Aorto-left atrial fistula. A reversible cause of acute refractory heart failure.

Fistulas between the aorta and left atrium, invariably a complication of aortic valvular endocarditis, are rare and infrequently diagnosed premortem. We describe a patient who presented with this entity and review the reports of five other patients for whom a diagnosis was made premortem. A number of causative organisms have been identified. The clinical course is characteristically one of rapidly progressive heart failure. Notably, only half of these fistulas were detected by transthoracic echocardiography, whereas all were identified by transesophageal echocardiography when utilized. Once the diagnosis is made, prompt surgical repair is required to avert the high mortality from rapidly developing refractory congestive heart failure.

Cirrhosis: a risk factor for cryptococcal peritonitis.

Cryptococcal peritonitis is usually associated with end-stage renal disease and peritoneal dialysis. Significant liver disease has not been well recognized as a risk factor for its development. We report two patients with cirrhosis who developed peritoneal infections with Cryptococcus neoformans. We also retrospectively review all cases of cryptococcal illness at the Ohio State University Medical Center from October 1990 to January 1994 and present a review of the literature regarding cryptococcal peritonitis associated with hepatic dysfunction. Cirrhotic patients with this entity present with subtle, nonspecific complaints resulting in delayed diagnoses, dissemination, and death. We suggest that clinicians maintain an increased awareness of this unusual but lethal entity in patients with liver impairment. Early and frequent abdominal paracenteses with bedside inoculations of fungal culture medium, India ink preparations, and serum cryptococcal antigen testing may hasten the diagnosis and institution of appropriate therapy.

Normal arterial blood gas in a patient with saddle pulmonary artery embolus: diagnosis by transesophageal echocardiography.

This article describes a patient with a large, main pulmonary artery thromboembolus with normal arterial blood gas results, including normal alveolar-arterial oxygen gradient. The diagnosis was established using transesophageal echocardiography and confirmed with pulmonary angiography. The patient subsequently underwent anticoagulation and eventually was discharged without complications.

Fulminant hepatic failure associated with etodolac use.

Etodolac is a new pyranocarboxylic acid nonsteroidal anti-inflammatory agent with a unique chemical structure indicated for use in patients with painful musculoskeletal disorders and rheumatoid disease. Hepatotoxicity, in the form of reversible elevations in transaminases or bilirubin, occurs rarely. We present the first reported case of fulminant hepatic failure related to etodolac.

Pulmonary hypertension and systemic hypotension as limitations to exercise in chronic heart failure.

The authors have previously shown that the resistance ratio (RR) is increased in patients with congestive heart failure (CHF), and that the patients with the highest RRs have an increased mortality. The authors hypothesized that CHF patients with the lowest maximum oxygen consumption and the most impaired Weber functional classification would have the highest RR. Eighty-four patients with chronic CHF underwent seated ergometric exercise to exhaustion. Hemodynamic and respiratory gas exchange parameters were measured at rest and peak exercise. Weber functional classifications (A through E) were determined from maximum oxygen consumptions, and patients were stratified to evaluate the RR. The RR increased progressively across Weber classifications at rest (A vs E; P < .001) and with maximum exercise (A vs E; P < .002). At rest, elevation in the RR was related to an increase in the pulmonary pressure gradient (A vs E; P < .002) secondary to increased mean pulmonary arterial pressures. With peak exercise, this elevation was secondary to a decrease in the systemic pressure gradient (A vs E; P < .001). Further analysis revealed that the progressive decrease in the systemic pressure gradient was due to progressively lower mean arterial pressures (A vs E; P < .001). Elevation of the RR, both at rest and peak exercise, predicts a more impaired exercise functional status in patients with chronic CHF. Increases in the RR at peak exercise were related to decreases in mean arterial pressure, most likely limiting perfusion to exercising skeletal muscle. The mechanism of poor exercise blood pressure response in these patients is unclear. Possible explanations include abnormal systemic baroreceptor function with inappropriate vascular adaptation, and a poor cardiac output response to a relative increase in right ventricular afterload in systemic vasodilation seen with exercise.