Triggers Of Acute Myocardial Infarction Research Articles

Severe infections as risk factors for acute myocardial infarction: a nationwide, Danish cohort study from 1987-2018

Abstract Aims Infections have been associated with acute myocardial infarction (AMI), but differences in risk between infection types and age groups are unclear. This study aims to investigate whether infections are associated with subsequent AMI and whether the risk differs across infection sites and age groups. Methods Nationwide registers were used to include 702596 adults hospitalized between 1987-2018 with either; pneumonia (n=344319), urinary tract infection (UTI) (n=270101), soft tissue/bone infection (n=66718), central nervous system infection (CNS) (n=17025), or endocarditis (n=4433). Patients were sex- and age-matched with two unexposed controls. Outcome was first-time AMI within ten years. A time-dependent cox proportional hazards model with cut-offs at 30 and 90 days was used for calculating adjusted hazard ratios (HR). Results Pneumonia, UTI, and soft tissue/bone infection were associated with increased relative rates of AMI compared to matched, unexposed controls. Highest relative rates were found within the first 0-30 days post-exposure; Pneumonia: HR 3.39 (95% CI 3.15-3.65), UTI: HR 2.44 (95% CI 2.21-2.70), Soft tissue/bone infection: HR 1.84 (95% CI 1.45-2.33). Relative rates decreased over time but remained significantly elevated throughout the follow-up period and was increased in all age groups. No association was found for CNS infection and for endocarditis only at 31-90 days, HR 2.28 (95% CI 1.20-4.33). Conclusion Acute infections are associated with increased relative rates of AMI across different infection sites and age groups with higher relative rates found for pneumonia. This indicates that some infections may act as a trigger for AMI with a site and/or pathogen specific risk.

Emotional Stress and Physical Exertion as Triggers of Acute Myocardial Infarction

Emotional Stress and Physical Exertion as Triggers of Acute Myocardial Infarction

Risk of Acute Myocardial Infarction in Patients with Gastroenteritis: A Nationwide Case-Control Study.

Gastroenteritis promotes the development of systemic inflammation and a hypercoagulable state. There are limited data regarding the association between gastroenteritis and acute myocardial infarction (AMI). We aimed to evaluate the risk of AMI after an episode of gastroenteritis. In this nested case-control study, we selected patients who were hospitalized for AMI (N = 103,584) as a case group during 2010–2017 and performed propensity score matching (case-control ratio 1:1) to select eligible controls from insurance research data in Taiwan. We applied multivariable logistic regressions to calculate adjusted odds ratios (ORs) with 95% confidence intervals (CIs) for the risk of AMI associated with recent gastroenteritis within 14 days before AMI. We also compared the outcomes after AMI in patients with or without gastroenteritis. A total of 1381 patients (1.3%) with AMI had a prior episode of gastroenteritis compared to 829 (0.8%) among the controls. Gastroenteritis was significantly associated with a subsequent risk of AMI (adjusted OR: 1.68, 95% CI: 1.54–1.83), which was augmented in hospitalizations for gastroenteritis (adjusted OR: 2.50, 95% CI: 1.20–5.21). The outcomes after AMI were worse in patients with gastroenteritis than in those without gastroenteritis, including increased 30-day in-hospital mortality (adjusted OR: 1.28, 95% CI: 1.08–1.52), medical expenditure, and length of hospital stay. Gastroenteritis may act as a trigger for AMI and correlates with worse post-AMI outcomes. Strategies of aggressive hydration and/or increased antithrombotic therapies for this susceptible population should be further developed.

ST-elevation Myocardial Infarction Indirectly Induced by Trauma

Myocardial infarction (MI) can be provoked by various conditions including blunt chest trauma or stress. We herein report a case of traumatic pneumothorax of the right side in which ST-segment elevation MI developed later, probably due to stress after trauma. A 63-year-old man presented with chest pain after trauma. Pneumothorax of the right chest accompanied by an 8th right rib fracture was confirmed on chest computed tomography. Although electrocardiography was considered nonspecific on presentation, at 40 minutes after presentation, prominent ST-segment elevation in the precordial and lateral leads were noted. A diagnosis of anterior acute MI was made. Emergency coronary angiography, performed after the insertion of a chest tube into the right chest cavity, revealed total occlusion of the left anterior descending coronary artery. Coronary recanalization was obtained by thrombus aspiration and stent implantation. The clinical course was uneventful. The present case highlights the importance of recognizing trauma not only as a direct trigger but also as an indirect trigger of acute MI.

