Risk Factor For Myocardial Infarction Research Articles

Novel Role of YAP1 in Regulating Blood Pressure and Vascular Tone

Introduction: Hypertension is a major risk factor for occlusive vascular diseases, myocardial infarction, heart failure, stroke, and chronic kidney disease. In the U.S., ~30% of adults suffer from hypertension. Merely half of the individuals with hypertension have their blood pressure under control, despite the wide range of antihypertensive medications available, indicating an urgent need for a better understanding of the underlying causes of hypertension to identify novel therapeutic strategies for its treatment and prevention. Recent genome-wide association study (GWAS) has identified an unexpected association between a loss-of-function SNP in the YAP1 gene locus and decreased blood pressure (BP). Moreover, de novo analysis of publicly available RNAseq data revealed that the vascular tissues of hypertensive mice treated with Ang-II exhibit increased YAP1 expression. Suggesting a novel role of YAP1 in blood pressure regulation. However, whether Vascular smooth muscle cell (VSMC) expressed YAP1 has a specific role in VSMC contraction and BP regulation remains completely unknown. Therefore, we hypothesized that YAP1 could play a key role in regulating blood pressure. Methodology: We have generated a novel inducible SM-specific- Yap1 Knockout ( YAP1 iKO) mouse model and employed a pharmacological inhibitor of YAP1, Verteporfin, to delineate the functional role of VSMC-expressed YAP1 in hypertension in regulating vascular tone and BP. Vascular reactivity experiments were performed using wire myography. BP was measured in ambulant mice via radiotelemetry. In vitro gain- and loss-of-function studies utilizing human coronary artery SMCs were conducted to examine the impact of YAP1 on contractility signaling components using western blotting. Results: Consistent with GWAS and RNAseq data, we found that YAP1 is upregulated in vascular tissues of spontaneously hypertensive rats (SHRs). Using aortic rings from WT mice, we discovered that Verteporfin significantly reduced vasoconstrictive responses to Phenylephrine or Serotonin but did not alter endothelium-dependent vasorelaxant responses to Acetylcholine, suggesting a specific role of YAP1 in VSMCs. Consistently, YAP1 iKO exhibited attenuated responses to vasoconstrictors in isolated conduit and resistance vessels. Importantly, radiotelemetry studies demonstrated for the first time that YAP1 iKO mice exhibit a hypotensive phenotype. Mechanistically, YAP1 gain- and loss-of-function studies in human VSMCs showed that YAP1 activates multiple signaling pathways that play a key role in VSMC contractility including RhoA/ROCK1/actin polymerization and PKC/ERK signaling pathways. Summary/Conclusion: This is the first study to demonstrate that inhibition of SM-specific-Yap1 expression regulates BP and vascular tone, likely via the regulation of contractile machinery components. Together, our data suggest that YAP1 is a promising novel therapeutic target for ameliorating hypertension. This work is supported by a grant from National Heart, Lung, and Blood Institute (R00HL153896). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Linking IL-6 and hsCRP among Indian patients with myocardial infarction

The association between serum interleukin-6 (IL-6) and highly sensitive C - reactive protein (hsCRP) as predictors of the risk factors for Myocardial Infarction. The study included a total of 50 patients with Myocardial Infarction, aged between 25 to 74 years. The levels of hsCRP were measured using the immunoturbidimetry method, while Interleukin 6 was estimated using the sandwich ELISA method. Statistical analysis was conducted using SPSS version 21.0, with p values calculated using Quartile ratio, ANOVA unpaired t-test, and Kaplan-Meier Curve Method. A p-value of less than 0.05 was considered statistically significant. All participants underwent a questionnaire, physical examination, medical history assessment, and laboratory tests. The results of the study showed that there was a significant correlation between IL-6 and hsCRP levels in the Quartile groups, as well as with lipid profiles. The Kaplan-Meier method also demonstrated a significant association between IL-6 and hsCRP levels in participants. The comparison of biomarkers further supported these findings. Thus, data shows that elevated levels of hsCRP and IL-6 could serve as valuable diagnostic markers for predicting Acute Myocardial Infarction. Our study strongly suggests that IL-6 could be a powerful marker in evaluating the Myocardial Infarction.

