Herz-Kreislauf-Erkrankungen sind weltweit die häufigste Todesursache. Adipositas und Diabetes mellitus zählen zu den wichtigsten beeinflussbaren kardiovaskulären Risikofaktoren, die über chronische Entzündung, Insulinresistenz, Dyslipidämie und Gefäßschäden die Entstehung der Atherosklerose fördern. Im Mittelpunkt einer wirksamen Prävention stehen Lebensstilmaßnahmen mit Ernährungsoptimierung und regelmäßiger körperlicher Aktivität, ggf. unter Einsatz digitaler Gesundheitsanwendungen. Reichen konservative Maßnahmen nicht aus, stehen indikationsabhängig medikamentöse Therapien wie SGLT2(„sodium-glucose linked transporter 2“)-Inhibitoren oder inkretinbasierte Medikamente und die metabolische Chirurgie zur Verfügung. Ergänzend sind eine konsequente Blutdruck- und Lipidsenkung essenziell. Langfristig lässt sich das kardiovaskuläre Risiko nur durch eine individualisierte, interdisziplinäre Prävention senken, die medizinische, verhaltensbezogene und gesellschaftliche Maßnahmen miteinander verbindet.
The no-reflow prediction in acute coronary syndrome (NORPACS) risk score was developed to predict the risk of no reflow after percutaneous coronary intervention (PCI). This study sought to investigate whether the NORPACS risk score predicts the outcome of patients with ST-segment elevation myocardial infarction (STEMI) treated with primary PCI (pPCI). This retrospective study included 1725 patients. Receiver operating characteristic curve analysis revealed 6 as the optimal NORPACS risk score cut-off value. Patients were thus dichotomized into two groups: high (≥ 6) NORPACS risk score (n = 765) and low (< 6) NORPACS risk score (n = 960). The frequency of in-hospital and all-cause mortality was significantly higher in the high NORPACS risk score group than in the low NORPACS risk score group. Compared with the baseline model, in the full model of binary logistic regression, the NORPACS risk score as both a continuous and a categorical variable emerged as an independent predictor of in-hospital mortality (odds ratio [OR]: 1.61, 95
Genetic disposition for cardiovascular disease (CVD) is a major determinant of aging-related traits, such as healthspan, dementia, and frailty. While rare monogenic disorders provide important mechanistic insights, most CVDs and aging-related traits are driven by the cumulative effects of numerous common genetic variants, resulting in a polygenic risk architecture. Analyses of genes and pathways affected by these variants revealed significant correlations in the genetic architectures of CVD and aging, which appear to promote each other bidirectionally. Thus, CVD and aging share common genetic mechanisms, linking inherited cardiovascular risk to frailty, dementia, reduced healthspan, and shortened lifespan—and, conversely, explaining why aging is the strongest risk factor for atherosclerosis. Advances in genome-wide association studies have also enabled the construction of a polygenic risk score (PRS), which quantifies inherited CVD risk and facilitates early risk stratification beyond conventional clinical assessment. Importantly, individuals at high polygenic risk for CVD derive greater benefit from preventive strategies, which reduce their lifelong burden of CVD risk and ultimately promote healthy aging. Therefore, personalizing clinical risk assessment by integrating genetic testing for both CVD and aging-related traits may be of clinical importance. Specifically, lifestyle modification and preventive therapies based not only on conventional risk assessment, but also on polygenic risks may offer an individualized life-course approach for precision prevention, shifting cardiovascular care from reactive disease management toward the promotion of healthy aging.
Extracorporeal cardiopulmonary resuscitation (ECPR) has emerged as a rescue strategy for selected patients with refractory cardiac arrest. However, identifying patients most likely to achieve neurologically meaningful survival remains challenging. Conventional selection criteria, including age, initial rhythm, witnessed arrest, bystander cardiopulmonary resuscitation (CPR), and no-flow and low-flow duration, are clinically useful but may be insufficient when interpreted as isolated thresholds. We conducted a narrative review of contemporary evidence on ECPR patient selection, incorporating randomized trials, observational studies, registries, systematic reviews and meta-analyses, and current guideline and consensus recommendations. Evidence was critically evaluated with particular attention to patient-level prognostic factors, arrest setting, dynamic physiological and metabolic variables, ECPR logistics, and system-level determinants of outcome. Current evidence supports a multidimensional rather than single-variable approach to ECPR candidacy. Favorable arrest characteristics, potentially reversible etiology, shorter low-flow duration, and preserved physiological reserve remain important; however, chronological low-flow time should be interpreted alongside the quality and effectiveness of ongoing CPR. Dynamic information—including transient return of spontaneous circulation, lactate kinetics, arterial pH, end-tidal carbon dioxide, and hemodynamic parameters—may further refine assessment of biological viability. Frailty, comorbidity burden, cerebral perfusion, and extracorporeal membrane oxygenation-related contraindications should also be incorporated into decision-making. Importantly, selection cannot be separated from system performance: Cannulation strategy, transport logistics, institutional experience, and the ability to establish extracorporeal circulation rapidly may substantially modify the likelihood of benefit. Differences between out-of-hospital and in-hospital cardiac arrest further limit the universal application of rigid eligibility criteria. Candidacy for ECPR should be viewed as a dynamic, probability-based assessment rather than a checklist of fixed thresholds. Integrating arrest characteristics, reversibility, evolving physiology, patient reserve, and system capability may provide a more clinically meaningful framework for identifying patients most likely to achieve neurologically favorable survival after ECPR.
Age is the strongest risk factor for cardiovascular disease, yet biological aging is increasingly recognized as a modifiable process. Animal studies over the past few decades have demonstrated that genetic, pharmacological, and dietary interventions can extend the healthspan and lifespan of animals by targeting conserved mechanisms of aging. Examining whether lifespan-extending interventions work in humans is challenging due to the long lifespan of our species. However, the development of biomarkers of biological aging or “aging clocks” has allowed for human trials where the rate of biological aging can be estimated. These surrogate markers now enable the first generation of human geroscience trials, in which interventions such as caloric restriction, rapamycin, taurine, plasma exchange, or nutritional strategies are evaluated for their ability to slow biological aging. Particularly relevant for cardiology are recently developed organ- and cell-specific aging clocks that estimate the biological age of the heart, vasculature, and cardiovascular cell types. These biomarkers may be suitable for improving cardiovascular risk prediction and providing surrogate outcomes for trials targeting cardiovascular aging. Together, these advances suggest that slowing biological aging could complement established cardiovascular prevention and treatment strategies in the future.
