Premature Myocardial Infarction Research Articles

Identification of a functional missense variant in the matrix metallopeptidase 10 (MMP10) gene in two families with premature myocardial infarction

A positive family history is a major independent risk factor for atherosclerosis, and genetic variation is an important aspect of cardiovascular disease research. We identified a heterozygous missense variant p.L245P in the MMP10 gene in two families with premature myocardial infarction using whole-exome sequencing. The aim of this study was to investigate the consequences of this variant using in-silico and functional in-vitro assays. Molecular dynamics simulations were used to analyze protein interactions, calculate free binding energy, and measure the volume of the substrate-binding cleft of MMP10-TIMP1 models. The p.L245P variant showed an altered protein surface, different intra- and intermolecular interactions of MMP10-TIMP1, a lower total free binding energy between MMP10-TIMP1, and a volume-minimized substrate-binding cleft of MMP10 compared to the wild-type. For the functional assays, human THP-1 cells were transfected with plasmids containing MMP10 cDNA carrying the p.L245P and wild-type variant and differentiated into macrophages. Macrophage adhesion and migration assays were then conducted, and pro-inflammatory chemokine levels were evaluated. The p.L245P variant led to macrophages that were more adherent, less migratory, and secreted higher levels of the pro-inflammatory chemokines CXCL1 and CXCL8 than wild-type macrophages. Thus, the p.L245P variant in MMP10 may influence the pathogenesis of atherosclerosis in families with premature myocardial infarction by altering protein - protein interactions, macrophage adhesion and migration, and expression of pro-inflammatory chemokines, which may increase plaque rupture. These results could contribute to the development of selective MMP10 inhibitors and reduce the risk of atherosclerosis in families with a history of premature myocardial infarction.

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.

The diagnostic value of genetic testing in familial hypercholesterolemia in patients with premature myocardial infarction

Objective: To evaluate the diagnostic value of gene testing in familial hypercholesterolemia (FH) in patients with premature myocardial infarction(PMI). Methods: This study was a single center cross-sectional study. A retrospective analysis was made on PMI patients who visited the People's Hospital of Peking University from May 1, 2015 to March 31, 2017. Clinical data of patients was collected and gene testing of FH related genes low density lipoprotein receptor (LDLR), proprotein convertase subtilisin/kexin type 9 (PCSK9), apolipoprotein B(APOB) and low density lipoprotein receptor adaptor protein 1(LDLRAP1) was carried out. Clinical diagnosis of FH patients was performed using Simon Broome criteria, DLCN criteria, and FH Chinese expert consensus. Results: There were 188 males (83.6%) among 225 PMI patients, and the age of the first myocardial infarction was (46.6±7.2) years old. Ten patients carried FH pathogenic or possibly pathogenic mutations (4.4%). Compared with Simon Broome standard, DLCN standard and FH Chinese expert consensus, gene testing increased the diagnostic rate of FH by 53.3%, 33.3% and 42.1% respectively. Conclusion: Gene testing is helpful to improve the diagnosis of FH, and it is important to start the standard treatment of FH as early as possible in patients with premature myocardial infarction.

Acute kidney injury prediction model utility in premature myocardial infarction

The incidence of premature myocardial infarction (PMI) has been rising and acute kidney injury (AKI) occurring in PMI patients severely impacts prognosis. This study aimed to develop and validate a prediction model for AKI specific to PMI patients. The MIMIC-Ⅲ-CV and MIMIC-Ⅳ databases were utilized for model derivation of PMI patients. Single-center data served for external validation. There were 571 and 182 AKI patients in the training set (n= 937) and external validation set (n= 292) cohorts, respectively. Finally, a 7-variable model consisting of: Sequential Organ Failure Assessment (SOFA) score, coronary artery bypass grafting (CABG), ICU stay time, loop diuretics, estimated glomerular filtration rate (eGFR) HCO3- and Albumin was developed, achieving an AUC of 0.85 (95% CI: 0.83-0.88) in the training set. External validation also confirmed model robustness. This model may assist clinicians in the early identification of patients at elevated risk for PMI. Further validation is warranted before clinical application.

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.

