Cause Of ST-elevation Myocardial Infarction Research Articles

ST-Elevation Myocardial Infarction Due to Coronary Vasospasm Associated with Eosinophilic Granulomatosis with Polyangiitis: A Case Report.

ST-elevation myocardial infarction (STEMI) can be caused by underlying coronary artery vasospasm (CAV) with or without associated atherosclerotic disease. Coronary artery vasospasm is a rare but potentially devastating manifestation of eosinophilic granulomatosis with polyangiitis (EGPA). We describe a 54-year-old male with a known history of EGPA and coronary artery disease presenting to the emergency department with chest pain and an inferior STEMI on electrocardiogram. He was ultimately taken for coronary angiography and found to have a discrete vasospastic lesion in the right coronary artery that was treated with intra-coronary nitroglycerin and calcium channel blockers. He was continued on immunosuppressant agents (prednisone and mepolizumab) for management of EGPA and followed up with outpatient cardiology and rheumatology for vasospastic angina. This case highlights a rare cause of STEMI, discusses the nuances in treatment of STEMI due to CAV, and provides background on pathophysiology and treatment of EGPA.

Trends in primary percutaneous coronary intervention for the treatment of acute coronary ST-elevation myocardial infarction in Latin American countries: insights from the CECI consortium.

ST-elevation myocardial infarction (STEMI) requires revascularization treatment, preferably via primary percutaneous coronary interventions (pPCI). There is a lack of data about contemporary management of STEMI in Latin America. This was a multicenter, multinational, prospective, and dynamic registry of patients undergoing pPCI in Latin America for STEMI (STEMI/LATAMI Registry) that was carried out in nine centers from five countries (Argentina, Ecuador, Venezuela, Bolivia, and the Dominican Republic) between June 2021 and June 2023. All interventionalists involved in the study were originally trained at the same institution (Centro de Estudios en Cardiología Intervencionista, Buenos Aires, Argentina). The primary objective was to evaluate procedural and in-hospital outcomes of pPCI in STEMI and in-hospital outcome in the Latin America (LATAM) region; as secondary endpoints, we analyzed the following subgroups: differences between pPCI vs. pharmaco-invasive or late presenters, gender, elderly and very elderly patients, cardiogenic shock outcomes, and causes of STEMI. In total, 744 STEMI patients who underwent PCI between June 2021 and June 2023 in five countries (nine centers) in our continent were included; 76.3% had a pPCI, 8.1% pharmaco-invasive PCI, and 15.6% had late STEMI PCI. There were no differences in region or center when we evaluated in-hospital and 30 days of death. The rate of procedural success was 96.2%, and the overall in-hospital mortality rate was 2.2%. In the subgroup of pPCI, mean symptom onset-to-balloon time was 295.3 ± 246 min, and mean door-to-balloon time was 55.8 ± 49.9 min. The femoral approach was chosen in 60.5%. In 3.0% of patients, the left main disease was the culprit artery, with 1.63 ± 1.00 stents per patient (564 drug-eluting stents and 652 bare metal stents), with 34 patients receiving only plain optimal balloon angioplasty. Definitive stent thrombosis was related to the infarct artery as the primary cause of STEMI in 7.5% of patients. The use of assistant mechanical devices was low, at 2.1% in the pPCI group. Women were older, with large numbers in very elderly age (≥90 years), greater mortality, and incidence of spontaneous coronary dissection as a cause of STEMI (p < 0.001, p < 0.001, p < 0.001, and p < 0.003, respectively). In suitable LATAM Centers from low/medium-income countries, this prospective registry in patients with STEMI, PCI performed by well-trained operators has comparable results to those reported in well-developed countries.

