Metabolic inflammation (metaflammation) is a key biological process linking obesity, insulin resistance, and chronic disease. This review integrates molecular and epidemiological evidence to explain how low-grade inflammation acts as both the cause and consequence of metabolic dysfunction. Adipose tissue functions as an immunometabolic organ, releasing cytokines and adipokines that disrupt insulin signaling and promote systemic complications. Major mediators—TNF-α, IL-6, CRP, leptin, resistin, and decreased adiponectin—constitute a proinflammatory network underlying metabolic syndrome, cardiovascular disease, and fatty liver. Using an integrative approach based on the DMAIC model (Define–Measure–Analyze–Improve–Control), this review synthesizes data from international and Latin American studies, emphasizing Mexico, Colombia, and Ecuador. Findings indicate that inflammation begins in adipose tissue and extends to the liver, skeletal muscle, cardiovascular system, and central nervous system, creating a self-perpetuating feedback loop. Regional data show high obesity and metabolic syndrome prevalence, driven by biological vulnerability and social factors such as diet, urbanization, and limited healthcare access. Effective management requires a multilevel strategy combining lifestyle modification, pharmacologic agents, targeted anti-inflammatory compounds, and public health interventions. Lifestyle change remains the cornerstone, supported by metabolic drugs and multidisciplinary programs. The evidence supports metaflammation as the unifying mechanism driving global metabolic disease. Recognizing it as a therapeutic and preventive target reframes clinical priorities, emphasizing the restoration of immunometabolic balance through integrative, context-specific action.

Background/Objectives: Lyme disease is a tick-borne zoonosis caused by Borrelia burgdorferi that can affect multiple organ systems. Although cardiovascular involvement is considered uncommon, it may lead to severe and potentially life-threatening complications, particularly conduction disturbances and inflammatory cardiac conditions. This review aims to describe the spectrum of cardiovascular manifestations documented in patients with Lyme disease, focusing on clinical presentation, diagnostic approaches, management strategies, and reported outcomes. Methods: A narrative literature review was performed using PubMed, MEDLINE, and Google Scholar. Articles published between January 2000 and July 2025 in English or Spanish were screened. Eligible studies included original research articles, systematic and narrative reviews, case series, and case reports describing confirmed Lyme disease with cardiovascular involvement. A total of 30 studies were included. The available evidence was predominantly based on case reports and small case series, with considerable heterogeneity in study design, patient populations, and reported outcomes. Data on clinical manifestations, diagnostic methods, treatment strategies, and outcomes were extracted and synthesized. Results: Atrioventricular conduction disturbances were the most frequently reported cardiovascular manifestation, ranging from first-degree block to complete heart block, often presenting abruptly with syncope or bradycardia. Other reported manifestations included atrial and ventricular arrhythmias, myocarditis, pericarditis, myopericarditis, valvular endocarditis, aortitis, and vasculitis. Diagnosis relied on a combination of clinical suspicion, epidemiologic exposure, serologic testing, electrocardiographic monitoring, and cardiac imaging. Most patients were treated with antimicrobial therapy, commonly intravenous ceftriaxone followed by oral doxycycline, with temporary pacemaker support required in selected cases. Overall, clinical outcomes were favorable when treatment was initiated promptly. Conclusions: Cardiovascular involvement in Lyme disease, although infrequent, encompasses a broad clinical spectrum with potentially serious consequences. Early recognition, appropriate diagnostic evaluation, and timely antimicrobial therapy are essential to ensure reversibility of cardiac manifestations and favorable outcomes. However, the available evidence is limited by heterogeneity and the predominance of low-level-evidence studies.