Premature acute myocardial infarction with ST segment elevation: a cohort study in the 2012-2022 decade

Premature acute myocardial infarction with ST segment elevation: a cohort study in the 2012-2022 decade

Plasma Haptoglobin as A Potential Biomarker for Coronary Artery Disease in Young Hypertensive Adults

INTRODUCTION: Uncontrolled hypertension is one of the recognized risk factors for coronary artery disease (CAD) in young adults, commonly underestimated owing to the young age. A novel biomarker to improve CAD risk assessment and hypertension management should be identified for this cohort. Thus, we had conducted a study to investigate plasma concentration and the role of haptoglobin in young hypertensive adults in the establishment of premature acute myocardial infarction (AMI). MATERIALS AND METHODS: A total of 120 male adults aged between 18 to 45 years enrolled into this cross-sectional study, divided into control, hypertensive, and acute myocardial infarction (AMI) groups. Blood samples were collected from all subjects, plasma concentrations of haptoglobin measured using enzyme-linked immunosorbent assays, and other CAD risk factors including high sensitivity C-reactive protein (hs-CRP) levels were analyzed. RESULTS: Plasma concentration of haptoglobin in the AMI group was the highest compared to hypertensive and control group (290.63±99.90 vs. 208.47±112.93 vs. 170.02±108.11 ng/ml, p&lt;0.006). There was a significant association between AMI and plasma haptoglobin concentration in hypertensive subjects independent of other known CAD risk factors (OR: 0.985, 95% CI 0.973-0.997, p=0.017). There was positive correlation between plasma haptoglobin and hs-CRP (r=0.0370, p&lt;0.001). CONCLUSION: Plasma haptoglobin is a potential biomarker to identify young hypertensive adults who are at risk of developing CAD.

Prevalent Variants in the LDLR Gene Impair Responsiveness to Rosuvastatin among Family Members of Patients with Premature Myocardial Infarction.

Familial hypercholesterolemia (FH) is an inherited metabolic disorder characterized by high levels of low-density lipoprotein cholesterol (LDL-c) from birth. About 85% of all FH cases are caused by pathogenic variants in the LDLR gene. Individuals with FH have increased cardiovascular risk, including a high risk of premature myocardial infarction (PMI). We conducted an opportunistic exome screening to identify variants in the LDLR gene among Vietnamese patients with PMI treated at a general hospital in southern Vietnam. A cascade testing for LDLR variants was conducted in their relatives within three generations, and the effects of the LDLR variant on the response to rosuvastatin treatment were also studied using a comparative before-and-after study design on those who were eligible. A total of 99 participants from the three generations of four PMI patients were recruited, mean age 37.3 ± 18.5 years, 56.6% males. Sanger sequencing revealed two variants in the LDLR gene: variant rs577934998 (c.664T>C), detected in 17 individuals within one family, and variant rs12710260 (c.1060+10G>C), found in 32 individuals (49.5%) in the other three families tested. Individuals harboring the variant c.664T>C had significantly higher baseline LDL-c and total cholesterol levels compared to those with variant c.1060+10G>C (classified as benign) or those without LDLR variants, and among the 47 patients subjected to a 3-month course of rosuvastatin therapy, those with variant c.664T>C had a significantly higher risk of not achieving the LDL-c target after the course of treatment compared to the c.1060+10G>C carriers. These findings provide evidence supporting the existence of pathogenic LDLR variants in Vietnamese patients with PMI and their relatives and may indicate the need for personalizing lipid-lowering therapies. Further studies are needed to delineate the extent and severity of the problem.

Trends in Premature Mortality from Acute Myocardial Infarction in American Indians/Alaska Natives in the United States from 1999 to 2020

Cardiovascular disease is the leading cause of mortality in American Indian and Alaska Native (AI/AN) groups. They are disproportionately found to have a higher rates of premature myocardial infarction (MI). The CDC WONDER (Centers for Disease Control and Prevention) was queried to identify premature MI deaths (female <65 years and male <55 years) occurring within the United States between 1999-2020. We investigated proportionate mortality trends related to premature MI among AI/ANs stratified by sex. Deaths attributed to AMI were identified using the International Classification of Diseases, 10th Revision, Clinical Modification (ICD-10) codes I21- I22. We compared the proportional mortality rate due to premature MI to that of non-AI/AN racial group, which comprised of all other races (Blacks, Whites, and Asian/Pacific Islander populations). In AI/ANs, we analyzed a total of 14,055 acute myocardial infarction (AMI) deaths of which 3,211 were premature MI deaths corresponding to a proportionate mortality rate of 22.8% (male 20.8%, female 26.2%). Non- AI/AN population had a lower proportionate mortality of 14.8% (male 13.7%, female 16%); p<0.01). On trend analysis, there was no significant improvement over time in the proportionate mortality of AI/ANs (19.8% in 1999 to 21.7% in 2020, p=0.09). Upon comparison of sex, proportionate mortality of premature MI in females showed a non-statistically significant increase from 21.6% in 1999 to 27.3% in 2020 [average annual percent change (AAPC) of 0.7; p=0.06)]. However, males had a statistically significant decrease in proportionate mortality of premature MI from 18.5% in 1999 to 18.2% in 2020 [AAPC of -0.8; p=0.01)]. AI/ANs have an alarmingly higher rate of proportionate mortality of premature MI compared to other races, with no improvement in the proportionate mortality rates over 20 years, despite an overall downtrend in AMI mortality. Further research to address the reasons for the lack of improvement in premature MI is needed to improve outcomes in this patient population.

