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Background Post-infarction cardiovascular remodeling and heart failure are the leading cause of myocardial infarction (MI)-driven death during the past decades. Experimental observations have involved intestinal microbiota in the susceptibility to MI in mice; however, in humans, identifying whether translocation of gut bacteria to systemic circulation contributes to cardiovascular events post-MI remains a major challenge. Results Here, we carried out a metagenomic analysis to characterize the systemic bacteria in a cohort of 49 healthy control individuals, 50 stable coronary heart disease (CHD) subjects, and 100 ST-segment elevation myocardial infarction (STEMI) patients. We report for the first time higher microbial richness and diversity in the systemic microbiome of STEMI patients. More than 12% of post-STEMI blood bacteria were dominated by intestinal microbiota ( Lactobacillus , Bacteroides , and Streptococcus ). The significantly increased product of gut bacterial translocation (LPS and d -lactate) was correlated with systemic inflammation and predicted adverse cardiovascular events. Following experimental MI, compromised left ventricle (LV) function and intestinal hypoperfusion drove gut permeability elevation through tight junction protein suppression and intestinal mucosal injury. Upon abrogation of gut bacterial translocation by antibiotic treatment, both systemic inflammation and cardiomyocyte injury in MI mice were alleviated. Conclusions Our results provide the first evidence that cardiovascular outcomes post-MI are driven by intestinal microbiota translocation into systemic circulation. New therapeutic strategies targeting to protect the gut barrier and eliminate gut bacteria translocation may reduce or even prevent cardiovascular events post-MI.

Moderately elevated blood levels of homocysteine are weakly correlated with coronary heart disease (CHD) risk, but causality remains uncertain. When folate levels are low, the TT genotype of the common C677T polymorphism (rs1801133) of the methylene tetrahydrofolate reductase gene (MTHFR) appreciably increases homocysteine levels, so \"Mendelian randomization\" studies using this variant as an instrumental variable could help test causality. Nineteen unpublished datasets were obtained (total 48,175 CHD cases and 67,961 controls) in which multiple genetic variants had been measured, including MTHFR C677T. These datasets did not include measurements of blood homocysteine, but homocysteine levels would be expected to be about 20% higher with TT than with CC genotype in the populations studied. In meta-analyses of these unpublished datasets, the case-control CHD odds ratio (OR) and 95% CI comparing TT versus CC homozygotes was 1.02 (0.98-1.07; p = 0.28) overall, and 1.01 (0.95-1.07) in unsupplemented low-folate populations. By contrast, in a slightly updated meta-analysis of the 86 published studies (28,617 CHD cases and 41,857 controls), the OR was 1.15 (1.09-1.21), significantly discrepant (p = 0.001) with the OR in the unpublished datasets. Within the meta-analysis of published studies, the OR was 1.12 (1.04-1.21) in the 14 larger studies (those with variance of log OR<0.05; total 13,119 cases) and 1.18 (1.09-1.28) in the 72 smaller ones (total 15,498 cases). The CI for the overall result from large unpublished datasets shows lifelong moderate homocysteine elevation has little or no effect on CHD. The discrepant overall result from previously published studies reflects publication bias or methodological problems.

Evidence indicates that the densely cultivated region of northeastern China acts as a source for the wind-borne agent of Kawasaki disease (KD). KD is an acute, coronary artery vasculitis of young children, and still a medical mystery after more than 40 y. We used residence times from simulations with the flexible particle dispersion model to pinpoint the source region for KD. Simulations were generated from locations spanning Japan from days with either high or low KD incidence. The postepidemic interval (1987–2010) and the extreme epidemics (1979, 1982, and 1986) pointed to the same source region. Results suggest a very short incubation period (<24 h) from exposure, thus making an infectious agent unlikely. Sampling campaigns over Japan during the KD season detected major differences in the microbiota of the tropospheric aerosols compared with ground aerosols, with the unexpected finding of the Candida species as the dominant fungus from aloft samples (54% of all fungal strains). These results, consistent with the Candida animal model for KD, provide support for the concept and feasibility of a windborne pathogen. A fungal toxin could be pursued as a possible etiologic agent of KD, consistent with an agricultural source, a short incubation time and synchronized outbreaks. Our study suggests that the causative agent of KD is a preformed toxin or environmental agent rather than an organism requiring replication. We propose a new paradigm whereby an idiosyncratic immune response, influenced by host genetics triggered by an environmental exposure carried on winds, results in the clinical syndrome known as acute KD.

