Rodolfo D. Benatti

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.

Heart failure in patients with human immunodeficiency virus infection: Epidemiology and management disparities.

BACKGROUND Persons living with HIV are at a higher risk of cardiovascular disease despite effective antiretroviral therapy and dramatic reductions in AIDS-related conditions. We sought to identify the epidemiology of heart failure (HF) among persons living with HIV in the United States in an era of contemporary antiretroviral therapy. METHODS Explorys is an electronic healthcare database that aggregates medical records from 23 healthcare systems nationwide. Using systemized nomenclature of medicine-clinical terms (SNOMED-CT), we identified adult patients (age>18), who had active records over the past year (September 2014-September 2015). We described the prevalence of HF in HIV patients by demographics and treatment and compared them to HIV-uninfected controls. RESULTS Overall, there were 36,400 patients with HIV and 12,208,430 controls. The overall prevalence of HF was 7.2% in HIV and 4.4% in controls (RR 1.66 [1.60-1.72], p<0.0001). The relative risk of HF associated with HIV infection was higher among women and younger age groups. Patients receiving antiretroviral therapy had only marginally lower risk (6.4% vs. 7.7%, p<0.0001) of HF compared to those who were untreated. Compared to uninfected patients with HF, HIV patients with HF were less likely to receive antiplatelet drugs, statins, diuretics, and ACE/ARBs (p<0.0001 for all comparisons). For patients with HIV and HF, receiving care from a cardiologist was associated with higher use of antiplatelets, statins, betablockers, ACE/ARBs, and diuretics. CONCLUSIONS Persons with HIV are at higher risk for HF in this large contemporary sample that includes both men and women. Although the prevalence of heart failure is higher in older HIV patients, the relative risk associated with HIV is highest in young people and in women. HIV patients are less likely to have HF optimally treated, but cardiology referral was associated with higher treatment rates.

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 1980s 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.

Platelet Inhibition With Ticagrelor for Left Ventricular Assist Device Thrombosis

Although considered standard therapy for Stage D heart failure since 2008, the continuous, axial flow HeartMate II (HMII) left ventricular assist device (LVAD) has recently been associated with unexpected rise in rates of pump thrombosis.1 With an incidence of 0.01 to 0.11 events per patient-year, LVAD thrombosis responds to intensification of antithrombotic therapy with unfractionated heparin (UFH), dual antiplatelet therapy with or without thrombolytics or glycoprotein IIb/IIIa inhibition in <50% of cases, and is associated with nearly 50% 6-month mortality.1 Therefore, surgical pump exchange or urgent transplantation remains the treatment of choice despite potential high risk and cost. Herein, we report the first successful experience using the potent P2Y12 ADP receptor inhibitor ticagrelor in addition to UFH and aspirin (acetylsalicylic acid [ASA]) to treat LVAD thrombosis and avoid pump exchange in 4 patients with confirmed or suspected HMII thrombosis. With institutional Instituitional Review Board approval, we reviewed medical records of 4 consecutive patients admitted to the cardiac intensive care unit at our institution with confirmed or suspected LVAD thrombosis. LVAD thrombosis was diagnosed in the presence of abrupt elevations of serum lactate dehydrogenase (LDH) to >900 mg/dL without (suspected LVAD thrombosis) or with (confirmed LVAD thrombosis) 1 of the following: (1) abnormal LVAD flows or power surges, (2) clinical symptoms of heart failure, or (3) supporting echocardiographic ramp study. We determined antiplatelet activity using VerifyNow P2Y12 assay, with values >230 P2Y12 reaction units (PRU) indicating nonresponder status. Patients were treated clinically using standard doses of medications based on clinical preference. ### Patient 1 A 28-year-old black man had HMII implanted as destination therapy for nonischemic cardiomyopathy before 7 days. Postsurgical course was complicated by slowly increasing LDH with peak of 980 U/L, requiring maintenance of UFH in addition to ASA 325 mg daily, dipyridamole, later switched to clopidogrel. Because LDH remained …

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

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.