Acute inferior myocardial infarction combined with papillary muscle rupture: A case report. / 急性下壁心肌梗死合并乳头肌断裂1例.

The incidence of acute myocardial infarction (AMI) is increasing. Acute papillary muscle rupture is one of the serious and rare mechanical complications of AMI, which occurs mostly in inferior and posterior myocardial infarction. A patient with acute inferior myocardial infarction developed pulmonary edema and refractory shock, followed by cardiac arrest. After cardiopulmonary resuscitation (CPR), revascularization of criminal vessels was carried out by emergency percutaneous transluminal coronary angioplasty (PTCA) under the support of intra-aortic balloon pump (IABP) and extra corporeal membrane oxygenation (ECMO). Although the patient was given a chance for surgery, his family gave up treatment due to unsuccessful brain resuscitation. It reminds that mechanical complications such as acute papillary muscle rupture, valvular dysfunction and rupture of the heart should be highly suspected when cardiogenic pulmonary edema and cardiogenic shock are difficult to correct in acute inferior myocardial infarction. Echocardiogram and surgery should be put forward when revascularization of criminal vessels is available.

Autoimmune limbic encephalitis mimicking inferior myocardial infarction on ECG.

A man in his 60s with prior history of coronary artery bypass graft was found collapsed, unresponsive on the floor by family. ECG demonstrated an inferior ST elevation myocardial infarction. However, coronary angiography was negative for a culprit lesion. A faciobrachial dystonic seizure was witnessed during his hospitalisation, ultimately leading to a diagnosis of leucine-rich glioma-inactivated 1 (LGI-1) autoimmune encephalitis. It is likely that neurogenic stunned myocardium led to this presentation.

Successful percutaneous coronary intervention with extracorporeal membrane oxygenation in a patient with acute inferior wall myocardial infarction complicated by electrical storm, cardiogenic shock, and cardiac arrest: a case report.

BACKGROUND: High-risk patients with coronary heart disease who develop acute myocardial infarction (AMI) have severe coronary lesions. If severe complications occur, such as malignant ventricular arrhythmia, cardiogenic shock, and cardiac arrest, implementation of emergency percutaneous coronary intervention (PCI) may be hindered, leading to a higher perioperative mortality rate. Extracorporeal membrane oxygenation (ECMO) can pave the way for rapid myocardial reperfusion therapy. When cardiac arrest occurs, hemodynamic support with ECMO can facilitate revascularization with PCI, which can increase the time available for further salvage and treatment and reduce intraoperative risk during PCI. CASE PRESENTATION: Herein, we report a case of a 61-year-old man with AMI who suffered electrical storm of sustained malignant ventricular fibrillation, cardiogenic shock, and cardiac arrest and was successfully treated with PCI with ECMO support. During PCI, repeated aspiration and removal of the right coronary artery thrombus were performed, and blood flow was restored after right coronary artery balloon dilation. One episode of defibrillation was delivered to restore sinus rhythm. Then, stents were implanted in the distal and proximal right coronary artery lesions to achieve revascularization. After PCI with ECMO support, irreversible malignant arrhythmia returned to sinus rhythm through coronary perfusion, which prevented death following unsuccessful cardiopulmonary resuscitation. After applying active treatments, including anti-shock, mechanical ventilation, anti-inflammation, and organ support, the patient was discharged after his condition and vital signs stabilized. The patient was followed up once a week after hospital discharge, and his cardiopulmonary function recovered well. CONCLUSIONS: With ECMO support, PCI should be performed immediately in patients with inferior wall AMI complicated by electrical storm of sustained ventricular fibrillation, cardiogenic shock, and cardiac arrest to facilitate stent placement, achieve complete revascularization, restore coronary perfusion, and avoid death.

Longitudinal Evaluation of Mitral Valve Leaflet Remodeling After Acute Myocardial Infarction: Serial Quantitation of Valve Geometry Using Real-Time 3-Dimensional Echocardiography.

