Subacute Anterior Myocardial Infarction Research Articles

Totally endoscopic trans-mitral removal of a left ventricular apical thrombus through right thoracotomy in a patient with subacute anterior myocardial infarction: a case report

BackgroundLeft ventricular thrombosis confers a life-threatening risk of systemic embolism; therefore, it requires prompt intervention. Although anticoagulation is the primary treatment, surgery is indicated in instances of large or/and mobile thrombus or when there is potential for recovery of ventricular contraction. However, standard left ventriculoplasty with thrombectomy carries risks of cardiac dysfunction due to left ventriculotomy.Case presentationA 70-year-old man developed chest pain and vomiting 3 weeks before presenting to our hospital. A chest radiograph showed substantial cardiomegaly and mild pulmonary congestion; N-terminal pro-brain natriuretic peptide (5698 ng/L) was substantially increased, and troponin T (56 ng/L) levels were slightly above reference values. Transthoracic echocardiography showed akinesis of the anteroseptal and apical segments with an ejection fraction reduced to approximately 20%. We diagnosed subacute myocardial infarction and initiated pharmacotherapy. On hospital day 7, coronary angiography revealed a left anterior descending artery lesion with 99% stenosis; percutaneous coronary intervention was successfully performed the next day. That same day, transthoracic echocardiography revealed a large mobile left ventricular apical thrombus without any left ventricular aneurysm, and heparin therapy was initiated. On hospital day 10, three-dimensional computed tomography confirmed the location of an apical thrombus, and we planned a fourth intercostal approach. A thrombectomy was performed on hospital day 11 using an endoscopic trans-mitral approach with a right thoracotomy to avoid a left ventriculotomy. The patient was discharged from intensive care on postoperative day 2 under heparin and warfarin therapy. The subsequent postoperative course was uneventful, and he was discharged on postoperative day 14 with a vitamin K antagonist. At the 6-month follow-up, there was no recurrence of thrombus in the left ventricle and Ejection Fraction had improved to 46%.ConclusionsTotally endoscopic thrombectomy via a trans-mitral approach through right thoracotomy was effective for a left ventricular thrombus. When concomitant coronary artery bypass grafting or left ventriculoplasty are not required, this procedure can be an effective option.

Coronary thrombus in 34-year-old female patient with 4G/4G polymorphism in the PAI-1 gene

Genetic factors and hypofibrinolytic state may contribute to the likelihood of developing in myocardial infarction (MI) in young women rather than traditional risk factors. High plasminogen-activator inhibitor-1 (PAI-1) level and PAI-1 gene polymorphism have been shown to be associated with thrombotic events such as myocardial infarction, deep venous thrombosis, and stroke. We determined 4G/4G polymorphism in a 34-year-old female patient with subacute anterior myocardial infarction and coronary thrombus in left anterior descending artery on coronary angiogram.

Sub-acute anterior myocardial infarction due to the discontinuation of warfarin in a patient with aortic valve prosthesis: what is the best treatment

Acute myocardial infarction (MI) is a common entity in patients due to the atherosclerotic plaque rupture or coronary embolism. We present a patient who had a mechanical aortic valve and was admitted to the hospital for a sub-acute anterior ST elevation myocardial infarction due to the discontinuation of warfarin. In case of persistent thrombus formation despite aggressive antithrombotic and anticoagulant therapy, thrombus aspiration, angioplasty and stenting should be preferred rather than conservative approach.

Hemarthrosis Caused by Enoxaparin at Patient Presenting with Acute Myocardial Infarction

Enoxaparin, a low-molecular-weight heparin, is one of the most useful anticoagulant. Treatment that have large using area including myocardial infarction. In this case a 65 years old male patient presenting with myocardial infarction and hemarthrosis caused by enoxaparin to be told. Patient admitted to the emergency service by angina and referred to us. After the first evaluation he hospitalized because of subacute anterior myocardial infarction. Including liver and renal function tests, platelets were normal. Medical treatment put in order. Enoxaparin was choosing as anticoagulant. During the treatments there was no problem but after last enoxaparin dose oedema was occurred at is left knee. We consulted him to orthopaedics. They did arthrocentesis to determine if it was hematoma or septic arthritis. Complete blood cells count evaluated. WBC 6.1, plt 45, Hb 10.6 detected. So it was hemarthrosis accepted. They recommend elastic bandage, elevation and cold execution. Enoxaparin treatment maintained. The day after oedema regressed. Coronary angiography done and stent implanted. Enoxaparin stopped Oedema followed by daily period, it gone back day by day. After the end of myocardial infarction treatment, he discharged.

