Coronary Vasospasm in Ischemic Heart Disease

Coronary Vasospasm in Ischemic Heart Disease Attilio Maseri and Sergio Chierchia Chest 1980;78;210-215 DOI 10.1378/chest.78.1_Supplement.210 The online version of this article, along with updated information and services can be found online on the World Wide Web at: http://chestjournal.chestpubs.org/content/78/1_Supplement/210

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Coronary

Vasospasm

*

.

in Ischemic

Heart

Disease Attilio

M.D.,

Maseri,

and Sergio

M.D.

Chierchia,

A series of objective documentations indicate the need to reconsider the traditional concept that angina can result only from increased myocardial metabolic demand in the presence of coronary obstruction. A sudden decrease in blood supply may cause transmural or subendocardial ischemia resulting in transient elevation or depression of the ST segment on the ECG. Coronary vasospasm is at present the only convincingly demonstrated cause of reduction of blood supply and it appears to be a common cause of spontaneous angina at rest which occurs in patients with extremely variable degrees of coronary atherosclerosis and is characterized by elevation or depression of the ST segment. Other causes of reduction of coronary blood supply, such as platelet

aggregation, may also play a role, but so far they could not be demonstrated in man. A provisional pathogenetic classification of angina may be useful for the management of anginal patients: (1) secondary angina, caused by an increase in myocardial demand above the fixed supply that has been limited by coronary atherosclerotic lesions (for which the approach is well-established); (2) primary angina, caused by other coronary or myocardial mechanisms that obviously require different diagnostic and therapeutic approaches. As was the case with hypertension, the classification may become more specific as the causes of primary angina are discovered. In several patients, angina caused by vasospasm coexists with typical secondary angina.

I)

pathogenetic

mechanisms

cause rence

of the of the

reversibility and attacks. Therefore,

wish

to discuss

uring the prevention

past 40 years, of ischemic

tered around sumption that sclerosis was

coronary the relation

and

a direct

angina

the

clinical

and

linear

pectoris,

death are explanation spite tween

was

widely

lack

coronary

sudden

and

accepted.

In

be-

the

disease,

clinical

a closer

relationship

and

the

high general

prevalence population

The

clinical

frequent,

look

clinical

between symptoms of

of coronary atherosclerosis relative to the number

wide

puzzling

facts

day-to-day

superimposed

all

point

variability to functional

on a variable

atherosclerosis

as a cause

severity

of acute

lends

itself

#{176}From the Cardiovascular Research ate Medical School, Hammersmith

best

210

requests: Road,

MASERI,

Dr.

London CHIERCHIA

Maseri, W12

OHS,

in our

underthe

events

to the

study

in

of the

Royal

Hospital,

Hammersmlth England

PostgraduLondon, EngHospital,

Pxcroius

The

definition

tion sient

of angina

our

given with

thinking

by the

Friedberg4

has

extrapolated

no-

that the only respectable cause of acute myocardial ischemia is the presence of

nary

atherosclerotic

blood crease

stenoses

supply that in myocardial

resulting

is unable demand.

ingrained coronary

to

in

that the very atherosclerotic

sponsible

for

the

tion

the

reduced

that

angina

by the stenosis was al demand. Angina, when

Clinical Careful

this

existence stenoses

syndrome coronary

exceeded thus,

threshold

trancoro-

a limited

meet excessive This concept was

tioned.5 Implicitly, the presence of atherosclerotic stenosis was automatically

fac-

land.

Reprint Ducane

advances

of

of coronary

clinical

Unit,

be-

pectoris.

ANCINA

only pectoris

events

heart disease based on of studies on the pathogenetic

deeply without

disease. Angina

acute

the frequent recurin this article, we

of

symptoms.

These

recent

of angina

conditioned

patients.

