Cause Of Acute Myocardial Infarction Research Articles

From Atherosclerosis to Spontaneous Coronary Artery Dissection: Defining a Clinical and Genetic Risk Spectrum for Myocardial Infarction.

Spontaneous coronary artery dissection (SCAD) has been increasingly recognized as a significant cause of acute myocardial infarction (AMI) in young and middle-aged women and arises through mechanisms independent of atherosclerosis. SCAD has a multifactorial etiology that includes environmental, individual, and genetic factors distinct from those typically associated with coronary artery disease. Here, we summarize the current understanding of the genetic factors contributing to the development of SCAD and highlight those factors which differentiate SCAD from atherosclerotic coronary artery disease. Recent studies have revealed several associated variants with varying effect sizes for SCAD, giving rise to a complex genetic architecture. Associated genes highlight an important role for arterial cells and their extracellular matrix in the pathogenesis of SCAD, as well as notable genetic overlap between SCAD and other systemic arteriopathies such as fibromuscular dysplasia and vascular connective tissue diseases. Further investigation of individual variants (including in the associated gene PHACTR1) along with polygenic score analysis have demonstrated an inverse genetic relationship between SCAD and atherosclerosis as distinct causes of AMI. SCAD represents an increasingly recognized cause of AMI with opposing clinical and genetic risk factors from that of AMI due to atherosclerosis, and it is often associated with complex underlying genetic conditions. Genetic study of SCAD on a larger scale and with more diverse cohorts will not only further our evolving understanding of a newly defined genetic spectrum for AMI, but it will also inform the clinical utility of integrating genetic testing in AMI prevention and management moving forward.

SPONTANEOUS CORONARY ARTERY DISSECTION (SCAD) WITH CARDIAC ARREST AT PRESENTATION: A SUBANALYSIS FROM THE DISCO REGISTRY

Abstract Introduction Spontaneous coronary artery dissection (SCAD) is a rare cause of acute myocardial infarction (AMI), which primarily affects young women without traditional cardiovascular risk factors, often presenting as sudden cardiac death. This study aims to investigate the prevalence, characteristics, predictors, and outcomes of cardiac arrest in SCAD patients. Methods The DISCO IT/SPA registry, an international retrospective multicenter study, enrolled 375 SCAD patients from 26 centers in Italy and Spain. Patients were categorized based on the presence or absence of cardiac arrest at admission. Data on demographics, clinical presentation, treatment, angiographic findings, and outcomes were collected. Angiograms were independently reviewed, and outcomes included major adverse cardiovascular events (MACE) and in–hospital bleeding. Results Among 375 SCAD patients, 20 (5.3%) presented with cardiac arrest. Both groups were similar in age, gender distribution, and conventional risk factors, except for a lower prevalence of dyslipidemia in the cardiac arrest group. ST–segment elevation myocardial infarction (STEMI) presentation and angiographic type 2b were independent predictors of cardiac arrest. Revascularization was more frequent in the cardiac arrest group. In–hospital outcomes, except for longer hospitalization, did not differ. On follow–up (average 21 months), MACE rates were similar between groups. Conclusions Cardiac arrest is a notable complication in SCAD, mostly presenting with ventricular fibrillation. The prognosis of SCAD patients presenting with cardiac arrest did not differ from those without, reporting a similar rate of events both in–hospital and during long–term follow–up. STEMI presentation and angiographic type 2b were identified as independent predictors of cardiac arrest in SCAD.

Abstract 1102: Post Gwas Functional Genomics Analysis To Identify Non-coding Single Nucleotide Polymorphisms Controlling The Risk Of Spontaneous Coronary Artery Dissection