Sub-acute anterior myocardial infarction due to the discontinuation of warfarin in a patient with aortic valve prosthesis: what is the best treatment

Sub-acute anterior myocardial infarction due to the discontinuation of warfarin in a patient with aortic valve prosthesis: what is the best treatment

Unsuccessful primary percutaneous coronary intervention leading to left ventricular pseudoaneurysm

Left ventricular (LV) pseudoaneurysm is usually a very rare complication of transmural myocardial infarction. It starts in a few weeks that following transmural infarction and it has various clinical presentations. Congestive heart failure, mitral regurgitation, ventricular tachyarrhythmia, systemic embolism and cardiac rupture are the most important manifestations. Here we discuss a 54-year-old woman who had a history of unsuccessful revascularization following subacute anterior myocardial infarction, admitted our institution with acute pulmonary edema. Echocardiography revealed a wide apical pseudoaneurysm with moderate mitral regurgitation. After medical stabilization of acute heart failure, open heart surgery advised to the patient.

Ventricular septal rupture: A rare post-myocardial infarction complication with a very high mortality rate

A 69-year-old diabetic and hypertensive man with no prior cardiovascular history was admitted to the emergency department complaining of dizziness and extreme fatigue. He had noticed worsening dyspnea for a few days without chest pain. The electrocardiogram showed deep Q waves with persistent ST-segment elevation in the anterior leads (Fig. 1a). Physical examination revealed a pansystolic murmur and systemic hypoperfusion signs including skin pallor and cold extremities and vital signs showed hypotension (85/66), sinus tachycardia (120 bpm) and low oxygen saturation (83% with ambient air). Troponine I (62 ug/L, n < 0.09 ug/L), creatine kinase (1447 U/L, n < 222 U/L) and LDH (2838 U/L, n < 240) were concordant with a sub-acute presentation. A transthoracic echocardiography (TTE) confirmed the suspicion of an extensive antero-septo-apical akinesia with an apical aneurysm and a severly impaired left ventricular ejection fraction (35%). The TTE also revealed a left-toright shunt (maximal systolic gradient of 28 mmHg) at the apex due to a 7 mm diameter ventricular septum rupture (VSR) (Fig. 1b). On the basis of these findings, we concluded to cardiogenic shock in the context of a VSR complicating a sub-acute anterior myocardial infarction (MI). An emergency coronary angiography revealed total occlusion of the mid left anterior descending coronary artery (LAD) (Fig. 1c) with no collateral flow. No revascularization was attempted since no significant benefit was

Coronary embolism in a patient with massive left atrial thrombus and mechanical valve thrombus: hybrid treatment with surgery and percutaneous intervention

A 67-year-old female was admitted to the emergency department with chest pain for the last 24 hours. She had a history of rheumatic mitral stenosis and had received a mechanical mitral valve (24-mm bi-leaflet St. Jude valve) three years ago. She had been inadequately anti-coagulated for the last two months. At the time of presentation, her international normalized ratio (INR) was 1.02. The electrocardiogram (ECG) revealed atrial fibrillation with a heart rate of 130 beats per minute, right bundle brunch block, and precordial ST segment elevation (Fig. A). Transthoracic echocardiography (TTE) revealed hypokinesis of the apex, apical and mid septal walls, with an ejection fraction of 40%, in normal range of mitral valve area of 2.3 cm2; the peak and mean transmitral gradients were 15 mmHg and 7 mmHg, respectively. Transesophageal echocardiography (TEE) showed up to 1.4 cm fibrillar thrombi on the mitral prosthetic valve and a huge thrombus completely filling the left atrial walls except for the mitral prosthetic valve line and extending to the right and left pulmonary vein ostia on the posterior wall and into the appendix (Fig. B, Video file 1*). Based on the symptom of chest pain and ECG findings, she was diagnosed as subacute anterior myocardial infarction and underwent coronary angiography, which revealed total occlusion of the proximal segment of the left anterior descending artery. The patient was anticoagulated with unfractionated heparin. Lesion wiring and predilatation were done using 2.0x12 and 2.5x20 mm balloons. A 2.75x32 mm bare metal stent was implanted (Fig. C). Heparin was infused for 10 days with adjustment of activated partial thromboplastin time (aPTT) level to 50-70 seconds. Because the follow-up TEE showed no regression of the thrombus on the mechanical valve or of the left atrial thrombus, surgical thrombectomy was planned. Median sternotomy was performed and huge left atrial thrombus fragments (7.5x3 cm, 6x4 cm, 6.5x5 cm, 1.7x0.7 cm, and 1.5x0.7 cm) were excised without mechanical valve replacement (Fig. D). The patient was discharged with optimal anticoagulation. She was asymptomatic and had normal mechanical valve functions on TTE examination at the twomonth follow-up. 784

RETRACTED: Successful treatment for a giant coronary saccular aneurysm complicated with myocardial infarction in a patient with Behcet's disease: Case report

We report on a 35-year-old man, with known Behcet's disease, who was admitted with the diagnosis of subacute anterior myocardial infarction. Coronary angiography revealed an isolated giant saccular aneurysm at the mid segment of left anterior descending coronary artery with a tight stenosis. The patient was successfully treated with covered stent on the first day of admission.

