Obstructive sleep apnea (OSA) causes recurrent apneas due to upper respiratory tract collapse, leading to sympathetic nervous system hyperactivation and increased cardiovascular risk. Moderate and severe forms of obstructive sleep apnea are associated with increased atrial volumes and affect left ventricular diastolic and then systolic function. Right ventricular ejection fraction can be accurately assessed via three-dimensional echocardiography, while bidimensional imaging can only provide a set of surrogate parameters to characterize systolic function (tricuspid annulus plane systolic excursion, right ventricular fractional area change, and lateral S’). Tissue Doppler imaging is a more sensitive tool in detecting functional ventricular impairment, but its use is limited by angle dependence and the unwanted influence of tethering forces. Two-dimensional speckle tracking echocardiography is considered more suitable for the assessment of ventricular function, as it is able to distinguish between active and passive wall motion. Abnormal strain values, a marker of subclinical myocardial dysfunction, can be detected even in patients with normal ejection fraction and chamber volumes. The left ventricular longitudinal strain is more affected by the presence of obstructive sleep apnea than circumferential strain values. Although the observed OSA-induced changes are subtle, the benefit of a detailed echocardiographic screening for subclinical heart failure in OSA patients on therapy adherence and outcome should be addressed by further studies.

The presence of a myocardial infarction at a younger age is of special interest, considering the psychological and socioeconomic impact, as well as long-term morbidity and mortality. However, this group has a unique risk profile, with less traditional cardiovascular risk factors that are not well studied. This systematic review aims to evaluate traditional risk factors of myocardial infarction in the “young”, highlighting the clinical implications of lipoprotein (a). We performed a comprehensive search using Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) standards; we systematically searched the PubMed, EMBASE, and Science Direct Scopus databases, using the terms: “myocardial infarction”, “young”, “lipoprotein (a)”, “low-density lipoprotein”, “risk factors”. The search identified 334 articles which were screened, and, at the end, 9 original research articles regarding the implications of lipoprotein (a) in myocardial infarction in the “young” were included in the qualitative synthesis. Elevated lipoprotein (a) levels were independently associated with an increased risk of coronary artery disease, especially in young patients, where this risk increased by threefold. Thus, it is recommended to measure the lipoprotein (a) levels in individuals with suspected familial hypercholesterolaemia or with premature atherosclerotic cardiovascular disease and no other identifiable risk factors, in order to identify patients who might benefit from a more intensive therapeutic approach and follow-up.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for the ongoing global coronavirus (COVID-19) pandemic. Although initially viewed as an acute respiratory illness, COVID-19 is clearly a complex multisystemic disease with extensive cardiovascular involvement. Emerging evidence shows that the endothelium plays multiple roles in COVID-19 physiopathology, as both a target organ that can be directly infected by SARS-CoV-2 and a mediator in the subsequent inflammatory and thrombotic cascades. Arterial stiffness is an established marker of cardiovascular disease. The scope of this review is to summarize available data on the acute and long-term consequences of COVID-19 on vascular function. COVID-19 causes early vascular aging and arterial stiffness. Fast, noninvasive bedside assessment of arterial stiffness could optimize risk stratification in acute COVID-19, allowing for early escalation of treatment. Vascular physiology remains impaired at least 12 months after infection with SARS-CoV-2, even in otherwise healthy adults. This raises concerns regarding the extent of arterial remodeling in patients with preexisting vascular disease and the potential development of a persistent, chronic COVID-19 vasculopathy. Long-term follow up on larger cohorts is required to investigate the reversibility of COVID-19-induced vascular changes and their associated prognostic implications.

Sustained physical activity induces morphological and functional changes in the cardiovascular system. While mostly physiological, they can also become a trigger for major adverse cardiovascular events, the most severe of which are sudden cardiac arrest and sudden cardiac death. Therefore, any novel method which can help more accurately estimate the cardiovascular risk should be considered for further studying and future implementation in the standard protocols. The study of biomarkers is gaining more and more ground as they have already established their utility in diagnosing ischemic cardiac disease or in evaluating cardiac dysfunction in patients with heart failure. Nowadays, they are being implemented in the screening of apparently healthy individuals for the assessment of the cardiovascular risk. The aim of this paper is to gather published data regarding the measurements of cardiac biomarkers in athletes, i.e., troponins, myoglobin, CK-MB, NT-proBNP, and D-Dimers, and their potential use in the field of sports cardiology.

Background and Objectives: Functional capacity (FC) assessed via cardiopulmonary exercise testing (CPET) is a novel, independent prognostic marker for patients with coronary artery disease (CAD). Neutrophil to lymphocyte ratio (NLR) and platelet to lymphocyte ratio (PLR) are two readily available predictors of systemic inflammation and cardiovascular event risk, which could be used as cost-effective predictors of poor FC. The purpose of this study was to evaluate the utility of NLR and PLR in predicting poor FC in patients with CAD and recent elective percutaneous coronary intervention (PCI). Materials and Methods: Our cross-sectional retrospective analysis included 80 patients with stable CAD and recent elective PCI (mean age 55.51 ± 11.83 years, 71.3% male) who were referred to a cardiovascular rehabilitation center from January 2020 to June 2021. All patients underwent clinical examination, cardiopulmonary exercise testing on a cycle ergometer, transthoracic echocardiography and standard blood analysis. Results: Patients were classified according to percent predicted oxygen uptake (% VO2 max) in two groups—poor FC (≤70%, n = 35) and preserved FC (>70%, n = 45). There was no significant difference between groups regarding age, gender ratio, presence of associated comorbidities, left ventricular ejection fraction and NLR. PLR was higher in patients with poor FC (169.8 ± 59.3 vs. 137.4 ± 35.9, p = 0.003). A PLR cut-off point of 139 had 74% sensitivity and 60% specificity in predicting poor FC. After multivariate analysis, PLR remained a significant predictor of poor functional status. Conclusions: Although CPET is the gold standard test for assessing FC prior to cardiovascular rehabilitation, its availability remains limited. PLR, a cheap and simple test, could predict poor FC in patients with stable CAD and recent elective PCI and help prioritize referral for cardiovascular rehabilitation in high-risk patients.

Obstructive sleep apnea (OSA) is characterized by repetitive upper airway collapse, chronic hypoxia and a proinflammatory phenotype. The purpose of our study was to evaluate readily available inflammatory biomarkers (C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), white blood cell count (WBC), red cell distribution width (RDW), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), mean platelet volume (MPV), WBC-to-MPV ratio (WMR) and lymphocyte-to-C-reactive protein ratio (LCR)) before and after CPAP in patients with moderate–severe OSA. We performed a prospective study that included patients with newly-diagnosed moderate–severe OSA. The control groups (patients without OSA and with mild OSA) were selected from the hospital polygraphy database. All subjects underwent routine blood panel, which was repeated in moderate–severe OSA patients after 8 weeks of CPAP. Our final study group included 31 controls, 33 patients with mild, 22 patients with moderate and 37 patients with severe OSA. CRP, ESR, NLR and WMR were correlated with OSA severity. After 8-week CPAP therapy, we documented a decrease in weight status, which remained statistically significant in both CPAP-adherent and non-adherent subgroups. Readily available, inexpensive inflammatory parameters can predict the presence of moderate–severe OSA, but are not influenced by short-term CPAP.