Early impairment of coronary flow reserve in young men with borderline hypertension

Abstract

Objectives: The purpose of this study was to investigate whether functional abnormalities in coronary vasomotion are present in young healthy asymptomatic men fulfilling the World Health Organization (WHO) criteria for borderline hypertension.

Background: Previous studies have reported reduced coronary flow reserve in middle-aged subjects with sustained hypertension and hypertension-induced microvascular heart disease or left ventricular hypertrophy.

Methods: Myocardial blood flow was measured at baseline and during dipyridamole-induced hyperemia by means of positron emission tomography and oxygen-15-labeled water in asymptomatic young men with borderline hypertension (group 1: n = 16, mean +/- SD age 37 +/- 4 years, 24-h ambulatory blood pressure 135 +/- 10/81 +/- 9 mm Hg) and matched healthy control subjects (group 2: n = 19, age 35 +/- 3 years, 24-h ambulatory blood pressure 119 +/- 8/69 +/- 8 mm Hg, p < 0.001). Left ventricular (LV) mass, dimensions and function were measured by echocardiography.

Results: LV mass, dimensions and diastolic function were similar in the study groups. Baseline myocardial blood flow was similar (0.83 +/- 0.21 vs. 0.80 +/- 0.22 ml/g per min, group 1 vs. group 2, respectively, p = NS), and a significant increase in flow was detected after dipyridamole infusion (0.56 mg/kg body weight in 4 min intravenously) in both groups. However, the flow response to dipyridamole was significantly lower in group 1, leading to lower hyperemic flow in group 1 than in group 2 (2.85 +/- 1.20 vs. 3.80 +/- 1.44 ml/g per min, respectively). Consequently, the coronary flow response was lower in hypertensive than in normotensive men (3.46 +/- 1.23 vs. 4.99 +/- 2.5 ml/g per min, group 1 vs. group 2, respectively, p < 0.05).

Conclusions: These results demonstrate reduced coronary reactivity present in young asymptomatic men with borderline hypertension and no signs of hypertension-induced angina or left ventricular hypertrophy. Because baseline basal myocardial blood flow was unchanged, the reduction in coronary flow reserve depends on an impaired maximal vasodilator capacity.