Ghulam Muhammad Mahar Medical College (غلام محمد مہر میڈیکل کالج) or GMMMC in short is the sixth public sector Medical college under the Government of Sindh where 100 meritorious students of tagged districts, including Sukkur, Khairpur and Ghotki are getting education every year. It is named after Sindh politician Ghulam Muhammad Khan Mahar.It is a constituent College of Shaheed Mohtarma Benazir Bhutto Medical University, located in the center of Sukkur city GMMMC is home to 500 students in the MBBS programs, with clinical rotations occurring at GMMMC Teaching Hospital, Government Anwar Piracha Teaching Hospital, SIUT Chablani Medical Center Sukkur, National Institute of Cardiovascular Diseases (NICVD), Sukkur satellite center. The school has a large and experienced faculty to support its mission of education, research, and clinical care. Faculty members hold appointments at basic sciences and clinical departments. There are about 114 full-time faculty members consisting of Lecturers, Assistant Professors, Associate Professors, and Professors at GMMMC..
Background:ST-segment elevation myocardial infarction (STEMI) continues to be a leading cause of cardiovascular (CV) morbidity and mortality worldwide, posing an ongoing clinical and public health burden. Although angiotensin-converting enzyme inhibitors (ACEIs) remain integral to guideline-recommended therapy following STEMI, recent evidence indicates that sacubitril/valsartan may offer superior cardioprotective benefits. This meta-analysis aims to systematically evaluate and compare the efficacy and safety of sacubitril/valsartan versus ACEIs in the management of patients with STEMI. Methods:PubMed and Cochrane databases were systematically searched from inception to July 2024 to identify randomized controlled trials (RCTs) comparing sacubitril/valsartan and ACEIs in patients with STEMI. Data were synthesized using a random-effects model to calculate risk ratios (RRs) and weighted mean differences (WMDs), each with 95% confidence intervals (CIs). A P-value < 0.05 was considered statistically significant. Results:A total of five RCTs comprising 4915 participants were included in the final analysis. Sacubitril/valsartan therapy was associated with a significant reduction in major adverse cardiovascular events (MACE) [RR: 0.66 (0.50, 0.86); P = 0.002] and hospitalizations for heart failure (HHF) [RR: 0.67 (0.49, 0.92); P = 0.01]. Treatment with sacubitril/valsartan also significantly improved left ventricular ejection fraction (LVEF) [WMD: 2.60 (1.53, 3.68); P < 0.00001] and reduced NT-proB-type natriuretic peptide (NT-proBNP) levels (WMD: -268.89 [-422.35, -115.42]; P = 0.0006). No significant differences were observed in the risk of recurrent myocardial infarction [RR: 1.02 (0.39, 2.71); P = 0.96), CV death [RR: 0.78 (0.61, 1.01); P = 0.06], or all-cause mortality [RR: 0.85 (0.68, 1.06); P = 0.15]. Safety analyses revealed no significant differences in the risk of cough [RR: 0.63 (0.15, 2.72); P = 0.54], hypotension [RR: 1.68 (0.97, 2.91); P = 0.06], worsening renal function [RR: 0.51 (0.22, 1.21); P = 0.13], or hyperkalemia [RR: 0.59 (0.17, 2.01); P = 0.40]. Conclusion:Sacubitril/valsartan therapy significantly reduces MACE and HHF and improves LVEF in patients with STEMI, without increasing the risk of adverse safety outcomes. Future well-powered randomized trials are needed to confirm these results and support clinical guideline recommendations.
