Mechanical complications of myocardial infarction

Mechanical complications after an acute infarction include 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 but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. 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.

Mechanical complications of myocardial infarction

10.1093/med/9780199687039.003.0045_update_002 ◽

2017 ◽

Author(s):

José López-Sendón ◽

Esteban López de Sá

Keyword(s):

Myocardial Infarction ◽

Left Ventricle ◽

Mitral Regurgitation ◽

Papillary Muscle ◽

Thrombus Formation ◽

Left Ventricular ◽

Free Wall ◽

Mechanical complications after an acute infarction include 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 but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. 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.

Mechanical complications of myocardial infarction

10.1093/med/9780199687039.003.0045 ◽

2015 ◽

Author(s):

José López-Sendón ◽

Esteban López de Sá

Keyword(s):

Myocardial Infarction ◽

Left Ventricle ◽

Mitral Regurgitation ◽

Papillary Muscle ◽

Thrombus Formation ◽

Left Ventricular ◽

Free Wall ◽

Mechanical complications after an acute infarction include 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 but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. 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.

Survival from Combined Left Ventricular Free Wall Rupture and Papillary Muscle Rupture Complicating Acute Myocardial Infarction

Journal of the American Society of Echocardiography ◽

10.1016/j.echo.2006.04.042 ◽

2007 ◽

Vol 20 (7) ◽

pp. 905.e1-905.e3

Author(s):

Carlos Enrique Sanchez ◽

Vipin B. Koshal ◽

Marc Antonchak ◽

Anne R. Albers

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Papillary Muscle ◽

Left Ventricular ◽

Ventricular Free Wall ◽

Free Wall ◽

Left Ventricular Free Wall ◽

Free Wall Rupture ◽

Left Ventricular Free Wall Rupture Followed by Papillary Muscle Rupture Combined with Acute Myocardial Infarction

Japanese Journal of Cardiovascular Surgery ◽

10.4326/jjcvs.39.129 ◽

2010 ◽

Vol 39 (3) ◽

pp. 129-132

Author(s):

Junko Kobayashi ◽

Hideo Yoshida ◽

Hideyuki Kato ◽

Toshihiko Suzuki ◽

Makoto Mohri ◽

...

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Papillary Muscle ◽

Left Ventricular ◽

Ventricular Free Wall ◽

Free Wall ◽

Left Ventricular Free Wall ◽

Free Wall Rupture ◽

P1322 Role of echocardiography in the assessment of mechanical complications of acute myocardial infarction: case report series

European Heart Journal - Cardiovascular Imaging ◽

10.1093/ehjci/jez319.763 ◽

2020 ◽

Vol 21 (Supplement_1) ◽

Author(s):

C Gonzalez Garay ◽

S K Farias Vergara ◽

M C Lopez Rincon ◽

B A Gaxiola Cadena ◽

A M Guzman Ayon

Keyword(s):

Coronary Artery ◽

Papillary Muscle ◽

Reperfusion Therapy ◽

Left Ventricular ◽

Free Wall ◽

Free Wall Rupture ◽

Muscle Rupture ◽

History Of

Abstract INTRODUCTION The incidence of the mechanical complications of acute myocardial infarction (AMI) has noticeably decreased throughout the world after the era of primary percutaneous coronary intervention (PCI); nonetheless, when they present, the mortality rate continues being high, requiring for their diagnosis an adequate clinical suspicion, followed by intensive care therapy and in most cases, surgical treatment. In the current report we present 4 cases of mechanical complications using transthoracic echocardiography (TTE) as diagnostic tool: a ventricular septal defect, a papillary muscle rupture, a left ventricular (LV) free wall rupture and a ventricular aneurysm. PATIENT 1: A 71-year-old male who presented with inferior AMI and no reperfusion therapy, complicated with transitory AV block, ventricular fibrillation and severe mitral regurgitation secondary to posteromedial papillary muscle rupture (Panel A). He followed surgery with biological mitral valve replacement and PCI of the right coronary artery (RCA). PATIENT 2: A 71-year-old male who presented with anterior AMI and no reperfusion therapy, suddenly showed signs of cardiogenic shock. The TTE demonstrated pericardial effusion associated with an image of thrombus fixed to the antero-apical wall of the LV of 21 mm in dimension, apical segments akinesia and left ventricular ejection fraction (LVEF) of 40% (Panel B). These findings concluded LV free wall rupture, that required urgent surgical repair of the apical region with sphacelated myocardium. PATIENT 3: A68-year-old male, with history of hospitalization 2 months prior for an event of acute coronary syndrome. Admitted again for chest pain, with a TTE that demonstrated a ventricular septal defect associated with intramyocardial dissection, apical thrombus of 17x11 mm in dimension, apical dyskinesis and LVEF of 30% (Panel C). Coronary angiography documented critical obstruction of proximal left anterior descending coronary artery (LAD) and chronic total occlusion of the RCA. He was taken to surgical repair of the defect and coronary artery bypass (CABG). PATIENT 4: A 77-year-old male, with a history of PCI in 2009 (unknown coronary vessel), presented with inferior AMI and no reperfusion therapy. TTE demonstrated an aneurysm in the basal inferior segment of 55x44 mm in dimension, partially thrombosed, with a neck of 23 mm, severe mitral regurgitation and LVEF of 45% (Panel D). Coronary angiography documented multivessel disease with unsuitable coronary anatomy for CABG. CONCLUSIONS The incidence of AMI mechanical complications has decreased noticeably to less than 1% in the era of primary PCI. These include free wall rupture (0.17%), papillary muscle rupture (0.26%) and LV free wall rupture (0.17%). Immediate echocardiographic assessment is needed when clinical findings suggest such complications; urgent treatment is fundamental to improve short term prognosis. Abstract P1322 Figure. Bidimensional TTE images.