​Comprehensive mendelian randomization analysis of plasma proteomics to identify new therapeutic targets for the treatment of coronary heart disease and myocardial infarction.

Ischemic heart disease is one of the leading causes of mortality worldwide, and thus calls for development of more effective therapeutic strategies. This study aimed to identify potential therapeutic targets for coronary heart disease (CHD) and myocardial infarction (MI) by investigating the causal relationship between plasma proteins and these conditions. A two-sample Mendelian randomization (MR) study was performed to evaluate more than 1600 plasma proteins for their causal associations with CHD and MI. The MR findings were further confirmed through Bayesian colocalization, Summary-data-based Mendelian Randomization (SMR), and Transcriptome-Wide Association Studies (TWAS) analyses. Further analyses, including enrichment analysis, single-cell analysis, MR analysis of cardiovascular risk factors, phenome-wide Mendelian Randomization (Phe-MR), and protein-protein interaction (PPI) network construction were conducted to verify the roles of selected causal proteins. Thirteen proteins were causally associated with CHD, seven of which were also causal for MI. Among them, FES and PCSK9 were causal proteins for both diseases as determined by several analytical methods. PCSK9 was a risk factor of CHD (OR = 1.25, 95% CI: 1.13-1.38, P = 7.47E-06) and MI (OR = 1.36, 95% CI: 1.21-1.54, P = 2.30E-07), whereas FES was protective against CHD (OR = 0.68, 95% CI: 0.59-0.79, P = 6.40E-07) and MI (OR = 0.65, 95% CI: 0.54-0.77, P = 5.38E-07). Further validation through enrichment and single-cell analysis confirmed the causal effects of these proteins. Moreover, MR analysis of cardiovascular risk factors, Phe-MR, and PPI network provided insights into the potential drug development based on the proteins. This study investigated the causal pathways associated with CHD and MI, highlighting the protective and risk roles of FES and PCSK9, respectively. FES. Specifically, the results showed that these proteins are promising therapeutic targets for future drug development.

Serum ferritin and the risk of myocardial infarction: A Mendelian randomization study.

The potential role of serum ferritin as a risk factor for myocardial infarction (MI) is controversial, necessitating a systematic exploration of the causal relationship between ferritin and MI through Mendelian randomization (MR) methods. Genetic data were derived from a genome-wide association study (GWAS), employing the inverse variance-weighted (IVW) method as the primary approach. Comprehensive sensitivity analyses were conducted to validate the robustness of the results. Evaluation of instrumental variables was performed using the F-statistic, and a meta-analysis was employed to assess the average gene-predicted effect between ferritin and MI. The MR study revealed a negative correlation between ferritin and MI. The odds ratios (ORs) in the IVW method were 0.83 [95% confidence interval (CI) = 0.72-0.97; P = .017] and 0.86 (95% CI = 0.72-1.02; P = .080). Additionally, meta-analysis consistently indicated a negative causal relationship between ferritin and MI, with no heterogeneity or horizontal pleiotropy, thereby indicating a negative correlation between ferritin levels and the risk of MI. The genetic evidence sheds light on the causal relationship between ferritin levels and MI risk, providing new perspectives for future interventions in acute myocardial infarction (AMI).

Prevalence of elevated lipoprotein(a) in cardiac rehabilitation patients - results from a large-scale multicentre registry in Germany.

