LEFT-VENTRICULAR FILLING PROFILES IN YOUNG WHITE-COAT HYPERTENSIVE PATIENTS WITHOUT HYPERTROPHY

This study was to assess left ventricular diastolic function in young white-coat hypertensive subjects <50 years of age without hypertrophy. Hypertensive patients (systolic or diastolic blood pressure greater t han or equal to 140 or greater than or equal to 90 mm Hg on all three visits) were defined as while coat if their average 24-hour blood pres sure was <127/81 mm Hg and at least 18/16 mm Hg lower than their avera ge office values. We chose three groups balanced for sex, age, and bod y mass index: 50 sustained hypertensives, 25 white-coat hypertensives, and 25 normotensives. Office blood pressure was similar in white-coat and sustained hypertensives. Ambulatory blood pressure was comparable in white-coat hypertensives and normotensives. Compared with normoten sives, white-coat hypertensives had more impaired diastolic function: increased ratio of late to early filling velocities, raised ratio of l ate to early time-velocity integral, prolonged deceleration time, and lengthened isovolumic relaxation time (P<.001, P<.001: P=.002, and P<. 001, respectively). No difference was noticed between white-coat and s ustained hypertensives. Compared with normotensives, white-coat hypert ensives had higher values of plasma and urine norepinephrine (P<.001 a nd P<.001, respectively), plasma and urine aldosterone (P<.001 and P=. 002, respectively), plasma renin activity (P=.04), total cholesterol ( P=.001): and LDL cholesterol (P<.001). No difference was observed betw een white-coat and sustained hypertensives. Within white-coat hyperten sives, 24-hour urinary aldosterone closely correlated with the ratio o f late to early filling velocities (P=.008), and plasma and 24-hour ur inary norepinephrine correlated well with total cholesterol (P=.037 an d P=.006, respectively). No correlation was detected within the sustai ned hypertensives and normotensives. Heightened neurohumoral activity clearly supported the progression of diastolic dysfunction and metabol ic abnormality in white-coat hypertensives.