Current concepts of Prinzmetal s variant form of angina ...

Current concepts of Prinzmetal's variant form of angina pectoris

Frederick A. H e u p l e r , J r . , M.D.

Department of Cardiology

Definit ion

Variant angina is a clinical-electrocardio-graphic syndrome first described by Prinzmetal et al1 in 1959. Al though others had described similar cases previously,2 - 7 Prinzmetal was the first to suggest that the clinical picture in these patients f o r m e d a discrete enti ty.

T h e essential characteristics of this syndrome are (1) r ecu r ren t attacks of angina unre la ted to exert ion which usually occur at rest or with nor-mal activity, (2) concomitant S -T segment eleva-tion in EKG leads reflect ing the area of myocar-dial ischemia, and (3) r e tu rn of the electrocardi-og ram to its previous appea rance following at-tacks (Table 1).

T h e pa t t e rn of chest pain is variable: it may follow an in termi t tent or stable course for months to years, it may present as accelerated angina over a shor t pe r iod , or it may appea r only in the immedia te pre infarc t ion or postin-farct ion per iod . 8 T h e first two pat terns are the ones we usually associate with the t e rm Prinzme-tal's variant ang ina . Perhaps the third g r o u p should be classified separately as peri- infarct ion Prinzmetal 's angina .

T h e episode of angina usually lasts less than 15 minutes , but may be p ro longed . It o f ten

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132 Cleveland Clinic Quar ter ly

Table 1. Definit ion of Prinzmetal 's var iant ang ina

I . E s s e n t i a l c h a r a c t e r i s t i c s A . R e c u r r e n t a n g i n a u n r e l a t e d to e x e r -

t i o n B . S - T s e g m e n t e l e v a t i o n d u r i n g a n g i n a C . N o r m a l i z a t i o n o f E K G b e t w e e n a n g i n a

e p i s o d e s I I . C o m m o n a s s o c i a t e d f i n d i n g s

A . P r e d i c t a b l e da i ly p a t t e r n o f r e s t p a i n B . L o n g p e r i o d s o f s p o n t a n e o u s r e m i s -

s ion C . T y p i c a l e x e r t i o n a l a n g i n a D . Pos i t ive s t ress tes t E . M a j o r a r r h y t h m i a s d u r i n g a n g i n a F . S y n c o p e d u r i n g a n g i n a G . T e r m i n a t i o n o f v a r i a n t p a t t e r n a f t e r

m y o c a r d i a l i n f a r c t i o n H . S u d d e n d e a t h

occurs at rest , with a predictable daily pa t te rn . T h e interval between pains may be minutes to years. In patients with long per iods between attacks, di-agnosis may be diff icul t due to the logistical problem of obtaining an e lect rocardiogram d u r i n g attacks.

In addit ion to rest pa in , typical ex-ert ional angina occurs in nearly 50% of patients, bu t it is usually a minor par t of the clinical picture.1 ' 8 -10

Stress tests a re also positive in nearly 50% of pat ients , 1 1 ' 1 2 showing ei ther S-T segment elevation13-17 o r , more commonly , S-T segment depres-sion.11 ' 1(i- 18

Dur ing attacks of variant angina , S-T segment elevation occurs in two or more EKG leads, and reciprocal S-T segment depress ion occurs in con-tralateral leads (Fig. 1A and B). With subsequent attacks, S-T segment ele-vation almost invariably occurs in the same EKG leads. Rarely, S-T seg-ment elevation may occur alternately in one set of EKG leads with one attack, and in a d i f f e r e n t set of leads with o the r attacks.19

T h e varying deg ree of S -T seg-

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m e n t elevation which occurs d u r i n g angina correlates roughly with the se-verity of attacks in any one patient .1

T h e r e may be barely percept ible ele-vation with mild attacks, and more than 5 m m elevation with severe at-tacks. Dur ing episodes of variant an-gina, 25% to 50% of patients will ex-per ience ma jo r a r rhy thmias , such as ventr icular tachycardia, ventr icular fibril lation, or complete hea r t block.1 ' it, 20-22 (jpigm 2). This may account for