Background: Spontaneous Coronary Artery Dissection (SCAD) is a non-atherosclerotic coronary artery disease and the leading cause of acute myocardial infarction in young females. SCAD results from the combination of genetic susceptibility and acquired triggering factors including inflammation and sex hormones. Three loci have been revealed by two large-scale genome-wide association studies (GWAS) in SCAD. However, GWAS only reveals the statistical associations between the genetic loci and diseases, and the biological mechanisms remain unknown. Methods: GWAS-reported tag single nucleotide polymorphisms (SNPs) and the linked haplotype SNPs were collected. Synthesized oligonucleotides representing the SNP alleles were subjected to electrophoretic mobility shift assays (EMSA) with nuclear proteins extracted from vascular endothelial cells (ECs), smooth muscle cells (SMCs) and fibroblasts. Hi-C analysis was performed to predict the potential target gene(s) based on chromatin interactions. The functionality of the SNP-associated target genes was examined in cultured vascular cells by RNA silencing. Results: The risk allele of tag SNPs in three genetic loci (chr1q21.2, 6p24.11 and 12q13.1) were associated with 1.5 to 1.8-fold higher risk of SCAD. Intronic, non-tag SNP rs7549396 (G/A) in chr1q21.2 locus was identified as the functional SNP in EMSA, given its consistent allele-imbalanced gel shifting pattern in ECs, SMCs and fibroblasts. Hi-C analysis in human aortic tissue identified a 490kb long-range chromatin interaction between SNP rs7549396 and the promoter of Annexin A9 (ANXA9), an extracellular matrix (ECM) and an inflammation-related protein potentially associated with the pathogenesis of SCAD. The knockdown of ANXA9 in vascular cells showed significant changes in inflammatory makers (IL-1β, vCAM-1 and CCL-2) and ECM degradation enzyme (MMP-1). Conclusions: Leveraging our post-GWAS functional genomics approach, we identified functional non-coding SNPs in disease-associated genetic locus and predicted a novel potential pathogenic gene ANXA9 for SCAD. Further studies on the functions of this SNP and its associated target gene ANXA9 will provide genetics and mechanistic explanation for this mysterious disease.

CircDiaph3 aggravates H/R-induced cardiomyocyte apoptosis and inflammation through miR-338-3p/SRSF1 axis

Acute myocardial infarction (AMI) is one of the most prevalent cardiovascular diseases, accounting for a high incidence rate and high mortality worldwide. Hypoxia/reoxygenation (H/R)-induced myocardial cell injury is the main cause of AMI. Several studies have shown that circular RNA contributes significantly to the pathogenesis of AMI. Here, we established an AMI mouse model to investigate the effect of circDiaph3 in cardiac function and explore the functional role of circDiaph3 in H/R-induced cardiomyocyte injury and its molecular mechanism. Bioinformatics tool and RT-qPCR techniques were applied to detect circDiaph3 expression in human patient samples, heart tissues of AMI mice, and H/R-induced H9C2 cells. CCK-8 was used to examine cell viability, while annexin-V/PI staining was used to assess cell apoptosis. Myocardial reactive oxygen species (ROS) levels were detected by immunofluorescence. Western blot was used to detect the protein expression of anti-apoptotic Bcl-2 while pro-apoptotic Bax and cleaved-Caspase-3. Furthermore, ELISA was used to detect inflammatory cytokines production. While bioinformatics tool and RNA pull-down assay were used to verify the interaction between circDiaph3 and miR-338-3p. We found that circDiaph3 expression was high in AMI patients and mice, as well as in H/R-treated H9C2 cells. CircDiaph3 silencing ameliorated apoptosis and inflammatory response of cardiomyocytes in vivo. Moreover, the knockdown of cirDiaph3 mitigated H/R-induced apoptosis and the release of inflammatory mediators like IL-1β, IL-6, and TNF-α in H9C2 cells. Mechanistically, circDiaph3 induced cell apoptosis and inflammatory responses in H/R-treated H9C2 cells by sponging miR-338-3p. Overexpressing miR-338-3p in H/R-treated cells prominently reversed circDiaph3-induced effects. Notably, miR-338-3p inhibited SRSF1 expression in H/R-treated H9C2 cells. While overexpressing SRSF1 abrogated miR-338-3p-mediated alleviation of apoptosis and inflammation after H/R treatment. To summarize, circDiaph3 aggravates H/R-induced cardiomyocyte apoptosis and inflammation through the miR-338-3p/SRSF1 axis. These findings suggest that the circDiaph3/miR-338-3pp/SRSF1 axis could be a potential therapeutic target for treating H/R-induced myocardial injury.

