Brief Communication

Dual Coronary Emboli in Peripartum Cardiomyopathy

Coronary emboli are rare but devastating events. We present the case of a 31-year-old woman with peripartum cardiomyopathy and mural thrombus. She was admitted with an acute, non-ST elevation myocardial infarction. Two emboli were seen on the coronary angiogram: one in the left anterior descending coronary artery and a second in the left circumflex artery. Each embolus resolved after local infusion of eptifibatide at the time of angiography. There has been 1 report in the English-language medical literature of a similar coronary embolic event in the setting of peripartum cardiomyopathy; however, in that case, only 1 embolus was found. Our case further documents embolic coronary occlusion as a consequence of peripartum cardiomyopathy. (Tex Heart Inst J 2004;31: 442-4)

Lyndon C. Box, MD Viktor Hanak, MD Joaquin G. Arciniegas, MD

W
Key words: Adult; coronary angiography; coronary thrombosis/complications/ diagnosis; echocardiography; electrocardiography; eptifibatide; female; human; myocardial diseases/ complications; myocardial infarction/diagnosis/therapy; platelet glycoprotein GPIIBIIIA complex; pregnancy complications, cardiovascular; thromboembolism/ diagnosis/etiology; ventricular function, left From: Department of Internal Medicine, Carraway Methodist Medical Center, Birmingham, Alabama Address for reprints: Lyndon C. Box, MD, 5000 San Jose Blvd., Apt. 18, Jacksonville, FL 32207 E-mail: lcbox@yahoo.com 2004 by the Texas Heart Institute, Houston

e know of only 1 prior report in the English-language medical literature of embolic myocardial infarction from a mural thrombus secondary to peripartum cardiomyopathy.1 We present a similar case, in which emboli were lodged in 2 coronary arteries; we believe it to be the 1st report of such a case. Our case confirms this series of events as a potential mechanism for acute myocardial infarction in young women.

Case Report
In January 2001, a 31-year-old woman presented at the emergency department of our institution after 30 minutes of chest pain, dyspnea, nausea, and vomiting. She was 4 weeks post partum; delivery of her infant had been induced because of preeclampsia. She reported having had lower extremity edema and increased fatigue during the interim, but no dyspnea, orthopnea, paroxysmal nocturnal dyspnea, or palpitations since delivery. There was no family history of cardiomyopathy. Of note, 8 years before this presentation, she had been evaluated for palpitations at another hospital, and an emergency room physician had mentioned to her that she had a large heart. At that time, she reported taking steroids for respiratory symptoms, but a specific medication was not recorded. The palpitations ceased after she stopped taking the medication. No further evaluation was performed. She was a smoker and occasionally used marijuana, but denied use of cocaine, amphetamines, or intravenous drugs. The patients electrocardiogram showed inferior Q waves with non-specific S-T changes. The cardiac serum troponin I level was 31.2 mg/dL; creatine phosphokinase, 1359 U/L; and creatine kinase myoglobin, 113.8 mg/dL. On the coronary angiogram (Fig. 1), there was an abrupt termination of the distal left anterior descending coronary artery (LAD), consistent with an embolus. A 2nd embolus was seen in the mid third of the circumflex artery. A 6F JL4 (Judkins left 4) catheter was positioned in the left main coronary artery, and eptifibatide was infused. Flow improved to TIMI grade III in the left circumflex artery, and faint filling could be seen beyond the LAD. A chest radiograph showed mild cardiomegaly and mild pulmonary congestion. Echocardiography showed left ventricular enlargement (end-diastolic diameter, 6.9 cm), severe global hypokinesis, and inferior akinesis; the estimated global ejection fraction was 0.20. In addition, the patient had mild left atrial enlargement, mild-to-moderate mitral regurgitation, and right heart dimensions at the upper limit of normal. A definite apical mural thrombus was seen. Results of a hypercoagulability evaluation were negative.
Volume 31, Number 4, 2004

442

Dual Coronary Emboli in Peripartum Cardiomyopathy

Fig. 1 An embolus is present in the left circumflex artery (large arrow) and the distal left anterior descending coronary artery (small arrow).