« • -J.J ;..,..: I : | : i 1 . 1 , ; I • j >.: ,

j r t • i • : . .; . i i . - i 1 ; • . ! . 1 . 1 . •

^ r n ^ l i ^ k i l i l i i ' t M l ¡ • i i f e - l i

F i g . 1. A , E K G d u r i n g s p o n t a n e o u s a t t a c k o f v a r i a n t a n g i n a . T h i s d e m o n s t r a t e s S - T seg-m e n t e l e v a t i o n in l e a d s I I , I I I , A V F , a n d V 6

a n d r e c i p r o c a l d e p r e s s i o n in l e a d s A V L , I , a n d V , - V 4 . B , E K G i m m e d i a t e l y a f t e r a t t a c k o f v a r i a n t a n g i n a s u b s i d e d . T h e S - T s e g m e n t s a r e i soe lec t r i c in all l e a d s a n d n o n e w Q waves h a v e a p p e a r e d .



Fall 1976 Variant fo rm of angina pectoris 133

3. DUR ING PAIN

4. DUR ING PAIN

1TIIIIHI4 W T O i r a r

! .À ,A/A L ,/\ U v W UjA— UAA) ; i-TW-Hi i H+H ri-H l^j-j+FTi i 11: • >: t ' A

F i g . 2. H o l t e r m o n i t o r s t r ips d e m o n s t r a t i n g P V C s a n d s h o r t r u n s o f ventr ic u l a r t a c h y c a r d i a d u r i n g an e p i s o d e o f va r i an t a n g i n a . S - T seg-m e n t e leva t ion is p r e s e n t d u r i n g a n g i n a , a n d t h e S - T s e g m e n t is isoelectr ic w h e n pa t i en t is f r e e o f p a i n .

an increased incidence of syncope and sudden death in these patients. Insertion of a pacemaker will prevent bradycardia and syncope in selected patients, but it does not prevent an-ginal episodes.

Acute myocardial infarction may eventually develop in patients with a stable history of variant angina, usu-ally in the area which demonst ra ted S-T segment elevation du r ing attacks of angina . Af ter infarct ion, most pa-tients do not cont inue to have attacks of variant angina.

Several syndromes of myocardial ischemia resembling variant angina have been described (Table 2). In pa-tients with otherwise typical variant angina, episodes of mild angina may occur without S-T segment elevation and , conversely, episodes of S-T seg-ment elevation may occur without pain », 13, IS, 23—25 Some patients never experience angina, but have episodes of syncope due to a major arrhyth-mia, which is preceded by S-T seg-

ment elevation.26-28 Such patients cannot properly be said to have var-iant angina, but the pathophysiology appears to be similar. Another g roup of patients has been identified who have typical exertional angina, but no angina at rest, and who develop S-T segment elevation on exercise tests.14, 17 It is noteworthy that the mortality in these patients is much higher than in those with S-T seg-ment depression.

Angiography in patients with major coronary artery obstructions

Prinzmetal postulated that most patients with this syndrome would have severe obstruction in the coro-nary artery pe r fus ing the portion of the myocardium reflected by the S-T segment elevation du r ing pain.1 Cor-onary ar ter iography has conf i rmed this impression in most patients.8 , 9-ii. is isj0t infrequent ly , they have ma-jo r obstructions in more than one coronary artery.

T h e appearance and distribution of the coronary artery obstructions in these patients are similar to those in patients with typical angina pectoris and to those with angina at rest asso-ciated with S-T segment depres-sion.29 One exception is that patients with variant angina rarely have been demonst ra ted to have isolated total obstruction with collaterals to the cor-onary artery per fus ing the area where S-T segment elevation oc-curs.18 Coronary spasm superim-

Table 2. Variations of Prinzmetal's variant angina

A. S - T s e g m e n t e leva t ion wi thou t a n g i n a B. S - T s e g m e n t e l e v a t i o n , a r r h y t h m i a , a n d

s y n c o p e w i t h o u t a n g i n a C . S - T s e g m e n t e l eva t ion on ly d u r i n g e x e r -

t ional a n g i n a



134 Cleveland Clinic Quar te r ly Vol. 43, No . 3

posed on fixed severe coronary ob-struct ion has been demons t r a t ed an-giographically d u r i n g attacks of var-iant a n g i n a . 2 5 , 3 0 , 3 1

