Background: The severity of coronary artery disease is a prognostic factor for major adverse cardiovascular events in patients diagnosed with acute myocardial infarction. ACE I/D polymorphism is one of the genetic factors that may affect the severity of coronary artery disease. This study aimed to investigate the association between ACE I/D genotypes and the severity of coronary artery disease in patients with acute myocardial infarction.Materials and methods: A single-center, prospective, observational study was conducted at the Department of Cardiology and Department of Interventional Cardiology, Cho Ray Hospital, Ho Chi Minh City, Vietnam from January 2020 to June 2021. All participants diagnosed with acute myocardial infarction underwent contrast-enhanced coronary angiography. The severity of coronary artery disease was determined by Gensini score. ACE I/D genotypes were identified in all subjects by using the polymerase chain reaction method.Results: A total of 522 patients diagnosed with first acute myocardial infarction were recruited. The patients' median Gensini score was 34.3. The II, ID, and DD genotype rates of ACE I/D polymorphism were 48.9%, 36.4%, and 14.7%, respectively. After adjusting for confounding factors, multivariable linear regression analysis showed that the ACE DD genotype was independently associated with a higher Gensini score compared with the II or ID genotypes.Conclusion: The DD genotype of the ACE I/D polymorphism was associated with the severity of coronary artery disease in Vietnamese patients diagnosed with first acute myocardial infarction.

The pathogenesis and prognosis of patients with acute myocardial infarction (AMI) may be influenced by both genetic and environmental factors. Findings on the relationship of polymorphisms in various genes encoding the renin-angiotensin-aldosterone system with coronary artery lesions and mortality in AMI patients are inconsistent. The aim of this study was to determine whether theAGTR1A1166C genetic polymorphism affects coronary artery lesions and 1-year mortality in post-AMI patients. Patients with their first AMI admitted to Cho Ray Hospital, Vietnam, from January 2020 to August 2021 were enrolled in this prospective clinical study. All participants underwent invasive coronary angiography and were identified as having the genotypes ofAGTR1A1166C by way of a polymerase chain reaction method. All patients were followed up for all-cause mortality 12 months after AMI. The association of theAGTR1A1166C polymorphism with coronary artery lesions and 1-year mortality was evaluated using logistic regression and Cox regression analysis, respectively. Five hundred and thirty-one AMI patients were recruited. The mean age was 63.9 ± 11.6 years, and 71.6% of the patients were male. There were no significant differences in the location and number of diseased coronary artery branches between the AA and AC+CC genotypes. The AC and CC genotypes were independently associated with ≥ 90% diameter stenosis of the left anterior descending (LAD) artery (odds ratio = 1.940; 95% confidence interval (CI): 1.059–3.552,p= 0.032). The 1-year all-cause mortality rate difference between patients with the AC and CC genotypes versus those with the AA genotype was not statistically significant (hazard ratio = 1.000, 95% CI: 0.429–2.328,p= 1.000). TheAGTR1A1166C genetic polymorphism is associated with very severe luminal stenosis of the LAD but not with mortality in AMI patients.

The prognostic role of the angiotensin-converting enzyme (ACE) insertion/deletion (I/D) genetic polymorphism in patients with acute myocardial infarction (AMI) is controversial and inconsistent across various study populations. This study evaluated the predictive validity of the ACE I/D variant based on 12-month all-cause mortality in Vietnamese patients after AMI. This was an observational, prospective study conducted among AMI patients at Cho Ray Hospital between January 2020 and September 2021. All participants were identified for ACE I/D polymorphism using the polymerase chain reaction method, with follow-up on survival status at 12 months from the date of admission. The proportions of II, ID, and DD genotypes of the ACE I/D variant were 49.5%, 35.9%, and 14.6%, respectively. All-cause mortality after 12 months occurred in 58 cases (10.6%). The ACE I/D polymorphism did not affect all-cause mortality in the dominant (P = .196), recessive (P = .827), homozygous (P = .515), and heterozygous (P = .184) models. A subgroup analysis by usage status of angiotensin-converting enzyme inhibitor/angiotensin II receptor blocker (ACEI/ARB) showed that in the non-ACEI/ARB group, patients with the DD genotype had a lower cumulative survival probability than patients with the II/ID genotypes (hazard ratio [HR] = 3.97, 95% confidence interval [CI]: 1.21–13.04; P = .023). Among patients with Global Registry of Acute Coronary Events (GRACE) scores below the median (153.5 points), those with DD genotype had a higher risk of mortality than those with the II/ID genotypes (HR = 3.35, 95% CI: 1.01–11.11; P = .049). The ACE I/D genetic polymorphism was found not to be associated with 12-month all-cause mortality in Vietnamese patients with AMI. However, it was associated with mortality in patients who did not use ACEI/ARB and also whose GRACE scores were below 153.5 points.

Heart failure is a growing public health issue with high mortality and hospitalization rates. Comprehensive management programs are needed to improve outcomes and reduce costs. In Vietnam, there are gaps in guideline-directed medical therapy, lack of a multidisciplinary approach, inadequate patient education, and poor continuity from inpatient to outpatient care. However, management programs are evolving with 29 hospitals having established programs. Initial results show improved use of medications, reduced hospitalizations and mortality, and better quality of life in some programs. Challenges remain around resources, costs, patient diversity, and lack of standardization. Standardization initiatives like EuroHeart are working to define common data sets and care standards internationally. Effective programs require optimized hospital treatment, comprehensive discharge planning, structured follow up, and patient selfmanagement support. Further government support, healthcare professional training, public education, research, and regional collaborations are needed to advance heart failure care in Vietnam.

Despite evidence of SGLT2 inhibitors in improving cardiovascular outcomes of heart failure with preserved ejection fraction (HFpEF), the heterogenous mechanism and characteristic multimorbidity of HFpEF require a phenotypic approach. Metabolic phenotype, one common HFpEF phenotype, has various presentations and prognoses worldwide. We aimed to identify different phenotypes of hypertensive-diabetic HFpEF, their phenotype-related outcomes, and treatment responses. The primary endpoint was time to the first event of all-cause mortality or hospitalization for heart failure (HHF). Among 233 recruited patients, 24.9% experienced primary outcomes within 12 months. A total of 3.9% was lost to follow-up. Three phenotypes were identified. Phenotype 1 (n = 126) consisted of lean, elderly females with chronic kidney disease, anemia, and concentric hypertrophy. Phenotype 2 (n = 62) included younger males with coronary artery disease. Phenotype 3 (n = 45) comprised of obese elderly with atrial fibrillation. Phenotype 1 and 2 reported higher primary outcomes than phenotype 3 (p = 0.002). Regarding treatment responses, SGLT2 inhibitor was associated with fewer primary endpoints in phenotype 1 (p = 0.003) and 2 (p = 0.001). RAAS inhibitor was associated with fewer all-cause mortality in phenotype 1 (p = 0.003). Beta blocker was associated with fewer all-cause mortality in phenotype 1 (p = 0.024) and fewer HHF in phenotype 2 (p = 0.011). Our pioneering study supports the personalized approach to optimize HFpEF management in hypertensive-diabetic patients.