CRT-100.24 The Impact of Sex on Clinical Cardiogenic Shock Outcomes Following ST-Elevation Myocardial Infarction Treated With Primary Percutaneous Intervention

Cardiogenic shock (CS) remains the leading cause of ST-elevation myocardial infarction (STEMI)-related mortality. Over the years, despite impressive mortality reduction during STEMI, CS mortality rates remained high and constant. Contemporary studies (e.g., SHOCK, SHOCK IABP-II and SHOCK-MVD) showed

“Too Young to Have a Broken Heart”: Spontaneous Coronary Artery Dissection Causing ST-Elevation Myocardial Infarction in a Young Adult: A Case Report

ST-elevation myocardial infarction (STEMI) rarely occurs among patients 18 to 34 years old. Spontaneous coronary artery dissection (SCAD) is a rare cause of STEMI and is frequently described among patients in peripartum period. SCAD has a high mortality rate if not recognized and treated immediately. We present a case of SCAD presenting as STEMI in a 19-year-old nonpregnant patient. A 19-year-old female with chronic kidney disease, complained of sudden onset substernal chest pain. Physical examination showed a blood pressure of 140/90 mm Hg, HR of 112 bpm, with note of rales, pedal edema, and cold clammy extremities. Electrocardiogram showed ST-elevation in leads V3 to V6. Cardiac troponin was elevated and echocardiography revealed left ventricular segmental hypokinesia and depressed systolic function. Patient was diagnosed with acute anterolateral wall STEMI. Coronary angiogram revealed total occlusion of the mid-segment of the left anterior descending artery (LAD), while the rest of the coronary arteries were strikingly normal. After initial balloon angioplasty and stenting of the mid LAD, coronary artery dissection was noted at the distal LAD. A stent was successfully deployed, achieving TIMI flow grade III with no residual stenosis. She remained stable and was discharged improved. STEMI rarely happens in the young adults. Moreover, literature highlights the rarity of STEMI caused by SCAD. SCAD usually occurs among young pregnant patients without risk factors for atherosclerosis. We highlighted the significance of suspecting SCAD among young patients who present with STEMI and prompt treatment with revascularization in clinical situations such as this case. SCAD remains to be a rare cause of STEMI. However, SCAD should be considered among young individuals with STEMI. Treatment is primarily medical unless there is persistent chest pain and/or ischemic ECG changes, hemodynamic instability, or unstable arrhythmia, where revascularization is necessary. J Med Cases. 2018;9(6):164-169 doi: https://doi.org/10.14740/jmc3052e

Spontaneous Coronary Artery Dissection Causing ST-Elevation Myocardial Infarction in a Young Adult: A Case Report

Introduction: ST-elevation myocardial infarction (STEMI) rarely occurs among patients 18 to 34 years old. Spontaneous coronary artery dissection (SCAD) is a rare cause of STEMI that is frequently described among patients in peripartum period. SCAD has a high mortality rate when not recognized and treated immediately. We present a case of SCAD presenting as STEMI in a nineteen-year-old non pregnant patient. Case: A nineteen-year-old female with chronic kidney disease complained of sudden-onset substernal chest pain. Physical examination showed blood pressure of 140/90 mmHg, heart rate of 112 beats per minute, with findings of of bibasilar rales, pedal edema and cold and clammy extremities. Electrocardiogram (ECG) showed ST-elevation in leads V3 to V6. Cardiac troponin was elevated, and echocardiography revealed left ventricular segmental hypokinesia and depressed systolic function. Patient was diagnosed with acute anterolateral wall STEMI. Coronary angiogram revealed total occlusion of the mid segment of the left anterior descending artery (LAD), while the rest of the coronary arteries were strikingly normal. After initial balloon angioplasty and stenting of the mid LAD, coronary artery dissection was noted at the distal LAD. A stent was successfully deployed, achieving thrombolysis-in-myocardial-infarction (TIMI) flow grade III with no residual stenosis. Patient remained stable and was discharged improved. Discussion: STEMI rarely happens in young adults. Moreover, literature highlights the rarity of STEMI caused by SCAD. SCAD usually occurs among young pregnant patients who have no risk factors for atherosclerosis. In this report, we highlight the importance of suspecting SCAD among young patients who present with STEMI and of prompt treatment with revascularization in similar clinical situations. Conclusion: SCAD remains a rare cause of STEMI, but it should be considered when young individuals present with STEMI. Treatment is primarily urgent revascularization especially if there is persistent chest pain or ischemic ECG changes, hemodynamic instability, or unstable arrhythmia. Keywords: spontaneous coronary artery dissection, SCAD, acute coronary syndrome, ACS, ST-elevation myocardial infarction, STEMI

Improving prevention: risk scores, imaging, and PCSK9 inhibitors.

