scholarly journals A Coronary Conundrum: Papillary Muscle Rupture and Ischemic Mitral Regurgitation Secondary to Coronary Thromboembolism in Antiphospholipid Syndrome

2019 ◽  
Vol 7 ◽  
pp. 232470961984224
Author(s):  
Amar Shere ◽  
Pradyumna Agasthi ◽  
Farouk Mookadam ◽  
Sudheer Konduru ◽  
Reza Arsanjani

Antiphospholipid syndrome (APS) is an autoimmune disorder that has a strong propensity for a hypercoagulable state and is known to be associated with venous and arterial thromboembolism. We describe an uncommon case of APS in the setting of non-Hodgkin’s lymphoma, with thromboembolism, and a rare complication after an uncommon etiology of myocardial infarction. This case highlights the importance of early and appropriate type of anticoagulation to reduce the morbidity and mortality in patients with APS.

1996 ◽  
Vol 4 (1) ◽  
pp. 60-62
Author(s):  
Ha Jong Won ◽  
Namsik Chung ◽  
Cho Seung Yun ◽  
Shim Won Heum ◽  
Kang Meyun Sik ◽  
...  

The complete rupture of a papillary muscle is a relatively rare complication of acute myocardial infarction and is generally considered to be rapidly fatal. We describe the multiplane transesophageal echocardiography features of a completely ruptured anterolateral papillary muscle complicating acute non-Q wave lateral myocardial infarction.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Calvin M Kagan ◽  
Benjamin Kenigsberg ◽  
Gaby WEISSMAN ◽  
Mark Hofmeyer ◽  
Samer S Najjar ◽  
...  

A 63-year-old male with numerous cardiac risk factors presented with two hours of rapidly progressing chest pain and shortness of breath. Exam was notable for respiratory distress requiring non-invasive mechanical ventilation and a holosystolic apical murmur radiating to the axilla. He had an elevated troponin and an electrocardiogram with anteroseptal ST depressions. He was diagnosed with a non-ST segment elevation acute coronary syndrome and taken for cardiac catheterization. Surprisingly, no occlusive epicardial disease was discovered. Left ventriculogram revealed engorgement of the left atrium and pulmonary arteries suggestive of severe mitral regurgitation. The mechanism of mitral regurgitation was unclear until transesophageal echocardiography showed a ruptured posteromedial papillary muscle with flail mitral valve, a picture classically caused by myocardial infarction. Cardiac MRI demonstrated preserved LV function with minor inferior apical hypokinesis, nonspecific endocardial late gadolinium enhancement in the inferior segments, and a small LV thrombus. An embolic myocardial infarction targeting a small territory involving posteromedial papillary muscle was thought most probable. The patient then underwent an uneventful mitral valve replacement and recovery. However, he returned two months later with severe biventricular dysfunction and cardiogenic shock with peripheral eosinophilia. Myocardial biopsy confirmed the diagnosis of eosinophilic myocarditis. An exhaustive workup for the etiology of his eosinophilia proved unrevealing; he was consequently diagnosed with the idiopathic subtype. The case highlights a rare but important clinical entity that has a varied phenotype. Our patient presented atypically with an acute papillary muscle rupture that mimicked an acute myocardial infarction, ultimately delaying diagnosis. As evidenced by our case, clinical suspicion of myocarditis should be high in all patients presenting with typical anginal symptoms with mechanical or circulatory compromise in the absence of acute coronary occlusion.


Author(s):  
José López-Sendón ◽  
Esteban López de Sá

Mechanical complications after an acute infarction involve different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies occurring in <1% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment (Ibanez et al, 2017). Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.


2017 ◽  
Vol 69 (11) ◽  
pp. 2443
Author(s):  
Michael Valentino ◽  
Alec Vishnevsky ◽  
Hetal Mehta ◽  
Paul Walinsky ◽  
Gregary Marhefka

2021 ◽  
Vol 2021 ◽  
pp. 1-5
Author(s):  
Akiko Kameyama ◽  
Hiroshi Imamura ◽  
Hiroshi Kamijo ◽  
Kanako Takeshige ◽  
Katsunori Mochizuki ◽  
...  

Papillary muscle rupture (PMR) is a rare and fatal complication of acute myocardial infarction (AMI). We report a case of acute mitral regurgitation (MR) due to PMR with pulmonary edema and cardiogenic shock following AMI with small myocardial necrosis. An 88-year-old woman was brought to our emergency department in acute respiratory distress, shock, and coma. She had no systolic murmur, and transthoracic echocardiography was inconclusive. Coronary angiography showed obstruction of the posterior descending branch of the right coronary artery. Although the infarction was small, the hemodynamics did not improve. Transesophageal echocardiography established papillary muscle rupture with severe mitral regurgitation 5 days after admission. Thereafter, the patient and her family did not consent to heart surgery, and she eventually died of progressive heart failure. Physicians should be aware of papillary muscle rupture with acute mitral regurgitation following AMI in patients with unstable hemodynamics, no systolic murmur, and no abnormalities revealed on transthoracic echocardiography.


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