Objectives: This randomized controlled trial aimed to compare the effects of rosuvastatin and a supervised resistance-band exercise program on lipid profile, anthropometric measures, blood pressure, and health-related quality of life in obese adults with dyslipidemia. Methodology: A randomized, parallel-group, active-controlled trial was conducted between October 2024 and April 2025. Participants received either rosuvastatin 5 mg daily (Group A) or a supervised resistance-band exercise program performed three times weekly for 10 weeks (Group B). Primary outcomes included changes in lipid profile parameters, while secondary outcomes included blood pressure, body mass index (BMI), waist-to-hip ratio, hip circumference, and quality of life assessed using the SF-36 questionnaire. Outcomes were measured at baseline, week 5, and week 10. Results: Both interventions were associated with significant improvements over time in cardiometabolic, anthropometric, and quality-of-life outcomes (p ≤ 0.005). Rosuvastatin resulted in significantly greater reductions in systolic and diastolic blood pressure, total cholesterol, and LDL cholesterol compared with resistance-band exercise (p < 0.001). In contrast, resistance-band exercise produced significantly greater improvements in body weight, BMI, waist-to-hip ratio, and hip circumference (p < 0.001). Improvements in quality of life modestly favored the exercise group (p = 0.046). No significant between-group differences were observed for triglycerides or HDL cholesterol. Conclusion: Both rosuvastatin and resistance-band exercise were effective in improving lipid profiles and cardiometabolic health in obese adults with dyslipidemia. Pharmacological therapy demonstrated superior lipid-lowering and blood pressure effects, whereas structured resistance exercise provided greater benefits for body composition and quality of life.
Objectives: To determine the frequency of pediatric myocarditis among admissions to a tertiary-care pediatric cardiology unit and to evaluate the clinical characteristics, laboratory findings, echocardiographic features, and short-term outcomes of children diagnosed with myocarditis in the post-COVID-19 era. Methodology: This descriptive cross-sectional study was conducted at the Pediatric Cardiology Department of The Children’s Hospital, Multan, Pakistan, from August 2025 to January 2026. Children aged up to 14 years admitted with newly diagnosed clinically suspected myocarditis were enrolled consecutively. Demographic characteristics, clinical manifestations, laboratory parameters, echocardiographic findings, COVID-19 exposure status, and in-hospital outcomes were recorded. Results: Among 892 pediatric admissions during the study period, 76 (8.5%) children were diagnosed with myocarditis. The median age was 2.00 years (IQR 1.00–3.75), and 43 (56.6%) children were male. Evidence of prior COVID-19 exposure or infection was identified in 36 (47.4%) children. The median left ventricular ejection fraction was 24.50% (IQR 16.25–28.00), indicating marked myocardial dysfunction. Fever (89.5%), respiratory distress (81.6%), and palpitations (64.5%) were the most frequent presenting symptoms. Elevated cardiac biomarkers and inflammatory markers were commonly observed. Inotropic support was required in 75 (98.7%) children. The overall in-hospital mortality rate was 17.1% (n=13). No statistically significant differences were observed between children with and without evidence of prior COVID-19 exposure or infection regarding demographic characteristics, clinical presentations, laboratory findings, echocardiographic parameters, mortality, or duration of hospital stay (p>0.05). Conclusion: Pediatric myocarditis represented a considerable burden among admissions to a tertiary-care pediatric cardiology unit during the post-COVID-19 period. Although evidence of prior COVID-19 exposure or infection was present in nearly half of the myocarditis cases, short-term clinical features and in-hospital outcomes were broadly comparable between children with and without evidence of COVID-19 exposure or infection. Early recognition and timely management remain essential to improve outcomes in pediatric myocarditis.
Objectives: To determine the frequency of maternal and fetal outcomes among pregnant women with cardiac disease presenting at Lady Reading Hospital and to explore the association of selected maternal comorbidities with adverse obstetric outcomes. Methodology: A descriptive cross-sectional study was conducted at the Department of Obstetrics and Gynaecology at Lady Reading Hospital. A total of 85 pregnant women with confirmed cardiac disease were recruited. Data regarding demographic characteristics, cardiac disease classification, maternal outcomes, and fetal outcomes were collected using medical records and patient interviews. Maternal outcomes included mode of delivery, postpartum hemorrhage, and maternal mortality, while fetal outcomes included preterm delivery, intrauterine growth retardation (IUGR), intrauterine fetal death (IUFD), and stillbirth. Results: The mean age of participants was 30.07 ± 6.00 years. Rheumatic heart disease was the most common cardiac disorder (40.0%), followed by congenital heart disease (32.9%). Normal vaginal delivery was the most frequent maternal outcome, observed in 35.3% of patients, followed by planned cesarean section in 23.5%. Postpartum hemorrhage occurred in 8.2% of participants, while maternal mortality was observed in 2.4%. Among fetal outcomes, intrauterine growth retardation was the most common complication (14.1%), followed by preterm delivery (11.8%), intrauterine fetal death (4.7%), and stillbirth (3.5%). No statistically significant associations were observed between smoking, hypertension, diabetes mellitus, and adverse maternal or fetal outcomes (p>0.05). Conclusion: Pregnancy complicated by cardiac disease was associated with considerable maternal and fetal morbidity in this study population. Although normal vaginal delivery remained the most frequent mode of delivery, adverse maternal and fetal outcomes, including postpartum hemorrhage, maternal mortality, IUGR, preterm delivery, IUFD, and stillbirth, were also observed. Early risk stratification, multidisciplinary management, and routine fetal growth monitoring may improve obstetric outcomes in this high-risk population.
Objectives: This study aimed to identify risk factors that may predict the severity of coronary artery disease (CAD) among patients with inflammatory bowel disease (IBD). Methodology: A case-control study was conducted on 110 participants, comprising 55 patients with IBD and 55 healthy controls. Cardiovascular risk was evaluated using the Framingham risk score, carotid intima-media thickness (CIMT), and coronary angiography quantified by the SYNTAX score. CAD severity was categorized as low (SYNTAX ≤22) or moderate-to-high (SYNTAX >22). Results: Patients with IBD exhibited significantly higher leukocyte counts, fasting blood glucose, C-reactive protein (CRP), CIMT, and SYNTAX scores compared to controls (p<0.05). Atherosclerotic plaques were also more prevalent in the IBD group (21.8% vs. 3.6%). Among participants with SYNTAX >22, age, diabetes mellitus (DM), hypertension (HTN), smoking, and IBD prevalence were significantly higher. Multivariate logistic regression identified DM (OR=5.26, p=0.022), HTN (OR=3.89, p=0.026), smoking (OR=4.52, p=0.024), and IBD (OR=2.77, p<0.001) as independent predictors of severe CAD. Conclusion: IBD is significantly associated with more severe CAD, reflected in higher SYNTAX scores and CIMT values, independent of traditional cardiovascular risk factors. These findings highlight the importance of incorporating chronic inflammation markers into cardiovascular risk assessment models for IBD patients.
