BACKGROUND: Few data exist regarding intraventricular flow patterns in the presence of left ventricular dysfunction. Therefore, we examined the relation between intracavitary left ventricular flow dynamics and the presence of ventricular contractile abnormalities using videodensitometric analysis of transpulmonary contrast echocardiography. METHODS AND RESULTS: Two-dimensional echocardiography was performed before, during, and after intravenous injection of sonicated albumin in 8 normal subjects, 22 patients with infarction, and 6 patients with dilated cardiomyopathy. Time-intensity curves were recorded, and disappearance half-times (in cardiac cycles) were measured for regions of interest at the mitral orifice (Ta) and mid-left ventricular cavity (Tb). We observed contrast enhancement of the left ventricular cavity in 28 of 36 patients. Ta and Tb were identical (19 beats) in all normal patients, but Tb was greater than Ta (19 versus 22 beats, P < .001) in patients with dyssynergy. Patients with dyssynergy were divided in three groups: group A, in whom Tb-Ta < or = 3; group B, in whom Tb-Ta > or = 4; and group C, which was composed of patients without contrast enhancement. Left ventricular end-diastolic dimension was similar in normal patients (46.1 mm) and group A patients (50.3 mm) but was less in each cohort than in groups B (58.7 mm) and C (64.1 mm) (all P < .01). Significant correlation was observed between Tb-Ta and both ejection fraction (r = -.67, P < .001) and wall motion index (r = .62, P < .001). CONCLUSIONS: Clearance of contrast from the mid-left ventricular cavity is prolonged in patients with left ventricular dysfunction. This prolongation may be related to increased left ventricular diastolic volume, impaired intracavitary mixing, or paradoxical systolic flow. Delayed left ventricular contrast washout may have implications regarding the formation of left ventricular thrombi.
BACKGROUND: Few data exist regarding intraventricular flow patterns in the presence of left ventricular dysfunction. Therefore, we examined the relation between intracavitary left ventricular flow dynamics and the presence of ventricular contractile abnormalities using videodensitometric analysis of transpulmonary contrast echocardiography. METHODS AND RESULTS: Two-dimensional echocardiography was performed before, during, and after intravenous injection of sonicated albumin in 8 normal subjects, 22 patients with infarction, and 6 patients with dilated cardiomyopathy. Time-intensity curves were recorded, and disappearance half-times (in cardiac cycles) were measured for regions of interest at the mitral orifice (Ta) and mid-left ventricular cavity (Tb). We observed contrast enhancement of the left ventricular cavity in 28 of 36 patients. Ta and Tb were identical (19 beats) in all normal patients, but Tb was greater than Ta (19 versus 22 beats, P < .001) in patients with dyssynergy. Patients with dyssynergy were divided in three groups: group A, in whom Tb-Ta < or = 3; group B, in whom Tb-Ta > or = 4; and group C, which was composed of patients without contrast enhancement. Left ventricular end-diastolic dimension was similar in normal patients (46.1 mm) and group A patients (50.3 mm) but was less in each cohort than in groups B (58.7 mm) and C (64.1 mm) (all P < .01). Significant correlation was observed between Tb-Ta and both ejection fraction (r = -.67, P < .001) and wall motion index (r = .62, P < .001). CONCLUSIONS: Clearance of contrast from the mid-left ventricular cavity is prolonged in patients with left ventricular dysfunction. This prolongation may be related to increased left ventricular diastolic volume, impaired intracavitary mixing, or paradoxical systolic flow. Delayed left ventricular contrast washout may have implications regarding the formation of left ventricular thrombi.