Advances in the Clinical Management of Acute Myocardial Infarction

Acute myocardial infarction is a kind of cardiovascular disease mainly caused by coronary artery stenosis, atherosclerosis or blockage of myocardial cell hypoxia and ischemic necrosis, and it is one of the most hazardous cardiovascular diseases around the world. In recent years, the incidence of acute myocardial infarction has been increasing year by year in our country as well as the trend of rejuvenation, which has aroused the great importance of various medical experts. This has also caused various medical experts to pay great attention to the treatment of acute myocardial infarction in the clinic through the treatment of acute myocardial infarction to carry out continuous in-depth exploration, summarized some of the treatment of acute myocardial infarction effective methods. In this paper, the causes of acute myocardial infarction are elaborated, and the treatment plan of acute myocardial infarction is summarized, hoping to provide certain reference for clinical research.

Spontaneous Coronary Artery Dissection and COVID-19: A Review of the Literature.

SARS-CoV-2 is responsible for the global coronavirus disease 2019 (COVID-19) pandemic. While the cardiovascular effects of COVID-19 have been thoroughly described, there are limited published studies in the literature establishing a connection between spontaneous coronary artery dissection (SCAD) and COVID-19. Cardiovascular manifestations include, among others, myocarditis, acute myocardial infraction, and thrombosis. In general, SCAD is an uncommon and underdiagnosed cause of acute myocardial infarction (AMI), particularly in younger women and in patients with underlying fibromuscular dysplasia (FMD). Many patients with SCAD often report significant emotional stress, especially in relation with job loss, during the week preceding their cardiac event. Moreover, the COVID-19 pandemic has led to societal stress and increased unemployment, factors that have been associated with cardiovascular morbidity. SCAD emerges as a rare manifestation of coronary artery disease, which a few recent case reports link to COVID-19. The aim of this article is to summarize the relevant data on the pathophysiology of COVID-19 and SCAD along with a review of the reported cases on acute coronary syndrome (ACS) following SARS-CoV2 infection and, thus, to provide insights about the relationship between COVID-19 and SCAD.

Thrombus architecture is influenced by the antiplatelet loading treatment in patients with acute myocardial infarction

BackgroundIntracoronary thrombus formation is a main cause of acute myocardial infarction triggered by platelet activation. However, there are no data on the impact of different treatment strategies with antiplatelet agents before percutaneous coronary intervention (PCI) on histological characteristics of thrombus formation. ObjectiveIn this study, we investigate the impact of preinterventional administration of the P2Y12-inhibitors clopidogrel and prasugrel on thrombus composition, highlighting significant changes associated with the antiplatelet pre-treatment. MethodsWe prospectively enrolled 104 consecutive patients with ST-segment elevation myocardial infarction (STEMI) undergoing immediate PCI and thrombus aspiration by immunohistochemical staining along with RNA-sequencing employing Nanostring analysis. Fifty-two patients were treated with either prasugrel loading (60 mg) or clopidogrel loading (600 mg) prior to PCI, respectively. ResultsIn Patients with STEMI, intracoronary thrombus architecture was significantly altered between patients pre-treated with prasugrel when compared to clopidogrel. Fibrin content of thrombi was significantly decreased (41.8 % versus 66.7 %, p = 0.009) after pre-treatment with prasugrel compared to clopidogrel. Furthermore, levels of MPO positive cells in intracoronary thrombi were significantly decreased in patients with prasugrel pre-treatment (90.5 versus 201.1, p = 0.014) indicating an association of antiplatelet pre-treatment and the inflammatory responses during thrombus formation. Most strikingly, we observed significant differences among both pre-treatment groups regarding altered RNA expression and signaling pathways of thrombo-inflammatory processes within the thrombotic material, which were independently associated with antiplatelet strategies. ConclusionsOur study elucidates the impact of antiplatelet pre-treatment on thrombus remodeling and architecture, thereby lowering the risk of recurrent adverse cardiovascular events in prasugrel-treated patients.

