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The Western Journal of Medicine logoLink to The Western Journal of Medicine
. 2000 Jan;172(1):47–48. doi: 10.1136/ewjm.172.1.47

Does “white coat hypertension” increase the risk for any adverse outcome from hypertension?

Joel A Simon 1
PMCID: PMC1070724  PMID: 10695445

Patients with “white coat hypertension” have elevated blood pressures when measured in health care settings but normal blood pressures otherwise. First described in 1940, white coat hypertension has been estimated to account for about 20% of all cases of hypertension.1 Unlike the consensus reached on the diagnosis and treatment of sustained hypertension—disseminated in periodic reports from the Joint National Committee on the Detection, Evaluation, and Treatment of High Blood Pressure—the diagnosis, treatment, and clinical implications of white coat hypertension remain uncertain and controversial.

Periodic monitoring of patients for evidence of early target organ damage or sustained hypertension is prudent

White coat hypertension is best diagnosed by obtaining normal average daytime blood pressure measurements, using 24-hour ambulatory blood pressure monitoring, in patients who have elevated blood pressures in health care settings. These monitors are often programmed to measure blood pressures every 15 to 30 minutes during a patient's usual daily activities. A daytime average blood pressure of greater than 135/85 mm Hg in an ambulatory person has been proposed as a reasonable cutoff for diagnosing the presence of hypertension. Unfortunately, population norms for average 24-hour daytime blood pressures have not been determined, and published studies have often used different definitions for white coat hypertension.2,3

Although not reported consistently, white coat hypertension has been associated in some studies with an increased risk of sustained hypertension4 and target organ damage, such as left ventricular hypertrophy.5 The actual risk posed by white coat hypertension on cardiovascular disease end points—such as stroke, myocardial infarction, and hypertensive nephropathy—however, remains unclear. To date, few prospective studies have been done of patients with white coat hypertension diagnosed by ambulatory blood pressure measurement. Khattar and colleagues in a recent study reported that white coat hypertension was an independent predictor of cardiovascular disease events during a period of 9 years of follow-up, but the risk of such events was lower than among patients with sustained hypertension.6 Other prospective studies of shorter duration have failed to observe any relation between white coat hypertension and an increased risk of cardiovascular morbidity.7

Data from follow-ups longer than 9 years are not available. In general, the risk for target organ damage and cardiovascular disease events associated with white coat hypertension appears to be intermediate between that of normotensive persons and patients with sustained hypertension.

For most practitioners, the biggest challenge remains the detection, treatment, and adequate control of sustained hypertension. Recent national survey data indicate that hypertension goes undetected in about 30% of people who have the disease, 50% of those whose hypertension is detected are not taking medication, and 70% of those taking antihypertensive medication continue to have blood pressures higher than 140/90 mm Hg.8

White coat hypertension may not be an entirely benign condition

Because white coat hypertension has a comparatively benign prognosis, at least in the short term, most authorities would, in the absence of evidence of target organ damage, defer pharmacologic treatment of patients having this diagnosis.

Nevertheless, white coat hypertension may not be an entirely benign condition, and periodic monitoring of patients for evidence of early target organ damage or sustained hypertension is prudent. A greater use of 24-hour ambulatory blood pressure monitoring is also warranted to identify the disorder and to prevent the unnecessary pharmacologic treatment of patients diagnosed as having it.

Figure 1.

Figure 1

References

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