Santiago Alberto Avila Ak

Arrhythmias and sudden cardiac death represent major challenges in sports cardiology because they may occur in apparently healthy athletes and may be related to structural heart disease, inherited channelopathies, coronary abnormalities, myocarditis, or other arrhythmogenic substrates. This study analyzed the principal factors associated with sudden cardiac death in athletes, with emphasis on cardiovascular preparticipation evaluation, electrocardiographic interpretation, characterization of ventricular arrhythmias, and perioperative cardiovascular management. An integrative review and analytical synthesis of clinical guidelines, consensus statements, epidemiological studies, systematic reviews, and relevant observational investigations was performed using evidence from recognized scientific databases and international cardiovascular societies. The findings demonstrated that sudden cardiac death is uncommon overall but is heterogeneously distributed, with higher incidence reported in specific groups such as male athletes, Black athletes, and Division I male basketball players. Hypertrophic cardiomyopathy, congenital coronary artery anomalies, myocarditis, arrhythmogenic cardiomyopathy, and inherited electrical disorders were identified among the principal underlying conditions. Athlete-specific electrocardiographic criteria reduced abnormal classifications while preserving the detection of clinically significant cardiovascular disease. The analysis of ventricular ectopy showed that morphology, complexity, exercise response, symptoms, and the presence of structural abnormalities are more clinically informative than arrhythmic burden alone. In the perioperative setting, high functional capacity does not eliminate cardiovascular risk, particularly in athletes with known or suspected arrhythmogenic substrates. Electrolyte disturbances, autonomic fluctuations, anesthetic agents, hypoxemia, hemodynamic changes, and surgical stress may facilitate perioperative rhythm disturbances. The evidence supports an integrated and individualized strategy combining preparticipation screening, targeted diagnostic testing, arrhythmic risk stratification, shared decision-making, and perioperative planning. This approach may improve the identification of high-risk athletes while avoiding unnecessary restrictions and promoting safer participation in sport and surgical care.

Cardiovascular multimorbidity in young adults is an increasingly relevant clinical and public health concern because multiple cardiovascular, metabolic, renal, behavioral, and psychosocial risk factors may coexist long before overt cardiovascular disease becomes clinically evident. This study analyzed the emerging burden of cardiovascular multimorbidity in young adults, emphasizing conventional and emerging risk factors, early detection strategies, and population-level consequences. An integrative literature review was conducted using recent epidemiological studies, prospective cohorts, systematic reviews, scientific statements, and contemporary cardiovascular risk frameworks. The evidence showed that obesity, dyslipidemia, hypertension, impaired glucose metabolism, nicotine exposure, physical inactivity, poor sleep, and psychosocial factors frequently cluster during early adulthood. Additional markers such as apolipoprotein B, lipoprotein(a), renal dysfunction, central adiposity, and cumulative low-density lipoprotein cholesterol exposure may provide complementary information regarding long-term cardiovascular vulnerability. The findings also demonstrated that short-term cardiovascular risk estimates may underestimate the lifetime impact of prolonged exposure to multiple risk factors in younger individuals. Early detection therefore requires a multidimensional approach integrating clinical, anthropometric, laboratory, behavioral, familial, and social information. From a population perspective, the early onset of multimorbidity may increase future cardiovascular events, chronic healthcare utilization, premature disability, and economic burden. A life-course approach to cardiovascular prevention, focused on early recognition and reduction of cumulative risk exposure, may improve long-term cardiovascular health and limit progression toward established cardiovascular disease.

Cardiovascular disease remains the leading cause of mortality worldwide despite substantial advances in lipid-lowering therapies. Although achieving recommended low-density lipoprotein cholesterol (LDL-C) targets significantly reduces cardiovascular risk, many patients continue to experience recurrent cardiovascular events, a phenomenon known as residual cardiovascular risk. Increasing evidence indicates that chronic low-grade inflammation is a major contributor to this persistent risk. This review analyzes current scientific evidence regarding the biological mechanisms, inflammatory biomarkers, and emerging therapeutic strategies associated with residual inflammatory risk beyond LDL cholesterol. The literature demonstrates that activation of the NLRP3 inflammasome and the interleukin-1β/interleukin-6 pathway plays a central role in endothelial dysfunction, plaque progression, and atherosclerotic instability. High-sensitivity C-reactive protein (hs-CRP) remains the most widely validated biomarker for identifying persistent inflammatory activity in clinical practice. Landmark clinical trials, including CANTOS, COLCOT, and LoDoCo2, have demonstrated that selective anti-inflammatory therapies reduce recurrent cardiovascular events independently of additional LDL-C lowering, whereas nonspecific anti-inflammatory approaches have shown limited benefit. Furthermore, obesity, type 2 diabetes mellitus, metabolic syndrome, and chronic kidney disease substantially amplify residual inflammatory risk through shared pathophysiological mechanisms. Current evidence supports a transition toward comprehensive cardiometabolic prevention integrating lipid management, lifestyle modification, metabolic optimization, and targeted anti-inflammatory therapy. Future precision medicine strategies incorporating inflammatory biomarkers and individualized risk assessment may further improve cardiovascular outcomes and reduce the global burden of atherosclerotic disease.

