COVID-19 has shown significant morbidity with the involvement of multiple systems, including the cardiovascular system. Cardiovascular manifestations in the acute phase can include myocardial injury itself, myocardial infarction, venous thromboembolic events, myocarditis, Takotsubo syndrome, and different arrhythmic events. Myocardial injury defined by the rise of cardiac biomarkers in blood has been found in multiple studies with a prevalence of about 20%. Its presence is related to worse clinical outcomes and in-hospital mortality. The mechanisms of myocardial injury have been the subject of intense research but still need to be clarified. The characterization of the cardiac affectation with echocardiography and cardiac magnetic resonance has found mixed results in different studies, with a striking incidence of imaging criteria for myocarditis. Regarding post-acute and chronic follow-up results, the persistence of symptoms and imaging changes in recovered COVID-19 patients has raised concerns about the duration and the possible significance of these findings. Even though the knowledge about this disease has increased incredibly in the last year, many aspects are still unclear and warrant further research.

The exact mechanisms leading to myocardial injury in the coronavirus disease 2019 (COVID-19) are still unknown. In this retrospective observational study, we include all consecutive COVID-19 patients admitted to our center. They were divided into two groups according to the presence of myocardial injury. Clinical variables, Charlson Comorbidity Index (CCI), C-reactive protein (CRP), CAC (COVID-19-associated coagulopathy), defined according to the ISTH score, treatment and in-hospital events were collected. Between March and April 2020, 331 COVID-19 patients were enrolled, 72 of them (21.8%) with myocardial injury. Patients with myocardial injury showed a higher CCI score (median (interquartile range), 5 (4–7) vs. 2 (1–4), p = 0.001), higher CRP values (18.3 (9.6–25.9) mg/dL vs. 12.0 (5.4–19.4) mg/dL, p ˂ 0.001) and CAC score (1 (0–2) vs. 0 (0–1), p = 0.001), and had lower use of any anticoagulant (57 patients (82.6%) vs. 229 patients (90.9%), p = 0.078), than those without. In the adjusted logistic regression, CRP, myocardial injury, CCI and CAC score were positive independent predictors of mortality, whereas anticoagulants resulted as a protective factor. Myocardial injury in COVID-19 patients is associated with inflammation and coagulopathy, resulting in a worse in-hospital prognosis. Treatment with anticoagulant agents may help to improve in-hospital outcomes.

Hypertrophic cardiomyopathy (HCM) can cause symptoms due to the obstruction of the left ventricle outflow tract (LVOT). Although pharmacological therapy is the first step for treating this condition, many patients do not fully respond to the treatment, and an invasive approach is required to manage symptoms. Septal reduction therapies include septal myectomy (SM) and alcohol septal ablation (ASA). ASA consists of a selective infusion of high-grade alcohol into a septal branch supplying the basal interventricular septum to create an iatrogenic infarction with the aim of reducing LVOT obstruction. Currently, SM and ASA have the same level of indication; however, ASA is normally reserved for patients of advanced age, with comorbidities or when the surgical approach is not feasible. Recent data suggests that there are no differences in short- and long-term all-cause mortality, cardiovascular mortality and sudden cardiac death between ASA and SM. Despite the greater experience and refinement of the technique gained in recent years, the most common complication continues to be complete atrio-ventricular block, requiring a permanent pacemaker. Septal reduction therapies should be performed in experienced centres with comprehensive programs.

Background: Long‐term outcomes of ST‐segment–elevation myocardial infarction in patients with diabetes have been barely investigated. The objective of this analysis from the EXAMINATION‐EXTEND (10‐Years Follow‐Up of the EXAMINATION trial) trial was to compare 10‐year outcomes of patients with ST‐segment–elevation myocardial infarction with and without diabetes. Methods and Results: Of the study population, 258 patients had diabetes and 1240 did not. The primary end point was patient‐oriented composite end point of all‐cause death, any myocardial infarction, or any revascularization. Secondary end points were the individual components of the primary combined end point, cardiac death, target vessel myocardial infarction, target lesion revascularization, and stent thrombosis. All end points were adjusted for potential confounders. At 10 years, patients with diabetes showed a higher incidence of patient‐oriented composite end point compared with those without (46.5% versus 33.0%; adjusted hazard ratio [HR], 1.31 [95% CI, 1.05–1.61]; P =0.016) mainly driven by a higher incidence of any revascularization (24.4% versus 16.6%; adjusted HR, 1.61 [95% CI, 1.19–2.17]; P =0.002). Specifically, patients with diabetes had a higher incidence of any revascularization during the first 5 years of follow‐up (20.2% versus 12.8%; adjusted HR, 1.57 [95% CI, 1.13–2.19]; P =0.007) compared with those without diabetes. No statistically significant differences were found with respect to the other end points. Conclusions: Patients with ST‐segment–elevation myocardial infarction who had diabetes had worse clinical outcome at 10 years compared with those without diabetes, mainly driven by a higher incidence of any revascularizations in the first 5 years. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT04462315.

Background: Myocardial fibrosis leads to ventricular dysfunction and worsened prognosis, especially after ST-segment elevation myocardial infarction (STEMI). Sodium–glucose cotransporter 2 inhibitors (SGLT2is) offer cardiovascular benefits by reducing markers of myocardial fibrosis and fibroblast activity. However, the effects of SGLT2i on myocardial fibrosis deposition among STEMI patients undergoing primary percutaneous coronary intervention (PCI) have not yet been evaluated. Study and Design: The effect of DAPAgliflozin on myocardial fibrosis and ventricular function in patients with STEMI (DAPA-STEMI) trial is a phase III, multicenter, randomized, double-blind, placebo-controlled trial. The study aims to assess the effects of dapagliflozin on myocardial fibrosis and ventricular function, evaluated using cardiac magnetic resonance (CMR), in STEMI patients undergoing primary PCI. Eligible patients were 30 to 85 years old and exhibited a left ventricular ejection fraction ≤ 50%. A total of 120 patients with STEMI were expected to be randomized 1:1 to receive dapagliflozin 10 mg or placebo daily for six months. The primary endpoint is the change in the extracellular volume fraction of the remote myocardium from baseline to six months, as measured by CMR. The secondary endpoints include changes in the circulating C-terminal propeptide of type I procollagen, N-terminal propeptide of type III procollagen, and Galectin-3 from baseline to six months. The study was stopped prematurely due to slow recruitment, with 54 enrolled patients, limiting the statistical power to detect changes in the primary endpoint between groups. Conclusions: The DAPA-STEMI trial will provide insights into the impact of dapagliflozin on myocardial fibrosis and ventricular remodeling in patients with STEMI undergoing primary PCI. Clinical Trial Registration Unique Identifier: NCT06619600