Objectives: To compare the angiographic, functional, and clinical outcomes of deferred versus immediate stenting strategies in patients presenting with ST-segment elevation myocardial infarction (STEMI) and high thrombus burden undergoing primary percutaneous coronary intervention (PCI). Methodology: This retrospective observational cohort study was conducted at the Department of Cardiology, Lady Reading Hospital, Peshawar, Pakistan, between January 2022 and December 2024. A total of 450 adult STEMI patients with angiographically confirmed high thrombus burden (TIMI thrombus grade ≥3) undergoing primary PCI were included. Patients were categorized into immediate stenting (n=218) and deferred stenting (n=232) groups. Deferred stenting involved initial reperfusion followed by delayed stent implantation after 24–72 hours of intensive antithrombotic therapy. The primary endpoint was the occurrence of no-reflow/slow-reflow phenomenon. Secondary outcomes included final TIMI flow grade 3 achievement, major adverse cardiac events (MACE) at 30 days and 6 months. Results: Deferred stenting was associated with a significantly lower incidence of no-reflow/slow-reflow compared with immediate stenting (5.2% vs. 28.9%, p<0.001). Final TIMI flow grade 3 achievement was significantly higher in the deferred group (94.8% vs. 71.1%, p<0.001). Patients undergoing deferred stenting demonstrated superior left ventricular systolic function (LVF) recovery both at discharge (49.7±5.6% vs. 44.2±7.1%, p<0.001) and at 6-month follow-up (55.3±5.3% vs. 50.2±5.6%, p<0.001). While 30-day MACE rates were not significantly different between groups (9.1% vs. 12.4%, p=0.252), the deferred stenting group showed significantly lower MACE rates at 6 months (10.8% vs. 20.2%, p=0.006). Conclusion: In STEMI patients with high thrombus burden, deferred stenting was associated with improved myocardial perfusion, better recovery of LVF, and lower mid-term adverse cardiovascular events compared with immediate stenting, without significant increase in bleeding or procedural complications. Deferred stenting may therefore represent a beneficial strategy in carefully selected high-risk patients undergoing primary PCI.
Cardiovascular disease (CVD) continues to impose a substantial burden on global health systems, with coronary artery disease (CAD) remaining the leading cause of morbidity and mortality worldwide. In Pakistan, this burden is particularly concerning, as CAD not only presents with high prevalence but also manifests at younger ages and often with increased clinical complexity. While conventional risk factors such as hypertension, diabetes mellitus, sedentary lifestyle, and tobacco use contribute significantly to disease progression, they do not fully account for the early onset and severity observed in many patients. This underscores the need to explore underlying genetic predispositions that may contribute to disease susceptibility [1,2]. In this context, the study by Pathan et al. [3] provides valuable insight into the genetic determinants of CAD. The authors focus on the Factor V Leiden (FVL) mutation, a well-characterized genetic variant associated with resistance to activated protein C and a resultant prothrombotic state. Although its role in venous thromboembolism is well established, the association between FVL and arterial thrombosis, including CAD, has remained inconsistent across different populations [4]. The findings of this case–control study are noteworthy. The authors demonstrate a statistically significant association between the FVL mutation and CAD, with the heterozygous GA genotype observed more frequently in CAD patients (15%) compared with controls (4%), corresponding to an approximately fourfold increased risk. Furthermore, the study reports a significant relationship between the presence of the mutant allele and angiographic severity, with higher frequencies of GA and AA genotypes among patients with multi-vessel disease. These findings suggest that the FVL polymorphism may not only contribute to disease susceptibility but may also be associated with more extensive coronary involvement. Importantly, the study also reaffirms the role of traditional cardiovascular risk factors, including hypertension, dyslipidemia, hyperglycemia, and elevated fibrinogen levels, all of which were significantly more prevalent among CAD patients. The coexistence of these metabolic abnormalities with prothrombotic genetic variants highlights a potential synergistic effect, contributing to enhanced thrombotic tendency and accelerated atherosclerotic progression. Notably, the independent association of the FVL polymorphism with CAD risk, even after adjustment for confounders, suggests that genetic predisposition may represent an additional layer of risk beyond conventional factors [5]. From a clinical perspective, these findings prompt important considerations. The concept of integrating genetic screening into cardiovascular risk assessment, particularly among younger individuals or those with a strong family history of CAD, aligns with the emerging paradigm of precision medicine. However, it is essential to interpret these results with caution. Current international guidelines do not support routine screening for FVL in CAD patients, and the evidence base remains insufficient to warrant immediate changes in clinical practice. Several limitations inherent to the study design must also be acknowledged. The relatively modest sample size and single-population focus may limit generalizability, while the case–control design precludes definitive causal inference. Additionally, CAD is a multifactorial and polygenic disorder, and the evaluation of a single genetic polymorphism may not fully capture the complexity of its genetic architecture. Nevertheless, this study makes a meaningful contribution to the growing body of literature exploring genetic determinants of CAD in South Asian populations. It reinforces the importance of population-specific research and highlights the potential role of thrombophilia-related genetic variants in cardiovascular disease pathogenesis. The work by Pathan et al. advances our understanding of the interplay between genetic and traditional risk factors in CAD. While further large-scale, multi-center, and longitudinal studies are required to validate these findings, this study provides an important step toward more individualized approaches to cardiovascular risk assessment and prevention. References Agosti P, Mancini I, Sadeghian S, Pagliari MT, Abbasi SH, Pourhosseini H, et al. Factor V Leiden but not the factor II 20210G> A mutation is a risk factor for premature coronary artery disease: a case-control study in Iran. Res Pract Thromb Haemost. 2023;7(1):100048-56. DOI: 10.1016/j.rpth.2023.100048 Athar M, Abduljaleel Z, Ghita IS, Albagenny AA, Halawani SH, Alkazmi MM, et al. Prevalence of the factor V Leiden mutation Arg534Gln in western region of Saudi Arabia: functional alteration and association study with different populations. Clin Appl Thromb Hemost. 2021;27:10. DOI: 10.1177/1076029620978532 Martin KA, Cushman M. Factor V Leiden. JAMA. 2025;333(22):2013. DOI: 10.1001/jama.2025.2420 Pathan AK, Waryah AM, Aziz Q, Nangrejo R, Siddiqui IA, Pathan AH. Association of Factor V Leiden (rs6025) Polymorphism with the Presence and Angiographic Severity of Coronary Artery Disease in a Pakistani Population: A Case–Control Study. Pak Heart J. 2026;59(02):317-325. DOI: 10.47144/phj.v59i2.3473 Cui Z, Zhao G, Liu X. Blood fibrinogen level as a biomarker of adverse outcomes in patients with coronary artery disease: A systematic review and meta-analysis. Medicine. 2022;101(33):e30117. DOI: 10.1097/md.0000000000030117
Ischemic heart disease (IHD) remains one of the leading global causes of death, primarily driven by atherosclerotic plaque progression and vascular dysfunction. Growing genomic and molecular evidence identifies A Disintegrin and Metalloproteinase with Thrombospondin Motifs-7 (ADAMTS7) as a key mediator in these pathological processes. ADAMTS7, a secreted zinc-dependent metalloproteinase, contributes to vascular smooth muscle cell migration by degrading extracellular matrix components such as cartilage oligomeric matrix protein (COMP). Several single-nucleotide polymorphisms, including the widely studied rs3825807 variant, have been associated with increased susceptibility to IHD, highlighting the genetic relevance of ADAMTS7. This narrative review synthesizes current literature on the genetic associations, molecular mechanisms, regulatory pathways, and translational implications of ADAMTS7 in ischemic heart disease. It further explores its emerging value as a biomarker and its potential as a therapeutic target for cardiovascular disease prevention and management.
