Cause Of Myocardial Infarction Research Articles

NON ATHEROSCLEROTIC SPONTANEOUS CORONARY ARTERY DISSECTION OF THE RIGHT CORONARY ARTERY IN EVOLUTION - WAS NORETHINDRONE THE CULPRIT

Non-Atherosclerotic Spontaneous Coronary Artery Dissection (NASCAD), a non-traumatic, non-iatrogenic separation of the coronary wall is a rare cause of myocardial infarction. Often seen in pregnancy, less than 10 cases have been reported with combined oral contraceptive (OCP) use and none with the

Comparative Study between Diabetic and non- Diabetic Patients Regarding Prevalence of Coronary Artery Disease and Plaque Composition by Multi-detector CT Coronary Angiography

Abstract Diabetes is known to be a major cardiovascular risk factor associated with significantly increased morbidity and mortality and particularly increased risk of major cardiac events especially myocardial infarction as a manifestation of highly incident coronary artery disease (CAD).This can lead to decreased life expectation and life quality. Major cause for myocardial infarction is plaque rupture. Prevalence of obstructive and non-obstructive plaques is increased in diabetic patients. Background and Objectives The prevalence of coronary heart disease in diabetic patients compared to non- diabetics and evaluating the composition of the plaque in diseased individuals in both groups by usage of multislice computed tomography (MSCT) angiography . Subjects and Methods A total of 80 consecutive MSCT angiography examinations were performed between August 2017 and June 2018. Of these, the patients were evaluated for the presence and type of atherosclerotic plaque and severity of luminal narrowing. Results Eighty (40 in the diabetic group and 40 in the non-diabetic group) patients underwent MSCT angiography with DM prevalence of 0.212 (95% Cl for AOR 0.056 -1.896). Among them, 20 patients (50 %) in the diabetic group and 14 patients (35 %) in the non-diabetic group had +ve coronary heart disease, 33.3 % had significant and moderately significant coronary narrowing on diabetic group and 31.3 % in non-diabetic group on MSCT angiography. Diabetic patients had more soft plaque compared with non-diabetic patients. Conclusion DM is not an independent factor for the disease occurrence in coronary artery disease but is a dependent factor in the association of other risk factors such as smoking ,hypertension and dyslipidemia.

Application of an OCT-based 3D reconstruction framework to the hemodynamic assessment of an ulcerated coronary artery plaque

The rupture of a vulnerable plaque, known as ulceration, is the most common cause of myocardial infarction. It can be recognized by angiographic features, such as prolonged intraluminal filling and delayed clearance of the contrast liquid. The diagnosis of such an event is an open challenge due to the limited angiographic resolution and acquisition frequency. The treatment of ulcerated plaques is an open discussion, due to the high heterogeneity and the lack of evidences that support particular strategies. Therefore, the therapeutic decision should follow a detailed investigation with angiography and intravascular imaging, such as optical coherence tomography (OCT), to locate the lesion, besides its geometric features and the lumen occlusion severity.The aim of this study is the application of a framework for the in-silico analysis of the disrupted hemodynamics due to an ulcerated lesion. The study employed a validated OCT-based reconstruction methodology and computational fluid dynamics (CFD) simulations for the computation of local hemodynamic quantities, such as wall shear stress.The reported findings, such as disrupted pre-operative flow conditions, proved the applicability of the developed framework for CFD analyses on complicated patient-specific anatomies that feature ulcerated plaques. The prediction of lesion expansion and the clinical decision making can benefit from a reliable computation of wall shear stress distributions that result from the peculiar anatomy of the lesion. The application of intravascular OCT imaging, high fidelity 3D reconstructions and CFD simulations might guide the treatment of such pathology.

