Despite the improvement in prognosis in patients with acute myocardial infarction (AMI), a significant proportion of survivors still experience heart failure (HF)-related adverse outcomes. Adverse left ventricular remodeling (LVR), which refers to a progressive dilation of left ventricular (LV) end-diastolic and end-systolic volumes, usually accompanied by a deterioration in LV systolic function, occurs frequently and underlies most cases of HF development after AMI. In this review, we discuss the current definitions of post-AMI LVR, the most appropriate imaging modalities for its detection, and the pathophysiological mechanisms by which Cardiac Rehabilitation (CR) can improve LVR—including exercise interventions, cardiovascular risk factors control, and pharmacological therapy optimization. Finally, we provide up-to-date recommendations for the follow-up and management of LVR in post-AMI patients enrolled in CR and outline future prospects on this topic.

Anxiety and depression are common after a myocardial infarction (MI), so psychological and psychiatric mental health (MH) interventions are recommended during Cardiac Rehabilitation Programs (CRP). We aim to evaluate anxiety and depression symptoms and quality of life in MI sufferers followed in a CRP without dedicated MH resources. We prospectively included 164 MI patients in our CRP without dedicated MH resources. Patient Health Questionnaire 2-item (PHQ-2) and Generalized Anxiety Disorder 2-item (GAD-2) questionnaires for depression and anxiety screening (altered if ≥3 points) and the 36-Item Short Form Survey Instrument (SF-36) to analyze four MH components and Mental Component Summary (MCS) were assessed at the beginning and after CRP. The mean age was 61.35 ± 10.76 years, and most patients were male (86.6%). A significant improvement in SF-36 mental components (from +5.94 ± 27.98 to +8.31 ± 25 points, p < 0.001) and SF-36-MCS (+1.85 ± 10.23 points, p = 0.02) was noted, as well as a reduction in depression and anxiety symptoms in PHQ-2 and GAD-2 (p < 0.001). However, 33 (20.1%) patients showed a positive screening for depression and/or anxiety at the end of the program. These patients were younger (56.6 ± 8.05 vs. 62.55 ± 11.05 years, p = 0.004) and showed significantly worse initial scores of SF-36 mental components, PHQ-2, and GAD-2 (p < 0.001). We conclude that a Phase 2 CRP without dedicated MH resources can achieve significant improvements in MH well-being after MI. However, one-fifth of the population had substantial depression and/or anxiety symptoms at the end of the program. This subset, characterized by worse initial MH scores, may benefit from specific MH interventions during CRP.

The use of N-terminal pro-brain natriuretic peptide (NT-proBNP) after ST-segment elevation acute myocardial infarction (STEMI) is unclear. We evaluated its prognostic significance after post-STEMI cardiac rehabilitation. The prognostic significance of NT-proBNP was tested upon completion of cardiac rehabilitation (median, 45 days post-STEMI) in an exploratory group (n = 105 patients with the researchers blinded to NT-proBNP values) and validated in the following 276 patients. Baseline and cardiac imaging variables including cardiovascular magnetic resonance (CMR) parameters were recorded. The primary endpoint was the occurrence of a first major adverse cardiac event (MACE: cardiac death, myocardial infarction, or re-admission for heart failure). In the exploratory group, a cut-off value of NT-proBNP >400 pg/mL emerged as a potent MACE predictor (37 % vs.17 %; hazard ratio [HR]: 6.8 [1.5-30.3], p = 0.01). In the study group, during a 203-week median follow-up, 88 (32 %) first MACEs were detected. NT-proBNP >400 pg/mL (n = 168, 61 %) associated with a higher MACE rate (46 % vs. 10 %, HR: 4.6 [2.3-8.9], p < 0.001) and, separately, with more cardiac deaths, myocardial infarctions, and re-admissions for heart failure (p < 0.05 for all comparisons). NT-proBNP improved the multivariate model for MACE prediction (area under the curve 0.81 vs. 0.72, p < 0.001). Analyzing all measurements performed during follow-up (n = 1018), the risk of transition to MACE was higher in case of NT-proBNP >400 pg/mL (14 % vs.3 %, p < 0.001). Even after comprehensive adjustment, NT-proBNP emerges as a potent, accessible and inexpensive tool for risk stratification of STEMI patients after completion of rehabilitation programs.

