Heart transplant outcomes in patients with Chagas cardiomyopathy in the United States.

BACKGROUND: Chagas cardiomyopathy (CC) is one of the chronic manifestations of Trypanosoma cruzi (T. cruzi) infection and is among the leading reasons for heart transplantation (HT) in Latin America. Chagas disease is also present in areas with large Hispanic communities in the United States. Our objective is to evaluate the outcomes of cardiac allograft recipients with the diagnosis of CC in the United States. METHODS AND RESULTS: We identified 25 adult patients with CC and 15 930 with idiopathic dilated cardiomyopathy (IDCMP) who underwent HT between 1987 and 2015. CC patients were mostly Hispanics, had lower mean pulmonary artery pressure (23 vs 29 mm Hg, P = .035) and lower BMI (24 vs 26, P = .007). Patients with CC were more likely to be supported with a total artificial heart (TAH) as bridge to transplant (P = .009). There were no statistical differences for overall mortality and graft survival between CC and IDCMP cardiac allograft recipients. Induction therapy and mycophenolate mofetil (MMF) use were associated with higher rate of infection in Chagas patients. CONCLUSIONS: Heart transplantation recipients with CC diagnosis appear to have similar outcomes to IDCMP patients. Induction therapy and MMF use may be associated with higher risk of infection in CC patients who underwent transplantation.

Heart Transplantation for Chagas Cardiomyopathy.

Chagas cardiomyopathy (CC) is one of the chronic manifestations of Trypanosoma cruzi (T. cruzi) infection and is a major public health disease in Latin America. Since it is a chronic systemic infection, Chagas disease was long considered a potential contraindication for transplantation because of the risk of recurrence with immunosuppression. However, early South American experience in the 1980's established the feasibility of heart transplantation (HT) in patients with Chagas disease. Indeed, the first cardiac transplant for a recipient with CC was performed in 1985 in Brazil. Chagas etiology of heart failure has become the third most common indication for HT in South America. T. cruzi reactivation post-transplant is a common issue that requires prophylactic surveillance but responds well to appropriate therapy. Chagas reactivation has been associated with the potency of the immunosuppressive protocol and occurs more frequently after rejection episodes. Yet, many important questions regarding the management of Chagas HT candidates and recipients remain unanswered. For example, biventricular systolic failure is frequent in end-stage CC, but its impact on the modality of mechanical circulatory bridging has not been described. Also, there is no consensus regarding the most adequate immunosuppressive regimen that balances the risk of graft rejection and disease reactivation. The real efficacy and safety of HT for end-stage CC will only be appreciated when a Latin American transplant registry is established. This review covers the current state of the art of HT for CC.

Left Ventricular Assist Devices or Inotropes for Decreasing Pulmonary Vascular Resistance in Patients with Pulmonary Hypertension Listed for Heart Transplantation.

BACKGROUND: Fixed pulmonary hypertension is common in patients with advanced heart failure and is a contraindication for heart transplantation. Left ventricular assist devices (LVAD) and inotropes have been used to reduce pulmonary vascular resistance (PVR) and allow transplantation. However, little is known about the efficacy of this strategy. METHODS: We queried the United Network for Organ Sharing registry for all adult patients (age ≥18 years) listed for primary heart transplantation (2008-2014) with PVR of >5 wood units (WU) or transpulmonary gradient >16 mmHg who were treated with LVAD or IV inotropes as status 1a, 1b, or 7. We compared waitlist mortality/delisting and absolute changes in hemodynamics between listing and transplantation. RESULTS: Of 18,009 patients listed during the study period, 1016 were included in the analysis (393 LVAD, 623 inotropes), with a mean age of 52.9 ± 11.6 years, 74% male, and 38% had ischemic etiology. Mean PVR was 5.7 ± 2.4 WU and transpulmonary pressure gradient 19.3 ± 5.3 mmHg. Compared with the inotrope group, LVAD patients were more likely listed as status 1A (32.8% vs 18.1%, P < .001), had lower PVR (5.3 WU vs 5.9 WU, P = .001), and higher cardiac output (4.1 vs 3.6 L/min, P < .001). After a mean of 239 days, PVR decreased by 1.71 WU in the LVAD group vs 1.85 WU in the inotrope group (P = .52). PVR normalization (<2.5 WU) occurred at similar rates among those treated with inotropes and LVAD (30.7% vs 35.6%, P = .228). Waitlist mortality was similar between LVAD and inotropes (adjusted P = .837). Absolute PVR and transpulmonary pressure gradient reductions correlated with time on the waitlist (P < .001 for both comparisons). CONCLUSION: Only about one-third of patients with fixed pulmonary hypertension achieve normalization of PVR before transplant with either LVAD or inotropes. Similar waitlist mortality was observed among patients bridged with either strategy.

Strain-time curve analysis by speckle tracking echocardiography in cardiac resynchronization therapy: Insight into the pathophysiology of responders vs. non-responders.

BACKGROUND: Patients with non-ischemic heart failure etiology and left bundle branch block (LBBB) show better response to cardiac resynchronization therapy (CRT). While these patients have the most pronounced left ventricular (LV) dyssynchrony, LV dyssynchrony assessment often fails to predict outcome. We hypothesized that patients with favorable outcome from CRT can be identified by a characteristic strain distribution pattern. METHODS: From 313 patients who underwent CRT between 2003 and 2006, we identified 10 patients who were CRT non-responders (no LV end-systolic volume [LVESV] reduction) with non-ischemic cardiomyopathy and LBBB and compared with randomly selected CRT responders (n = 10; LVESV reduction ≥15%). Longitudinal strain (εlong) data were obtained by speckle tracking echocardiography before and after (9 ± 5 months) CRT implantation and standardized segmental εlong-time curves were obtained by averaging individual patients. RESULTS: In responders, ejection fraction (EF) increased from 25 ± 9 to 40 ± 11% (p = 0.002), while in non-responders, EF was unchanged (20 ± 8 to 21 ± 5%, p = 0.57). Global εlong was significantly lower in non-responders at pre CRT (p = 0.02) and only improved in responders (p = 0.04) after CRT. Pre CRT septal εlong -time curves in both groups showed early septal contraction with mid-systolic decrease, while lateral εlong showed early stretch followed by vigorous mid to late contraction. Restoration of contraction synchrony was observed in both groups, though non-responder remained low amplitude of εlong. CONCLUSIONS: CRT non-responders with LBBB and non-ischemic etiology showed a similar improvement of εlong pattern with responders after CRT implantation, while amplitude of εlong remained unchanged. Lower εlong in the non-responders may account for their poor response to CRT.