Combined Impact of Migraine and Pregnancy-Induced Hypertension on Long-term Risk of Premature Myocardial Infarction and Stroke.

Migraine and pregnancy-induced hypertension (PIH) are known to increase cardiovascular risk on their own. However, evidence is limited on the combined impact of migraine and PIH on risk of cardiovascular disease. The aim of this study was to examine the combined impact of migraine and PIH on risk of premature (age 60 years and younger) major adverse cardiovascular and cerebrovascular events (MACCE), a composite end point consisting of myocardial infarction, stroke, or death due to one of these diseases. We conducted a population-based cohort study in Denmark (1996-2018) among women who had delivered at least one child. This population was stratified into 4 cohorts: women with neither migraine nor PIH, women with migraine, women with PIH, and women with both migraine and PIH. As a measure of absolute risk, we computed the 20-year cumulative incidence of premature MACCE, treating death by other causes than myocardial infarction and stroke as a competing risk. We used Cox regression to compute 20-year adjusted hazard ratios (HRs) of premature MACCE. Women with neither migraine nor PIH served as the comparison cohort. The 20-year absolute risk of premature MACCE was 1.3% (95% CI 1.2%; 1.3%) for women without migraine and without PIH (n = 1,288,541), 2.2% (95% CI 2.0%; 2.4%) for women with migraine (n = 54,827), 2.8% (95% CI 2.6%; 3.1%) for women with PIH (n = 49,008), and 3.1% (95% CI 2.1%; 4.4%) for women with both migraine and PIH (n = 3,140). The adjusted HR of premature MACCE was 1.66 (95% confidence interval [CI] 1.50-1.84) for women with migraine, 2.76 (95% CI 2.52-3.03) for women with PIH, and 2.41 (95% CI 1.61-3.61) for women with both migraine and PIH. Migraine and PIH separately increased the risk of premature MACCE. The risk of premature MACCE among women who had both migraine and PIH was similar to that among women with PIH only.

Investigating the Smoker's Paradox: Aortic Stenosis Patient Outcomes in Smokers

BackgroundSmoking is a major risk factor for premature atherosclerosis, myocardial infarction (MI), heart failure (HF), and sudden cardiac death. Studies suggest that smokers lose at least a decade of life expectancy compared to non-smokers. Despite these well-documented risks, the short-term mortality rates following acute coronary syndromes (ACSs) or related HF are lower in current smokers than non-smokers, a phenomenon known as the smoker's paradox. This study aimed to examine the influence of smoking on in-hospital outcomes for patients diagnosed with aortic stenosis (AS) in the United States and ascertain the presence of the smoker's paradox in this patient population. MethodsIn this study, we utilized the National Inpatient Sample (NIS) for the year of 2020 to identify all patients who were admitted for a principal diagnosis of aortic stenosis (AS). Subsequently, we isolated those patients with an ICD-10 code indicating smoking or tobacco use. To examine associations, both logistic and linear regression analyses were employed while adjusting for potential confounding factors. Our findings were considered significant if the 2-tailed p-value was 0.05 or lower. ResultsIn 2020, there were 102,615 hospitalizations with a principal diagnosis of aortic stenosis, 41,689 (40.6%) of these cases involved patients with a secondary diagnosis of smoking history or use. After accounting for factors such as age, race, gender, hospital bed size, location, teaching status, insurance coverage, income level, and Elixhauser comorbidities, we found that patients who smoked and had AS demonstrated a lower rate of in-hospital mortality (aOR 0.64, 95% CI 0.51 – 0.81), mechanical ventilation (aOR 0.77, 95% CI 0.67- 0.88), vasopressor initiation (aOR 0.79, 95% CI 0.64- 0.95), mechanical circulatory support (aOR 0.56, 95% CI 0.34-0.91), and hemodialysis initiation (aOR 0.56, 95% CI 0.47-0.67) when compared to non-smoking patients with AS (Figure 1). ConclusionOur study demonstrated that patients with a primary diagnosis of aortic stenosis (AS) and a history of smoking or tobacco use had significantly lower odds of in-hospital mortality, mechanical ventilation, vasopressor use, mechanical circulatory support, and hemodialysis initiation compared to their non-smoking counterparts with AS. To comprehensively understand the smoker's paradox and its influence on clinical outcomes for patients hospitalized with AS, it is crucial to carry out larger, methodologically rigorous investigations. Such studies will aid in revealing the underlying mechanisms and reasons behind the persistence of this paradox, despite its apparent contradiction, ultimately enhancing our understanding and informing more effective patient care strategies.

