TY - JOUR
T1 - Mechanisms of coronary artery spasm
AU - Lanza, Gaetano Antonio
AU - Careri, Giulia
AU - Crea, Filippo
PY - 2011
Y1 - 2011
N2 - The term coronary artery spasm (CAS) refers to a sudden,
intense vasoconstriction of an epicardial coronary artery
that causes vessel occlusion or near occlusion. Although CAS
may be involved in other coronary syndromes, it represents
the usual cause of variant angina.
The variant form of angina was first described in 1959 by
Prinzmetal et al,1 who used this term to indicate that angina
attacks, unlike the most common form of effort angina,
occurred at rest and were associated with ST-segment elevation,
rather than ST-segment depression, on the ECG (Figure
1). Because myocardial ischemia occurred in the absence of
any change in myocardial oxygen demand, the authors
hypothesized that it was caused by an increased tonus of
vessels at the level of coronary stenoses.1
Some years later, in fact, coronary angiography, performed
during spontaneous angina attacks, demonstrated that CAS is
the usual cause of variant angina.2 4 Coronary angiography
also showed that CAS could occur at the site of a stenosis
(either minor or severe) or in angiographically normal coronary
arteries,5 usually at a localized segment of an epicardial
artery (focal spasm) (Figure 2).6 However, sometimes CAS
involves 2 or more segments of the same (multifocal spasm)
or of different (multivessel spasm) epicardial coronary arteries,
or may also involve diffusely one or multiple coronary
branches.7
Careful assessment of clinical history and 24- to 72-hour
ambulatory ECG monitoring are usually sufficient to achieve
the diagnosis of variant angina, whereas the use of provocative
tests of CAS (eg, intravenous ergonovine, intracoronary
ergonovine, or acetylcholine administration) is required in
about 10% of patients.7
Transmural myocardial ischemia caused by occlusive CAS
can be complicated by malignant ventricular arrhythmias,8,9
which can result in sudden death, or, if prolonged, by acute
myocardial infarction.10 Accordingly, a prompt diagnosis
would be essential to prevent these serious complications,
even though calcium antagonists are very effective in preventing
CAS.11,12 However, the diagnosis of variant angina is
often overlooked for several months after its manifestation.7
Sixty years after the first description of variant angina, the
causes and the mechanisms of CAS are still poorly defined.
The research in this field has indeed been refrained by several
factors, including the low incidence of the disease and the
considerable efficacy of nonspecific vasodilator therapy.12
However, in 10% to 20% of patients, CAS is refractory to
standard treatment, or high doses of calcium antagonists are
needed to effectively prevent its recurrence. Thus, elucidating
the mechanisms responsible for CAS could make treatment of
difficult or refractory cases easier.13
In this article, we review the state of knowledge regarding
the etiopathogenesis of CAS in patients with the clinical
syndrome of Prinzmetal variant angina.
AB - The term coronary artery spasm (CAS) refers to a sudden,
intense vasoconstriction of an epicardial coronary artery
that causes vessel occlusion or near occlusion. Although CAS
may be involved in other coronary syndromes, it represents
the usual cause of variant angina.
The variant form of angina was first described in 1959 by
Prinzmetal et al,1 who used this term to indicate that angina
attacks, unlike the most common form of effort angina,
occurred at rest and were associated with ST-segment elevation,
rather than ST-segment depression, on the ECG (Figure
1). Because myocardial ischemia occurred in the absence of
any change in myocardial oxygen demand, the authors
hypothesized that it was caused by an increased tonus of
vessels at the level of coronary stenoses.1
Some years later, in fact, coronary angiography, performed
during spontaneous angina attacks, demonstrated that CAS is
the usual cause of variant angina.2 4 Coronary angiography
also showed that CAS could occur at the site of a stenosis
(either minor or severe) or in angiographically normal coronary
arteries,5 usually at a localized segment of an epicardial
artery (focal spasm) (Figure 2).6 However, sometimes CAS
involves 2 or more segments of the same (multifocal spasm)
or of different (multivessel spasm) epicardial coronary arteries,
or may also involve diffusely one or multiple coronary
branches.7
Careful assessment of clinical history and 24- to 72-hour
ambulatory ECG monitoring are usually sufficient to achieve
the diagnosis of variant angina, whereas the use of provocative
tests of CAS (eg, intravenous ergonovine, intracoronary
ergonovine, or acetylcholine administration) is required in
about 10% of patients.7
Transmural myocardial ischemia caused by occlusive CAS
can be complicated by malignant ventricular arrhythmias,8,9
which can result in sudden death, or, if prolonged, by acute
myocardial infarction.10 Accordingly, a prompt diagnosis
would be essential to prevent these serious complications,
even though calcium antagonists are very effective in preventing
CAS.11,12 However, the diagnosis of variant angina is
often overlooked for several months after its manifestation.7
Sixty years after the first description of variant angina, the
causes and the mechanisms of CAS are still poorly defined.
The research in this field has indeed been refrained by several
factors, including the low incidence of the disease and the
considerable efficacy of nonspecific vasodilator therapy.12
However, in 10% to 20% of patients, CAS is refractory to
standard treatment, or high doses of calcium antagonists are
needed to effectively prevent its recurrence. Thus, elucidating
the mechanisms responsible for CAS could make treatment of
difficult or refractory cases easier.13
In this article, we review the state of knowledge regarding
the etiopathogenesis of CAS in patients with the clinical
syndrome of Prinzmetal variant angina.
KW - coronary spasm
KW - coronary spasm
UR - http://hdl.handle.net/10807/5703
U2 - 10.1161/CIRCULATIONAHA.111.037283
DO - 10.1161/CIRCULATIONAHA.111.037283
M3 - Article
SN - 0009-7322
VL - 124
SP - 1774
EP - 1782
JO - Circulation
JF - Circulation
ER -