Cardiorenal syndrome associated with type 2 diabetes mellitus has emerged as a major global health challenge due to its increasing prevalence, complex pathophysiology, and significant impact on morbidity and mortality. The interaction between cardiovascular disease, chronic kidney disease, and metabolic dysfunction creates a bidirectional cycle of organ damage mediated by inflammation, oxidative stress, endothelial dysfunction, neurohormonal activation, and fibrosis. This review analyzes current evidence regarding the mechanisms linking diabetes with cardiovascular and renal deterioration, emphasizing the concept of the cardiorenal-metabolic continuum. A comprehensive review of contemporary literature was conducted using international scientific databases and clinical practice guidelines. The findings indicate that recent therapeutic advances, particularly sodium-glucose cotransporter-2 inhibitors, glucagon-like peptide-1 receptor agonists, and non-steroidal mineralocorticoid receptor antagonists, have significantly improved cardiovascular and renal outcomes while reducing disease progression and hospitalization rates. Despite these advances, substantial challenges remain regarding early diagnosis, treatment accessibility, therapeutic implementation, and healthcare disparities. These challenges are especially relevant in Latin American countries, including Mexico, Colombia, and Ecuador, where the burden of diabetes and chronic kidney disease continues to rise. Current evidence supports the adoption of integrated multidisciplinary approaches focused on early detection, comprehensive risk assessment, and evidence-based therapeutic interventions. The transition from organ-centered management toward a cardiorenal-metabolic model represents a fundamental paradigm shift that may contribute to improved patient survival, preservation of organ function, and enhanced quality of life.

Cardiorenal syndrome (CRS) represents a complex bidirectional interaction between the cardiovascular and renal systems in which dysfunction of one organ may induce or worsen dysfunction of the other. The increasing global prevalence of heart failure, chronic kidney disease, hypertension, obesity, and diabetes mellitus has significantly contributed to the growing clinical and epidemiological burden of CRS. This review aimed to analyze the principal pathophysiological mechanisms, diagnostic approaches, and contemporary therapeutic strategies associated with cardiorenal syndrome through an evidence-based analysis of current scientific literature. The study was developed as a narrative and analytical review using scientific evidence obtained from internationally recognized databases, including PubMed, Scopus, Web of Science, and high-impact journals in nephrology, cardiology, and internal medicine. The analysis focused on hemodynamic alterations, neurohormonal activation, venous congestion, inflammatory pathways, endothelial dysfunction, oxidative stress, diagnostic biomarkers, pharmacological therapies, and multidisciplinary management approaches. The reviewed evidence demonstrated that CRS is a multifactorial systemic condition involving complex interactions between cardiac and renal dysfunction. Venous congestion, activation of the renin–angiotensin–aldosterone system, sympathetic nervous system stimulation, chronic inflammation, and endothelial injury were identified as major contributors to disease progression. Biomarkers such as NT-proBNP, cystatin C, NGAL, and KIM-1 showed important diagnostic and prognostic value, although integrated clinical evaluation remains essential. Contemporary therapeutic strategies, particularly sodium-glucose cotransporter-2 inhibitors, demonstrated substantial cardiovascular and renal protective effects. Multidisciplinary care models were also associated with improved patient outcomes and optimization of long-term management. In conclusion, cardiorenal syndrome should be understood as a highly dynamic and multisystemic condition requiring integrated cardiovascular and renal assessment. Early diagnosis, evidence-based therapy, preventive medicine, and multidisciplinary collaboration remain fundamental for improving prognosis and reducing the global burden associated with CRS.