Patient demographics and clinical characteristics among patients with a premature myocardial infarction and lipoprotein(a) measurement: a retrospective analysis of the South Tyneside and Sunderland NHS Foundation Trust in the UK

Patient demographics and clinical characteristics among patients with a premature myocardial infarction and lipoprotein(a) measurement: a retrospective analysis of the South Tyneside and Sunderland NHS Foundation Trust in the UK

Sex and racial disparities in proportional mortality of premature myocardial infarction in the USA from 1999-2020

Abstract Background The incidence of premature myocardial infarction (PMI) (females &amp;lt;65 years and males &amp;lt;55 years) is increasing. We investigated proportional mortality trends related to PMI stratified by sex, race, and ethnicity from 1999-2020. Methods The CDC WONDER (Center for Disease Control and Prevention Wide-Ranging Online Data for Epidemiologic Research) was queried to identify PMI deaths occurring within the U.S. between 1999- 2020. We calculated trends in the proportional mortality of PMI using the Joinpoint regression analysis. Results From 1999-2020, we identified a total of 3,017,826 AMI-related deaths. Of these 373,317 were PMI deaths, corresponding to proportional mortality of 12.5% (male 12%, female 14%). On trend analysis, the proportional mortality of PMI increased from 10.5% in 1999 to 13.2% in 2020 [AAPC of 1.0 (0.8 to 1.2, p&amp;lt;0.01)] with a significant increase in females from 10% in 1999 to 17% in 2020 [AAPC of 2.4 (1.8 to 3.0, p&amp;lt;0.01)] and no significant change in males, 11% in 1999 to 10% in 2020 [AAPC of -0.2 (-0.7 to 0.3, p=0.4)]. There was a significant increase in proportional mortality in both Blacks (18% in 1999 to 21% in 2020) and Whites (10% in 1999 to 12% in 2020), with no statistical difference among American Indian or Alaska Native, Asian or Pacific Islander, or Hispanics. Conclusion Over the last 2 decades there has been a significant increase in the proportional mortality of PMI in females and black population in spite of the overall downtrend in AMI-related mortality.AMI mortalityAMI mortality based on race

Mitochondrial heteroplasmy as a marker for premature coronary artery disease: analysis of the poly-C tract of the control region sequence

Abstract Mitochondrial DNA (mtDNA) differs from the nuclear genome in many aspects: a maternal inheritance pattern, being more prone to acquire somatic novo mutations, accumulative with age; and the possible coexistence of different mtDNA alleles (heteroplasmy). Mitochondria are key cellular organelles responsible for energy production, involved in complex mechanisms, including atherosclerosis. In this scenario, we aimed to evaluate mtDNA variants that could be associated with premature cardiovascular disease. We evaluated 188 consecutive patients presenting with premature myocardial infarction with ST elevation (STEMI) confirmed by coronary angiogram. mtDNA polymorphisms and clinical data were evaluated and compared with 271 individuals from the same population (control group). Tobacco consumption (80.85% vs 21.21%, p&amp;lt;0.01) and dyslipidemia (38.83% vs 28.41%, p=0.02) were significant more frequent among STEMI patients. Besides, C16223T mtDNA mutation and poly-C heteroplasmy were significantly more frequent among premature STEMI cases than in controls. The OR associated C16223T mtDNA mutation with an increased presence of cardiovascular risk factors. Our data suggest that mtDNA C16223T mutation and poly-C heteroplasmy may be associated with unstable atherosclerosis disease. Moreover, the presence of cardiovascular risk factors (CVRFs) was associated to C16223T mtDNA mutation, with a cumulative effect. Protective mitochondrial pathways are potential therapeutic targets. Thus, preventing exposure to the damaging mechanisms associated to CVRFs is of the utmost importancemtDNA sanger analysisBaseline characteristics.