Lipoprotein(a) (Lp(a)) is an independent risk factor for myocardial infarction and aortic valve stenosis. European guidelines recommend assessing it at least once in a lifetime, particularly in premature atherosclerotic heart disease. A non-interventional registry was conducted at MEDIAN rehabilitation facilities in Germany to assess the frequency of Lp(a) testing in referring acute care hospitals and the prevalence of elevated Lp(a) levels in aortic valve stenosis or premature myocardial infarction. All consecutive patients referred after coronary intervention or aortic valve surgery were included in four cohorts: aortic valve intervention (cohort 1), current/previous myocardial infarction at < 60 years of age (cohorts 2a/2b), and myocardial infarction at ≥ 60 years of age (control). The analysis included 3393 patient records (cohort 1, n = 1063; cohort 2a, n = 1351; cohort 2b, n = 381; control, n = 598). Lp(a) had been determined at the referring hospital in 0.19% (cohort 1), 4.96% (cohort 2a), 2.36% (cohort 2b), and 2.01% (control) of patients. Lp(a) levels were > 50 mg/dL or > 125 nmol/L in 28.79% (cohort 1), 29.90% (cohort 2a), and 36.48% (cohort 2b; p < 0.001) compared to 24.25% (control). Family history of premature cardiovascular disease was reported in 13.45% (cohort 1), 38.56% (cohort 2a), and 32.81% (cohort 2b) compared to 17.89% (control; p < 0.05 for each comparison). Lp(a) had been rarely assessed in acute management of aortic valve stenosis or premature myocardial infarction despite expanding scientific evidence and guideline recommendation. Given the above-average incidence of elevated Lp(a) levels, awareness for Lp(a) has to increase substantially to better identify and manage high-risk patients.

Spontaneous coronary artery dissection in a young woman with signs of connective tissue dysplasia and hereditary thrombophilia: clinical case

BACKGROUND: Spontaneous coronary artery dissection (SCAD) is a disease that develops unrelated to intracoronary intervention, atherosclerosis, aortic dissection, or mechanical trauma and causes a false lumen (intramural hematoma) in the wall of the coronary artery (CA) with impaired blood flow in it and myocardial ischemia in the affected region of the CA. SCAD most often develops in young and middle-aged adults (aged ≤50 years); among women, it becomes the culprit in 24%–35% of cases of acute myocardial infarction (MI). SCAD is a risk factor for MI, and incorrect interpretation of the angiographic picture and intravascular imaging methods can lead to incorrect tactics of patient behavior.&#x0D; CLINICAL CASE DESCRIPTION: This article presents a clinical case of SCAD leading to the development of MI in a young woman with concomitant connective tissue dysplasia and hereditary thrombophilia. The angiographic disease course resembled focal atherosclerosis, and in the course of invasive management, complications had arisen, confirming the probable genesis of coronary artery obstruction.&#x0D; CONCLUSION: SCAD is a complex disease, with a sudden onset and an ambiguous prognosis. In most cases, SCAD develops in young women in the absence of cardiovascular factors. It is difficult to diagnose because its signs and symptoms are similar to more common diseases, mainly MI. SCAD can masquerade as focal stenosis on an angiogram, mimicking an atherosclerotic plaque. The «gold standard» for diagnosing SCAD is optical coherence tomography (OCT). OCT enables the visualization of the state of all coronary artery walls and elucidates the pathogenetic mechanisms of MI. If performing OCT is impossible after diagnostic coronary angiography in young patients in suspected cases, the likelihood of DST and SCAD risk must be assessed to avoid errors in choosing treatments. The technical accessibility of intracoronary imaging methods reduces the frequency of diagnostic and, consequently, treatment errors.

Association of different milk fat content with coronary artery disease and myocardial infarction risk: A Mendelian randomization study.