Coarctation of the aorta (CoA) represents a significant proportion of congenital heart disease and remains a major cause of morbidity in early life. Timely intervention is essential, particularly in neonates where ductal closure may precipitate rapid clinical deterioration. Although surgical repair has traditionally been considered the standard of care, catheter-based interventions, including balloon dilatation, have gained increasing acceptance in selected patient populations. The study by Javed et al. provides important data regarding the immediate and short-term outcomes of balloon dilatation in neonates and infants, with a particular focus on age-related differences [1]. The authors report a significant reduction in transcoarctation gradient following balloon dilatation, confirming the effectiveness of the procedure in relieving obstruction. This finding is consistent with prior studies demonstrating that balloon angioplasty can achieve rapid hemodynamic improvement, particularly in critically ill patients requiring urgent intervention [2,3]. The observed reduction in median gradient and the acceptable rate of immediate procedural success support the role of balloon dilatation as a therapeutic option in early life.A key strength of this study is the comparison between neonates and infants. The results demonstrate that infants have significantly higher procedural success rates and better short-term outcomes compared to neonates. Lower post-procedure gradients and greater gradient reduction in infants suggest that anatomical and physiological factors associated with age play an important role in procedural efficacy. Neonates often present with smaller vessel size, increased vascular fragility, and associated arch hypoplasia, all of which may limit optimal balloon expansion and contribute to suboptimal results [4,5]. The study further highlights a clinically important issue: the risk of recoarctation. The overall recoarctation rate at six months was 23.47%, with a substantially higher incidence in neonates compared to infants. This observation is consistent with previously published data indicating that younger age at intervention is associated with increased risk of restenosis [6,7]. The identification of age as an independent predictor of recoarctation through multivariable analysis strengthens the validity of this finding and emphasizes the importance of age-specific treatment strategies. From a clinical perspective, these findings suggest that while balloon dilatation provides effective short-term relief, its durability in neonates remains limited. In this subgroup, the procedure may be more appropriately considered as a palliative or bridging intervention rather than definitive therapy. In contrast, infants appear to derive greater benefit, with improved procedural success and lower rates of recurrence, supporting the use of balloon dilatation as a more definitive option in selected cases. The safety profile reported in this study is reassuring. The low rate of major complications indicates that balloon dilatation can be performed safely in experienced centers. This is particularly relevant in settings where surgical resources may be limited or where critically ill patients may not be optimal candidates for immediate surgery [3,8]. In addition to hemodynamic outcomes, the study provides data on clinical improvement, including resolution of heart failure symptoms, improved feeding, and stabilization of vital parameters. These outcomes are clinically meaningful and reinforce the benefit of timely intervention. The greater degree of clinical improvement observed in infants further supports the influence of age on both physiological recovery and overall outcomes [9]. Despite its strengths, several limitations should be considered. The study is based on a single-center experience, which may limit generalizability. The ambispective design introduces potential limitations related to retrospective data collection. Furthermore, the follow-up period of six months is relatively short and does not allow assessment of long-term outcomes such as late recoarctation, aneurysm formation, or persistent hypertension. Future studies with longer follow-up and multicenter collaboration would be valuable. Another consideration is the role of anatomical factors such as arch hypoplasia and lesion morphology. Although arch hypoplasia was not identified as an independent predictor of recoarctation in this study, this may be related to sample size limitations. More detailed anatomical assessment may help refine risk stratification [10]. Balloon dilatation is an effective and relatively safe intervention for native CoA in early life, particularly in infants. However, the higher rate of recoarctation in neonates underscores the need for careful patient selection and close follow-up. Further research is required to evaluate long-term outcomes and optimize age-specific treatment strategies. References Javed S, Shaikh AS, Korejo HB, Kumari V, Ahsan AK, Rafique N. Immediate and Short-Term Outcomes of Balloon Dilatation for Native Coarctation of the Aorta in Neonates and Infants at a Tertiary Care Center. Pak Heart J. 2026;59(02):461-9. DOI: 10.47144/phj.v59i2.3523 Rao PS, Galal O, Smith PA, Wilson AD. Five- to nine-year follow-up results of balloon angioplasty of native aortic coarctation in infants and children. J Am Coll Cardiol. 1996;27(2):462-70. DOI: 10.1016/0735-1097(95)00479-3 Arora HS, Vidya P, Ghosh AK, Mishra SC, Shouche S, Sethi BS, et al. Midterm safety and outcome of balloon angioplasty of native aortic coarctation in neonates and young infants. Ann Pediatr Cardiol. 2022;15(2):121-7. DOI: 10.4103/apc.apc_197_21 Chetan D, Mertens LL. Challenges in diagnosis and management of coarctation of the aorta. Curr Opin Cardiol. 2022;37(1):115-22. DOI: 10.1097/HCO.0000000000000934 Stephens EH, Feins EN, Karamlou T, Anderson BR, Alsoufi B, Bleiweis MS, et al. Management of neonates and infants with coarctation of the aorta. Ann Thorac Surg. 2024;118(2):527-44. DOI: 10.1016/j.athoracsur.2024.04.012 Liang CD, Su WJ, Chung HT, Hwang MS, Huang CF, Lin YJ, Chien SJ, Lin IC, Ko SF. Balloon angioplasty for native coarctation of the aorta in neonates and infants with congestive heart failure. Pediatr Neonatol. 2009;50(4):152-7. DOI: 10.1016/S1875-9572(09)60054-1 Sandoval JP, Kang SL, Lee KJ, Benson L, Asoh K, Chaturvedi RR. Balloon Angioplasty for Native Aortic Coarctation in 3- to 12-Month-Old Infants. Circ Cardiovasc Interv. 2020;13(11):e008938. DOI: 10.1161/CIRCINTERVENTIONS.120.008938 Hysko K, Bertram H, Bobylev D, Horke A, Hansmann G. Advances in the treatment of neonatal coarctation of the aorta. Pediatrics. 2025;155(3):e2024067434. DOI: 10.1542/peds.2024-067434 Amoozgar H, Bahmanpour N, Farhadi P, Edraki MR, Borzouee M, Ajami G, et al. Balloon angioplasty for native coarctation in children: immediate outcome and follow-up. Int Cardiovasc Res J. 2015;9(1):e10542. https://brieflands.com/journals/ircrj/articles/10542 Vasile CM, Laforest G, Bulescu C, Jalal Z, Thambo JB, Iriart X. From Crafoord's End-to-End Anastomosis Approach to Percutaneous Interventions: Coarctation Management Strategies and Reinterventions. J Clin Med. 2023;12(23):7350. DOI: 10.20944/preprints202310.1295.v1
