Vimal Mehta

Aims: The impact of tirzepatide and dulaglutide on major adverse cardiovascular events (MACE) and heart failure (HF) outcomes according to HF status is unknown. Methods and results: Patients with type 2 diabetes (T2D) and atherosclerotic cardiovascular disease were treated with tirzepatide up to 15 mg or dulaglutide 1.5 mg weekly (average 4 years). The incidence of MACE-3 [cardiovascular (CV) death, myocardial infarction (MI), stroke], MACE-4 (CV death, MI, stroke, coronary revascularization) and composite of all-cause or CV death and hospitalization or urgent visits for HF were analysed in patients with and without a history of HF. A history of HF (20.3%) was associated with more coronary artery disease and prior MI. Incidences of event categories were higher in the HF group. The hazard ratio (HR) for all-cause death or hospitalization or urgent visits for HF on tirzepatide vs. dulaglutide was 0.83 [95% confidence interval (CI) 0.70–0.99] in patients with HF and 0.88 (95%CI 0.78–1.00) without HF. The HR for CV death or hospitalization or urgent visits for HF was 0.85 (95%CI 0.70–1.03) and 0.96 (95%CI 0.83–1.12), for MACE-3 0.90 (95%CI 0.76–1.08) and 0.93 (95%CI 0.83–1.04), and for MACE-4 0.81 (95%CI 0.69–0.95) and 0.91 (95%CI 0.83–1.00) in patients with and without HF, respectively. The patient-reported outcomes of APPADL and EQ-5D-5L visual analogue scores improved and were higher on tirzepatide in both groups. Conclusion: With overall non-inferiority established, this exploratory analysis revealed lower rates of the composite of all-cause death or HF events, or MACE-4 among patients with T2D and HF treated with tirzepatide compared with dulaglutide.

Aims: In severe rheumatic mitral stenosis (MS) with sinus rhythm, left atrial appendage (LAA) dysfunction increases thromboembolic risk, yet clinical guidelines provide no recommendations, and its assessment via transoesophageal echocardiography is not feasible for routine or repeated use. This study assessed whether left atrial (LA) strain imaging could non-invasively predict LAA contractile dysfunction. Methods and results: We prospectively enrolled 138 patients with severe rheumatic MS in sinus rhythm who underwent transthoracic and transoesophageal echocardiography. Left atrial appendage inactivity was defined as LAA emptying velocity < 25 cm/s. Left atrial reservoir strain (LASr), conduit, and contractile strain were quantified using speckle-tracking echocardiography. Multivariable logistic regression and receiver operating characteristic analyses were performed to evaluate predictors of LAA inactivity. Left atrial appendage inactivity was observed in 108 patients (78.2%), and LAA thrombus was detected in eight patients (5.8%)—all in sinus rhythm. In multivariate analysis, LASr was the strongest independent predictor of LAA inactivity [odds ratio: 0.61 per 1% increase; 95% confidence interval (CI): 0.50–0.75; P < 0.0001]. Left atrial reservoir strain yielded an area under the ROC curve of 0.950 (95% CI: 0.911–0.989), with a threshold of ≤22.95% showing a sensitivity of 93.5% and specificity of 90% for predicting LAA inactivity. Impaired LA strain identified patients with elevated fibrinogen, D-dimer, and the presence of LAA thrombus. Conclusion: Left atrial strain imaging provides a robust non-invasive predictor of LAA dysfunction in severe rheumatic MS patients in sinus rhythm. These findings support the potential clinical utility of LA strain in improving risk stratification and guiding anticoagulation decisions in this under-recognized high-risk population.

Left ventricular (LV) pseudoaneurysm, a rare occurrence, develops when a ruptured ventricle is encapsulated by the pericardium or scar tissue. Unlike free intrapericardial rupture, which often results in cardiac tamponade and fatal outcome, there are instances where the cardiac rupture remains contained, forming a pseudoaneurysm and averting immediate tamponade. We describe a 43-year-old male who underwent successful surgical repair of LV rupture following inferior wall myocardial infarction that resulted in the formation of a large pseudoaneurysm. The diagnostic challenges encountered and the technical difficulties that were seen while performing the repair of the defect are being described. As the diagnosis can be challenging, swift and precise identification of LV pseudoaneurysm is paramount due to significant risk of rupture and mortality. Consequently, surgical intervention is advised as the preferred treatment for pseudoaneurysm repair. The potential dangers of rupture far outweigh the inherent risks associated with surgery, emphasizing the urgency of timely intervention.