Amrit Malik

Reduced hospitalizations in severe, refractory congestive heart failure with peritoneal dialysis: a consecutive case series.

BACKGROUND Peritoneal dialysis (PD) for long-term management of diuretic resistant volume overload in heart failure (HF) may provide potential benefit with few adverse consequences. We examined the impact of PD on clinical status hospitalizations, and complications of therapy in severe end-stage HF. METHODS A consecutive case series of 10 transplant ineligible patients receiving PD solely for HF volume management between 2007 and 2011 was evaluated with clinical data reviewed pre- and post-PD initiation. RESULTS The mean ejection fraction (EF) pre-PD was 24.5 ± 6.0% with the majority of patients having NYHA class IIIB symptoms and moderate-severe right ventricular dysfunction. 9/10 patients were Stage 3 chronic kidney disease (CKD) or worse. After PD initiation, average weight loss was almost 7 kg (p = 0.016) with improvement in diuretic response, peripheral edema, and functional class. There was a significant decrease in re-hospitalization from an average of 3.2 ± 2.5 to 0.1 ± 0.3 admissions per patient (p = 0.007) and reduced average length of stay from 37 ± 36.7 to 0.78 ± 2.3 days (p = 0.019). SUMMARY Objective criteriabased institution of PD for the treatment of diuretic refractory severe-end-stage HF was well tolerated and demonstrated favorable outcomes; these included improved clinical status, reduced hospitalizations and length of stay, with very few and easily treatable PDrelated complications. PD appears to be a viable option in refractory, end-stage congestive heart failure (CHF).

Gender-related gene expression in response to dietary fatty acids and predisposition to atherosclerosis and cardiovascular disease

Abstract There is now overwhelming evidence that nutritional genomics has the potential to change dietary guidelines and personal dietary recommendations. While the field of nutrigenomics determines the impact of nutrients on the genome, proteome and metabolome, nutrigenetics, involves understanding the role of genetic variation in the interaction between diet and disease. It is evident that nutrigenetics has the potential to provide the basis for personalized dietary recommendations based on the individual’s genetic makeup. Although men and women share in common most of their genetic information, significant differences in susceptibilities to complex diseases such as atherosclerosis and cardiovascular disease exist. Accordingly, this review discusses the modulation of gene expression by dietary fatty acids in a gender-specific manner, which may open new approaches in dietary intervention of atherosclerosis and cardiovascular disease that are linked to sex.

Serum sickness after antithymocyte globulin administration in a cardiac transplant patient.

CLINICAL HISTORY A 57-year-old gentleman with allo-geneic heart transplantation for nonischemic cardiomyopathy developed nonspecific graft dysfunction 3 years posttransplant. He had no documented cellular or antibody-mediated rejection, graft vasculopathy, and donor-specific antibodies on panel reactive antibody testing. Plasmapheresis and IV immunoglobulin infusions were initiated in addition to increases in maintenance immuno-suppression therapy with no significant impact on his reduced ejection fraction. Because of recurrent presentations of decompensated heart failure despite escalation of care, ATG therapy was initiated with 75 mg of IV rabbit ATG daily for 3 days followed by 50 mg IV for 1 day. Nine days after IV thymoglobulin therapy, he presents with fever, chills, lip swelling, and myalgias. Physical examination revealed mild congestive heart failure and an erythematous and pruritic maculopapular rash. He had tender polyarthritis in his extremities with significant restriction to active and passive range of motion (Fig. 1). Laboratory investigations revealed mild leukocytosis, elevated C-reactive protein, and acute renal insufficiency with no evidence of active sediments on urinalysis. Cytomegalovirus testing was unremarkable. Based on this inflammatory presentation and clinical context, he was diagnosed with SS secondary to IV ATG and started on IV methylprednisolone 1 g daily for 6 days. Failing to show significant improvement at 48 hours, plasmapheresis was initiated for 5 days with marked symptomatic relief after the first exchange. He was discharged home on his 10th day of admission with complete resolution of his presenting symptoms.