671 Myocardial Infarction Due to Left Main Coronary Artery Compression in Eisenmenger’s Syndrome

Compression of the left main coronary artery (LMCA) is increasingly recognised as a cause of angina, myocardial infarction and sudden death in patients with pulmonary hypertension [[1]Gailé N. Saia F. Pallazini M. et al.Left Main Coronary Artery Compression in Patients With Pulmonary Arterial Hypertension and Angina.JACC. 2017; 69: 2808-28017Crossref Scopus (70) Google Scholar,[2]Demerouti E.A. Manginas A.N. Athanassoupoulos G.D. et al.Complications leading to sudden cardiac death in pulmonary artery hypertension.Resp Care. 2013; 58: 1246-1254Crossref PubMed Scopus (50) Google Scholar]. Here we report a case of myocardial infarction with severe left ventricular dysfunction due to LMCA compression in a patient with Eisenmenger’s Syndrome. A 63-year-old female with Eisenmenger’s Syndrome due to a ventricular septal defect (VSD) and patent ductus arteriosus (PDA) presented with increasing dyspnoea over several weeks. Echocardiography illustrated severe global left ventricular systolic dysfunction (EF 17%), an unrestricted 12mm VSD, dilated and hypertrophied right ventricle with moderate tricuspid and pulmonary regurgitation. Estimated RV systolic pressure was 112mmHg. An ECG was revealed ST-elevation in aVR with widespread ST depression, with an elevated serum troponin of 6.7ug/L (<0.04). The patient had normal coronary angiography 2 years prior. Repeat coronary angiography revealed severe ostial LMCA stenosis due to extrinsic pulmonary artery compression, with the remaining vessels disease free. Percutaneous intervention to the LMCA was performed with a zotarolimus drug eluting stent with excellent angiographic result. Anti-platelets and up-titration of heart failure therapy was initiated. 2 years after discharge, she remains stable with a LVEF of 40% and NHYA Class II symptoms at home with her husband. In patients with pulmonary hypertension, progressive symptoms are often attributed to worsening pulmonary resistance or right heart dysfunction/ischaemia [[1]Gailé N. Saia F. Pallazini M. et al.Left Main Coronary Artery Compression in Patients With Pulmonary Arterial Hypertension and Angina.JACC. 2017; 69: 2808-28017Crossref Scopus (70) Google Scholar,[3]Gómez A. Bialostozky D. Zajarias A. et al.Right ventricular ischaemia in patients with primary pulmonary hypertension.JACC. 2001; 38: 1137-1142Crossref Scopus (179) Google Scholar]. LMCA compression represents an important and treatable cause of myocardial infarction and LV dysfunction with excellent medium-term outcomes.

Coronary embolism causing myocardial infarction after heart valve surgery

Introduction. Coronary embolism can rarely be a cause of myocardial infarction. It is usually associated with atrial fibrillation, dilated cardiomyopathy, bacterial endocarditis and underlying hypercoagulable state, as well as heart surgery. Case report. We reported a case of a patient with severe mitral and tricuspid regurgitation, with no underlying coronary artery disease. The patient underwent heart valve surgery, and the immediate postoperative course was uneventful. Five days after the operation, the patient sustained cardiac arrest, which was followed by a successful cardiopulmonary resuscitation. Electrocardiography showed atrial fibrillation with a significant ST segment elevation in the inferior leads. Urgent coronary angiography revealed a total occlusion of the right coronary artery, thus percutaneous coronary intervention was performed, after which flow restoration through the artery was achieved. The patient was discharged with triple antithrombotic therapy on the 20th postoperative day. Conclusion. Heart surgery could be followed by unexpected and potentially fatal complications, coronary embolism being one of them. In such case, the prompt and adequate reaction by the whole medical team is crucial for a patient's survival and recovery.

