Diastolic Blood Pressure in Coronary Artery Disease
Thomas Weber, MD; Johann Auer, MD; Bernd Eber, MD; Michael F. O'Rourke, MD
Thomas Weber, MD
From Klinikum Wels, Wels, Austria, and St. Vincent's Clinic, Sydney, Australia.
Johann Auer, MD
Bernd Eber, MD
Michael F. O'Rourke, MD
Potential Financial Conflicts of Interest: Dr. O'Rourke is a funding director of AtCor Medical, a manufacturer of systems for pulse-wave form analysis.
Messerli and colleagues (1) provide new insights into the J-curve discussion in hypertensive patients with coronary artery disease (CAD). Briefly, they observed an increase in all-cause mortality and myocardial infarctions with lower diastolic blood pressure in patients from the International Verapamil-Trandolapril Study (INVEST) (2), hypertensive patients with CAD, who were treated with a verapamil sustained-release–based or atenolol-based strategy. The authors mention impaired coronary perfusion, increased pulse pressure and arterial stiffness, and underlying chronic illness as possible pathophysiologic mechanisms.
Clearly, we cannot speculate on the latter mechanism, but we would like to support the 2 other explanations. First, the mean patient age in INVEST was 66 years. Generally in this age group, isolated systolic hypertension is by far the most common phenotype of hypertension (3), a condition characterized by widened pulse pressure, increased arterial stiffness, increased or premature arterial wave reflections (therefore decreased diastolic blood pressure), and impaired coronary perfusion (4, 5). In the original publication, more than 50% of patients had “controlled” diastolic blood pressure at baseline, suggesting isolated systolic hypertension. A complementary analysis in patients with isolated systolic hypertension, if they had been identified at baseline, would be very interesting. Second, Chirinos and colleagues (6), as well as our group (7), recently observed that increased arterial wave reflections, one of the main pathophysiologic principles contributing to an increased pulse pressure in patients with isolated systolic hypertension, are accompanied by an increase in major adverse cardiovascular events, including myocardial infarction and death, in patients with CAD. In the Chirinos and colleagues' paper (6), as well as in a previous study showing a relationship between increased arterial wave reflections and the presence and extent of CAD (8), a lower diastolic blood pressure was a predictor of the unfavorable end point. Moreover, in the latter study, systolic blood pressure was identical in patients with and without CAD, and the statistically significant difference in pulse pressure was mediated mainly by a lower diastolic blood pressure in the CAD group. In other words, the only clue to the altered arterial characteristics in patients with CAD was a lower diastolic blood pressure. Of note, most patients with CAD in that study were treated hypertensive patients with a mean age of 63.8 years and, therefore, were similar to those in the INVEST patient population.