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Lee, J.M.,Park, J.,Kang, J.,Jeon, K.H.,Jung, J.h.,Lee, S.E.,Han, J.K.,Kim, H.L.,Yang, H.M.,Park, K.W.,Kang, H.J.,Koo, B.K.,Kim, S.H.,Kim, H.S. Elsevier/North-Holland Biomedical Press 2015 INTERNATIONAL JOURNAL OF CARDIOLOGY Vol.184 No.-
Background: Studies have reported conflicting results regarding efficacy of mechanical hemodynamic support using intra-aortic balloon pump (IABP) or percutaneous ventricular assisted device (pVAD) in patients undergoing high-risk PCI. We performed a Bayesian network meta-analysis comparing the safety and efficacy of mechanical hemodynamic support devices and medical therapy (MT). Methods and results: RCTs comparing overall mortality of IABP versus MT or IABP versus pVAD in high-risk PCI populations were included. The primary endpoint was overall mortality, using the longest available follow-up in each study. This analysis included 2843 patients from 13 trials. In network meta-analysis, overall survival benefit was not significant with IABP (RR 0.84, 95% CrI 0.56-1.24) or pVAD (RR 0.95, 95% CrI 0.42-2.06), compared with MT. IABP or pVAD also did not show early survival benefit compared with MT. In terms of bleeding, pVAD was the worst (versus IABP: RR 29.4, 95% CrI 5.99-221.0; versus MT: RR 41.7, 95% CrI 8.19-330.0), which was mainly driven by the higher incidence of bleeding in the ECMO and TandemHeart, while IABP was worse than MT (RR 1.41, 95% CrI 1.01-2.08). The incidence of acute limb ischemia or vascular complication was not different between treatment groups. Conclusions: In this meta-analysis, routine elective use of IABP or pVAD did not reduce mortality, while it increased bleeding, compared with MT in high-risk PCI population or even in the patients with cardiogenic shock. Thoughtful selection of appropriate patients and balancing the risk and benefit should be the prerequisites to the use of mechanical hemodynamic support devices.
Kim, S.J.,Kim, W.,Woo, J.S.,Ha, S.J.,Kang, W.Y.,Hwang, S.H.,Kang, D.G.,Lee, S.U.,Cho, S.K.,Im, J.S.,Kim, W. Elsevier/North-Holland Biomedical Press 2012 INTERNATIONAL JOURNAL OF CARDIOLOGY Vol.158 No.1
Background: Several studies have demonstrated that adenosine and nicorandil protect the myocardium against angioplasty-related myocardial injury. We conducted a prospective study to investigate the myocardial protective effects of combination therapy with intracoronary adenosine and nicorandil. Methods: We enrolled 213 consecutive patients with stable or unstable angina who were scheduled for non-urgent PCI for de-novo coronary lesions. Patients were randomized into group I (control saline, n=55), group II (adenosine 50μg, n=54), group III (nicorandil 4mg, n=54), or group IV (adenosine-nicorandil combination, n=50). Serial assessments of CK-MB were used to assess myocardial necrosis before and after PCI. The primary endpoint was the incidence of myocardial necrosis (elevation of CK-MB), and the secondary endpoints were the changes in serum CK-MB and cTnI levels and the incidence of post-procedural myocardial infarction (MI). Results: No significant differences were observed among the four groups with regard to baseline or angiographic characteristics. No major adverse events related to adenosine and nicorandil were observed. There were no significant differences in the incidence of post-procedural myocardial necrosis among the four groups (10.9, 14.8, 14.8, and 14.0%, respectively, p=0.9). There were no significant differences in the incidence of post-procedural MI among groups (p=0.6). In multivariate regression analysis, multivessel stenting, median stent length, and the presence of a compromised side branch were independent predictors of myonecrosis. Conclusions: Pretreatment with intracoronary adenosine, nicorandil, or the combination of the two drugs did not reduce the incidences of myocardial necrosis or MI after non-urgent PCI in patients with low-risk angina pectoris.
