Abstract

Hypertensive heart disease, characterized by left ventricular (LV) hypertrophy, left atrial enlargement, and LV dysfunction, represents a relatively advanced stage of hypertension-mediated organ damage (HMOD) typically associated with unrecognized or inadequately controlled systemic hypertension. However, a growing amount of evidence supports the view that subtle cardiac morphofunctional abnormalities such as LV concentric remodeling and mild impairment in LV relaxation can develop very early in the natural history of hypertension. Furthermore, an increased risk of initial cardiac HMOD has also been reported for long-held innocent conditions such as prehypertension and white coat hypertension (WCH). WCH is a common condition in which blood pressure (BP) measured in the medical environment is elevated while ­out-of-office BP (i.e., home and/or ambulatory BP [ABP]) is ­normal.1 The relationship between WCH and cardiac HMOD, an intermediate step linking hypertension with overt cardiovascular disease, has been investigated by numerous individual studies and their meta-analyses. Pooled data from 25 studies, including a total of 7.382 untreated individuals (2.493 true normotensives, 1.705 WCH, and 3.184 sustained hypertensives), showed that LV mass index (LVMI) gradually increased from normotensive, WCH, to sustained hypertensive patients. A meta-regression analysis restricted to WCH group documented a significant direct correlation between LVMI and office systolic BP (r = 0.42, P < 0.01); this was not the case for daytime systolic BP (r = 0.18, P = 0.17). Of note, the meta-analysis suggested that LV relaxation (in parallel with a greater left atrial size) but not LV ejection fraction (LVEF) was impaired in WCH.2

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