Primary Percutaneous Coronary Intervention in Patients With Spontaneous Coronary Artery Dissection vs Coronary Artery Disease

BackgroundSpontaneous coronary artery dissection (SCAD) is a rare cause of acute myocardial infarction. Revascularization in SCAD remains very challenging and therefore is not recommended as the initial management strategy in stable SCAD without high-risk features. ObjectivesThe aim of this study was to compare in-hospital mortality and 30-day readmission rates between patients with SCAD with ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PPCI) and patients with STEMI without SCAD undergoing PPCI. MethodsThis study was conducted using the administrative minimum dataset of the Spanish National Health System (2016-2020). Risk-standardized in-hospital mortality ratios and readmission ratios were calculated, and results were adjusted using propensity score (PS) analyses. ResultsA total of 65,957 episodes of PPCI were identified after exclusions. The crude in-hospital mortality rate was 4.8%. Of these, 315 (0.5%) were SCAD PPCI and 65,642 were non-SCAD PPCI. SCAD PPCI patients were younger and more frequently women than non-SCAD PPCI patients. Crude mortality (5.7% vs 4.8%), risk-standardized in-hospital mortality ratio (5.3% vs 5.3%), and PS-adjusted (315 pairs) mortality (5.7% vs 5.7%) were similar in SCAD PPCI and non-SCAD PPCI patients. In addition, crude (3% vs 3.3%) and PS-adjusted (297 pairs) 30-day readmission rates (3% vs 4%) were also similar in both groups. ConclusionsPPCI, when indicated in patients with STEMI and SCAD, has similar in-hospital mortality and 30-day readmission rates compared with PPCI for atherothrombotic STEMI. These findings support the value of PPCI in selected patients with SCAD.

Spontaneous coronary artery dissection in women with acute myocardial infarction: is there a new role for autoimmunity?

Spontaneous coronary artery dissection (SCAD) is an uncommon cause of acute myocardial infarction in women and has an unclear pathophysiology. Autoantibodies (AAs) targeting angiotensin-II receptor type 1 (AT1R) and endothelin-1 receptor type A (ETAR) have known detrimental effects on endothelial function. We investigated the prevalence of these AAs in SCAD-affected female patients. Female patients diagnosed at coronary angiography with myocardial infarction and SCAD were consecutively enrolled. Autoantibodies targeting angiotensin-II receptor type 1 and ETAR-AA titres and seropositivity prevalence were compared between SCAD patients, ST-elevation myocardial infarction (STEMI) patients, and healthy women. Ten women with SCAD and 20 age-matched controls (10 women with STEMI and 10 healthy women) were included. Six out of 10 (60%) women with myocardial infarction and SCAD were seropositive for AT1R-AAs and ETAR-AAs. In contrast, only one (10%) healthy woman and one (10%) STEMI patient were seropositive for AT1R-AAs (P = 0.03 and P = 0.03, respectively). One STEMI patient was seropositive for ETAR-AAs, while none of the healthy women was found to be seropositive (P = 0.03 and P = 0.01, respectively). The median AA titre was significantly higher in SCAD patients than in healthy women (P = 0.01 for AT1R-AAs; P = 0.02 for ETAR-AAs) and STEMI patients (P < 0.001 for AT1R-AAs; P = 0.002 for ETAR-AAs). Autoantibodies targeting angiotensin-II receptor type 1 and ETAR-AA seropositivity is significantly higher in SCAD women with myocardial infarction than in healthy women or female patients with STEMI. Our findings, corroborated by previous data in the literature and biological plausibility, suggest a possible role for AT1R-AAs and ETAR-AAs in the pathophysiology of SCAD in women with acute myocardial infarction and should warrant further studies with larger sample sizes.