Numerous observational studies have investigated on the correlation of whole, semi-skimmed, and skimmed milk with coronary artery disease (CAD) and myocardial infarction (MI) risk; However, no consensus has been reached and evidence on any causal links between these exposures and outcomes remains unclear. This study aimed to conduct univariate and multivariate Mendelian randomization (MR) analyses, using publicly released genome-wide association study summary statistics (GWAS) from the IEU GWAS database, to ascertain the causal association of milk with various fat content with CAD and MI risk. For the exposure data, 29, 15, and 30 single-nucleotide polymorphisms for whole milk, semi-skimmed milk, and skimmed milk, respectively, obtained from 360,806 Europeans, were used as instrumental variables. CAD and MI comprised 141,217 and 395,795 samples, respectively. We used inverse variance weighted (IVW), weighted median, MR-Egger regression, and MR Pleiotropy Residual Sum and Outlier analyses to determine whether pleiotropy and heterogeneity could skew the MR results. Sensitivity tests were conducted to verify the robustness of the results. After adjusting for false discovery rates (FDR), we discovered proof that skimmed milk intake is a genetically predicted risk factor for CAD (odds ratio [OR] = 5.302; 95% confidence interval [CI] 2.261-12.432; P < 0.001; FDR-corrected P < 0.001) and MI (OR = 2.287; 95% CI 1.218-4.300; P = 0.010; FDR-corrected P = 0.009). Most sensitivity assessments yielded valid results. Multivariable MR for CAD and MI produced results consistent with those obtained using the IVW method. There was no causal relationship between whole or semi-skimmed milk, and CAD or MI. Our findings indicate that the consumption of skimmed milk may increase the risk of CAD and MI. This evidence may help inform dietary recommendations for preventing cardiovascular disease. Further studies are required to elucidate the underlying mechanisms.

Equivalent density of calcium deposits – a new diagnostic pattern for atherocalcinosis

Objective. To assess the density of the calcified substrate of atherosclerotic plaques of the carotid arteries using data from the computed tomography of patients with multifocal atherosclerosis. Material and methods. In 251 patients with verified atherosclerosis of the coronary and carotid arteries, with a high prevalence of angina pectoris, a history of myocardial infarction and modifiable cardiovascular risk factors, multislice computed tomography (MSCT) of the carotid arteries was performed to assess the calcium index and determine the equivalent density of calcium deposits (EDCD). A morphological sub-study of the material from the removed atherosclerotic plaques was carried out using scanning electron microscopy (SEM) in 12 patients. Results. According to the MSCT data, we identified 5 main types of calcium deposit location in the thickness of the atherosclerotic plaque. We noted that totally calcified plaques were associated with carotid artery stenosis by more than 30 %. According to the SEM data, we identified 2 leading patterns: diffuse and compact types of microcalcification. There was a statistically significant association of a low level of EDCD with a diffuse type of calcification both in vivo (p=0.010) and ex vivo (p=0.008). Patients, having carotid artery EDCD less than 0.21 mg/mm3, reported a significantly higher incidence of type 2 diabetes mellitus (p=0.0001) and a history of stroke (p=0.021). When comparing the MSCT data on the calcium deposit density and their localization in the atherosclerotic plaque, we noted a statistically significant predominance of low EDCD with superficial calcification of the plaque (p=0.002). Conclusion. The use of a calculated indicator of the equivalent density of calcium deposits of the atherosclerotic substrate allows us to non-invasively obtain new data on the structure of plaques. The observed association of the superficial distribution of calcification with low calcification density according to the MSCT data may indicate potential plaque instability.

Clopidogrel induced reduction in neutrophil count: An overlooked beneficial effect?

Complement-stimulated neutrophils are able to adhere to the endothelium and damage endothelial cells both in vitro and in vivo. These blood cells participate in the early stages, growth and complications of atherosclerotic plaques. Recent findings, based on mendelian randomization analysis, support the concept that high neutrophil counts are a causal risk factor for ischemic heart disease and myocardial infarction . Clopidogrel decreases leukocyte count and inflammatory markers in patients with acute coronary syndromes; this off-target effect, which is independent of the antiplatelet action, may help explaining secondary prevention data showing a superiority of clopidogrel over aspirin in reducing new cardiovascular events.

Age and healthy lifestyle behavior’s disparities and similarities on knowledge of myocardial infarction symptoms and risk factors among public and outpatients in a resource-limited setting, cross-sectional study in greater Gaborone, Botswana

