Acute Anteroseptal Myocardial Infarction Research Articles

A case report: anteroseptal ST elevation due to acute isolated right ventricular infarction

BackgroundElectrocardiogram (ECG) is the first diagnostic tool physicians use in diagnosing acute myocardial infarction (MI). In this case report, we present a case where the initial ECG diagnosis was that of an acute anteroseptal MI but emergency coronary angiography showed that the infarct-related artery was a small non-dominant right coronary artery (RCA) instead of the anticipated left anterior descending artery (LAD). Isolated right ventricular (RV) infarction from a non-dominant RCA is rarely seen in clinical practice, and it may exhibit ECG changes that can be confused with an acute anteroseptal MI. It is important to appreciate the subtle differences in the ECG changes that occur in either of these two types of MI for appropriate diagnosis and treatment.Case presentationA 49-year-old non-smoking male with prior coronary stent implantation in LAD presented with acute chest pain and his pre-hospital ECG indicated an anteroseptal STEMI possibly due to stent thrombosis, but an emergency angiogram showed patent LAD and Circumflex arteries. There was however thrombotic occlusion of the right, non-dominant coronary artery, which was revascularized with a drug-eluting stent. The patient’s chest pain and ST elevations resolved, and subsequent echo showed moderate RV systolic dysfunction in keeping with RV myocardial infarction.DiscussionRV myocardial infarction is usually due to an occlusion of the dominant RCA proximal to the origin of its RV wall branch, which often results in inferior ST elevation with reciprocal anterior ST depression. The ST elevation over V1 which would accompany RV infarction is often masked due to the more dominant electrical forces of inferior and posterior LV wall infarction. Our case demonstrates that in isolated RV infarction due to non-dominant proximal RCA occlusion, anterior ST elevation can be seen over V1-3, being most prominent in V1, which overlies the right ventricle, and resolved after restoring flow to the RCA. Spatial vector analysis of the ECG or right-sided ECG leads would be helpful to aid the diagnosis of RV infarction when clinical suspicion is present, for example when there is significant hypotension, raised jugular venous pressure but clear lung fields or deterioration after nitrate administration.

Cardiac toxicity of EGFR – 3rd generation TKI in patients with metastatic non-small cell lung cancer. Case report and literature data update

Purpose: The incidence of bronchopulmonary cancer has increased significantly in recent decades, especially in developed countries, and today it is the leading cause of death in men and the 3rd in women. The toxicities of tyrosine kinase inhibitor therapy are varied, with cardiac toxicities at the top of the pyramid. Because of the occurrence of these toxicities, depending on their intensity, the dose must be reduced or even treatment stopped. Patient and method: We present the case of a 72-year-old patient, diagnosed in 2019 with non-small bronchopulmonary neoplasm with histology of adenocarcinoma with EGFR mutation, stage IV. Results: In the oncology committee, it is decided to start targeted therapy with tyrosine kinase inhibitors of the first generation, Erlotinib, with a partial response to the treatment in the imaging evaluations, continued treatment until November 2020 when the T790M resistance mutation is detected. According to the new NCCN guidelines, therapy with the third-generation EGFR-TKI, Osimertinib, is initiated. In September 2021, the patient developed a non-ischemic acute antero-septal myocardial infarction that was complicated by LV apical aneurysm and severe LV systolic dysfunction, associated with therapy with tyrosine kinase inhibitors. Osimertinib treatment is stopped and third-line treatment with Vinorelbine is initiated. Conclusions: Investigation and permanent monitoring of patients, in treatment with 3rd generation tyrosine kinase inhibitors, who may develop cardiac toxicities, but also a good management of these toxicities, lead to both increased survival and improved status of performance.

