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Left ventricular filling profiles in young white-coat hypertensive patients without hypertrophy
Insights
White-coat hypertension in individuals under 50, even without hypertrophy, shows impaired left ventricular diastolic function. This dysfunction is linked to heightened neurohumoral activity and metabolic changes.
Area of Science:
- Cardiology
- Hypertension Research
- Diastolic Dysfunction
Background:
- White-coat hypertension (WCH) is characterized by elevated office blood pressure (BP) but normal out-of-office BP.
- The impact of WCH on left ventricular (LV) diastolic function, particularly in younger individuals without cardiac hypertrophy, requires further investigation.
Purpose of the Study:
- To assess left ventricular diastolic function in young white-coat hypertensive subjects (<50 years) without cardiac hypertrophy.
- To compare diastolic function and neurohumoral markers between sustained hypertensives, white-coat hypertensives, and normotensives.
Main Methods:
- Three balanced groups were studied: sustained hypertensives (n=50), white-coat hypertensives (n=25), and normotensives (n=25).
- Office and 24-hour ambulatory BP monitoring were performed.
- Echocardiography assessed left ventricular diastolic function.
- Plasma and urine levels of norepinephrine, aldosterone, and renin activity, along with lipid profiles, were measured.
Main Results:
- White-coat hypertensives exhibited impaired diastolic function compared to normotensives, including increased E/A ratio, prolonged deceleration time, and lengthened isovolumic relaxation time.
- No significant differences in diastolic function were observed between white-coat and sustained hypertensives.
- White-coat hypertensives showed higher plasma and urine norepinephrine and aldosterone, elevated plasma renin activity, and increased total and LDL cholesterol compared to normotensives.
Conclusions:
- Young white-coat hypertensive individuals without hypertrophy demonstrate significant diastolic dysfunction.
- Heightened neurohumoral activity and metabolic abnormalities are associated with diastolic dysfunction in white-coat hypertension.
- These findings suggest that WCH may represent an early stage of hypertensive heart disease.
Abstract:
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 > or = 140 or > or = 90 mm Hg on all three visits) were defined as white coat if their average 24-hour blood pressure was < 127/81 mm Hg and at least 18/16 mm Hg lower than their average office values. We chose three groups balanced for sex, age, and body 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 normotensives, white-coat hypertensives had more impaired diastolic function: increased ratio of late to early filling velocities, raised ratio of late 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 sustained hypertensives. Compared with normotensives, white-coat hypertensives had higher values of plasma and urine norepinephrine (P<.001 and 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 between white-coat and sustained hypertensives. Within white-coat hypertensives, 24-hour urinary aldosterone closely correlated with the ratio of late to early filling velocities (P=.008), and plasma and 24-hour urinary norepinephrine correlated well with total cholesterol (P=.037 and P=.006, respectively). No correlation was detected within the sustained hypertensives and normotensives. Heightened neurohumoral activity clearly supported the progression of diastolic dysfunction and metabolic abnormality in white-coat hypertensives.