Multivessel Acute Coronary Thrombosis and Occlusion —
An Unusual Cause of Cardiogenic Shock

Coronary angiography in the early phase of ST-elevation acute myocardial infarction (STEMI) usually identifies total thrombotic occlusion of a single infarct-related artery.¹ However, simultaneous acute occlusion of all major epicardial coronary arteries is extremely unusual.² We present a case of STEMI and cardiogenic shock associated with multiple large thrombi treated successfully by thrombus aspiration and balloon inflations.

Case Report. A 44-year old physician was transferred urgently to our catheterization unit 3 hours after a syncopal episode associated with chest pain and massive ST-segment elevation both in the anterior and inferior electrocardiographic leads (Figure 1). His past medical history included chronic alcoholism and heavy smoking for 25 years. The patient denied any history of hypertension, diabetes mellitus, dyslipidemia, cocaine abuse, chest trauma or previous angina. He was treated in the ambulance with intravenous fluids, 5 mg of metoprolol, 325 mg of chewable aspirin and an intramuscular injection of 50 mg of thiamine. On admission, he was conscious, restless, pale and sweating. His systolic blood pressure was 60 mmHg. He had a heart rate of 145 beats per minute and a respiratory rate of 24 per minute. The cervical veins were engorged and the lungs clear. Cardiac auscultation revealed typical gallop rhythm without murmurs. Neither hepatosplenomegaly nor deep vein thrombosis was detected.

As shown in Figure 2, immediate diagnostic coronary angiography revealed thrombotic occlusion of both the right coronary artery (RCA) and the proximal left anterior descending artery (LAD), with TIMI flow grade 1 and 0, respectively. Two large nonocclusive mobile thrombi were identified in the mid segment of the left circumflex (CX) artery, without flow disturbances or vessel wall narrowing (Figure 2B).

Following the clinical and angiographic findings, an intra-aortic balloon pump was inserted and 5,000 units of unfractionated heparin, 600 mg of clopidogrel, and a bolus of eptifibatide (180 μg/kg) were administered. Transthoracic echocardiography (TTE) excluded the presence of left-sided masses, inter-atrial septal defect or patent foramen ovale. Immediate wiring and dilatation of the LAD using a 2 x 20 mm Maverick balloon (Boston Scientific Corp., Natick, Massachusetts) did not result in improved coronary flow, and an Export aspiration catheter (Medtronic Inc., Minneapolis, Minnesota) was inserted. After the first aspiration run in the LAD, the TIMI flow improved to grade 2, and a thrombotic mass was noticed in the collection cup. At this time, 125,000 units of urokinase and repeated boluses of 36 μg of adenosine were injected into the left coronary system. Following the third aspiration run, the TIMI flow grade in the LAD improved to grade 3 (Figure 2F) in the absence of significant vessel wall narrowing.

We then decided to treat the RCA. After two aspiration runs in the RCA, the TIMI flow improved to grade 3 (Figure 2D), and 125,000 units of urokinase were injected into the vessel as well. The last vessel to be treated was the CX. After wiring and a single aspiration run, both large thrombi disappeared, and no significant vessel wall narrowing was noticed by repeated coronary injections (Figure 2E). Since TIMI flow grade 3 was recorded in all major epicardial vessels associated with myocardial blush grade 2, the patient was transferred back to the coronary care unit. Blood tests showed a white blood cell count of 14.46/ml, a hemoglobin level of 16.7 g/dl, a platelet count of 559,000/ml, and a peak creatine kinase level of 4,450 units. Postprocedure left ventricular function analysis by TTE showed anterior wall hypokinesis with an estimated global left ventricular ejection fraction of 35%. Hematological evaluation of hypercoagulability, including lupus anticoagulant, anti-cardiolipin IgM and IgG were negative. Creactive protein was 12 mg/L, homocysteine and folic acid levels were 19.5 mg% (upper normal limit is 15.5) and 6 mg/dl (normal range: 3.1–12.4 mg/dl), respectively. The patient refused a transesophageal echocardiographic evaluation. Seven days postadmission, repeat coronary angiography showed near-normal coronary vessels. As presented in Figure 3, intravascular ultrasound (IVUS) of the proximal LAD showed an eccentric fibro-fatty plaque with a luminal cross-sectional area of 6.1 mm² without any evidence of plaque rupture. IVUS evaluation of both the CX and RCA did not reveal any atheromatous plaques.

Discussion. We presented an unusual case of multivessel acute thrombotic occlusion in STEMI leading to cardiogenicshock. Our patient was successfully treated, primarily by thrombus aspiration and by balloon inflations. An IABP was inserted and kept in place for several hours only, with rapid and uneventful recovery of our patient.

The concept of multiple plaque ruptures in acute coronary syndrome (ACS), otherwise termed “pancoronaritis” syndrome, was recently described by Virmani et al, Falk and others.^3–5 Previous studies using both angioscopy and IVUS showed that multiple plaque ruptures are frequent (up to 75% ofcases) in ACS, and can be detected in the three major coronary trunks.^6,7 Maehara et al evaluated 300 plaque ruptures in 257 arteries in 254 patients with ACS during preintervention IVUS.⁸ Multiple ruptures were observed in 39 of 254 patients (15%), 36 of those in the same artery.⁸ Thrombi were more common in patients with unstable angina or myocardial infarction (p = 0.02) and in multiple ruptures (p = 0.04). The plaque rupture site contained the minimum luminal area site in only 28% of patients.⁸

Since emboli to the coronary tree as well as blood coagulopathy were found to be highly unlikely by physical examination and TTE evaluation, the case described here probably validates the concept that ACS may potentially involve the entire coronary tree, even in the absence of angiographically significant vessel wall narrowing. We did not evaluate the patient for the presence of the 20210A prothrombin allele, which was recently found to be an inherited risk factor for ACS among patients who have a limited extent of coronary disease on angiography, or who lack major metabolic and acquired risk factors.⁹ Yet, hematological evaluation for the most common causes of blood coagulopathy in this patient were negative. However, one may also hypothesize that in our patient, a cascade of events started with acute plaque rupture and LAD occlusion (the only artery with atheroma by IVUS). The acute LAD occlusion led to severe hypotension and cardiogenic shock with severely reduced coronary perfusion pressure, blood stasis and multiple thrombi formation.

In conclusion, our patient is demonstrative of the versatility of the clinical and angiographic presentation of ACS and cardiogenic shock. We suggest that IABP insertion and rapid thrombus aspiration should be used as the primary therapeutic modalities in such complicated cases.

References

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8. Maehara A, Mintz GS, Bui AB, et al. Morphologic and angiographic features of coronary plaque rupture detected by intravascular ultrasound. J Am Coll Cardiol 2002;40:904-910.

9. Burzotta F, Paciaroni K, De Stefano V, et al. Increased prevalence of the G20210A prothrombin gene variant in acute coronary syndromes without metabolic or acquired risk factors or with limited extent of disease. Eur Heart J 2002;23:26–30.