Papillary Muscle Rupture After Acute Inferior Myocardial Infarction.
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ABSTRACT:
SUBMITTER: Singam NSV
PROVIDER: S-EPMC8717755 | biostudies-literature | 2021 Sep
REPOSITORIES: biostudies-literature
Publications
Papillary Muscle Rupture After Acute Inferior Myocardial Infarction.
Singam Narayana Sarma V NSV Ghafghazi Shahab S
Texas Heart Institute journal 20210901 4
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Project description:A 52-year-old man presented with acute onset of chest pain and was found to have an inferolateral ST-segment elevation myocardial infarction and acute mitral regurgitation due to papillary muscle rupture. This case describes a rare, potentially fatal mechanical complication of acute myocardial infarction. (Level of Difficulty: Beginner.).
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Project description:A 73-year-old woman in cardiogenic shock was referred to our hospital because of papillary muscle rupture immediately after the onset of acute myocardial infarction (MI). She had undergone emergent percutaneous coronary intervention and mitral valve replacement. Serial creatine kinase and creatine kinase MB levels indicated that she had acute phase MI on arrival. Pathological findings showed coagulative necrosis of the papillary muscle, which was characteristic evidence of the consequence of prolonged ischemia. We describe herein an unusual case of complete rupture of the posterior papillary muscle occurring immediately after the development of MI. <Learning objective: Mechanical complications of acute myocardial infarction (AMI) such as left ventricular free wall rupture, interventricular wall rupture, and papillary muscle rupture (PMR) commonly occur 2 to 7 days after the onset of AMI. We describe a case of PMR immediately after AMI, which may cause a silent and severe ischemic event a few days before the onset of PMR. This is a rare case of PMR immediately after AMI.>.
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Project description:Papillary muscle rupture is a catastrophic condition, of which most cases manifest posterior papillary muscle rupture. Anterior papillary muscle rupture is a rare condition. Particularly, anterior papillary muscle rupture due to acute myocardial microinfarction of the small high lateral branch is extremely rare. Since papillary muscle rupture can occur even in such a small branch or small area due to myocardial infarction, echocardiographic and/or ventriculographic confirmation is essential in cases of sudden worsening of heart failure. Herein, we report the case of anterior papillary muscle rupture with a good outcome. A 61-year-old man was admitted to our hospital with cardiogenic shock. Echocardiography revealed severe mitral regurgitation due to papillary muscle rupture. Coronary angiography demonstrated high-grade stenosis in the high lateral branch. However, no other significant stenoses were found. Emergency mitral valve replacement was performed. The patient was discharged 19 days after surgery without any complications.
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Project description:A 75-year-old man was admitted to the emergency department for a late-presenting myocardial infarction. The coronary angiography revealed a thrombotic occlusion of the circumflex artery. He presented a rapid hemodynamic and respiratory deterioration as a result of a severe mitral regurgitation with a flail anterior leaflet due to a partial tear of the medial papillary muscle (PM). Given the patient's comorbidities, a percutaneous mitral valve repair with two-dimensional (2D)/3D transesophageal echocardiography was performed, deploying two MitraClips. MitraClip implantation may be considered in an acute setting of PM tear as an alternative for surgical treatment in selected patients.
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Project description:Ventricular septal rupture is a rare and potentially fatal complication of transmural myocardial infarction. Early identification utilising transthoracic echocardiography significantly improves long term outcomes in these patients. We report on a case of a 77-year-old male who presented with signs and symptoms of cardiac failure and a loud systolic murmur. The patient underwent an initial point-of-care ultrasound which revealed evidence of a transmural myocardial infarction and a high suspicion of an apical ventricular septal rupture. A complete transthoracic echocardiogram confirmed the septal rupture diagnosis and the patient subsequently underwent surgical repair of the ventricular rupture. This case highlights the role of echocardiography in decreasing adverse outcomes in patients with ventricular septal rupture.