Anabolic Androgenic Steroids-Induced Acute “Tombstone” ST-Segment Elevation Myocardial Infarction

Anabolic-androgenic steroids (AAS) are frequently used to treat a wide variety of pathological medical conditions including but not limited to hypogonadism, aplastic anemia, and metastatic breast cancer. Nonetheless, the abuse of AAS continues to rise among professional and recreational athletes despite their deleterious adverse effects. Here, we report a 34-year-old male, with a history of nonmedical use of AAS for 2 months, who had persistent severe retrosternal chest pain. His electrocardiogram was suggestive of acute anteroseptal ST-segment elevation myocardial infarction. He underwent urgent coronary angiography which revealed a thrombotic burden in the left anterior descending artery without underlying atherosclerosis.

Assessment of Regional Wall Motion Abnormality in Patients with Acute Anteroseptal ST Segment Elevation Myocardial Infarction

Post myocardial infarction (MI) short and long term clinical outcome is largely determined by the size of the infarcted area. It is generally assumed that as the lead involvement in the 12 lead electrocardiography (ECG) is less in anteroseptal ST segment elevation myocardial infarction (AS-STEMI), where ST segment elevation (STE) is limited to leads V1 to V3, myocardial damage is likely to be less. This study was intended to assess regional wall motion abnormality (RWMA) in acute anteroseptal STEMI patients. 90 patients with AS-STEMI admitted in between October 2012 and September 2013, were included. For each patient, a transthoracic echocardiogram (TTE) was performed within 24-48 hours of MI and was interpreted by an independent investigator blinded to the patient’s ECG data.The mean (± SD) age of the patients was 51.57 (± 12.02) years with mean (± SD) age of the patients was 52.58 (± 12.02) years with a range of 23 - 80 years. There were 91.1% male and 8.9% female. The mean (± SD) EF% was 38.80 %( ± 5.78). All the segments of left ventricle, except basal and mid inferolateral segments, were affected in anteroseptal STEMI. So, the term AS-STEMI may be a misnomer, as it implies that only the anteroseptal segments of the left ventricle are involved. This study shows that regional dysfunction in patients with AS-STEMI extends beyond the anteroseptal region and may be it is as much extensive as extensive anterior myocardial infarction. So, any patients with anterior wall involvement should be treated with utmost importance.
 University Heart Journal Vol. 15, No. 1, Jan 2019; 28-33

Incidence of left ventricular thrombus formation in acute and chronic anteroseptal myocardial infarction

Incidence of left ventricular thrombus formation in acute and chronic anteroseptal myocardial infarction

Spontaneous closure of ventricular septal perforation following percutaneous coronary intervention for acute myocardial infarction

We report on an 84-year-old woman with anteroseptal acute myocardial infarction. Emergency coronary angiography revealed the occlusion of proximal left anterior descending artery without collateral circulation, and percutaneous coronary intervention...

O16-3 - A Case of Intractable Ventricular Fibrillation after Acute Myocardial Infarction Successfully Treated with Central Extracorporeal Membrane Oxygenation

The patient was a 42-year-old man with acute anteroseptal myocardial infarction which was treated with percutaneous coronary intervention at the other hospital. On the 9th hospital day, he suffered from intractable ventricular fibrillation; an extracorporeal mambrane oxygenation (ECMO) was inserted from the femoral. The patient was then transferred to our hospital. He was treated with catecholamines, water-loading, transfusion and continuous renal replacement therapy for cardiac shock and acute kidney injury, although, progressive anemia and expanding retroperitoneal hematoma remained. The results of computed tomography and internal pressure of the bladder suggested that he should have abdominal compartment syndrome. The ECMO was replaced from the femoral to central cannulation, which led to successful bleeding control, and removed one week later. The patient was treated with medications and rehabilitation therapy. Two months later, his renal function was improved; the patient was discharged on the 105th hospital day. Here, we report the suggestive case with some literature reviews.

Case of a Large Dissecting Intramyocardial Hematoma Treated Conservatively

Case of a Large Dissecting Intramyocardial Hematoma Treated Conservatively

Acute Anteroseptal Myocardial Infarction after a Negative Exercise Stress Test.