3. The

the

ischemic of a series

mechanisms

association and

of quantitative

of

of these

anatomic

discrepancies:1

lesions

symptomatic

this

and

statistical heart

that

disease2,3

in the

tors,

taught

puzzling

anatomic

2.

infarction,

standing conclusions

disease

concept

a well-defined

atherosclerosis

many

the

and

cen-

the asathero-

of the

In fact,

by

of ischemic

1. The the

one.

overwhelming

manifestation

on coronary

manifestations

myocardial

coronary

reveals

atherosclerosis, between

accompanied

of the

diagnosis, therapy, heart disease have

on flow

of angina was quesa

coronary held re-

the

assump-

reserve

by increased will consistently

inso

caused myocardidevelop

is exceeded.

Observations history

of

anginal

the following puzzling symptoms often varies CHEST,

patients

facts: (1) the in different days 78: 1, JULY, 1980


often

reveals

severity or weeks SUPPLEMENT

of or

at different tion

times

causing can

exertion

toms;

(3)

cause physician. According

the

angina

occurs

by

the

hypothesis

that

only

demand

for

to

a variable

similar

attributed

work

loads:

to increased

noncardiac

or

of

thus,

heart

the

by

only

the

cause

of debe

myocardial

angina

rate,

at rest

contractility,

blood pressure, or ventricular volume. phy did not disclose any stenosis, the sidered

without

in myocardial angina should

level

Continuous

symp-

or

the

If arteriograwas con-

pain

angiogram

not

satisfac-

tory. Yet about were impressed angina

a

and

coronary

century ago,7 by the apparently

suspected

vessels

attacks. scientific hypothesis

that

might

famous primitive

a spastic

clinicians onset

for

the

This hypothesis fell into disrepute approach to medicine prevailed and pathologists who could

atherosclerotic evidence of

lesions altered

were coronary

unable to vasomotor

of anginal

sequence of events ably similar to that sudden In the

angina

characterized

pression several

of the authors

by

ST segment, since 1930.’

did

1970s toting

continuous in cardiac care

of angina

was

elevation

not

rather

already Only

described in the

electrocardiographic units illustrate

rare.14”3

Its

than

deby mid-

moththis form

that

dramatic

electrocar-

diographic changes, its occurrence in patients normal coronary arteries,16 and some isolated, sional angiographic spasm17’18 reproposed vasospasm

on for

spasm,

patients

clinical extreme “variant”

ischemia angina

that

Recently,

rather

angina spectrum caused

provided

by both

a “proved large series

than

disease. SUPPLEMENT

stimulus of ischemic

Thus, and

the heart

of patients

that

we

monitored,

measurements

were

some-

More

echocardiographic

recently,

that

increased

by

of

rather

than

it can

it exceeded

the

in term

medicine, clear

cut the

of

that

flow

useful

and

any

it is so large

that

of the

patient,

practical

point

other

provide

an

fields angina

for

approaches

types and

of

immediate

“secondary” therapeutic

from all other diagnostic

of

angina.2

from

to

no de-

classifi-

“secondary”

between

diagnostic

canrest

pathogenetic

borrowed meant

separation

at

angina can to increased

for the

and

of the

demand

reserve

a provisional

only

onset

the represent

angina

stenosis. Since “secondary”

“primary” is

at to

be proven

“primary,”

pressure

of ischemia.

a cause

we considered to propose

of

blood

in myocardial

coronary

by critical be considered

by

findings

and

consequence

as

at

occasional rate

assumed

the

accepted

cation

this

an increase

unless

view,

are

measurements

cause

mand,

segment

rest

attacks

anginal

from

isolated incorrectly

limited longer

ST

demand was contradicted It is conceivable that heart

pain,

longer,

of

left ac-

resulted

chest

be

onset

of

that

values

obtained

the

pain which, and often was

not preceded by an increase dimensions. Thus, the traditionally

misconception

are

of angina therapeutic

which ap-

proaches. Transient

only one transient

in episodes

absent.’4’2

well established require specific hyof

similar

depression.

