scholarly journals P181 An uncommon mechanism of severe mitral regurgitation due to infective endocarditis mimicking acute myocardial infarction

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
A Collevecchio ◽  
G Simeti ◽  
M Previtero ◽  
S Iliceto ◽  
D Muraru ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infective Endocarditis ◽  
Mitral Regurgitation ◽  
Coronary Arteries ◽  
Papillary Muscle ◽  
Distal Part ◽  
Troponin I ◽  
Blood Cultures ◽  
Coronary Syndrome

Abstract A 53-year-old man, smoker, with diabetes mellitus, presented to the Emergency Department because of intense chest and abdominal pain, accompanied by dyspnea and high fever (39.5 °C) in the previous 4 days. Physical examination revealed an apical holosystolic murmur, with no signs of peripheral or pulmonary edema. An ECG showed sinus rhythm (90 bpm), complete right bundle branch block and minimal ST elevation in the inferior leads. A transthoracic echocardiography showed a mild reduction in left ventricle ejection fraction (EF 44%) due to akinesia of the infero-lateral wall, and mild mitral regurgitation (MR) due to mitral valve prolapse. An abdominal ultrasound ruled out signs of acute cholecystitis. Blood cultures were collected, and an empirical antibiotic therapy was started. Urgent blood exam showed high Troponin I (72000 ng/L) and high C-reactive protein (290 mg/L). An acute coronary syndrome was suspected based on clinical, ECG and echocardiography exam, and the patient underwent coronary angiography (Figure 1, Panel A) that showed no significant coronary stenosis, except for two small filling defects in the very distal part of both the left anterior descendent and the circumflex coronary arteries suspected for coronary emboli. The patient was then admitted in the coronary care unit, but after just a few hours his clinical and hemodynamic condition deteriorated. A transesophageal echocardiography was performed to rule out mechanical complications related to the acute myocardial infarction and revealed severe MR (Panel D), elongated, hyperechogenic and dysfunctioning antero-lateral papillary muscle (ALPM) with an abnormal mobility suggestive for myocardial abscess, and a mobile mass attached on the aortic valve suggestive for vegetation (Panel B and C). Due to the worsening hemodynamic status, the patient underwent urgent cardiac surgery. Histological analysis confirmed the presence of an abscess of the ALPM due to Staphylococcus Aureus. The patient died after a week because of cerebral hemorrhage. Autopsy reported multiple lungs, renal and cerebral embolic septic infarctions. Learning points coronary artery embolization and papillary muscle abscess are very rare and often fatal consequences of infective endocarditis (IE). High (otherwise unexplained) fever and signs of embolism are minor Duke modified criteria for IE that should lead the physician to look for major criteria, such as positive blood cultures or echocardiography suggestive for IE. Emboli seen in the very distal part of the coronary arteries might have caused the ALPM abscess. Abstract P181 Figure

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

Circulation ◽  
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 ◽  
Papillary Muscle Rupture ◽  
St Segment Elevation ◽  
Coronary Syndrome ◽  
Muscle Rupture

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.

scholarly journals Paraoxonase-1 55 LL Genotype Is Associated with No ST-Elevation Myocardial Infarction and with High Levels of Myoglobin

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Francesca Marchegiani ◽  
Liana Spazzafumo ◽  
Maurizio Cardelli ◽  
Mauro Provinciali ◽  
Francesco Lescai ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Troponin I ◽  
Paraoxonase 1 ◽  
Ischemic Damage ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Coronary Syndrome ◽  
St Elevation ◽  
Serum Paraoxonase

It is well known that serum paraoxonase (PON1) plays an important role in the protection of LDL from oxidation. PON1 55 polymorphism is currently investigated for its possible involvement in cardiovascular diseases. The objective of our study is to verify if PON1 55 polymorphism is associated with risk of acute coronary syndrome (ACS) and with biochemical myocardial ischemia markers, such as troponin I, creatine kinase (CK)-MB, myoglobin, and C-reactive protein. We analysed PON1 55 polymorphism in a total of 440 elderly patients who underwent an ACS episode: 98 patients affected by unstable angina (UA), 207 AMI (acute myocardial infarction) patients affected by STEMI (ST elevation), and 135 AMI patients affected by NSTEMI (no ST elevation). We found that individuals carrying PON1 55 LL genotype are significantly more represented among AMI patients affected by NSTEMI; moreover, the patients carrying LL genotype showed significantly higher levels of myoglobin in comparison to LM + MM carriers patients. Our study suggests that PON1 55 polymorphism could play a role in the pathogenesis of cardiac ischemic damage. In particular, the significant association between PON1 55 LL genotype and the occurrence of a NSTEMI may contribute to improve the stratification of the cardiovascular risk within a population.