Angiography in patients with no ma-jor coronary artery obstructions

Patients with no ma jo r obstruct ions (more than 50%) demons t r a t ed by se-lective coronary a r te r iography consti-tu te a small s u b g r o u p of all pat ients with variant angina . More t han 30 such cases have been repor ted . 9 - 1 1 , 1 5 ,

16, 19-22, 32-46 A l though a few of these were said to have normal coronary ar ter ies , most have had at least mild (up to 30%) obstruct ions. In this sub-g r o u p , the attacks of variant angina a re probably d u e to severe coronary spasm super imposed on a mild ob-struction .

In at least 20 such pat ients , reversi-ble, severe coronary spasm with S-T segment elevation and chest pain has been demons t r a t ed d u r i n g angiogra-p h y . » - 25. 32, 34-36, 42, 44, 46, 47 J n m Q s t Q f

these , the spasm occurred in the r ight coronary ar tery . T h e location of the spasm may vary f r o m one sec-tion of the ar tery to ano the r on sub-sequent injections. Corona ry spasm may ex tend several cent imeters a long an ar tery , o r it may p r o d u c e a shor t , discrete, annu la r constr ict ion. It may involve m o r e than one ar tery . Spasm of a coronary ar tery may p r o d u c e an a p p e a r a n c e which is angiographical ly identical to a f ixed organic obstruc-t ion. T h e ma jo r d i f f e rence between these two types of coronary ar tery na r rowing is that the deg ree of spasm tends to vary with subsequent injec-tions, whereas the d e g r e e of f ixed obstruct ion remains stable. T h e spasm generally responds rapidly to ni t roglycerin. If ni troglycerin is given to such patients p r ior to coro-

nary a r t e r iography , it may prevent the occur rence of spasm d u r i n g cath-eterization. T h e r e f o r e , we do not r e c o m m e n d its rou t ine use be fo re coronary a r t e r iography in pat ients in w h o m we suspect coronary spasm plays a significant role.

"Mal ignant" coronary spasm, which is associated with S-T segment changes and ang ina , should be dif-fe ren t ia ted f r o m "benign" o r "cathe-te r - induced" spasm not associated with chest pain o r EKG changes . T h e t e rm benign coronary spasm is pre-f e r r e d to the t e rm ca the te r - induced spasm fo r two reasons: (1) this type of spasm may occur be fo re the catheter is in t roduced into a coronary ar tery , and (2) mal ignant spasm with angina and S-T segment changes may be in-duced by ca the ter manipula t ion in a coronary ar tery . Benign coronary spasm occurs in about 1% of all pa-tients u n d e r g o i n g coronary arteriog-raphy , and is of n o clinical signifi-cance, as fa r as we know, except that occasionally it may be mistaken for a fixed organic coronary ar tery ob-struction.4 8 , 49

Rarely coronary spasm may be in-duced by withdrawal of nitrates a f te r pro longed occupational exposure . Angina and myocardial infarct ion have been r e p o r t e d in workers who are chronically exposed to nitrates in the m a n u f a c t u r e of explosives. Se-vere coronary spasm with normal coronary ar ter ies has been docu-mented occasionally in such pa-tients.50, 51

Since weeks may pass between spontaneous attacks of variant an-gina, provocative tests fo r inducing malignant coronary spasm at the time of coronary ang iography can be help-ful in conf i rming the diagnosis. Either e p i n e p h r i n e or methachol ine



Fall 1976

chloride may induce coronary spasm and attacks of variant angina; atro-pine has been said to prevent and abolish such attacks.47- 52 Yasue et al52

were able to precipitate attacks of an-gina and coronary spasm with metha-choline chlor ide in 3 of 10 patients with variant angina .