Analysis of Patient Perceptions of Possible Triggers of Acute Myocardial Infarction

Studies using case-crossover methodology have shown that stressors such as physical exertion, emotional stress, heavy meals, and respiratory infection can trigger acute myocardial infarction (AMI). However, patients may differ in their perception of what triggered their heart attack, which in turn influences the potential for a triggered acute risk prevention strategy. In this prospective, observational cohort study, adult patients with AMI and confirmed obstructive coronary disease underwent interviews which included an open-ended question asking what they thought may have triggered their AMI. Of 874 patients, 399 (45.7%) identified a possible trigger, while 475 (54.3%) did not identify a trigger. Possible triggers included emotional stress (24.7%), physical exertion (10.9%), non-respiratory illnesses (3%), heavy meals (2.3%), medication changes (1.5%), alcohol (1.4%), fatigue (1.4%), respiratory infection (0.8%), sexual activity (0.3%), cocaine (0.1%), and caffeine (0.1%). Smoking was identified as a possible trigger by 56 patients (6.4%). 55 patients (6.1%) identified >1 possible trigger. Prior beta blocker use was associated with a lower likelihood of identifying emotional stress as a trigger (OR 0.53, 95% CI 0.29–0.96, p=0.035). Almost half of patients (45.7%) identified a possible trigger of AMI, although 6.4% who identified smoking may have been uncertain regarding what would generally be regarded as a chronic risk factor. Emotional stress was the most frequently identified trigger (24.7%), with reduced reporting by those on prior beta blockers. Further study of triggers and their modifiers may provide insight into novel approaches to prevention.

FROM NOSE BLOCK TO HEART BLOCK: A CASE OF INFLUENZA A CAUSING COMPLETE HEART BLOCK

SESSION TITLE: Medical Student/Resident Cardiovascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Influenza is associated with cardiac complications such as myocarditis, congestive heart failure, and sudden death in hospitalized patients. It is also known to cause conduction blocks and cardiac arrest secondary to asystole and ventricular fibrillation. This is often overlooked as a cause of rhythm disorders due to the paucity of knowledge, and the rarity of the condition. CASE PRESENTATION: A 58-year-old female with a history first-degree atrioventricular block (AVB) presented with shortness of breath and cough for 3 days. On admission, she was febrile with a temperature of 100.5 degrees F and a normal chest x-ray. She tested positive for influenza A H1 N1. Her electrocardiogram (EKG) showed first-degree AVB with a PR interval of 300ms. However, on day 2, she had a syncopal episode and the telemetry strip revealed bradycardia with a 4.5-second pause. Her EKG showed a second-degree Mobitz type II that degenerated into a complete heart block. Electrophysiology was consulted, she underwent transvenous pacing. Her echocardiogram showed normal systolic function and chamber size, with no valvular abnormalities. She had an FDG positive emission tomography-cardiac sarcoidosis study which found no increased uptake to suggest an inflammatory/infiltrative process. She also had negative ischemia work up 6 months before hospitalization. The AVB was attributed to influenza after ruling out other causes. She subsequently underwent implantation of a dual-chamber his pacemaker with non-selective His bundle pacing. DISCUSSION: The pathogenesis of conduction disorders in influenza is believed to be secondary to myocarditis and inflammatory infiltrates pressing the conduction pathway with consequent necrosis in experimental models. It has also been hypothesized that inflammatory cytokines alter the electrical properties of endothelial cells which could explain why our patient had a complete heart block, without evidence of myocarditis (1). Hypoxia can cause AVB however, our patient was not hypoxic when the syncopal episode occurred. Hence, it is important to keep a close eye on patients admitted with influenza with an already compromised conduction system as there is a risk of potential worsening due to the inflammatory cytokines. Although the treatment of influenza is relatively simple, delay in initiating treatment may be fatal. Epidemiological studies have demonstrated decreased cardiovascular mortality in high-risk patients following influenza vaccination, so it is vital to educate patients about the importance of vaccination (2). CONCLUSIONS: Patients with an already compromised conduction system are at risk of worsening conduction blocks when faced with an inflammatory trigger. Most cases of conduction blocks secondary to influenza are temporary and resolve without a permanent pacemaker, however, cases with high degree block/complete heart block may warrant implantation of a permanent pacemaker. Reference #1: Warren-Gash C, Smeeth L, Hayward AC. Influenza as a trigger for acute myocardial infarction or death from cardiovascular disease: a systematic review. Lancet Infect Dis. 2009;9(10):601-10. Reference #2: Mamas MA, Fraser D, Neyses L. Cardiovascular manifestations associated with influenza virus infection. Int J Cardiol. 2008;130(3):304-9. DISCLOSURES: No relevant relationships by Ayesha Azmeen, source=Web Response No relevant relationships by Dimitrios Drekolias, source=Web Response No relevant relationships by Naga Vaishnavi Gadela, source=Web Response No relevant relationships by Jason Jacob, source=Web Response No relevant relationships by Mahati Paravathaneni, source=Web Response

