Elsevier

The Lancet

Volume 348, Issue 9028, 7 September 1996, Pages 654-657
The Lancet

Early Report
White-coat hypertension as a cause of cardiovascular dysfunction

https://doi.org/10.1016/S0140-6736(96)02303-3Get rights and content

Summary

Background

The increasing use of 24 h ambulatory blood pressure monitoring has allowed diagnosis of white-coat hypertension, in which blood pressures are higher on clinic measurements than on ambulatory monitoring. Treatment is not generally thought to be necessary for this disorder. However, there is evidence that patients with white-coat hypertension develop renal impairment and left ventricular hypertrophy. We undertook this study to assess whether white-coat hypertension, in the absence of cardiovascular structural abnormalities, is associated with cardiovascular functional abnormalities.

Methods

Cardiovascular function was assessed by ultrasonography in three groups of patients classified as normotensive, persistently hypertensive, or white-coat hypertensive (23, 20, and 22 patients, respectively) on the basis of ambulatory blood pressure monitoring, carried out for 28 h with recordings taken every 15 min during the day and every 20 min during the night, and clinic measurements, made with a semi-automatic oscillometric device.

Results

Similar abnormalities of diastolic left ventricular function were identified in the patients with persistent hypertension and those with white-coat hypertension; both groups differed in these indices from the normotensive group (E/A ratios 0·94 [SD 0·23], 1·06 [0·21], and 1·24 [0·31] respectively; ANOVA p<0·005). In addition, the white-coat and persistently hypertensive groups, when compared with the normotensive group, showed similar abnormalities of elasticity, compliance, and stiffness (stiffness index 4·32 [1·90], 4·53 [1·38], and 3·27 [0·95] respectively; ANOVA p<0·05) of the large arteries.

Interpretation

Functional cardiovascular abnormalities were identified in white-coat hypertensive patients who had no identifiable structural abnormalities. Such functional abnormalities can be reversed by antihypertensive treatment. We propose that patients with white-coat hypertension might benefit from antihypertensive treatment as well as those with persistent hypertension. This hypothesis should be addressed in prospective clinical trials.

Introduction

Most clinical trials of antihypertensive treatment have relied on conventional clinic measurement of blood pressure to identify hypertensive patients and to demonstrate the benefits of blood pressure reduction.1 However, 20–40% of individuals with borderline clinic hypertension can be reclassified as normotensive during daytime ambulatory monitoring,25 and these trials inevitably included some such individuals with white-coat hypertension. However, controversy remains about the precise definition of white-coat hypertension. For example, one definition is a raised diastolic pressure (90–104 mm Hg) at clinic but normal daytime ambulatory blood pressure (below the 90th percentile of a normotensive control group)2 and another is a mean clinic blood pressure at least 6 mm Hg higher than the ambulatory mean.3 Nevertheless, the inclusion of white-coat hypertensive patients in the studies cited did not prevent the demonstration of significant reductions in cardiovascular disease. Irrespective of the definition, and despite the recognition that the presence of medical personnel influences blood pressure,6 the general assumption is that the inclusion of white-coat hypertensive patients may have diluted the overall magnitude of the benefits of a drug treatment found in previous studies. Another possibility is that the white-coat hypertensive patients also benefited from active treatment–this idea is the substance of our hypothesis. The main aim of our pilot study was the non-invasive measurement of a range of indices of cardiovascular function in patients referred for evaluation of their hypertension, to find out whether patients with white-coat hypertension differ from patients with hypertension or normotensive individuals in terms of known markers of hypertensive cardiovascular disease.

Section snippets

Methods

65 consecutive patients referred for assessment of hypertension were asked for written informed consent to take part in this study, which was approved by the local ethics committee. Eligible patients were aged 45–75 years, had no evidence of clinically significant disease (including cardiovascular or cerebrovascular disease, atrial fibrillation, or significant heart valve disease, insulin-dependent diabetes, renal impairment, or liver disease); and were not receiving antihypertensive treatment

Statistical analysis

Three groups of patients were defined on the basis of ambulatory blood pressure monitoring profiles and clinic recordings: persistently hypertensive patients who had a diastolic pressure of 95 mm Hg or more both at the clinic and on daytime ambulatory monitoring; white-coat hypertensive patients who had a diastolic pressure of 95 mm Hg or more at the clinic but not on ambulatory blood pressure monitoring; and normotensive patients who had a diastolic pressure 95 mm below Hg at all times. These

Results

There were no significant differences in sex distribution, age, weight, or height between the groups of patients (table 1). By definition, clinic blood pressures were higher in persistently and white-coat hypertensive patients than in the normotensive patients, and ambulatory blood pressure monitoring pressures were higher in persistently hypertensive patients than in either of the other groups (figure 1). There were no significant differences in heart rate or pulse pressure between groups.

Discussion

Our main finding was that similar abnormalities of cardiovascular function–including reduced arterial elasticity and left ventricular diastolic dysfunction–occur in patients with white-coat hypertension and those with persistent hypertension.

Both the persistently and white-coat hypertensive patients had larger arteries than the normotensive patients, as has been previously described.11 Although these differences might simply reflect higher blood pressures at the time of the ultrasonographic

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