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The implications of serum enzymes and coagulation activities in postinfarction myocardial rupture
Shi-Min Yuan1, Hua Jing, Jacob Lavee
1Department of Cardiothoracic Surgery, Affiliated Hospital of Taishan Medical College, Taian 27100, Shandong Province, People's Republic of China. shi_min_yuan@yahoo.com
Insights
Postinfarction myocardial rupture significantly elevates serum enzymes and coagulation markers, except fibrinogen. These biomarker profiles aid in diagnosing, treating, and predicting outcomes in rupture patients.
Area of Science:
- Cardiology
- Biochemistry
- Medical Diagnostics
Background:
- Cardiovascular diseases and serum enzyme/coagulation activity associations are known in myocardial infarction.
- Alterations in these biomarkers specifically in postinfarction myocardial rupture are underreported.
Purpose of the Study:
- To investigate and present the profiles of serum enzymes and coagulation activities in patients experiencing postinfarction myocardial rupture.
Main Methods:
- Study included 19 patients undergoing surgical repair for postinfarction myocardial rupture (2004-2008).
- Classified rupture types: free wall, papillary muscle, ventricular septal, and double structure.
- Analyzed laboratory findings including serum enzymes and coagulation activities.
Main Results:
- Coagulation markers and serum enzymes (except fibrinogen) significantly increased post-rupture.
- Significant differences in D-dimer, PTT, LDH, CK, and CK-MB between survivors and non-survivors.
- Elevated Troponin I levels observed early after rupture onset or surgical repair.
Conclusions:
- Myocardial rupture causes marked elevations in serum enzymes and coagulation activities, excluding fibrinogen.
- Biomarker evaluation can assist in diagnostic and treatment decisions.
- These markers may help in assessing the clinical prognosis of myocardial rupture patients.
Objective:
Associations between cardiovascular diseases and serum enzymes or coagulation activities have been sufficiently documented in patients with myocardial infarction. However, the alterations of these biomarkers in patients with postinfarction myocardial rupture have rarely been reported. The aim of this study is to present the profiles of the markers in patients with postinfarction myocardial rupture.
Methods:
From 2004 to 2008, 19 consecutive patients were referred to this hospital for surgical repair of postinfarction myocardial rupture. Eight (42.1%) patients had free wall rupture, 5 (26.3%) had papillary muscle rupture, 5 (26.3%) had ventricular septal rupture, and 1 (5.3%) had double structure (ventricular septum + free wall) rupture. Thirteen patients survived the operation, and 6 died. Laboratory findings including serum enzymes and coagulation activities were collected and analyzed.
Results:
The coagulation markers and serum enzymes except for fibrinogen increased significantly after the development of myocardial rupture. Statistical differences in D-dimer, partial thromboplastin time, peak lactate dehydrogenase, peak creatine kinase and creatine kinase fraction MB were found between non-survivors and survivors. Troponin I values were elevated significantly during the early days after the onset or surgical repair of myocardial rupture. Multivariant regression analysis did not show any significant relationship between creatine phosphokinase fraction MB (Y) and D-dimer (X1) or fibrinogen (X2).
Conclusion:
Myocardial rupture leads to extremely high serum enzyme and coagulation activities except for fibrinogen after the onset. The evaluation of these biomarkers may help in making diagnostic and treatment decisions and in judging the clinical prognosis of such patients.
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