P1736 An unexpected cause of ventricular tachycardia in a young patient

Abstract Introduction Hypoplastic coronary artery disease (HCAD) refers to a congenital underdevelopment of one or more coronary arteries, which are greatly reduced in diameter or length. It is a rare congenital abnormality which has rarely been documented in living patients and which may lead to myocardial infarction (MI) and sudden cardiac death (SCD). This case describes an otherwise healthy young male, which was admitted in the emergency department (ED) for repeated sustained ventricular tachycardia (VT) and was thereby diagnosed with an isolated hypoplasia of the left circumflex coronary artery (CX). Investigations revealed scar-related tachycardia, due to a prior silent myocardial infarction caused by HCAD. These findings were suggested by echocardiography and coronary angiography and were later confirmed by magnetic resonance and 3D cardiac mapping. Case Report A 34-year-old male patient was admitted to the intensive care unit with recurrent sustained VT causing hemodynamic instability. After receiving two electric shocks and amiodarone in the ambulance, the patient became hemodynamically stable. There was no remarcable medical history besides a syncopal fall 5 years before and no symptoms prior to the current event. Initial physical examination, ECG and laboratory testing were normal. Echocardiography revealed a dilated left ventricle with akynesia of the lateral wall and a mildly reduced ejection fraction (EF = 45%), moderate mitral regurgitation due to restriction of the posterior mitral leaflet. A subsequent emergent coronary angiography was therefore performed, which showed no sign of atherosclerotic lesions, yet it revealed a hypoplastic CX, without compensatory collateral vessels supplying the lateral wall. Cardiac MR demonstrated delayed enhancement with transmural necrosis and no viability in the lateral wall of the LV, suggesting a long-standing MI. Therefore, the final diagnosis was scar-related VT, due to a prior silent MI caused by HCAD. The management of this patient included implantation of an ICD in the secondary prevention of SCD. Moreover, we performed an EPS, which identified a scar at the level of the lateral and inferolateral LV walls as a substrate for VT (electroanatomic 3D voltage mapping) and of the critical istmus (3D activation mapping). The next step was radiofrequency ablation of the critical isthmus, with no inducibility of the VT after the procedure. After 6-months follow-up, there was no recurrence of the VT. Conclusion Finding the cause of myocardial infarction in a young patient with VT can be very challenging. We emphasise the role of imaging for the diagnosis and management of these patients. HCAD is a rare congenital anomaly, which can lead to progressive fibrosis in the territory with poor blood supply, MI and SCD. Although it is a rare condition, it should be considered in young adults who present with MI and/or SCD. Abstract P1736 Figure. Investigations

Association between genetic variants and risk of myocardial infarction among young Moroccan population

The causes of Myocardial Infarction (MI) may depend on environemental and genetic risk factors in young patients. The aim of the study was to describe the risk factors and genetic features in young patients with MI and compare these findings to those identified in older patients. This prospective study was conducted within the Department of Cardioloy in conjunction with the cellular pathology lab at the University Hospital of Casablanca between November 2012 and August 2017. Patients aged less than 45 years with MI (group I) were compared to patients older than 55 years with MI (group II). The genetic study focused on the contribution of 8 genes. We included 140 patients of which 70 were ≤ 45 years. The mean age of the younger cohort was 37.87 years vs. 64.21 years in group (II) .Both groups were predominantly male. In group (I), smoking was the most frequent risk factor 61.8% vs. 38.2% ( P = 0.007). Hypertension was common in group II (60,7% vs. 39,3%; P = 0.02). No statistically significant differences were observed between the groups in terms of diabetes,obesity and dyslipidemia. This study demonstrated an association of genetic predisposition factors involved in lipid metabolism (APOAV genotypes, APOE), endothelial dysfunction (MTHFR gene variants, eNOS) and coagulation cascade (FV genes, FII). The analysis revealed six polymorphisms with a significant correlation to an increased risk of MI in young subjects. There were no statistically significant correlations between the FV gene polymorphisms and risk factors such as age,gender, diabetes, smoking, and dyslipidemia. However, a statistically significant correlation regarding hypertension and obesity was identified ( P = 0.02 and P = 0.032 respectively) The results in this study indicate that genetic variations, although uncommon, are correlated to an increased risk of MI in this cohort. Further studies are needed to further investigate this conclusion.

A064 Spontaneous Coronary Artery Dissection: The Diagnostic Utility of Computed Tomography Coronary Angiography