scholarly journals Takotsubo cardiomyopathy: case report

2017 ◽  
Vol 95 (7) ◽  
pp. 663-668
Author(s):  
Marina G. Matveeva ◽  
G. E. Gogin ◽  
M. N. Alekhin
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Left Ventricle ◽  
Coronary Arteries ◽  
Takotsubo Cardiomyopathy ◽  
Left Ventricular ◽  
Classical Type ◽  
Coronary Microvascular Dysfunction ◽  
Apical Ballooning Syndrome ◽  
Coronary Syndrome

This article reports a clinical case of Takotsubo cardiomyopathy manifest clinically, biochemicaly, electrocardiographically, and echocardiographicalyas acute myocardial infarction. The diagnosis was based on finding intact coronary arteries and rapid positive dynamics of instrumental and laboratory data. Takotsubo cardiomyopathy (CMP) (stress-associated CMP, apical ballooning syndrome) is a rare reversible disease developing after acute emotional and physical stress. Its prevalence is estimated at 1-2% of all cases of acute myocardial infarction. It most commonly affects postmenopausal women. The clinical picture is similar to that of acute coronary syndrome with transient hypo- and akinesiaof apical and middle segments of the left ventricle (LV) in combination with hyperkinesia of its basal myocardial segment in the absence of stenosis or a spasm of coronary arteries. The precise pathophysiology of the disease is unknown; several hypotheses are proposed including enhancedsympathoadrenal activity, catecholamine multivesselepicardial coronary artery spasm, coronary microvascular dysfunction, catecholamine cardiotoxicity and catecholamine-mediated myocardial stunning. The Mayo Clinic diagnostic criteria are most widely used in clinical practice: transient hypokinesia, akinesia, or dyskinesia of left ventricular mid-segments with or without apical involvement; regional wall motion abnormalities extending beyond the region of blood supply of a single epicardialartery; a stressful event oftenbut not always present in the medical history in the absence of obstructive coronary disease or angiographic evidence of acute plaque rupture; new electrocardiographic abnormalities (either ST-segment elevation and/or T-wave inversion) or modest elevation in cardiac troponin 1 level; the absence of pheochromocytoma and myocarditis. Takotsubo cardiomyopathyhas been classified into 3 types based on the involvement of the left ventricle: classical type, reverse type and mid-ventricular type; lesions of right ventricle are also described. Specific treatment of the disease is unavailable, and the main purpose of therapy is normalization of LV systolic function. The prognosis of Takotsubo cardiomyopathyis favorable, complete clinical recovery is observed in 95,5% of the cases, the average time of recovery is between 2 and 3 weeks.

scholarly journals Diagnostic Pitfalls in Papillary Muscle Rupture-Associated Acute Mitral Regurgitation after Acute Myocardial Infarction

2021 ◽  
Vol 2021 ◽  
pp. 1-5
Author(s):  
Akiko Kameyama ◽  
Hiroshi Imamura ◽  
Hiroshi Kamijo ◽  
Kanako Takeshige ◽  
Katsunori Mochizuki ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Mitral Regurgitation ◽  
Papillary Muscle ◽  
Transthoracic Echocardiography ◽  
Heart Surgery ◽  
Systolic Murmur ◽  
Papillary Muscle Rupture ◽  
Muscle Rupture ◽  
Acute Mitral Regurgitation

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.

Severe Mitral Regurgitation Following Acute Myocardial Infarction and Ruptured Papillary Muscle

Circulation ◽  
1968 ◽  
Vol 37 (4s2) ◽  
Author(s):  
ANDREW G. MORROW ◽  
LAWRENCE S. COHEN ◽  
WILLIAM C. ROBERTS ◽  
NINA S. BRAUNWALD ◽  
EUGENE BRAUNWALD
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Mitral Regurgitation ◽  
Papillary Muscle ◽  
Severe Mitral Regurgitation
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