BACKGROUND: Recent animal studies have suggested that mitral valve (MV) leaflet remodeling can occur even without significant tethering force and that the postinfarct biological reaction would contribute to the histopathologic changes of the leaflet. We serially evaluated the MV remodeling in patients with anterior and inferior acute myocardial infarction (MI), by using 2- and 3-dimensional transthoracic echocardiography. Additional histopathologic examinations were performed to assess the leaflet pathology. METHODS: Sixty consecutive first-onset acute MI (anterior MI, n=30; inferior MI, n=30) patients who underwent successful primary percutaneous coronary intervention were examined (1) before primary percutaneous coronary intervention, (2) at 6-month follow-up, and (3) at follow-up 1 year or later after onset. MV complex geometry including MV leaflet area and thickness was analyzed using dedicated software. Additional histopathologic study compared 18 valves harvested during surgery for ischemic mitral regurgitation (MR). RESULTS: MV area and thickness incrementally increased during the follow-up period. MV leaflet area significantly increased (anterior MI: 5.59 [5.28-5.98] to 6.54 [6.20-7.26] cm2/m2, P<0.001; inferior MI: 5.60 [4.76-6.08] to 6.32 [5.90-6.90] cm2/m2, P<0.001), and leaflet thickness also increased (anterior MI: 1.09 [0.92-1.24] to 1.45 [1.28-1.60] mm/m2, P<0.001; inferior MI: 1.15 [1.03-1.25] to 1.44 [1.27-1.59] mm/m2, P<0.001); data represent onset versus ≥1 year. Larger annuls, larger tenting, and a reduced leaflet area/annular ratio with smaller coaptation index were observed in patients with persistent ischemic MR compared with those without significant ischemic MR. Histopathologic examinations revealed that MV thickness was significantly greater in chronic ischemic MR compared with acute ischemic MR (1432.6±490.5 versus 628.7±278.7 µm; P=0.001), with increased smooth muscle cells and fibrotic materials. CONCLUSIONS: MV leaflet remodeling progressed both in area and thickness after MI. This is the first clinical study to record the longitudinal course of MV leaflet remodeling by serial echocardiography.

Type 2 Myocardial Infarction Resulted from the Left Thoracic Stomach.

The universal definition of myocardial infarction (MI) provides five subtypes of acute myocardial infarction (AMI). We present an interesting case of a type 2 myocardial infarction caused by the dilation of the left thoracic stomach.

Type 2 myocardial infarction resulted from the left thoracic stomach

Abstract The universal definition of myocardial infarction (MI) provides five subtypes of acute myocardial infarction (AMI). We present an interesting case of a type 2 myocardial infarction caused by the dilation of the left thoracic stomach.

Effects of Myocardial Perfusion Defect on the Frontal QRS-T Angle in Anterior Versus Inferior Myocardial Infarction.

Objective The frontal QRS-T angle on a 12-lead electrocardiogram (ECG) has recently become accepted as a variable of ventricular repolarization. We compared the effects of myocardial perfusion defect (MPD) on the frontal QRS-T angle between anterior and inferior myocardial infarction (MI) using single-photon emission computed tomography. Methods The frontal QRS-T angle was defined as the absolute value of the difference between the frontal plane QRS axis and T-wave axis. A QRS-T angle more than 90° was considered abnormal. Patients Forty-two patients with anterior MI and 42 age- and sex-matched patients with inferior MI were enrolled. For controls, 42 age- and sex-matched patients with no MPD were selected. Results The mean frontal QRS-T angles in anterior MI, inferior MI and control subjects were 94.7±46.2°, 26.7±22.1° and 27.0±23.2°, respectively. Compared with controls, the frontal QRS-T angle was larger in anterior MI subjects (p<0.001), and similar in value to that in inferior MI subjects (p=0.69). An abnormal QRS-T angle was frequent in the anterior MI subjects than the inferior MI subjects (55% vs. 2%, p<0.001). In anterior MI subjects, MPD was significantly associated with the T-wave axis (ρ=0.46, p=0.002) and QRS-T angle (ρ=0.47, p=0.002), but was not with the QRS axis (ρ=0.07, p=0.66). In inferior MI subjects, there were no associations between MPD and the ECG variables. Conclusion Our data suggest that the frontal QRS-T angle in inferior MI subjects is not increased as evidently as that in anterior MI subjects.

