The Association Between Cardiac Rupture and Early Mortality Among Women With Myocardial Infarction Treated With Thrombolytics

1998 ◽  
Vol 31 (2) ◽  
pp. 379A
Author(s):  
R Becker
Keyword(s):  
Myocardial Infarction ◽  
Early Mortality ◽  
Cardiac Rupture

scholarly journals The association between cardiac rupture and early mortality among women with myocardial infarction treated with thrombolytics

1998 ◽  
Vol 31 ◽  
pp. 379
Author(s):  
Richard C. Becker ◽  
Sumita D. Paul ◽  
Frederick A. Spencer ◽  
Steven P. Ball ◽  
Elliott M. Antman
Keyword(s):  
Myocardial Infarction ◽  
Early Mortality ◽  
Cardiac Rupture

C-Reactive Protein as a Predictor of Infarct Expansion and Cardiac Rupture After a First Q-Wave Acute Myocardial Infarction

Circulation ◽  
1997 ◽  
Vol 96 (3) ◽  
pp. 778-784 ◽  
Author(s):  
Toshihisa Anzai ◽  
Tsutomu Yoshikawa ◽  
Hiroto Shiraki ◽  
Yasushi Asakura ◽  
Makoto Akaishi ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Rupture ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Infarct Expansion ◽  
Q Wave

M-Complex: The Electrocardiographic Sign of Impending Cardiac Rupture following Myocardial Infarction

1972 ◽  
Vol 17 (10) ◽  
pp. 319-325 ◽  
Author(s):  
M. Afzal Mir
Keyword(s):  
Myocardial Infarction ◽  
Chest Pain ◽  
Coronary Care Unit ◽  
Progressive Increase ◽  
Injury Pattern ◽  
Cardiac Rupture ◽  
Time Of Death ◽  
St Segment ◽  
Coronary Care ◽  
Electrocardiogram Ecg

Out of 284 patients admitted to the Coronary-Care Unit, 60 patients showed an acute monophasic injury pattern (M-Complex) on their initial electrocardiogram (ECG). There were 13 fatalities on the first day of myocardial infarction; 6 from the M-complex group. Three of these 6 patients died with cardiac rupture. The ECG features of these 3 patients were compared with the 3 non-rupture patients. A progressive increase in the elevated R-ST segment of the M-complex with an upward ‘pull’ of the R-ST junction, proved to be an ominous ECG sign of impending cardiac rupture in patients with protracted chest pain and persistent hypertenison. The 3 non-rupture patients remained in a hypotensive state from admission to the time of death. Atrioventricular block and A-V junctional tachycardia were the commonest rhythm disturbances in patients dying with cardiac rupture.

Cardiac Rupture in Acute Myocardial Infarction

2009 ◽  
Vol 205 (1-6) ◽  
pp. 11-16 ◽  
Author(s):  
Sten Rasmussen ◽  
Arne Leth ◽  
Erik Kjøller ◽  
Asger Pedersen
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Rupture

scholarly journals Targeted Deletion of Class A Macrophage Scavenger Receptor Increases the Risk of Cardiac Rupture After Experimental Myocardial Infarction

Circulation ◽  
2007 ◽  
Vol 115 (14) ◽  
pp. 1904-1911 ◽  
Author(s):  
Kenichi Tsujita ◽  
Koichi Kaikita ◽  
Takanori Hayasaki ◽  
Tsuyoshi Honda ◽  
Hironori Kobayashi ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Interleukin 10 ◽  
Experimental Myocardial Infarction ◽  
Cardiac Rupture ◽  
Infarcted Myocardium ◽  
Factor Α ◽  
Necrosis Factor

Background— Class A macrophage scavenger receptor (SR-A) is a macrophage-restricted multifunctional molecule that optimizes the inflammatory response by modulation of the activity of inflammatory cytokines. This study was conducted with SR-A–deficient (SR-A −/− ) mice to evaluate the relationship between SR-A and cardiac remodeling after myocardial infarction. Methods and Results— Experimental myocardial infarction (MI) was produced by ligation of the left coronary artery in SR-A −/− and wild-type (WT) male mice. The number of mice that died within 4 weeks after MI was significantly greater in SR-A −/− mice than in WT mice ( P =0.03). Importantly, death caused by cardiac rupture within 1 week after MI was 31% (17 of 54 mice) in SR-A −/− mice and 12% (6 of 51 mice) in WT mice ( P =0.01). In situ zymography demonstrated augmented gelatinolytic activity in the infarcted myocardium in SR-A −/− mice compared with WT mice. Real-time reverse transcription–polymerase chain reaction at day 3 after MI showed that the expression of matrix metalloproteinase-9 mRNA increased significantly in the infarcted myocardium in SR-A −/− mice compared with WT mice. Furthermore, SR-A −/− mice showed augmented expression of tumor necrosis factor-α and reduction of interleukin-10 in the infarcted myocardium at day 3 after MI. In vitro experiments also demonstrated increased tumor necrosis factor-α and decreased interleukin-10 expression in activated SR-A −/− macrophages. Conclusions— The present findings suggest that SR-A deficiency might cause impairment of infarct remodeling that results in cardiac rupture via insufficient production of interleukin-10 and enhanced expression of tumor necrosis factor-α and of matrix metalloproteinase-9. SR-A might contribute to the prevention of cardiac rupture after MI.

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