Prinzmetal's Angina or Variant

Angina Pectoris

DISORDER OF THE
CARDIOVASCULAR SYSTEM
DEFINITION
Variant angina pectoris is a clinical
syndrome that usually occurs at rest and is
associated with reversible ST-segment
elevation without enzymatic evidence of
acute MI.
Vasospasm
This syndrome is caused by coronary
vasospasm, w/ch can be prevented or
reversed by nitroglycerin.
The spasm may be segmental in nature or
involve the entire artery.
Angiograph Studies
Although it can develop in px w/ normal
coronary arteries, most px have
angiographically significant atherosclerotic
CAD.
Px w/ variant angina are at
risk of MI and sudden
death.
PATHOPHYSIOLOGY
Vasospasm usually happens at the site of,
or in close proximity to, an atherosclerotic
plaque.
 Nicotine, cocaine, hyperventilation,
exercise, cold exposure, handgrip,
histamine, vasopressin, and platelet-
mediated vasoactive
substances(thromboxane) may induce
vasospasm in px w/ variant angina.
 Hypercholesterolemia also implicated in
vasospasm, since elevated cholesterol
levels impair endothelial function and
lower the threshold to ergonovine-induce
vasospasm.
CLINICAL MANIFESTATION
Chest discomfort usually occurs at rest or
during ordinary activities that are not
associated w/ a substantial increase in
cardiac work, most ischemic episodes are
not preceded by rise in heart rate or blood
pressure.
Transient coronary artery spasm.
 Focal spasm is most common in the right
coronary artery, and it may occur at one or
more sites in one artery or in multiple
arteries simultaneously.
The location and radiation are similar to
those of stable angina, but the duration is
somewhat longer.
The discomfort follows a circadian pattern,
manifesting predominantly in the early
morning.
Cardiac examination is usually normal in
the absence of ischemia.
 Variant angina is related to heavy cigarette
smoking and also has been associated
with migraine headaches and Raynaud's
phenomenon.
There also has been an association with
aspirin-induced asthma.
 Coronary angiography demonstrates
transient coronary spasm as the diagnostic
hallmark of Prinzmetal's angina.
Atherosclerotic plaques, which do not
usually cause critical obstruction, in at
least one proximal coronary artery occur in
the majority of patients, and in them
spasm usually occurs within 1 cm of the
plaque.
 Even though variant angina by definition is
associated with ST-segment elevation
during an ischemic episode, coronary
artery spasm can manifest initially as ST-
segment depression or T-wave inversion.
Ventricular tachycardia is common during
prolonged episodes of ST-segment
elevation, whether painful or silent.
The clinical diagnosis of variant angina is
made with the detection of transient ST-
segment elevation with rest pain.
DIAGNOSIS
All patients with variant angina should undergo coronary
arteriography.
Intravenous or intracoronary administration
of ergonovine is helpful in eliciting spasm
in patients with normal coronary arteries or
minor atherosclerotic changes. Ergonovine
induces coronary vasospasm in more than
90% of patients with variant angina; in
contrast, fewer than 1% of patients with
atypical chest pain and no CAD have
ergonovine-induced vasospasm.
A negative ergonovine test effectively rules out coronary
spasm as a cause for angina.