Spontaneous coronary artery dissection (SCAD) is an important cause of myocardial infarction in young to middle aged women. The utility of computed tomography coronary angiography (CTCA) in the diagnosis of SCAD has not been well established. We sought to investigate the correlation of invasive coronary angiography to CTCA in SCAD, and its use in follow-up. Consecutive patients who underwent CTCA following a diagnosis of SCAD on coronary angiography between 2010 and 2018 at our institute were included. CTCA was reported independently by two cardiologists: one with knowledge of the SCAD location, and a second blinded. A total of 32 patients with 38 non-contiguous SCAD lesions were included in our study (65.6% female, mean age 50.5±8.8 years). The left circumflex artery was most commonly affected (34.2%), and 27 lesions (71.1%) affected the distal or branch coronary vessel. The majority of SCAD lesions (78.9%) were type-2 SCAD according to the Saw classification. CTCA was performed post-SCAD at a median of 40.5 days, and 25 of 38 lesions (25.8%) were unhealed. The number of days post-SCAD till CTCA was significantly less for unhealed versus healed lesions (median 30 vs 104 days, U=73.5, p=0.005). In the blinded reporting, 18 of 25 unhealed lesions were correctly identified (sensitivity 72%), while 7 of 13 healed lesions were correctly reported as negative for dissection (specificity 53.8%). The predictive accuracy of CTCA to assess healing of SCAD increases with time. Due to the CTCA limitations of spatial resolution and the predilection for distal coronary vessels in coronary dissection, there is moderate accuracy in blinded diagnosis using CTCA, although its likely role may lie in follow-up surveillance, or symptomatic patients post-SCAD.

275 A Novel Method for Detecting Coronary Artery Dissection Using Computed Tomography Coronary Angiography

Spontaneous coronary artery dissection (SCAD) is an uncommon and underdiagnosed condition, which is increasingly recognised as an important cause of myocardial infarction. Computed tomography coronary angiography (CTCA) is an emerging non-invasive tool for assessment of SCAD, not yet recommended as first-line imaging due to its lower temporal and spatial resolution compared to catheter coronary angiography. A 34-year-old female with no medical history presented with chest pain and inferolateral ST-segment elevation on electrocardiogram (ECG). Catheter coronary angiography revealed coronary artery dissection involving the left main, left anterior descending and circumflex arteries. Computed tomography angiogram revealed multifocal carotid and vertebral artery dissection, with renal artery beading, suggesting fibromuscular dysplasia. A follow-up CTCA was performed using a prospective ECG-gated dual source high-pitch helical scanner (Siemens, High Definition Flash, Forchheim, Germany). The scan was repeated 13 seconds later without further contrast. This “double-scan” had the unique effect of showing contrast “staining” in the false lumen of the dissection, occurring as a result of residual contrast not yet washed out from the first scan. The findings of this “double-scan” technique appears analogous to the contrast staining of the false lumen observed on catheter coronary angiography. Depending on the type of scanner and mode of use, obtaining more than two scans following the contrast bolus may be possible. However, the timing of repeat scans may need to vary depending on the flow characteristics of false lumen filling and haemodynamics. Further research is required to determine how to best apply this novel utility.

A review on the biomechanics of coronary arteries

Globally, cardiovascular diseases are seen as one of the largest economic burdens on society and the single largest cause of death, with atherosclerosis the leading cause of myocardial infarction (heart attack). Due to the complex interactions in the coronary vasculature, medical imaging technology is unable to recognise correlations between artery and fluid mechanics and disease initiation and progression, hence, biomechanical analysis of coronary arteries in patient-specific models is necessary to provide critical information in clinical settings; large variability in modelling approaches, parameters and results still, however, hamper accurate and reliable model development. This review aims to assist in filling that gap by presenting an overview of research efforts to date, from both theoretical and experimental perspectives, to assist in addressing the challenge of developing a reliable and accurate biomechanical model of human coronary arteries. Studies have been categorised primarily on their approach, either purely theoretical, purely experimental/clinical or a combined theoretical and experimental/clinical approach as well as then divided into structural, fluid, and fluid–structure interaction (FSI) analysis. From research efforts to date it is clear that the development of FSI models to incorporate the effects of shear-thinning, non-Newtonian flows in viscoelastic, realistic artery and plaque morphologies developed from in vivo, high resolution imaging is critical for accurate determination of disease initiation/progression, including atherosclerosis, plaque formation, and failure mechanisms. The inclusion of micro-constituents such as micro-calcification, endothelial cell layer, collagen cross-linking, vascular smooth muscle cell contractility and constitutive blood equations also affects stress magnitude, distribution and failure mechanisms and should be adequately accounted for. A set of appendices are also provided where studies are summarised and assessed based on their approach to modelling and are categorised by considering the imaging modality used, methodology, material and blood properties, type of coronary artery, approach to the study (theoretical, experimental, in vitro & in vivo), number of patients/specimens and a general description. It is hoped this review will assist in furthering the field of coronary artery biomechanics and contribute to developing accurate and reliable patient-specific models capable of improving our understanding of cardiovascular biomechanics and hence, the initiation/progression of related diseases to address the growing global morbidity, mortality and economic challenge of cardiovascular disease and myocardial infarction.