Objective: This study aimed to determine the prevalence of significant left main (LM) and proximal left anterior descending (pLAD) coronary artery disease and to identify factors associated with their presence in patients presenting with acute inferior wall myocardial infarction (IWMI). Methodology: A prospective observational cross-sectional study was conducted at a tertiary care cardiac center between February and August 2022. Ninety-six consecutive adult patients presenting with acute IWMI underwent coronary angiography and were included in the analysis. Significant coronary artery disease was defined as ≥50% stenosis in the LM coronary artery and ≥70% stenosis in the pLAD artery. Results: A total of 96 patients were enrolled, including 63 males (65.6%) and 33 females (34.4%), with a mean age of 57.8 ± 10.4 years. Isolated LM disease was identified in 1 patient (1.0%), isolated pLAD disease in 44 patients (45.8%), and combined LM and pLAD involvement in 6 patients (6.3%). Overall, pLAD involvement was present in 52.1% of patients, while LM involvement was observed in 7.3%. Hypertension (52.1%) and diabetes mellitus (37.5%) were the most prevalent cardiovascular risk factors. Multivariable logistic regression demonstrated that hypertension (adjusted OR = 1.96, 95% CI: 1.10–3.50; p = 0.01), diabetes mellitus (adjusted OR = 2.67, 95% CI: 1.30–5.51; p = 0.001), and family history of coronary artery disease (adjusted OR = 3.09, 95% CI: 1.43–6.82; p < 0.001) were independently associated with the presence of LM and/or pLAD disease. Conclusion: Significant proximal LAD involvement was common among patients presenting with acute IWMI, whereas left main coronary artery disease occurred less frequently. Traditional cardiovascular risk factors, particularly hypertension, diabetes mellitus, and family history of coronary artery disease, were independently associated with the presence of LM and/or pLAD disease.
Objectives: To identify patient-related and operational factors associated with prolonged door-to-balloon time (DTBT) and to evaluate the association between prolonged DTBT and in-hospital outcomes among patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI) in a Level II catheterization laboratory. Methodology: This prospective observational analytical study included consecutive adult patients presenting with acute STEMI and undergoing primary PCI during office hours. Participants were categorized into DTBT ≤90 minutes and DTBT >90 minutes. Data regarding demographic characteristics, cardiovascular risk factors, clinical severity indicators, operational workflow delays, and in-hospital outcomes were collected. Major adverse cardiovascular events (MACE) were defined as a composite of in-hospital death, heart failure, cardiogenic shock, cardiac arrest, and clinically significant arrhythmia. Results: A total of 120 patients were included, of whom 91 (75.8%) were male, with a mean age of 56.3 ± 12.3 years. Thirty patients (25.0%) experienced prolonged DTBT (>90 minutes). Patients with prolonged DTBT had significantly higher rates of heart failure (30.0% vs 2.2%), cardiogenic shock (13.3% vs 1.1%), cardiac arrest (10.0% vs 1.1%), arrhythmia (30.0% vs 3.3%), in-hospital mortality (13.3% vs 0%), and MACE (60.0% vs 6.7%) compared with patients achieving DTBT ≤90 minutes (all p<0.05). Delay in ECG acquisition, delay in consent, and Cath lab occupancy remained independently associated with prolonged DTBT in adjusted analyses. Prolonged DTBT was also independently associated with MACE (adjusted OR 19.94; 95% CI 6.40–62.06). Conclusion: A considerable proportion of STEMI patients undergoing primary PCI experienced prolonged DTBT, and delayed reperfusion was associated with significantly worse in-hospital outcomes. Early ECG acquisition, streamlined emergency consent procedures, and improved Cath lab workflow management may represent important quality improvement targets in resource-limited Level II catheterization laboratories.
Objectives: To evaluate the clinical characteristics, angiographic findings, management strategies, and in-hospital outcomes of patients with previous CABG presenting with ACS. Methodology: This prospective observational cohort study was conducted between November 2024 and October 2025. Consecutive adult patients with a history of CABG presenting with ACS were enrolled. Data regarding clinical characteristics, treatment strategies, procedural details, and in-hospital outcomes were collected prospectively. Results: A total of 279 patients were included, with a mean age of 64.5 ± 8.2 years; 87.8% were male. Hypertension and diabetes mellitus were present in 83.9% and 70.6% of patients, respectively. Unstable angina was the most common presentation (57.0%), followed by NSTEMI (30.1%) and STEMI (12.9%). Angiography demonstrated extensive native coronary artery disease involving the LAD (96.9%), LCX (93.4%), and RCA (91.7%). Saphenous vein graft obstruction was most frequently observed in SVG-RCA (52.4%) and SVG-OM1 (38.9%), whereas arterial graft failure was less common. PCI was performed in 41.6% of patients, achieving a procedural success rate of 95.7%. In-hospital mortality was low (1.4%), while acute kidney injury (3.6%), life-threatening arrhythmias (3.9%), and stroke (0.4%) occurred infrequently. Multivariable analysis identified Killip class III/IV as an independent predictor of composite in-hospital adverse events (adjusted OR 45.65, 95% CI 1.82–1145.59; p=0.020). Conclusion: Patients with prior CABG presenting with ACS constitute a high-risk population characterized by extensive native coronary artery disease, significant graft pathology, and multiple cardiovascular comorbidities. Nevertheless, contemporary management strategies, including selective PCI and optimized medical therapy, are associated with favorable short-term outcomes and low in-hospital mortality.
Ischemic heart disease (IHD) remains the leading global cause of morbidity and mortality, driven by a complex interplay of atherosclerosis, inflammation, endothelial dysfunction, thrombosis, and oxidative stress. Despite notable declines in mortality in high-income regions, the burden of IHD continues to rise in low- and middle-income countries, where risk factors, healthcare disparities, and environmental exposures compound disease progression. The molecular mechanisms that underlie plaque initiation, progression, and destabilization are increasingly recognized as crucial therapeutic targets. However, important gaps persist—particularly in understanding how inflammatory pathways, oxidative stress, and immune activation converge to cause myocardial injury and adverse cardiovascular events. This narrative review synthesizes current evidence on the molecular and pathophysiological basis of IHD, elaborating on atherosclerotic plaque biology, coronary artery narrowing, thrombosis development, myocardial ischemia and infarction, and the interconnected inflammatory and oxidative stress pathways central to disease evolution. Emerging therapeutic opportunities—including inflammasome inhibitors, targeted anti-inflammatory agents, endothelial modulators, and mitochondrial-protective strategies—are highlighted in relation to their potential to complement conventional lipid-lowering and antithrombotic therapy. Future research must focus on translating molecular insights into personalized treatment strategies to support earlier diagnosis, better risk stratification, and improved clinical outcomes for diverse global populations.