A more sensitive provocative test has been recently developed at the Cleveland Clinic Hospital . On the r ecommenda t ion of P roudf i t , of ou r g roup , e rgonovine maleate was first adminis tered in December 1972, as a provocative agent for patients with variant angina and no ma jo r coro-nary obstructions.4 6 In o u r experi-ence since t hen , this d r u g has repro-duced attacks of angina and S-T seg-ment elevation in 10 of 13 patients with a history of variant angina and no major coronary obstruct ions, and provoked severe coronary spasm in 12 of 13 (Fig. 3A-D). Ergonovine ma-leate is highly specific for this g r o u p of patients: it did not induce severe coronary spasm or angina in more than 50 pat ients who did not have the Prinzmetal s y n d r o m e . This provoca-tive test is not r e c o m m e n d e d for pa-tients with variant angina who have fixed, severe coronary ar tery ob-structions because of the possibility of inducing myocardial infarc t ion. T h e use of any provocative agent for in-

Var iant f o r m of angina pectoris 135

F i g . 3 . S e q u e n c e o f a n g i o g r a p h i c c h a n g e s in R C A in I . A O p r o j e c t i o n . A , S p o n t a n e o u s s p a s m wi th 9 5 % o b s t r u c t i o n in p r o x i m a l o n e t h i r d ; a n g i n a a n d S - T s e g m e n t e l e v a t i o n in l e a d s I I , I I I , a n d A V F . B , A f t e r n i t r o g l y c e r i n , o n l y s l igh t n a r r o w i n g in p r o x i m a l o n e t h i r d ; n o c h e s t p a i n ; E K G n o r m a l . C , S p a s m wi th 9 5 % o b s t r u c t i o n in p r o x i m a l o n e t h i r d i n d u c e d by e r g o n o v i n e m a l e a t e ; a n g i n a a n d S - T seg-m e n t e l e v a t i o n in l e a d s I I , I I I , a n d A V F . D , A f t e r s e c o n d n i t r o g l y c e r i n , m i l d d i f f u s e n a r -r o w i n g t h r o u g h o u t ; n o ches t p a i n ; F.KG n o r -m a l . F i g . 3 A t o D .




duc ing attacks of Prinzmetal 's var iant angina is potentially dangerous and is r e c o m m e n d e d only for use by car-diologists, p referably in a cardiac lab-oratory with the necessary equ ipmen t and personnel to m a n a g e any compli-cations.

Natural history of Prinzmetal's var-iant angina

Because of the scarcity of patients with variant ang ina , it is necessary to combine the exper ience of several centers to assess the clinical course of this synd rome . In one such study by Bentivoglio et al,53 90 cases were col-lected f r o m the l i te ra ture . Myocar-dial infarc t ion developed in 22 pa-tients within m o n t h s a f t e r the onset of symptoms, and 13 others died sud-denly . Th i s comprises a combined in-cidence of m a j o r cardiac events of 39%. At this t ime, not e n o u g h pa-tients have been catheter ized a n d fol-lowed fo r a sufficient length of t ime to be certain of the na tura l history of variant angina in relation to the pres-ence and severity of co ronary ar tery obstruct ions . But , as a g r o u p , pa-tients with the Prinzmetal synd rome compr ise a high risk subset in the g r o u p of patients with ischemic hea r t disease.

Patients with episodes of variant angina a p p e a r i n g in the immedia te pos t infarc t ion per iod have a h igher incidence of re infarc t ion a n d dea th than o the r patients with myocardial infarct ion. 5 4 Patients with the syn-d r o m e of exercise- induced S -T seg-m e n t elevation, bu t without the typi-cal clinical picture of Prinzmetal 's an-gina, also have a poor prognosis . O f the 10 patients followed f o r m o r e than 1 year by For tu in and Friesin-ger , 1 7 f o u r died within 2 years, and a nonfa ta l myocardial infarc t ion devel-o p e d in a fifth pa t ient .