Coronary Embolism and Myocardial Infarction: A Scoping Study.

Coronary embolism is a cause of acute myocardial infarction (AMI)in which obstructive foci enter the coronary circulation, block normal blood flow and precipitate ischemia. Precise studies focusing on patient population affected, pathophysiological mechanisms, and treatment strategies are scanty, in spite of a reported prevalence estimated at 2.9%. As the understanding of myocardial infarction without evidence of coronary artery disease continues to grow, an in-depth review of this previously seldomly reported subtype of coronary ischemia was in order. Patients suffering coronary embolism are 15 to 20 years younger than traditional AMI patients with a slight predominance towards male sex, which resembles the gender data of the populations affected by non-traditional myocardial infarction in published reports. While the expected prevalence rate of cardiovascular disease risk factors such as hypertension and hyperlipidemia are present, this population also has a relatively high prevalence of atrial fibrillation and valve pathology, especially endocarditis. Initial presentation is indistinguishable from other causes of myocardial infarction however fever is commonly present, when endocarditis with valvular involvement is the primary cause of the coronary embolism. Mechanical thrombectomy is the mainstay of treatment, followed by percutaneous coronary intervention. Mortality is the highest in patients who do not receive targeted treatment for the coronary embolism, particularly if only antimicrobial agents or anticoagulation without thrombolytic agents are employed. The unique features of coronary embolism highlighted in this historical study justify further examination in contemporary patient populations.

Spontaneous coronary artery dissection: update 2019.

Spontaneous coronary artery dissection (SCAD) is an important cause of myocardial infarction (MI) in women with few or no conventional cardiovascular risk factors. Lack of awareness about this condition among healthcare providers had led to significant underdiagnosis and misdiagnosis in this relatively young patient population. The current review summarizes the contemporary data on cause, management strategies and outcomes of SCAD. SCAD is not as rare as previously thought, accounting for up to 4% of all acute coronary syndromes. It is frequently linked with predisposing factors, such as fibromuscular dysplasia or other vasculopathies, and is often triggered by physical or emotional stress. Due to more fragile vessel architecture, coronary angiography as the first-line diagnostic tool should be performed meticulously to avoid iatrogenic dissection. Intravascular imaging may be required if angiographic findings are uncertain. Unless patients have high-risk features such as ongoing ischemia, recurrent chest pains, left main artery dissection, ventricular arrhythmias, or hemodynamic instability, a conservative treatment strategy is favored over revascularization. Close monitoring is essential after a SCAD-event as recurrent cardiovascular events post-SCAD are frequent.

Galanthamine improves myocardial ischemia-reperfusion-induced cardiac dysfunction, endoplasmic reticulum stress-related apoptosis, and myocardial fibrosis by suppressing AMPK/Nrf2 pathway in rats

Myocardial ischemia/reperfusion (I/R) injury is an important cause of myocardial infarction and heart failure after cardiovascular surgery. Galanthamine (Gal) is an important Amaryllidaceae alkaloid with anti-acetylcholinesterase and anti-inflammatory activity. The purpose of this study was to investigate the role of Gal in myocardial I/R injury. In this study, an animal model of myocardial I/R injury was constructed, and the rats were divided into five groups (n=10): the sham, I/R model, I/R + Gal (1 mg/kg), I/R + Gal (3 mg/kg), and I/R + Aspirin (20 mg/kg) groups. The expression of related proteins was detected by Western blotting and Immunohistochemistry, and Histological lesion was detected by HE staining. Results showed that Gal improves I/R-induced cardiac dysfunction in rats. Moreover, Gal inhibits I/R-induced endoplasmic reticulum stress (ERS)-related apoptosis by suppressing the expression of CHOP, Cleaved caspase 12, and caspase 3, and promoting the expression of CADD34 and BiP in rats. Furthermore, Gal mitigates I/R-induced myocardial fibrosis through restraining the expression of α-SMA and Collagen I in rats. Mechanically, Gal promoted the expression of AMPKα1, Nrf2 and HO-1. However, AMPK inhibitor Compound C exhibited the opposite effects. Collectively, this finding suggests that Gal improves I/R-induced cardiac dysfunction, ERS-related apoptosis, and myocardial fibrosis by activating AMPK/Nrf2 pathway in myocardial I/R rats. Given this evidence, Gal may be a potential therapeutic drug for the treatment of I/R injury.

