To investigate the no reflow risk factors after percutaneous coronary intervention in ST elevation myocardial infarction patients. Sample size, mean±standard deviation (SD) or frequencies (percent) of normal and no reflow groups were extracted from each study. Of 27 retrospective and prospective studies, we found that increasing risks of no reflow were associated with advanced age, male, family history of coronary artery disease, smoking, diabetes mellitus, hypertension, delayed reperfusion, killip class ≥2, elevated blood glucose, increased creatinine, elevated creatine kinase (CK), higher heart rate, decreased left ventricular ejection fraction (LVEF), collateral flow ≤1, longer lesion length, multivessel disease, reference luminal diameter, initial thrombolysis in myocardial infarction (TIMI) flow, and high thrombus burden. Moreover, initial TIMI flow ≤1 and high thrombus burden had the greater impact on no reflow (OR95%CI=3.83 [2.77-5.29], p<0.0001 and 3.69 [2.39-5.68], p<0.0001, respectively). Our meta-analysis reveals that initial TIMI flow ≤1 and high thrombus burden are the most impacted no reflow risk factors.

Atherosclerosis occurs as a result of low-density lipoprotein (LDL) deposits oxidation. Endothelial dysfunction is an early process of atherosclerosis. Restoring endothelial lining back to normal by endothelial progenitor cells (EPCs) is critical for slowing or reversing vascular disease progression. Oxidative stress from hydrogen peroxide (H₂O₂) is increased in dyslipidemia so that antioxidant agent is required to prevent destruction of blood vessels. This study aims to report Ganoderma lucidum polysaccharide peptide (PsP) effects in atherogenic process by measuring H₂O₂ level, IL-10 level, and EPC number in blood serum, and also intima-media thickness of aorta in dyslipidemia Wistar rat model by giving them a hypercholesterol diet (HCD). The study was an experimental in vivo post-test with control group design. Thirty-five Wistar rats (Rattus norwegicus) were divided into five groups (normal diet group, HCD group, and hypercholesterol groups that received 50 mg/kg, 150 mg/kg, and 300 mg/kg bodyweight PsP). Each treatment group showed significant results for the administration of PsP using the one-way analysis of variance test (p<0.050) for the reduction of H₂O₂ (p = 0.003), levels of IL-10 (p = 0.027), number of EPC in the blood serum (p = 0.011), and the intima-media thickness of the aorta (p = 0.000). PsP from G. lucidum is a potent antioxidant and may prevent atherogenesis process in patients with dyslipidemia. The optimum doses of PsP in this study is 300 mg/kg bodyweight. Further studies are required to determine the antioxidant effects of PsP G. lucidum and its benefits in the management of dyslipidemia.

Objectives: The aim of the study was to evaluate the correlation between left ventricular hypertrophy and the gene polymorphism of angiotensin-converting enzyme (ACE) intron deletion (I/D) and ACE G2350A. Methods: Information related to the sample size and genotype frequencies was extracted from each study. Results: Our results found that the D allele (p = 0.0180) and DD genotype (p = 0.0110) of ACE I/D had a significant association with increasing the risk of left ventricular hypertrophy, whereas the I allele (p = 0.0180), but not II (p = 0.1660) and ID genotypes (p = 0.1430), was associated with decreasing the risk of left ventricular hypertrophy. On other hand, we found that the A allele (p = 0.0020) and GA genotype of ACE G2350A (p = 0.0070) had the correlation with increasing the risk of left ventricular hypertrophy. Conclusions: Our meta-analysis reveals that the D allele of ACE I/D and the A allele of ACE G2350A are associated with increasing the risk of left ventricular hypertrophy.

Objective: To determine the correlation between complete blood count and the risk of coronary heart disease (CHD). Material and Methods: All CHD patients treated in Aisyiyah Hospital during January 2011 to December 2017 were enrolled for the study. Information related to demographic, clinical, and complete blood count were extracted from medical record. Multiple logistic regression test was employed to evaluate the correlation between complete blood count and CHD incidence. In addition, a meta-analysis was also conducted to summarize findings from other regions. Results: A total of 516 CHD patients and 102 controls were included in our study. We found that elevated hemoglobin (OR 95%CI=4.92 [2.02-12.01], p=0.002), leukocyte (OR 95 CI=5.35 [3.17-9.03], p=0.001), hematocrit (OR 95%CI=2.31 [1.40-3.83], p=0.010), eosinophil (OR 95%CI= 2.78 [1.68-4.26], p=0.001), and monocyte (OR 95%CI=1.31 [0.80-2.16], p=0.023) were associated with the incidence of CHD. Furthermore, our meta-analysis revealed that elevated levels of leukocyte, eosinophil, and monocyte increased the risk of CHD approximately 3.57, 5.34, and 2.77 times, respectively. Conclusion: There is strong evidence that elevated levels of leukocyte, eosinophil, and monocyte are the risk factor for CHD.