The importance of the clinical observer in the development of a white-coat effect in African-American patients with hypertension.

INTRODUCTION: As the office-awake blood pressure (BP) difference (white-coat effect) in African-Americans has not been evaluated, we studied the ethnicity, professional status (nurse versus doctor) and sex of the observer on the white-coat effect in African-American patients with hypertension. METHODS: Seated clinical BP measurements were obtained in random order by an African-American male research physician, a Caucasian male research physician, and a Caucasian female nurse who is of similar age and clinical experience. Within 1 week, ambulatory BP recordings were performed. RESULTS: A total of 65 African-American patients [54+/-13 years, 55% women, body mass index (BMI) 31+/-6 kg/m, 62% on drug therapy, 28% current smokers] participated in the study. Twenty-two percent had a systolic white-coat effect >20 mmHg and 49% had a diastolic white-coat effect >10 mmHg (average of all observers). Although there were no differences in the magnitude of the white-coat effect among the three study observers, the primary physician's diastolic white-coat effect was significantly greater than that of the African-American physician (14+/-12 vs. 9+/-12, P=0.05), but not the systolic white-coat effect (16+/-16 vs. 10+/-16 mmHg, P=0.09). BMI positively correlated with the systolic and diastolic white-coat effect (r=0.30, P=0.02 and r=0.41, P=0.0001), but this correlation was true only for female patients in multiple regression analyses. BMI significantly predicted the systolic (P=0.043) and diastolic (P=0.004) white-coat effects. CONCLUSION: A white-coat effect is relatively common in African-American patients with hypertension and is the largest when the observer is their usual doctor. The clinical observer's ethnicity or sex does not play an important role in generating a white-coat effect in African-American patients with hypertension.

Primary hyperaldosteronism associated with hypertensive emergencies.

There is growing awareness of primary hyperaldosteronism as a cause of secondary hypertension. Usually, it manifests as hypertension and hypokalemia, or as resistant hypertension. Much less often, primary hyperaldosteronism may be detected after a hypertensive emergency has developed. We highlight this association by reporting on eight patients with a clinical diagnosis of primary hyperaldosteronism whose course was complicated by a hypertensive crisis. In all patients, an elevated serum aldosterone, was accompanied by a suppressed plasma renin activity despite the presence of a hypertensive crisis. A good outcome was obtained either with laparoscopic adrenalectomy (1 patient) or with an antihypertensive drug regimen that included an antialdosterone agent (7 patients). The differential diagnosis of hypertensive emergencies should include primary hyperaldosteronism.