Physiology of Prinzmetal's variant angina

Prinzmetal 's var iant angina ap-pears to be associated with m o r e se-vere myocardial ischemia than typical exert ional angina . In exper imenta l studies on dogs , S -T segment eleva-tion occur red 25 to 35 seconds a f t e r comple te occlusion of a coronary ar-tery, and this was observed in the central , severely ischemic a rea , whereas S-T segment depress ion oc-cu r r ed in the m o r e per iphera l and less severely ischemic myoca rd ium. As the severe ischemia in the central a rea was lessened by release of the occlusion, S -T segment elevation was replaced by S -T segment depression be fo re r e t u r n i n g to normal . 5 5

T o de t e rmine whe the r episodes of variant angina are associated with an increase in cardiac work , Guazzi et al23 r eco rded con t inuous EKGs and intraar ter ia l pressures in f o u r pa-tients with variant angina . Dur ing 38 anginal episodes in these pat ients , no change in blood pressure o r pulse p receded the S-T segment changes and angina . A similar study by Mas-eri et al25 conf i rms these results. Since an increase in pulse o r blood pressure o r bo th is the ma jo r de ter -minan t of an increase in cardiac work , these Findings make it highly unlikely that episodes of variant an-gina a re secondary to an increase in cardiac work . T h e y are consistent with the theory that acute changes in d i ame te r of the coronary ar tery , such as may be caused by spasm, are re-sponsible fo r the physiologic events in Prinzmetal 's variant angina (Fig.

4).

Since the severity of f ixed coronary obstruct ions is highly variable in pa-tients with variant ang ina , it appea r s that the relative contr ibut ion of fixed



Fall 1976 Variant f o r m of angina pectoris 137

Fixed coronary obstruction (mild to severe)

+

Superimposed transient coronary narrowing

(e.g., by spasm or thrombus) 1 Severe myocardial ischemia

(without increased cardiac work)

J \ S-T segment elevation Angina

Fig. 4. Phys io logic s e q u e n c e in P r i n z m e t a l ' s v a r i a n t a n g i n a .

obstruct ion a n d of spasm-induced obstruct ion may vary f r o m one pa-tient to ano the r , bu t that the combi-nat ion of the two is operat ive in most patients (Fig. 5).

Assuming tha t the combinat ion of fixed obstruct ion and supe r imposed spasm under l ies all o r most cases of Prinzmetal 's var iant ang ina , the mechanism which precipi tates the spasm is not u n d e r s t o o d . I t is not yet certain whe the r the severe coronary spasm in pat ients with mild coronary obstructions is t r iggered by the auto-nomic nervous system, h u m o r a l fac-tors, increased sensitivity of the coro-nary ar tery to vasoconstrictive stim-uli, or by a combinat ion of these.3 3 ' 45' 52,56 j t m a y b e that ^ e physiologic mechanism which t r iggers coronary spasm in pat ients with mild, f ixed coronary obstruct ions is d i f f e ren t f r o m that in pat ients with severe, Fixed obstruct ions.

T h e physiologic events in patients with Prinzmetal 's var iant angina a re in m a r k e d contrast to those in pa-tients with exert ional ang ina and in patients with angina at rest associated with S-T segment depress ion: in these latter two g roups , an increase in blood pressure o r pulse o r both usually precedes the onset of EKG changes and angina (Fig. 6).

Medical treatment of Prinzmetal's variant angina

It is diff icult to evaluate the effect of t r ea tmen t in patients with Prinz-metal 's variant angina . Spon taneous variations in f requency of angina are the ru le in these pat ients , especially in the s u b g r o u p with no ma jo r coro-nary obstruct ions . Periods of daily at-tacks fo r m o n t h s may al ternate with per iods of months , or even years, when no attacks occur . In patients with f ixed coronary ar tery obstruc-tions, many au thors have r epo r t ed favorable responses to the c o m m o n modes of the rapy , including vasodi-lators a n d propranolol . 5 7 In almost all pat ients , nitroglycerin will rapidly

100

Degree of coronary

obstruction

Predominant Predominant f ixed spasm

obstruction

* Range of obstruction necessary to produce variant angina

Fig. 5. A n g i o g r a p h i c f i n d i n g s in P r i n z m e t a l ' s v a r i a n t a n g i n a .

extracardiac stimulus (exertion, emotion, cold a ir , meals)

increased pulse and/or increased blood pressure

I increased pressure-rate product

I increased cardiac work

I myocardial ischemia

(with or without EKG changes)

I angina

Fig. 6. Physio logica l s e q u e n c e in typical an -g i n a p e c t o r i s .