Pharmacogenomics has emerged as an essential component of personalized therapy in internal medicine, offering a framework to understand how genetic variability influences drug response, safety, and treatment effectiveness. This review synthesizes international evidence to identify clinically relevant gene–drug interactions, evaluate global implementation strategies, and examine their applicability to healthcare systems in Mexico, Colombia, and Ecuador. The analysis demonstrates that cytochrome P450 enzymes—particularly CYP2C19, CYP2D6, and CYP3A4—continue to play a dominant role in predicting therapeutic outcomes, with strong evidence supporting interactions such as CYP2C19–clopidogrel, CYP2D6–codeine, and SLCO1B1–simvastatin. These associations consistently appear in international guidelines and represent high-impact opportunities for improving cardiovascular, psychiatric, and oncologic care. Global implementation models from North America, Europe, and Asia highlight the importance of structured policies, laboratory capacity, and electronic health record integration, while emerging experiences from Africa and Southeast Asia emphasize scalable, resource-adapted strategies. In Latin America, Mexico demonstrates the highest readiness for pharmacogenomic adoption, followed by Colombia with promising institutional initiatives, and Ecuador with early-stage development requiring capacity-building. The review also discusses the expansion of pharmacogenomics into multi-omic approaches, including epigenetics and nutrigenomics, which are expected to refine predictive accuracy but require advanced informatic infrastructure and clinician training. Overall, pharmacogenomics provides a powerful opportunity to enhance therapeutic precision, reduce adverse drug reactions, and promote equitable and efficient healthcare delivery. Its successful implementation in Latin America will depend on coordinated policy development, investment in infrastructure, and the integration of genomic education into clinical training programs.

Recent developments in electrocardiographic signal analysis have redefined the diagnostic and prognostic landscape of cardiac arrhythmias. This review synthesizes current international evidence on advanced ECG-centered analytical strategies for early detection and risk stratification, incorporating studies published between 2021 and 2025 and contextualizing their applicability within healthcare systems in Mexico, Colombia, and Ecuador. The collective literature demonstrates that early identification of atrial fibrillation achieves consistently high diagnostic accuracy, supported by robust waveform characterization, rhythm-based modeling, and recognition of subtle conduction irregularities. Comparable approaches applied to supraventricular and ventricular arrhythmias also yield strong performance despite higher morphological variability. In contrast, prognostic assessment of ventricular instability and sudden cardiac death presents greater complexity; however, recent investigations highlight meaningful advances based on dynamic features such as beat-to-beat variability, QRS complexity, repolarization heterogeneity, and ectopic burden. Evidence further underscores the decisive impact of monitoring duration, with 7–14-day ambulatory patches markedly outperforming conventional ECG and short Holter recordings in detecting intermittent arrhythmic episodes. A multidimensional interpretive framework—integrating atrial conduction markers, repolarization indices, autonomic modulation, and electrical instability signatures—emerges as essential for achieving clinically relevant predictive performance. Finally, the review highlights expanding feasibility for regional adoption in Latin America, supported by progressive improvements in infrastructure, workflow integration, and clinical capacity. Overall, the findings reflect a pivotal transition toward enhanced ECG analysis as a central component of contemporary arrhythmia evaluation, with substantial implications for early diagnosis, risk prediction, and long-term patient outcomes.

In Mexico, since June 2025, human cases of myiasis caused by Cochliomyia hominivorax (the screwworm) have been identified, prompting health authorities to issue a surveillance alert for potential infections by this fly. Here we report the identification and interdisciplinary management of a case of nasal myiasis caused by Lucilia sericata. In September 2025, a 40-year-old Hispanic man was admitted to the emergency room due to an altered mental status; after a 17-day hospital stay, nasal larvae were detected. The larvae were submitted for morphological identification by microscopy and molecular identification by polymerase chain reaction, using ITS-2 and 16S loci as nuclear and mitochondrial markers, respectively; the amplicons were purified and sequenced, and a Bayesian phylogenetic analysis was performed. Morphological analysis showed that they were L. sericata larvae at different developmental stages (1st to 3rd instars). Molecular analysis confirmed the morphological result, as phylogenetic inferences showed a clear grouping of the sequences within the L. sericata cluster. While remaining vigilant for possible human cases of myiasis caused by C. hominivorax, here, we confirmed by morphological and molecular analysis the identification of an unexpected case of nasal myiasis caused by L. sericata, demonstrating the importance of care in all aspects of thorough epidemiological surveillance and the interdisciplinary management to address these alerts and any related cases.