Disease relevance of Heart Rupture

• Temporary administration of PA inhibitor-1 or the matrix metalloproteinase-inhibitor TIMP-1 completely protected wild-type mice against rupture but did not abort infarct healing, thus constituting a new approach to prevent cardiac rupture after acute myocardial infarction [1].
• CONCLUSIONS: Cardiac rupture, left ventricular aneurysmal formation, and 1-year cardiac death were associated with an elevation of serum CRP early after AMI, suggesting that elevation of CRP levels after AMI may predict infarct expansion [2].
• To assess the efficacy of volume expansion and pharmacologic support in cardiac tamponade due to cardiac rupture, a model of hemorrhagic cardiac tamponade was developed and treatment with rapid saline infusion and dobutamine was compared with rapid saline infusion alone in 15 closed chest dogs [3].
• We report a case of subacute cardiac rupture with frank pericardial effusion receiving thrombolytic and glycoprotein IIb/IIIa inhibitor therapies [4].
• The rates of ventricular arrhythmia, rates of cardiac rupture, and blood pressures in the 2 strains were similar after MI [5].

High impact information on Heart Rupture

• Inhibition of plasminogen activators or matrix metalloproteinases prevents cardiac rupture but impairs therapeutic angiogenesis and causes cardiac failure [1].
• Targeted deletion or pharmacological inhibition of MMP-2 prevents cardiac rupture after myocardial infarction in mice [6].
• In patients with cardiac rupture, peak CRP levels were higher than in those without rupture (P=.001); peak CK levels were not predictive [2].
• Hemodynamic efficacy of rapid saline infusion and dobutamine versus saline infusion alone in a model of cardiac rupture [3].
• We hypothesized that testosterone may adversely affect remodeling after MI, exaggerating the inflammatory response and increasing cardiac rupture, whereas estrogen may be cardioprotective, attenuating early remodeling and reducing rupture rate [7].

Chemical compound and disease context of Heart Rupture

• A partial defect in technetium-99m pyrophosphate image suggesting cardiac rupture following acute myocardial infarction [8].
• Surgical repair of the cardiac rupture, mediastinal irrigation with povidone-iodine, and broad-spectrum antibiotics resulted in the patient's recovery [9].
• The patient improved after therapy with cefotaxime; however, cardiac rupture occurred on the sixth postoperative day [10].
• Seven patients with cardiac rupture from blunt trauma were encountered at the University Hospital, University of Alabama School of Medicine, in a 15-year period [11].
• The effect of antiplatelet therapy with glycoprotein IIb-IIIa receptor blockers (abciximab) on cardiac rupture is unknown [12].

Anatomical context of Heart Rupture

• It is postulated that eosinophils rich in arylsulfatase B, peroxidase, glucuronidase, beta-glycerophosphatase, major basic protein, and eosinophilic cationic protein may further weaken the necrotic myocardium and, in part, determine whether acute myocardial infarction will eventually result in cardiac rupture [13].

Gene context of Heart Rupture

• Urokinase type PA (u-PA) and PA inhibitor type 1 (PAI-1) seem to modulate cardiac rupture and infarct healing [14].
• Peri-infarct pursestring for repair of subacute cardiac rupture [15].
• Of these 1,250 patients studied, 12 patients (0.96%) had cardiac rupture (ventricular septal defect [VSD], three patients; left ventricular [LV] free wall rupture, nine patients] after d-PCI, with a mean (+/- SD) time of occurrence of 52.3 +/- 36.2 h [16].
• Cardiac rupture from blunt trauma with atrial septal defect [17].
• Since matrix metalloproteinases (MMPs) play an important role in infarct healing, tissue repair and extracellular matrix (ECM) remodeling post-MI, we studied the temporal relationship of MMP expression and inflammatory response to cardiac rupture after acute MI [18].

References