Heart failure (HF) is a global health challenge characterized by the heart’s inability to satisfy metabolic demands, driven by renin–angiotensin–aldosterone system (RAAS) overactivation, a neurohormonal imbalance, and emerging mechanisms like the gut–heart axis and mitochondrial dysfunction. Affecting over 6 million adults in the US alone, HF incurs a 5-year mortality rate of 50% and escalating costs projected to double by 2030. This review examines HF’s molecular paradigms, integrating established pathways with advances in omics, stem cell therapy, genetic modification, and personalized medicine. The RAAS blockade remains central, yet its efficacy is limited in HF with preserved ejection fraction (HFpEF). Stem cell therapies (mesenchymal and induced pluripotent stem cells) show regenerative potential but face poor retention (<10% survival at 30 days). CRISPR/Cas9 offers precision, though off-target effects persist. The gut microbiome, via trimethylamine N-oxide, exacerbates inflammation, while omics technologies promise biomarkers for tailored treatments. Challenges include translating these innovations into practice, particularly for HFpEF. Future directions involve novel HFpEF therapies, enhanced stem cell delivery, precise genetic tools, and microbiome interventions, supported with artificial intelligence. By 2030, these advances could shift HF management toward regeneration, contingent on overcoming translational barriers through global collaboration.

Background: Anterior ST‐elevation myocardial infarction (STEMI) is frequently associated with severe complications, such as myocardial dysfunction and conduction abnormalities. Complete atrioventricular block (CAVB), especially when combined with bifascicular block, is a rare but critical presentation that reflects extensive myocardial damage, often linked to proximal left anterior descending (LAD) artery occlusion. Case Presentation: A 76‐year‐old male with a history of hypertension, diabetes mellitus, and dyslipidemia presented to the emergency department with a 6‐day history of gastrointestinal symptoms and recurrent syncope. On arrival, he exhibited bradycardia, hypotension, and mottling, progressing to cardiac arrest. The return of spontaneous circulation was achieved after one cycle of advanced cardiovascular life support. Electrocardiography revealed CAVB with a ventricular escape rhythm displaying right bundle branch block morphology, left anterior fascicular block, and anterior ST‐segment elevation. Emergency interventions included endotracheal intubation, Swan–Ganz catheterization, transvenous pacing, and vasopressor support. Echocardiography demonstrated severe left ventricular systolic dysfunction with an ejection fraction of 25%. Coronary angiography identified critical proximal stenoses in the LAD and circumflex arteries, managed with percutaneous coronary intervention and stent placement. Persistent conduction abnormalities and systolic dysfunction necessitated implantation of a cardiac resynchronization therapy defibrillator (CRT‐D). Despite extensive rehabilitation efforts, the patient died after 60 days of hospitalization. Discussion: This case highlights the importance of rapid recognition and intervention in anterior STEMI complicated by CAVB and bifascicular block, signaling significant proximal LAD involvement. Advanced therapeutic options, including CRT‐D, are crucial for addressing these rare, life‐threatening conduction disturbances. The fatal outcome underscores the need for vigilant follow‐up and individualized preventive strategies to improve prognosis in such complex STEMI cases.

Heart failure (HF) is a global health challenge characterized by the heart’s inability to satisfy metabolic demands, driven by renin-angiotensin-aldosterone system (RAAS) overactivation, neurohormonal imbalance, and emerging mechanisms like the gut-heart axis and mitochondrial dysfunction. Affecting over 6 million adults in the US alone, HF incurs a 5-year mortality rate of 50% and escalating costs projected to double by 2030. This review examines HF’s molecular paradigms, integrating established pathways with advances in omics, stem cell therapy, genetic modification, and personalized medicine. RAAS blockade remains central, yet its efficacy is limited in HF with preserved ejection fraction (HFpEF). Stem cell therapies (mesenchymal and induced pluripotent stem cells) show regenerative potential but face poor retention (10% survival at 30 days). CRISPR/Cas9 offers precision, though off-target effects persist. The gut microbiome, via trimethylamine N-oxide, exacerbates inflammation, while omics technologies promise biomarkers for tailored treatments. Challenges include translating these innovations into practice, particularly for HFpEF. Future directions involve novel HFpEF therapies, enhanced stem cell delivery, precise genetic tools, and microbiome interventions, supported by artificial intelligence. By 2030, these advances could shift HF management toward regeneration, contingent on overcoming translational barriers through global collaboration.