Download the Issue @ a Glance podcast Subscribe to the EHJ Podcast ![Graphic][1] Prevention is better than cure: this old saying is still valid today. We have made enormous progress with this approach, but we can, indeed must, improve further beyond current guidelines.1 Thus, a summary of the recent achievements as provided by M. John Chapman from INSERM in Paris, France in ‘ The year in cardiology 2015: prevention ’2 is very timely. The authors note that a further improvement in the prevention of cardiovascular disease is of critical importance, as coronary heart disease still represents the most common cause of death worldwide,3 associated with impaired quality of life, reduced life expectancy, and socio-economic cost. The year 2015 has witnessed dramatic progress in cardiovascular prevention on several fronts. Notably, this includes first event reduction in high-risk patients in general practice followed by the introduction of comprehensive strategies to attenuate modifiable risk factors, including lifestyle and dietary habits. Beyond that, secondly, hybrid imaging4 to detect subclinical atherosclerosis, with potential improvement in risk prediction and management, has improved management. Thirdly, it is now clear that plaque rupture and thin-cap fibroatheroma5,6 are the major cause of ST-elevation myocardial infarction. The emergence of ‘omics’ technologies to identify new causal biofactors also opens up new avenues. Monoclonal antibodies targeting proprotein convertase subtilisin/kexin type 9 (or PCSK9)7 not only further reduce LDL-cholesterol, but preliminary findings strongly suggest that they also reduce cardiovascular events. Furthermore, the EMPA-REG OUTCOME trial using the novel antihyperglycaemic agent, empagliflozin,8 a selective sodium–glucose co- transporter inhibitor, significantly reduced cardiovascular mortality; also, the recent PATHWAY-2 and PATHWAY-3 trials using spironoloactone as add-on therapy in resistant hypertension, and amiloride plus hydrochlorothiazide in hypertensive patients requiring a diuretic, respectively, showed markedly better blood pressure control; and, finally, … [1]: /embed/inline-graphic-1.gif

Spontaneous Coronary Artery Dissection/Intramural Haematoma in Young Women with ST-Elevation Myocardial Infarction: "It Is Not Always a Plaque Rupture Event".

Spontaneous coronary artery dissection (SCAD) is an unusual, but increasingly recognized, cause of ST-elevation myocardial infarction (STEMI), especially among younger patients without conventional risk factors for coronary artery disease (CAD). Although dissection of the coronary intima or media is a hallmark finding, hematoma formation within the vessel wall is often present. It remains unclear whether dissection or hematoma is the primary event, but both may cause luminal stenosis and occlusion. The diagnosis of SCAD is made principally with invasive coronary angiography, although adjunctive intracoronary imaging modalities may increase the diagnostic yield. In STEMI patients, the decision whether to pursue primary percutaneous coronary intervention (PCI) or appropriate conservative medical therapy is based on clinical presentation, the extent of the dissection, the critical anatomy involvement, and the amount of ischaemic myocardium at risk. In this case report, we present two cases of young women with SCAD and STEMI, successfully treated with primary PCI. We briefly illustrate the characteristic aspects of the angiographic presentation and intravascular ultrasound-guided treatment. SCAD should always be considered in young STEMI patients without conventional risk factors for CAD with primary angioplasty to be required in patients with ongoing myocardial ischemia.