Abstract 14517: apoE Receptor-2-R952Q Variant in Macrophages Potentiates Hyperlipidemia and Atherosclerosis in LDL Receptor-Knockout Mice via Increased Secretion of Soluble LDL Receptor-Related Protein-1

Introduction and objective: Apolipoprotein E Receptor-2 (apoER2) is a type I transmembrane receptor in the LDLR family expressed in vascular smooth muscle cells (VSMC), endothelium, and macrophages. An apoER2 mutation referred to as apoER2-R952Q (R952Q) is associated with elevated plasma triglyceride levels and increased risk of premature coronary artery disease and myocardial infarction in humans. This study investigated the role of the R952Q mutation of apoER2 in modulating disease development. Methods and Results: We generated R952Q-expressing mice using a CRISPR-directed approach. This mouse line was crossed with the LDLR knockout mouse line and the progenies were fed a high cholesterol diet for 16 or 24 weeks. Results showed that unlike apoER2 knockout, the accelerated atherosclerosis R952Q variant mice exhibited was linked to increased plasma lipid levels. Considering apoER2's expression, which is notably absent in hepatocytes, we investigated the impact of R952Q myeloid cells on disease progression via bone marrow transplant. Results showed that wildtype apoER2 mouse recipients of R952Q bone marrow recapitulated the elevated plasma lipid level phenotype while R952Q mouse recipients of wildtype apoER2 bone marrow did not. Due to the absence of LDLR in our model, we investigated LRP1’s role in the context of myeloid-specific R952Q and found an increase in the production of hypercholesterolemia-associated soluble LRP1 (sLRP1) in the plasma of high cholesterol diet-fed mice with myeloid-specific R952Q. sLRP1 may compete with cell-surface LRP1 in lipoprotein clearance, suggesting a novel mechanism by which the R952Q mutation in macrophages may increase plasma lipid levels, thereby accelerating atherosclerosis. Conclusion: The R952Q mutation in apoER2 accelerates atherosclerosis via overproduction of soluble LRP1, a gain-of-function mechanism in macrophages resulting in hypercholesterolemia.

Abstract 16988: Conventional and Regionally Distinctive Risk Factors for First-Onset Myocardial Infarction in Bangladesh. The Bangladesh Risk of Acute Vascular Events (BRAVE) Study

Background: South Asians may be particularly susceptible to premature myocardial infarction (MI) owing both to classic cardiovascular risk factors and distinctive practices more common in South Asian populations. Hypothesis: Identifying modifiable risk factors for MI in South Asian populations should inform prevention strategies. Goal: To study conventional risk factors and several distinctive South Asian characteristics and practices in relation to the likelihood of first-ever MI in Bangladesh. Methods: In a case-control study involving 8,133 first MI cases and 8,122 controls, we calculated odds ratios (ORs) for MI (adjusted, when appropriate, for age, sex, smoking status, history of diabetes, history of hypertension, family history of MI, and LDL-cholesterol) and assessed their potential public health impact using population attributable fractions (PAFs). Results: The mean (SD) age of first MI was 53 (11) years. Adjusted ORs (95% CIs) were 2.75 (2.53-2.99) for cigarette smoking, 2.33 (2.08-2.60) for parental history of MI, 2.26 (2.07-2.48) for history of hypertension, 1.79 (1.61-1.98) for history of diabetes, and 1.61 (1.55-1.67) per 1-SD higher LDL-cholesterol. The highest PAFs (95% CIs) were for current cigarette smoking (48.9% [46.1%-51.6%]), higher LDL-cholesterol (32.4% [30.2%-34.4%]) and history of hypertension (14.7% [13.2%-16.1%]). As for regionally distinctive practices, ORs were 4.05 (3.15-5.21) with biri smoking, 2.04 (1.48-2.81) with chewing tobacco, and 1.26 (1.05-1.51) with parental history of first cousin marriage. Conclusion: In a large case-control study, we confirmed the relevance of several conventional risk factors to risk of first-onset MI in the Bangladesh population. We also identified significant associations with MI of practices distinctive to South Asian populations, including indigenous modes of tobacco consumption and parental first-cousin marriage, apparently independent of conventional risk factors. These findings should help identify opportunities for cardiovascular disease prevention in South Asia that embrace both conventional and regionally distinctive risk factors.

