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

Tohru Fukai, Samon Koyanagi, Akira Takeshita

Research output: Contribution to journalArticle

59 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)1305-1311
Number of pages7
JournalAmerican Heart Journal
Volume126
Issue number6
DOIs
StatePublished - Jan 1 1993
Externally publishedYes

Fingerprint

Coronary Vasospasm
Coronary Stenosis
Myocardial Infarction
Unstable Angina
Ergonovine
Myocardial Reperfusion
Coronary Balloon Angioplasty
Thallium
Creatine Kinase
Coronary Angiography

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Role of coronary vasospasm in the pathogenesis of myocardial infarction : Study in patients with no significant coronary stenosis. / Fukai, Tohru; Koyanagi, Samon; Takeshita, Akira.

In: American Heart Journal, Vol. 126, No. 6, 01.01.1993, p. 1305-1311.

Research output: Contribution to journalArticle

@article{61e075ca77934840a84041e877ee2dfc,
title = "Role of coronary vasospasm in the pathogenesis of myocardial infarction: Study in patients with no significant coronary stenosis",
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.",
author = "Tohru Fukai and Samon Koyanagi and Akira Takeshita",
year = "1993",
month = "1",
day = "1",
doi = "10.1016/0002-8703(93)90527-G",
language = "English (US)",
volume = "126",
pages = "1305--1311",
journal = "American Heart Journal",
issn = "0002-8703",
publisher = "Mosby Inc.",
number = "6",

}

TY - JOUR

T1 - Role of coronary vasospasm in the pathogenesis of myocardial infarction

T2 - Study in patients with no significant coronary stenosis

AU - Fukai, Tohru

AU - Koyanagi, Samon

AU - Takeshita, Akira

PY - 1993/1/1

Y1 - 1993/1/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0027138621&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027138621&partnerID=8YFLogxK

U2 - 10.1016/0002-8703(93)90527-G

DO - 10.1016/0002-8703(93)90527-G

M3 - Article

C2 - 8249786

AN - SCOPUS:0027138621

VL - 126

SP - 1305

EP - 1311

JO - American Heart Journal

JF - American Heart Journal

SN - 0002-8703

IS - 6

ER -