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Coronary segmental responses to acetylcholine and bradykinin in patients with atherosclerotic risk factors
1First Department of Internal Medicine, Hiroshima University School of Medicine, Japan.
Insights
Coronary endothelial dysfunction in patients with hypertension or high cholesterol is complex. Bradykinin
Area of Science:
- Cardiovascular Medicine
- Endothelial Function Research
- Vascular Biology
Background:
- Coronary endothelial dysfunction is a key factor in cardiovascular disease.
- Hypertension and hypercholesterolemia are significant risk factors for endothelial dysfunction.
- Assessing endothelial function in patients with normal coronary arteries is crucial.
Purpose of the Study:
- To investigate the characteristics of coronary endothelial dysfunction.
- To evaluate vascular responses to acetylcholine and bradykinin in patients with risk factors.
- To understand the heterogeneity of endothelial dysfunction in normal coronary arteries.
Main Methods:
- Quantitative angiography to measure epicardial coronary artery diameters.
- Infusion of acetylcholine, bradykinin, and nitroglycerin into the left coronary ostium.
- Inclusion of 19 patients with hypertension and/or hypercholesterolemia and normal coronary arteries.
Main Results:
- Acetylcholine induced both vasoconstriction and vasodilation in coronary segments.
- Bradykinin significantly dilated both vasoconstricted and vasodilated segments.
- Bradykinin-induced dilation was more pronounced in segments that initially vasodilated to acetylcholine.
Conclusions:
- Coronary endothelial dysfunction is a heterogeneous process in patients with cardiovascular risk factors.
- Impaired endothelium-dependent dilation involves muscarinic and B2-kinin receptors.
- Findings highlight the complex nature of endothelial dysfunction in hypertension and hypercholesterolemia.
Abstract:
This study was designed to elucidate the nature of coronary endothelial dysfunction in patients with hypertension and/or hypercholesterolemia and normal smooth coronary arteries by evaluating the coronary vascular responses to acetylcholine and bradykinin. The study included 19 patients (10 men; age [mean +/- SD] 61 +/- 9 years) with angiographically normal smooth coronary arteries and either hypertension (n = 7) and/or hypercholesterolemia (n = 13). Patients received acetylcholine (3 or 30 microg/min) infusions followed by bradykinin (0.5, 1.5, 2.5 microg/min) and nitroglycerin (200 microg/min) infusions into the left coronary ostium. Epicardial coronary artery diameters were measured by quantitative angiography. Angiography detected both vasoconstricted and dilated segments following acetylcholine infusion. Bradykinin significantly dilated both types of segments (p <0.001, respectively). However, bradykinin-induced dilation was significantly greater in segments exhibiting acetylcholine-induced vasodilation than in those exhibiting vasoconstriction (p <0.01 in the proximal portion and p <0.02 in the distal portion). Nitroglycerin-induced dilation was similar in all segments. These results suggest that coronary endothelial dysfunction may be a heterogeneous process in patients with coronary risk factors. Moreover, the mechanism underlying diminished endothelium-dependent dilation involves not only the muscarinic receptor, but also B2-kinin receptor.