Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiac rupture is a catastrophic complication of acute myocardial infarction with highly mortality rate. Three types of rupture are ventricular free wall rupture( VFR), ventricular septal rupture( VSR), and papillary muscle rupture( PMR). A combination of any 2 types of rupture is called ventricular double rupture (VDR), and very rare. We report a case of VDR (VSR and VFR) after acute myocardial infarction. A 76-year-old female with heart failure was admitted to our hospital. Echocardiography showed an apical VSR and pericardial effusion. She was diagnosed with VDR and emergent operation was performed. During operation, the site of VFR was right ventricle, which was the same infarction area of VSR. VSR was closed by infarction exclusion technique, concurrently excluding the site of VFR. VFR was successfully repaired by mattress sutures. Post-operative course was good without heart failure, though residual shunt was remained. The patient survived and was discharged from our hospital.
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PMID:[Ventricular septal rupture and right ventricular free wall rupture after acute myocardial infarction]. 2391 34

The natural peptide N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP) decreases inflammation in chronic diseases such as hypertension and heart failure. However, Ac-SDKP effects on acute inflammatory responses during myocardial infarction (MI) are unknown. During the first 72 hours post-MI, neutrophils, M1 macrophages (pro-inflammatory), and M2 macrophages (pro-resolution) and release of myeloperoxidase (MPO) and matrix metalloproteinases (MMP) are involved in cardiac rupture. We hypothesized that in the acute stage of MI, Ac-SDKP decreases the incidence of cardiac rupture and mortality by preventing immune cell infiltration as well as by decreasing MPO and MMP expression. MI was induced by ligating the left descending coronary artery in C57BL/6 mice. Vehicle or Ac-SDKP (1.6 mg/kg/d) was infused via osmotic minipump. Cardiac immune cell infiltration was assessed by flow cytometry, cardiac MPO and MMP levels were measured at 24-48 hrs post-MI. Cardiac rupture and mortality incidence were determined at 7 days post-MI. In infarcted mice, Ac-SDKP significantly decreased cardiac rupture incidence from 51.0% (26 of 51 animals) to 27.3% (12 of 44) and mortality from 56.9% (29 of 51) to 31.8% (14 of 44). Ac-SDKP reduced M1 macrophages in cardiac tissue after MI, without affecting M2 macrophages and neutrophils. Ac-SDKP decreased MMP-9 activation in infarcted hearts with no changes on MPO expression. Ac-SDKP prevents cardiac rupture and decreases mortality post-acute MI. These protective effects of Ac-SDKP are associated with decreased pro-inflammatory M1 macrophage infiltration and MMP-9 activation.
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PMID:Ac-SDKP decreases mortality and cardiac rupture after acute myocardial infarction. 2936 96


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