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Myocardial injury and LV systolic/diastolic dysfunction at week 8 was alleviated by co-administered rosuvastatin, but not by carvedilol. It is unclear whether the cardioprotective effect of rosuvastatin is attributed to a suppression of oxidative stress induced by doxorubicin, because carvedilol did not exhibit a cardioprotective effect despite its antioxidant effects.

Background :A recent study has shown that triple anti-platelet therapy (cilostazol+clopidogrel+aspirin) resulted in a significantly lower restenosis rate after coronary stenting than did conventional therapy (clopidogrel+aspirin). However, the anti-platelet effects of cilostazol, when combined with clopidogrel and aspirin, have not been evaluated.Methods :Low dose cilostazol (50 mg/BID) was given to 47 patients who had already been taking clopidogrel (75 mg/day) and aspirin (100 mg/day) for more than 1 month subsequent to coronary stenting due to AMI and unstable angina. Markers of platelet activation, P-selectin and activated GPIIb/IIIa on platelets, were measured at baseline and 2 weeks after cilostazol treatment. We empirically divided patients into tertiles (low, n=16; moderate, n=14; high group, n=17), according to the baseline P-selectin expression. We then performed a comparative assessment of the anti-platelet effects of cilostazol at baseline and after 2 weeks of cilosatzol administration.Results :P-selectin was significantly decreased after 2 weeks of cilostazol treatment in total patients (n=47, 3.2±2.4% to 2.0±1.9%, p=0.03). This inhibition of P-selectin expression was mainly achieved in the moderate and high P-selectin groups (low group; 1.4±0.5 to 1.9±1.3%, p>0.05, moderate group; 2.5±0.3 to 1.3±0.3%, p<0.05, high group; 5.4±2.7 to 2.7±2.8%, p<0.05). Activated GPIIb/IIIa was not significantly changed (13.5% to 17.6%, p>0.05). Underlying disease, cardiovascular risk factors, concomitant medication including statin, and hsCRP were not related to the degree of P-selectin expression.Conclusion :Our data demonstrated that cilostazol treatment in addition to conventional anti-platelet therapy provides more effective suppression of platelet P-selectin expression in patients with relatively high platelet activity.

After 4 hours of abstinence from smoking, CFR and CVRI in smokers were similar to those of nonsmokers. However, consecutively smoking two cigarettes acutely reduced CFR and increased CVRI. These findings suggested that smoking could reduce coronary blood flow immediately, even in healthy people.

Renin-angiotensin system (RAS) blockers have shown clinical outcomes superior to those of the beta (β)-blocker atenolol, despite similar reductions in the peripheral blood pressure (BP), perhaps because of different impacts on central hemodynamics. However, few comparative studies of RAS blockers and newer vasodilating β-blockers have been performed. We compared the central hemodynamic effects of losartan and carvedilol in a prospective, randomized, open, blinded end point study. Of the 201 hypertensive patients enrolled, 182 (49.6±9.9 years, losartan group=88 and carvedilol group=94) were analyzed. Carotid-femoral pulse wave velocity (cfPWV), aortic augmentation index (AIx), AIx corrected for a heart rate (HR) of 75 beats per minute (AIx@HR75) and central BP were measured noninvasively at baseline and after a 24-week treatment regimen with losartan or carvedilol. After 24 weeks, there were no between-group differences in the brachial BP, cfPWV, AIx@HR75 or central BP changes, except for a more favorable AIx effect with losartan. The changes in all measured metabolic and inflammatory parameters were also not significantly different between the two groups, except for uric acid. Losartan and carvedilol showed generally comparable effects on central hemodynamic indices, metabolic profile, inflammatory parameters and peripheral arterial pressure with a 24-week treatment.

Although amiodarone appears to have few pro-arrhythmic effects, torsade de pointes (TdP) has been observed during long-term drug administration, usually in conjunction with electrolyte disturbances, a change in drug dosage, or concomitant drug therapy. We report two cases of amiodarone-induced TdP shortly after administration of a low dose of oral amiodarone, in the absence of predisposing factors.

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