Metabolic syndrome is currently recognized as a major multisystem disorder associated with significant cardiovascular, renal, endocrine, and inflammatory complications. The present review aimed to analyze the pathophysiological mechanisms, epidemiological characteristics, cardiovascular and renal outcomes, and current therapeutic perspectives associated with metabolic syndrome through an integrative analysis of recent scientific literature. A narrative and integrative review methodology based on the Scientific Method and a Process-Based Approach was employed using peer-reviewed publications indexed in PubMed, Scopus, and internationally recognized medical journals. The analyzed evidence demonstrated that insulin resistance, visceral obesity, chronic low-grade inflammation, oxidative stress, endothelial dysfunction, and neurohormonal activation constitute the principal mechanisms underlying multisystem deterioration in metabolic syndrome. Cardiovascular complications including coronary artery disease, heart failure, hypertension, and cerebrovascular disease were strongly associated with metabolic dysfunction. Additionally, chronic kidney disease progression appeared closely linked to glomerular hyperfiltration, fibrosis, inflammatory injury, and endothelial impairment. Epidemiological findings from Mexico, Colombia, and Ecuador revealed increasing prevalence patterns associated with obesity, sedentary lifestyles, nutritional transition, and socioeconomic disparities. The review also identified the importance of multidisciplinary therapeutic strategies involving lifestyle modification, cardiovascular risk reduction, glycemic control, renal protection, and emerging pharmacological therapies such as GLP-1 receptor agonists and SGLT2 inhibitors. Overall, metabolic syndrome should be understood as a systemic cardiometabolic disorder requiring comprehensive clinical management, preventive medicine strategies, and continued scientific investigation to reduce long-term morbidity and mortality.

Cardiovascular disease remains the leading cause of mortality worldwide, and traditional risk stratification models based on static variables are often insufficient to explain the complexity of cardiometabolic disorders. In this context, metabolic flexibility—defined as the ability of the organism to adapt substrate utilization according to physiological demands—has emerged as a relevant integrative concept linking endocrinology and cardiovascular disease. This review analyzes metabolic flexibility as a central mechanism in cardiovascular risk, exploring its physiological basis, its relationship with insulin resistance and metabolic disorders, and its implications in cardiovascular pathology. Evidence shows that impaired metabolic flexibility is associated with altered substrate utilization, mitochondrial dysfunction, systemic inflammation, and increased cardiovascular risk. These alterations contribute to inefficient myocardial energy metabolism, vascular dysfunction, and disease progression. Additionally, current therapeutic strategies that improve metabolic regulation have demonstrated significant cardiovascular benefits, supporting the relevance of metabolic pathways in disease prevention and management. The analysis also highlights the importance of considering metabolic flexibility in populations with a high burden of cardiometabolic disease, particularly in Latin American countries such as Mexico, Colombia, and Ecuador.

Cardiovascular disease remains the leading cause of global morbidity and mortality, despite significant advances in lipid management and risk factor control. Emerging evidence indicates that cardiometabolic dysfunction and chronic low-grade inflammation act synergistically to accelerate early vascular injury long before the onset of overt clinical events. This review integrates contemporary epidemiological data, mechanistic insights, biomarker analyses, and randomized clinical trial evidence to examine the cardiometabolic–inflammatory–vascular axis as a unified framework for early cardiovascular risk assessment. Population-level data confirm the sustained global expansion of cardiovascular burden, paralleled by increasing prevalence of metabolic syndrome and insulin resistance. Inflammatory biomarkers such as high-sensitivity C-reactive protein and interleukin-6 demonstrate graded associations with incident cardiovascular events, independent of traditional risk factors. Arterial stiffness emerges as a measurable intermediate phenotype reflecting cumulative metabolic and inflammatory exposure, with higher quartiles associated with substantially increased event rates. Furthermore, randomized trials targeting inflammatory pathways show reductions in major adverse cardiovascular events in selected high-risk populations, supporting inflammation as a modifiable contributor to atherosclerotic progression. The integration of inflammatory biomarkers into traditional prediction models yields modest but consistent improvements in discrimination and risk stratification. These findings collectively support a paradigm shift toward earlier biological detection of vascular dysfunction. Such an approach is particularly relevant for regions experiencing rapid growth in cardiometabolic risk, including Mexico, Colombia, and Ecuador. Advancing cardiovascular prevention will require integrative strategies that combine metabolic control, inflammatory assessment, and early vascular evaluation within a precision-based framework.