Superimposed spasm

Fixed obstruction

Spectrum of angiographic f indings



138 Cleveland Clinic Quar te r ly Vol. 43, N o . 3

abor t attacks of ang ina . In patients with no m a j o r co rona ry obstruct ion, the e f fec t of medical t r ea tmen t var-ies. Most au tho r s r e p o r t improve-m e n t with isosorbide d ini t ra te , but it is o f t en ineffect ive. Propranolo l is less effective in these pat ients , and it may even increase their symp-toms.8 ' 52 Initial exper ience with nife-dipine , which is no t yet commercially available in the Un i t ed States, ap-pears promising. 4 5

Because of the small n u m b e r of patients with variant angina in any one insti tution, most r epor t s of medi-cal t r ea tmen t a re anecdota l a n d in-volve few pat ients . Despite medical t r ea tmen t , the morbid i ty and mortal-ity in pat ients with this syndrome is h igh .

Surgical treatment of Prinzmetal's variant angina

T h e surgical t r e a t m e n t of variant angina in pat ients with severe, fixed coronary obstruct ions must be con-sidered separately f r o m surgical t r ea tmen t in pat ients with no ma jo r coronary obstruct ions because the re-sults a re so d i f f e r e n t .

T h e r e is still some controversy con-cern ing the use of coronary bypass surgery fo r pat ients with variant an-gina and severe, fixed coronary ob-structions. Patients who have the poorest symptomat ic results a f t e r surgery usually have occluded bypass graf ts o r persis tent , severe coronary obstruct ions which have not been by-passed.9 , n ' 37 If a pa t en t bypass g ra f t with no anastomotic na r rowing and with good r u n o f f is placed in the se-verely (more than 70%) obstructed coronary ar tery supply ing the area of myocardial ischemia in a pat ient with Prinzmetal 's var iant ang ina , relief of the Pr inzmetal s y n d r o m e is virtually

invariable.1 2 , 16, 24, 53, 58 T h e exper i -ence with bypass surgery f o r severe, fixed obstruct ions in pat ients with var iant angina in J a p a n a p p e a r s to be totally at variance with the exper i -ence in the Uni ted States. O n e au-tho r repor t s that n o n e of the n ine pat ients so t rea ted had relief of symptoms , even t hough pos topera-tive coronary ang iography in some pat ients demons t r a t ed pa ten t bypass graf ts . 4 5 Since the patency ra te of sa-p h e n o u s vein graf ts at the Cleveland Clinic is usually m o r e than 80%, a n d that of in ternal m a m m a r y ar tery graf ts approaches 95%, o u r cu r r en t practice is to consider bypass surgery in any pat ient with variant ang ina a n d severe, fixed coronary ar tery ob-struct ions.

Bypass surgery has been appl ied in a small n u m b e r of pat ients with var-iant angina secondary to mal ignant coronary spasm.39"41, 59 As opposed to those pat ients with variant angina and severe, fixed obstructions, most pat ients with variant angina asso-ciated with normal or mildly to mod-erately na r rowed coronary ar ter ies cont inue to have symptoms despi te successful bypass surgery. Th i s may be because spasm occurs distal to the g ra f t or in o the r n o n g r a f t e d vessels. T h e indication f o r bypass g r a f t sur-gery in pat ients with variant ang ina d u e to mal ignant spasm in the ab-sence of significant fixed coronary obstruct ion remains uncer ta in at this t ime.