Impacto del polvo sahariano en la incidencia de síndrome coronario agudo

Introduction and objectivesAsian desert dust has recently been recognized as a trigger for acute myocardial infarction. The inflow of dust from the Sahara into Spain impairs air quality due to an increase in particulate matter concentrations in the ambient air. The aim of the present study was to elucidate whether Saharan dust events are associated with the incidence of acute coronary syndrome (ACS) in patients living near North Africa, the major global dust source. MethodsWe prospectively collected data on hospitalizations due to ACS in 2416 consecutive patients from a tertiary care hospital (Canary Islands, Spain) from December 2012 to December 2017. Concentrations of particulate matter with an aerodynamic diameter 10 microns or smaller (PM10) and reactive gases were measured in the European Air Quality Network implemented in the Canary Islands. We applied the time-stratified case crossover design using conditional Poisson regression models to estimate the impact of PM10 Saharan dust events on the incidence of ACS. ResultsThe occurrence of Saharan dust events observed 0 to 5 days before the onset of ACS was not significantly associated with the incidence of ACS. Incidence rate ratios (IRR) of PM10 levels 1, 2, 3, 4 and 5 days before ACS onset (for changes in 10μg/m3) were 1.27 (95%CI, 0.87-1.85), 0.92 (95%CI, 0.84-1.01), 0.74 (95%CI, 0.45-1.22), 0.98 (95%CI, 0.87-1.11), and 0.95 (95%CI, 0.84-1.06), respectively. ConclusionsExposure to Saharan desert dust is unlikely to be associated with the incidence of ACS.

Impact of Saharan dust on the incidence of acute coronary syndrome

Introduction and objectivesAsian desert dust has recently been recognized as a trigger for acute myocardial infarction. The inflow of dust from the Sahara into Spain impairs air quality due to an increase in particulate matter concentrations in the ambient air. The aim of the present study was to elucidate whether Saharan dust events are associated with the incidence of acute coronary syndrome (ACS) in patients living near North Africa, the major global dust source. MethodsWe prospectively collected data on hospitalizations due to ACS in 2416 consecutive patients from a tertiary care hospital (Canary Islands, Spain) from December 2012 to December 2017. Concentrations of particulate matter with an aerodynamic diameter 10 microns or smaller (PM10) and reactive gases were measured in the European Air Quality Network implemented in the Canary Islands. We applied the time-stratified case crossover design using conditional Poisson regression models to estimate the impact of PM10 Saharan dust events on the incidence of ACS. ResultsThe occurrence of Saharan dust events observed 0 to 5 days before the onset of ACS was not significantly associated with the incidence of ACS. Incidence rate ratios (IRR) of PM10 levels 1, 2, 3, 4 and 5 days before ACS onset (for changes in 10μg/m3) were 1.27 (95%CI, 0.87-1.85), 0.92 (95%CI, 0.84-1.01), 0.74 (95%CI, 0.45-1.22), 0.98 (95%CI, 0.87-1.11), and 0.95 (95%CI, 0.84-1.06), respectively. ConclusionsExposure to Saharan desert dust is unlikely to be associated with the incidence of ACS.

