Association of short-term exposure to air pollution with myocardial infarction with and without obstructive coronary artery disease

2020 ◽  
pp. 204748732090464 ◽  
Author(s):  
Masanobu Ishii ◽  
Tomotsugu Seki ◽  
Koichi Kaikita ◽  
Kenji Sakamoto ◽  
Michikazu Nakai ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Acute Myocardial Infarction ◽  
Air Pollution ◽  
Coronary Artery ◽  
Coronary Arteries ◽  
Odds Ratio ◽  
Short Term ◽  
Short Term Exposure ◽  
Artery Disease

Background Air pollution including particulate matter with an aerodynamic diameter ≤2.5 µm (PM2.5) increases the risk of acute myocardial infarction. However, whether short-term exposure to PM2.5 triggers the onset of myocardial infarction with nonobstructive coronary arteries, compared with myocardial infarction with coronary artery disease, has not been elucidated. This study aimed to estimate the association between short-term exposure to PM2.5 and admission for acute myocardial infarction, myocardial infarction with coronary artery disease, and myocardial infarction with nonobstructive coronary arteries. Design This was a time-stratified case-crossover study and multicenter validation study. Methods This study used a nationwide administrative database in Japan between April 2012–March 2016. Of 137,678 acute myocardial infarction cases, 123,633 myocardial infarction with coronary artery disease and 14,045 myocardial infarction with nonobstructive coronary arteries were identified by a validated algorithm combined with International Classification of Disease (10th revision), diagnostic, and procedure codes. Air pollutants and meteorological data were obtained from the monitoring station nearest to the admitting hospital. Results In spring (March–May), the short-term increase of 10 µg/m3 in PM2.5 2 days before admission was significantly associated with admission for acute myocardial infarction, myocardial infarction with nonobstructive coronary arteries, and myocardial infarction with coronary artery disease after adjustment for meteorological variables (odds ratio 1.060, 95% confidence interval 1.038–1.082; odds ratio 1.151, 1.079–1.227; odds ratio 1.049, 1.026–1.073, respectively), while the association was not significant in other variables. These associations were also observed after adjustment for other co-pollutants. The risk for myocardial infarction with nonobstructive coronary arteries (vs myocardial infarction with coronary artery disease) was associated with an even lower concentration of PM2.5 under the current environmental standards. Conclusions This study showed the seasonal difference of acute myocardial infarction risk attributable to PM2.5 and the difference in the threshold of triggering the onset of acute myocardial infarction subtype.

scholarly journals P1443 Sex differences of coronary physiology can be justified by fractional myocardial mass

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
H Y Kim ◽  
K H Kim ◽  
J H Choi
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Acute Myocardial Infarction ◽  
Coronary Artery ◽  
Gender Difference ◽  
Coronary Arteries ◽  
Clinical Presentation ◽  
Lower Prevalence ◽  
Myocardial Mass ◽  
Artery Disease

Abstract Background Women has lower prevalence of coronary artery disease but has higher mortality from acute myocardial infarction. The gender difference in the anatomical-physiological relationship may elucidate the gender difference in the clinical presentation of coronary artery disease. Purpose We hypothesized that the gender difference in the anatomical-physiological relationship may elucidate the gender difference in the clinical presentation of coronary artery disease. Background Women has lower prevalence of coronary artery disease but has higher mortality from acute myocardial infarction. The gender difference in the anatomical-physiological relationship may elucidate the gender difference in the clinical presentation of coronary artery disease. Methods In this multicenter registry, 482 patients who underwent coronary CT angiography and fractional flow reserve (FFR) measurement were enrolled. Fractional myocardial mass (FMM, a vessel-specific amount of myocardium) and %FMM (fraction of FMM to whole myocardial mass) was measured in major coronary arteries and branches. FFR and quantitative coronary angiography (QCA) were interrogated in the subset of 772 vessels. The severity of physiological or anatomical stenosis was assessed by FFR and diameter stenosis (DS), respectively. Results In the analysis of all major epicardial arteries (N = 3,833), FMM was lower in women compared to men (p < 0.01, all), but %FMM was similar between women and men (p = NS, all). Among physiologically assessed 772 vessels, compared to men (N = 587), vessels of women (N = 185) showed smaller dimension (reference diameter (RD) = 2.90 ± 0.65 vs 3.14 ± 0.69 mm, minimal luminal diameter (MLD) = 1.30±.0.57 vs 1.40 ± 0.57 mm (p < 0.05, all), similar severity of stenosis (DS = 55% vs 55% p = NS), and higher FFR (0.81 ± 0.13 vs 0.78 ± 0.15, p < 0.001). In subgroup analysis according to the tertiary categories of DS, RD, and MLD, vessels of women showed higher FFR and lower FMM. Generalized estimating equations modeling demonstrated that gender, DS, RD, MLD, and location in left anterior descending artery were not (p = NS, all) but FMM/MLD were significant predictors for FFR ≤ 0.80 (p = 0.021). Conclusions Compared to men, coronary arteries of women are smaller and supply smaller amount of myocardium even after adjusting for vessel size, which may explain overall higher FFR value of women. This gender difference in anatomical-physiological relationship may explain the gender difference in the clinical coronary artery disease. Abstract P1443 Figure.

scholarly journals High retinoic acid receptor-related orphan receptor A gene expression in peripheral blood leukocytes may be related to acute myocardial infarction

2021 ◽  
Vol 49 (6) ◽  
pp. 030006052110196
Author(s):  
Heyu Meng ◽  
Jianjun Ruan ◽  
Xiaomin Tian ◽  
Lihong Li ◽  
Weiwei Chen ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Acute Myocardial Infarction ◽  
Coronary Artery ◽  
Peripheral Blood ◽  
Retinoic Acid Receptor ◽  
Stable Coronary Artery Disease ◽  
Orphan Receptor ◽  
Blood Leukocytes ◽  
Artery Disease

