Infective Endocarditis Presenting as Complete Heart Block With an Unexpected Finding of a Cardiac Abscess and Purulent Pericarditis.

Intracardiac abscess resulting in complete heart block is an infrequent complication of infective endocarditis. Most presentations of endocarditis are limited to valvular and perivalvular structures, with varying degrees of heart block occurring in the minority of cases. We report a case of endocarditis manifesting as chest pain associated with ST segment elevation and complete heart block. The patient expired unexpectedly within a few hours of presentation. Postmortem examination revealed an atrial septal abscess, purulent pericardial collection, and fibrinous pericarditis. Spread of the abscess into the atrial septum was postulated to be the cause of the complete heart block. In endocarditis, the ominous development of heart block and a poor response to antibiotic therapy imply significant extension of the infection. Management therefore requires prompt ventricular pacing with consideration for valve replacement and possible pericardial drainage.

Prevalence and risk factors of pulmonary hypertension in patients with elevated pulmonary venous pressure and preserved ejection fraction.

Pulmonary hypertension (PH) is a well-recognized complication of left-sided heart failure with preserved left ventricular systolic function that portends a worse prognosis. The identification of risk factors may provide insight into possible mechanisms for the development of PH in this population. Targeting these risk factors could possibly attenuate the development of PH. The limited data available regarding the prevalence of PH and its risk factors in patients with heart failure with preserved left ventricular systolic function are based on echocardiography. To further study this, an institutional database was searched for all patients who underwent right-sided and left-sided cardiac catheterization with ventriculography from October 1996 to September 2007 who met the following criteria: left ventricular end-diastolic pressure (LVEDP) >15 mm Hg, a left ventricular ejection fraction > or =50%, and no significant left-sided cardiac valvular disease. The demographic, clinical, and hemodynamic data of these patients were then analyzed. Of 455 patients who met these criteria, 239 (52.5%) had PH, defined as mean pulmonary artery pressure >25 mm Hg. Using multivariate logistic regression, PH was strongly and independently associated with LVEDP > or =25 mm Hg (odds ratio 4.3), morbid obesity (odds ratio 3.4), and atrial arrhythmias (odds ratio 3.1). Other significant associations were age > or =80 years, chronic obstructive pulmonary disease, and dyspnea on exertion. In conclusion, PH is a frequent finding in patients with elevated LVEDPs and preserved left ventricular systolic function. Factors associated with its development are LVEDP > or =25 mm Hg, morbid obesity, atrial arrhythmias, age > or =80 years, chronic obstructive pulmonary disease, and dyspnea on exertion.

Non-invasive detection of pulmonary hypertension prior to renal transplantation is a predictor of increased risk for early graft dysfunction.

BACKGROUND: Early graft dysfunction is a significant complication after renal transplantation and is a marker of adverse outcomes. Although multiple predictors of graft dysfunction have been previously described, the reported prevalence of pulmonary hypertension (pulmonary HTN) in the dialysis population (40-50%), along with biologic and physiologic principles, led us to hypothesize that pulmonary HTN might be an additional risk factor for early graft dysfunction. METHODS: We performed a retrospective study that screened all adult renal transplants performed at our institution over a 3-year period and limited the evaluation to those subjects who had an estimated pulmonary artery systolic pressure on a preoperative echocardiogram report (n = 55). The primary outcome of this study was to investigate the impact of pulmonary HTN on early graft dysfunction using a combined endpoint of delayed graft function or slow graft function. RESULTS: Among patients receiving a living donor kidney, early graft dysfunction was not observed regardless of pulmonary HTN status. However, among patients receiving a deceased donor kidney, pulmonary HTN was found to be associated with a significant increased risk of early graft dysfunction (56 vs 11.7%, P = 0.01). Univariate and multivariable logistic regression supported this observation as an independent risk factor beyond potential confounding recipient, donor and graft-based risk factors for early graft dysfunction (P < 0.05). CONCLUSION: Pulmonary HTN detected on non-invasive imaging prior to renal transplantation appears to be an independent predictor of early graft dysfunction among those patients who receive a deceased donor kidney.