Objectives: This study aimed to compare the clinical characteristics, risk factors, management strategies, and in-hospital outcomes of young acute coronary syndrome (ACS) patients (≤45 years) with those of older adults, addressing a significant evidence gap in the region. Methodology: This cross-sectional study included all consecutive patients presenting with ACS. Data were collected on demographics, cardiovascular risk factors, clinical presentation, angiographic findings, treatment modalities, and in-hospital outcomes. Comparative analyses between age groups were performed, and multivariable logistic regression identified predictors of in-hospital mortality. Results: Among 310 ACS patients, 23.2% were ≤45 years. Young adults demonstrated a distinctive risk profile characterized by significantly higher prevalence of khat chewing, smoking, and family history of premature coronary artery disease, whereas diabetes mellitus was more common among older adults (p < 0.05). Younger patients more frequently underwent coronary angiography and PCI, while older patients were managed more conservatively (p < 0.05). Single-vessel disease was predominant in younger individuals, contrasting with greater multivessel involvement in older patients. Although overall complication and mortality rates were comparable between groups, older adults exhibited higher GRACE scores and more frequent heart failure. Independent predictors of in-hospital mortality—including low systolic blood pressure, elevated serum creatinine, reduced LVEF, multivessel disease, and delayed symptom-to-door time—were consistent across age groups. PCI was independently protective. Conclusion: Young Yemeni adults with ACS exhibit unique behavioral and familial risk patterns but share similar mortality risk predictors with older patients. These findings highlight an urgent need for targeted prevention strategies addressing modifiable behaviors—especially smoking and khat chewing.
Objectives: Premature coronary artery disease (PCAD) in individuals younger than 45 years carries significant clinical and socioeconomic implications. This study aimed to evaluate serum tetranectin (TN) as a potential non-invasive biomarker for diagnosing PCAD and predicting its severity. Methodology: A case–control study was conducted including 84 PCAD patients undergoing elective coronary angiography and 84 age- and sex-matched controls with normal coronary findings. Serum TN levels were measured using ELISA, and severity of coronary stenosis was determined by SYNTAX and Gensini scoring systems. Results: Serum TN levels were significantly lower in PCAD patients than in controls (87.7 [32.5–381.3] vs. 153.1 [58.1–608.8], P < 0.001). TN levels demonstrated strong negative correlations with both SYNTAX (r = –0.882, P < 0.001) and Gensini (r = –0.836, P < 0.001) scores. ROC analysis showed excellent discriminatory accuracy for predicting high SYNTAX scores (AUC = 0.970, cutoff ≤54.2 ng/mL). Multivariate regression confirmed TN as an independent predictor of PCAD (OR = 0.995, P = 0.008) and of severity indices. Conclusion: Serum TN is a promising biomarker for the non-invasive diagnosis and risk stratification of PCAD. Its strong inverse correlation with coronary severity scores and echocardiographic dysfunction supports its potential utility in early detection and disease monitoring.
Objective: Postoperative delirium (POD) is a common neuropsychiatric complication following cardiac surgery and is associated with adverse clinical outcomes, prolonged hospitalization, increased healthcare costs, and long-term cognitive impairment. This study aimed to determine the frequency of postoperative delirium and identify factors associated with its occurrence among patients undergoing elective cardiac surgery at a tertiary cardiac center in Pakistan. Methodology: A prospective observational cohort study was conducted between 10 January 2026 and 10 April 2026. A total of 184 adult patients aged 30–80 years undergoing elective cardiac surgery were enrolled through consecutive sampling. Demographic, clinical, surgical, and perioperative data were collected using a structured study proforma. Postoperative delirium was assessed twice daily using the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU) during hospitalization. Results: Among the 184 patients included in the study, postoperative delirium developed in 40 patients, yielding a frequency of 21.7%. The median time to delirium onset was postoperative day 2 (IQR: 1–3 days). Factors significantly associated with POD included age >50 years (OR=2.65, 95% CI: 1.01–6.94; p=0.031), low educational status (OR=2.05, 95% CI: 1.05–4.04; p=0.041), hypertension (OR=2.28, 95% CI: 1.02–5.11; p=0.031), diabetes mellitus (OR=2.61, 95% CI: 1.17–5.80; p=0.011), previous stroke (OR=5.63, 95% CI: 1.96–16.20; p<0.001), heart failure (OR=3.66, 95% CI: 1.68–7.96; p=0.001), current smoking (OR=2.11, 95% CI: 1.00–4.44; p=0.041), reduced preoperative ejection fraction (p=0.002), prolonged cardiopulmonary bypass duration >120 minutes (OR=3.69, 95% CI: 1.76–7.72; p<0.001), prolonged cross-clamp time >90 minutes (OR=2.78, 95% CI: 1.22–6.31; p=0.011), ICU stay >5 days (OR=4.09, 95% CI: 1.95–8.57; p<0.001), and postoperative anticholinergic medication use (OR=4.57, 95% CI: 2.10–9.93; p<0.001). Conclusion: Postoperative delirium occurred in approximately one-fifth of patients undergoing elective cardiac surgery and was associated with several demographic, clinical, and perioperative factors. Recognition of these associated factors may facilitate early identification of high-risk patients and support the development of targeted preventive and monitoring strategies in cardiac surgical practice.
Objectives: To determine the association between active smoking and ST-elevation myocardial infarction (STEMI) among patients presenting with acute coronary syndrome (ACS) in a tertiary care hospital setting. Methodology: This comparative cross-sectional study was conducted in the Department of Cardiology, Jinnah Hospital Lahore, Pakistan, from April to October 2020. A total of 240 adult patients presenting with ACS were enrolled, including 120 active smokers and 120 non-smokers. Demographic characteristics, cardiovascular risk factors, smoking status, and ACS subtype were recorded using a structured proforma. ACS was classified into STEMI, NSTEMI, and unstable angina according to the Fourth Universal Definition of Myocardial Infarction. Results: The mean age of smokers and non-smokers was 44.23 ± 9.54 years and 42.72 ± 10.68 years, respectively. Male patients constituted 76.6% of smokers and 70.0% of non-smokers. STEMI was the most frequent ACS subtype and was observed in 70.8% of smokers compared with 65.0% of non-smokers. Smokers also demonstrated significantly lower BMI compared to non-smokers (20.3 ± 1.9 kg/m² vs. 23.1 ± 2.1 kg/m²; p < 0.001). Multivariable logistic regression analysis demonstrated that active smoking was independently associated with higher odds of STEMI presentation (adjusted OR = 1.85; 95% CI: 1.13–3.02; p < 0.05). Other variables including age, gender, diabetes mellitus, dyslipidemia, and BMI did not show statistically significant associations with STEMI. Conclusion: Active smoking was significantly associated with STEMI presentation among patients with ACS. These findings reinforce the role of smoking as an important and preventable cardiovascular risk factor. Strengthening smoking cessation programs, public awareness campaigns, and preventive cardiovascular strategies may help reduce the burden of STEMI and adverse cardiovascular outcomes in high-risk populations.
