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Loss of flow-dependent coronary artery dilatation in patients with hypertension
I Antony1, G Lerebours, A Nitenberg
1Service d'Explorations Fonctionnelles, Centre Hospitalier et Universitaire Xavier Bichat, Paris, France.
Insights
Flow-mediated coronary artery dilation is impaired in hypertensive patients. This loss of function may hinder the heart
Area of Science:
- Cardiovascular Physiology
- Hypertension Research
- Coronary Artery Disease
Background:
- Essential hypertension is linked to abnormal endothelium-dependent coronary responses to acetylcholine.
- Previous studies show flow-dependent dilation in normal coronary arteries.
- This study investigates if flow-dependent dilation is impaired in hypertensive patients.
Purpose of the Study:
- To test the hypothesis that flow-dependent coronary artery dilation is impaired in patients with essential hypertension.
- To compare coronary vasomotor response to increased blood flow between hypertensive patients and control subjects.
Main Methods:
- Quantitative angiography and intracoronary Doppler flow velocity measurements were used.
- Coronary blood flow and artery diameter changes were assessed after papaverine-induced vasodilation.
- The left anterior descending coronary artery (LAD) and circumflex artery (LCx) were analyzed in 14 hypertensive patients and 10 controls.
Main Results:
- Control subjects showed significant LAD dilation (17.0%) with a 521% increase in blood flow.
- Hypertensive patients exhibited no significant LAD dilation (-0.4%) despite a 406% increase in blood flow.
- Both groups responded similarly to isosorbide dinitrate, indicating preserved smooth muscle function.
Conclusions:
- Flow-mediated coronary dilation is lost in hypertensive patients.
- This impairment may compromise the normal coronary response to increased myocardial metabolic demand.
- Findings suggest a specific endothelial dysfunction in hypertensive coronary arteries.
Background:
Abnormal endothelium-dependent coronary response to acetylcholine has been shown in patients with essential hypertension. We tested the hypothesis that flow-dependent dilatation, which has been shown in normal human coronary arteries, is impaired in hypertensive patients.
Methods And Results:
The coronary vasomotor response to maximal increase of blood flow induced by papaverine was studied in 10 control subjects and in 14 hypertensive patients with no other risk factors and angiographically normal coronary arteries. After the injection of papaverine in the midportion of the left anterior descending coronary artery (LAD), the diameter of the proximal LAD (LAD1) was measured by quantitative angiography, whereas that of the proximal circumflex artery (LCx) served as control segment. Estimates of coronary blood flow in the distal LAD (LAD2) were calculated by intracoronary Doppler flow velocity measurements. An increase in LAD2 blood flow of 521 +/- 41% (P < .001) in control subjects was associated with a 17.0 +/- 3.3% dilatation of the LAD1 (P < .001) and with no significant change in the diameter of the LCx. In hypertensive patients, despite a comparable increase in LAD2 blood flow of 406 +/- 32% (P < .001), the LAD1 failed to dilate (-0.4 +/- 0.6%, NS). The dilative response to isosorbide dinitrate was similar in control subjects and hypertensive patients (30.0 +/- 4.1%, P < .001 and 21.9 +/- 1.9%, P < .001, respectively).
Conclusions:
Thus, the flow-mediated coronary dilatation is lost in hypertensive patients, and this may impair normal dilatation observed in response to an increase in myocardial metabolic demand.