Ki, Y.J.,Choi, D.H.,Lee, Y.M.,Lim, L.,Song, H.,Koh, Y.Y. Elsevier/North-Holland Biomedical Press 2014 INTERNATIONAL JOURNAL OF CARDIOLOGY Vol.175 No.3
Objective: The aim of this study was to determine the associations of brachial-ankle pulse wave velocity (baPWV), high-sensitivity cardiac troponin T (hs-cTnT) and N-terminal pro-B type natriuretic peptide (NT-proBNP) with the development of adverse outcomes after percutaneous coronary intervention (PCI). Methods: The baPWV, hs-cTnT and NT-proBNP were analyzed in 372 patients who underwent PCI. The primary endpoint was cardiac death. Results: There were 21 events of cardiac death during a mean of 25.8months of follow-up. When the baPWV cut-off level was set to 1672cm/s using the receiver operating characteristic curve, the sensitivity was 85.7% and the specificity was 60.1% for differentiating between the group with cardiac death and the group without cardiac death. Kaplan-Meier analysis revealed that the higher baPWV group (≥1672cm/s) had a significantly higher cardiac death rate than the lower baPWV group (<1672cm/s) (11.4% vs. 1.4%, log-rank: P<0.0001). This value was more useful in patients with myocardial injury (hs-cTnT≥0.1ng/mL) or heart failure (NT-proBNP≥450pg/mL). Conclusions: The results of this study show that high baPWV is a predictive marker for cardiac death after PCI.
Choi, S.H.,Jung, S.Y.,Yoo, S.Y.,Yoo, S.M.,Kim, D.Y.,Kang, S.,Baek, S.H.,Kwon, S.M. Elsevier/North-Holland Biomedical Press 2013 INTERNATIONAL JOURNAL OF CARDIOLOGY Vol.169 No.1
Backgrounds: Although the rescue of cellular senescence during ex vivo expansion of human-derived cardiac progenitor cells (hCPC) is critical for the application of autologous stem cell therapy in cardiovascular disease, the underlying molecular pathways during replicative senescence in hCPC have not been fully defined. Thus, we examined whether the regulation of mitogen-activated protein kinases activation could facilitate the recovery of human c-kit-positive hCPCs (hCPC<SUP>c-kit+</SUP>) and whether senescence is reactive oxygen species (ROS)-dependent or -independent. Methods and results: To investigate the molecular pathways of replicative cellular senescence, we first evaluated cellular senescence in ex vivo-expanded hCPC<SUP>c-kit+</SUP> by using senescence-associated β-galactosidase (SA-β-gal) activity with enlarged cytoplasm and observed increased expression of cell senescence-related pivotal molecules, including TP53, cleavage Mdm2 (cMdm2), and Mdm2. Unexpectedly, we found that the extracellular signal-regulated kinase (ERK) was markedly activated in aged hCPC<SUP>c-kit+</SUP>, with reduced proliferative activity. SA-β-gal activity and cytoplasm size in senescent hCPC<SUP>c-kit+</SUP> were significantly reduced, with reduced TP53 and cMdm2 expression after treatment with a specific ERK inhibitor (U0126). We examined whether the signaling in ERK inhibitory rescue of hCPC<SUP>c-kit+</SUP> senescence is ROS-dependent. Interestingly, the increased ROS level was not changed after treatment with a specific ERK inhibitor. Similarly, the increased expression levels of endogenous antioxidant enzymes, e.g., peroxiredoxin (Prdx)-1 and 2, in senescent hCPC<SUP>c-kit+</SUP> were not changed after treatment with a specific ERK inhibitor. Conclusions: From the above results, we conclude that the specific inhibition of ERK during cellular senescence might rescue bioactivities of senescent hCPC<SUP>c-kit+</SUP> in a ROS-independent manner.