chest

which

a particular

vasospasm.’4 the

coronary coronary coronary

represents of acute

understanding

CHEST, 78: 1, JULY, 1980

of of

became study of

the

showed

to a broader

basis.

angina

entity, “variant” of a continuous

myocardial clue

a scientific

“variant” However,

pothesis.”19 these

documentations the hypothesis

was

was remarkdog following

at the onset of a late phenomenon

The

with occa-

and

These

studies.23

hypothesis

in vasomotor tone et al8 for a form of

attacks in the

and

series

Therefore,

of an increase by Prinzmetal

on a large series showed that the

times increased however, was

not was

large

by an increased measurements.

of angina.

in heart

we never observed an increase in heart rate or blood pressure before the onset of the ST segment changes in any of the episodes recorded in agreement with

of Angina

hypothesis reproposed

ligation

were rate or

attacks

recording of ventricuand automatic analy-

tape

in anginal observed

elevation

caused objective

only

The

coronary

of ST segment

of patients

the

system performed our institutionsl,m

cepted

that

Form

sis by computer of patients in

obtain any tone in

on the basis actual proof

monitoring

blood pressure.2#{176} Continuous lar pressures on magnetic

was

generalized but without

“Variant”

consistently

changes ventricular

accepted hypothesis cause

not

showed

of supply was of a reasonable the

Demand

angina showed that preceded by increase

studies

Thus, the theory of inbeyond the possibility

it was

“variant”

when the on clinical document

their necropsy specimens. creased myocardial demand and

Myocardial

hemodynamic

with

other of

disturbance

be responsible

of Increased

heavy

at rest patient

The Myth

of exer-

and without

was an excessive increase the variable threshold for

attributed

level

widely,

be performed

often

to the

(2)

vary

recognizable

any

was

day;

may

sometimes

and

angina mand,

of the

angina

Reduction

of Coronary

201Thallium myocardial gina at rest provided the

first

mentation

angina

that

“variant”

Blocd

scintigraphy during andirect systematic docuwas

a massive regional reduction of more, it showed that also angina CORONARY YASOSPASM

Supply

IN ISCHEMIC


associated flow.27 at rest

with Furtherwith ST

HEART DISEASE

211

segment

depression

reduction

was

of coronary

associated

blood

with

allowed

that

consistently

a reduction

of flow

the

be

by

caused

nary

blood

crease

of angina by

an

the

chest

of coroexcessive

and/or

Vasospasm

mentation

by

Mechanisms

by

were

angiography.

occasional,

design.17”8’3#{176} Subsequently,

tematic recurrent

angiographic anginal

test3”32 strating

In

angiographic

observed

experience,

but

always

pump

func-

cf Coronary

Spasm

responsible

features

of coronary

are

the

following: 1. It usually involves a long segment of a vessel, but it may involve more than one vessel, and it can be occlusive with or without distal filling, or subocclusive

with

slow

filling

visible branches. 2. It may involve able

severity

graphically greater ably

phases

an

and

or diffuse

to all

extremely

vari-

lesions,

with

both

and

different

extensions phases

may of the

episodes, and it may and T wave changes

of the

same

episode

vary

same cause during

and

in

considerepisode

and

variable ST successive

successive

epi-

sodes.

gina

because

it is searched

it is usually evident

that coronary in association

more

in this

severe

syndrome.

subcritical organic plete obstruction,

in ST segment

Thus,

212

the

MASERI,

first

more

intensively

hence,

In patients

stenoses, hardly

vasomotor tone involving impair blood flow in the result

for and

vasospasm is most with “variant” anand

more with

readily critical

or

the stenotic subendocardial

segment regions

may and

in

convincingly

CHIERCHIA

documented

cause

of

to the

of

autonomic of

the

disease. were

“variant”

Increase responsible

sponand

test

from during

Transient

altera-

responsible but

the

cannot yet be substances,

may also be involved feed-back mechanisms

for data

in

considered released

in the genesis of vasospasm.

in sympathetic alpha-tone was shown to be for cold-induced angina.38 Our present, knowledge

prising

given

tence

of coronary

vasosapasm.19’39

Role

of Coronary

Spasm

in this

the

recent

coronary hypothesis,”19

12-lead

EGGs

are

thermore,

the

role

siderably

if we

field

for

taken

vasospasm;

myocardial in ST

segment

variability observed

of the threshold in some patients.