Postinfarction intramyocardial dissection, an interesting case report and systematic review.

Intramyocardial dissection (IMD) with ventricular septal rupture (VSR) following myocardial infarction (MI) is a rare subacute form of cardiac rupture. The evidence available in this regard is scarce. We aimed to share our experience and conduct a systematic review of previous cases. We searched the literature and performed a systematic review of previous cases. A total of 37 cases of IMD with VSR were included (1 our original and 36 literature cases). Mean age was 68 ± 8 years and 20 (54.1%) patients were male. Anterior and inferior MI were observed in 14 (37.8%) and 23 (62.2%) cases, respectively. The dissected area was the septum, RV, both septum and RV, or LV apex in 21 (56.8%), 9 (24.3%), 5 (13.5%), and 2 (5.4%), respectively. Apicoseptal and inferoseptal VSR were observed in 15 (40.5%) and 22 (59.5%) cases, respectively. At least one occluded artery was observed in 29 (90.6%) of cases. Reperfusion therapy was done for 15 (40.5%) cases before the VSR occurred. Surgery, percutaneous, and medical therapy were done for 26 (70.3%), 3 (8.1%), and 7 (18.9%) cases, respectively. The mortality rate was significantly higher in the medical versus surgical-treated group (85.7% versus 42.3%, P = .027). There was a trend to higher mortality in the group with dissection of both septum and RV (P = .15). We concluded that echocardiography has a critical role in diagnosing this complication. Surgery is mandatory in IMD with VSR.

Type-A aortic dissection manifesting as acute inferior myocardial infarction: 2 case reports.

RATIONALE: Acute Type-A aortic dissection (AD) is a challenging clinical emergency. Despite advances in diagnosis and surgical techniques, the high surgical mortality rate of the condition persists. As a result of similarities in clinical symptoms, AD can mimic acute myocardial infarction (AMI). In this paper, we report 2 cases of patients with acute AD manifesting as inferior AMI. PATIENT CONCERNS: Two patients with undetected AD were misdiagnosed with AMI; in such patients, the administration of thrombolytic therapy has disastrous consequences. DIAGNOSES: The patients were initially diagnosed with AMI in the emergency room, and then diagnosed with AD during catheterization. INTERVENTIONS: The patients were transferred to the cardiac catheterization laboratory for primary coronary angiography. The initial attempt to selectively engage the coronary ostium was unsuccessful. Subsequent computed tomography angiography (CTA) confirmed AD from the aortic root to the abdominal aorta and dissection violations of the coronary ostium. The patients underwent emergency aortic root replacement. OUTCOMES: One patient recovered and was discharged 2 weeks later. At a 1-year follow-up examination, CTA indicated that this patient had made a full recovery. The other patient died 6 days after surgery. LESSONS: As a result of similarities in clinical symptoms, AD can mimic AMI. Rapid diagnosis and treatment of AD is crucial. Difficulty during catheter engagement should raise the suspicion of acute Type-A AD.

[Inferior myocardial infarction: first Moroccan study of 103 cases]. / Infarctus du myocarde inférieur: première série marocaine, à propos de 103 cas.

Myocardial infarction (MI) is a major cause of cardiovascular mortality. Inferior MI accounts for 30-50% of infarctions but it is associated with a favorable prognosis compared to anterior infarct. This study aimed to study the epidemiological, clinical, electrical, echocardiographic, angiographic features of inferior MI, as well as its complications and its therapeutic approaches. Over a period of 3 years, we admitted 720 patients with STEMI, of whom 103 with inferior STEMI, reflecting a rate of 14.3%. There was a clear male predominance, with an average age of 58 years (men) and 62 years (women). Smoking was the main risk factor for cardiovascular disease (57.28% of patients were smokers). Right ventricular infarction was found in 11.65% of cases. Half of these patients had hemodynamic instability. Third-degree atrioventricular block was diagnosed in 12.6% of patients. Therapeutic approach was based on thrombolysis (7 patients) and coronary angiogram (42 patients). Inferior MI was caused by right coronary lesion in 53% of cases and circumflex artery occlusion in 47% of cases. Right coronary is responsible for right ventricular infarction in 100% of cases. Coronary angioplasty was performed in 18 patients after coronary angiogram. Eleven patients underwent transluminal coronary angioplasty in the right coronary while 2 patients underwent transluminal coronary angioplasty in the circumflex artery. Early mortality at 30 days was 1.94%. In the right ventricular infarction group mortality rate was about 17%.