The patient recovered slowly and was discharged after 2 weeks of hospital care. At the 6-month followup visit, the patient continued to be in New York Heart Association functional class III despite optimal therapy for congestive heart failure.

proach, which allows diagnostic data to be gathered and potential therapy to be provided without the added risk of more aggressive strategies. In any case, reperfusion needs to be documented angiographically, and further adjunctive therapy may be necessary. The negative results of the hypercoagulability evaluation in our patient further support cardiomyopathy as the cause of her mural thrombus and emboli. Her poor ventricular function was likely the result of peripartum cardiomyopathy. No other possible cause was elicited. The echocardiogram strongly suggested a recent subacute process, due to the severe, symmetric, global left ventricular dysfunction and enlargement with relatively mild atrial enlargement. The patient had been told previously that she had a large heart, which left the diagnosis of peripartum cardiomyopathy open to question (if a strict National Institute of Health definition were followed*). Nevertheless, we believe that the finding of an enlarged heart was dubious, since it was judged from a chest radiograph in an emergency room setting. Furthermore, an interim of 8 years without symptoms makes it unlikely that she had significant cardiomyopathy before her pregnancy. The incidence of coronary emboli in peripartum cardiomyopathy is unknown. Although the condition is likely to be exceedingly rare, it should be considered by anyone evaluating a patient with peripartum cardiomyopathy and chest pain. Early recognition can lead to rapid effective treatment and limit the extent of myocardial infarction.
*National Institutes of Health Office of Rare Diseases defines peripartum cardiomyopathy as cardiac failure of unknown origin occurring within the final month of pregnancy or within 5 months of delivery, with no known heart disease before the final month of pregnancy. This is best confirmed by echocardiography showing left ventricular systolic dysfunction.8

Discussion
Thrombus formation and arterial emboli are known sequelae of peripartum cardiomyopathy,2- 6 but there is only 1 reported case of such a patient with embolism of the coronary arteries.1 Our case supports this mechanism as a cause of myocardial infarction. The presence of 2 emboli in separate arteries eliminates the possibility that a process within the arteries was the cause, and therefore substantiates emboli from a mural thrombus as the primary mechanism. Reperfusion with eptifibatide may have been serendipitous, since glycoprotein IIb/IIIa inhibitors are not, strictly speaking, fibrinolytic agents. There has been documentation of clot dissolution with these agents, particularly in the setting of fresh or ongoing thrombosis.7 No clinical trials are available to guide therapy for a unique patient such as ours (with multiple emboli and presumably no underlying coronary disease), but the initiation of reperfusion therapy (standard with myocardial infarction) is indicated. In similar patients who present at centers that can provide immediate percutaneous intervention, local eptifibatide may achieve reperfusion without mechanical therapy or use of thrombolytic agents. The return of flow to both vessels in our patient supports the efficacy of this apTexas Heart Institute Journal

References
1. Dickfield T, Gagliardi JP, Marcos J, Russell SD. Peripartum cardiomyopathy presenting as an acute myocardial infarction. Mayo Clin Proc 2002;77:500-1. 2. Hodgman MT, Pessin MS, Homans DC, Panis W, Prager RJ, Lathi ES, Criscitiello MG. Cerebral embolism as the initial manifestation of peripartum cardiomyopathy. Neurology 1982;32:668-71. 3. Bassaw B, Ariyanayagam DC, Roopnarinesingh S. Peripartum cardiomyopathy and arterial embolism. West Indian Med J 1992;41:79-80. 4. Janssens U, Klues HG, Hanrath P. Successful thrombolysis of right atrial and ventricle thrombi in a patient with peripartum cardiomyopathy and extensive thromboembolism. Heart 1997;78:515-6. 5. Carlson KM, Browning JE, Eggleston MK, Gherman RB. Peripartum cardiomyopathy presenting as lower extremity arterial thromboembolism. A case report. J Reprod Med 2000;45:351-3.

Dual Coronary Emboli in Peripartum Cardiomyopathy

443

6. Rester BT, Warnock JL, Patel PB, McMullan MR, Skelton TN, Collop NA. Lysis of a left ventricular thrombus with recombinant tissue plasminogen activator. Chest 2001;120: 681-3. 7. Collet JP, Montalescot G, Lesty C, Weisel JW. A structural and dynamic investigation of the facilitating effect of glycoprotein IIb/IIIa inhibitors in dissolving platelet-rich clots. Circ Res 2002;90(4):428-34.

8.

Pearson GD, Veille JC, Rahimtoola S, Hsia J, Oakley CM, Hosenpud JD, et al. Peripartum cardiomyopathy: National Heart, Lung, and Blood Institute and Office of Rare Diseases (National Institutes of Health) workshop recommendations and review. JAMA 2000;283:1183-8.

444

Dual Coronary Emboli in Peripartum Cardiomyopathy

Volume 31, Number 4, 2004