However, the in

was documented it may be one

the

very

fact

demonstration “primary”

con-

following: of a conischemia

at rest,

(3)

nocturnal,

vasospasm

and in of the for

that of

angina

Fur-

absence of episodes crisis, is not caused

demand;

and

pain.’4 the

angina

depression;

vasospasm gina,40’4’

ex-

expands

one extreme myocardial

diurnal, postprandial, in the tachycardia of hypertensive increased

chest spasm

to accept

(2)

rare

with

during

willing

surexis-

can be considered a to be frequent when

of coronary

are

be very

Syndromes

which,

spasm appears

not

of the

in Angina

(1) “variant” angina is just tinuous spectrum of acute by

should

acceptance

angina,

ceptions,14 “proved

spasm

sug-

frequent

held

angina,n.36

limited

to

the

ergonovine

tone

same

in the vary con-

of symptoms

support of this hypothesis conclusive. Vasoconstrictor

led

depression.

anginal

in the

ergonovine,

from

waning

response phases

tions

result

in the absence of comdetectable changes in

critical

during

or following

and

changing

caused

It is our belief frequently reported

leads

of spasm

as judged

waxing

“Variant”

stenoses

same

demonstration

in time

taneous

angio-

atherosclerotic

90 percent.

severity

in different segment

with

of atherosclerotic

than during

run-off

vessels

normal

3. Its

and

the

transient,

tone are likely to be of electrocardio-

gest the presence of localized hypersensitivity same vessel. This hypersensitivity must

from platelets,37 and/or in the

relevant

vasospasm

spontaneously

attacks

in spontaneous most

branch,

different of

in

the

for

vasomotor recurrence

changes and

siderably

of demonspasm was

the

and cause with or

arrhythmias

attacks

the

for the occurrence of the ergonovine

to that

our

than a sys-

with frequent pretreatment

greatly the possibility Ergonovine-induced

to be similar

episodes.33

these

chance

undertook

study of patients attacks by avoiding

enhanced vasospasm.

shown

by

we

with nitrates and by waiting attack.2’ The introduction

of coroits docu-

Initially,

more

be variable alterations

of ventricular

mechanisms

graphic

coronary

observations

reduction

inThe

of the possible existence stimulated interest in

may

increase

resulting

tion.14’21’22

demand.

The awareness nary vasospasm

a transient

The

impairment

pain

severe

increase in coronary multiple.27’34 The

Coronary

to be tone.

coronary flow electrocardiographic

without with

appears

vasomotor

to

appear

reduction

than

angina

in regional variable

of the dichanges.

at rest

transient

rather

in myocardial

preceded

independently and of T wave

episodes a sudden,

supply,

of coronary us to demonstrate

monitoring

of ischemic episodes of the ST segment

Therefore,

“primary” in coronary

More recently, continuous sinus oxygen saturation29 onset rection

a regional

supply.

only the should

coronary

exertional causes

for

of

suggest

anthe

angina

intensive role

CHEST, 78: 1, JULY, 1980


can

(4)

exertional

of by

search coronary that

an

SUPPLEMENT

open

approach

minded

might

nisms

responsible

cording

to our clinical than vasospasm,

quent

for

disclose

“primary” impression, are likely

MYoCAIWIAL

other

CoNcLusIoN

mecha-

ac-

which,

angina

though to exist.