A myocardial infarction is a rare complication which can occur after an exercise stress test. We report a 48-year-old male who was referred to the Mildura Cardiology Practice, Victoria, Australia, in August 2014 with left-sided chest pain. He underwent an exercise stress test which was negative for myocardial ischaemia. However, the patient presented to the Emergency Department of the Mildura Base Hospital 30 minutes after the test with severe retrosternal chest pain. An acute anteroseptal ST segment elevation myocardial infarction was observed on electrocardiography. After thrombolysis, he was transferred to a tertiary hospital where coronary angiography subsequently revealed significant left anterior descending coronary artery stenosis. Thrombus aspiration and a balloon angioplasty were performed. The patient was discharged three days after the surgical procedure in good health.

Myocardial Infarction in a Young Patient After Acute Exposure to Carbon Monoxide.

Carbon monoxide (CO) is an odorless, colorless, clear gas that attaches to the hemoglobin (Hb). Its affinity for Hb is approximately 200 times higher than that of oxygen, and CO blocks the capacity of Hb to carry oxygen (1). One of the most important effects of CO is tissue hypoxia, especially in the parts of tissues with the highest demand for oxygen and the lowest metabolic stores, such as the brain and heart, which are therefore more vulnerable. CO intoxications are usually expressed as neurological events, but cardiological events can also occur (2). Myocardial injury may arise via electrical, functional, and morphological changes in the heart through severe general tissue hypoxia; there may be a direct toxic effect on the myocardial mitochondria promptly after exposure, or this may be delayed for several days (3). CO can induce a tendency toward coronary vasospasm and thrombus formation by slowing the bloodstream, increasing the permeability of the vessel walls, and increasing platelet aggregability and polycythemia; these factors are also responsible for myocardial damage in patients with CO poisoning (4). In addition, oxygen radical formation and subsequent lipid peroxidation, as well as induction of cellular apoptosis, are also potential explanations for the cardiotoxicity of CO (2, 5). Cardiac involvement encompassing angina attack, myocardial infarction, heart failure, cardiogenic shock, and arrhythmias, such as ventricular extrasystoles, atrial fibrillation, bradycardia, and atrioventricular block in CO poisoning was first noted by Lippi (5). However, 50% or more of the circulating form of carboxyhemoglobin can lead to patchy myocardial necrosis, a CO-Hb level of ≥ 25% is considered an indication for the use of hyperbaric oxygen or advanced treatment (6, 7). Acute myocardial infarction (AMI) is a clinical condition occurring suddenly but resulting from a long-term decrease in the amount of oxygen present in the myocardium. Its most common cause is atherosclerotic disease of the coronary arteries. AMI associated with CO poisoning occurs very rarely. In this letter, a young person who did not have known coronary atherosclerotic disease and had AMI due to exposure to CO is presented with the aim of drawing attention to the fact that CO poisoning which occurs commonly throughout the world may lead to AMI. A 27-year-old male patient lost consciousness while struggling against fire in the workplace and entered cardiac arrest. After undergoing resuscitation by the 112 emergency service, he was brought to emergency intubated with unconscious and admitted. Upon admission to the hospital, ventilation with 100% oxygen was continued. The patient’s Glasgow coma score was 4, and noradrenaline infusion was initiated owing to hypotension. Arterial blood gas analysis was performed, and a CO-Hb value of 22% was detected. On initial electrocardiogram (ECG), ventricular tachycardia and other alterations were observed. The patient was diagnosed with anteroseptal AMI. Emergency angiographic and primary percutaneous interventions were performed; it was observed that Left anterior descending (LAD) as completely obstructed, (Figures 1 and 2) and a stent was placed (Figures 3 and 4). The patient further stabilized and was prepared for and transferred to hyperbaric oxygen therapy. Thorax computed tomography (CT) was taken and pneumothorax and trachea rupture was observed, probably due to resuscitation. No intervention was considered necessary except for chest tube insertion by the Chest Surgery Department The patient was extubated on the 11th day after admission to intensive care unit and transferred to the infectious diseases clinic. Identifying cardiotoxicity in patients with CO poisoning can be difficult. This report of a rare case should remind physicians