Hybrid closure of postinfarction ventricular septal rupture enlargement after transcathether closure with Amplatzer occluder

Ventricular septal rupture (VSR) is nowadays a rare complication of myocardial infarction (MI), but with a mortality rate still very high. Urgent surgical correction is recommended, although in specific cases percutaneous closure of a post-infarct VSR is a therapeutic option or a bridge to surgical correction. We report a case of an 80-year-old woman, with a subacute anterior MI with an antero-septal VSR. Rapid clinical deterioration in a high-surgical-risk patient led us to attempt percutaneous VSR closure at day 8 post MI. A 16-mm Amplatzer post-infarction (PI) muscular VSD closed the defect with intra-cardiac echocardiography guidance, that allowed conscious sedation. Clinical and haemodynamic improvement was immediate. Unfortunately, a small orifice distal to the device persisted, which enlarged to 8 mm over the following days, with a Qp/Qs shunt of 1.9. At day 17 post MI, the VSR was surgically closed by suturing the Amplatzer device to the septum. A residual shunt was evident, but with no progression, being the patient discharged in NYHA class I. Percutaneous closure of a post-MI VSR as a bridge to surgery is a therapeutic option in patients with high surgical risk, allowing haemodynamic stabilization and thus gaining time for a further surgical intervention if needed, improving these patients grim prognosis. Intra-cardiac echocardiography for monitoring the percutaneous procedure instead of a transoesophageal approach, as well as the surgical technique, make this case unique.

The Importance of Cardiac Biomarkers on Remodelling After Myocardial Infarction

BackgroundThe purpose of this study is to evaluate the importance of tenascin-C ( TNC), N-terminal pro brain natriuretic peptide (NT-proBNP) and C-reactive protein (CRP) on LV remodelling after myocardial infarction (MI).MethodsFifty-seven stable patients with subacute anterior MI who had total or subtotal occlusion in the infarct-related left anterior desending artery in coronary angiography were enrolled the study. 18 of patients who had total occlusion received only medical theraphy, 19 of patients who had total occlusion received successful PCI+ medical theraphy and 20 of patients who had subtotal occlusion received successful PCI+ medical theraphy. Left ventricular volumes and ejection fractions (EF) were measured with echocardiography. Serum TNC, NT-proBNP and CRP levels were measured at admission and a month after treatment.ResultsThere was significant increase in LV end-diastolic volume (LVEDV) and LV end-systolic volume (LVESV) baseline to follow-up in total-PCI group. Baseline to follow-up; a borderline significant increase was observed in LVEDV in the total-medical group. No significant difference was seen in LV volumes and EF in the subtotal-PCI group. NT-proBNP, TNC and CRP levels were decreased in all groups. The decrease in NT-proBNP and CRP values were significant in the total-medical and subtotal-PCI group but in the total-PCI group they were not significant. The decrease of TNC was significant in all groups but the lowest decrease was seen in the total-PCI group.ConclusionTNC, NT-proBNP and CRP reflect LV remodelling in accordance with echocardiography after MI.KeywordsTenascin-C; NT-pro BNP; CRP; Remodelling; Myocardial infarction

Acute myocardial infarction due to a large coronary aneurysm in Behçet’s disease

A 32-year-old man with Behcet’s disease presented with typical chest pain of 36-hour onset. His physical examination was normal. Levels of cardiac enzymes and troponin I were increased. Electrocardiography showed ST-segment depression in precordial leads. An emergency invasive intervention was initiated with the diagnosis of subacute anterior myocardial infarction. Coronary angiography showed a large aneurysm in the proximal segment of the left anterior descending artery with TIMI 0 flow (Fig. A). The large aneurysm was also demonstrated by multislice computed tomography (Fig. B, C). The patient underwent an emergency surgical intervention for repair of the coronary aneurysm. Behcet syndrome is a vasculitis that can affect all the arteries and veins. Coronary artery aneurysms are uncommon in Behcet’s disease. Ali Dogan Ahmet Celik† Serap Dogan# Ibrahim Ozdogru

The Relationship between Tenascin-C Levels and the Complexity of Coronary Lesion after Myocardial Infarction