Salvage of Simultaneous Acute Coronary Closure and Retroperitoneal Bleeding Using Veno-Arterial Extracorporeal Membrane Oxygenation and Chronic Total Occlusion Percutaneous Coronary Intervention Techniques in a Patient with ST-Segment Elevation Myocardial Infarction.

Iatrogenic coronary artery dissection is a feared complication of percutaneous coronary intervention as it can potentially lead to severe myocardial ischemia, arrhythmias, shock, and death. Bailout-stenting or less often, emergent coronary artery bypass graft surgery may be needed for restoring antegrade flow. We describe a case of inferior ST-segment elevation acute myocardial infarction with preserved antegrade coronary flow. Percutaneous coronary intervention was complicated by acute right coronary artery closure during guide catheter engagement. Attempts for re-entry into the right coronary artery true lumen failed. Attempts to obtain right femoral arterial access resulted in retroperitoneal hematoma. The patient developed refractory ventricular fibrillation and could not be defibrillated. Veno-arterial extracorporeal membrane oxygenation was started using surgical right femoral cutdown for the venous cannula and the left common femoral artery for the arterial cannula. A dissection strategy with a knuckled guidewire was used around previously placed stents followed by successful re-entry into the distal right coronary artery using the Stingray system. The venous cannula was changed to the internal jugular vein and the right common femoral artery and vein were surgically repaired. The patient was decannulated two days later and was eventually discharged from the hospital neurologically intact.

Association between coronary dominance and acute inferior myocardial infarction: a matched, case-control study.

BACKGROUND: Previous studies have found a connection between left coronary artery dominance and worse prognoses in patient with acute coronary syndrome, which remains a predominant cause of morbidity and mortality globally. The aim of this study was to investigate whether coronary dominance is associated with the incidence of acute inferior myocardial infarction (MI). METHODS: Between January 2011 and November 2014, 265 patients with acute inferior MI and 530 age-matched and sex-matched controls were recruited for a case-control study in the Second Affiliated Hospital of Xi'an Jiaotong University in Xi'an, China. All participants underwent coronary angiography. The exclusion criteria included history of coronary artery bypass graft surgery, chronic or systemic diseases (including hepatic failure, kidney failure, hypothyroidism and Grave's disease), ventricular fibrillation, and known allergy to iodinated contrast agent. Patients with left- or co-dominant anatomies were placed into the LD group and those with right-dominant anatomy were included in the RD group. The association of acute inferior MI and coronary dominant anatomy were assessed using multivariable conditional logistic regression, and to estimate the odds ratio (OR) and 95% confidence interval (95%CI). RESULTS: Distributions of right dominance were significantly different between the acute inferior MI group and control group (94.0% vs. 87.9%, P = 0.018). Univariable conditional logistic regression revealed that right dominance may be a risk factor for the incident acute inferior MI (OR: 2.137; 95% CI: 1.210-3.776; P = 0.009). After adjusting for baseline systolic blood pressure, heart rate, smoking status, diabetes mellitus, hypertension, hyperlipidaemia, and family history of coronary artery disease, results of multivariate conditional logistic regression showed that right dominance was associated with the incidence of acute inferior MI (OR: 2.396; 95% CI: 1.328-4.321; P = 0.004). CONCLUSIONS: Right coronary dominance may play a disadvantageous role in the incidence of acute inferior MI. However, further studies are needed to verify our findings, especially with regard to the underlying mechanisms.

