Role of coronary vasospasm in the pathogenesis of myocardial infarction: Study in patients with no significant coronary stenosis

doi:10.1016/0002-8703(93)90527-G

American Heart Journal

Volume 126, Issue 6, December 1993, Pages 1305-1311

https://doi.org/10.1016/0002-8703(93)90527-G Get rights and content

Abstract

The role of coronary vasospasm in the pathogenesis of myocardial infarction is unclarified. Among 212 patients with myocardial infarction in whom percutaneous transluminal coronary angioplasty (PTCA) or coronary thrombolysis was not performed at the acute stage, 21 patients (10%) showed no significant coronary stenosis (the degree of stenosis was less than 50% of the luminal diameter) by coronary angiography 4 weeks after myocardial infarction. Among them, 11 (52%) had preinfarction angina at rest, including two with variant angina, and nine (43%) had postinfarction angina at rest. Intracoronary ergonovine maleate induced coronary vasospasm in 12 (75%) of 16 patients examined. Coronary vasospasm occurred in the infarct-related coronary arteries in all patients, and importantly, multivessel coronary vasospasm occurred in 11 patients (69%). The infarct size was relatively small in these patients: (1) seven patients (33%) had Q wave myocardial infarction while 14 patients (67%) had non-Q wave myocardial infarction; (2) peak creatine phosphokinase (CPK) was lower than 1000 IU/ml in all patients; and (3) thallium-201 (TI-201) scintigraphic study showed no perfusion defect in 8 of 18 patients. There was only one patient with congestive heart failure and no patient died. These results suggest that coronary vasospasm may play an important role in the pathogenesis of myocardial infarction in patients without significant coronary stenosis. The relatively small infarct size suggests that coronary reperfusion occurred in the early stages of myocardial infarction.

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Citation Excerpt :
The prevalence of MI in patients with variant angina can be derived from the data obtained by H. Yasue et al., according to which the survival rate of patients with variant angina at 1, 3, 5, and 10 years was 98%, 97%, 97%, and 93%, respectively, whereas the survival rate without MI at 1, 3, 5, and 10 years was 86%, 85%, 83%, and 81%, respectively [324]. The role of coronary vasospasm in the pathogenesis of MI was established in the work of T. Fukai et al., who showed that intracoronary ergonovine maleate induced coronary vasospasm in 75% of patients with MI and no significant coronary stenosis [325]. Furthermore, coronary vasospasm occurred in the infarct-related coronary arteries in all patients, and, importantly, multi-vessel coronary vasospasm occurred in 69% of patients [325].
In 2006, Takotsubo syndrome (TTC) was described as a distinct type of stress-induced cardiomyopathy (stress cardiomyopathy). However, when thinking about Takotsubo cardiomyopathy from the viewpoints of the AHA and ESC classifications, 2 possible problems may arise.
The first potential problem is that a forecast of disease outcome is lacking in the ESC classification, whereas the AHA only states that ‘outcome is favorable with appropriate medical therapy’. However, based on the literature data, one can make a general conclusion that occurrence of myocardial lesions in TTC (i.e., myocardial fibrosis and contraction-band necrosis) causes the same effects as in other diseases with similar levels of myocardial damage and should not be considered to have a lesser impact on mortality. To summarise, TTC can cause not only severe complications such as pulmonary oedema, cardiogenic shock, and dangerous ventricular arrhythmias, but also damage to the myocardium, which can result in the development of potentially fatal conditions even after the disappearance of LV apical ballooning.
The second potential problem arises from the definition of TTC as a stress cardiomyopathy in the AHA classification. In fact, the main factors leading to TTC are stress and microvascular anginas, since, as has been already discussed, coronary spasm can cause myocardium stunning, resulting in persistent apical ballooning.
Thus, based on this review, 3 distinct types of stress cardiomyopathies exist (variant angina, microvascular angina, and TTC), with poor prognosis. Adding these diseases to the classification of cardiomyopathies will facilitate diagnosis and preventive prolonged treatment, which should include intensive anti-stress therapy.
2012 ACCF/AHA focused update incorporated into the ACCF/AHA 2007 guidelines for the management of patients with unstable angina/Non-ST-Elevation myocardial infarction: A report of the american college of cardiology Foundation/American Heart Association task force on practice guidelines
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Citation Excerpt :
Infants, elderly patients, and patients with hepatic dysfunction lack sufficient plasma cholinesterase to metabolize the drug (1003) and therefore are at high risk of adverse effects with cocaine use. The basis for coronary spasm has been demonstrated in both in vitro (1003) and in vivo (999,1004–1008) experiments in animals and humans. Reversible vasoconstriction of rabbit aortic rings has been demonstrated with cocaine in concentrations of 10−3 to 10−8 mol per liter.
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2011, Journal of the American College of Cardiology

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Role of coronary vasospasm in the pathogenesis of myocardial infarction: Study in patients with no significant coronary stenosis

Abstract

Am J Cardiol

Am J Cardiol

J Am Coll Cardiol

Am Heart J

J Am Coll Cardiol

Am J Med

Am J Cardiol

The nature and clinical features of myocardial infarction with normal coronary arteriogram

Circulation

Myocardial infarction in nine patients with radiologically patent coronary arteries

N Engl J Med

Coronary spasm and thrombosis associated with myocardial infarction in a patient with nearly normal coronary arteries

Circulation

Coronary spasm producing coronary thrombosis and myocardial infarction

N Engl J Med

Coronary vasospasm as a possible cause of myocardial infarction: a conclusion derived from the study of “preinfarction” angina

N Engl J Med

Variant angina culminating in coronary thrombosis and myocardial infarction

Chest

Arteriographic evidence of coronary arterial spasm in acute myocardial infarction

Circulation