The increase of tenascin-C levels after myocardial infarction has been demonstrated by previous studies. The relationship between tenascin-C and the grade of stenosis in the infarct-related coronary artery was indeterminate. The aim of this study was to evaluate the relationship between tenascin-C levels and total occlusion after acute myocardial infarction. Fifty-nine patients with subacute anterior myocardial infarction were divided into two groups according to their having a totally or subtotally occluded left anterior desending artery. Plasma tenascin-C, troponin I, CK-MB, uric acid, mean platelet volume, and lipid profile levels were also measured. The history of the smoking rate, hypertension and diabetes mellitus were similar in both groups. Hemoglobin, mean platelet volume, serum creatinine, CK-MB, troponin I, serum lipid profile and uric acid levels were similar in the two groups. The CRP and tenascin-C levels were significantly higher in the total occlusion group. Tenascin-C levels were highest in patients with proximal LAD total occlusion and lowest in patients with subtotal LAD occlusion. The tenascin-C levels were correlated with the grade of stenosis (r = 0.602, p < 0.001). This study demonstrates that higher tenascin-C levels were related with the total occlusion and inflammation after MI.

Short-Term Left Ventricular Remodeling After Revascularization in Subacute Total and Subtotal Occlusion With the Infarct-Related Left Anterior Descending Artery.

BackgroundLarge randomized studies revealed that percutaneous coronary intervention has no clinical benefit in patients with total occlusion. The purpose of this study is to evaluate left ventricular remodelling after PCI for total and subtotal infarct-related left anterior desending artery in stable patients who have not received trombolytic theraphy.MethodsSixty stable patients with subacute anterior myocardial infarction who have total or subtotal occlusion in the infarct-related left anterior descending artery were enrolled the study (20 patient in the total-medical group, 20 patient in the total-PCI group and 20 patient in the subtotal-PCI group). All patients’ left ventricular diameters, volumes and ejection fractions measured at admission and after a month.ResultsThe necrotic segment number in scintigraphy were similar in three groups. In the total-PCI group, there were significant increases in left ventricular diastolic diameter, left ventricular end-diastolic volume and left ventricular end-systolic volume at first month. A borderline significant increase was observed in LVEDV in the total-medical group at first month. No significant difference was seen in all echocardiographic parameters in the subtotal-PCI group at a month after discharge. The percentage of increase in LVEDV was significantly higher and the percentage of increase in LVESV was borderline significantly higher in the total-PCI group than the other groups.ConclusionsIn stable patients, PCI for total occlusion in the subacute phase of anterior MI causes an increase in LV remodeling. Nevertheless PCI for subtotal occlusion in the subacute phase of anterior MI may prevent LV remodeling.

The longest documented left main coronary artery

The left main coronary angiography (LMCA) ranges from 3 to 6 mm in diameter and may be up to 10 to 15 mm in length in humans. We here report a case of the longest LMCA (38 mm) in a 60-year-old woman with subacute anterior myocardial infarction. In coronary angiography and coronary computerized tomography LMCA was measured to be 38 mm long.

Energetic differences between viable and non-viable myocardium in patients with recent myocardial infarction are not an effect of differences in wall thinning— a multivoxel 31P-MR-spectroscopy and MRI study

To evaluate multivoxel (31)P-MR spectroscopy (MRS) for assessment of energy metabolism in patients with myocardial infarction (MI) in correlation to left ventricular (LV) wall thickness and the outcome of revascularization. Thirty patients with subacute anterior myocardial infarction and planned revascularization were enrolled. 3D-chemical shift imaging was applied to determine PCr/ATP ratios in two areas: infarcted/anterior and noninfarcted/septal myocardium. MRI was used to evaluate LV function and wall thickness, and was repeated 6 months after revascularization to assess myocardial viability. Fifteen volunteers were controls. Fifteen patients showed normalization of wall motion abnormalities after revascularization (Group 1; viable), 15 not (Group 2; non-viable). Regarding infarcted/anterior myocardium, Group 2 had lower PCr/ATP ratios (0.81 +/- 0.60 vs 1.17 +/- 0.25), and PCr/ATP ratios were reduced in both groups compared to controls (1.45 +/- 0.29). Regarding noninfarcted/septal myocardium, again Group 2 had lower ratios (0.93 +/- 0.53 vs 1.31 +/- 0.38); however, compared to controls (1.51 +/- 0.32) a reduction of PCr/ATP ratios was only found in Group 2. For both myocardial regions, no correlations between PCr/ATP ratios and LV wall thickness were detected. The more severe energetic alteration in irreversibly damaged myocardium is not an effect of differences of wall thinning. Additional alterations of noninfarcted, adjacent myocardium can be detected.