-cause mortality after HTx.