Pediatric myocarditis remains one of the most challenging conditions encountered in clinical cardiology. Its presentation is often nonspecific, its diagnosis frequently elusive, and its clinical course highly variable, ranging from complete recovery to fulminant heart failure, arrhythmias, transplantation, or death. Consequently, clinicians continue to face difficult decisions regarding diagnostic evaluation, therapeutic intensity, and long-term surveillance of affected children [1]. In this context, the study by Jamil et al.[2] provides valuable local evidence regarding the burden, clinical characteristics, and short-term outcomes of pediatric myocarditis in Pakistan during the post-COVID-19 era. In a region where epidemiological and outcome data remain limited, this report offers important insights into a disease that continues to impose substantial clinical and healthcare challenges. Since the emergence of the COVID-19 pandemic, increasing attention has focused on myocardial involvement in children following SARS-CoV-2 infection. Reports have documented rises in myocarditis diagnoses associated with acute COVID-19 infection, post-infectious inflammatory syndromes, and multisystem inflammatory syndrome in children (MIS-C) [3]. Against this backdrop, the findings reported by Jamil et al. are particularly noteworthy. Among 892 pediatric cardiology admissions, 76 children were diagnosed with myocarditis, accounting for 8.5% of all admissions, while nearly half demonstrated evidence of prior SARS-CoV-2 exposure. Although hospital-based proportions should not be interpreted as population incidence rates, the observed burden underscores the considerable impact that myocarditis continues to exert on tertiary pediatric cardiac services in Pakistan. The severity of illness observed in this cohort deserves particular attention. The reported median left ventricular ejection fraction of only 24.5% reflects profound myocardial dysfunction at presentation. Furthermore, nearly all patients required inotropic support, and the observed mortality rate of 17.1% highlights the potentially devastating nature of the disease [4]. These findings reinforce a well-recognized clinical reality: pediatric myocarditis frequently presents late in its course, often after significant ventricular dysfunction and hemodynamic compromise have already developed. Such challenges may be further amplified in resource-limited environments where delays in referral, limited diagnostic capabilities, and restricted access to advanced heart failure therapies can adversely affect outcomes. An especially important observation from this study is the absence of significant differences in clinical presentation, laboratory findings, echocardiographic characteristics, or short-term outcomes between children with and without evidence of prior COVID-19 exposure. While SARS-CoV-2 has been clearly associated with myocardial injury, myocarditis, and MIS-C, these findings suggest that once clinically significant myocarditis develops, disease severity and short-term outcomes may be determined more by the extent of myocardial inflammation and ventricular dysfunction than by the specific infectious trigger itself. Although this interpretation should be approached cautiously given the modest sample size and observational design, it raises important questions regarding the pathophysiological similarities shared by myocarditis of different etiologies. The study also draws attention to a persistent challenge faced by healthcare systems across many low- and middle-income countries: limited access to advanced diagnostic technologies. Contemporary international guidelines recognize cardiac magnetic resonance imaging (CMR) as the preferred non-invasive modality for confirming myocardial inflammation, while endomyocardial biopsy remains the diagnostic reference standard in carefully selected cases [5]. However, both investigations remain unavailable or inaccessible in many resource-constrained settings. Consequently, clinicians often rely on a pragmatic combination of clinical assessment, cardiac biomarkers, electrocardiography, and echocardiography, as was done in this study. Although such approaches are often necessary, they may increase diagnostic uncertainty and potentially lead to both underdiagnosis and overdiagnosis. These realities highlight the urgent need for practical, evidence-based diagnostic algorithms tailored specifically for resource-limited environments. Another noteworthy finding is the predominance of very young children, with a median age of only two years. This contrasts with several reports from high-income countries, where myocarditis and COVID-19-related myocardial involvement have often been described more frequently among older children and adolescents. Whether this age distribution reflects regional epidemiological differences, distinct infectious etiologies, referral patterns, healthcare-seeking behavior, or demographic characteristics remains uncertain. Future multicenter studies incorporating broader geographic representation will be necessary to better understand these differences. Several limitations of the study merit consideration. The single-center design, relatively small sample size, absence of advanced imaging confirmation, and reliance on clinically based diagnostic criteria limit generalizability. Most importantly, the lack of long-term follow-up leaves unanswered questions regarding ventricular recovery, persistent systolic dysfunction, arrhythmia burden, exercise capacity, quality of life, and progression to dilated cardiomyopathy. These outcomes are particularly relevant because the consequences of pediatric myocarditis may extend far beyond hospital discharge, with some children experiencing chronic cardiovascular sequelae despite apparent early recovery. Nevertheless, this study provides an important contribution to the limited literature on pediatric myocarditis from South Asia. Beyond documenting disease burden, it highlights the realities of managing severe myocardial inflammation in resource-constrained settings, where clinicians must frequently make critical decisions without access to advanced diagnostic or therapeutic resources. The findings serve as a timely reminder that myocarditis remains a significant cause of pediatric morbidity and mortality and underscore the importance of early recognition, prompt referral, and strengthened pediatric cardiac care services. As the post-COVID-19 era continues to evolve, collaborative multicenter registries, standardized diagnostic pathways, and longitudinal outcome studies will be essential to better define the epidemiology, risk factors, and long-term consequences of pediatric myocarditis in low- and middle-income countries. Generating such evidence will be crucial not only for improving clinical outcomes but also for informing health policy and resource allocation aimed at reducing the burden of this potentially life-threatening disease. References Law YM, Lal AK, Chen S, Čiháková D, Cooper LT Jr, Deshpande S, et al. Diagnosis and management of myocarditis in children: a scientific statement from the American Heart Association. Circulation. 2021;144(6): e123–e135. DOI:10.1161/CIR.0000000000001001 Jamil M, Arshad MS, Adnan M, Mehwish F. Frequency, Clinical Characteristics, and Short-Term Outcomes of Pediatric Myocarditis in the Post-COVID-19 Era: A Tertiary Care Experience from Pakistan. Pak Heart J. 2026;59(03):1-2. DOI: 10.47144/phj.v59i3.3612 Patel T, Kelleman M, West Z, Peter A, Dove M, Butto A, et al. Comparison of multisystem inflammatory syndrome in children-related myocarditis, classic viral myocarditis, and COVID-19 vaccine-related myocarditis in children. J Am Heart Assoc. 2022;11:e024393. DOI: 10.1161/JAHA.121.024393 Williams JL, Jacobs HM, Lee S. Pediatric Myocarditis. Cardiol Ther. 2023;12(2):243-260. DOI: 10.1007/s40119-023-00309-6 Dawood I, Alhussein ST, Wadi WY, Abdalgadir RA, Mohammed SS, Ahmed EH. Viral myocarditis in pediatrics: A review of current diagnostic methods and future directions. Ann Pediatr Card. 2025;18:42-8. DOI: 10.4103/apc.apc_236_24
Objectives: To evaluate whether persistent post-recovery ST-segment depression (PPRSTD ≥4 minutes) during exercise testing (ET) predicts double-vessel coronary artery disease (2VD) and to assess its value in localizing critical coronary lesions. Methodology: This prospective cohort study enrolled 86 consecutive patients with chronic stable angina (CSA, CCS class II) undergoing ET and scheduled coronary angiography (C. Ang.) between January 2017 and February 2018. Fourteen patients were excluded based on predefined criteria, leaving 72 patients (mean age 40–60 years; 39 males, 33 females) for final analysis. Of these, 33 exhibited ≥4 minutes PPRSTD, and 39 had <4 minutes. C. Ang. findings were classified by vessel involvement (LMS, LAD, LCX, RCA), lesion site (ostial, proximal, mid), and vessel dominance. Statistical analysis included Chi-square, Fisher’s exact test, odds ratios (OR), and measures of association (Yule’s Q, Cramér’s V). Results: Patients with ≥4 minutes PPRSTD were strongly associated with double-vessel disease involving the LAD and dominant RCA, predominantly affecting proximal or ostial segments (11 vs. 0; p <0.001). Sensitivity and specificity were 63.9% and 100%, respectively, with PPV 33.3% and NPV 100%. A very strong positive correlation was observed (Yule’s Q = 0.945, Cramér’s V = 0.462). No significant association was found between ≥4 minutes PPRSTD and LMS or triple-vessel disease. Male patients were disproportionately represented in the ≥4 minutes group. Conclusion: Persistence of ≥4 minutes PPRSTD after ET is a reliable non-invasive predictor of LAD and dominant RCA double-vessel disease with proximal critical lesions. This marker provides valuable prognostic information for risk stratification and localization of CAD prior to angiography.