less

fre-

INFABCtLON

Objective measurements and appropriate investigations have led to the concept that acute transient myocardial ischemia can be caused by different pathogenetic mechanisms, and that often, coronary atherosclerotic stenosis may be the bystander rather

Although

the

cardial

pathogenetic

infarction

markable

are

that

attacks initiated

in

vasospasm may rupture or hemorrhage, blood

tion

and

stagnation, initiate

which opening

may

cause

filling

occlusion.M alterations

of

an

occludes

infarct

than

a vessel

stenosis.

at

Coronary

acute

site

old

does

intracoronary

early

not

injection

with a recent report, of factors interacting

suggesting to produce

drome

is complex.

possibility

spasm further

may initiate studies, but

mechanisms fions

Thus,

myocardial also in this

such

as

be

carefully

should

the

Potentially with

matic

and

fore,

if we

elevation acceptable comes spectable would risk

fatal “variant”

of the ST landmark

and

a specific

are

In our frequent

ischemic

segment strong

than tendency no clue in some

in pasympto-

episodes.’4

to accept

the

segment may of coronary

experience, in patients

frequent during

There-

conclusion

that

atherosclerotic

be considered vasospasm,

an it be-

may well be a redeath. Its prevention of the patients at prevention

arrhythmias with elevation

are much of the ST have a but we

as to why those patients and not

tend

arrhythmias

CHEST, 78: 1, JULY, 1980 SUPPLEMENT

nisms relevant tions

should

investigation and

ischemia role in the

of

heart

often, andemand.

other

they of the

relief of not have

heart the

disease under-

atherosclerosis,

of the

because genesis

reduction

toward

of

for the therapy

for does

of ischemic

orientated

the

at the

appear to reantagonist”

surgery spasm

bypass

mechanisms

of coronary

vasospasm to “calcium

coronary

of the

of

aim

Medical because increased

be

not

responsible

metabolic demand caused solely by

prevention

should

also

towards

only

for and

identification

be directed

with well

both patient

patient

episodes.

necessarily

re-

of coronary

the

but

ischemic

vasospasm of

mechanisms

of research.

to the

of the mechanisms

for

coronary

lines

towards

Coronary caused by

toward

failor can

but

mechanisms possible

appear clinical

of mecha-

to play manifesta-

a

disease.

of vaso-

in those with depression and to recur in the same patient, in others.

also

on the

of new

stenosis, of

standing

ventricular

arrhythmias

manifestations

approach only

not

maniischemia

have profound implications management of the anginal

directed

should

clinical

acute

with

clinical

development

a rationale. Research

by

of coronary prognosis belikely to be less

myocardial

concepts

the

identification

hand,

is caused

asymptomatic.

diagnostic

not

other

possible

with

itself

Empirically, patients spond remarkably

both

for

for the

of the

pai&4’2’

expanding for

myocardial

the

ischemia

transient

completely

These

drugs.4648 symptoms

arrhythmias

therapy

chest

of myocardial gina is not

DEATH

angina,

manifest

be

one

acute

can

should

altera-

for

On

Other

be respon-

coronary bed than in one jeopardized by coronary atheroFinally, angina pectoris should now

only

occurrence

deserves possible

myocardial

evident that vasospasm cause of sudden require the identification

spasm. more

have occur

willing

vaso-

considered.

asymptomatic are

that

the syn-

also

death.

myocardial

without

The at

and

may

a normal

of

artery disease the practical of

that this

in severely lesions.

remain

reversi-

infarction field, other

primitive

SUDDEN

tients

phase

of nitrates,43

variance mosaic

pectoris,

acute

sponsible

percent

appear

when

patient.