Impact of Temperature Variation on Acute Myocardial Infarction in Karachi, Pakistan.

IntroductionEnvironmental triggers of acute myocardial infarction (AMI) have gained mounting evidence from various geographies of the world. However, due to geographic variations in seasonal temperature and other metrological parameters, it is difficult to generalize the findings in one population to another population with different climatic conditions. Therefore, the aim of this study was to assess the relationship between meteorological parameters and the number of primary percutaneous coronary intervention (PCI) procedures for AMI at a tertiary care cardiac hospital in Karachi, Pakistan.MethodsFor this cross-sectional study, data was obtained on the number of primary PCI procedures conducted at the National Institute of Cardiovascular Diseases (NICVD) Karachi, Pakistan during 1st June 2016 to 31st May 2018. Daily meteorological data of the Karachi region for the same period was obtained from the Pakistan Meteorological Department. It consists of temperature, atmospheric pressure, and relative humidity. Based on the weather conditions of Karachi, the data was divided into two seasons; summer (April to October) and winter (November to March). Multiple linear regression analysis was performed taken the number of primary PCI performed as regressand and time trend, average temperature, temperature variation, and relative humidity as regressors.ResultsA total of 115,494 hospital admissions were recorded during the study period out of which rate of primary PCI was 10.5% (12,107). A negative relationship between average temperature and number of primary PCI was observed with standardized regression coefficients of -0.13 (p < 0.001) on the overall regression model. A similar significant negative relationship of average temperature was observed on the regression model for the cold season with standardized regression coefficients of -0.17 (p < 0.001). While no such relationship was observed for the warm season.ConclusionThe average daily temperature was found to be negatively related to the number of primary PCI. Subgroup analysis revealed that the average daily temperature had a significant negative relationship with the number of primary PCI in the cold season; however, no such impact was observed in the warm season.

Emotional Triggers of Acute Myocardial Infarction

Emotional Triggers of Acute Myocardial Infarction

Christmas, national holidays, sport events, and time factors as triggers of acute myocardial infarction: SWEDEHEART observational study 1998-2013

ObjectivesTo study circadian rhythm aspects, national holidays, and major sports events as triggers of myocardial infarction.DesignRetrospective observational study using the nationwide coronary care unit registry, SWEDEHEART.SettingSweden.Participants283 014 cases of myocardial...

Alcohol binge- A striking trigger for acute myocardial infarction

Alcohol binge- A striking trigger for acute myocardial infarction

Triggering of Acute Myocardial Infarction by a Heavy Meal

Triggering of Acute Myocardial Infarction by a Heavy Meal

The Emotional, Environmental, Physical and Chemical Triggers of Acute Myocardial Infarction: An Analytical Demographic Study

Objective: Acute triggers are external stimuli that produce acute pathophysiologic changes directly leading to the onset of myocardial infarction (MI). Acute myocardial infarction (AMI) is one of the main causes of mortality. Recent studies have confirmed the impact of acute triggers on the occurrence of AMI, but have not evaluated their differences in terms of demographic characteristics. This study was conducted to investigate the impact of acute triggers on AMI in various demographic groups. Methods: This is an analytical cross-sectional study on 269 patients affected by AMI in two hospitals in 2015 and 2016 in Iran. To attain the goals of the study, acute triggers were divided into four groups of emotional, environmental, physical, and chemical. A researcher-developed questionnaire and interview were used to collect data. The risk and control periods were also evaluated for each trigger. The data were analyzed by descriptive statistics and inferential statistics such as statistical logistic regression and McNemar’s test using SPSS 21. The P-value was set at 0.05. Results: The results showed that sudden exposure to hot/cold weather in men (P=0.03, OR=3.4), underlying diseases (P=0.03, OR=1.8), heavy activities (P=0.03, OR=1.6) and consuming tea/coffee in men (P=0.01, OR=1.8) increased the chance of AMI. It was also discovered that triggers such as pulmonary infections, overeating and/or eating high-fat foods that are not dependent on demographic variables promoted the chance of AMI (P<0.05). Conclusion: All people - regardless of age, sex, and the presence/lack of underlying illness - are at risk of developing MI in the face of respiratory infections, overeating, and intake of high-fat foods. Also, sudden exposure to hot and / or cold weather, heavy activity and high consumption of coffee and/or tea, can increase the risk of MI in men.

