Myocardial rupture after myocardial infarction is related to the perfusion status of the infarct-related coronary artery

Cheriex, Emile C.; Swart, Hans de; Dijkman, L. W. N.; Havenith, Miek G.; Maessen, Jos G.; Engelen, Domien J; Wellens, Hein J.J.

doi:10.1016/0002-8703(95)90309-7

Cited by 42 publications

(25 citation statements)

References 19 publications

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Section: Discussionmentioning

confidence: 92%

“…4,5 Rupture typically occurs in an area that has been infarcted without successful reperfusion. 6 There was an increased occurrence noted in patients treated with thrombolytic therapy versus patients who underwent coronary intervention (3.3% vs. 1.8%).5 Complete rupture of the left ventricular free wall is suggested by the development of sudden right heart failure and shock due to hemopericardium with resultant electromechanical dissociation. Incomplete, or subacute, rupture occurs when organized thrombus and pericardium seal the perforation forming a pseudoaneurysm.…”

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confidence: 99%

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Man feeling tired and “lousy” five days following myocardial infarction

Popescu¹

2006

TMF

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A 70 year-old male presents to his cardiologist's office with complaints of feeling fatigued and "lousy". His past medical history is significant for HTN and HL, but until a recent hospitalization, he was non-compliant with his outpatient medical regimen. Of note, he also has a history of heavy alcohol consumption and a 30 pack-year smoking history. The patient reports that he was recently discharged after acute myocardial infarction (AMI) from an outside hospital. At that time, he underwent a diagnostic cardiac catheterization, but no intervention was performed secondary to 100% RCA stenosis and technical difficulties. He was sent home on clopidogrel, aspirin, metoprolol, lisinopril and simvastatin. He currently appears tired and anxious, however he has no symptoms of chest pain, dyspnea, orthopnea, diaphoresis, or lightheadedness; he does report that his primary symptoms leading him to admission was chest pain and shortness of breath.On physical exam, the patient's blood pressure is 75/56 mmHg with a heart rate of 89 beats per minute, respiratory rate is 18, and his room air oxygen saturation is 98%. Cardiac exam revealed a new apical systolic murmur best heard at the posterior axillary line radiating towards to the scapula with an S3 present. JVP was estimated to be 20 cm H2O. Lung exam demonstrated bibasilar crackles. Peripheral extremities were warm with no lower extremity edema.Initial laboratory data include a creatinine of 2.7 mg/dL (baseline 1.3 mg/dL), hemoglobin of 11.8 g/dL, a white blood cell count of 12,500 cells/mm3 without left shift or band forms, and troponin of 5.89 ng/mL. EKG revealed a normal sinus rhythm with ST elevations in leads II, III, aVF and ST depressions throughout the lateral precordial leads suggesting ongoing inferolateral ischemia or injury.The patient was admitted to the Cardiac Care Unit (CCU) for further medical management. He received fluid boluses for BP support. Aspirin and statin therapy were continued and additionally, therapeutic intravenous heparin was initiated. Clopidogrel was held due to a potential need for surgical intervention. Beta blocker and ACE inhibitor were discontinued secondary to hypotension.Cardiac catheterization reports were obtained from the outside hospital and demonstrated a 100% RCA stenosis. Additionally, there was diffuse disease throughout the coronary arteries including a 50% LAD, 50% LCx, 50% OM1, and 60% D2 stenosis with an ejection fraction of 35%. An echocardiogram obtained upon admission to this institution visualized a mobile echodensity attached to the chordal region of the anterior mitral leaflet suggestive of partial papillary muscle rupture leading to anterior leaflet prolapse, as well as systolic dysfunction due to multiple segmental wall motion abnormalities. Doppler evaluation confirmed severe, posteriorlaterally directed mitral regurgitation with a "shoulder" sign, suggestive of severe, acute MR likely secondary to papillary muscle rupture.Due to the patient's acute renal failure, RCA angioplasty was not performed despite persis...

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Section: Discussionmentioning

confidence: 92%

mentioning

confidence: 99%

Man feeling tired and “lousy” five days following myocardial infarction

Popescu¹

2006

TMF

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“…Late rupture may occur within two weeks of an acute myocardial infarction with no preferential infarction site. 12 The left ventricle is more frequently involved than the right ventricle 13 and myocardial rupture is less common in patients with a patent infarct-related artery 14 ; rupture typically occurs in an infarcted area without successful reperfusion. Complete rupture usually leads to sudden cardiac death from cardiac tamponade.…”

Section: Discussionmentioning

confidence: 99%

Cardiac Rupture in Embolic Myocardial Infarction after Implantation of a Valved Aortic Conduit

Lamm

Auer

Maurer

et al. 2008

Heart, Lung and Circulation

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“…Firstly, ventricular rupture is usually seen after a transmural myocardial infarction without reperfusion, whereas our patient showed reperfusion. This has been described by Cheriex et al [1]. They hypothesised that thrombolysis may be an important pathogenic factor since this may result in a hemorrhagic infarction that enhances local weakening and rupture, particularly when thrombolysis is started late (after 6 h).…”

mentioning

confidence: 84%