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Clinical Significance of Coronary Vasomotor Tone in Myocardial Ischemia

Juan Carlos Kaski, Attilio Maseri

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Abstract

Our understanding of the pathogenic mechanisms underlying chronic stable angina, unstable angina and Prinzmetal’s variant angina has increased in recent years. There is now general agreement that dynamic coronary stenoses may contribute to these ischemic syndromes [15, 24, 25]. Dynamic stenoses can be caused by increase of coronary vasomotor tone, coronary thrombosis or by a combination of the two. The thrombotic component confers to the anginal syndromes the feature of instability and the tendency to evolve towards myocardial infarction [18, 32]. It is now generally accepted that an episodic increase of the vasomotor tone of epicardial coronary arteries is not only the cause of variant angina but may also be a pathogenic component in other more common anginal syndromes [15,18, 24, 25, 32, 50, 77]. Although the terms “coronary spasm” and “coronary vasoconstriction” are frequently used synonymous in medical literature to indicate increases in coronary vasomotor tone, a distinction between the two is necessary, as the difference between coronary spasm, as seen in variant angina, and the coronary vasoconstriction commonly observed in chronic stable angina is not only one of degree, but it seems to reflect also different underlying mechanisms.

About this research paper

What this paper is about

Our understanding of the pathogenic mechanisms underlying chronic stable angina, unstable angina and Prinzmetal’s variant angina has increased in recent years. There is now general agreement that dynamic coronary stenoses may contribute to these ischemic syndromes [15, 24, 25]. Dynamic stenoses can be caused by increase of coronary vasomotor tone, coronary thrombosis or by a combination of the two. The thrombotic component confers to the anginal syndromes the feature of instability and the tendency to evolve towards myocardial infarction [18, 32]. It is now generally accepted that an episodic increase of the vasomotor tone of epicardial coronary arteries is not only the cause of variant angina but may also be a pathogenic component in other more common anginal syndromes [15,18, 24, 25, 32, 50, 77]. Although the terms “coronary spasm” and “coronary vasoconstriction” are frequently used synonymous in medical literature to indicate increases in coronary vasomotor tone, a distinction between the two is necessary, as the difference between coronary spasm, as seen in variant angina, and the coronary vasoconstriction commonly observed in chronic stable angina is not only one of degree, but it seems to reflect also different underlying mechanisms.

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Available abstract

Our understanding of the pathogenic mechanisms underlying chronic stable angina, unstable angina and Prinzmetal’s variant angina has increased in recent years. There is now general agreement that dynamic coronary stenoses may contribute to these ischemic syndromes [15, 24, 25]. Dynamic stenoses can be caused by increase of coronary vasomotor tone, coronary thrombosis or by a combination of the two. The thrombotic component confers to the anginal syndromes the feature of instability and the tendency to evolve towards myocardial infarction [18, 32]. It is now generally accepted that an episodic increase of the vasomotor tone of epicardial coronary arteries is not only the cause of variant angina but may also be a pathogenic component in other more common anginal syndromes [15,18, 24, 25, 32, 50, 77]. Although the terms “coronary spasm” and “coronary vasoconstriction” are frequently used synonymous in medical literature to indicate increases in coronary vasomotor tone, a distinction between the two is necessary, as the difference between coronary spasm, as seen in variant angina, and the coronary vasoconstriction commonly observed in chronic stable angina is not only one of degree, but it seems to reflect also different underlying mechanisms.

Key concepts: Medicine, Cardiology, Internal medicine, Angina, Vasomotor, Vasoconstriction, Coronary arteries, Myocardial infarction

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