Abstract 14124: A Marked Increase in Myocardial Oxidative Stress Associated With Sympathetic Hyperactivity is Related to Transient Myocardial Dysfunction in Patients With Takotsubo Cardiomyopathy

Introduction: Sympathetic hyperactivity is considered as one of the most likely pathogenic mechanism in takotsubo cardiomyopathy (TC). However, little is known about the relationship between sympathetic hyperactivity and myocardial oxidative stress (OS). Hypothesis: We hypothesized that cardiac sympathetic hyperactivity was associated with cardiac myocardial OS, and OS related to transient myocardial dysfunction in patients with TC compared with acute anteroseptal myocardial infarction (AMI). Methods: In 8 TC patients and 8 AMI patients (NYHA 3), ECG, echocardiography, cardiac catheterization and serial measurements of plasma catecholamines, urinary (U) 8-hydroxy-2’-deoxyguanosine (8-OHdG) as a marker of OS and plasma CPK were performed for two weeks from onset. Results: Blood sampling from coronary sinus (CS) and aorta (Ao) at 1st day showed that norepinephrine (NE) levels and 8-OHdG level in CS were significantly higher than those in Ao and peripheral blood, indicating that an increase in myocardial OS was associated with cardiac sympathetic hyperactivity. NE levels in peripheral blood were peaked out at 1st day and 2-times higher in TC than in AMI within a week, while the max CPK value in TC was significantly lower than that in AMI. Dual scintigraphy of 201Tl and 123I-meta-iodobenzylguanidine was performed at 7th day showed that cardiac sympathetic nervous injury was much larger than myocardial perfusion damage in all TC patients. U-8OHdG level (ng/mg Cr; normal range:<10.0) in TC was elevated in parallel with the profile of plasma NE level (1st day: 65.6±24.5, 4th day: 19.1±8.3, 7th day: 16.4±9.1), while it was decreased to almost normal range after percutaneous coronary intervention for left anterior descending artery in AMI (1st day: 24.3±13.8, 4th day: 9.8±3.4, 7th day: 12.3±2.7). Interestingly, difference in serum 8-OHdG levels (CS vs Ao) in TC increased proportionally with wall motion score (WMS) as an index of LV dysfunction (R=0.93, p<0.001), while difference in serum NA levels (CA vs Ao) in TC did not. U-8OHdG level in TC was positively correlated with WMS at each day (1st day, 7th day). Conclusions: These findings suggest that myocardial OS induced by cardiac sympathetic hyperactivity may play a critical role in transient LV dysfunction in TC.

Abstract 11749: Prognostic Value of Left Ventricular Global Longitudinal Strain and Ejection Fraction in Patients With Non-ischemic and Ischemic Heart Disease

Background: Both Left ventricular (LV) global longitudinal strain (GLS) and LV ejection fraction (LVEF) are useful parameters for assessment of LV function. The aim of this study is to confirm the prognostic value of them in patients with non-ischemic and ischemic heart disease. Methods: We studied 179 patients (DCM group: Age 61±15 years, 70 females, LVEF 33±9%) with non-ischemic dilated cardiomyopathy and heart failure symptom, and 97 patients (MI group: Age 66±13 years, 18 females, LVEF 45±7%) who were successfully treated with percutaneous coronary intervention for acute anteroseptal myocardial infarction. Echocardiography was used for LV GLS derived from 2D speckle-tracking method and LVEF with modified Simpson’s method. Outcome was assessed according to death and re-hospitalization with heart failure in the follow-up period. Results: 40 patients in DCM group and 10 patients in MI group experienced at least one event. In these 2 groups, significant differences in GLS and LVEF were found between patients with and without cardiac events (p<0.05). Kaplan-Meier analysis showed patients with worse GLS had an unfavorable outcome in both DCM and MI groups (p<0.05), but LVEF did not associated with outcome. Conclusion: LV GLS has the potential to predict the outcome with higher sensitivity than LVEF in patients with heart disease regardless of ischemic etiology.