Objective This study aimed to investigate whether differential expression of the retinoic acid receptor-related orphan receptor A ( RORA) gene is related to occurrence of acute myocardial infarction (AMI). Methods This was a retrospective study. White blood cells of 93 patients with acute myocardial infarction and 74 patients with stable coronary artery disease were collected. Reverse transcription quantitative polymerase chain reaction and western blotting were used to measure RORA mRNA and protein expression, respectively. Results RORA mRNA expression levels in peripheral blood leukocytes in patients with AMI were 1.57 times higher than those in patients with stable coronary artery disease. Protein RORA levels in peripheral blood of patients with AMI were increased. Binary logistic regression analysis showed that high expression of RORA was an independent risk factor for AMI, and it increased the risk of AMI by 2.990 times. Conclusion RORA expression levels in patients with AMI is significantly higher than that in patients with stable coronary artery disease. High expression of RORA is related to AMI and it may be an independent risk factor for AMI.

Prospective Analysis after Coronary-artery Bypass Grafting: Platelet GP IIIa Polymorphism (HPA-1b /PlA2) Is a Risk Factor for Bypass Occlusion, Myocardial Infarction, and Death

2000 ◽  
Vol 83 (03) ◽  
pp. 404-407 ◽  
Author(s):  
Michael Klein ◽  
Hans Dauben ◽  
Christiane Moser ◽  
Emmeran Gams ◽  
Rüdiger Scharf ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Risk Factor ◽  
Coronary Artery ◽  
Odds Ratio ◽  
Bypass Surgery ◽  
Artery Bypass ◽  
Bypass Grafting ◽  
Hereditary Risk ◽  
Artery Disease

SummaryRecently, we have demonstrated that human platelet antigen 1b (HPA-1b or PlA2) is a hereditary risk factor for platelet thrombogenicity leading to premature myocardial infarction in preexisting coronary artery disease. However, HPA-1b does not represent a risk factor for coronary artery disease itself. The aim of our present study was to evaluate the role of HPA-1b on the outcome in patients after coronaryartery bypass surgery. We prospectively determined the HPA-1 genotype in 261 consecutive patients prior to saphenous-vein coronaryartery bypass grafting. The patients were followed for one year. Among patients with bypass occlusion, myocardial infarction, or death more than 30 days after surgery, the prevalence of HPA-1b was significantly higher than among patients without postoperative complications (60 percent, 6/10, vs. 24 percent, 58/241, p <0.05, odds ratio 4.7). Using a stepwise logistic regression analysis with the variables HPA1b, age, sex, body mass index, smoking (pack-years), hypertension, diabetes, cholesterol and triglyceride concentration, only HPA-1b had a significant association with bypass occlusion, myocardial infarction, or death after bypass surgery (p = 0.019, odds ratio 4.7). This study shows that HPA-1b is a hereditary risk factor for bypass occlusion, myocardial infarction, or death in patients after coronary-artery bypass surgery.

Abstract 13804: Clinical Profile and Outcomes of Myocardial Infarction With Non-obstructive Coronary Arteries in Older Adults

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Ara H Rostomian ◽  
Derek Q Phan ◽  
Mingsum Lee ◽  
Ray X Zadegan
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Los Angeles ◽  
Coronary Arteries ◽  
Medical Center ◽  
Invasive Coronary Angiography ◽  
Obstructive Coronary Artery Disease ◽  
Kaiser Permanente ◽  
Artery Disease

Introduction: Myocardial Infarction with non-obstructive coronary artery disease (MINOCA) is found in 5%-6% of patients with acute myocardial infarction (AMI). As such, the diagnosis and management of AMI patients with non-obstructive coronary artery disease (NOCAD) poses a challenge as compared to patients with MI with coronary artery disease (MICAD). Hypothesis: To evaluate the characteristics and outcomes of MINOCA in older patients as compared with MICAD patients, with and without revascularization. Methods: This was a retrospective observational study of patients ≥80 years old who underwent invasive coronary angiography (ICA) for AMI between 2009-2019 at Kaiser Permanente Los Angeles Medical Center. MINOCA was defied as <50% stenosis of coronary arteries on angiography with a troponin level ≥0.05 ng/ml. Patients with MINOCA vs MICAD were compared. Multivariate logistic regression was used to identify independent predictors of MINOCA and Kaplan-Meier survival analysis was used to analyze all-cause mortality between cohorts. Results: A total of 259 patients with MINOCA (mean ± SD age 83.8±2.7 years, 68% female) and 687 patients with MICAD (84.7±3.4 years, 40% female) were analyzed. Younger age (odds ratio [OR]=1.11; 95% confidence interval [CI]=1.05-1.18), female sex (OR=3.14; CI=2.20-4.48), black race (OR=2.53; CI=1.61-3.98), no history of prior stroke (OR=1.56; CI=1.06-2.33), atrial fibrillation or flutter (OR=2.04; CI:1.38-3.02), lower troponin levels (OR=1.08; CI:1.03-1.11), and lower triglyceride levels per 10 mg/dl increments (OR=1.06; CI:1.03-1.11) increased the odds of having MINCOA as compared to MICAD. At median follow-up of 2.4 years, MINOCA was associated with a lower rate of death (44.8% vs 55.2%, p<0.01) compared to un-revascularized MICAD, but no difference (31.3% vs 40.4%, p=0.68) when compared to re-vascularized MICAD. Conclusions: Patients age ≥80 years with MINOCA have fewer traditional risk factors compared to their counterparts with MICAD and fewer deaths compared to un-revascularized MICAD, but similar mortality compared to revascularized MICAD

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