Derivation and Validation of Spontaneous Coronary Artery Dissection Prediction Score in Patients With Myocardial Infarction

Spontaneous coronary artery dissection (SCAD) is an important cause of acute myocardial infarction (AMI); however, the prevalence of SCAD and its predictors in AMI are unknown. We sought to derive and validate a simple score that can help predict SCAD in patients with AMI. We analyzed the Nationwide Readmissions Database and created a risk score for SCAD in patients with an index hospitalization for AMI. We used a multivariate logistic regression analysis to determine the independent predictors of SCAD, and each was assigned points proportional to its regression coefficient. Among 1,155,164 patients with AMI, 8,630 (0.75%) had SCAD. Based on the derivation cohort, the independent predictors of SCAD were fibromuscular dysplasia (odds ratio [OR] 67.0, 95% confidence interval [CI] 42.0 to 107.9, p <0.01), Marfan or Ehlers-Danlos syndrome (OR 4.7, 95% CI 1.7 to 12.5, p <0.01), polycystic ovarian syndrome (OR 5.4, 95% CI 3.0 to 9.8, p <0.01), female gender (OR 1.99, 95% CI 1.9 to 2.1, p <0.01), and aortic aneurysm (OR 1.41, 95% CI 1.1 to 1.7, p <0.01). The SCAD risk score included fibromuscular dysplasia (5 points), Marfan or Ehlers-Danlos syndrome (2 points), polycystic ovarian syndrome (2 points), female gender (1 point), and aortic aneurysm (1 point). The C-statistics of the score were 0.58 (derivation cohort) and 0.61 (validation cohort). In conclusion, the SCAD score is an easy bedside clinical tool that can help clinicians identify patients with AMI who are at risk for SCAD.

St-elevation myocardial infarction in a healthy 16-year-old adolescent: a clinical case

Background. Diagnosis of acute myocardial infarction (AMI) in pubertal patients is a diagnostic challenge, as individuals of such a young age usually do not have traditional risk factors for coronary heart disease (CHD) and, as a result, are at increased risk of misdiagnosis.Objective. To describe a clinical case of AMI in a 16-yearold patient against the background of complete well-being.Design and methods. A 16-year-old patient, against the background of complete well-being, developed pressing pains in the chest, which stopped on their own after a few hours. During hospitalization, in addition to an increase in the level of troponin, the results of other laboratory and instrumental studies did not confirm the version of AMI, as a result of which other cardiac and non-cardiac causes of the development of chest pain formed the basis of the diagnostic search. This was the reason for the delayed diagnosis and endovascular treatment of thrombotic occlusion of the right coronary artery, and, as a result, the formation of an area of persistent hypokinesia of the lower parts of the left ventricle. Further search for possible causes of AMI, including the analysis of genetically associated conditions, did not yield results.Results. This publication describes a case of acute inferior myocardial infarction with ST segment elevation and thrombotic occlusion of the right coronary artery in a 16-year-old adolescent and the impact of an irrational diagnostic process on long-term prognosis.Conclusion. The presented clinical case demonstrates the importance of including the diagnosis of AMI in the process of differential diagnosis of acute chest pain, even in adolescent patients.

Chronic or Changeable Infarct Size after Spontaneous Coronary Artery Dissection.

Spontaneous coronary artery dissection (SCAD) could be the cause of acute myocardial infarction (AMI) and sudden cardiac death. Clinical presentations can vary considerably, but the most common is the elevation of cardiac biomarkers associated with chest discomfort. Different pathological etiology in comparison with Type 1 AMI is the underlying infarct size in this population. A 42-year-old previously healthy woman presented with SCAD. Detailed diagnostical processing and treatment which were performed could not prevent myocardial injury. The catheterization laboratory was the initial place for the establishment of a diagnosis and proper management. The management process can be very fast and sometimes additional imaging methods are necessary. Finding predictors of SCAD recurrence is challenging, as well as predictors of the resulting infarct scar size. Patients with recurrent clinical symptoms of chest pain, ST elevation, and complication represent a special group of interest. Therapeutic approaches for SCAD range from the "watch and wait" method to complete revascularization with the implantation of one or more stents or aortocoronary bypass grafting. The infarct size could be balanced through the correct therapeutical approach, and, proper multimodality imaging would be helpful in the assessment of infarct size.