Left Ventricular and adjacent Right ventricular Pseudoaneurysms post acute myocardial infarction communicating via a Ventricular Septal Defect

10.22541/au.160812826.67804259/v1 ◽

2020 ◽

Author(s):

Kevin Kang ◽

John Wilson ◽

Jeffrey Friedel ◽

Angel Flores

Keyword(s):

Myocardial Infarction ◽

Right Ventricular ◽

Color Doppler ◽

Fatal Outcome ◽

Left Ventricular ◽

Inferior Wall ◽

Muscle Rupture ◽

Echocardiographic Images

The rare but deadly post myocardial infarction (MI) mechanical complications are categorized as ventricular free wall rupture, ventricular septal rupture (VSD) and papillary muscle rupture in decreasing order of incidence. The incidence of the mechanical complications has been mitigated by early revascularization in recent years but mortality remains high. The cardiac rupture if contained by clot, scar and pericardium leads to a LV pseudoaneurysm that delays or diminishes the fatal outcome. Mechanical complications and pseudoaneurysm are recognized by echocardiography. We report a previously unreported occurrence of a pseudoaneurysm involving the adjacent walls of both the ventricles, LV basal and inferoseptal walls and the adjacent right ventricular inferior wall (RV). The LV and RV communicated via a hole in the pseudoaneurysmal wall. The echocardiographic images initially showed the LV pseudoaneurysm bulging into the RV rather than into the pericardium. The color Doppler showed shunting through the LV pseudoaneurysm into the RV creating an unusual VSD. The CT angiograms corroborated the echo findings. The LV pseudoaneurysm had a tear in it and this led to bleeding not into pericardium but into the adjacent RV pseudoaneurysm, hence creating a very unusual VSD. Subsequently, our patient went for surgical repair of pseudoaneurysm and the surgical findings confirmed the imaging findings that there was a massive LV pseudoaneurysm from the inferior and inferoseptal walls, the adjacent RV wall was involved with the pseudoaneurysm and a communication between LV pseudoaneuysm sac and the RV was seen. Such pathology has not been described in the past.

Abstract 14887: Look Beyond the Coronaries: A Rare Cause of Acute Papillary Muscle Rupture

Circulation ◽

10.1161/circ.142.suppl_3.14887 ◽

2020 ◽

Vol 142 (Suppl_3) ◽

Author(s):

Calvin M Kagan ◽

Benjamin Kenigsberg ◽

Gaby WEISSMAN ◽

Mark Hofmeyer ◽

Samer S Najjar ◽

...

Keyword(s):

Myocardial Infarction ◽

Mitral Valve ◽

Mitral Regurgitation ◽

Papillary Muscle ◽

Invasive Mechanical Ventilation ◽

Lv Function ◽

St Segment Elevation ◽

Coronary Syndrome ◽

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.

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

Journal of Investigative Medicine High Impact Case Reports ◽

10.1177/2324709619842247 ◽

2019 ◽

Vol 7 ◽

pp. 232470961984224

Author(s):

Amar Shere ◽

Pradyumna Agasthi ◽

Farouk Mookadam ◽

Sudheer Konduru ◽

Reza Arsanjani

Keyword(s):

Myocardial Infarction ◽

Mitral Regurgitation ◽

Antiphospholipid Syndrome ◽

Papillary Muscle ◽

Rare Complication ◽

Autoimmune Disorder ◽

Ischemic Mitral Regurgitation ◽

Muscle Rupture ◽

Uncommon Case

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.