P5538Safety and efficacy of acetylcholine provocation test for diagnosis of vasospastic angina in young patients

Abstract Background Vasospastic angina (VSA) is considered as a cause of myocardial infarction with nonobstructive coronary arteries. Given the previous reports of higher incidence of cardiovascular events in young VSA patients, early diagnosis and optimal treatment are important for these patients. While acetylcholine provocation test (ACh test) for VSA diagnosis is well reported, ACh test among young patients is not as commonly performed, therefore its safety and usefulness for this patient subset have not been fully evaluated. Purpose The purpose of this study was to evaluate the safety and the proportion of positive results of ACh test for young patients. Methods Data from patients who underwent ACh test in our institution from May 2012 to September 2018 were retrospectively analyzed. A total of 669 patients were enrolled and divided into 2 groups according to age: Young group (Age≤50, n=106); and Senior group (Age&gt;50, n=563). Results The senior group had a higher incidence of hypertension, dyslipidemia, diabetes mellitus, and coronary artery disease. On the other hand, the young group had a significantly higher incidence of current smoker and tendency of daily alcohol. The rate of positive ACh test was similar, and there were no significant differences in major or minor complications between the 2 groups. Patient characteristics and outcome Young group Senior group p (n=106) (n=563) Age (years) 42.8±7.3 68.0±9.0 &lt;0.001 Male (%) 56.6 52.2 0.407 Current smoker (%) 34.9 15.4 &lt;0.001 Daily alcohol (%) 31.1 22.9 0.070 Hypertension (%) 33.0 66.6 &lt;0.001 Dyslipidemia (%) 50.0 68.4 &lt;0.001 Diabetes (%) 12.3 20.8 0.047 ACh positive (%) 52.8 49.9 0.581 Minor adverse event (%) 4.7 5.9 0.820 Major adverse event (%) 0.9 1.4 1.000 Major adverse event: composite of death, ventricular fibrillation, sustained ventricular tachycardia (VT), myocardial infarction and stroke. Minor adverse event: non-sustained VT and paroxysmal atrial fibrillation. Conclusion ACh provocation test for young patients can be safely performed, and the rate of positive results was similar to that of senior patients. In young patients suspected of having VSA, ACh test should be actively performed to identify optimal medical therapy for prevention of cardiovascular events. Acknowledgement/Funding None

TCT-467 In-Hospital and Long-Term Outcomes Among Patients With Spontaneous Coronary Artery Dissection Presenting With Ventricular Tachycardia and/or Fibrillation

Spontaneous coronary artery dissection (SCAD) is an important cause of myocardial infarction (MI) in young to middle-aged women. Ventricular tachycardia and/or ventricular fibrillation (VT/VF) may complicate up to 10% of SCAD presentation, and the long-term outcomes are unknown. The authors

Revascularization in Patients With Spontaneous Coronary Artery Dissection and ST-Segment Elevation Myocardial Infarction

