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Coronary circulation in arterial hypertension
1Medizinische Klinik und Poliklinik B-Kardiologie, Pneumologie und Angiologie, Heinrich-Heine-Universität Düsseldorf, F.R.G.
Insights
Hypertension impairs coronary vasodilator reserve, leading to reduced blood flow and potential myocardial ischemia, independent of left ventricular hypertrophy. This vascular alteration is a key finding in hypertensive patients with angina and normal coronary arteries.
Area of Science:
- Cardiology
- Vascular Physiology
- Hypertension Research
Background:
- Arterial hypertension is a primary cause of congestive heart failure and a significant risk factor for coronary artery disease (CAD).
- Coronary reserve is often impaired in hypertensive individuals, even without diagnosed CAD.
- The underlying cause of this reduced coronary reserve (left ventricular hypertrophy vs. vascular alterations) requires investigation.
Purpose of the Study:
- To investigate whether reduced coronary reserve in hypertensive patients is linked to left ventricular hypertrophy (LVH) or primary vascular changes.
- To quantify coronary reserve and resistance in hypertensive patients with angina and normal coronary angiograms.
- To compare these parameters with those of normotensive individuals.
Main Methods:
- Coronary reserve was assessed in 31 hypertensive patients and 12 normotensive controls.
- Coronary resistance was measured before and after intravenous dipyridamole administration.
- Coronary blood flow was quantified using the argon gas chromatographic method; LV muscle mass was determined by ventriculography.
Main Results:
- Hypertensive patients exhibited 20% higher coronary resistance and 40% lower maximal coronary blood flow post-dipyridamole compared to controls.
- Minimal coronary resistance increased by 112% and coronary reserve was reduced by 37% in hypertensive subjects (p < 0.001).
- No significant correlation was found between impaired coronary reserve and left ventricular muscle mass (r = 0.024).
Conclusions:
- Hypertension significantly impairs coronary vasodilator reserve, independent of left ventricular hypertrophy.
- This impairment is characterized by increased coronary resistance and reduced maximal flow, contributing to myocardial ischemia.
- Findings suggest primary vascular alterations are responsible for reduced coronary reserve in hypertensive patients.
Abstract:
Arterial hypertension is the most common cause of congestive heart failure and an important risk factor in coronary artery disease (CAD). However, even in the absence of CAD, coronary reserve is frequently impaired in hypertensive patients. To study whether the reduced coronary reserve is due to the degree of left ventricular hypertrophy (LVH) or is a consequence of primary vascular alterations, coronary reserve was determined in 31 hypertensive patients (age of 56 +/- 10 years; systolic/diastolic blood pressure of 167 +/- 18/98 +/- 9 mm Hg) with angina pectoris and normal coronary angiogram. Coronary reserve was determined by measuring coronary resistance before and after dipyridamole (0.5 mg/kg of body weight i.v.). Coronary blood flow was measured quantitatively by the gas chromatographic argon method. LV muscle mass was measured by ventriculography. Twelve normotensive patients (age of 52 +/- 8 years) were studied for comparison. Coronary resistance was 20% higher in hypertensive than in normotensive patients, whereas coronary blood flow at rest was not significantly different. The maximal coronary blood flow after dipyridamole was 40% lower in hypertensive than in normotensive patients; accordingly, minimal coronary resistance was significantly increased by 112% in hypertensive patients (p less than 0.0005). Coronary reserve was reduced by 37% (p less than 0.001) in hypertensive patients compared with normotensive patients. Between the impairment in coronary reserve and left ventricular muscle mass, no significant correlation (r = 0.024, n.s.) was found. The impaired coronary vasodilator reserve is reflected by episodes of transient myocardial ischemia during ST-segment monitoring.