BackgroundWe tested whether objectively measured indices of obstructive sleep apnoea (OSA) and sleep quality are associated with coronary artery calcification (CAC) prevalence independent of obesity, a classic confounder.Methods1465 Multi-Ethnic Study of Atherosclerosis participants (mean age 68 years), who were free of clinical cardiovascular disease, had both coronary CT and in-home polysomnography and actigraphy performed. OSA categories were defined by the Apnea-Hypopnea Index (AHI). Prevalence ratios (PRs) for CAC >0 and >400 (high burden) were calculated.ResultsParticipants with severe OSA (AHI ≥30; 14.6%) were more likely to have prevalent CAC, relative to those with no evidence of OSA, after adjustment for demographics and smoking status (PR 1.16; 95% CI 1.06 to 1.26), body mass index (1.11; 1.02 to 1.21) and traditional cardiovascular risk factors (1.10; 1.01 to 1.19). Other markers of hypoxaemia tended to be associated with a higher prevalence of CAC >0. For CAC >400, a higher prevalence was observed with both a higher arousal index and less slow-wave sleep. Overall, associations were somewhat stronger among younger participants, but did not vary by sex or race/ethnicity.ConclusionsIn this population-based multi-ethnic sample, severe OSA was associated with subclinical coronary artery disease (CAC >0), independent of obesity and traditional cardiovascular risk factors. Furthermore, the associations of the arousal index and slow-wave sleep with high CAC burden suggest that higher nightly sympathetic nervous system activation is also a risk factor. These findings highlight the potential importance of measuring disturbances in OSA as well as sleep fragmentation as possible risk factors for coronary artery disease.

Human pluripotent stem cell-derived cardiomyocytes (CMs) are a promising tool for cardiac cell therapy. Although transplantation of induced pluripotent stem cell (iPSC)-derived CMs have been reported in several animal models, the treatment effect was limited, probably due to poor optimization of the injected cells. To optimize graft cells for cardiac reconstruction, we compared the engraftment efficiency of intramyocardially-injected undifferentiated-iPSCs, day4 mesodermal cells and day8, day20 and day30 purified iPSC-CMs after initial differentiation by tracing the engraftment ratio (ER) using in vivo bioluminescence imaging. This analysis revealed the ER of day20 CMs was significantly higher compared to other cells. Transplantation of day20 CMs into the infarcted hearts of immunodeficient mice showed good engraftment and echocardiography showed significant functional improvement by cell therapy. Moreover, the imaging signal and ratio of Ki67-positive CMs at 3 months post injection indicated engrafted CMs proliferated in the host heart. Although this graft growth reached a plateau at 3 months, histological analysis confirmed progressive maturation from 3 to 6 months. These results suggested that day20 CMs had very high engraftment, proliferation and therapeutic potential in host mouse hearts. They also demonstrate this model can be used to track the fate of transplanted cells over a long time.

Educational attainment is widely used as a surrogate for socioeconomic status (SES). Low SES is a risk factor for hypertension and high blood pressure (BP). To identify novel BP loci, we performed multi-ancestry meta-analyses accounting for gene-educational attainment interactions using two variables, “Some College” (yes/no) and “Graduated College” (yes/no). Interactions were evaluated using both a 1 degree of freedom (DF) interaction term and a 2DF joint test of genetic and interaction effects. Analyses were performed for systolic BP, diastolic BP, mean arterial pressure, and pulse pressure. We pursued genome-wide interrogation in Stage 1 studies (N = 117 438) and follow-up on promising variants in Stage 2 studies (N = 293 787) in five ancestry groups. Through combined meta-analyses of Stages 1 and 2, we identified 84 known and 18 novel BP loci at genome-wide significance level (P < 5 × 10-8). Two novel loci were identified based on the 1DF test of interaction with educational attainment, while the remaining 16 loci were identified through the 2DF joint test of genetic and interaction effects. Ten novel loci were identified in individuals of African ancestry. Several novel loci show strong biological plausibility since they involve physiologic systems implicated in BP regulation. They include genes involved in the central nervous system-adrenal signaling axis (ZDHHC17, CADPS, PIK3C2G), vascular structure and function (GNB3, CDON), and renal function (HAS2 and HAS2-AS1, SLIT3). Collectively, these findings suggest a role of educational attainment or SES in further dissection of the genetic architecture of BP.

Background Coronary heart disease (CHD) mortality rates have been decreasing in Turkey since the early 1990s. Our study aimed to determine how much of the CHD mortality decrease in Turkey between 1995 and 2008 could be attributed to temporal trends in major risk factors and how much to advances in medical and surgical treatments. Methods The validated IMPACT CHD mortality model was used to combine and analyse data on uptake and effectiveness of CHD treatments and risk factor trends in Turkey in adults aged 35–84 years between 1995 and 2008. Data sources were identified, searched and appraised on population, mortality and major CHD risk factors for adults those aged 35–84 years. Official statistics, electronic databases, national registers, surveys and published trials were screened from 1995 onwards. Results Between 1995 and 2008, coronary heart disease mortality rates in Turkey decreased by 34% in men and 28% in women 35 years and over. This resulted in 35,720 fewer deaths in 2008. Approximately 47% of this mortality decrease was attributed to treatments in individuals (including approximately 16% to secondary prevention, 3% angina treatments, 9% to heart failure treatments, 5% to initial treatments of acute myocardial infarction, and 5% to hypertension treatments) and approximately 42% was attributable to population risk factor reductions (notably blood pressure 29%; smoking 27%; and cholesterol 1%). Adverse trends were seen for obesity and diabetes (potentially increasing mortality by approximately 11% and 14% respectively). The model explained almost 90% of the mortality fall. Conclusion Reduction in major cardiovascular risk factors explained approximately 42% and improvements in medical and surgical treatments explained some 47% of the CHD mortality fall. These findings emphasize the complimentary value of primary prevention and evidence-based medical treatments in controlling coronary heart disease.

