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Just as Hippocrates vowed his life to practicing the highest standards of medicine, cardiovascular disease fellowship program directors strive not only to provide comprehensive training for our fellows, but also to support them for long-term success in both professional and personal lives. Pregnancy

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.

We show that spironolactone use was associated with an increased rate of all-cause hospitalizations, but no difference in hospitalizations for heart failure or pulmonary arterial hypertension, in patients with World Health Organization Group 1 pulmonary arterial hypertension. A possible reason for this finding is confounding from retrospective study design.

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 pulmo-nary 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.

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 (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.