White-coat hypertension

THE LANCET

threshold of ambulatory blood pressure (daytime below 130/80 mm Hg) or self-measured blood pressure. Until further prospective long-term studies are available on the natural history of white-coat hypertension a reasonable recommendation could be to seek frequent blood-pressure checks, postponing treatment, regardless of clinic measurements, if one is certain of the absence of targetorgan damage. Paolo Verdecchia, *Giuseppe Schillaci, Claudia Borgioni, Antonella Ciucci, Carlo Porcellati Ospedale Generale R Silvestrini, Area Omogenea di Cardiologia e Medicina, Perugia; and *Ospedale Beato G Villa, 06062 Città della Pieve, Italy

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Glen SK, Elliot HL, Curzio JL, Lees KR, Reid JL. White-coat hypertension as a cause of cardiovascular disfunction. Lancet 1996; 348: 654–57. Verdecchia P, Schillaci G, Boldrini F, Zampi I, Porcellati C. Variability between current definitions of ‘normal’ ambulatory blood pressure: implications for the assessment of white-coat hypertension. Hypertension 1992; 20: 555–62. Verdecchia P, Porcellati C, Schillaci G, et al. Ambulatory blood pressure: an independent predictor of prognosis in essential hypertension. Hypertension 1994; 24: 793–801. Verdecchia P, Schillaci G, Borgioni C, et al. Identification of subjects with white-coat hypertension and persistently normal ambulatory blood pressure. Blood Press Monitor 1996; 1: 217–22. Pickering TG. White-coat hypertension. Curr Opin Nephr Hypertens 1996; 5: 192–98.

SIR—There is accumulating evidence that patients with white-coat hypertension may go on to develop bloodpressure related end-organ damage despite normal 24 h ambulatory blood pressure monitoring (ABPM). To try to explain this paradox we have studied treadmill performance in patients with white-coat hypertension, looking for relations between the white-coat effect, staged exercise blood pressure, and echocardiographic left-ventricular mass index. 16 male and nine female patients (mean age 45 [SD14]) without symptoms and with a normal 24 h mean ABPM of 130(7)/81(5) mm Hg were studied. The daytime ABPM was similar to that in Glen and colleagues study 1 (147–121/93–75 mm Hg). Clinic blood pressure was raised at 164(26)/105(11) mm Hg. We defined the white-coat effect as the difference between the clinic BP and the mean 24 h ABPM. Echocardiography was used to calculate leftventricular mass index.2 Five males and four females had left-ventricular hypertrophy (Ä134 and 110 g/m 2, respectively); the index ranged widely (67–187 g/m2). Treadmill exercise testing was done by a Bruce protocol and stage 2 systolic blood pressure was measured although patients exercised to exhaustion. The exercise blood pressure at this submaximal level was chosen because it has been shown to be of prognostic value in hypertensive patients.3 17 patients exhibited exaggerated exercise blood pressure rises above 200 mm Hg. In hypertensive patients this would suggest future cardiovascular risk.4 There was a significant correlation between exercise blood pressure and leftventricular mass index (r=0·49, p=0·014), a relation seen in established hypertension but not in normotensive patients. 5 This index was not related to clinic blood pressure or to mean 24 h or daytime ABPM. There was a strong relation between the white-coat effect and stage 2 exercise blood pressure (r=0·70, p<0·001). There was a significant negative correlation between exercise blood pressure and transmitral peak E/A (r=20·47, p<0·03). This may suggest that exercise blood pressure rises in parallel to increasing diastolic dysfunction, though the exercise time in this group was normal (10·9 [2·6] min). Extending the observation of Glen and colleagues, we suggest that exercise-related rises in blood pressure

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contribute to a cumulative blood pressure load which with time may produce end-organ damage. *P O Lim, R J MacFadyen, T M MacDonald *Hypertension Unit, Department of Clinical Pharmacology, University of Dundee, Ninewells Hospital and Medical School, Dundee DD1 9SY, UK

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Glen SK, Elliot HL, Curzio JL, Lees KR, Reid JL. White-coat hypertension as a cause of cardiovascular dysfunction. Lancet 1996; 348: 654–57. Devereux R, Reichek R. Echocardiographic determination of left ventricular mass in man: anatomic validation of the method. Circulation 1977; 55: 613–18. Mundal R, Kjeldsen SE, Sandvik L, Erikssen G, Thaulow E, Erikssen J. Exercise blood pressure predicts cardiovascular mortality in middle-aged men. Hypertension 1994; 24: 56–62. Lim PO, MacFadyen RJ, Clarkson PBM, MacDonald TM. Impaired exercise tolerance in hypertensive patients. Ann Intern Med 1996; 124: 41–55. Fagard R, Amery A. Physical exercise in hypertension. In: Laragh JH, Brenner BM, eds. Hypertension: pathophysiology, diagnosis, and management, 2nd ed. New York: Raven, 1995: 2669–81.

Authors’ reply SIR—The original title of our paper was “Is white coat hypertension a cause of cardiovascular functional abnormalities? An hypothesis to be tested”. Despite the above criticisms and differences of opinion there remains a consensus that further outcome studies are required to test this hypothesis. Whilst the particular level of diastolic blood pressure will certainly influence the categorisation of the patient groups we chose 95 mm Hg based on the threshold for initiation of treatment recommended by the World Health Organization and the International Society of Hypertension and from the data in a large study of white-coat hypertension. This choice was detailed in the article and it was intended to allow our results to be interpreted clinically in the context of initiating antihypertensive treatment in a patient found to be hypertensive in the clinic but not according to the daytime ambulatory blood pressure average. At the time the results from the PAMELA study were not available, and we realised that any arbitrary threshold was unlikely to meet with universal approval. Krakoff and Phillips seem to misunderstand our method of classification whereby the clinic reading was derived from a series of three visits to the hospital, with recordings under standardised conditions, and with classifying value derived from an average of three final recordings at the third visit. As Kristensen and Høegholm indicated, the threshold we chose led to the inclusion, in the white-coat group, of individuals who might be classified as persistent hypertensives according to alternative criteria—but they overlook the fact that this threshold would also have led to the inclusion in the normotensive group of patients who otherwise might be classified as hypertensive. Irrespective of the definition, there is a close comparability between the daytime and night-time values in the white coat and normotensive groups and these are significantly different from the corresponding values in the persistent hypertensives. We accept that the absence of left-ventricular hypertrophy in patients with white-coat hypertension predicts a relatively low rate of cardiovascular morbidity and mortality but the new data from Verdecchia et al identify an intermediate level of risk, as we suggested from our results, even though this contrasts with the opinions expressed by Krakoff and Phillips. Again, however, this is likely to be a problem of definition. With respect to the standardisation procedures for the functional cardiovascular measurements we accept that there are limitations in our technique but, again in the absence of an accepted procedure, we standardised our measurements by allowing for the slope of the relation between blood

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