Pathologic f indings in patients with Prinzmetal's variant angina

T h e coronary arteries of patients with variant angina do not demon-strate distinctive pathologic changes , such as abnormal innervat ion or in-creased muscle thickness in the arte-



Fall 1976

rial wall. T h e y have typical a thero-sclerotic obstruct ions similar to those f o u n d in pat ients with exert ional an-gina or myocardial infarc t ion. Au-topsies in patients with variant angina and angiographically mild coronary ar tery obstruct ions have d e m o n -strated a variety of f indings in the coronary arter ies: some arteries were repor ted as no rma l , and others showed a spec t rum f r o m mild to 75% narrowing.1 0 ' 15' 20> 3(i T h e reason for the discrepancy between the angio-graphic f ind ing of mild obstruction and the autopsy f ind ing of severe ob-struction is not obvious at this t ime. It is possible that a severe obstruction was not detected d u r i n g angiogra-phy. Or , it may be that at autopsy the severity of a f ixed, mode ra t e obstruc-tion was overest imated because the coronary ar tery collapsed in the post-m o r t e m state, making the l umen ap-pear smaller. At least mild coronary atherosclerosis is almost invariably f o u n d at autopsy in any pat ient with the syndrome of variant ang ina , even if the vessels were in t e rp re ted as an-giographically no rma l .

Summary T h e syndrome of Prinzmetal 's var-

iant angina consists of r ecu r ren t at-tacks of angina unre la ted to exert ion and accompanied by reversible S-T segment elevation. Variant angina is associated with a high risk of s u d d e n dea th and myocardial infarc t ion. Coronary spasm plays a major role in inducing attacks. Ergonovine ma-leate has been used as a provocative test for patients with no major coro-nary obstructions. Medical therapy is moderately effective in relieving symptoms. Coronary bypass surgery should be considered for any patient with severe, fixed obstruct ions, but is

Variant fo rm of angina pectoris 139

usually ineffective in patients with mild obstructions associated with ma-l ignant coronary spasm. T h e pa tho-genesis of the coronary spasm in these patients is poorly u n d e r s t o o d .

References 1. P r i n z m e t a l M, K e n n a m e r R , Merl iss R , e t

al: A n g i n a p e c t o r i s . I . A v a r i a n t f o r m o f a n g i n a p e c t o r i s ; p r e l i m i n a r y r e p o r t . A m J M e d 27: 3 7 5 - 3 8 8 , 1959.

2 . P a r k i n s o n J : E l e c t r o c a r d i o g r a p h i c c h a n g e s d u r i n g b r i e f a t t a c k s o f a n g i n a p e c t o r i s ; t h e i r b e a r i n g o n t h e o r i g i n a l p a i n . L a n c e t 1: 1 5 - 1 9 , 1931.

3 . R a n d i e s FS , F r a d k i n N F : E l e c t r o c a r d i -o g r a p h i c a l t e r a t i o n s r e s e m b l i n g t h o s e p r o -d u c e d by m y o c a r d i a l i n f a r c t i o n o b s e r v e d d u r i n g a s p o n t a n e o u s a t t a c k o f a n g i n a p e c t o r i s . A n n I n t e r n M e d 28: 6 7 1 - 6 7 6 , 1948.

4 . R o c s l e r H , D r e s s l e r W : T r a n s i e n t e l e c t r o -c a r d i o g r a p h i c c h a n g e s i d e n t i c a l w i th t h o s e o f a c u t e m y o c a r d i a l i n f a r c t i o n a c c o m p a n y -i n g a t t a c k s o f a n g i n a p e c t o r i s . A m H e a r t J 47: 5 2 0 - 5 2 6 , 1954.

5 . S a n a z a r o PJ : T r a n s i e n t e l e c t r o c a r d i -o g r a p h i c c h a n g e s s i m u l a t i n g a c u t e m y -o c a r d i a l i n f a r c t i o n ; i n t e r p r e t a t i o n o f t h e i r s i g n i f i c a n c e a n d r e p o r t o f a ca se . A m H e a r t J 51: 149-155 , 1956.

6 . S i ege l M L , Feil H : E l e c t r o c a r d i o g r a p h i c s t u d i e s d u r i n g a t t a c k s o f a n g i n a p e c t o r i s a n d o f o t h e r p a r o x y s m a l p a i n . J Clin I n -ves t 10: 7 9 5 - 8 0 6 , 1931.

7. W i l s o n F N , J o h n s t o n F D : T h e o c c u r r e n c e in a n g i n a p e c t o r i s of e l e c t r o c a r d i o g r a p h i c c h a n g e s s i m i l a r in m a g n i t u d e a n d in k i n d t o t h o s e p r o d u c e d by m y o c a r d i a l i n f a r c -t i o n . A m H e a r t J 22: 6 4 - 7 4 , 1941.