Impact of reperfusion therapy and infarct localization on frequency of premature ventricular beats in acute myocardial infarction.

To determine the impact of infarct localization and types of reperfusion therapy on the frequency of ventricular premature beats (VPBs) in patients with acute myocardial infarction (AMI) and reduced left ventricular ejection fraction (LVEF). A total of 705 patients with acute ST elevation myocardial infarction (STEMI) were divided according to the infarct localization (anteroseptal, anterolateral, inferior and posterior) and reperfusion therapy (fibrinolysis or percutaneous coronary intervention with stenting) into two groups: LVEF<45% was an experimental group and LVEF>45% was a control group. The occurrence of VPBs<10 per hour was defined as a non-significant, and the occurrence of VPBs>10 per hour defined as a significant. In patients with fibrinolysis therapy and LVEF<45% significant number of VPBs were in anteroseptal (p=0.017), anterolateral (p<0.001) and posterior AMI (p<0.001), but in patients with percutaneous coronary intervention (PCI) and LVEF<45% significant number of VPBs were only in anteroseptal AMI (p=0.001) localization. In patients with reduced ejection fraction in AMI, treatment with PCI method has a better antiarrhythmic effect compared to fibrinolysis treatment.

Manifestation of latent left ventricular outflow tract obstruction caused by acute myocardial infarction: An important complication of acute myocardial infarction

BackgroundAlthough transient left ventricular outflow tract (LVOT) obstruction is reported as a complication with acute myocardial infarction (AMI), the mechanisms and features of LVOT obstruction in AMI are unclear. Methods and resultsHerein, we present two cases of transient LVOT obstruction with anteroseptal AMI. The features of these two cases were one-vessel disease (1-VD) of the left anterior descending artery (LAD) and maintenance of blood flow to the major septal branch (SB). Moreover, LVOT obstruction was revealed after dobutamine infusion in the chronic phase and the aorto-septal angle was low in these two cases, meaning that latent LVOT obstruction was due to sigmoid-shaped septum. ConclusionsLatent LVOT obstruction would be manifested in the acute phase of AMI. 1-VD of LAD and the maintenance of major SB blood flow are important factors with respect to the manifestation of latent LVOT obstruction.

Acute myocardial infarction in a 28-year-old man from embolized left atrial myxoma

Atrial myxoma has been reported as source of coronary emboli, a rare complication, causing acute myocardial infarction (MI). We report case of a 28-year-old male, who presented with acute chest pain, radiating to left arm, with sweating and palpitation. Transthoracic echocardiography (TTE) showed an irregular homogenous pedunculated mass of size 3.7 × 2.1 cm attached to the interatrial septum towards the base of the anterior mitral leaflet, prolapsing into left ventricle (LV) during diastole, but not obstructing the flow. Emergency coronary angiography revealed a tubular lesion (thrombus containing) in left anterior descending (LAD) coronary artery. The patient was diagnosed as acute anteroseptal MI due to LAD coronary artery embolization originating from left atrial myxoma. Coronary artery bypass graft (CABG) along with surgical resection of friable myxomatous mass was done. Histopathological examination was consistent with atrial myxoma. Present case justifies that atrial myxomas should be considered as a differential diagnosis while dealing with MI in young patients.

Very Late Stent Thrombosis After Four Year with Sirolimus Coated Stent

Coronary stents are very important place with decreased restenosis rates. Very late stent trombosis is a problem of drug eluting stents but underlying mechanism is not fully understood. Protection of very late stent trombosis can achieved by optimal use of dual antiplatalet therapy and pay attention while novel stent design project. In this case report we present a very late stent trombosis with the diagnosis of acute anteroseptal myocardial infarction.

