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Updated: Jun 19, 2026

Measurement of Myocardial Lactate Production for Diagnosis of Coronary Microvascular Spasm
Published on: September 17, 2021
Myocardial ischemia and coronary microvascular vasomotion: the impact of hypercholesterolemia
Tatsuya Komaru1, Kunio Shirato
1Tohoku University Graduate School of Medicine, Department of Cardiovascular Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai 980-8574, Japan. komaru@cardio.med.tohoku.ac.jp
Insights
Coronary microvascular dilation protects the heart during ischemia. Hypercholesterolemia impairs this defense by disrupting vasodilator signaling, likely via redox mechanisms, increasing heart injury risk.
Area of Science:
- Cardiovascular Physiology
- Vascular Biology
- Myocardial Ischemia
Background:
- Coronary microvascular dilation is a key defense against heart injury during myocardial ischemia.
- Ischemic myocardium releases both vasodilatory and vasoconstrictor signals.
- Hypercholesterolemia is linked to microvascular dysfunction without atherosclerotic lesions.
Purpose of the Study:
- To review the mechanisms of ischemic vasodilation.
- To discuss the impact of hypercholesterolemia on coronary microvascular regulation.
- To explore the role of redox-sensitive mechanisms in impaired vasodilation.
Main Methods:
- Review of existing literature on ischemic vasodilation.
- Analysis of bioassay studies on hypercholesterolemia and microvascular function.
- Discussion of redox-sensitive pathways in cardiovascular regulation.
Main Results:
- Ischemic myocardium-derived factors mediate vasodilation.
- Hypercholesterolemia severely impairs vasodilator signal transduction to coronary microvessels.
- Redox-sensitive mechanisms are implicated in this impairment.
Conclusions:
- Understanding ischemic vasodilation is crucial for cardiovascular health.
- Hypercholesterolemia significantly compromises the heart's protective microvascular response.
- Targeting redox mechanisms may offer therapeutic potential for hypercholesterolemia-induced microvascular dysfunction.
Abstract:
Coronary microvascular dilation in response to myocardial ischemia is an important defense mechanism for minimizing heart injury. Since myocardial ischemia is an intense stimulus for a living body, many biologic signals that affect the vascular tone are activated. Recent evidence demonstrated that among them, ischemic myocardium-derived factors play dominant roles as mediators of ischemic vasodilation, and that ischemic myocardium releases vasoconstrictor signals simultaneously. Hypercholesterolemia, a major risk factor for coronary atherosclerosis, is known to produce microvascular dysfunction, although it does not produce atherosclerotic lesions at the microvascular level. A recent bioassay study demonstrated that the vasodilator signal transduction from the myocardium to coronary microvessels is severely impaired in hypercholesterolemia. It is likely that redox-sensitive mechanisms play a major role in the impairment of the defensive responses. The present understanding of the mechanism of ischemic vasodilation and the impact of hypercholesterolemia on coronary microvascular regulation shall be discussed in this review.
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