Spontaneous coronary artery dissection: an unpredictable event.

Spontaneous coronary artery dissection (SCAD) is an under-recognized cause of acute coronary syndrome that predominantly affects women in adulthood and is the leading cause of acute myocardial infarction in pregnancy. The most common clinical presentation is ST-segment elevation myocardial infarction (STEMI) or non-STEMI, followed by cardiogenic shock (∼2%), sudden cardiac death (0.8% in autopsy series), cardiac arrest, ventricular arrhythmias (∼5%), and Takotsubo syndrome. The prevalence of SCAD in the general population is largely uncertain due to underdiagnosis. Oral contraceptives, post-menopausal therapy, and infertility treatments are recognized associated factors. The pathological substrates (fibromuscular dysplasia) and triggers (especially emotional stress) are commonly present in affected women. The few cases with a precise genetic aetiology occur in the context of syndromic and non-syndromic connective tissue diseases. The only true certainty in SCAD is the overwhelming prevalence in women. The first event as well as the recurrence (up to 30%, which varies depending on the definition) is largely unpredictable. The treatment strategy is highly individualized and requires extensive additional study in order to optimize outcomes and prevent major adverse cardiovascular events in affected individuals. We have known about SCAD for nearly a century, but we still do not know how best to prevent, diagnose, and treat it, making SCAD a highly important and unmet clinical need.

Prevalence of Anxiety, Depression, and Distress in SCAD and Non-SCAD AMI Patients: A Comparative Study.

Spontaneous coronary artery dissection (SCAD) is an increasingly recognized cause of acute myocardial infarction (AMI), particularly in younger women without classic cardiac risk factors. Spontaneous coronary artery dissection is considered to be particularly stressful; however, few studies have quantified SCAD survivor stress levels. This study compared anxiety, depression, and distress levels in SCAD and non-SCAD AMI patients. A sample of 162 AMI (35 [22%] SCAD) patients was recruited from hospitals and via social media, in Australia and the United States. All had had their AMI in the past 6 mo. Participants completed an online questionnaire comprising the Generalized Anxiety Disorder-2 (GAD2), Patient Health Questionnaire-2 (PHQ2), Kessler-6 (K6), and Cardiac Distress Inventory (CDI). T-tests, χ 2 tests, Mann-Whitney tests, and analysis of covariance were used to compare SCAD and non-SCAD samples. Logistic regression was used to identify the unique predictors of anxiety, depression, and distress, controlling for relevant confounders. Patients with SCAD were more commonly female and significantly younger than non-SCAD patients. Patients with SCAD scored significantly higher on the GAD2, PHQ2, K6, and CDI and a significantly larger proportion was classified as anxious, depressed, or distressed using these instruments. In logistic regression, together with mental health history, having had a SCAD-AMI predicted anxiety, depression, and distress, after controlling for female sex, younger age, and other confounding variables. This study supports the view that anxiety, depression, and distress are more common after SCAD-AMI than after traditional AMI. These findings highlight the psychosocial impacts of SCAD and suggest that psychological support should be an important component of cardiac rehabilitation for these patients.

Embolic myocardial infarction associated with patent foramen ovale: a case series

A patent foramen ovale (PFO) is a fairly common mild cardiac defect that causes a shunting across the atrial septum. PFO is also a known risk factor for cryptogenic stroke. Much less frequently, PFO is associated with non-cerebral systemic embolic events. The article describes a case series of paradoxical embolism of the coronary arteries (CA), which caused myocardial infarction (MI). The presence of PFO was confirmed by imaging techniques. Subsequently, the patients underwent successful endovascular closure of the PFO. Thus, paradoxical CA embolism is a rare and underdiagnosed cause of acute MI. It should be considered in patients with MI and a low risk of atherosclerotic coronary artery disease. However, in most cases, it is not possible to verify the source of the embolism. The significance of occluder implantation as one of the treatment tactics requires further clarification.

