Primary Stenting in a Patient with Acute Myocardial Infarction and Primary Antiphospholipid Syndrome
- Volume 14 - Issue 4 - April, 2002
- Posted on: 8/1/08
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Antiphospholipid syndrome (APS) is an uncommon thrombotic disorder characterized by antiphospholipid antibodies (aPL). The syndrome may be associated with arterial or venous thrombosis, thrombocytopenia, recurrent fetal loss, skin lesions, neurological complications and retinal occlusion.1 Premature myocardial infarction may also be seen as a part of APS. In coronary artery bypass graft (CABG) operations and coronary balloon angioplasty (PTCA), APS may lead to complications such as bypass graft closure2 and early failure of PTCA.3,4 Although the patients with APS frequently have positive lupus anticoagulant activity, only a minority of these patients have satisfying diagnostic criteria for systemic lupus erythematosis (SLE). Thus, APS without the clinical features of SLE is called primary antiphospholipid syndrome.5 We present a case of primary stenting in a patient with primary APS who had recurrent coronary thrombosis without any other thrombotic disorder.
Case Report. A 38-year-old man who was referred to our center from another hospital was admitted to the coronary care unit (CCU) with chest pain and history of five times defibrillation within the last 2 hours. He had electrocardiography (ECG) performed 1 hour prior to admission; it showed ST-segment elevation in leads V2–6, I and aVL and ST-segment depression in leads III and aVF (Figure 1A). Anterior wall myocardial infarction was considered to be the diagnosis based upon this ECG. The patient had no history of heart disease and no risk factors except smoking. His blood pressure was 110/70 mmHg and heart rate was 70 beats/minute. Physical examination was completely normal. We performed a new ECG; it showed ST-segment elevation in II, III and aVF and ST-segment depression in I, aVL and V1–2 (Figure 1B). We diagnosed acute inferior wall myocardial infarction and administered intravenous streptokinase. We detected successful clinical reperfusion signs. The patient was treated with aspirin, beta-blocker and heparin after thrombolytic therapy.
After an uneventful follow-up period, we performed coronary angiography on the tenth day of admission. Left main coronary artery (LMCA) was normal, the proximal left anterior descending coronary artery (LAD) had eccentric plaque, the circumflex artery was normal and the right coronary artery (RCA) showed moderate (50–70%) stenosis in the mid-segment. Left ventriculography was normal. We planned an exercise stress test to evaluate the significance of the stenosis in the RCA and discharged the patient.
The patient was re-admitted 5 days later with atypical chest pain. There were no diagnostic ECG changes during chest pain. Exercise stress test was performed 2 days later. There were no clinical symptoms or significant changes in ST segment during the treadmill period. During the recovery phase, he suffered severe chest pain and the monitor of the treadmill device showed ST-segment elevation in leads V2–6. Ventricular fibrillation then developed. After defibrillation and transfer to the CCU, ST-segment elevation was observed in II, III and aVF. We diagnosed acute inferior reinfarction and performed emergency coronary angiography. The RCA was totally obstructed at the point where we detected moderate stenosis in the previous angiography (Figure 2A) and the proximal LAD had subocclusive thrombus at the location where we detected eccentric plaque in the previous coronary angiography (Figure 2B). The patient underwent PTCA with successful recanalization. A few minutes after PTCA, we detected a new thrombus formation at the occlusion site and decided to implant a coronary stent. We finished the procedure after successful implantation of a 2.5 x 18 mm AVE GFX stent (Arterial Vascular Engineering, Inc., Santa Rosa, California). Ticlopidine 250 mg twice daily was added to treatment.
We administered continuous intravenous heparin for 7 days after stent placement and performed a control angiography on day 7. The stent in the RCA was completely patent and the proximal LAD had only eccentric plaque. Because of the recurrence of myocardial infarction and thrombus formation in 2 different coronary arteries at the same time, additional blood tests were performed after the discontinuation of heparin. Results of routine biochemical tests, including lipid profile, hemoglobin and blood platelet count (220,000/mm3), were within normal limits. Prothrombin time and activated partial thromboplastin time were normal. Protein C, protein S and fibrinogen levels were normal. Antinuclear antibody, anti-DNA and lupus anticoagulant were negative. Biological syphilis test was negative. IgG aPL was 10 GPL units (normal, < 4 GPL units) and IgM aPL was 12 MPL units (normal, < 7 MPL units). We planned to repeat hematological tests 3 months later and discharged the patient with aspirin, ticlopidine and beta-blocker. After an asymptomatic period of 3 months, we repeated the blood tests. IgG and IgM aPL were still elevated at 10 GPL units and 13 MPL units, respectively. Other test results were within normal limits.
