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Unrecognized myocardial infarction (MI) is an MI that remains undetected in the acute phase and is associated with an unfavourable prognosis. With this systematic review and meta-analysis, we evaluated the burden of cardiovascular risk factors in individuals with unrecognized MI. We searched general population-based cohort studies diagnosing unrecognized MI by electrocardiogram or myocardial imaging up to 24 November 2023. Pooled mean differences (MDs) or risk ratios (RRs) with 95% confidence intervals (CIs) were determined, and random-effects meta-analyses were performed. Fourteen cohort studies were included involving 200 450 individuals (mean age 62.8 ± 9.9 years, 56.0% women), among which 4322 (2.2%) experienced unrecognized MI (mean age 66.3 ± 8.2 years, 47.8% women) and 4653 (2.1%) recognized MI (mean age 68.5 ± 7.3 years, 33.8% women). Compared to individuals without MI, those with unrecognized MI had higher body mass index (MD 0.27, 95% CI 0.16–0.39) and systolic blood pressure (MD 4.48, 95% CI 2.81–6.15) levels, and higher prevalence of hypertension (RR 1.27, 95% CI 1.06–1.51) and diabetes mellitus (RR 1.67, 95% CI 1.36–2.06). Furthermore, individuals with unrecognized MI had lower prevalence of hypertension (RR 0.92, 95% CI 0.88–0.97) and diabetes mellitus (RR 0.80, 95% CI 0.70–0.92). Individuals with unrecognized MI are characterized by a substantial burden of metabolic risk factors. Our findings suggest insufficient recognition and management of cardiovascular risk factors among individuals with unrecognized MI. [ABSTRACT FROM AUTHOR]

This article discusses the challenges in identifying vulnerable atherosclerotic plaques that can cause myocardial infarctions. The concept of the "vulnerable plaque" originated in the 1980s and refers to plaque rupture and plaque erosion as the main mechanisms of myocardial infarction. The authors propose using plasma cell-free DNA methylation as a potential non-invasive biomarker to detect plaque-specific methylation signatures in patients at risk for myocardial infarction. They aim to develop a polymerase chain reaction (PCR)-based assay to quantify DNA methylation and assess its performance compared to whole genome methylation sequencing. The successful implementation of a plaque biomarker could greatly impact healthcare by enabling targeted detection of dangerous plaques in both men and women. [Extracted from the article]

Ischaemic heart disease (IHD) is a complex disorder and a leading cause of death and morbidity in both men and women. Sex, however, affects several aspects of IHD, including pathophysiology, incidence, clinical presentation, diagnosis as well as treatment and outcome. Several diseases or risk factors frequently associated with IHD can modify cellular signalling cascades, thus affecting ischaemia/reperfusion injury as well as responses to cardioprotective interventions. Importantly, the prevalence and impact of risk factors and several comorbidities differ between males and females, and their effects on IHD development and prognosis might differ according to sex. The cellular and molecular mechanisms underlying these differences are still poorly understood, and their identification might have important translational implications in the prediction or prevention of risk of IHD in men and women. Despite this, most experimental studies on IHD are still undertaken in animal models in the absence of risk factors and comorbidities, and assessment of potential sex-specific differences are largely missing. This ESC WG Position Paper will discuss: (i) the importance of sex as a biological variable in cardiovascular research, (ii) major biological mechanisms underlying sex-related differences relevant to IHD risk factors and comorbidities, (iii) prospects and pitfalls of preclinical models to investigate these associations, and finally (iv) will provide recommendations to guide future research. Although gender differences also affect IHD risk in the clinical setting, they will not be discussed in detail here. [ABSTRACT FROM AUTHOR]