Acute Myocardial Infarction of the Left Main Coronary Artery Secondary to Embolism

There are few reported cases of left main artery embolism and is usually fatal, the importance of atrial fibrillation as a cause of acute myocardial infarction and the treatment these patients should be offered, this case highlights the challenges faced during the management of this rare condition due to lack of clear-cut guidelines describing an evidence-based approach [1]. We describe the case of of LMCA thrombus that presented as ST-elevation myocardial infarction (STEMI) in a patient with paroxysmal atrial fibrillation who was successfully treated with thrombus aspiration is presented. We highlight the importance of intravascular imaging to determine the underlying putative mechanism.

Treatment Approach of Acute Coronary Thrombosis without Dissection in a Bleeding Patient with Multiple Trauma.

Trauma is one of the causes of acute myocardial infarction (AMI). In the literature, coronary dissection or vasospasm is thought to play a role in the aetiology of AMI, but the presence of coronary thrombosis without coronary dissection is uncommon. If bleeding pathologies occur in addition to traumatic coronary thrombosis, this may make the situation more complicated. A 32-year male patient was brought to a tertiary emergency service due to a car accident. We detected femoral shaft fracture, hemothorax, subdural haemorrhage, and coronary thrombosis without dissection in the patient. A chest tube was inserted and emergency coronary angiography was performed. Total occlusion of the left anterior descending artery (LAD) was detected. Balloon angioplasty was done and a stent was applied to the LAD. Acetyl salicylic acid and clopidogrel were started despite his bleeding pathologies. In trauma patients, coronary thrombosis without coronary dissection may occur with bleeding pathologies. Electrocardiography should be performed in patients with chest trauma. Thrombosis-bleeding balance should be carefully evaluated during treatment and treatment should be determined by taking this situation into consideration. Key Words: Coronary thrombosis, Multiple trauma, Bleeding, Angioplasty, Antiplatelet therapy.

Abstract 12162: Acute Myocardial Infarction Caused by Spontaneous Coronary Artery Dissection of the First Septal Perforator

A 68 year old female with hyperlipidemia and tobacco use presented with acute, substernal, chest pressure that occurred during yard work. She had no prior history of coronary artery disease or stable angina. Electrocardiograms (ECG) did not have ischemic changes but high sensitivity troponin was elevated at 285 ng/L and peaked at 1308 ng/L. Therapy was started for acute coronary syndrome and nitroglycerin drip for continued discomfort. Echocardiogram showed ejection fraction of 61% and akinesis of the infero-septum at the mid-ventricle. Coronary angiogram showed diffuse narrowing of the large first septal branch artery (S1) concerning for coronary intramural hematoma. No other significant coronary artery disease was present. Cardiac magnetic resonance (CMR) confirmed hypokinesis of the septum and subendocardial delayed enhancement in the interventricular septum at the mid ventricle suggestive of an isolated septal perforator infarct. She was conservatively managed and discharged 48 hours later. Four days later she had recurrent chest pressure and was re-admitted. Her ECG showed J-point elevation in the anteroseptal leads. Repeat coronary angiogram showed unchanged type 2 spontaneous coronary artery dissection of S1 and a small coronary cameral fistula between the distal septal branch and the right ventricle. The diagnosis of spontaneous coronary artery dissection of the first septal branch is rare and may be missed on angiogram. CMR in addition to invasive coronary angiography aides in the evaluation of this rare cause of acute myocardial infarction and changes clinical management decisions including observation time and evaluation for fibromuscular dysplasia.

Abstract 12681: GWAS Meta-Analysis in SCAD, a Women Predominant Ischemic Heart Disease, Reveals Common Variants and Genes Related to Artery Integrity and Tissue-Mediated Coagulation

