THROMBUS FORMATION IN NON CULPRIT CORONARY ARTERY AFTER THROMBOLYSIS FOR ACUTE MYOCARDIAL INFARCTION

MS. MOURALI, F. EL AYECH, S. HANNECHI, A. ZAROUI, H. ALOUI, F. MGHAIETH, R. MECHMECHEService des Explorations Fonctionnelles et de Réanimation Cardiologiques. Hôpital La Rabta. Tunis

CONCLUSION :Simultaneous coronary occlusion should be always a consideration in patients

presenting with AMI. Different mechanisms has been postulated which exact

pathogenesis is still not well understood. Here we especially mention the systemic

and loco-regional acute pro-thrombotic and inflammatory states, diffuse

destabilization of atherosclerotic plaques leading to pan coronaritis phenomenon,

intravenous cocaine abuse… In our patient, the possibility that thrombolytic

therapy for AMI may be related to an increase hypercoagulable state is not

excluded.

CONCLUSION :Simultaneous coronary occlusion should be always a consideration in patients

presenting with AMI. Different mechanisms has been postulated which exact

pathogenesis is still not well understood. Here we especially mention the systemic

and loco-regional acute pro-thrombotic and inflammatory states, diffuse

destabilization of atherosclerotic plaques leading to pan coronaritis phenomenon,

intravenous cocaine abuse… In our patient, the possibility that thrombolytic

therapy for AMI may be related to an increase hypercoagulable state is not

excluded.

INTRODUCTION:Coronary plaque rupture and acute thrombosis are the main initial mechanisms of

acute myocardial infarction (AMI). Multiple intrinsic and extrinsic factors can cause

plaque instability. Previously reported, although uncommon, multiple simultaneous

coronary occlusion in AMI is still poorly understood. We report a case in our hospital

who presented an antero-septal myocardial infarction associated with thrombus

formation in circumflex coronary artery (Cx).

INTRODUCTION:Coronary plaque rupture and acute thrombosis are the main initial mechanisms of

acute myocardial infarction (AMI). Multiple intrinsic and extrinsic factors can cause

plaque instability. Previously reported, although uncommon, multiple simultaneous

coronary occlusion in AMI is still poorly understood. We report a case in our hospital

who presented an antero-septal myocardial infarction associated with thrombus

formation in circumflex coronary artery (Cx).

CASE REPORTCASE REPORT : :We report a case of a 44-year-old male, smoker having no other coronary risk factor

was admitted to our emergency department with symptoms of vomiting, sweating

and retrosternal chest pain radiating to the left arm, all started 1H before

presentation. His initial 12 lead electrocardiogram showed upwardly concave ST

segment elevation in anteroseptal leads with no ST segment depression, and

pathological Q waves on the inferior leads was noted (ECG.1).

CASE REPORTCASE REPORT : :We report a case of a 44-year-old male, smoker having no other coronary risk factor

was admitted to our emergency department with symptoms of vomiting, sweating

and retrosternal chest pain radiating to the left arm, all started 1H before

presentation. His initial 12 lead electrocardiogram showed upwardly concave ST

segment elevation in anteroseptal leads with no ST segment depression, and

pathological Q waves on the inferior leads was noted (ECG.1).

E F

DISCUSSION :In most cases of acute ST elevation MI, a single culprit vessel is often found.

However, multivessel occlusion, although uncommon, can occur. Multiple mechanisms

has been postulated. Plaque rupture occur from either primary disruption of the

fibrous cap mediated by inflammation or as a result of intraluminal forces extrinsic

influence by sympathetic tones and cathecolamines. Those 2 mechanisms can be

widespread through the coronary vasculature resulting in multiple simultaneous

events in multiple coronaries leading to “pan-coronaritis”. Goldstein et Al.

demonstrated the presence of multiple unstable plaques and overlying thrombi in

patient with acute MI. In his cohort, up to 32.8%of patients with acute MI had thrombi

in non culprit arteries. 25-50% of patients who died of acute MI had multiple coronary

thrombosis. Different cases of multiple coronary thrombosis has been reported by

Hamada et Al. in a patient with systemic thrombocytosis, by Stenberg et Al. in a

patient with IV cocaine abuse, by Suzuki et Al. in a patient with suspected corornary

spasm..

ACS may be associated with a systemic acute pro-thrombotic condition, possibly

involving inflammatory mechanisms as well, which are not confined to a single spot in

the coronary circulation. Thrombolytic therapy begun early during AMI can restore

myocardial blood flow , coronary reflow may then reduce the extent of myocardial

necrosis and preserve contractile function in myocardial segments that might

otherwise be lost. Yet, reocclusion after recanalization may negate these beneficial

effects. In our patient the possibility that thrombolytic therapy for AMI is related to

hypercoagulable state or the possibility of embolization of the proximal "clot in lysis”

to a multistenosis Cx artery are both not excluded.

DISCUSSION :In most cases of acute ST elevation MI, a single culprit vessel is often found.