Environmental triggers of acute myocardial infarction: results of a nationwide multiple-factorial population study.

The objective of this study was to study the independent environmental triggers of ST-elevation myocardial infarction (STEMI) in a multifactorial environmental population model. Daily counts of all STEMI patients who underwent urgent percutaneous coronary intervention over the period 2006-2009 in Belgium were associated with average daily meteorological data and influenza-like illness incidence data. The following meteorological measures were investigated: particulate matter less than 10 μM (PM10) and less than 2.5 μM (PM(2.5)), ozone, black smoke, temperature and relative humidity. During the study period a total of 15,964 STEMI patients (mean age 63, 75% male) were admitted with a daily average admission rate of 11 ± 4 patients. A multivariate Poisson regression analysis showed that only the temperature was significantly correlated with STEMI, with an 8% increase in the risk of STEMI for each 10°C decrease in temperature (adjusted incidence risk ratio (IRR) 0.92, 95% CI 0.89-0.96). The effects of temperature were consistent among several subpopulations but the strongest effect was seen in diabetic patients (IRR 0.85, 95% CI 0.78 -0.95). There was a trend for an incremental risk of STEMI for each 10 μg/m³ PM(2.5) increase and during influenza epidemics with IRR of 1.02 (95% CI 1.00-1.04) and 1.07 (95% CI 0.98-1.16), respectively. In a global environmental model, low temperature is the most important environmental trigger for STEMI, whereas air pollution and influenza epidemics only seem to have a modest effect.

Triggering of acute myocardial infarction by respiratory infection.

Respiratory infection has been associated with an increased short-term risk of myocardial infarction (MI). However, previous studies have predominantly been conducted without angiographic confirmation of MI. The possibility can therefore not be excluded that raised troponin levels or electrocardiogram abnormalities that may be seen with respiratory infections are due to non-ischaemic causes. To investigate the association between respiratory infection and angiographically confirmed MI. Interviews were conducted within 4 days of hospitalisation in 578 patients with angiographically confirmed MI, to assess for recent exposure to respiratory infection symptoms and the usual annual frequency of these symptoms. Using case-crossover methodology, exposure to respiratory infection prior to the onset of MI was compared against the usual frequency of exposure in the past year. Symptoms of respiratory infection were reported by 100 (17%) and 123 (21%) within 7 and 35 days, respectively, prior to MI. The relative risk (RR) for MI occurring within 1-7 days after respiratory infection symptoms was 17.0 (95% confidence interval (CI) 13.2-21.8), and declined with subsequent time periods. In a subgroup analysis, the RR tended to be lower in groups taking regular cardiac medications. For those who reported milder, upper respiratory tract infection symptoms, the RR for the 1-7-day time period was 13.5 (95% CI 10.2-17.7). These findings confirm that respiratory infection can trigger MI. Further study is indicated to identify treatment strategies to decrease this risk, particularly in individuals who may have increased susceptibility.

Abstract MP071: Genetic Modification of Triggers of Acute Myocardial Infarction: Results From a Case-crossover Study in Costa Rica

