Xin Wei

Background: Inferior ST-segment elevation myocardial infarction (STEMI) complicated by right ventricular involvement (RVMI) leads to right-heart-dominant failure and a higher incidence of cardiogenic shock (CS). Evidence guiding the choice between inotropic agents in this specific phenotype remains limited. Methods: This single-center retrospective cohort study included 211 patients with inferior STEMI and suspected RVMI treated with either dobutamine (n = 55) or milrinone (n = 156) between June 2009 and June 2025. The primary outcome was 30-day mortality. Secondary outcomes included duration of inotropic support and hospital length of stay. Confounding and missing data were addressed using multiple imputation, multivariable Cox regression, inverse probability of treatment weighting, and sensitivity analyses. Results: The dobutamine group had more severe hemodynamic and electrical instability, while the milrinone group exhibited greater left ventricular dysfunction. The 30-day mortality rates were 25.5% for dobutamine and 29.5% for milrinone. No significant difference was found in unadjusted (HR 0.863; 95% CI 0.475–1.570; P = 0.632) or multivariable-adjusted Cox analysis (HR 0.612; 95% CI 0.316–1.187; P = 0.153), with results remaining consistent across multiple sensitivity and propensity-based analyses. Notably, among survivors, the duration of inotropic support was significantly shorter in the dobutamine group (3.1 vs. 5.0 days; adjusted β = −1.805; 95% CI −3.147 to −0.463; P = 0.009). Conclusion: In patients with inferior STEMI and suspected RVMI, no statistically significant difference in 30-day mortality was detected between dobutamine and milrinone, though the study was underpowered to establish equivalence. Dobutamine was associated with a shorter duration of support among survivors despite its application in more unstable patients. Inotrope selection should therefore be individualized based on the patient’s hemodynamic phenotypes.

Background: Ventricular septal rupture (VSR) following acute myocardial infarction (AMI) creates an abrupt left-to-right shunt that can progress to cardiogenic shock (CS). Once CS develops, mortality increases dramatically and delayed repair becomes less feasible. Intra-aortic balloon pumps (IABPs) are widely used to facilitate delayed repair; however, whether initiating IABP before CS onset improves survival remains unclear. Methods: We retrospectively analyzed 124 patients with AMI-related VSR (2009–2024), categorized by IABP timing relative to CS onset (defined as first catecholamine administration) into pre-CS, post-CS, and no-IABP groups. The primary outcome was all-cause mortality within 90 days after AMI onset. Kaplan–Meier curves and Cox proportional hazards models were applied, with subgroup analyses by CS status. Results: The 90-day survival rate was 68.2% in the pre-CS IABP group, 14.3% in the post-CS group, and 35.1% in the no-IABP group. Pre-CS IABP was associated with significantly lower mortality compared with no-IABP (adjusted HR = 0.401, 95% CI 0.174–0.925, p = 0.032) and post-CS IABP (adjusted HR = 0.369, 95% CI 0.149–0.910, p = 0.030). In the CS subgroup, IABP use did not improve survival (19.4% vs. 17.6%, p = 0.365). Among non-CS patients, IABP use was independently associated with lower mortality (85.7% vs. 50.0%, p = 0.027; adjusted HR = 0.178, 95% CI 0.040–0.801, p = 0.025). Conclusions: Given the retrospective design and limited sample size, these findings are hypothesis-generating. Early IABP use was associated with improved short-term survival, an effect not observed once CS had developed. These findings support early risk stratification to identify high-risk patients who may benefit from timely hemodynamic support.