However, multivessel occlusion, although uncommon, can occur. Multiple mechanisms

has been postulated. Plaque rupture occur from either primary disruption of the

fibrous cap mediated by inflammation or as a result of intraluminal forces extrinsic

influence by sympathetic tones and cathecolamines. Those 2 mechanisms can be

widespread through the coronary vasculature resulting in multiple simultaneous

events in multiple coronaries leading to “pan-coronaritis”. Goldstein et Al.

demonstrated the presence of multiple unstable plaques and overlying thrombi in

patient with acute MI. In his cohort, up to 32.8%of patients with acute MI had thrombi

in non culprit arteries. 25-50% of patients who died of acute MI had multiple coronary

thrombosis. Different cases of multiple coronary thrombosis has been reported by

Hamada et Al. in a patient with systemic thrombocytosis, by Stenberg et Al. in a

patient with IV cocaine abuse, by Suzuki et Al. in a patient with suspected corornary

spasm..

ACS may be associated with a systemic acute pro-thrombotic condition, possibly

involving inflammatory mechanisms as well, which are not confined to a single spot in

the coronary circulation. Thrombolytic therapy begun early during AMI can restore

myocardial blood flow , coronary reflow may then reduce the extent of myocardial

necrosis and preserve contractile function in myocardial segments that might

otherwise be lost. Yet, reocclusion after recanalization may negate these beneficial

effects. In our patient the possibility that thrombolytic therapy for AMI is related to

hypercoagulable state or the possibility of embolization of the proximal "clot in lysis”

to a multistenosis Cx artery are both not excluded.

After administration of aspirin 250mg, unfractionated heparin 5000 UI IV, clopidogrel

600mg and nitro-derivatives 6mg, intravenous thrombolytic therapy for anteroseptal

myocardial infarction was initiated with streptokinase, 1500000UI on 45 minutes. 30

minutes after thrombolytic initiation, patient still had chest pain, and the

electrocardiogram noted a total resolution of ST segment in anteroseptal leads, with

emergence of a complete right bundle branch block and unexpected ST segment

elevation of less than 2mm in the inferior leads (ECG.2).

After administration of aspirin 250mg, unfractionated heparin 5000 UI IV, clopidogrel

600mg and nitro-derivatives 6mg, intravenous thrombolytic therapy for anteroseptal

myocardial infarction was initiated with streptokinase, 1500000UI on 45 minutes. 30

minutes after thrombolytic initiation, patient still had chest pain, and the

electrocardiogram noted a total resolution of ST segment in anteroseptal leads, with

emergence of a complete right bundle branch block and unexpected ST segment

elevation of less than 2mm in the inferior leads (ECG.2).

Percutaneous recanalization of occluded Cx was attempted, evidenced a severe

multistenosis artery and was complicated with anterograde dissection extending from

the Cx to a big marginal branch (FIG.2), scaled by 2 bare metal stents. The procedure

final aspect showed a patent artery with TIMI 3 flow. Peak creatine kinase level was

6300 IU and maximum troponin I elevation was 432 ng/ml. Post procedure

electrocardiogram showed Q waves and inverted T waves in inferior leads, with no

more ST elevation or depression. Echocardiography revealed moderately hypokinetic

anterior wall and akinesia in inferior wall with left ventricular ejection fraction about

45%. Patient was discharged home 10 days later on aspirin, plavix, statin,

angiotensin converting enzyme inhibitor and betablocker.

Percutaneous recanalization of occluded Cx was attempted, evidenced a severe

multistenosis artery and was complicated with anterograde dissection extending from

the Cx to a big marginal branch (FIG.2), scaled by 2 bare metal stents. The procedure

final aspect showed a patent artery with TIMI 3 flow. Peak creatine kinase level was

6300 IU and maximum troponin I elevation was 432 ng/ml. Post procedure

electrocardiogram showed Q waves and inverted T waves in inferior leads, with no

more ST elevation or depression. Echocardiography revealed moderately hypokinetic

anterior wall and akinesia in inferior wall with left ventricular ejection fraction about

45%. Patient was discharged home 10 days later on aspirin, plavix, statin,

angiotensin converting enzyme inhibitor and betablocker.

90 minutes after thrombolytic initiation, the patient noted regression of the chest

pain, clinical examination was unremarkable with no electrocardiogram changes, after

which, the patient was transferred to the intensive care unit for further monitoring. 4

hours after thrombolytic initiation, the patient reported a recurrent angina. Cardiac

catheterization was promptly performed and coronary angiography showed a single

vessel disease with widely both patent left anterior descending and right coronary

arteries, and proximal circumflex coronary artery occlusion (FIG.1).

90 minutes after thrombolytic initiation, the patient noted regression of the chest

pain, clinical examination was unremarkable with no electrocardiogram changes, after

which, the patient was transferred to the intensive care unit for further monitoring. 4

hours after thrombolytic initiation, the patient reported a recurrent angina. Cardiac

catheterization was promptly performed and coronary angiography showed a single

vessel disease with widely both patent left anterior descending and right coronary

arteries, and proximal circumflex coronary artery occlusion (FIG.1).

FIG. 1 FIG. 2

ECG 2

ECG 1