Objectives In this cross-sectional study from Botswana, we investigated knowledge of myocardial infarction (MI) symptoms and risk factors among the general public and outpatients with MI risk factors based on age and lifestyle behaviors, in addition to assessing associations with sociodemographic and MI risk factors.Method Open-ended questionnaires about 8 MI symptoms and 10 risk factors, were administered by research assistants to a representative selection of outpatients (n = 525) and the public (n = 2248). Weight and height were measured in all participants and BMI was calculated. Knowledge scores were compared between the two groups. We examined whether sociodemographic and MI risk factors had impact on the scores. Analyses were further adjusted for lifestyle behavior (smoking status, dietary status and physical activities).ResultsThe valid response rate was 97.9% comprising 97.8% for the public (n = 2199) and 98.1% for outpatients (n = 515). Public respondents (35.2 ± 12.3 years) were younger than outpatients (38.5 ± 12.6 years). The public comprised 56.9% females while outpatients 54.6%.In general, outpatients had higher knowledge of MI symptoms than the public, with mean scores ± SD of 3.49 ± 2.84 vs 2.80 ± 2.54. Outpatients also had higher knowledge score of MI risk factors than the public, with mean scores, 5.33 ± 3.22 vs 3.82 ± 3.07. For MI symptoms, outpatients were more aware than the public for chest pains among all ages, for arm pain/ numbness, neck/ jaw pain radiating to/ from chest, and feeling sick or looking pallor on the skin among those aged 35–49 years.Among both the public and outpatients, lower knowledge of both MI symptoms and risk factors was associated with primary education, not residing/working together, history of hypertension, no history of heart disease/stroke, and obesity. There were similarities and disparities on MI knowledge among respondents with various numbers of healthy lifestyle behaviours.ConclusionResults call for urgent educational campaigns on awareness and knowledge of MI and using strategies based on age and lifestyle behavior.

Levels of Protein S in Saudi Patients with Myocardial Infarction

A heart attack - also known as a myocardial infarction (MI) or acute myocardial infarction (AMI)—happens when blood supply to a part of the heart stops, resulting in heart muscle damage. Coronary artery disease is the leading cause of MI. Risk factors include smoking, diabetes, lack of exercise, obesity, high blood pressure, poor diet, and excessive alcohol consumption. Protein S, a vitamin K-dependent protein, functions as a cofactor for activated protein C (APC), allowing it to inactivate factors Va and VIIIa more effectively. This study examines levels of protein S in Saudi patients with myocardial infarction. A case-control study was performed to estimate the level of protein S in Saudi patients with MI. A total of 150 samples (2.5/mL of venous blood) from patients with MI and healthy controls (n = 50) were obtained and analyzed using an enzyme-linked immunosorbent assay (ELISA) sandwich. Patients’ mean protein S levels were within normal ranges (86.19.63 and 76.2030.64, respectively). Patients and controls had no significant difference in mean antithrombin (ATIII) and protein C levels (p-value = 0.26, 0.2, and 0.19, respectively). The findings also revealed that certain samples had low ATIII (8.7%) and protein C levels (11.3% ). From this study, we conclude that protein S deficiency was not found to be a major risk factor for MI.

Factors Associated With Myocardial Infarction in a Rural Population With Peripheral Arterial Diseases.

Peripheral arterial disease (PAD) studies in rural populations are limited. The incidence of myocardial infarction (MI) is higher in patients with PAD. This study examined the association between sociodemographic and clinical risk factors and MI in patients with PAD in Central Appalachia, comprising of 230 counties across six states in the United States. Data from electronic medical records of 13,455 patients with PAD were extracted from a large health system in Central Appalachia. Bivariate and logistic regression analyses were conducted. The final sample consisted of 5574 patients with PAD, of whom 24.85% were also diagnosed with MI. The mean age was 71 ± 11.23years, and the majority were male (56.40%). After adjusting for confounders, patients with hypertension had three times higher odds of MI (adjusted Odds Ratio [aOR] = 3.21; 95% CI: 2.50-4.14) compared with those without hypertension. The likelihood of MI increased by 51% among patients with diabetes (aOR = 1.51; 95% CI: 1.33-1.71), 34% among ever-smokers (aOR = 1.34; 95% CI: 1.18-1.52), and 45% in males (aOR = 1.45; 95% CI: 1.27-1.65). Hypertension, diabetes, smoking, and male sex were identified as significant risk factors for MI. Screening and effective management of these risk factors in rural areas could potentially prevent MI incidence among patients with PAD.