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Project description:A previously healthy 61-year-old man presented to the emergency department with chest pain and dyspnoea for 6 hours. Examination revealed distress with an apical pansystolic murmur. Initial electrocardiogram showed sinus tachycardia and ST elevation in leads II, III, and aVF compatible with an inferior ST-elevation myocardial infarction. Point-of-care echocardiography in the emergency department showed a flail anterior mitral leaflet and severe mitral regurgitation, leading to a provisional diagnosis of papillary muscle rupture. Emergency cardiac catheterization showed 100%, 80%, and 70% occlusion of the middle right coronary, left anterior descending, and left circumflex arteries, respectively. An emergency triple vessel coronary artery bypass grafting and mitral valve replacement was performed. Posteromedial papillary muscle rupture resulting in mitral regurgitation was confirmed intraoperatively. The patient recovered uneventfully. In the absence of primary percutaneous coronary intervention, thrombolysis decisions should be made with extreme caution if mechanical complications of ST-elevation myocardial infarction are suspected.
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Project description:ObjectiveMyocardial rupture is a fatal complication of acute myocardial infarction (AMI). Early diagnosis of myocardial rupture is feasible when emergency physicians (EPs) perform emergency transthoracic echocardiography (TTE). The purpose of this study was to report the echocardiographic features of myocardial rupture on emergency TTE performed by EPs in the emergency department (ED).MethodsThis was a retrospective and observational study involving consecutive adult patients presenting with AMI who underwent TTE performed by EPs in the ED of a single academic medical center from March 2008 to December 2019.ResultsFifteen patients with myocardial rupture, including eight (53.3%) with free wall rupture (FWR), five (33.3%) with ventricular septal rupture (VSR), and two (13.3%) with FWR and VSR, were identified. Fourteen of the 15 patients (93.3%) were diagnosed on TTE performed by EPs. Diagnostic echocardiographic features were found in 100% of the patients with myocardial rupture, including pericardial effusion for FWR and a visible shunt on the interventricular septum for VSR. Additional echocardiographic features indicating myocardial rupture were thinning or aneurysmal dilatation in 10 patients (66.7%), undermined myocardium in six patients (40.0%), abnormal regional motions in six patients (40.0%), and pericardial hematoma in six patients (40.0%).ConclusionEarly diagnosis of myocardial rupture after AMI is possible using echocardiographic features on emergency TTE performed by EPs.
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Project description:The natural peptide N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP) decreases inflammation in chronic diseases such as hypertension and heart failure. However, Ac-SDKP effects on acute inflammatory responses during myocardial infarction (MI) are unknown. During the first 72 hours post-MI, neutrophils, M1 macrophages (pro-inflammatory), and M2 macrophages (pro-resolution) and release of myeloperoxidase (MPO) and matrix metalloproteinases (MMP) are involved in cardiac rupture. We hypothesized that in the acute stage of MI, Ac-SDKP decreases the incidence of cardiac rupture and mortality by preventing immune cell infiltration as well as by decreasing MPO and MMP expression. MI was induced by ligating the left descending coronary artery in C57BL/6 mice. Vehicle or Ac-SDKP (1.6 mg/kg/d) was infused via osmotic minipump. Cardiac immune cell infiltration was assessed by flow cytometry, cardiac MPO and MMP levels were measured at 24-48 hrs post-MI. Cardiac rupture and mortality incidence were determined at 7 days post-MI. In infarcted mice, Ac-SDKP significantly decreased cardiac rupture incidence from 51.0% (26 of 51 animals) to 27.3% (12 of 44) and mortality from 56.9% (29 of 51) to 31.8% (14 of 44). Ac-SDKP reduced M1 macrophages in cardiac tissue after MI, without affecting M2 macrophages and neutrophils. Ac-SDKP decreased MMP-9 activation in infarcted hearts with no changes on MPO expression. Ac-SDKP prevents cardiac rupture and decreases mortality post-acute MI. These protective effects of Ac-SDKP are associated with decreased pro-inflammatory M1 macrophage infiltration and MMP-9 activation.
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Project description:A previously asymptomatic 53-year-old male presented 5 days after an acute anterior wall myocardial infarction, who was fibrinolytic naïve, with worsening dyspnea. Transthoracic echocardiographic evaluation revealed rupture of the interventricular septum and pseudoaneurysm of the left ventricle, confirmed by angiography. Coronary angiogram revealed multivessel disease. The patient underwent successful closure of ventricular septal rupture with repair of pseudoaneurysm and saphenous vein grafts to posterior descending branch of right coronary artery and obtuse marginal branch of left circumflex artery. Double ventricular ruptures following acute myocardial infarction are very rare with a reported incidence of 0.3% from various series in the revascularization era. They are also associated with exceedingly high mortality rates reaching up to 50%, even when intervened emergently.
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