Background: Depression and impaired health-related quality of life are common after acute myocardial infarction (AMI) and have been associated with worse clinical and functional outcomes. However, local data describing these dimensions during the post-infarction period in public healthcare settings remain limited. Methods: We conducted a cross-sectional observational study using data from the Prospective Myocardial Infarction Registry (REPRIM), including patients with ST-segment elevation myocardial infarction (STEMI) treated in a public tertiary care setting in Chile between 2019 and 2020. Health-related quality of life was assessed 30 days after the index event using the SF-36 questionnaire, and depressive symptoms were evaluated with the 17-item Hamilton Depression Rating Scale (HAM-D). Associations between quality of life and depressive symptoms were explored using multivariable linear regression models adjusted for age, sex, diabetes mellitus, hypertension and left ventricular ejection fraction, and mortality was described during the available follow-up. Results: During the study period, 121 patients with acute myocardial infarction were identified. Of the 100 patients included in REPRIM, 68 met the criteria for this subanalysis (alive at 30 days, successful contact and complete questionnaire data). Most patients exhibited at least mild depressive symptoms (94.1%), with a median HAM-D score of 12 (interquartile range 10–15). Higher depressive symptom severity was significantly associated with lower physical (PCS) and mental (MCS) component scores of the SF-36 in unadjusted analyses ( ρ = −0.46 and ρ = −0.58, respectively; p < 0.001) and remained independently associated after multivariable adjustment [ β = −1.26 [95% CI −2.06 to −0.46] for PCS; β = −1.50 [95% CI −2.40 to −0.61] for MCS; both p < 0.01]. Patients with moderate or higher depressive symptoms had significantly worse quality-of-life scores compared with those with mild symptoms. Mortality analyses were descriptive due to the limited number of events. Conclusions: In this cross-sectional study of STEMI survivors treated in a public hospital, depressive symptoms were highly prevalent at 30 days and were consistently associated with poorer physical and mental health-related quality of life. These findings highlight the substantial burden of depressive symptoms early after myocardial infarction and support the relevance of integrating mental health and quality-of-life assessment into post-infarction follow-up within public healthcare systems, while acknowledging the limitations of our small, single-centre study.

Backround: Acute heart failure (AHF) is a severe condition with high mortality, with variable data depending on the region. The objective of the study was to describe its mortality in a high-complexity hospital in Santiago, Chile, and the associated factors. Methods: A retrospective study was conducted with 184 patients admitted between 2017 and 2019, aged over 18, and diagnosed with AHF by a cardiology resident. Clinical, sociodemographic, and therapeutic variables were recorded. Regression models and descriptive statistics were used. Results: The 12-month mortality rate was 22.7%, of which 35% were due to cardiac causes. The associated risk factors were age (HR 2.28, 95%CI: 1.22-4.23; p<0.05), plasma creatinine at admission (OR 1.87, 95%CI: 1.16-3.40; p<0.05), ProBNP over 4140 pg/mL (RR 2.0, 95%CI: 1.02-4.13; p<0.05), chronic kidney disease (OR 5.44, 95%CI: 1.5-9.3; p<0.05), and atrial fibrillation or flutter (OR 2.74, 95%CI: 1.30-5.76; p<0.05). The use of angiotensin-converting enzyme inhibitors (ACEi) and beta-blockers (BB) at discharge were protective for mortality (OR 0.45, 95%CI: 0.21-0.94; p<0.05 and OR 0.27, 95%CI: 0.09-0.79; p<0.05, respectively), as was a ProBNP level below 3220 pg/mL (RR 0.54, 95%CI: 0.28-0.96; p<0.05). Conclusions: AHF is associated with high one-year mortality in Chile, with significant relevance of patient history and admission tests. The use of ACEi and BB at discharge was associated with improved survival, highlighting the importance of optimized management during hospitalization and at discharge to improve prognosis.