Myocardial infarction in patients with HIV infection: incidence, risk factors, pathogenesis, clinical performance and treatment

HIV infection increases the risk of premature myocardial infarction (MI) and other atherosclerotic cardiovascular diseases, which are the main noncommunicable cause of death in HIV-infected patients. The review presents the analysis of recent literature on the incidence, prevalence and risk factors of MI in HIV-infected people. It established that MI is associated with the combined effects of traditional cardiovascular risk factors, HIV infection and the cardiometabolic effects of antiretroviral therapy. Pathogenetic features of acute coronary syndrome in HIV infection under conditions of systemic immune-mediated inflammation, hypercoagulation and direct exposure to the virus are highlighted. The clinical features and coronary damage in MI are described. Methods of treating MI are compared. We concluded that the volume and quality of care for patients with HIV and MI is insufficient. From the perspective of possible drug interactions with antiretroviral therapy, effectiveness and safety of methods for secondary prevention of MI was analyzed.

Expression levels and clinical significance of ferroptosis-related genes in patients with myocardial infarction

Myocardial infarction (MI) is the most serious type of cardiovascular disease and the leading cause of cardiac death.Ferroptosis is one of the newly discovered programmed cell death modes in MI, but its mechanism of action in MI has not been clarified.In this study, we analyzed the expression changes of ferroptosis-related genes in MI and explored the potential mechanisms of ferroptosis-related functions in myocardial infarction. Public data sets GSE19339, GSE97320 and GSE141512 were retrieved from the Gene Expression Omnibus (GEO) Datasets public database. After data preprocessing, differentially expressed genes were screened, and differentially expressed ferroptosis-related genes associated with myocardial infarction were obtained. The biological function and signaling pathway enrichment analysis were performed to establish the PPI interaction network specific to heart tissue, and the differential diagnosis significance of differentially expressed ferroptosis-related genes associated with myocardial infarction was analyzed by ROC curve and decision tree model.A total of 317 genes showed significant changes in expression levels in patients with myocardial infarction, including 205 down-regulated genes and 112 up-regulated genes.Gene Ontology (GO) enrichment analysis and functional classification of Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling pathways showed that these genes were mainly involved in signaling pathways or biological functions related to inflammation and apoptosis.Five differentially expressed ferroptosis-related genes (SLC2A3, EPAS1, HMOX1, ATM, FANCD2) were obtained, all of which played key biological functions in cardiac tissue function. SLC2A3, EPAS1, HMOX1, ATM and FANCD2 genes all had good diagnostic value for myocardial infarction (P < 0.05). The increase of SLC2A3, EPAS1 and HMOX1 are risk factors for myocardial infarction, while ATM and FANCD2 are protective factors.Decision tree analysis showed that SLC2A3, HMOX1, ATM, FANCD2 gene had higher net yield in diagnosing myocardial infarction. In summary, the mechanism of ferroptosis is involved in the occurrence and progression of myocardial infarction. In this study, five differentially expressed ferroptosis-related genes associated with myocardial infarction were retrieved, which may be good biomarkers of ferroptosis after MI.These findings also suggest that the differential expression of ferroptosis-related genes associated with myocardial infarction has significant diagnostic significance for myocardial infarction.

Sex differences in the association between insulin resistance and non-fatal myocardial infarction across glycaemic states