BackgroundSpontaneous coronary artery dissection (SCAD) is an increasingly recognized cause of myocardial infarction (MI) in younger women, often treated conservatively due to revascularization risks. Revascularization outcomes are largely unknown in SCAD presenting with ST-segment elevation myocardial infarction (STEMI). ObjectivesThe purpose of this study was to compare revascularization strategies and outcomes of STEMI-SCAD with STEMI atherosclerosis (STEMI-ATH). MethodsConsecutive STEMI patients were retrospectively analyzed (2003 to 2017) at 2 regional STEMI programs (Minneapolis Heart Institute and Cedars-Sinai Smidt Heart Institute) with 3-year outcomes. ResultsAmong 5,208 STEMI patients, SCAD was present in 53 (1%; 93% female). SCAD prevalence was 19% in female STEMI patients age ≤50 years. Compared with STEMI-ATH, STEMI-SCAD patients were younger (age 49 ± 10 years vs. 63 ± 13 years), were more often female (93% vs. 27%), and had more frequent cardiogenic shock (19% vs. 9%); all p ≤ 0.03. In STEMI-SCAD, the culprit artery was more commonly left main (13% vs. 1%) or left anterior descending (47% vs. 38%); both p = 0.003. Acute revascularization was lower in STEMI-SCAD (70% vs. 97%); p < 0.001. In STEMI-SCAD, acute revascularization included percutaneous coronary intervention (PCI), n = 33 (62%), or bypass grafting, n = 4 (8%); PCI success was 91%. Those with revascularization were more likely to have shock, left main culprit, proximal dissection, and initial TIMI (Thrombolysis In Myocardial Infarction) flow grade 0 to 1. The 3-year survival was 98% for STEMI-SCAD versus 84% for STEMI-ATH; p < 0.001. ConclusionsSTEMI-SCAD represents an important STEMI subset, particularly among younger women, characterized by significantly greater frequency of left main or left anterior descending culprit and cardiogenic shock than STEMI-ATH. Primary PCI is successful in most STEMI-SCAD patients, with low 3-year mortality.

Mtdna Mutations Associated With Myocardial Infarction

Background and Aims: Myocardial infarction is one of clinical manifestations of coronary heart disease. In some cases, the cause of myocardial infarction may be atherosclerotic plaques which occurred in the human aorta. The association of mtDNA mutations with atherosclerotic lesions in human arteries was previously detected by our research group. The aim of the study was to detect mutations mtDNA associated with myocardial infarction.

Is Plaque Rupture Always Responsible in Acute Coronary Syndrome?

The majority cause of myocardial infarction is the atherothrombotic event, mainly cause by plaque rupture. Since the 20th century, it was found that the plaque rupture was not the solely condition responsible for the acute coronary syndrome. With the invention of more sensitive myocardial biomarker, a series of guideline was written as guideline for the definition of myocardial infarction. This review discuss about the consensus in the Universal Definition of Myocardial Infarction.

A young man with acute anterior wall myocardial infarction after Cannabis abuse: Identification of perivascular edema of the culprit lesion after plaque rupture using cardiovascular magnetic resonance tomography

Canabis abuse is a rare but well-known und increasing cause of myocardial infarction in young people, predominantly in the male sex. Although the exact pathophysiological mechanism is not completely understood, several hypotheses have been proposed: coronary artery spasm due to alpha-adrenergic receptor stimulation; premature atherosclerosis with „classical “plaque formation and rupture resulting in thrombus formation with complete vessel closure. The latter model is supported by the fact that concomitant cigarette smoking is usual in cannabis drug abusers and represents a classical cardiovascular risk factor [1].

Current state-of-play in spontaneous coronary artery dissection

For over 80 years, spontaneous coronary artery dissection (SCAD) has been recognised as a cause of myocardial infarction. SCAD is described as a non-iatrogenic, non-atherosclerotic coronary artery dissection, resulting in formation of a false lumen or intramural haematoma in the coronary artery wall that compresses the true lumen, often compromising myocardial blood flow. In early literature, the incidence of SCAD in acute coronary syndrome (ACS) was underestimated. Recent advances in awareness and widespread early angiographic investigation in ACS has led to important shifts in our understanding of the prevalence, predisposing causes, natural history, aetiology, clinical and angiographic features, management, and prognosis of SCAD. It is now well understood that SCAD predominantly affects women and is responsible for around 20% of ACS presentations in females below the age of 60. Despite this, SCAD is still often overlooked and misdiagnosed as atherosclerotic disease. Misdiagnosis is multifactorial; with contributing factors including a low clinical index of suspicion, particularly in young females, a lack of clinician familiarity with angiographic variants, and limitations of angiography. Although increasing evidence suggests that optimal management is distinct from atherosclerotic coronary artery disease, many questions remain unanswered regarding the pathogenesis and optimal treatment of SCAD, heralding prospective research to answer these questions. This review aims to give a current clinical perspective on SCAD and highlight the importance of familiarity and vigilance with this condition when diagnosing and treating ACS.