Aims The effects of testosterone on cardiovascular disease (CVD) as reported in literature have been ambiguous. Recently, the interplay between testosterone and oestradiol as assessed by testosterone/oestradiol (T/E2) ratio was suggested to be better informative on the normal physiological balance. Considering the role in CVD, we hypothesized that a low T/E2 ratio in men with CVD is associated with increased inflammation, a more unstable plaque and a worse cardiovascular outcome. Methods and results Testosterone and oestradiol concentrations were determined in blood samples of 611 male carotid endarterectomy patients included in the Athero-Express Biobank Study. T/E2 ratio was associated with baseline characteristics, atherosclerotic plaque specimens, inflammatory biomarkers, and 3 year follow-up information. Patients with low T/E2 ratio had more unfavourable inflammatory profiles compared with patients with high T/E2 as observed by higher levels of C-reactive protein [2.81 μg/mL vs. 1.22 μg/mL (P  < 0.001)] and higher leucocyte counts [8.98*109/L vs. 7.75*109/L (P  = 0.001)] in blood. In atherosclerotic plaques, a negative association between T/E2 ratio and number of neutrophils [ B = −0.366 (P  = 0.012)], plaque calcifications [OR: 0.816 (P  = 0.044)], interleukin-6 (IL-6) [ B = −0.15 (P  = 0.009)], and IL-6 receptor [ B = −0.13 (P  = 0.024)] was found. Furthermore, in multivariate Cox regression analysis, low T/E2 ratio was independently associated with an increased risk for major cardiovascular events (MACE) during 3 year follow-up [hazard ratio 1.67 (95% confidence interval 1.02–2.76), P  = 0.043]. In men with elevated body mass index (BMI), these effects were strongest. Conclusion In male patients with manifest atherosclerotic disease, low T/E2 ratio was associated with increased systemic inflammation, increased inflammatory plaque proteins, and an increased risk of future MACE as compared to men with normal T/E2 ratio. These effects are strongest in men with elevated BMI and are expected to be affected by aromatase activity in white fat tissues. Normalization of T/E2 ratio may be considered as target for the secondary prevention of CVD in men. [ABSTRACT FROM AUTHOR]

Aims Epidemiological evidence indicates a protective effect of light to moderate alcohol consumption compared to non-drinking and heavy drinking. Although several mechanisms have been suggested, the effect of alcohol on atherosclerotic changes in vessel walls is unclear. Therefore, we explored the relationship between alcohol consumption and common carotid intima media thickness, a marker of early atherosclerosis in the general population. Methods Individual participant data from eight cohorts, involving 37,494 individuals from the USE-IMT collaboration were used. Multilevel age and sex adjusted linear regression models were applied to estimate mean differences in common carotid intima-media thickness (CIMT) with alcohol consumption. Results The mean age was 57.9 years (SD 8.6) and the mean CIMT was 0.75 mm (SD 0.177). About, 40.5% reported no alcohol consumed, and among those who drank, mean consumption was 13.3 g per day (SD 16.4). Those consuming no alcohol or a very small amount (<5 g per day) had significantly lower common CIMT values than those consuming >10 g per day, after adjusting for a range of confounding factors. Conclusion In this large CIMT consortium, we did not find evidence to support a protective effect of alcohol on CIMT. [ABSTRACT FROM AUTHOR]

Background: In patients with established cardiovascular disease, high levels of the extracellular vesicle (EV)-derived proteins cystatin C, CD14, and α2-antiplasmin predict recurrent cardiovascular events. We examined whether these proteins are associated with the extent of vascular disease., Methods: In 1062 patients from the SMART (Secondary Manifestations in ARTerial disease) study, EVs were isolated from plasma at baseline. Cystatin C, CD14, and α2-antiplasmin were measured in these vesicles using a multiplex assay. The extent of vascular disease burden was determined by a sum score that incorporates history and current presence of clinically manifest coronary, cerebrovascular, peripheral arterial, and abdominal aneurysm disease, and parameters of atherosclerosis that were assessed during the SMART screening protocol (ankle-brachial index, common carotid intima-media thickness, carotid stenosis, and aorta diameter). The relation between EV protein levels and extent of vascular disease was evaluated using ordinal multivariable regression models., Results: EV-derived CD14 was significantly associated with the number of affected vascular territories (OR 2.4, 95% CI 1.4-4.1) as represented by the sum score, independently of cardiovascular risk factors. Cystatin C and α2-antiplasmin EV levels did not show an independent association with vascular disease extent. When investigating parameters of the sum score separately, we did not observe a strong association between any of the EV-derived proteins and the markers of atherosclerosis., Conclusions: EV-derived CD14 levels are strongly correlated to the extent of vascular disease, but not specifically to markers that reflect atherosclerosis burden, in patients with manifest cardiovascular disease., (© The European Society of Cardiology 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav.)