Shin, S.Y.,Park, J.I.,Park, S.K.,Barrett-Connor, E. Elsevier/North-Holland Biomedical Press 2015 INTERNATIONAL JOURNAL OF CARDIOLOGY Vol.181 No.-
Background: Exercise electrocardiography in asymptomatic adults has been criticized because of relatively poor accuracy predicting future heart disease risk, but studies may have been too short. We investigated if integrated analysis of graded exercise tolerance tests (GXT) predicted long-term coronary heart disease (CHD) and all-cause mortalities among community-dwelling older adults. Methods and results: From 1972 to 1974, 1789 adult residents of a predominantly Caucasian, middle- to upper-middle-class southern California community participated in a clinical evaluation that included a GXT; 52.4% (N=939) of those who had baseline GXT were followed up to 2010-up to 36years-for vital status, CHD and all-cause mortality. Multiply adjusted hazard ratios of an abnormal graded GXT were 1.65 (95% CI 0.78-3.49) and 1.56 (95% CI 1.15-2.11) for CHD and all-cause mortality, respectively. An integrated analysis hazard ratio was calculated based on the following GXT findings: significant ST change, inability to achieve target heart rate [THR], abnormal heart rate recovery [HRR], and chronotropic incompetency [ChI]. Compared to those with 0 or 1 abnormality, participants with 2 or more positive findings had significantly higher CHD (HR 2.18) and all-cause (HR 1.92) mortalities. Participants with 3 or more positive findings showed even higher hazard ratios-CHD (HR 6.16) and all-cause (HR 2.49) mortalities. When adjusted for any of 3 Framingham risk models, the integrated electrocardiographic model correlated well with CHD and all-cause mortalities. Conclusions: An integrated analysis of electrocardiographic and non-electrocardiographic measures of GXT is useful in predicting long-term CHD and all-cause mortalities in an asymptomatic middle-aged population.
Association between aortic calcification and stable obstructive coronary artery disease
Kim, E.J.,Yong, H.S.,Seo, H.S.,Lim, S.Y.,Kim, S.W.,Kim, M.N.,Kim, Y.K.,Poddar, K.L.,Ramasamy, S.,Na, J.O.,Choi, C.U.,Lim, H.E.,Kim, J.W.,Kim, S.H.,Lee, E.M.,Rha, S.w.,Park, C.G.,Oh, D.J. Elsevier/North-Holland Biomedical Press 2011 INTERNATIONAL JOURNAL OF CARDIOLOGY Vol.153 No.2
Background: Coronary artery calcification (CAC) is correlated with aortic calcification (AC) and predicts coronary atherosclerosis as well as obstructive coronary artery disease (OCAD). This study aims to investigate whether AC predicts OCAD independent of CAC and its incremental value in predicting OCAD with CAC. Methods: Among the consecutive patients who underwent 64-slice multidetector CT (MDCT), we enrolled 120 stable OCAD (luminal narrowing ≥50%) patients and 120 controls without OCAD, matched for cardiovascular risk factors. CAC, thoracic AC, and OCAD were determined by MDCT. Results: The prevalence of AC and CAC were significantly higher in OCAD patients than in controls (64% vs. 48%, p=0.019; 57% vs. 32%, p<0.001, respectively). There is a significant correlation between AC and CAC scores in the overall study population (r=0.528, p<0.001). In univariate analysis, the odds ratios (ORs) of AC and CAC in predicting OCAD were 1.91 (95% CI, 1.14-3.21) and 2.82 (95% CI, 1.67-4.78), respectively. When an adjustment was made for each other, AC did not maintain a significant association with OCAD, whereas CAC persisted the association (OR, 2.52; 95% CI, 1.42-4.47). Both AC and CAC present as compared to both absent was found to be a more potent predictor for OCAD (OR, 3.37; 95% CI 1.78-6.36, p<0.001) than CAC alone. Conclusions: The presence of AC was associated with stable OCAD independently from cardiovascular risk factors, but the association seemed to be based on the close correlation between AC and CAC. However, AC might have an incremental value with CAC for predicting OCAD.