Subject(s)
Peptic Ulcer Perforation/complications , Pneumopericardium/diagnostic imaging , Stomach Ulcer/complications , Aged , Echocardiography, Transesophageal , Fistula/complications , Gastric Fistula/complications , Heart Diseases/complications , Humans , Male , Pneumopericardium/etiology , RadiographyABSTRACT
The recognition of dysfunctional but viable myocardium after acute myocardial infarction (MI) may be of importance for both patient prognostication and the decision for revascularization. Low-dose dobutamine echocardiography (LDDE) has been shown to be a reliable technique in detecting reversibility of dysfunctional myocardium. The aim of the present study was to assess by LDDE possible time-dependent changes in myocardial viability and to evaluate the value of LDDE used in the postinfarction period. Twenty-seven patients with acute MI underwent LDDE on day 6, 30, and 90. At LDDE day 6, 41% of the affected segments showed a positive response to LDDE. At later examination on day 30 and 90, only 32% and 18%, respectively, of the dysfunctioning segments responded to dobutamine stimulation, with a significant decline in response (p < 0.0001), indicating loss of viability. Spontaneous segmental outcome was significantly better for LDDE-responding segments than for nonresponding segments (p = 0.0001). This study indicated that myocardial viability may be temporary and that a time-dependent loss of viability may take place during the first months after MI.
Subject(s)
Dobutamine , Myocardial Infarction/physiopathology , Female , Humans , Male , Middle Aged , Myocardial Contraction/drug effects , Myocardial Infarction/diagnostic imaging , Predictive Value of Tests , Prognosis , Sensitivity and Specificity , Time Factors , UltrasonographyABSTRACT
A 44-year-old woman was seen on three separate occasions for acute pulmonary edema which had developed 30 minutes after ingestion of a single hydrochlorothiazide-amiloride (Moduretic) tablet. Eighteen cases of hydrochlorothiazide-induced pulmonary edema have been reported previously. Clinical findings and investigations in the present and previous cases indicate a noncardiogenic cause for the pulmonary edema. Increased pulmonary vascular permeability is probably involved. So far, attempts to demonstrate an immunological mechanism have failed and the pathophysiology remains uncertain. The reaction may be difficult to differentiate from left ventricular failure in patients with cardiac disease. Attention should be drawn to this severe but rare side effect of a frequently used diuretic.
