Pulmonary hemodynamic effects of dipyridamole infusion in patients with normal and elevated pulmonary artery systolic pressure receiving PB127.

BACKGROUND: Intravenous administration of microspheres used as ultrasound contrast agents may potentially alter pulmonary hemodynamics. PB127 (POINT Biomedical Corp., San Carlos, CA) is an investigational ultrasound perfusion-imaging agent used in conjunction with dipyridamole to diagnose coronary artery disease. The effects of PB127 alone or in combination with dipyridamole on pulmonary hemodynamics have not been described. METHODS: We studied 20 patients, including 10 with elevated screening pulmonary artery systolic pressure (>35 mm Hg). Doppler-derived pulmonary hemodynamics were determined before and after continuous infusion of PB127 (0.175 mg/kg diluted in 5% dextrose) or 5% dextrose. Patients then received dipyridamole (0.56 mg/kg) and hemodynamics were again assessed. RESULTS: During PB127/dextrose infusion, there were no significant changes in pulmonary hemodynamics compared with baseline. After dipyridamole, there were small increases in pulmonary artery systolic pressure and in pulmonary flow and a reduction in pulmonary vascular resistance. These changes occurred in patients with normal and elevated pulmonary artery systolic pressure. CONCLUSION: PB127 infusion does not alter pulmonary hemodynamics. Mild alterations of pulmonary hemodynamics occur after dipyridamole administration.

Myocardial contrast echocardiographic estimates of infarct size predict likelihood of left ventricular remodeling after acute anterior wall myocardial infarction.

OBJECTIVES: We sought to determine the utility of myocardial contrast echocardiography (MCE) in predicting left ventricular (LV) remodeling (LVR) in patients with a recent anterior wall myocardial infarction and residual regional LV akinesis. BACKGROUND: Although recent studies have shown that MCE predicts recovery of regional and global LV systolic function after myocardial infarction, the relationship between myocardial perfusion patterns and likelihood of subsequent LVR has not been extensively studied. METHODS: In all, 50 patients (mean age 62 years) underwent contrast-enhanced echocardiography for determination of LV volumes and ejection fraction, and MCE, 2 days after admission, with follow-up contrast-enhanced echocardiography 6 months later. LVR was defined as greater than 15% increase in LV end-diastolic volume index at follow-up. RESULTS: LVR occurred in 19 patients (38%) (group 1), with stable LV volumes in 31 patients (62%) (group 2). Routine clinical and angiographic variables did not differ between groups 1 and 2. Both transmural extent of infarction and number of abnormally perfused myocardial segments (assessed by MCE) predicted LVR. LVR occurred in 55% of patients with transmural perfusion defects, and was less common in those with subendocardial perfusion defects or normal perfusion (31% and 21%, respectively). The mean percent increase in LV size was significantly greater for transmural infarcts (15 +/- 7%) versus subendocardial infarcts or normal perfusion (-1 +/- 8 and 8 +/- 8, respectively). When more than 5 myocardial segments were abnormally perfused, remodeling always occurred and was extensive. CONCLUSIONS: MCE markers of infarct size are useful in predicting subsequent risk of LVR after myocardial infarction. Routine performance of MCE studies in select patients early after infarction may be helpful in further refining risk stratification.