Objectives: To compare the frequency of angiographic no-reflow (NR) between left anterior descending (LAD) and non-left anterior descending (non-LAD) infarct-related arteries in patients undergoing primary percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI). Methodology: This prospective observational comparative study was conducted between September 2025 and February 2026. A total of 192 consecutive STEMI patients undergoing primary PCI were enrolled and categorized according to the angiographically identified infarct-related artery into LAD (n=96) and non-LAD (n=96) groups. Demographic, clinical, angiographic, and procedural characteristics were recorded using a structured proforma. Angiographic no-reflow was defined as final thrombolysis in myocardial infarction (TIMI) flow grade 0–2 after successful mechanical opening of the culprit vessel in the absence of residual stenosis, dissection, visible thrombus, or coronary spasm. Comparative analyses were performed using appropriate univariate tests. Results: Among the 192 participants, the mean age was 51.3±7.4 years and 76.0% were male. Patients with LAD-related STEMI were significantly older and more frequently diabetic than those with non-LAD infarctions. Overall, angiographic no-reflow occurred in 54 (28.1%) patients. The frequency of no-reflow was significantly higher in the LAD group compared with the non-LAD group (36.5% versus 19.8%, p=0.010). After adjustment for age, diabetes mellitus, time to presentation, baseline TIMI flow, thrombus burden, lesion morphology, stent length, and stent diameter, LAD involvement remained independently associated with no-reflow (adjusted odds ratio 2.0; 95% confidence interval 1.0–4.1; p=0.047). Delayed presentation, high thrombus burden, and longer stent length were also independently associated with no-reflow. Conclusion: LAD-related STEMI was associated with a significantly higher frequency of angiographic no-reflow compared with non-LAD culprit vessel STEMI during primary PCI. The association persisted after adjustment for important clinical and procedural variables.
Abstract Congenital heart disease (CHD) is the most common congenital anomaly worldwide, affecting approximately 1 in every 100 live births. Advances in prenatal diagnosis, neonatal care, cardiac surgery, catheter-based interventions, and lifelong follow-up have transformed CHD from a fatal childhood condition into a chronic disease spanning the entire lifespan. Despite these achievements, congenital heart disease remains largely overlooked in national and global non-communicable disease (NCD) strategies, which predominantly focus on cardiovascular diseases of adulthood, diabetes, chronic respiratory diseases, and cancer. This omission is particularly detrimental in low- and middle-income countries (LMICs), where delayed diagnosis, limited specialized services, financial barriers, and inadequate workforce capacity continue to contribute to preventable mortality and lifelong disability. As survival improves globally, the number of adults living with congenital heart disease now exceeds the pediatric population, creating an emerging public health challenge. Integrating congenital heart disease into national NCD frameworks would facilitate comprehensive planning for prevention, early detection, specialized treatment, workforce development, sustainable financing, registries, and lifelong care. This editorial highlights why congenital heart disease should be recognized as the next global health priority and outlines practical recommendations for policymakers. Editorial Congenital heart disease is no longer a rare pediatric condition but a major global health challenge [1,2]. Advances in medical care have transformed CHD into the largest population of survivors with lifelong congenital cardiovascular disease, creating new responsibilities for health systems [3-5]. For decades, global non-communicable disease (NCD) strategies have concentrated on four major disease groups—cardiovascular disease, diabetes mellitus, chronic respiratory diseases, and cancer [6]. These priorities have undoubtedly improved health outcomes worldwide. However, an important and growing population has remained largely invisible within national health agendas: individuals living with congenital heart disease (CHD). Congenital heart disease is the commonest congenital anomaly, affecting nearly 1.35 million newborns annually worldwide [1,2]. Improvements in fetal diagnosis, neonatal intensive care, cardiac surgery, interventional cardiology, and medical management have dramatically increased survival [3-5]. Today, more than 90% of children born with CHD in high-income countries survive into adulthood [3-5]. Consequently, congenital heart disease has evolved from a pediatric disorder into a lifelong chronic cardiovascular disease requiring continuous multidisciplinary care [3,5,7]. Yet, national NCD strategies rarely acknowledge this changing epidemiology. A Growing but Neglected Global Health Burden: Although rheumatic heart disease has received increasing recognition within global cardiovascular health initiatives, congenital heart disease has remained underrepresented despite its substantial burden [6,8]. Every year, hundreds of thousands of children die because they lack timely diagnosis or access to definitive treatment [2,9]. Many survivors experience chronic heart failure, pulmonary hypertension, arrhythmias, infective endocarditis, stroke, neurodevelopmental impairment, or repeated hospitalizations that significantly reduce quality of life [5,7]. The disparity is greatest in low- and middle-income countries (LMICs), where nearly 90% of children with congenital heart disease are born [2,9-11]. Unfortunately, specialized pediatric cardiac centers, trained congenital cardiologists, congenital cardiac surgeons, advanced imaging facilities, and pediatric intensive care units remain scarce across many regions. The result is an unacceptable gap between disease burden and healthcare capacity. Congenital Heart Disease Fits the Definition of a Chronic Non-Communicable Disease: The exclusion of congenital heart disease from NCD policies is increasingly difficult to justify. Modern congenital heart disease fulfills every characteristic of a chronic non-communicable disease [5-7]: Lifelong disease requiring continuous follow-up Recurrent need for specialist healthcare Substantial healthcare expenditure Progressive complications throughout life Impact on education, employment, pregnancy, and mental health Requirement for multidisciplinary coordinated care Many adults with repaired congenital heart disease require repeated interventions, electrophysiology procedures, heart failure management, pulmonary hypertension therapy, cardiac transplantation