Heart failure with preserved ejection fraction (HFpEF) is common in type 2 diabetes mellitus (T2D), leading to high morbidity and mortality. Managing HFpEF in diabetic patients is challenging with limited treatments. Sodium-glucose co-transporter 2 (SGLT2) inhibitors and glucagon-like peptide-1 receptor agonists (GLP1-RA) have shown potential cardiovascular benefits. This meta-analysis compares the effects of GLP1-RA and SGLT2 inhibitors on HFpEF in T2D patients. We conducted a meta-analysis of randomized controlled trials (RCTs) and observational studies evaluating GLP1-RA and SGLT2 inhibitors’ impact on HFpEF in T2D patients. Databases searched included PubMed, MEDLINE, and Cochrane Library up to July 2024. Primary outcomes were changes in left ventricular ejection fraction (LVEF), myocardial fibrosis (extracellular volume fraction, ECV), and functional capacity (6-minute walk test, 6MWT). Secondary outcomes included HbA1c, body weight, and systolic blood pressure (SBP). Twelve studies with 3,428 patients (GLP1-RA: 1,654; SGLT2 inhibitors: 1,774) were included. Both GLP1-RA and SGLT2 inhibitors significantly improved LVEF compared to placebo (GLP1-RA: mean difference [MD] 2.8%, 95% confidence interval [CI] 1.5 to 4.1, p < 0.001; SGLT2 inhibitors: MD 3.2%, 95% CI 2.0 to 4.4, p < 0.001). SGLT2 inhibitors significantly reduced myocardial fibrosis (MD -3.5%, 95% CI -4.2 to -2.8, p < 0.001) more than GLP1-RA (MD -2.3%, 95% CI -3.0 to -1.6, p < 0.001). Functional capacity improved significantly with both treatments (GLP1-RA: MD 45 m, 95% CI 30 to 60, p < 0.001; SGLT2 inhibitors: MD 50 m, 95% CI 35 to 65, p < 0.001). Secondary outcomes showed reductions in HbA1c (GLP1-RA: MD -1.1%, 95% CI -1.4 to -0.8, p < 0.001; SGLT2 inhibitors: MD -1.0%, 95% CI -1.3 to -0.7, p < 0.001) and body weight (GLP1-RA: MD -2.5 kg, 95% CI -3.1 to -1.9, p < 0.001; SGLT2 inhibitors: MD -2.0 kg, 95% CI -2.6 to -1.4, p < 0.001). Both treatments significantly lowered SBP (GLP1-RA: MD -5.2 mmHg, 95% CI -6.5 to -3.9, p < 0.001; SGLT2 inhibitors: MD -4.8 mmHg, 95% CI -6.0 to -3.6, p < 0.001). GLP1-RA and SGLT2 inhibitors significantly benefit HFpEF management in T2D patients. SGLT2 inhibitors reduce myocardial fibrosis more effectively, while both improve LVEF, functional capacity, and metabolic parameters. These therapies should be integral to HFpEF management in diabetic patients. Further research is needed on long-term outcomes and potential combined therapy effects.

Background: Sodium–glucose co-transporter 2 (SGLT2) inhibitors offer cardiovascular benefits in patients with heart failure, yet their direct effects on myocardial fibrosis—particularly in heart failure with preserved ejection fraction (HFpEF) and type 2 diabetes (T2D)—remain underexplored. This study investigates the antifibrotic impact of dapagliflozin in diabetic HFpEF patients, with a focus on its potential as a disease-modifying therapy. Methods: In a multicenter, double-blind, placebo-controlled trial, 100 patients with HFpEF and T2D were randomized (1:1) to receive dapagliflozin 10 mg daily or placebo for 12 months. Stratification was performed by baseline extracellular volume fraction (ECV). Myocardial fibrosis was assessed using cardiac MRI-derived ECV at baseline, 6 months, and 12 months. Secondary endpoints included changes in left ventricular mass index (LVMI), HbA1c, and 6-min walk test (6MWT) distance. Results: Dapagliflozin significantly reduced myocardial fibrosis (mean ΔECV: − 3.5% [95% CI − 4.2 to − 2.8]) compared to placebo (− 0.8% [95% CI − 1.3 to − 0.4]; p < 0.001). Additional benefits included greater reductions in LVMI (− 8.2 g/m² vs. − 2.1 g/m²; p = 0.002), improved glycemic control (HbA1c: − 1.2% vs. − 0.4%; p = 0.01), and enhanced functional capacity (+ 45 m vs. + 10 m in 6MWT; p = 0.01). Conclusions: Dapagliflozin demonstrated a significant reduction in myocardial fibrosis and improvements in cardiac structure, metabolic control, and exercise tolerance in HFpEF patients with T2D. These findings support the evolving role of SGLT2 inhibitors as validated components of guideline-directed therapy, with potential disease-modifying effects through targeted myocardial fibrosis regression.