BackgroundFemales are generally less prone to cardiovascular (CV) events than males, but this protection is trumped by diabetes. The mechanism behind the increased relative risk in females with diabetes is not fully understood. Insulin resistance (IR) is suggested to be a more important contributor to CV morbidity in females than in males. We aim to investigate differences in the association between IR indexes (Homeostatic Model Assessment of IR - HOMA-IR, visceral adiposity index – VAI, and triglycerides/high-density lipoprotein-cholesterol - TG/HDL-C index), and a first non-fatal myocardial infarction (MI) across different glycaemic states.MethodsIR indexes were calculated in a population with (n = 696) and without (n = 707) a first non-fatal MI, free from known diabetes. MI cases were investigated at least six weeks after the event. All participants were categorized by an oral glucose tolerance test as having normal glucose tolerance, impaired fasting glucose, impaired glucose tolerance, or newly diagnosed diabetes. Comparison of proportion of glycaemic states by sex was tested by chi-square test. The associations between sex, a first non-fatal MI, IR indexes, and traditional CV risk factors were analysed by multivariate logistic regression models. Continuous variables were logarithmically transformed.ResultsOf the total population 19% were females and 81% males, out of whom 47% and 50% had a first non-fatal MI, respectively. Compared with males, females were older, less often smokers, with lower body mass index and higher total cholesterol and high-density lipoprotein cholesterol levels. The proportion of glycaemic states did not differ between the sexes (p = 0.06). Females were less insulin resistant than males, especially among cases and with normal glucose tolerance. In logistic regression models adjusted for major CV risk factors including sex, the associations between VAI and TG/HDL-C index and a first non-fatal MI remained significant only in females (odds ratios and 95% confidence intervals: 1.7, 1.0-2.9, and 1.9, 1.1–3.4 respectively).ConclusionsThese results support the assumption that IR indexes based on anthropometrics and lipid panel, i.e., VAI and TG/HDL-C, could be a better measure of IR and CV-predictor for non-fatal MI in females, even without glycaemic perturbations.

Should a recent SARS-CoV-2 infection be considered a risk or prognostic factor for ST-segment elevation myocardial infarction?

The aim of the study was to assess whether a recent SARS-CoV-2 infection could by itself be a risk or prognostic factor for ST-segment elevation myocardial infarction (STEMI). An observational study in unvaccinated patients with STEMI confirmed by cardiac catheterization was conducted. A recent or concurrent SARS-CoV-2 infection was identified by the presence of serum IgG against the nucleocapsid protein, or a positive polymerase chain reaction test on nasopharyngeal swabs. Baseline cardiovascular risk factors, clinical STEMI severity, main catheterization findings, and occurrence of major adverse cardiovascular events (MACE) during hospitalization were compared between study subgroups. Of a total of 89 patients recruited, 14 (16%) had a recent SARS-CoV-2 infection. Patients with STEMI and recent SARS-CoV-2 infection had a markedly lower frequency of high blood pressure (20% versus 55%; P = 0.03) as well as a tendency to have fewer comorbidities. Regarding the clinical presentation, there were no differences in the severity of the STEMI. Furthermore, the main findings during cardiac catheterization including the atherosclerotic burden and the number of vessels affected, as well as the occurrence of MACE during follow-up, were not significantly different between the groups. A recent SARS-CoV-2 infection appears to facilitate the triggering of STEMI, as these patients have fewer traditional cardiovascular risk factors than their uninfected counterparts. However, this does not seem to affect the clinical presentation or the in-hospital course of STEMI patients.

Традиционные и нетрадиционные факторы риска развития инфаркта миокарда в молодом возрасте

In a world that is constantly changing, the emergence of certain diseases, such as cardiovascular disorders (CVD), is also changing. It is evident that there are unique characteristics of premorbid background, risk factors, pathogenesis, and course of CVD in young individuals compared to older individuals. Currently, there are no effective measures for primary prevention of CVD in young patients, and the use of risk-metric resources is limited due to their focus on elderly patients. Traditional risk factors for CVD are typically used to create an objective patient profile and determine the appropriate diagnostic pathway Non-traditional risk factors may not be immediately apparent, but they also play a role in the development of cardiac disorders in young patients and should be taken into consideration. Physicians should exercise caution when considering both traditional and non-traditional risk factors in young patients with chest pain This may necessitate more detailed monitoring of the patient's condition Timely medical care and management of comorbidities can significantly improve prognosis and maintain work capacity, which is particularly important at a young age. A personalized approach to the management of young patients is required for all of these entities Therefore, the issue of cardiovascular disease in young patients is currently urgent KEYWORDS: myocardial infarction, young patients, traditional risk factors, non-traditional risk factors FOR CITATION: Karetnikova V.N., Neeshpapa A.G., Peganova Kh.A. Traditional and non-traditional risk factors for myocardial infarction in young adults. Russian Medical Inquiry. 2024;8(1):26–30 (in Russ.). DOI: 10.32364/2587-6821-2024-8-1-4.

