White‐Coat Hypertension: A True Cardiovascular Risk?

White-coat hypertension (WCH) is a condition in which blood pressure (BP) rises in the medical setting, apparently as a result of anxiety. It is a common phenomenon, with about one third of all patients presenting with elevated BP in outpatient clinics. It is generally assumed that WCH causes no more than a 15 mm Hg increase in systolic and/or a 7 mm Hg increase in diastolic BP in otherwise normotensive patients and returns to baseline values in subsequent visits to a medical provider. A typical patient is generally a nonsmoking, higher-aged woman. Currently, there are no reliable prognostic data available for WCH, as patients are often treated on the basis of elevated office BP and large prospective randomized trials are lacking. In the article “The Impact of White-Coat Hypertension on Cardiac Mechanics,” Tadic and colleagues1 examine the effect of WCH and sustained arterial hypertension (SHT) on right ventricular (RV) and left ventricular (LV) remodeling. Multilayer longitudinal strain was determined by modified two-dimensional strain speckle tracking for the left and right ventricle. Overall, the investigators reproduced previous findings on the effects of hypertension on LV and RV deformation. They also concluded that deformational changes start in RV subendocardium as they were lower in subendocardial but not myocardial and subepicardial layers of the right ventricle in patients with WCH compared with normotensives. Interestingly, these changes happened despite preserved RV structure. The study has several limitations, however. The major limitation is the small size of the study population. Furthermore, the differences between patients with WCH and controls for the strain parameters were not substantial. Nonetheless, these findings remain interesting because they: (1) provide insight into the sequences of events in cardiac pathology, and (2) may implicate the need for antihypertensive therapy in WCH, particularly if future studies show that these structural abnormalities of subendocardium can advance to myocardium and result in diastolic and potentially systolic dysfunction. Several other studies have shown an increased cardiovascular (CV) risk in WCH compared with normotensive patients. In a clinical study by the author, using echocardiographic measurement of strain, LV longitudinal and circumferential strains were significantly lower in patients with white-coat hypertension compared with normotensive controls. These values were lowest in patients with SHT.2 In a meta-analysis of 29,100 participants (13,538 normotensive patients, 4806 with WCH and 10,756 with SHT, mean age of 59 years) followed-up for a period of 8 years, patients with WCH were shown to have higher rates of CV morbidity and mortality.3 However, all-cause mortality and stroke rates were only significantly increased in patients with SHT but not those with WCH as compared with normotensive patients. CV events were also higher in patients with WCH in a US study population. In this multiethnic study of 3000 US citizens (almost half African Americans), comprised of 3.3% WCH patients, WCH was independently associated with increased aortic pulsed wave velocity, cystatin C, and urinary albumin-to-creatinine ratio. WCH was independently associated with higher CV events compared with the normotensive group, even after adjustment for traditional CV risk factors (adjusted hazard ratio, 2.09; 95% confidence interval [CI], 1.05–4.15). In a Finnish longitudinal study comparing patients with WCH5 (142 participants with office BP ≥140/90 mm Hg and home BP <135/85 mm Hg) with normotensive patients (528 participants with BP <135/85 mm Hg), the rate of progression to SHT increased from 18% to 52% (P<.0001) during 11-year follow-up. The multivariable-adjusted relative risk for WCH developing to SHT compared with normotensives was 2.8 (95% CI, 2.2–3.6; P<.0001). In a Japanese study of 1464 (31.8% men; mean age, 60.6±10.8 years) randomly selected individuals from the general population of Ohasama, 212 experienced a first-time stroke during a 17.1-year period. The adjusted HR for stroke in WCH patients (n=19/137) was 1.38 (0.82–2.32; 95% CIs) compared with those with normal BP.6 WCH has also been associated with increased 24-hour pulse pressure (PP) and target organ damage.7 Not all patients with WCH are at risk for developing SHT or CV complications. The real questions are which patients from this group are at increased risk for developing sustained HTN and how can one identify the risk factors among these patients in order to prevent complications. The answer to these questions requires prospective studies, possibly complemented by human genetic studies. Finally, prospective studies are needed to see whether medical interventions can prevent the CV complications associated with WCH. Currently, any approach would only be empirical. In patients with low risk for CV morbidity, nonpharmacologic treatment should be considered. In this case, however, the patient must be followed closely, including using out-of-office BP measurements. In patients with multiple CV risk factors and/or target organ damage, drug therapy may need to be considered. The latter is obviously quite controversial at this point.