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Abstract Background Chronic obstructive pulmonary disease (COPD) is projected to become the third cause of mortality worldwide. COPD shares several pathophysiological mechanisms with cardiovascular disease, especially atherosclerosis. However, no definite answers are available on the prognostic role of COPD in the setting of ST elevation myocardial infarction (STEMI), especially during COVID-19 pandemic, among patients undergoing primary angioplasty, that is therefore the aim of the current study. Methods In the ISACS-STEMI COVID-19 registry we included retrospectively patients with STEMI treated with primary percutaneous coronary intervention (PCI) between March and June of 2019 and 2020 from 109 high-volume primary PCI centers in 4 continents. Results A total of 15,686 patients were included in this analysis. Of them, 810 (5.2%) subjects had a COPD diagnosis. They were more often elderly and with a more pronounced cardiovascular risk profile. No preminent procedural dissimilarities were noticed except for a lower proportion of dual antiplatelet therapy at discharge among COPD patients (98.9% vs. 98.1%, P = 0.038). With regards to short-term fatal outcomes, both in-hospital and 30-days mortality occurred more frequently among COPD patients, similarly in pre-COVID-19 and COVID-19 era. However, after adjustment for main baseline differences, COPD did not result as independent predictor for in-hospital death (adjusted OR [95% CI] = 0.913[0.658–1.266], P = 0.585) nor for 30-days mortality (adjusted OR [95% CI] = 0.850 [0.620–1.164], P = 0.310). No significant differences were detected in terms of SARS-CoV-2 positivity between the two groups. Conclusion This is one of the largest studies investigating characteristics and outcome of COPD patients with STEMI undergoing primary angioplasty, especially during COVID pandemic. COPD was associated with significantly higher rates of in-hospital and 30-days mortality. However, this association disappeared after adjustment for baseline characteristics. Furthermore, COPD did not significantly affect SARS-CoV-2 positivity. Trial registration number: NCT 04412655 (2nd June 2020).

Background: During the coronavirus disease 2019 (COVID-19) pandemic, concerns have been arisen on the use of renin-angiotensin system inhibitors (RASI) due to the potentially increased expression of Angiotensin-converting-enzyme (ACE)2 and patient's susceptibility to SARS-CoV2 infection. Diabetes mellitus have been recognized favoring the coronavirus infection with consequent increase mortality in COVID-19. No data have been so far reported in diabetic patients suffering from ST-elevation myocardial infarction (STEMI), a very high-risk population deserving of RASI treatment. Methods: The ISACS-STEMI COVID-19 registry retrospectively assessed STEMI patients treated with primary percutaneous coronary intervention (PPCI) in March/June 2019 and 2020 in 109 European high-volume primary PCI centers. This subanalysis assessed the prognostic impact of chronic RASI therapy at admission on mortality and SARS-CoV2 infection among diabetic patients. Results: Our population is represented by 3812 diabetic STEMI patients undergoing mechanical reperfusion, 2038 in 2019 and 1774 in 2020. Among 3761 patients with available data on chronic RASI therapy, between those ones with and without treatment there were several differences in baseline characteristics, (similar in both periods) but no difference in the prevalence of SARS-CoV2 infection (1.6% vs 1.3%, respectively, p = 0.786). Considering in-hospital medication, RASI therapy was overall associated with a significantly lower in-hospital mortality (3.3% vs 15.8%, p

Objective: Treatment of chronic total occlusion (CTO) with everolimus-eluting bioresorbable vascular scaffold (BVS) is safe and effective at short-term follow-up (FU). The current study investigated clinical and angiographic outcomes after treatment of CTO with BVS at >1 year. Methods: Thirty patients who underwent successful recanalization of 35 CTOs were included in this study. Quantitative coronary angiography (QCA) was performed at median FU period of 402 days. Clinical endpoints analyzed included all-cause mortality, cardiac death, non-fatal target vessel myocardial infarction, target vessel revascularization (TVR), symptom-driven target lesion revascularization (TLR), and BVS thrombosis. Results: QCA analysis revealed in-scaffold minimal luminal diameter of 2.14+-0.50 mm and late lumen loss (LLL) of 0.38+-0.54 mm. One cardiac death, 5 cases with TVR, and 3 cases with TLR were detected at median FU time of 542 days. No BVS thrombosis was observed. Conclusion: The Absorb BVS was safe and effective in the treatment of CTO with acceptable LLL at mid-term FU, comparable to drug eluting stents.