Left Ventricular Aneurysm After Post-Infarction Ventricular Septal Defect Repair.

The surgical indication and optimal approach for ischemic mitral regurgitation with ventricular septal defect remain uncertain. Very few studies have reported the occurrence of left ventricular aneurysms after repair of ischemic ventricular septal defects. We report a case of a left posterior ventricular aneurysm that developed after an urgent operation to repair an acute ischemic posterior ventricular septal defect using the double-patch sandwich technique via a right ventriculotomy.

Evaluation of right atrial volumes and functions by real-time three-dimensional echocardiography in patients after acute inferior myocardial infarction.

BACKGROUND: Right ventricle (RV) involvement causes acute systolic and diastolic functional alterations in the RV in patients after inferior myocardial infarction (IMI), which may result in an increase in left ventricle (LV) end-diastolic and right atrial (RA) pressure. In our study, we sought to evaluate RA volumes and mechanical functions using real-time three-dimensional echocardiography (RT3DE) in IMI patients with or without RV involvement. METHODS: Ninety-six consecutive patients with IMI (mean age: 59.7 ± 10.2 years, 60 female) were included. RV myocardial involvement (RVMI) was defined as the presence of a culprit lesion at the proximal portion of the first RV marginal branch in coronary angiography. The study population was divided into two groups: IMI (58.3%) and IMI + RVMI (41.7%). Patients were evaluated using conventional two-dimensional echocardiography (2DE) and RT3DE. RESULTS: In RT3DE measurements, IMI + RVMI patients had significantly higher RA phasic volumes and worse conduit mechanical function. A receiver operating characteristic (ROC) curve analysis revealed that an RT3DE RA maximum volume (Vmax) index > 27.9 mL/m2 was an independent predictor of RV involvement in patients after acute IMI, with a sensitivity of 80.0% and a specificity of 89.3%. CONCLUSIONS: Right ventricle involvement may cause an increase in RA phasic volumes and deterioration of conduit function in patients with acute IMI.

Clinical and echocardiographic factors associated with mitral plasticity in patients with chronic inferior myocardial infarction.

Aims: Ischaemic mitral regurgitation (IMR) is consequence of left ventricular (LV) remodelling after myocardial infarction. In some cases, the mitral valve enlarges to compensate for LV remodelling and tenting, improving its coaptation; a process termed 'plasticity'. We sought to identify clinical and echocardiographic factors associated with plasticity in patients with chronic inferior myocardial infarction (CII). Methods and results: This study included 91 revascularized CII patients and 46 controls. Plasticity and IMR severity were evaluated by 2D transthoracic echocardiography. Compared with controls, CII patients were older (59 vs. 25 years) and mostly men (80% vs. 46%), both P < 0.001. Chronic inferior myocardial infarction patients also had significant LV remodelling: larger LV volumes, larger mitral tenting areas, larger coaptation depths, longer mitral leaflets and chords, and worse mitral regurgitation (all P ≤ 0.03). Of 91 CII patients, 60 had mitral plasticity (longer anterior and posterior leaflets and longer posterior chords, all P < 0.001), despite not exhibiting significantly larger LV volumes, tenting area or coaptation depth, when compared with patients with no plasticity. Contralateral (anterior) papillary muscle-to-annulus length tended to be increased in CII plasticity patients (P = 0.05). Also they had less moderate and severe IMR (both P < 0.04) compared with non-plasticity CII patients. Multivariate analysis demonstrated independent associations between plasticity and smoking [odds ratio (OR) 0.03, 0.002-0.57; P = 0.019], duration of type-2 diabetes (OR 1.19, 1.007-1.42; P = 0.04) and haemoglobin (OR 2.17, 1.25-3.76; P = 0.005). Conclusion: Mitral plasticity results in less moderate and severe IMR. Longer time-duration of diabetes mellitus and higher haemoglobin level are independently associated with mitral plasticity, while smoking independently associates with no plasticity. Increased anterior papillary muscle-to-annulus length in CII patients with plasticity suggests complex LV remodelling mechanisms are involved in plasticity.