Delayed closure of postinfarction ventricular septum defect in a patient with single vessel disease

Abstract A 65-year-old patient with a systolic murmur that developed five days after acute anteroseptal myocardial infarction was referred to our Institution. He had previously been treated with fibrinolytic therapy. The patient was in a stable hemodynamic condition when admitted, with sustained diuresis. Blood gas analysis revealed normal parameters, whereas a chest X-ray showed signs of pulmonary congestion. Transthoracic echocardiography revealed a 1.5×1.2 cm post-infarction ventricular septum defect (VSD) in the apical part of the septum. Because the patient’s hemodynamic conditions were stable, we decided to postpone the operative treatment to allow scarring of the infarcted area to make VSD repair feasible, thereby increasing the chance for success. Operative treatment was performed three weeks after admission. We performed closure of the VSD with a bovine pericardial patch. The patient was discharged in good condition and remained well three months after the surgery.

Electrocardiographic impacts of lung resection

IntroductionElectrocardiographic (ECG) changes accompanying lung resection have not been well investigated previously in a large controlled series of human adults. Thus, our current investigation was undertaken for a better understanding of the ECG changes associated with lung resection. Materials and MethodsMedical records of 117 patients who underwent lung resection (segmentectomy, lobectomy, or pneumonectomy) were reviewed. Their clinical course and ECGs were compared during early, intermediate and late postoperative course (<1month, 1month to 1year and >1year post-op respectively). ResultsPatients in the acute postoperative phase had higher heart rate, increased maximum P-duration and P-dispersion, increased incidence of atrial arrhythmias and frequent ST-T changes. P-vector and QRS-vector were significantly affected after the lung resections; the correlation being most consistent between the anatomical displacements and the QRS-vector in the majority of patients. The axial shifts also demonstrated a characteristic temporal relationship after left pneumonectomy (a leftward deviation in the acute, normal or slight rightward deviation in the intermediate and a rightward deviation in the late postoperative course). The precordial R/S transition is often affected due to the mediastinal shifts and the ECGs in patients after left lung resection may simulate acute anteroseptal myocardial infarction due to a delayed R/S transition. ConclusionThe understanding and recognition of the expected ECG findings after lung resection are imperative to avoid confusing these changes with other acute cardiopulmonary events which would prevent unnecessary further investigational work-up. These ECG changes are often dynamic and may bear a temporal relationship to the dynamic post-surgical changes in the thoracic anatomy.

Isolated right ventricular myocardial infarction misdiagnosed as anteroseptal myocardial infarction on ECG: a case report

In this article, we present a case with isolated right ventricular myocardial infarction (MI) who underwent coronary angiography on suspicion of acute anteroseptal MI detected on ECG; however, occlusion of the proximal right coronary artery (RCA) was detected. A female patient aged 65 years was brought to the emergency room due to loss of consciousness 1 hour before. From the patient's history, it was understood that she had undergone stent placement to her proximal RCA 5 days before. On ECG, a decreasing elevation in ST segment elevation from V1 to V4 was seen, and pathologic Q waves were present at DIII and AVF. A complete AV block was detected on ECG. In the coronary angiography, thrombosis of the stent in the proximal RCA was seen. Stenosis detected in the mid-left anterior descending artery was 50% and at the distal part was 60%. The circumflex coronary artery was found normal. Percutaneous transluminal coronary angioplasty was performed to the 95% thrombotic lesion in the stent of the proximal RCA, and full patency was established. In our case, a decreasing elevation in the ST segment elevation from V1 to V4 was seen. Right ventricular MI usually occurs by an acute stenosis of the non-dominant proximal RCA branch that does not receive collateral flow. In our case, RCA was codominant and an acute stenosis of the stent in the proximal RCA was present. The occlusion of the non-dominant RCA can appear as isolated right ventricular MI without causing a left ventricular infarct, since it does not feed the left ventricle.

Emergency surgery for extrinsic coronary compression after percutaneous pulmonary valve implantation

Coronary artery compression is a rare and potentially fatal complication after percutaneous pulmonary valve implantation. We report on a case of an acute antero-septal non-ST myocardial infarction secondary to the partial laceration of the conduit and the creation of a thrombus giving an extrinsic compression of left anterior descendent coronary artery after Melody valve implantation.