OBJECTIVES: This study investigated 1) the role of left ventricular diastolic nonuniformity in hypertensive left ventricular diastolic dysfunction, and 2) the effects of a calcium channel antagonist on diastolic nonuniformity in hypertensive and normotensive subjects. BACKGROUND: Augmented left ventricular diastolic nonuniformity contributes to diastolic dysfunction in hypertrophic cardiomyopathy. Impaired left ventricular diastolic function with preserved systolic function has been recognized in hypertension. Therefore, abnormal ventricular regional nonuniformity might also be involved in hypertensive diastolic dysfunction in a milder form of hypertrophy. METHODS: Thirteen patients with established hypertension underwent radionuclide ventriculography before and after nifedipine administration. Indexes of left ventricular function were derived by computer analysis of the time-activity curve. After a computer subdivided the left ventricle into four regions, a time-activity curve of each region was constructed to determine an index of left ventricular diastolic nonuniformity. This index was calculated as the sum of the absolute values of time difference between global and regional peak filling in the septal, the apical and the lateral region. Ten normotensive subjects were studied for comparison. Echocardiography was performed in both groups. RESULTS: The two groups were matched for age, gender, heart rate, echocardiographic dimensions and systolic function. In the hypertensive group, left ventricular diastolic filling indexes were impaired, with a negative correlation between peak filling rate and the diastolic nonuniformity index. Although the change in ejection fraction after nifedipine administration was similar in the two groups, the increase in peak filling rate was larger in the hypertensive patients. The diastolic nonuniformity index decreased after nifedipine in the hypertensive but not in the control group. This decrease correlated with improved peak filling rate in the hypertensive group. CONCLUSIONS: In hypertensive patients with preserved systolic function, left ventricular diastolic nonuniformity increases, causing early diastolic dysfunction. Decreased diastolic nonuniformity after pharmacologic intervention contributes to lessened ventricular filling dysfunction, regardless of changes in loading conditions in hypertension. Thus, diastolic nonuniformity is an important determinant of left ventricular filling abnormality and might be a target of pharmacologic intervention in hypertensive patients.
OBJECTIVES: This study investigated 1) the role of left ventricular diastolic nonuniformity in hypertensive left ventricular diastolic dysfunction, and 2) the effects of a calcium channel antagonist on diastolic nonuniformity in hypertensive and normotensive subjects. BACKGROUND: Augmented left ventricular diastolic nonuniformity contributes to diastolic dysfunction in hypertrophic cardiomyopathy. Impaired left ventricular diastolic function with preserved systolic function has been recognized in hypertension. Therefore, abnormal ventricular regional nonuniformity might also be involved in hypertensive diastolic dysfunction in a milder form of hypertrophy. METHODS: Thirteen patients with established hypertension underwent radionuclide ventriculography before and after nifedipine administration. Indexes of left ventricular function were derived by computer analysis of the time-activity curve. After a computer subdivided the left ventricle into four regions, a time-activity curve of each region was constructed to determine an index of left ventricular diastolic nonuniformity. This index was calculated as the sum of the absolute values of time difference between global and regional peak filling in the septal, the apical and the lateral region. Ten normotensive subjects were studied for comparison. Echocardiography was performed in both groups. RESULTS: The two groups were matched for age, gender, heart rate, echocardiographic dimensions and systolic function. In the hypertensive group, left ventricular diastolic filling indexes were impaired, with a negative correlation between peak filling rate and the diastolic nonuniformity index. Although the change in ejection fraction after nifedipine administration was similar in the two groups, the increase in peak filling rate was larger in the hypertensivepatients. The diastolic nonuniformity index decreased after nifedipine in the hypertensive but not in the control group. This decrease correlated with improved peak filling rate in the hypertensive group. CONCLUSIONS: In hypertensivepatients with preserved systolic function, left ventricular diastolic nonuniformity increases, causing early diastolic dysfunction. Decreased diastolic nonuniformity after pharmacologic intervention contributes to lessened ventricular filling dysfunction, regardless of changes in loading conditions in hypertension. Thus, diastolic nonuniformity is an important determinant of left ventricular filling abnormality and might be a target of pharmacologic intervention in hypertensivepatients.