Background: Haemorrhagic stroke (HS) is a major cause of mortality in post-menopausal women (PM), who face heightened risk due to vascular aging. While overall stroke mortality has declined, recent data show slowing progress and persistent racial and regional disparities, necessitating reassessment of long-term trends. Methods: We analysed U.S. mortality data (1999–2023) from CDC WONDER for women aged ≥55 years (PM). HS deaths were identified using ICD-10 code I61. Age-adjusted (AAMR) and crude mortality rates (CMR) were calculated, stratified by race/ethnicity, region, and place of death. Trends were assessed with Joinpoint regression, reporting APC, AAPC, 95% CI, significance at p<0.05. Sensitivity analysis used overall U.S. adult HS mortality for comparison. Results: Overall PM AAMR declined (AAPC = -2.16%*), from 36.5 (1999) to 21.2 (2023). Two phases emerged: rapid decline (APC = -3.43%*) from 1999–2012, then slower decline (APC = -0.63%*) from 2012–2023. Sensitivity analysis showed overall mortality declined from 10.1 to 6.3 (AAPC = -1.90*), with early reductions (APC = -3.49%*) and stabilization post 2012 (APC = 0.12%), confirming similar plateauing trends and highlighting that PM women remain disproportionately affected. All racial groups declined significantly. American Indian/Alaska Natives (-2.15%*), Asian/Pacific Islanders (-3.20%*) and Hispanics (-2.13%*) had steep early declines that flattened after 2012, Whites (-2.20%*) showed strong early reductions with slower declines after 2011, and non-Hispanic Black women had highest rates (42.4→26.0) with slowest decline (-1.99%*). Mortality decreased across all ages (55–64, 65–74, 75–84, 85+) but spiked in 2020/2021, most in oldest cohorts. All census regions declined (AAPCs: -2.35%* Northeast, -1.92%* Midwest, -2.24%* South, -2.27%* West), with early reductions slowing after 2010–2012. Most deaths occurred in inpatient facilities (75%) Conclusions: HS mortality in PM women fell substantially since 1999, with trends similar to overall adult mortality but slowed after 2012. Trends in postmenopausal women mirror the general population but at higher mortality, underscoring heightened burden. Non-Hispanic Black women remain most affected, with highest rates and slowest decline, and regional disparities persist. Surges in 2020–2021, especially in oldest women, underscore fragile gains. Equity-focused, targeted public health strategies are urgently needed to address disparities and sustain prevention.
Cardiac troponin elevation is central to the diagnosis of myocardial injury, but its clinical interpretation remains challenging when type 1 myocardial infarction is absent. This systematic review evaluated the clinical and prognostic significance of elevated cardiac troponin in adults without type 1 myocardial infarction, with particular emphasis on type 2 myocardial infarction, critical illness-related myocardial injury, suspected acute coronary syndrome populations with minor myocardial injury, and acute or chronic heart failure-related myocardial injury. A systematic search of PubMed/MEDLINE, Scopus, and Web of Science identified six eligible clinical studies. The included evidence comprised prospective and retrospective cohort studies, secondary biomarker analyses of randomized trials, and trial-derived heart failure cohorts. Across heterogeneous clinical settings, troponin elevation was consistently associated with adverse outcomes, including all-cause mortality, cardiovascular mortality, heart failure hospitalization, cardiovascular death or heart failure rehospitalization, and greater clinical severity. In type 2 myocardial infarction and critical illness, troponin elevation identified high-risk patients despite the absence of classic plaque-rupture acute coronary syndrome. In heart failure populations, troponin appeared to function as a dynamic marker of myocardial stress, residual risk, and treatment-responsive injury. High-sensitivity assays further suggest that troponin may convey prognostic information across a continuum rather than only above binary diagnostic thresholds. These findings support a phenotype-based approach in which troponin elevation outside type 1 myocardial infarction is interpreted according to mechanism, clinical context, biomarker trajectory, and follow-up needs. Although current evidence does not define a uniform treatment pathway, it indicates that troponin-positive patients without type 1 myocardial infarction should not be considered low risk solely because acute coronary syndrome has been excluded. Future prospective studies should determine which troponin-positive phenotypes benefit most from structured cardiovascular reassessment, targeted investigation, and post-discharge surveillance.
Background:Ventricular arrhythmias (VAs) remain a leading cause of sudden cardiac death (SCD) in patients with ischemic and nonischemic cardiomyopathy, driven substantially by sympathetic nervous system overactivity and elevated catecholamine tone. Beta-adrenergic receptor blockers have been a cornerstone of pharmacotherapy for decades, yet their antiarrhythmic efficacy extends well beyond simple heart rate reduction. Objective:This narrative review synthesizes current evidence on the antiadrenergic mechanisms by which beta-blockers suppress ventricular arrhythmogenesis, evaluates their clinical impact in ischemic and nonischemic cardiomyopathy populations, delineates differential effects among specific beta-blocker agents, and details their safety profiles and clinical limitations.