Background: The clinical value of B-type natriuretic peptide (BNP) or N-terminal pro-B-type natriuretic peptide (NT-proBNP)-guided therapy for improving outcomes in patients with heart failure (HF) remains controversial. Thus, this meta-analysis synthesizes the available evidence from randomized controlled trials (RCTs) to determine whether a biomarker-guided strategy reduces all-cause mortality and HF-related hospitalizations compared with clinically guided management. Methods: This systematic review followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. We conducted a systematic search of PubMed, Embase, the Cochrane Library, and Web of Science databases from inception to May 2025 for RCTs comparing biomarker-guided versus clinically guided management in patients with HF. Pooled risk ratios (RRs) were calculated using a random-effects model. We performed extensive supplementary analyses, including a subgroup analysis, sensitivity analysis, and trial sequential analysis (TSA). Results: We included 17 articles (reporting on 17 distinct RCTs) comprising 5069 patients. The primary meta-analysis showed that biomarker-guided therapy was associated with a significant reduction in all-cause mortality (RR 0.84, 95% confidence interval (CI) 0.73–0.96; I2 = 12.2%) and HF-related hospitalizations (RR 0.79, 95% CI 0.65–0.96; I2 = 53.7%). However, the robustness of these findings was undermined by subsequent analyses. Meanwhile, a sensitivity analysis restricted to studies with a low risk of bias rendered the mortality benefit non-significant (RR 0.90, 95% CI 0.79–1.03). Egger's test indicated potential publication bias (p = 0.0285), and TSA suggested the cumulative evidence was insufficient to draw a definitive conclusion. Conclusions: Although there is a trend toward benefit, the existing evidence for biomarker-guided HF therapy is deemed “very low” quality based on the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) assessment. The results were compromised by methodological deficiencies in primary studies and potential publication bias. Therefore, the evidence is inadequate to support the routine use of this strategy in clinical practice. Further large-scale, high-quality RCTs are warranted. The PROSPERO Registration: CRD420250652134, https://www.crd.york.ac.uk/PROSPERO/view/CRD420250652134.

Background: Fulminant type 1 diabetes (FT1D) is a rare but life-threatening subtype of type 1 diabetes. The concurrence of FT1D with myocarditis is uncommon and attracts further clinical attention. Case Presentation: A 33-year-old female was transferred by a local hospital to West China Hospital because of altered consciousness, abrupt onset of hyperglycemia with ketoacidosis, significantly increased cardiac biomarkers, and ST segment elevations. Her random blood glucose at the local hospital was 50.19 mmol/L. Insulin infusion and fluid resuscitation were started immediately before referral. On admission, her random blood glucose was 14.17 mmol/L. HbA1C and glycosylated albumin (GA) were 6.3% and 21.45%, respectively. Her fasting C-peptide level was 0.022 nmol/L. Anti-Glutamic Acid Decarboxylase (anti-GAD) antibody was 25.06 IU/mL. FT1D was diagnosed based on the 2012 New Diagnosis Criteria of FT1D. Electrocardiogram showed significant ST segment elevation in leads II, III, aVF, and V3-V6. Echocardiography revealed a mildly reduced left ventricular ejection fraction (LVEF) of 46%. Coronary angiography displayed no abnormality. Cardiac magnetic resonance imaging revealed areas of increased signal intensity in the interventricular septum, basal and mid inferolateral walls, and apical inferior wall and subepicardial late gadolinium enhancement (LGE), particularly in the lateral aspects of the left ventricle on T2-weighted imaging (T2WI). Acute myocarditis was diagnosed based on the European Society of Cardiology 2013 Task Force Criteria. She was treated with insulin, fluid resuscitation, and supportive care, leading to rapid recovery of ketoacidosis and cardiac function. At the four-month follow-up, she remained on insulin therapy with good glycemic control but persistent low C-peptide levels. Conclusion: This case report raises awareness about FT1D, determines the differential diagnosis of acute cardiac presentations in an FT1D patient, and highlights clinical reasoning so that clinicians can recognize and manage similar presentations on time.

Myocardial infarction with non-obstructive coronary arteries (MINOCA) is a rare cause of heart attack, which may not receive sufficient attention from patients during post-discharge treatment, especially among those with normal coronary angiography results. We present the case of a 65-year-old woman who was readmitted to the hospital with ventricular septal rupture (VSR) complicated by ventricular aneurysm, occurring 2 weeks after myocardial infarction. During the initial admission, coronary angiography revealed normal coronary arteries, leading to a diagnosis of MINOCA. Epicardial coronary vasospasm or coronary embolism was considered as potential causes; however, the patient did not adhere to standardized treatment upon initial discharge. The delayed VSR led to a decline in cardiac function but did not result in severe hemodynamic impairment. Following correction of heart failure with medications, the patient underwent percutaneous VSR repair 19 days after diagnosis and was discharged with a favorable recovery. The occurrence of delayed VSR complicated with ventricular aneurysm in patients with MINOCA is rare, highlighting the possibility of serious complications in MINOCA cases. Both cardioprotective therapies and cause-targeted therapies are essential in the management of patients with MINOCA.