Objectives. Premature myocardial infarction (PMI) is an uncommon disease, and its incidence varies between 2% and 10%, rising, depending on genetic susceptibility under the influence of lifestyle. The purpose of this study was to investigate the association between SIRT1 single nucleotide polymorphisms (SNPs), SIRT1, and eNOS (endothelial nitric oxide synthase) protein expressions, total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) in young patients with premature ST-elevation myocardial infarction (STEMI). Methods. Genotyping of the three single-nucleotide polymorphisms (rs7895833 A > G in the promoter region, rs7069102 C > G in intron 4, and rs2273773 C > T in exon 5) in SIRT1 gene was performed in 108 consecutive patients (87.0% were men with a mean age of 40.74 ± 3.82 years) suffering from ST-elevation myocardial infarction at the age of ≤45 and 91 control subjects. Results. The risk for myocardial infarction was increased by 2.31 times in carriers of CC or CG genotypes. SIRT1 protein levels were enhanced and endothelial nitric oxide synthase levels were diminished in ST-elevation myocardial infarction patients regardless of the underlying gene variant. There was no correlation between SIRT1 expression and the amount of endothelial nitric oxide synthase, total antioxidant status, total oxidant status, and oxidative stress index levels in patients and in the control group either. Conclusions. SIRT1 single-nucleotide polymorphisms were associated with premature myocardial infarction, which affected the SIRT1 and endothelial nitric oxide synthase protein expression, irrespective of the underlying SIRT1 genotype.

Resumo Fundamento O fenômeno de no-reflow coronário (CNP, do inglês Coronary no-reflow phenomenon) está associado a um risco aumentado de eventos cardiovasculares adversos maiores (ECAM). Objetivo Este estudo teve como objetivo avaliar a relação entre os níveis séricos da Molécula-1 de lesão renal (KIM-1) e o CNP em pacientes com infarto agudo do miocárdio com supradesnivelamento do segmento ST (IAMCSST). Métodos Este estudo incluiu um total de 160 pacientes (113 homens e 47 mulheres; média de idade: 61,65 ± 12,14 anos) com diagnóstico de IAMCSST. Os pacientes foram divididos em dois grupos, o grupo reflow (GR) (n = 140) e o grupo no-reflow (GNR) (n = 20). Os pacientes foram acompanhados durante um ano. Um valor de p

Objective: The present study was an investigation of the effect of statins on the expression of circulating sirtuin 1 (SIRT1) and endothelial nitric oxide synthase (eNOS) proteins, and on the distribution of single nucleotide polymorphisms (SNPs) of the SIRT1 gene in patients with a history of premature myocardial infarction (PMI). Methods: A total of 108 patients who had suffered from a premature ST-elevation myocardial infarction (STEMI) under the age of 45 years were enrolled in this study. While 79 patients had been taking statins since the index event, 29 patients had not been treated with statins post myocardial infarction (MI) or the therapy had been withdrawn at the 4-week follow-up control. The control group consisted of 91 healthy patients without a previous cardiovascular event. The levels of SIRT1 and eNOS protein; oxidative stress markers, like total antioxidant status (TAS), total oxidant status (TOS), and the oxidative stress index (OSI); as well as the distribution of the SNPs rs7069102 and rs2273773 were measured and analyzed. Results: A significant increase in the SIRT1 level (p