To study the incidence and structure of periodontal disease in elderly Moscow residents suffering from permanent coronary heart disease, as well as examine the oral cavity and tooth structure in patients with generalized periodontitis and coronary heart disease. Stage 1 (studying the incidence and structure of periodontal diseases) enrolled 330 patients over 50 years old: Group 1 consisted of 180 patients (102 males and 78 females) with stable coronary heart disease; Group 2 consisted of 150 dental patients (90 males and 60 females) with periodontal pathology without associated coronary heart disease. Stage 2 enrolled 216 patients with generalized periodontitis (studying features of the generalized periodontitis course depending on the coronary heart disease presence): Group 1 consisted of 145 patients with coronary heart disease and generalized periodontitis (79 males and 66 females), Group 2 consisted of 71 patients with generalized periodontitis but without coronary heart disease (40 males and 31 females). It has been established that 172 (95.6%) patients with coronary heart disease had periodontal disease with a predominance of generalized periodontitis in its structure, present in 145 (84.3%) people with coronary heart disease. A more severe clinical course distinguishes generalized periodontitis in patients with coronary heart disease than those without comorbid coronary heart disease. Moreover, it is characterized by a higher mean number of tooth loss (6.21±0.16 vs 4.83±0.12 teeth, p <0.05), more teeth defects (54.69±2.25% vs 21.15±1.27%, p <0.05), higher caries intensity level (11.07±0.32 vs 8.55±0.41, p < 0,05), clinical attachment loss (5.76±0.09 mm vs 4.85±0.10 mm, p < 0.05), and greater depth of periodontal pockets (4.80±0.17 mm vs 3.64±0.21 mm, p < 0.05). Coronary heart disease is a favorable prerequisite for the development and progression of periodontal pathology.

Patients with chronic obstructive pulmonary disease complicated with coronary heart disease are a major public health problem, but it has not been widely accepted by the public or health professionals, the purpose of this study is to conduct a meta-analysis of the literature reports on the risk of coronary heart disease in patients with chronic obstructive pulmonary disease. Data sources are PubMed and Web of Science searched up to August 2021. Design is meta-analysis. Literature searches yielded 8877 records, meta-analysis showed that the risk of coronary heart disease in chronic obstructive pulmonary disease patients was 1.24 times higher than that in non-chronic obstructive pulmonary disease patients (HR=1.24,95% CL 1.16-1.32). The findings suggest that patients with chronic obstructive pulmonary disease are at a higher risk of developing coronary heart disease than non-chronic obstructive pulmonary disease patients.

Background： Patients with premature triple-vessel disease （PTVD） have a higher risk of recurrent coronary events and repeat revascularization： however, the long-term outcome of coronary artery bypass grafting （CABG）, percutaneous coronary intervention （PCI）, and medical therapy （MT） alone for PTVD patients is controversial. The aim of this study is to evaluate the long-term outcome of PTVD patients among these three treatment strategies, to find out the most appropriate treatment methods lbr these patients. Methods： One thousand seven hundred and ninety-two patients with PTVD （age： men 〈50 years and women _〈60 years） were enrolled between 2004 and 2011. The primary end point was all-cause death. The secondary end points were cardiac death, myocardial infarction, stroke, or repeat revascularization. Results： PCI, CABG, and MT alone were performed in 933 （52.1%）, 459 （25.6%）, and 400 （22.3%） patients. Both PCI and CABG were associated with lower all-cause death （4.6% vs. 4.1% vs. 15.5%, respectively, P 〈 0.01） and cardiac death （2.8% vs. 2.0% vs. 9.8%, respectively, P 〈 0.01 ） versus MT alone. The rate of repeat revascularization in the CABG group was significantly lower than those in the PCI and MT groups. After adjusting for baseline factors, PCI and CABG were still associated with similar lower risk of all-cause death and cardiac death versus MT alone （all-cause death： hazard ratio [HR]： 0.35, 95% confidence interval [CI]： 0.23-0.53, P 〈 0.01 and HR： 0.35, 95% CI： 0.18-0.70, P= 0.003, respectively, and cardiac death： HR： 0.32, 95% CI： 0.19-0.54, P〈 0.01 and HR： 0.36, 95% CI：0.14-0.93, P = 0.03, respectively）. Conclusions： PCI and CABG provided equal long-term benefits for all-cause death and cardiac death for PTVD patients. Patients undergoing MT alone had the worst long-term clinical outcomes.