anginal

vasospasm,

coronary vasospasm, the presence atherosclerosis adversely influences cause the effects of vasospasm are

ure

simply

90

even

in the

sudden

and

which

likely

which an

angina

festations

of late repreventa more

in the

sometimes

by

of

vasospasm

infarction even

appears

for

culprit

as coronary

be considered

pro-

In turn, ischemia in the myocardium

a thrombus

the

to

sible

devastating already sclerotic

aggrega-

leading

the

such

infarction

damage, associated

in spite vasospasm,

collaterals,

via

re-

appears to be other transient

platelet

circle

than

factors,

anginal

intimal which

favor

may become irreversible of the vessel. A diffuse

distal

appears

recurrent

cause

a vicious

longed, diffuse vascular may cause metabolic

myo-

mechanisms which control or irreversibility of corounknown, but it seems rea-

that

with

of

it

with

at rest, myocardial infarction by coronary vasospasm like

sonable plaque

ble

obscure,

still,

patients

ischemic episodes the the duration, reversibility, nary vasospasm are still

ing

mechanisms

to

REFERENCES 1 Maseri A. Expanding views on coronary artery disease: role of vasospasm and other modulatory factors. In: Hegyeli R, ed. Atherosclerosis reviews, vol 7: Measurement and control of cardiovascular risk factors. New York: Raven Press, 1980:271-79.

CORONARY VASOSPASM IN ISCHEMIC HEART DISEASE


213

2 Ehrlich

3

4

5 6 7 8

9

10

11

12 13

14

15

16

17

JC, Shinohara T. Low incidence of coronary thrombosis in myocardial infarction: restudy by serial block technique. Arch Pathol 1964; 78:432. Baroldi C. Acute coronary occlusion as a cause of myocardial infarct and sudden coronary heart death. Am J Cardiol 1965; 16:859-80. Friedberg CK. Diseases of the heart. Philadelphia: Saunders, 1966:700. James TN. Angina without coronary disease. Circulation 1970; 42:189-91. Lathan, PM. Collected works. London: New Syndenliam Society, 1876:445-80. Osler W. Lumleian lectures on angina pectoris. Lancet 1910; 1:697-702. Prinzmetal M, Kennarner R, Merliss B, Wads T, Bor N. Angina pectons: I. A variant form of angina pectoris. Am J Med 1959; 27:375-88. Parkinson J, Bedford DE. Electrocardiographic changes during brief attacks of angina-pectoris. Lancet 1931; 1: 15-19. Brow GR, Holman DV. Electrocardiographic study during a paroxysm of angina pectoris. Am Heart J 1933; 9:259-64. Penati F. Le modificazioni dell’elettrocardiogramma nelle crisi di angina di petto ed ii loro significato nella patogenesidelle crisi stesse. Minerva Med 1934; 2:289-98. Secondari E. Studio elettrocardiografico dell’attacco anginoso. Cuore e Circolazione 1938; 22:341-54. Wilson EM, Johnston FD. The occurrence in angina pectoris of electrocardiographic changes similar in magnihide and in kind to those produced by myocardial infarction. Am Heart J 1941; 22:375-88. Maseri A, Seven S, De Nes M, et al. “Variant” angina: one aspect of a continuous spectrum of vasospastic myocardial ischemia: pathogenetic mechanism, estimated incidence, clinical and coronarographic findings in 138 patient. Am J Cardiol 1978; 42:1019-35. Cherrier F, Neiman JL, Groussin P, Aliot E, Cuillierg M, Benissel J. Pninzmetal angina: a study of 100 cases. In: Kaltenbach M, Lichtlen P, Balcon R, Bussman WD, eds. Third symposium on coronary heart disease. Stuttgart: Georg Thieme Publishers, 1978:191-98. Cheng TO, Bashour T, Kelser GAJ Jr, Weiss L, Bacos J. Variant angina pectoris with normal coronary arteriograms: a variant of the variant. Circulation 1973; 47:47685. Dhurandar RW, Watt DL, Silver MD, Trimble AS, Adelman AG. Prinzmetal’s variant form of angina with arteriographic evidence of coronary arterial spasm. Am J Cardiol 1972; 30:902-05.