Introduction: Spontaneous coronary artery dissection (SCAD) is an understudied cause of acute myocardial infarction due to hematoma formation in coronary arteries primarily affecting women. It is not known to what extent SCAD is genetically distinct from other cardiovascular diseases, including atherosclerotic coronary artery disease (CAD). Methods and Results: Through a meta-analysis of 8 GWAS (1917 cases, 9292 controls of European ancestry), we identified 17 risk loci, including 12 new. Functional annotations pointed at enrichment in enhancer marks of arteries, specifically smooth muscle cells, and strong candidate genes, such as tissue factor gene ( F3 ) on Chr1 near rs1146473 (OR=1.32, P=5.8 х10 -9 ). F3 is novel for SCAD or any cardiovascular disease. The risk allele correlated with F3 lower expression in arteries, supporting a mechanism consistent with hematoma formation. Bayesian gene regulatory networks constructed from expression and genetics data indicated the extracellular matrix organization in arteries as the biological function where most prioritized genes clustered (e.g. COL4A1/A2, HTRA1, and TIMP3 ). Overall, we report substantial polygenicity for SCAD (LDSC: h 2 SNP = 0.71 ± 0.11) and shared genetics with several neurovascular diseases (e.g intracranial aneurysm). Intriguingly, for 6 loci, colocalization analyses showed that SCAD and CAD are likely to share the same causal variants but involve opposite risk alleles (e.g COL4A1/A2 ). In addition, a negative genetic correlation was found between SCAD and CAD (rg=-0.12; P=3.7х10 -3 ), including after conditioning on BP (mt-COJO: rg CAD/SBP =-0.19, P=4.6х10 -6 ). Mendelian randomization analyses indicated higher BP to associate with increased risk for SCAD (beta IVW-SBP =0.05, P=7.6х10 -6 , beta IVW-DBP =0.10, P=1.9х10 -6 ) and CAD (beta IVW-SBP =0.04, P=8.6х10 -49 ; DBP: beta IVW-DBP =0.06, P=1.6х10 -44 ) but not BMI, lipids, or type 2 diabetes, which we confirmed as genetic risk factors for CAD Conclusions: Our results set the stage for future investigation of novel biological pathways relevant to both SCAD and CAD and potential therapeutic and preventive strategies specifically targeting this ischemic disease predominantly affecting women.

Abstract 15587: Combined Spontaneous Coronary Artery Dissection and Takotsubo Cardiomyopathy in a Patient With Chest Pain

Introduction: Spontaneous coronary artery dissection (SCAD) and Takotsubo cardiomyopathy (TCM) are uncommon non-atherosclerotic causes of acute myocardial infarction (MI). These patients have fewer cardiovascular risk factors than those who have atherosclerotic MI. Clinical presentation in both subsets of MI is identical due to which diagnosis requires echocardiography and coronary angiography. The incidence of TCM and SCAD in the same patient is scarce and only documented in a few case reports and a case series. Case presentation: We present the case of a 50-year-old female with a past medical history of hypertension, hypothyroidism, and median arcuate ligament syndrome. She presented to the emergency department with intermittent chest pain radiating to her upper back, both arms, and her left jaw and it was associated with nausea. On examination, she was tachycardic, tachypneic, and anxious. She had normal heart sounds with no chest tenderness. Her EKG demonstrated ST-elevations in leads II, III, aVF, V4, V5, and V6. Laboratory results showed elevated high sensitivity troponin of 11,949 (pg/ml) and 30,256 (pg/ml) four hours later. The patient underwent emergent coronary angiography, which revealed diffuse tubular stenosis suggestive of type 2 SCAD in the second obtuse marginal artery but otherwise normal coronary anatomy with minimal stenosis. Left ventriculogram showed antero-apical, apical, and infero-apical hypokinesis and basal hyperkinesis, suggestive of Takotsubo cardiomyopathy. Transthoracic echocardiogram (TTE) completed 48 hours later demonstrated improved contractility with lateral wall hypokinesis. The patient was managed conservatively with medical management, and she was discharged on aspirin, plavix, carvedilol, isosorbide mononitrate, and losartan. Conclusions: SCAD and TCM are uncommon diagnoses that can rarely co-exist. TTE can help diagnose TCM in patients with chest pain and elevated cardiac biomarkers. Non-occlusive coronary vasculature is a diagnostic criterion per the proposed Mayo Clinic criteria. This case highlights the importance of coronary angiography in patients with TCM for assessment of potential co-existent coronary vascular pathology; SCAD in our case.