The patient was diagnosed to have primary APS according to the Harris criteria.6 Long-term warfarin treatment was started to prevent recurrence of thrombotic events. Control coronary angiography performed 6 months after stenting revealed a patent stent in the RCA (Figure 3A) and an eccentric lesion of 20–30% in the proximal LAD (Figure 3B); the other coronary arteries were normal. Patient follow-up was uneventful for 18 months after stent implantation.
Discussion. APS is characterized by venous or arterial thrombosis or both. Cardiac manifestations may include coronary artery7–15 or bypass venous graft occlusion,2 valvular disorder,16 pulmonary hypertension17 and large intracardiac thrombus mimicking mixoma.18 Vaarala et al. reported that antibodies against cardiolipin could be considered an independent risk factor for myocardial infarction.19 Transient aPL antibody production may be seen after acute myocardial infarction as an immune response.20 In our patient, antibodies were still high 3 months after the myocardial infarction. In the literature, we found 10 patients diagnosed with primary APS and myocardial infarction (Table 1). There were 6 females and 4 males, ranging in age from 20–62 years. Seven of the 10 patients had a history of additional thrombotic events, such as deep venous thrombosis, cerebral infarction or pulmonary embolism.7–13 Coronary angiography revealed normal coronary anatomy and myocardial infarction was thought to be due to microvascular disease in 3 of the patients.8,9,12 Five of the patients received thrombolytic therapy. Successful reperfusion was reported in all patients.4,7,10,12,15 Literature review revealed that 3 patients were revascularized by invasive procedures. One of these had an inferior infarction and was initially reperfused with thrombolytic therapy. PTCA was then performed at the culprit lesion. Despite a successful procedure, restenosis and de novo occlusive lesions were observed in other coronary vessels during the short-term follow-up period. The authors emphasized that PTCA for coronary occlusion of APS was unsuccessful.4 Takeuchi et al. performed primary PTCA to the RCA of a patient with APS and inferior myocardial infarction. The patient underwent long-term warfarin therapy. Control angiography performed 3 months later revealed no stenotic lesion or thrombus in the RCA. This was the first case of APS associated with myocardial infarction treated with primary PTCA as a revascularization procedure in the literature.14 Jankowski et al. performed coronary stent implantation in a patient with myocardial infarction and primary APS after the infarction healed. They reported that this was the first stent placement in a patient with primary APS.15
Our patient differs from the others in many aspects. Precordial ST-segment elevation associated with severe chest pain was followed by inferior ST-segment elevation and precordial ST-segment depression. The patient underwent primary PTCA for recanalization of the infarct-related artery when similar clinical and ECG settings repeated 5 days after hospital discharge. The RCA was found to be occluded and the LAD had a subocclusive thrombus in the proximal segment. The thrombus observed in the proximal LAD was probably responsible for the precordial ST-segment elevation as the first change on ECG. After the anticoagulation for 7 days, no thrombus was observed during the control coronary angiography. The existence of 2 different thrombotic lesions in 2 different coronary arteries at the same time and the recurrence of this process 15 days later is highly interesting, and to our knowledge is a rare event. We administered streptokinase to the patient during the first event of myocardial infarction and proved complete reperfusion. The patient underwent primary PTCA during the second event, which occurred in-hospital. Enlargement of thrombus was detected a few minutes after the balloon removal into the guiding catheter. Therefore, we performed stent placement on the culprit lesion. The stent was completely patent according to coronary angiography performed 6 months later. To our knowledge, this is the first primary stent implantation in a patient with primary APS and acute myocardial infarction.
The possible mechanisms of thrombosis in APS include effects of aPL on platelet membranes, on endothelial cells and on clotting components such as prothrombin, protein C and protein S.6 The outcome of PTCA in patients with primary APS is not yet clear. There are favorable and unfavorable reports about this procedure.3,4,14 There is only one report about stent placement in patients with primary APS as mentioned above.15 We performed successful primary stenting and saw that the result was good through the 6-month follow-up period. Although the most important factor is optimal stent placement to prevent in-stent thrombosis, prothrombotic state may lead to thrombotic complications in patients with primary APS. Since there is strong evidence that the thromboses in APS tend to recur, prophylactic and prolonged anticoagulant therapy is required.21 Several reports emphasized that therapeutic INR target in preventing recurrent thromboses in patients with primary APS should be higher than in other hypercoagulant states.15,22,23
In summary, we described a middle-aged man with primary APS who had recurrent myocardial infarctions caused by thrombus formation in two different coronary arteries at the same time. To our knowledge, this is the first case whose occluded RCA was treated with primary stent implantation. In young patients with myocardial infarction, APS should be considered as a possible cause of coronary occlusion. Thrombolytic therapy and interventions such as stent implantation seem to be effective revascularization procedures and must be followed by anticoagulant therapy.