Systolic anterior motion (SAM) of the mitral valve is classically associated with hypertrophic cardiomyopathy (HCM); however, it may rarely occur in the absence of left ventricular hypertrophy (LVH), particularly in the setting of acute myocardial ischemia. This phenomenon remains poorly understood and poses diagnostic and therapeutic challenges. We report the case of a 54-year-old woman presenting with non-ST-elevation myocardial infarction (NSTEMI). Transthoracic echocardiography showed a non-dilated left ventricle (LV end-diastolic diameter 45 mm), preserved systolic function (left ventricular ejection fraction (LVEF) 63%; end-diastolic volume 115 mL, end-systolic volume 42 mL), apical akinesia, and compensatory basal hyperkinesis. There was no LV hypertrophy (interventricular septum 8 mm; lateral wall 7 mm). SAM of the mitral valve was present, resulting in moderate mitral regurgitation and a dynamic left ventricular outflow tract (LVOT) gradient of 30 mmHg. The right ventricle was normal in size and function. Cardiac magnetic resonance imaging demonstrated apical myocardial edema on T2-weighted sequences and a punctiform transmural late gadolinium enhancement in the inferomedial segment on phase-sensitive inversion recovery (PSIR) sequences, with no evidence of cardiomyopathy or structural substrate that could explain LVOT obstruction. Coronary angiography revealed a significant mid-left anterior descending artery lesion, successfully treated with drug-eluting stent implantation. Medical management included betablocker therapy and careful volume optimization, with avoidance of inotropes. Follow-up transesophageal echocardiography at three weeks confirmed complete resolution of SAM, mitral regurgitation, LVOT gradient, and apical wall-motion abnormalities. This case illustrates a rare, ischemia-induced and reversible form of SAM without LVH. LVH was excluded based on echocardiographic wall thickness measurements below established thresholds (interventricular septum 8 mm and lateral wall 7 mm), well under the diagnostic cutoff for LVH (>11 mm), likely mediated by transient apical dysfunction and basal hyperkinesis, altering ventricular geometry and flow dynamics.

Introduction: Pharmacological therapies are recommended for individuals with obesity. Semaglutide, a glucagon‐like peptide‐1 receptor agonist (GLP‐1), and tirzepatide, a dual glucose‐dependent insulinotropic polypeptide and GLP‐1 receptor agonist (GIP/GLP‐1), are among the leading pharmacological options for obesity treatment. This network meta‐analysis (NMA) aims to evaluate the comparative efficacy of these two agents in reducing body weight and improving glycemic parameters. Methods: Pairwise comparisons within the NMA were conducted using a frequentist approach in RCTs comparing tirzepatide or semaglutide versus placebo, as well as tirzepatide versus semaglutide at their maximum dosages (15 and 2.4 mg, respectively). Results: A total of 28 RCTs were included, comprising 34 367 participants, 39.6% of whom were women and with a mean age of 57.8 ± 8.95 years. Tirzepatide demonstrated superiority over semaglutide in percentage weight reduction (mean difference [MD] 6.10%; 95% CI: 3.64, 8.57), absolute weight loss (MD 4.55 kg; 95% CI: 1.28, 7.83), BMI reduction (MD 1.71 kg/m ² ; 95% CI: 0.08, 3.34), and waist circumference reduction (MD 2.89 cm; 95% CI: 1.25, 4.53). Regarding glycemic parameters, tirzepatide was also more effective than semaglutide in reducing HbA1c (MD 0.33%; 95% CI: 0.20, 0.46) and fasting blood glucose (MD 10.39 mg/dL; 95% CI: 4.48, 16.29). Conclusion: In this NMA, tirzepatide appeared to be superior to semaglutide in both body weight reduction and improvement of glycemic indices.

Background/Objectives: Oral anticoagulation therapy (OAC) is crucial for reducing the risk of ischemic complications in patients with atrial fibrillation (AF). However, OAC also increases the risk of major bleeding events. The optimal management of OAC in patients with AF undergoing transaortic valve implantation (TAVI) is unclear. This study aimed to compare the efficacy and safety of OAC interruption vs. continuation in patients with AF scheduled for TAVI. Methods: PubMed, EMBASE, and Cochrane were searched to include all pertinent randomized and observational studies. The primary endpoint was the occurrence of net adverse clinical events (NACE), a composite of all-cause death, major vascular complications, and major bleeding at 30-day follow-up. Secondary endpoints included all-cause death, cardiovascular death, major vascular complications, major bleeding, any bleeding, stroke, non-fatal myocardial infarction, and the need for red-packed blood transfusion. Results: A total of three studies and 2773 patients were included in the analysis (1314 were allocated to continuation of OAC therapy and 1459 to interruption of OAC therapy during TAVI). The two study groups experienced a similar rate of NACE (OR = 0.89 [95% CI 0.61 to 1.31], I² = 77%, p = 0.56) compared to the OAC-interruption group. No significant differences were observed in the rate of all-cause death (p = 0.21), cardiovascular death (p = 0.35), major vascular complications (p = 0.84), major bleeding events (p = 0.47), total bleeding events (p = 0.62), or non-fatal MI (p = 0.55). Interestingly, the OAC-continuation group experienced a lower occurrence of stroke (OR = 0.62 [95% CI 0.39 to 0.97], I² = 0%, p = 0.04) and the need for red packed blood cells (OR = 0.66 [95% CI 0.50 to 0.86], I² = 20%, p < 0.01) compared to the OAC-interruption group. Conclusions: In patients with AF undergoing TAVI, there was no significant difference between interruption and continuation of OAC in terms of NACE, composite of all-cause death, major vascular complications, or major bleeding at 30-day follow-up. Of interest, the OAC-continuation group patients experienced lower rates of stroke and the need for blood transfusion.

Background: Current ESC guidelines recommend the use of oral anticoagulant therapy in patients with atrial fibrillation to reduce the risk of arterial embolization. Recently, Factor XIa inhibitors were investigated as an alternative to the commonly used DOACs. Aims: This systematic review and meta-analysis aim to assess whether Factor XIa inhibitors lead to lower risks of bleeding compared to DOACs in patients with atrial fibrillation. Methods: PubMed, Cochrane, and EMBASE were searched. The primary endpoint was the occurrence of a composite of Major or clinically relevant non-major bleeding. Secondary endpoints included death from any cause, cardiovascular death, any adverse effects, any serious adverse effects, minor bleeding, stroke, or systemic embolism. Results: A total of 3 studies met the inclusion criteria and were included in the qualitative and quantitative analysis, comprising 16,772 patients. Factor XIa inhibitors were associated with significantly fewer major or clinically relevant non-major bleedings than DOACs (RR = 0.40 [95% CI [0.32, 0.51]), I² = 3%, p < 0.00001). There were no differences between Factor XIa inhibitors and DOACs regarding the occurrence of death (RR = 0.83 [95% CI 0.63, 1.08]), I² = 0%, (p = 0.15) and cardiovascular death (RR = 1.09 [95% CI 0.74, 1.63]), I² = 0%, (p = 0.65). Interestingly, the risk of stroke and systemic embolism was higher among the patients exposed to factor XIa inhibitors compared to the DOACs group RR = 6.05 [95% CI [1.02, 35.94]), I² = 5%, (p = 0.05). Conclusions: Factor XIa inhibitors are superior to DOACs in terms of bleeding complications. However, this meta-analysis shows a significantly higher risk of stroke or systemic embolism as compared to commonly used DOACs.