8 . R u g g e r o l i C W , C o h n K , L a n g s t o n M: P r i n z m e t a l ' s v a r i a n t a n g i n a : a p a t h o p h y s i -o log ica l a n d cl inical k a l e i d o s c o p e . ( A b s t r ) A m J C a r d i o l 33: 167, 1974.

9 . B o d e n h e i m e r M , L i p s k i J , D o n o s o E , e t a l : P r i n z m e t a l ' s v a r i a n t a n g i n a : a cl inical a n d e l e c t r o c a r d i o g r a p h i c s t u d y . A m H e a r t J 87: 3 0 4 - 3 1 3 , 1974.

10. C o s b y R S , G i d d i n g s J A , S e e J R , e t al: V a r -i a n t a n g i n a : case r e p o r t s a n d c r i t i q u e . A m J M e d 53: 7 3 9 - 7 4 2 , 1972.

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20 . G i a n e l l y R , M u g l e r F, H a r r i s o n D C : P r i n z -m e t a l ' s v a r i a n t o f a n g i n a p e c t o r i s w i th o n l y s l i gh t c o r o n a r y a t h e r o s c l e r o s i s . C a l i f o r n i a M e d 108: 129 -132 , 1968.

21 . K e r i n N , S c h w a r t z H : P r i n z m e t a l a n g i n a w i t h t r a n s i e n t c o m p l e t e h e a r t b l o c k . A r c h I n t e r n M e d 134: 5 4 2 - 5 4 4 , 1974.

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23 . G u a z z i M , F i o r e n t i n i C , Po l e se A , e t al: C o n t i n u o u s e l e c t r o c a r d i o g r a p h i c r e c o r d -i n g in P r i n z m e t a l ' s v a r i a n t a n g i n a p e c t o r i s ; a r e p o r t o f f o u r ca se s . B r H e a r t J 32: 6 1 1 -616, 1970.

24 . K o s s o w s k y W A , M o h r B D , S u m m e r s D M , e t a l : F u r t h e r v a r i a n t p a t t e r n s wi th P r i n z -m e t a l a n g i n a p e c t o r i s . C h e s t 66: 6 2 2 - 6 2 7 , 1974.

25. M a s e r i A , M i m m o R , C h i e r c h i a S, e t al: C o r o n a r y a r t e r y s p a s m as a c a u s e o f a c u t e m y o c a r d i a l i s c h e m i a in m a n . C h e s t 68: 6 2 5 - 6 3 3 , 1975.

26. L a s s e r R P , d e la Paz N S : R e p e t i t i v e t r a n -s i e n t m y o c a r d i a l i s c h e m i a , P r i n z m e t a l t y p e , w i t h o u t a n g i n a p e c t o r i s , p r e s e n t i n g wi th S t o k e s - A d a m s a t t a c k s . C h e s t 64: 3 5 0 -352, 1973.

27 . G o r f i n k e l H J , I n g l e s b y T V , L a n s i n g A M , e t al: S - T s e g m e n t e l e v a t i o n , t r a n s i e n t l e f t -p o s t e r i o r h e m i b l o c k , a n d r e c u r r e n t v e n -t r i c u l a r a r r h y t h m i a s u n a s s o c i a t e d w i t h p a i n ; a v a r i a n t o f P r i n z m e t a l ' s a n g i n a l syn-d r o m e . A n n I n t e r n M e d 79: 7 9 5 - 7 9 9 , 1973.

28 . P r c h k o v V K , M o o k h e r j e e S, Sch iess W , e t a l : V a r i a n t a n g i n a l s y n d r o m e , c o r o n a r y a r t e r y s p a s m , a n d v e n t r i c u l a r f i b r i l l a t i on in a b s e n c e o f c h e s t p a i n . A n n I n t e r n M e d 81: 8 5 8 - 8 5 9 , 1974.

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a n g i n a p e c t o r i s c a u s e d by c o r o n a r y a r t e r y s p a s m . A m J M e d 56: 2 6 9 - 2 7 4 , 1974.

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