Background: Coffee intake and heavy physical exertion are triggers of acute myocardial infarction (AMI). It is hypothesized that their triggering effects can be modified by genetic variation. Methods: The study population consisted of incident cases (n=1354 for coffee intake, and n=1101 for heavy physical exertion) of nonfatal AMI recruited in Costa Rica between 1994 and 2004. Coffee intake and heavy physical exertion were assessed with validated questionnaires. Blood samples were collected and genotyping was conducted. We used a case-crossover design to estimate the relative risks (RRs) and 95% confidence intervals (CIs) of AMI associated with each trigger stratified by the genotypes of each SNP included. Chi-square tests of homogeneity of RR across genotypic strata were used to assess effect modification by genetic factors. We included SNPs from both candidate genes (candidate SNPs) and previous genome-wide association studies (GWAS SNPs) related to the pathophysiological pathways of the triggering effects. Specifically, the candidate SNPs were from select genes related to sympathetic nervous system, renin-angiotensin system, caffeine metabolism, and habitual coffee consumption. The GWAS SNPs were those previously found to be associated with AMI/coronary artery disease, lipid metabolism, blood pressure, heart rate, blood coagulation, matrix metalloproteinase, and adhesion molecules. A p-value of 0.05 was considered statistically significant at first. We then performed Bonferroni correction and false discovery rate (FDR) adjustment to account for multiple testing. Results: Among the SNPs associated with AMI/coronary artery disease, rs10483853 significantly modified the triggering effect of coffee, and rs10507130 was significant for heavy physical exertion. Among the SNPs associated with blood pressure, rs935334 was significant for both triggers. Among the SNPs associated with heart rate, rs9398652, rs1541010 and rs1395479 were significant for coffee intake, and rs17287293 and rs223116 were significant for heavy physical exertion. Among the SNPs associated with blood coagulation, rs4460176, rs565229, and rs12367822 were significant for coffee intake, and rs2731672, rs10489087, rs647316, rs2138852, rs1473247, rs12367822 and rs1671152 were significant for heavy physical exertion. The two SNPs associated with serum matrix metalloproteinase (rs11225434 and rs495366) both significantly modified the triggering effect of heavy physical exertion. No SNPs remained statistically significant after Bonferroni correction or FDR adjustment. Conclusions: We identified several potential genetic modifiers of the triggering effects of coffee intake and heavy physical exertion on AMI. Among them, heart rate and blood coagulation traits appeared to be more important. Replication studies in other populations will help confirm and expand our findings.

Physical Activity and Anger or Emotional Upset as Triggers of Acute Myocardial Infarction: The INTERHEART Study.

Physical exertion, anger, and emotional upset are reported to trigger acute myocardial infarction (AMI). In the INTERHEART study, we explored the triggering association of acute physical activity and anger or emotional upset with AMI to quantify the importance of these potential triggers in a large, international population. INTERHEART was a case-control study of first AMI in 52 countries. In this analysis, we included only cases of AMI and used a case-crossover approach to estimate odds ratios for AMI occurring within 1 hour of triggers. Of 12 461 cases of AMI 13.6% (n=1650) engaged in physical activity and 14.4% (n=1752) were angry or emotionally upset in the case period (1 hour before symptom onset). Physical activity in the case period was associated with increased odds of AMI (odds ratio, 2.31; 99% confidence interval [CI], 1.96-2.72) with a population-attributable risk of 7.7% (99% CI, 6.3-8.8). Anger or emotional upset in the case period was associated with an increased odds of AMI (odds ratio, 2.44; 99% CI, 2.06-2.89) with a population-attributable risk of 8.5% (99% CI, 7.0-9.6). There was no effect modification by geographical region, prior cardiovascular disease, cardiovascular risk factor burden, cardiovascular prevention medications, or time of day or day of onset of AMI. Both physical activity and anger or emotional upset in the case period were associated with a further increase in the odds of AMI (odds ratio, 3.05; 99% CI, 2.29-4.07; P for interaction <0.001). Physical exertion and anger or emotional upset are triggers associated with first AMI in all regions of the world, in men and women, and in all age groups, with no significant effect modifiers.

Triggering of Acute Myocardial Infarction by Respiratory Infection

Triggering of Acute Myocardial Infarction by Respiratory Infection

Climate and environmental triggers of acute myocardial infarction.

Over the past few decades, a growing body of epidemiological and clinical evidence has led to heightened concerns about the potential short- and long-term deleterious effects of the environment on cardiovascular health, including the risk for acute myocardial infarction (AMI). This review highlights the increased risk of AMI caused by exposure to air pollution and cold temperatures. These factors should be considered modifiable risk factors in the prevention of cardiovascular disease. The current body of knowledge about the biological mechanisms linking environmental changes to atherothrombotic events and the impact of climate change on cardiovascular health are discussed. Finally, recommendations for prevention and public policy are presented.