Key result
Morning systolic blood pressure surge was an independent predictor of both left ventricular mass and carotid intima-media thickness in elderly Japanese patients with treated hypertension.
Why the study?
Does morning blood pressure surge predict cardiovascular remodeling in elderly treated hypertensive patients?
Does morning blood pressure surge predict cardiovascular remodeling in elderly treated hypertensive patients?
Answers are grounded in this paper and cite their sources.
An excessive morning blood pressure surge is associated with adverse cardiovascular remodeling in treated hypertensive patients, though methodological limitations currently hamper its routine clinical application.
The well-documented morning increase in the incidence of acute coronary syndromes, sudden cardiac death, and ischemic stroke has been linked to diurnal changes in several physiological variables, including blood pressure (BP), heart rate, adrenergic activity, and platelet aggregability. It is therefore biologically plausible that an exaggerated BP increase during the early morning hours may cause progression of cardiovascular remodeling and atherosclerosis, and predict future cardiovascular morbidity and mortality. Several years ago, we described a hypertensive patient who, during a 24-h noninvasive ambulatory BP monitoring, developed an ischemic stroke in the early morning shortly after a large, sudden BP rise.1 In the following years, a large morning surge has been linked with a significantly increased risk of stroke,2 intracerebral hemorrhage,3 and total cardiovascular events4 in some, but not all,5,6 prospective studies. In the current issue of the Journal, Yano et al.7 report the results of a cross-sectional study carried out in 197 elderly Japanese patients with treated hypertension. In these subjects, morning systolic BP surge, defined as the top quartile of the distribution of the difference between the mean systolic BP 2 h after waking and the average of three readings centered on the lowest sleep BP (“sleep-trough” morning surge), was an independent predictor of both left ventricular mass and carotid intima–media thickness. Notably, the above relations were independent of average 24-h BP values and day–night BP change. Although the adverse cardiovascular consequences of an excessive morning BP surge had been already described in cohorts of mainly untreated subjects,2–4 this study is the first to be specifically carried out in treated hypertensive subjects. Based on the results of Yano's7 and other studies, is it time to add morning BP surge to the list of valuable pieces of clinical information yielded from ambulatory BP monitoring, along with 24-h average BP and nocturnal BP reduction? A few methodological points should be addressed in this regard. First, the prospective studies that reported an adverse prognostic value of early morning BP surge are based on relatively small numbers of events, ranging between 27 and 44 (refs. 2,3,4). On the contrary, other large prospective studies have either found a neutral5 or even a protective6 effect of a large morning surge on the future incidence of cardiovascular events, which mirrors the adverse cardiovascular consequences of a flattened day–night BP rhythm. A second important issue is the unavoidable collinearity between morning BP surge and nocturnal BP reduction. As expected, in this study a high morning BP surge was strongly related to nocturnal BP decline, and the subjects who had both excessive morning BP surge and excessive nocturnal BP fall (extreme dippers) showed adverse cardiac remodeling. Interestingly, when day–night BP changes were examined as a continuous rather than categorical variable, a low percent nocturnal BP decline was also related with cardiac and vascular hypertrophy. This provocative finding suggests that both a low and a high nocturnal BP reduction might have an independent effect on cardiovascular remodeling, but clearly more data are needed in this regard. Third, there is no agreement on which of the many proposed definitions best identifies morning BP surge. In this study, left ventricular mass had an association with high “sleep-trough,” but not with “waking” morning surge (the latter defined as the difference between average 2-h systolic BP after waking minus average 2-h systolic BP before waking). Fourth, the clinical utility of the morning BP surge obtained from a single ambulatory BP monitoring is limited by its rather poor reproducibility, with reported κ statistics ≤0.33 and ≤0.20 over the short and long term, respectively.8 The results of Yano et al.7 reinforce the view that an excessive morning BP surge could have adverse consequences on cardiovascular remodeling. Currently, differences in definitions and the limitations inherent in intermittent noninvasive ambulatory BP monitoring hamper the routine clinical application of this promising measure of circadian BP variation. Further studies in larger populations are needed to better elucidate the prognostic significance of an abnormal morning BP increase, and to demonstrate whether its pharmacological correction entails cardiovascular benefits. The authors declared no conflict of interest.
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Schillaci et al. (2009) conducted an editorial in Treated hypertension (n=197). Morning blood pressure surge was evaluated on Left ventricular mass and carotid intima-media thickness. Morning systolic blood pressure surge was an independent predictor of both left ventricular mass and carotid intima-media thickness in elderly Japanese patients with treated hypertension.
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