18

Oliva RB, Potts DE, Pluss RG. Coronary arterial spasm in Prinzmetal angina: documentation by coronary arteriography. N EngI J Med 1973; 288:745-51. 19 Meller J, Pichard A, Dack S. Coronary arterial spasm in Pninzmetal’s angina: a proved hypothesis. Am J Cardiol 1978; 37:938-40. 20 Guazzi M, Polese A, Fiorentini C, Magrini C, Bartorelli C. Left ventricular performance and related haemodynamic changes in Pninzmetal’s variant angina pectonis. Br Heart J 1971; 33:84-94. 21 Maseri A, Mimmo R, Chierchia S, Marchesi C, Pesola A, L’Abbate A. Coronary spasm as a cause of acute myocardial ischemia in man. Chest 1975; 68:825-33. 22

Chierchia not caused

and 214

S, Marchesi C, Maseri A. Evidence of angina by increased myocardial metabolic demand patterns of electrocardiographic and hemodynainic

MASERI, CHIERCHIA

alterations during “primary” angina. In: Maseri A, Klassen GA, Lesch M, eds. Primary and secondary angina pectoris. New York: Grune & Stratton, 1978:145-55. 23 Guazzi M, Polese A, Fiorentini C, Magrini F, Olivari MT, Bartorelli C. Left and right heart hemodynamics during spontaneous angina pectoris: comparison between angina with S-T segment depression and angina with S-T segment elevation. Br Heart J 1975; 37:401-13. 24 Distante A, L’Abbate A, Maseni A, Landini L, Michelassi C. Echocardiographic changes in vasospastic angina. In: Lancee CT, ed. Echocardiography. Boston: Martinus Nijhof Publishers, 1979:119-24. 25 Maseri A. Preface. In: Maseri A, Klassen GA, Lesch M, eds. Primary and secondary angina pectoris. New York: Grune & Stratton, 1978:13-14. 26 Mason A. Pathogenetic mechanisms of angina pectonis: expanding views. Br Heart j, in press. 27 Maseri A, Parodi 0, Severi S. Pesola A. Transient transmural reduction of myocardial blood flow, demonstrated by thallium-201 scintigraphy, as a cause of variant angina. Circulation 1976; 54:280-88. 28 Parodi 0, Maseni A. Assessment of acute chest pain syndrome by thallium-201 heart imaging. In: Donath A, Righetti A, eds. Progress in nuclear medicine. Basel: S Karger, in press. 29 Chierchia S, Brunelli C, Simonetti I, et al. Sequence of events in angina at rest: primary reduction in coronary

flow. 30

31

32

33 34

35

Circulation

1980;

81:759-67

Censini GG, Di Giorgi S, Murad-Netto S, Black A. Arteriographic demonstration of coronary artery spasm and its release after the use of a vasodilator in a case of angina pectoris and in the experimental animal. Angiology 1962; 13:550-53. Schroeder JS, Bolen JL, Quint BA et al. Provocation of coronary spasm with ergonovine maleate. Am J Cardiol 1977; 40:487-91. Curry BC, Pepine CJ, Sabom MB, Feldman RL, Christie LG, Conti CR. Effects of ergonovine in patients with or without coronary artery disease. Circulation 1977; 56:80309. Maseri A, L’Abbate A, Pesola A, et al. Coronary vasospasm in angina pectoris. Lancet 1977; 1:713-17. Maseri A, Seven S, Chierchia 5, Parodi 0, Biagini A. Characteristics and pathogenetic mechanism of “primary” angina at rest. In: Maseri A, Klassen GA, Lesch M, eds. Primary and Secondary Angina Pectonis. New York: Grune & Stratton, 1978:265-73. Yasue H, Touyama M, Kato H, Tanaka S, Akiyaina F.