This study aimed to assess the time course of circulating neutrophil and lymphocyte counts and their ratio (NLR) in ST-segment elevation myocardial infarction (STEMI) and coronavirus disease (COVID)-19 and explore their associations with clinical events and structural damage. Circulating neutrophil, lymphocyte and NLR were sequentially measured in 659 patients admitted for STEMI and in 103 COVID-19 patients. The dynamics detected in STEMI (within a few hours) were replicated in COVID-19 (within a few days). In both entities patients with events and with severe structural damage displayed higher neutrophil and lower lymphocyte counts. In both scenarios, higher maximum neutrophil and lower minimum lymphocyte counts were associated with more events and more severe organ damage. NLR was higher in STEMI and COVID-19 patients with the worst clinical and structural outcomes. A canonical deregulation of the immune response occurs in STEMI and COVID-19 patients. Boosted circulating innate (neutrophilia) and depressed circulating adaptive immunity (lymphopenia) is associated with more events and severe organ damage. A greater understanding of these critical illnesses is pivotal to explore novel alternative therapies.

Extracellular matrix (ECM) changes after myocardial infarction (MI) need precise regulation, and next-generation sequencing technologies provide omics data that can be used in this context. We performed a meta-analysis using RNA-sequencing transcriptomic datasets to identify genes involved in post-MI ECM turnover. Eight studies available in Gene Expression Omnibus were selected following the inclusion criteria. We compare RNA-sequencing data from 92 mice submitted to permanent coronary ligation or sham, identifying differentially expressed genes (p-value < 0.05 and Log2FoldChange ≥ 2). Functional enrichment analysis was performed based on Gene Ontology biological processes (BPs). BPs implicated in response to extracellular stimulus, regulation of ECM organization, and ECM disassembly were detected soon after ischemia onset. ECM disassembly occurred between days one to seven post-MI, compared with ECM assembly from day seven onwards. We identified altered mRNA expression of 19 matrix metalloproteinases and four tissue inhibitors of metalloproteinases at post-infarcted ECM remodeling and altered transcriptomic expression of 42 genes encoding 26 collagen subunits at the fibrotic stage. To our knowledge, this is the first meta-analysis using RNA-sequencing datasets to evaluate post-infarcted cardiac interstitium healing, revealing previously unknown mechanisms and molecules actively implicated in ECM remodeling post-MI, which warrant further validation.

We aimed to assess the correlation of cardiovascular magnetic resonance (CMR)-derived epicardial adipose tissue (EAT) with infarct size (IS) and residual systolic function in ST-segment elevation myocardial infarction (STEMI). We enrolled patients discharged for a first anterior reperfused STEMI submitted to undergo CMR. EAT, left ventricular (LV) ejection fraction (LVEF), and IS were quantified at the 1-week (n = 221) and at 6-month CMR (n = 167). At 1-week CMR, mean EAT was 31 ± 13 mL/m². Patients with high EAT volume (n = 72) showed larger 1-week IS. After adjustment, EAT extent was independently related to 1-week IS. In patients with large IS at 1 week (>30% of LV mass, n = 88), those with high EAT showed more preserved 6-month LVEF. This association persisted after adjustment and in a 1:1 propensity score-matched patient subset. Overall, EAT decreased at 6 months. In patients with large IS, a greater reduction of EAT was associated with more preserved 6-month LVEF. In STEMI, a higher presence of EAT was associated with a larger IS. Nevertheless, in patients with large infarctions, high EAT and greater subsequent EAT reduction were linked to more preserved LVEF in the chronic phase. This dual and paradoxical effect of EAT fuels the need for further research in this field.