Author + information
- Gian Battista Danzi, MD∗ ( and )
- Cesare Cuspidi, MD
- ↵∗Division of Cardiology, Ospedale Santa Corona, Via XXV April, 38, Pietra Ligure, Savona 17027, Italy
In a recent issue, McEvoy et al. (1) examined the relationship between diastolic blood pressure (DBP) with subclinical myocardial damage (using high-sensitivity cardiac troponin T) and with coronary heart disease (CHD), stroke, or death (1). They concluded that particularly among subjects with systolic blood pressure ≥120 mm Hg, and thus elevated pulse pressure, low DBP was associated with subclinical myocardial damage and coronary events.
In this insightful analysis, a very low DBP coupled with a high pulse pressure seemed to be very deleterious and these results put new perspective on studies that support lower targets for blood pressure lowering therapy (2).
It has been shown that overaggressive antihypertensive treatment, that leads to low DBP and thus hypoperfusion of the coronary arteries, results in cardiac ischemic events (3). McEvoy et al. (1) focused their attention on DBP as the predominant determinant of coronary perfusion. However, it should be remarked that several factors in addition to DBP, such as perfusion time, vessel wall diameter, and vasomotor tone, may importantly affect coronary blood flow. It has been reported that any increase in heart rate (HR) impinges on diastolic time more than on systolic time, reduces the perfusion time, and leads to subendocardial ischemia, especially in patients with coronary artery disease (4). Furthermore, a large body of evidence indicates that high HR can be considered a strong predictor of cardiovascular morbidity and mortality in different clinical settings (4). In their report, the authors, unfortunately, did not address the association of HR with subclinical myocardial damage and events across the various DBP categories. Considering that HR is a simple parameter that strongly correlates with diastolic coronary flow it should be routinely taken into account for refining risk stratification of CHD in treated hypertensive patients.
Please note: Both authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- 2017 American College of Cardiology Foundation
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