assessment, and lifelong surveillance. Their healthcare needs resemble those of patients with other chronic cardiovascular diseases already included within NCD frameworks. Why National NCD Strategies Matter? Inclusion within national NCD strategies extends beyond symbolic recognition. It determines health financing, workforce planning, service delivery, data collection, and political commitment. Recognition of congenital heart disease as a national NCD priority would encourage governments to establish: National congenital heart disease registries Newborn pulse oximetry screening programs Prenatal cardiac screening pathways Regional referral networks Dedicated pediatric and adult congenital heart disease centers Specialized workforce training Sustainable financing mechanisms Lifelong transition services from pediatric to adult care. Such policies are especially important for countries where specialized congenital cardiac services remain centralized, forcing families to travel long distances for diagnosis and treatment [6,12,13]. The Challenge in Low and Middle Income Countries: The challenges faced by LMICs differ substantially from those in high-income countries. Delayed diagnosis, malnutrition, pulmonary vascular disease, limited catheterization facilities, shortage of pediatric cardiac surgeons, inadequate intensive care resources, and financial hardship frequently convert treatable congenital heart defects into irreversible disease. Many countries continue to rely on a few tertiary centers that struggle with overwhelming patient volumes. Rural populations often remain undiagnosed until advanced complications develop. Without incorporation into national health planning, these inequities are unlikely to improve [8-11]. Congenital Heart Disease and Universal Health Coverage: Universal Health Coverage (UHC) aims to ensure that all individuals receive essential health services without financial hardship. Congenital heart disease perfectly aligns with this principle. Early diagnosis and timely intervention are among the most cost-effective investments in cardiovascular medicine. Repairing a ventricular septal defect or transposition of the great arteries during infancy allows children to become healthy, productive adults who contribute economically and socially for decades. Conversely, delayed treatment frequently results in irreversible pulmonary vascular disease, lifelong disability, repeated hospitalization, and substantially higher healthcare costs. Investment in congenital heart disease is therefore not only ethically imperative but economically rational [12,13]. The Need for Global Policy Change: The World Health Organization and international cardiovascular societies have successfully elevated hypertension, ischemic heart disease, stroke, and rheumatic heart disease within global health priorities. A similar coordinated effort is now required for congenital heart disease. Future national NCD action plans should explicitly incorporate congenital heart disease through measurable indicators, dedicated funding, surveillance systems, workforce development, research support, and quality improvement programs. Partnerships between governments, academic institutions, international organizations, patient advocacy groups, and professional societies will be essential for achieving these objectives [6,12,13]. Conclusion As countries strive to achieve Universal Health Coverage and the Sustainable Development Goals, congenital heart disease can no longer remain outside national non-communicable disease agendas. Recognizing CHD as a lifelong chronic cardiovascular disease is not merely a semantic change—it is a public health imperative that will determine whether millions of children born with congenital heart defects survive, thrive, and contribute to society. The time has come for governments, professional societies, and international organizations to move beyond episodic care and establish comprehensive national strategies that ensure equitable access to prevention, early diagnosis, definitive treatment, lifelong follow-up, and high-quality outcomes for every individual living with congenital heart disease [5,6,12,13]. References van der Linde D, Konings EEM, Slager MA, Witsenburg M, Helbing WA, Takkenberg JJM, et al. Birth prevalence of congenital heart disease worldwide: a systematic review and meta-analysis. J Am Coll Cardiol. 2011;58(21):2241-7. DOI: 10.1016/j.jacc.2011.08.025 Zimmerman MS, Smith AGC, Sable CA, Echko MM, Wilner LB, Olsen HE, et al. Global, regional, and national burden of congenital heart disease, 1990–2017. Circulation. 2020;141(9):717-27. DOI: 10.1016/S2352-4642(19)30402-X Marelli AJ, Ionescu-Ittu R, Mackie AS, Guo L, Dendukuri N, Kaouache M. Lifetime prevalence of congenital heart disease in the general population. Circulation. 2014;130(9):749-56. DOI: 10.1161/CIRCULATIONAHA.113.008396 Gilboa SM, Devine OJ, Kucik JE, Oster ME, Riehle-Colarusso T, Nembhard WN, et al. Congenital heart defects in the United States. Circulation. 2016;134(2):101-9. DOI: 10.1161/CIRCULATIONAHA.115.019307 Stout KK, Daniels CJ, Aboulhosn JA, Bozkurt B, Broberg CS, Colman JM, et al. 2018 AHA/ACC Guideline for the Management of Adults With Congenital Heart Disease. Circulation. 2019;139:e698-e800. DOI: 10.1161/CIR.0000000000000603 World Health Organization. Global Action Plan for the Prevention and Control of Noncommunicable Diseases 2013–2030. Geneva: WHO; 2013. Available at: https://www.who.int/publications/i/item/9789241506236 Baumgartner H, De Backer J, Babu-Narayan SV, Budts W, Chessa M, Diller GP, et al. 2020 ESC Guidelines for the management of adult congenital heart disease. Eur Heart J. 2021;42(6):563-645. DOI: 10.1093/eurheartj/ehaa554 World Health Organization. Cardiovascular Diseases. Geneva: World Health Organization; 2025. Available at: https://www.who.int/news-room/fact-sheets/detail/cardiovascular-diseases-(cvds) Zühlke L, Mirabel M, Marijon E. Congenital heart disease and rheumatic heart disease in Africa. Circulation. 2013;128:2714-23. DOI: 10.1136/heartjnl-2013-303896 Saxena A. Congenital heart disease in India: A status report. Indian J Pediatr. 2018;85:874-82. DOI: 10.1007/BF02724185 Watkins DA, Johnson CO, Colquhoun SM, Karthikeyan G, Beaton A, Bukhman G, et al. Global, regional, and national burden of rheumatic heart disease and congenital heart disease. Lancet Glob Health. 2020;8:e153-e161. DOI: 10.1056/NEJMoa1603693 World Health Organization. Universal Health Coverage (UHC): Key Facts. Geneva: WHO; 2025. Available at: https://www.who.int/news-room/fact-sheets/detail/universal-health-coverage-(uhc) United Nations. Transforming Our World: The 2030 Agenda for Sustainable Development. New York: United Nations; 2015. Available at: https://sdgs.un.org/2030agenda
