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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study determines the usefulness of electrocardiography in the emergency room for assessing the risk of cardiac rupture after acute anterior myocardial infarction (MI). The presence of ST segment elevation on the admission 12-lead electrocardiography was evaluated in 325 consecutive anterior MI patients. A forward-stepwise logistic regression analysis for cardiac rupture was performed with the covariates of age, gender, hypertension, history of MI, reperfusion therapy by coronary angioplasty, and ST segment elevations in leads I, aVL, V1-V6. Cardiac rupture occurred in 16 patients, including 7 with left ventricular free wall rupture (FWR) and 9 with ventricular septal perforation (VSP). For FWR, ST elevation in lead aVL was the only independent predictor (odds ratio = 12.1, P = .0215). For VSP, female gender (odds ratio = 5.32, P = .0201) was the independent predictor. In conclusion, in patients with acute anterior MI, ST segment elevation in lead aVL on the admission electrocardiography is a significant risk factor for left ventricular FWR.
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PMID:Cardiac rupture and admission electrocardiography in acute anterior myocardial infarction: implication of ST elevation in aVL. 1069 Nov 74

Methamphetamine (MA) not only affects the nervous system but also has cardiac toxicity and immunosuppressive properties. This manuscript will provide support that there is a relationship between MA use and heart disease as well as immune dysfunction. The cardiovascular manifestations of acute MA use include tachycardia, atrioventricular arrhythmias, myocardial ischemia, myocardial ischemia and hypertension, resulting in cardiac lesions. Chronic use of MA causes cardiomyopathy including cellular infiltration, myocardial hypertrophy, myocardium rupture and fibrosis. The increased catecholamine levels are responsible for the cardiac lesions induced by MA. The additional problem with MA use is its potential to disrupt the immune system function leading to suppression of mitogen-stimulated lymphocyte, a reduction in circulating lymphocyte numbers and alternation T-lymphocyte cytokine secretion as well as B cell proinflammatory cytokine secretion. Concomitant MA use and Human Immunodeficiency Virus (HIV) infection not only enhances immunosuppression associated with HIV but also increases the heart disease occurrence with a coincidentally complication of AIDS or AIDS medications.
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PMID:Heart disease, methamphetamine and AIDS. 1273 29

Cardiac rupture is a fatal complication of myocardial infarction that may involve especially the left ventricular free wall, the ventricular septum and the papillary muscle, but also the right ventricular free wall and more rarely the atrium. This complication is responsible for 10-15% of in-hospital deaths after ST-elevation myocardial infarction. Advanced age, female sex, first infarction and hypertension (in the acute phase of infarction) are the most important risk factors for cardiac rupture. It occurs typically between 4 and 7 days after the infarction but it may also develop within the first 24-48h, particularly in patients undergoing fibrinolytic therapy and in cardiac patients with the following characteristics: 1) recent coronary artery occlusion, 2) transmural necrosis, 3) poor collateral circulation, and 4) minimal or absent myocardial fibrosis. Cardiac rupture should be suspected when sudden or rapidly progressive hemodynamic deterioration occurs. After prompt diagnosis and stabilization, the patient can be operated. The high mortality rate between 5 and 14 days post-infarction justifies the urgency of surgical repair, which includes infartectomy and the employment of a Dacron patch and biological glues. Also percutaneous strategies have recently been used in patients with high surgical risk. The most frequently performed surgical techniques for the treatment of cardiac rupture are described below. By now early diagnosis and surgical treatment are crucial for successful outcome.
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PMID:[Surgical treatment of early complications after ST-elevation myocardial infarction]. 2141 30

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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