To describe the epidemiology of acute pancreatitis in a tertiary care center in Oman. A retrospective study evaluated all adults (>18 yrs) who presented with first attack of acute pancreatitis to SQUH from 1(st) of January 2006 to 31(st) of December 2012. One hundred seventy-four patients were found. The mean age of the cohort was 44 ± 11 years. 54% (n=95) were male and 45% (n=79) were female. Majority of the cases were mild (n=131) compared to moderate (n=29) and severe (n=14). Sixty six percent (n=116) of the cases were secondary to alcohol and biliary tract diseases. Alcoholic pancreatitis occurred in 53% of the males whereas biliary pancreatitis occurred in 51% of the females. Pancreatitis recurred in 40% (n=71) of the cases, especially in alcoholic pancreatitis. 56 patients (32%) had complications, especially in the severe cases. The data about acute pancreatitis in Oman was similar to the Western countries. Pancreatitis occurred in males more than females. Alcoholic pancreatitis was more common in males, whereas biliary pancreatitis was more common in females. Alcoholic pancreatitis re-occurred in nearly half of the cases. Severe cases were associated with more complications and recurrence.

Emerging evidence suggests a significant link between the gut microbiome and cardiovascular health, yet its role in the pathophysiology of heart failure has been underexplored. This systematic review and meta-analysis synthesize available research on how gut microbiota influence heart failure, offering new insights into therapeutic interventions. We conducted a comprehensive search of multiple databases for studies published up to the present, focusing on observational and experimental research that examines the relationship between the gut microbiome and heart failure outcomes. Eligibility criteria included studies on humans with diagnosed heart failure, assessments of microbiome composition, and reported cardiovascular outcomes. Quality assessment was performed using standardized tools, and meta-analysis was conducted to quantify the impact of microbiome diversity and composition on heart failure progression and response to treatment. The analysis included 25 studies encompassing 3200 patients with heart failure. Specific microbial profiles, particularly an increased abundance of Firmicutes and decreased Bacteroidetes, were associated with worsened heart failure conditions. Correlations were found between microbial diversity indices and clinical markers such as left ventricular ejection fraction (LVEF) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels. Mechanistic insights suggested that microbial metabolites, such as short-chain fatty acids and trimethylamine-N-oxide (TMAO), play a critical role in modulating inflammatory pathways and cardiac function. This review highlights the gut microbiome as a potential target for innovative therapeutic strategies in heart failure management. Modulating gut microbiota composition and diversity through dietary interventions, probiotics, or microbiome transplantation could offer new avenues for improving cardiovascular outcomes in heart failure patients. Integrative approaches in cardiovascular healthcare should consider the gut-heart axis for comprehensive disease management.

Objective: To determine the incidence and pattern of thyroid dysfunction (TD) in patients on chronic amiodarone therapy.Methods: A retrospective study which evaluated 59 patients who had received amiodarone therapy regularly for at least 12 months from a period of 3 years from October 2007 to October 2010. The patients were followed-up at the cardiac clinic at Sultan Qaboos University Hospital, Muscat, Oman.Results: The mean age of the cohort was 63 ± 13 years ranging from 27 to 98 years. Fifty-one percent (n = 30) of the patients were female. There were 11 (19%) cases of thyroid dysfunction (TD). Seven (12%) patients were hypothyroid, 3 (5%) had hyperthyroidism and 1 (2%) patient had sub-clinical hypothyroidism; no cases of sub-clinical hyperthyroidism were noted. Female gender and presence of anti-thyroid peroxidase antibodies were significantly associated with amiodarone-induced hypothyroidism (p = 0.001) while age, amiodarone dose and duration of therapy were not correlated with the development of TD (all p-values > 0.05).Conclusion: Amiodarone-induced thyroid dysfunction is prevalent. Hypothyroidism was more frequent and seen more in female patients and those who had positive anti-thyroid peroxidase antibodies. Initial screening and periodic monitoring of thyroid function is mandatory for all patients on amiodarone therapy.