Adjunctive loading dose of cilostazol in preventing periprocedural myocardial infarction.

INTRODUCTION: Periprocedural myocardial infarction (PMI) is a common complication of percutaneous coronary intervention (PCI). This study evaluated the safety and efficacy of adjunctive loading dose of cilostazol in preventing PMI in patients with acute coronary syndrome (ACS). METHODS: A total of 113 patients with ACS undergoing PCI were randomized to receive loading doses of dual (aspirin plus clopidogrel; DAPT group; n=57) or triple antiplatelet therapy (aspirin plus clopidogrel plus cilostazol; TAPT group; n=56). The loading and maintenance doses were 100 and 50 mg bid for cilostazol. Patients in the TAPT group received adjunctive cilostazol for 1 week. Cardiac biomarkers were measured before PCI, 8 and 24 hours after PCI to determine the incidence of PMI. RESULTS: There was no significant difference in the incidence of PMI between the TAPT and DAPT groups (32.1% vs 47.4%, P=.098). However, in the antiplatelet-naïve subgroup, TAPT significantly lowered the incidence of PMI compared to DAPT (17.9% vs 42.9%, P=.042). In the antiplatelet-treated subgroup, the incidences of PMI were comparable (46.4% vs 51.7%, P=.698). Multivariable logistic analysis showed that antiplatelet-treated (vs antiplatelet-naïve) (hazard ratio [HR]: 2.45; 95% confidence interval [CI]: 1.09-5.52; P=.030) subgroup was independently associated with PMI. However, TAPT (vs DAPT) (HR: 0.51; 95% CI: 0.23-1.14; P=.102) was not an independent protective factor of PMI. CONCLUSIONS: The present single-center, randomized study indicates that TAPT with adjunctive cilostazol was not associated with lower incidence of PCI-related PMI in patients with ACS. Further study with large study population is needed to get definite conclusions.

Cardioprotective effects of traditional Chinese medicine Guanmaitong on acute myocardial infarction.

Guanmaitong (GMT) is a traditional Chinese herbal compound that has been used for the treatment of coronary heart disease (CHD) and other cardiovascular diseases. However, the efficacy of GMT in treating cardiovascular diseases remains unclear. The aim of the present study was to investigate the protective mechanisms and identify the targeted proteins and signaling networks associated with the physiological activity of GMT in a rat model of acute myocardial infarction (AMI). Sprague-Dawley rats were randomly allocated into five groups: Control group (sham-operated), the model group, and small, medium, and large dosage GMT groups. The rat model of AMI was established via ligation of the coronary artery. The results indicate that GMT was able to reduce myocardial infarction size and improve the activities of tumor necrosis factor-α (TNF-α), intercellular adhesion molecule 1 (ICAM-1) and interleukin-1. Furthermore, the reduced apoptotic index of the GMT-treated cardiocytes (P<0.05 vs. model group) was in accordance with the downregulated expression of Bax and the upregulated expression of Bcl-2. In conclusion, GMT may exert a protective potential against myocardial infarction injury by inhibiting apoptosis and inflammation of cardiomyocytes, and may offer a promising adjunct treatment for CHD.

[Effects and potential mechanisms of short-term use of simvastatin on myocardial no-reflow after ischemia-reperfusion in rats].

OBJECTIVE: The main objective of this study is to assess the the effect of simvastatin (sim) on myocardial no-reflow (NR) and explore the possible potential mechanisms. METHODS: Adult male Wistar rats were randomized into sham group (n = 12), I/R (90 min ischemia via coronary ligation/120 min reperfusion, n = 18) and I/R plus sim group (20 mgxkg(-1)xd(-1) sim pretreated via gavage beginning 3 days before I/R, n = 18). After reperfusion, area at risk/area of left ventricular (RA/LVA), area of NR, determined by the area not perfused by thioflavin-S/area at risk (NA/RA) and area of myocardial infarction/area at risk (MIA/RA) were measured. Myocardium homogenate was used to determine the activity of eNOS, iNOS and MPO, and the content of NO and MDA. Myocardial immunohistochemistry was performed to determine the positive index of NF-kappaB p65 in cardiomyocytes and arteriole. RESULTS: The NR and myocardial infarction areas in I/R plus sim group were significantly smaller than those in I/R group (34.10 +/- 7.05 vs. 52.09 +/- 6.89, 78.80 +/- 7.60 vs. 90.13 +/- 5.72, each P < 0.05) while the ischemia area was similar between the 2 groups (P > 0.05). The myocardial activities of iNOS and MPO, the contents of NO and MDA were significantly lower while eNOS activity was significantly higher in I/R plus sim group than those in I/R group (5.02 +/- 1.64 vs. 9.19 +/- 2.89, 586.21 +/- 126.97 vs. 744.49 +/- 137.53, 257.72 +/- 93.43 vs. 384.10 +/- 40.68, 72.10 +/- 18.56 vs. 111.84 +/- 38.58, 7.08 +/- 1.74 vs. 3.72 +/- 0.98, all P < 0.05). The positive index of NF-kappaB p65 in cardiocytes and arteriole at left ventricular wall near the area of myocardial infarction was significantly lower in I/R plus sim group than that in I/R group (21.59 +/- 10.5 vs. 34.32 +/- 9.55, 27.27 +/- 13.19 vs. 44.91 +/- 15.06, each P < 0.05). CONCLUSION: Simvastatin could improve myocardial NR after ischemia-reperfusion by attenuating endothelial dysfunction and inhibiting inflammation and neutrophil activation.