The Use of Intranasal Fentanyl for the Palliation of Incident Dyspnea in Advanced Congestive Heart Failure: A Pilot Study

Background: Dyspnea is distressing in palliative patients with end-stage heart failure and many are hospitalized to optimize this symptom. We hoped to conduct a pilot study to determine whether the administration of intranasal fentanyl would decrease activity-induced dyspnea in this patient population. Methods: Patients performed two 6-minute walk tests with and without the administration of 50 μg of intranasal fentanyl. Vital signs were recorded before and after each walk, as were participant reported dyspnea and adverse events scores. Results: Twenty-four patients were screened, 13 were deemed eligible, and 6 completed the study. Dyspnea scores changed from a mean of 6.00 immediately after the walk without fentanyl to a mean of 3.83 after the walk with fentanyl (P = .048). Mean respiratory rate decreased from 21.0 to 18.7 (P = .034) breaths per minute and was considered a favorable outcome by the participants. Distance walked did not significantly increase with the fentanyl pretreatment (136.0-144.2 m; P = .283), although the participants reported feeling better while walking a similar distance. Conclusions: In this pilot study, the preadministration of intranasal fentanyl prior to activity in palliative, end-stage hospitalized heart failure patients, safely reduced tachypnea, and the feeling of shortness of breath. This approach may help palliate advanced heart failure patients by alleviating symptoms brought on by exertional activities.

End of life decisions in heart failure: to turn off the intracardiac device or not?

Purpose of review Heart failure is a significant public health concern around the world. Implantable cardioverter defibrillators with or without cardiac resynchronization therapy (CRT-D) have proven survival benefit. As patients progress to end-stage disease, management shifts to palliative care, and cardiologists are often confronted with how to best manage these devices. Recent findings Studies suggest that up to one-third of patients with an implantable cardioverter defibrillator receive painful shocks in the last 24 h of life. Disabling pacing or resynchronization devices may further weaken the heart function and expedite death, particularly if the patient has no underlying ventricular rhythm. Is it ethical or legal to discontinue functions of the implantable device? The discussion and the decision to be made are whether to continue both pacing and tachyarrhythmia therapies, disable tachyarrhythmia therapies while maintaining pacing, or discontinue both. Summary The decision to disable all or parts of the device function is ultimately up to the patient. To avoid painful shocks near the end of life, it is recommended that tachyarrhythmia therapies be turned off when the patient is being treated palliatively. After informed discussion, withdrawing the resynchronization or pacing device option is also acceptable if requested by the patient regardless of the potential outcomes.

Functional Adaptation During the Development of Cardiac Hypertrophy and Heart Failure in Females

Cardiac hypertrophy is an adaptive response of the heart to hemodynamic overload, during which terminally differentiated cardiomyocytes increase in size without undergoing cell division. Although the hypertrophic response may serve to maintain cardiac function for a certain period, prolonged hypertrophy becomes detrimental, resulting in cardiac dysfunction and heart failure. It is well known that both cardiac hypertrophy and heart failure are associated with cardiac remodeling as a consequence of the activation of β-adrenoceptor systems and apoptotic pathways; however, gender disparities in the type and extent of cardiac hypertrophy and occurence of cardiac dysfunction exist. The risk of death from heart failure in women lags about 10 years behind men, but the gap in the incidence rates is narrowed with advancing age. The mechanisms for the gender differences in the development of cardiac hypertrophy and heart failure as well as the mechanisms involved in cardioprotection in adult females are not completely understood. This article highlights some of the gender-related differences in the β-adrenergic system and cardiomyocyte apoptosis with respect to cardiac remodeling in cardiac hypertrophy and heart failure. Furthermore, the role of ovaries and estrogen replacement therapy in attenuating changes in β-adrenergic system, cardiomyocyte apoptosis, and cardiac remodeling during hypertrophy and failing stages of the female heart are also discussed.