Pninzmetal’s

variant form of angina alpha-adrenergic receptor-mediated spasm: documentation by coronary Heart J 1976; 91:148-55. 36 Ricci DR, Orlick AE, Cipriano PR, son DC. Altered adrenergic activity

spasm:

37

insight

into mechanism

Guthaner

DF,

in coronary

based

on study

of artery Am Harriarterial

of coronary

hemodynamics and the electrocardiogram. Am J Cardiol 1979; 43:1073-79. Ellis EF, Oelz 0, Roberts U II, et al. Coronary arterial smooth muscle contraction by a substance released from platelets: evidence that it is thromboxane A2. Science 1976; 193:1135-37.

38 Mudge GH Jr, Grossman W, Millis wald E. Reflex increase in coronary patients with ischemic heart disease. 39

as a manifestation coronary arteniography.

295:1333-37. Hills LD,

Braunwald CHEST,

R, Lesch M, Braunvascular resistance in

N EngI J Med

E. Coronary-artery 78: 1, JULY, 1980


spasm.

1976; N Engl

SUPPLEMENT

J Med 40

Specchia arterial elevation

1979; 41

Yasue

Tanaka patients induced

1978;

ence

299:702.

C, spasm in

de

Servi S, Falcone C, et as a cause of exercise-induced patients with variant angina.

al. Coronary ST-segment Circulation

59:948-54. H,

Omote

S, Takizawa

A,

Nagao

M,

Miwa

K,

S. Circadian variation of exercise capacity in with Prinzmetal’s variant angina: role of exercisecoronary arterial spasm. Circulation 1979; 59:

938-48. 42. Maseri A, L’Abbate A, Baroldi C, et al. Coronary vasospasm as a possible cause of myocardial infarction: a conclusion derived from the study of “perinfarction” angina. N EngI J Med 1978; 299:1271-77. 43 Maseri A, L’Abbate A, Baroldi G, et a!. Coronary vasospasm as a possible cause of myocardial infarction. Flor-

CHEST, 78: 1, JULY, 1980 SUPPLEMENT

International Meeting on Myocardial Infarction, 8-12, 1979, in press. 44 Oliva PB, Breckinridge JC. Arteriographio evidence of coronary arterial spasm in acute myocardial infarction. Circulation 1977; 56:366. 45 Baroldi C. Diflerent types of myocardial necrosis in coronary heart disease: a pathophysiologic review of their functional significance. Am Heart J 1975; 89:742-52. 46 Parodi 0, Maseni A, Simonetti I. Management of unstable angina at rest by verapamil: a double-blind cross-over study in CCU. Br Heart J 1979; 41:167-74. 47 Muller JE, Gunther SJ. Nifedipine therapy for Prinzmetal angina. Circulation 1978; 57:137-39. 48 Distante A, Maseri A, Seven S, et a!. Management of vasospastic angina at rest with continuous infusion of isosorbide dinitrate. Am J Cardiol 1979; 44:533-39. May

CORONARY VASOSPASM

IN ISCHEMIC


HEART DISEASE

215

Coronary Vasospasm in Ischemic Heart Disease Attilio Maseri and Sergio Chierchia Chest 1980;78; 210-215 DOI 10.1378/chest.78.1_Supplement.210 This information is current as of July 12, 2011 Updated Information & Services Updated Information and services can be found at: http://chestjournal.chestpubs.org/content/78/1_Supplement/210 Permissions & Licensing Information about reproducing this article in parts (figures, tables) or in its entirety can be found online at: http://www.chestpubs.org/site/misc/reprints.xhtml Reprints Information about ordering reprints can be found online: http://www.chestpubs.org/site/misc/reprints.xhtml Citation Alerts Receive free e-mail alerts when new articles cite this article. To sign up, select the "Services" link to the right of the online article. Images in PowerPoint format Figures that appear in CHEST articles can be downloaded for teaching purposes in PowerPoint slide format. See any online figure for directions.
