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Drug-eluting stents (DES) are considered the treatment of choice for most patients with obstructive coronary artery disease when percutaneous intervention (PCI) is feasible. However, stent thrombosis seems to occur more frequently with DES and occasionally is associated with resistance to anti-platelet drugs. We have experienced a case of recurrent stent thrombosis in a patient with clopidogrel resistance. A 63-year-old female patient suffered from acute myocardial infarction and underwent successful PCI of the left anterior descending coronary artery (LAD) with two DESs. She was found to be hyporesponsive to clopidogrel and was treated with triple anti-platelet therapy (aspirin 100 mg, clopidogrel 75 mg, and cilostazol 200 mg daily). Three days after discharge, she developed chest pain and was again taken to the cardiac catheterization laboratory, where coronary angiography (CAG) showed total occlusion of the mid-LAD where the stent had been placed. After intravenous administration of a glycoprotein IIb/IIIa inhibitor, balloon angioplasty was performed, resulting in Thrombolysis In Myocardial Infarction (TIMI) III antegrade flow. The next day, however, she complained of severe chest pain, and the electrocardiogram showed marked ST-segment elevation in V1-V6, I, and aVL with complete right bundle branch block. Emergent CAG revealed total occlusion of the proximal LAD due to stent thrombosis. She was successfully treated with balloon angioplasty and was discharged with triple anti-platelet therapy.

HMG-CoA reductase inhibitors (statins) reduce major adverse cardiac events (MACE) and mortality in patients with acute coronary syndrome. We investigated whether early statin therapy would be effective at reducing MACE in patients with acute myocardial infarction (AMI).A total of 1,159 patients were analyzed. They were grouped by initiation time of statin administration after admission as follows: group I; n = 945, ≤ 48 hours, group II; n = 214, > 48 hours.Cardiovascular risk factors and noncardiac comorbidities were not different between the two groups. ST-elevation MI as initial diagnosis was more prevalent in group I (68.4% versus 59.3%, P = 0.013). In-hospital mortality was not different in the two groups (0.8% versus 0.5%, P = 0.483). In one-year clinical follow-up, MACE and repercutaneous coronary intervention were lower in group I (17.8% versus 24.6%, P = 0.016, 10.2% versus 15.5%, P = 0.021, respectively). However, there was no difference in mortality (3.8% versus 4.7%, P = 0.319). In multivariate analysis, statin initiation within 48 hours after admission was an independent predictor of one-year MACE (OR 1.49, 95% CI = 1.00-2.21, P = 0.045).Consequently, early statin therapy within 48 hours after admission reduced MACE at one-year follow-up in patients with AMI.

Background: Myocardial bridge (MB) is regarded as a common benign lesion on coronary angiography (CAG). It is known to be harmless but may cause several cardiac events and recurrent hospitalization, so in the present study the long-term clinical course of patients with isolated MB and predictors of readmission were investigated. Methods and Results: Total 684 patients (343 males, 60.5±11.2 years) with persistent chest pain without critical stenosis on CAG were enrolled. The patients were divided into 2 groups according to the presence of MB. Clinical follow-up was performed with respect to readmission after baseline CAG. At a mean follow-up of 37 months, 92 patients (13.3%) were re-admitted because of 79 recurrent chest pain refractory to medication (11.5%), 8 myocardial infarctions (1.2%), 1 life-threatening arrhythmia (0.1%) and 4 deaths (0.6%). There was a significant higher incidence of readmission in the MB group (P=0.038). In multivariate analysis, long MB (hazard ratio (HR) 2.780; 95% confidence interval (CI) 1.070-7.218, P=0.036) and spontaneous vasospasm in CAG (HR 2.335; 95%CI 1.055-5.171, P=0.037) were the predictors of readmission. Moreover, additional use of aspirin or statin decreased the readmission rate. Conclusions: This study suggests that MB on non-occlusive CAG is not benign and may cause recurrent chest pain, myocardial infarction or life-threatening arrhythmia. Especially, patients with a long MB and vasospasm on CAG need intensive medical therapy, including antiplatelet treatment. (Circ J 2010; 74: 538 - 543)