a 29 year old male was admitted to keimyung university hospital in 1987 with a continous substernal chest pain of three days duration .
he had been previously admitted in because of pain , chills , a tingling sensation and raynaud s phenomenon of the left hand and both feet . at that time
peripheral arterial mapping indicated that the left brachial and radial arterial pulsations were weaker than the right , and the popliteal and dorsalis pedis arterial pulsations were absent in both .
the laboratory findings included wbc , 12,800/cu mm with 25% eosinophils ( 3,000/cu mm ) , hematocrit , 45% ; ast , 17 iu/1 ; aso titer , 125 u ; c - reactive protein , negative ; cryoglobulin and cryofibrinogen , negative ; serum ige level , zero ; hbs antigen , negative .
the electrocardiogram taken on admission , revealed a normal sinus rhythm with no abnormal q waves and st segments .
1 ) showed a segmental luminal narrowing of the profunda brachii and brachial arteries with thin , tree root shaped collaterals .
the femoral angiogram revealed luminal narrowing and a corrugated appearance of the left popliteal artery and prominent sural artery , which resembled a spider leg or vine tendrill .
buerger s disease was easily confirmed on the basis of the clinical features and angiographic findings .
six months prior to readmission , he began smoking again , and three months later , anterior chest discomfort following heavy exercise or consumption of alcohol was noted .
after 3 days of episodes of severe substernal chest pain which continued for several hours and did not subside even with rest , he presented at keimyung university hospital to an evaluation of the chest pain . upon admission
the patient s vital sign were blood pressure : 130/80 mmhg , body temperature : 36.8c , and pulse rate 78/minitue .
the peripheral arterial pulsations on both sides of the upper and lower extremities were symmetric , but the pulsations of the popliteal and dorsalis pedis arteries , which were absent on the first admission , were present but weak , the laboratory results included wbc , 6,300/cu mm with eosinophils 14% ( 910/cu mm ) ; hematocrit , 39.3% ; esr , 20 mm / hour ; creatinine kinase , 84.0 u / l ; asparate transaminase , 15.4 u / l ; lactic dehydrogenase , 158.4 u / l ; total cholesterol , 109 mg / dl ; total protein , 7.2 mg / dl and uric acid 5.9 mg / dl .
2 ) displayed a sinus rhythm with abnormal q wavese and an elevation of more than 1 mm in the st segments in lead i , avl and v2 - 5 .
two weeks after the substernal chest pain episode , left ventriculography and coronary angiography were performed , and the left ventriculogram revealed hypokinetic or akinetic movement in the anterior region .
3 ) in the right and left anterior oblique projections demonstrated partial segmental occlusion of the proximal left anterior descending artery ( 42% of the luminal area ) , complete occlusion of the first diagonal brach of the left anterior descending artery in the distal portion , and irregular and tortous contour of the right coronary artery without obvious luminal narrowing .
conservative management included the administration of nitrate , beta - blocker and calcium channel blocker .
leo buerger first described thromboangitis obliterans ( buerger s disease ) as a progressive peripheral insufficiency occuring primarily in young male smokers , many authors have reported on this unique clinicopathologic disease entity .
this disease has a geographic and ethnic prevalence , especially among indians , jews and orientals . in korea ,
buerger s disease is a much more prevalent peripheral vascular occlusive disease than arteriosclerotic obliterans .
although there have been occasional reports of involvement of the mesenteric and cerebral arteries and rarely of the coronary arteries , myocardial infarction , as a clinical feature , is an extremely rare event in buerger s disease .
however , shionoya et al , reported that on autosy a patient buerger s disease showed atheromatous changes in the coronary and abdominal aorta , and also that patients with buerger s disease were susceptible to the arteriosclerotic process .
our patient s electrocardiomgram showed an extensive anterior wall infarction , and the coronary angiogram revealed a partially occluded proximal portion of the left anterior descending artery , further proof of an anterior myocardial infarction .
it is widely accepted that a myocardial infarction is the result of either a totally or critically occluded ( less than 25% of the luminal area ) coronary artery .
recently , several mechanisms have been proposed as possible cause of the myocardial infarction in patients with normal or near normal coronary arteries . in 1983 ,
rosenblatt and selzer suggested three possible mechanisms to explain such a discrepancy ; 1 ) a myocardial infarction is produced by a coronary arterial spasm ; 2 ) coronary lesions may cause myocardial infarctions , but their presence is not noted on a subsequent coronary angiogram ; and 3 ) an occlusive lesion , present at the time of infarction , has disappeared due to recanalization or lysis of the thrombus .
coronary arteriographic studies in our patient revealed a 42% luminal narrowing of the left anterior descending artery , which was greater than the critical level of acute myocardial infarction .
thus we suspected that other mechanisms , such as coronary vasospasm or recanalization , might be the cause of a transmural infarction with arteriosclerosis .
another finding which supports the suggestion of a coronary vasospasm , as a cause of an acute myocardial infarction , is raynaud s phenomenon which was observed in the patient prior to the myocardial infarction .
ciraulo et al , reported that migrain or raynaud s phenomenon was more frequently associated with coronary vasospasm and resulted in myocardial infarction in patients with normal coronary arteries .
based on these reports , we sugges that the coronary vasospastic phenomenon was involved in this case .
the etiology of buerger s disease , though still obscure , is correlated with cigarette smoking .
most of the patients cited in the literature were cigarette smokers who experienced a slowdown in the progression of disease inwhen they stopped smoking . in 1983 , adar et al reported that patients with buerger s disease exhibited a cellular sensitivity to human type i or type iii antigens ( or both ) and developed antibodies to anticoagulants , suggesting that immunologic factors were involved in the etiology of the disease .
other aspects of the disease are the genetic predisposition and the noted prevalence of hla - a9 and hla - b5 in many affected persons and of hla - a9 and hla - w10 in japanese patients . in 1985 , ferguson et al , reported a case of buerger s disease associated with idiopathic hypereosinophilia and suggested that eosinophilia might be involved in the pathogenesis of buerger s disease .
they proposed a wherein long term smoking incited an allergic reaction with hypereosinophilia in some patients .
it is interesting to note that on both admission , our patient presented hypereosinophilia with a normal ige level and other immunologic data , but these results might not be consistent with ferguson s report .
the treatment of buerger s disease is rather simple & specific ; the patients should stop smoking .
when our patient stopped smoking and followed conservative management for the myocardial infarction , his chest pain subsided . in conclusion , a myocardial infarction is a possibility in buerger s disease due to coronary vasospasm and coronary arteriosclerosis .
 a twenty - nine year old male smoker with a three year history of buerger s disease was admitted with excruciating precordial chest pain . 
 the electrocardiogram indicated an anterior transmural infarction , and he also exhibited hypereosinophilia.a coronary angiogram disclosed a partial segmental occlusion of the left anterior descending artery at the proximal portion . 
 he was discharged without any complications after conservative managment . 
REPORT OF A CASE
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