The outcome of primary percutaneous coronary intervention for stent thrombosis causing ST-elevation myocardial infarction

There are very few scientific data about the effectiveness of primary percutaneous coronary intervention (PCI) in patients with ST-elevation myocardial infarction (STEMI) due to stent thrombosis (ST). The purpose of the present study is to investigate the efficacy and outcome of primary PCI for STEMI due to ST in the largest consecutive patient population with ST reported to date. A total of 2,644 consecutive STEMI patients undergoing primary PCI were retrospectively enrolled into the present study. The primary end point of this study was successful angiographic reperfusion defined as postprocedural Thrombolysis In Myocardial Infarction grade III flow. The secondary end points were cardiovascular death and reinfarction. Stent thrombosis was the cause of STEMI in 118 patients (4.4%). In patients with ST, angiographic success (postprocedural Thrombolysis In Myocardial Infarction grade III flow) was worse than in patients with de novo STEMI (76.3% vs 84.8%, P = .01). Patients with ST had significantly higher incidence of in-hospital cardiovascular mortality than patients with de novo STEMI (10.2% vs 5.3%, P = .02). In-hospital reinfarction rate was similar in both groups. In addition, long-term (mean 22 months) cardiovascular mortality and reinfarction rates were significantly higher in patients with ST compared with those without (17.4% vs 10.5%, P = .02 and 15.6% vs 9.5%, P = .03, respectively). Primary PCI for treatment of ST is less effective, and these patients are at increased risk for in-hospital and long-term mortality compared with patients undergoing primary PCI due to de novo STEMI.

Total occlusion of the infarct-related coronary artery correlates with brachial artery flow-mediated dilation in patients with ST-elevation myocardial infarction

Occlusion of the coronary artery is the main cause of ST-elevation myocardial infarction (STEMI). In some patients, it is followed by early spontaneous thrombolysis. In this study, we tried to determine whether spontaneous thrombolysis in the infarct-related artery (IRA) correlates with the state of the endothelium, which we assessed using the brachial artery flow-mediated dilation (FMD) test. 52 patients with STEMI were included in the study. Based on the results of coronary angiography performed during the first three days of STEMI, the patients were divided into two groups: Group I (n=33), consisting of patients with remaining total occlusion of the IRA, and Group II (n=19), consisting of patients with spontaneous thrombolysis. We assessed the endothelial function, using the brachial artery FMD test. In Group I, during the first three days of STEMI, brachial artery FMD results were significantly lower than those in Group II: 5.41+/- (3.23-7.41)% versus 10.81+/-(8.00-14.89)%, respectively; P=0.000036. After 7-14 days, this difference disappeared because of significant elevation of the FMD levels in the first group. Group I was characterized by higher levels of high sensitive C-reactive protein (CRP), cholesterol, and cholesterol-LDL and lower usage of angiotensin-converting enzyme (ACE) inhibitors before STEMI. The data presented above reveal that spontaneous coronary thrombolysis in patients with acute STEMI is associated with a preserved endothelium-dependent vasodilator response in the brachial artery. It can depend on the levels of hs-CRP, of fasting glucose, and of ACE-inhibitors from previous treatment.

Thrombolytic therapy in acute myocardial infarction

Thrombolytic therapy represents the major advancement for the treatment of acute myocardial infarction (MI) that has been achieved in recent years. Based on the recognition of acute totally occlusive intracoronary thrombosis as the primary cause of ST-elevation MI, thrombolytics were evaluated alone or in combination with antithrombotics for the treatment of acute MI. Streptokinase, APSAC and t-PA were the first "standard" regimens evaluated. The "accelerated" t-PA infusion was introduced as the "gold standard" thrombolytic regimen with the GUSTO trial, and was administered in combination with aspirin and intravenous heparin. Many newer thrombolytics have been developed with the expectation to further decrease acute MI mortality, to decrease bleeding complications or to facilitate drug administration. The introduction of platelet glycoprotein IIb/IIIa inhibitors in clinical pharmacology has added a novel drug category for potential use for primary thrombolysis or in combination with thrombolytics. Conceptualizing thrombolytic and anti-thrombotic combination regimens will optimize treatment of acute MI in the future.