Evaluation of Arterial Stiffness Parameters and the Growth Differentiation Factor-15 Level in Patients with Premature Myocardial Infarction.

Myocardial infarction (MI) is increasing at a younger age. Growth differentiation factor-15 (GDF-15) has been implicated in several key mechanisms of atherogenesis. Arterial stiffness parameters, including pulse wave velocity (PWV) and the augmentation index (AIx), can indicate the presence or progression of atherosclerosis. The aim of this study is to evaluate the GDF-15 level and arterial stiffness parameters in patients with premature MI. Thirty patients aged ≤45 years (mean age: 39 ± 5 years, 23 male) who recovered from a MI and 15 age and sex-matched subjects were consecutively included. The serum GDF-15 concentration levels and arterial stiffness parameters of the patients and controls were measured. GDF-15 levels were significantly higher in patients with premature MI, while there were no significant differences in PWV and AIx between the groups. The GDF-15 level was correlated negatively with high-density lipoprotein (HDL) cholesterol and positively with uric acid levels. Both GDF-15 (p = 0.046, odds ratio: 1.092, 95% confidence interval: 1.003-1.196) and HDL cholesterol (p = 0.037, odds ratio: 0.925, 95% confidence interval: 0.859-0.995) were found as independent factors associated with premature MI. GDF-15 could be a risk factor for premature MI. Further studies are needed to elucidate the central role of GDF-15 in the pathophysiology of early atherosclerosis and MI in the young population.

Age and gender-based categorization of very premature, premature, and non-premature acute myocardial infarction: A comparison of clinical and angiographic profile and in-hospital outcomes

BackgroundIn this study, we aimed to assess and compare the distribution of demographic and clinical characteristics and composite adverse clinical outcomes after primary percutaneous coronary intervention (PCI) among “very premature”, “premature”, and “non-premature” patients with “ST-segment elevation acute coronary syndrome (STE-ACS)” presented at a tertiary care center. MethodsWe included consecutive patients diagnosed with STE-ACS undergoing primary PCI. The “very premature” was defined as ≤40 years for males and ≤ 45 years for females, “premature” as <55 years for males and < 65 years for females, and “non-premature” as ≥55 years for males and ≥ 65 years for females. Clinical characteristics, angiographic patterns, and hospital course were compared among the three groups. ResultsIn a sample of 4686 patients, 78.8%(3691) were male, and the average age was 55.6 ± 11 years. In total, 12%(561) were categorized as very premature, 38.3%(1797) as premature, and 49.7%(2328) as non-premature. The distribution of clinical characteristics in very premature, premature, and non-premature groups were as follows; hypertension in 44.6% vs. 53.5% vs. 54.9%; p < 0.001, diabetes in 30.3% vs. 36.8% vs. 35.5%; p = 0.018, smoking in 29.6% vs. 23.3% vs. 26.3%; p = 0.005, obesity in 19.4% vs. 18.4% vs. 15.3%; p = 0.008, single vessel diseases in 58.8% vs. 37.8% vs. 28.8%; p < 0.001, and composite adverse clinical outcomes in 14.1% vs. 16.7% vs. 21.8%; p < 0.001, respectively. ConclusionIn conclusion, we have a substantial burden of premature STE-ACS. Very premature STE-ACS was found to be associated with a better prognosis, but a substantial burden of composite adverse clinical outcomes was also observed.

Premature myocardial infarction: A population-based cohort study

Premature myocardial infarction: A population-based cohort study

Chromosome Y Haplogroup R Was Associated with the Risk of Premature Myocardial Infarction with ST-Elevation: Data from the CholeSTEMI Registry.

Cardiovascular disease (CVD) is the leading cause of death worldwide, with coronary artery disease (CAD) being one of its main manifestations. Both environmental and genetic factors are widely known to be related to CAD, such as smoking, diabetes mellitus, dyslipidemia, and a family history of CAD. However, there is still a lack of information about other risk factors, especially those related to genetic mutations. Sex represents a classic CAD risk factor, as men are more likely to suffer CAD, but there is lack of evidence with regard to sex-specific genetic factors. We evaluated the Y chromosome haplogroups in a cohort of young Spanish male patients who suffered from STEMI. In this cohort, haplogroup R was significantly more frequent in STEMI patients.