Risk Factors of Myocardial Infarction among Patients Admitted to Al-Wahdah Teaching Hospital, Yemen

Risk Factors of Myocardial Infarction among Patients Admitted to Al-Wahdah Teaching Hospital, Yemen

The occurrence of ST elevation myocardial infarction (STEMI) and non-STEMI in patients with post traumatic stress disorder (PTSD) using the large nationwide inpatient sample (NIS).

PTSD leads to increased levels of stress hormones and dysregulation of the autonomic nervous system which may trigger cardiac events. The goal of this study is to evaluate any association between PTSD and the occurrence of STEMI and NSTEMI using a large database. Using the Nationwide Inpatient Sample (NIS) and ICD-9 codes from 2005 to 2014 (n=1,621,382), we performed a univariate chi-square analysis of in-hospital occurrence of STEMI and NSTEMI in patients greater than 40 years of age with and without PTSD. We also performed a multivariate analysis adjusting for baseline characteristics including age, gender, diabetes, race, hyperlipidemia, hypertension, and tobacco use. The 2005-2014 dataset contained 401,485 STEMI patients (745, or 0.19%, with PTSD) and 1,219,897 NSTEMI patients (2,441, or 0.15%, with PTSD). In the 2005 dataset, 0.5% of PTSD patients had STEMI compared to 1.0% of non-PTSD patients (OR=0.46, 95% C.I., 0.36-0.59). Similarly, 0.6% of patients with PTSD and 2.2% of patients without PTSD had NSTEMI (OR=0.28, 95% C.I., 0.23-0.35). In the 2014 dataset, 0.3% of PTSD patients had STEMI compared to 0.7% of non-PTSD patients (OR=0.43, 95% C.I., 0.35-0.51). Similarly, 1.4% of patients with PTSD versus 2.9% of patients without PTSD had NSTEMI (OR=0.48, 95% C.I., 0.44-0.52). Similar trends were seen throughout the ten-year period. After adjusting for age, gender, diabetes, race, hyperlipidemia, hypertension, and tobacco use, PTSD was associated with a lower occurrence of STEMI (2005: OR=0.50, 95% C.I., 0.37-0.66; 2014: OR=0.35, 95% C.I., 0.29-0.43) and NSTEMI (2005: OR=0.44, 95% C.I., 0.34-0.57; 2014: OR=0.63, 95% C.I., 0.58-0.69). Using a large inpatient database, we did not find an increased occurrence of STEMI or NSTEMI in patients diagnosed with PTSD, suggesting that PTSD is not an independent risk factor for myocardial infarction.

Biological Signaling Network in Myocardial Infarction in Young Adults. A Study of Transcriptome Analysis

Background: Myocardial infarction (MI) is the common manifestation of coronary heart disease that develops from occlusion of coronary arteries. Several risk factors of MI were identified, but data pertaining to genetics and molecular mechanisms involved in the development of MI is limited. Therefore, the present study attempts to analyze the peripheral blood transcriptome information of MI patients and unveil the key genes involved in the pathogenesis of MI. Methods: Total RNA was extracted from the blood sample for illumine sequencing, and raw data obtained were subjected to quality control (QC) using the FastQC tool, followed by trimming of raw data by the fastp tool. Further processed high-quality data were aligned onto the human reference genome using HISAT2 aligner. Gene quantification was done using the feature Counts plugin in the subread package. The raw read counts were given as input to the differential expression analysis (DESeq2) R package for the computation of differentially expressed genes. Gene set enrichment analysis for gene ontology was done using the clusterProfiler R package. Results: A total of 609 genes were significantly expressed in the present study, of which 561 genes were upregulated and 48 genes were downregulated. This study presents overall changes in genes involved in different categories such as biological processes, molecular functions, and cellular components in responses to MI. Conclusions: The significantly deregulated genes identified in the present study not only indicate the molecular and cellular changes but also suggest the scope for the detection of specific gene markers for MI.