Addition of cilostazol to aspirin therapy for secondary prevention of cardiovascular and cerebrovascular disease in patients undergoing percutaneous coronary intervention: A randomized, open-label trial.

BACKGROUND: Patients with established coronary artery disease are at increased risk for future ischemic events and require secondary prevention for systemic vascular disease. We performed a randomized clinical trial to evaluate the impact of cilostazol on cardiovascular and cerebrovascular disease in patients undergoing percutaneous coronary intervention. METHODS: A total of 514 patients who had undergone coronary stent implantation >6 months previously and were thought to no longer need dual antiplatelet therapy with aspirin and a thienopyridine were randomly assigned to receive aspirin plus cilostazol therapy or aspirin therapy alone after discontinuation of thienopyridine therapy. The primary efficacy end point was a composite of all-cause death, myocardial infarction, stroke, or cardiovascular or cerebrovascular revascularization at 2 years after randomization. The main safety end point was major or minor bleeding, according to the Thrombolysis in Myocardial Infarction bleeding definition. RESULTS: At 2 years, follow-up clinical data were available for 98.1% of patients. The primary efficacy end point occurred in 13.9% of the aspirin plus cilostazol group versus 22.1% of the aspirin-only group (hazard ratio 0.61, 95% CI 0.40-0.93, P = .021). The rate of major or minor bleeding was not significantly different between the aspirin plus cilostazol and aspirin-only groups (1.6% and 4.0%, respectively, hazard ratio 0.40, 95% CI 0.13-1.28, P = .12). CONCLUSIONS: In patients who underwent coronary stent implantation, the addition of cilostazol to aspirin therapy was associated with lower rates of cardiovascular and cerebrovascular events at 2 years compared with aspirin monotherapy.

Chronic pericardial constriction induced severe ischemic hepatitis manifesting as hypoglycemic attack.

Ischemic hepatitis, otherwise known as "shock liver", is characterized by a massive, but transient increase in serum transaminase levels, usually associated with cardiac failure. A patient who did not have a predisposition to hypoglycemia was discovered at home with disturbed consciousness caused by hypoglycemia. She had been diagnosed as having constrictive pericarditis several years earlier and had developed ischemic hepatitis. Though the high serum transaminase levels were rapidly normalized, severe jaundice gradually developed and the patient finally died of multiple organ failure. Hypoglycemia, which is considered secondary to reduced gluconeogenesis in the exhausted liver, is a rare complication of constrictive pericarditis.

Intracoronary transplantation of non-expanded peripheral blood-derived mononuclear cells promotes improvement of cardiac function in patients with acute myocardial infarction.

BACKGROUND: Transplantation of non-expanded peripheral blood mononuclear cells (PBMNCs) enhances neovessel formation in ischemic myocardium and limbs by releasing angiogenic factors. This study was designed to examine whether intracoronary transplantation of PBMNCs improves cardiac function after acute myocardial infarction (AMI). METHODS AND RESULTS: After successful percutaneous coronary intervention (PCI) for a ST-elevation AMI with occlusion of proximal left anterior descending coronary artery within 24 h, patients received an intracoronary infusion of PBMNCs within 5 days after PCI (PBMNC group). PBMNCs were obtained from patients by COBE spectra-apheresis and concentrated to 10 ml, 3.3 ml of which was infused via over-the-wire catheter. The global left ventricular ejection fraction (LVEF) change from baseline to 6 months followup in th ePBMNC group that underwent standard PCI for similar AMI [corrected]. The primary endpoint was the global left ventricular ejection fraction (LVEF) change from baseline to 6 months' follow-up. The data showed that the absolute increase in LVEF was 7.4% in the control group and 13.4% (p=0.037 vs control) in the PBMNC group. Cell therapy resulted in a greater tendency of DeltaRegional ejection fraction (EF) or significant improvement in the wall motion score index and Tc-99m-tetrofosmin perfusion defect score associated with the infarct area, compared with controls. Moreover, intracoronary administration of PBMNCs did not exacerbate either left ventricular (LV) end-diastolic and end-systolic volume expansion or high-risk arrhythmia, without any adverse clinical events. CONCLUSION: Intracoronary infusion of non-expanded PBMNCs promotes improvement of LV systolic function. This less invasive and more feasible approach to collecting endothelial progenitor cells may provide a novel therapeutic option for improving cardiac function after AMI.