Depressive symptoms are associated with clinical outcomes in heart failure with reduced ejection fraction.

AIMS: The objective of this study was to examine associations between elevated depressive symptoms and increased risk of adverse clinical events patients with heart failure and reduced ejection fraction (HFrEF), as well as the potential contribution of health behaviours. METHODS AND RESULTS: One hundred forty-two men and women with HFrEF were enrolled through heart failure (HF) clinics and followed over time. At baseline and 6 months, depressive symptoms were assessed by the Beck Depression Inventory-II (BDI-II) and HFrEF disease activity by B-type natriuretic peptide (BNP). The Self-Care of Heart Failure Index (SCHFI) was used to assess HF self-care behaviours. Proportional hazards regression models assessed the contribution of depressive symptoms and HFrEF disease biomarkers on death or cardiovascular hospitalization. Over a median follow-up period of 4 years, 42 patients (30%) died, and 84 (60%) had cardiovascular hospitalizations. A 10-point higher baseline BDI-II score was associated with a 35% greater risk of death or cardiovascular hospitalization. Higher baseline BDI-II scores were associated with poorer HF self-care maintenance behaviours (R = -0.30, P < 0.001) and fewer daily steps (R = -0.19, P = 0.04), suggesting that elevated depressive symptoms may diminish important health behaviours. Increases in plasma BNP over 6 months were associated with worse outcomes. Changes in BDI-II and plasma BNP over 6 months were positively related (R = 0.25, P = 0.004). CONCLUSIONS: This study confirms that elevated depressive symptoms are associated with an increased likelihood of adverse clinical outcomes in patients with HFrEF. Poor health behaviours may contribute to the adverse association of elevated depressive symptoms with the increased hazard of adverse clinical outcomes.

Association of Depression Symptoms and Biomarkers of Risk on Clinical Outcomes in HFrEF.

BACKGROUND: Prior studies have demonstrated an association of depression with adverse clinical outcomes in patients with HFrEF, but the possible mechanisms responsible for the association are not unserstood. METHODS: 142 men and women with HFrEF were enrolled through HF clinics and followed over time. At baseline and 6-months, depression was assessed by the Beck Depression Inventory (BDI-II) and disease activity by B-type natriuretic peptide (BNP). Proportional Hazards Regression Models assessed the contribution of depressive symptoms and HFrEF disease biomarkers on death or cardiovascular hospitalization. RESULTS: Over a median follow-up period of 4 years, 42 patients (30%) died, and 84 (60%) had cardiovascular hospitalizations. A 10-point higher baseline BDI-II score was associated with a 35% higher hazard of death or cardiovascular hospitalization. Greater baseline BDI-II scores were associated with poorer HF self-care maintenance (R=-0.30, p<0.001) and fewer daily steps (R=-0.19, p=0.04), suggesting that depression may adversely affect important health behaviors. Increases in plasma BNP over 6 months were associated with worse outcomes. Changes in BDI-II score and plasma BNP over 6 months were positively correlated (R=0.25, p=0.004). CONCLUSIONS: This study underscores the importance of elevated depression symptoms and their association with an increased likelihood of adverse clinical outcomes in patients with HFrEF. Health behaviors may play a greater role than direct biobehavioral pathways in the adverse effects of depression on the HF disease trajectory and resultant clinical outcomes.

Unexpected case of chagas disease reactivation in endomyocardial biopsy for evaluation of cardiac allograft rejection.

Acute Chagas disease reactivation (CDR) after cardiac transplantation is a well-known phenomenon in endemic countries of Central and South America and Mexico, but is rare outside of those countries. In this report, we describe a case of a 49-year-old male who presented 25 weeks after heart transplant with clinical features concerning for acute rejection, including malaise, anorexia, weight loss, and fever. His immunosuppression therapy included tacrolimus, mycophenolate, and prednisone. An endomyocardial biopsy revealed lymphocytic and eosinophilic inflammation, myocyte damage, and rare foci of intracellular organisms consistent with Trypanosoma cruzi amastigotes. The patient had no known history of Chagas disease. Upon additional questioning, the patient endorsed bites from reduviid bugs during childhood in El Salvador. Follow-up serum PCR testing was positive for T. cruzi DNA. Tests for other infectious organisms and donor specific antibodies were negative. This case illustrates the striking clinical and histologic similarities between acute cellular rejection and acute CDR with cardiac involvement in heart transplant patients, and thus emphasizes the importance of pre-transplant testing for Chagas in patients with epidemiologic risk factors.

Heart Failure: Advanced Refractory Heart Failure.

End-stage heart failure (HF) is associated with an extremely poor prognosis. Progressive and/or persistent HF signs and symptoms in the setting of optimal therapy is the hallmark of more advanced disease. Physicians must be able to recognize patients with features of refractory HF to aid in timely evaluation for advanced therapy options. Left ventricular assist device implantation and heart transplantation prolong survival in patients with end-stage HF, but are options only for select patients. Timely referral for evaluation is necessary to prevent secondary irreversible end-organ dysfunction and to ascertain whether there are factors that can be addressed and corrected. All patients with end-stage HF should be offered referral for palliative care to aid in symptom management and improve quality of life. In addition, for patients who are not candidates for advanced therapy options, hospice should be discussed. In some cases, palliative home inotrope infusion can be considered for symptom management.

Five-year Outcomes of Pulmonary Hypertension With and Without Elevated Left Atrial Pressure in Patients Evaluated for Kidney Transplantation.

BACKGROUND: Pulmonary hypertension (PH) is frequently reported in patients with advanced chronic kidney disease and is associated with early allograft failure and death. However, the causes of PH are heterogeneous, and patient prognosis may vary by etiologic subtype. METHODS: Data from the University of North Carolina Cardiorenal Registry were examined to determine associations between PH, with or without elevated left atrial pressure (eLAP), and mortality in candidates for kidney transplantation. PH and eLAP were determined by Doppler echocardiography and by tissue Doppler imaging, respectively. RESULTS: From 2006 to 2013, 778 registry patients were screened preoperatively by echocardiography. Most patients were black (64%) and men (56%); the mean age was 56 years. PH was identified in 97 (12%) patients; of these, eLAP was prevalent in half. During a median follow-up of 4.4 years, 179 (23%) received a kidney transplant, and 195 (25%) died. After adjustments for demographics, comorbidities, dialysis vintage, and kidney transplantation, PH was associated with twice the 5-year mortality (hazard ratio [HR] = 2.11; 95% confidence interval [CI]: 1.48-3.03), with stronger associations in the absence of eLAP (HR = 2.87; 95% CI: 1.83-4.49) than with eLAP (HR = 1.11; 95% CI: 0.57-2.17), P for interaction = 0.01. CONCLUSIONS: The mortality risk associated with PH among patients with advanced chronic kidney disease appears to differ by etiology. Patients with PH in the absence of eLAP are at high risk of death and in need of focused attention. Future research efforts should investigate potential strategies to improve outcomes for these patients.

The Value of Bedside Echocardiogram in the Setting of Acute and Chronic Pulmonary Embolism.

Echocardiography is valuable in the evaluation and risk stratification of patients with acute and chronic pulmonary embolism (PE). Patients with acute PE who have echocardiographic evidence of right ventricular dilatation and/or right ventricular dysfunction have a worse prognosis. A minority of patients with acute PE can develop chronic thromboembolic pulmonary hypertension. Patients with chronic thromboembolic pulmonary hypertension often have echocardiographic evidence of elevated pulmonary arterial pressures, right ventricular hypertrophy, right ventricular dysfunction, and/or left ventricular impaired relaxation.

Pulmonary hypertension: types and treatments.

Pulmonary arterial hypertension (PAH) is a panvasculopathy that affects the distal pulmonary arteries and leads to restricted blood flow. This increased afterload leads to adaptive mechanisms of the right ventricle, with eventual failure once it can no longer compensate. Pulmonary hypertension from associated conditions, most importantly left heart disease, i.e. heart failure, can also lead to the same sequela. Patients often experience early vague symptoms of dyspnea and exercise intolerance, and thus PH can elude clinicians until right heart failure symptoms predominate. Evidence-based treatment options with pulmonary vasodilators are available for those with PAH and should be employed early. It is essential that patients be accurately categorized by their etiology of PH, as treatment strategies differ, and can potentially be dangerous if employed in the wrong clinical scenario.

Current approaches to antiarrhythmic therapy in heart failure.

Atrial fibrillation (AF) is exceedingly common in patients with heart failure (HF), as they share common risk factors. Rate control is the cornerstone of treatment for AF; however, restoration of sinus rhythm should be considered when more than minimal symptoms are present. Life-threatening ventricular arrhythmias are responsible for the primary mode of death in patients with NYHA I, II, or III HF. Although implantable cardioverter defibrillators protect against sudden cardiac arrest, many patients will present with VT or ICD shocks. Antiarrhythmic drug therapy beyond beta-blocker therapy remains fundamental to the termination of acute VT and the prevention of ICD shocks.

Heart failure with preserved ejection fraction: an ongoing enigma.

Heart failure with preserved ejection fraction (HFpEF) is a complex clinical syndrome based on traditional heart failure symptoms with documentation of increased left ventricular filling pressures and preserved left ventricular ejection fraction. The exact mechanisms that induce HFpEF are not known. End-diastolic ventricular stiffness does not seem to be acting alone. Substantial mortality exists compared with healthy age-matched controls, as well as significant health care expenditures on hospitalizations and readmissions. This article reviews the epidemiology, pathophysiology, and treatment of heart failure with preserved ejection fraction (HFpEF). Current practice guidelines focus on remedying volume overload, aggressively controlling hypertension, and treatment of comorbid conditions that contribute to decompensation.