Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Low-dose aspirin (acetylsalicylic acid; ASA), inhibiting platelet thromboxane production in favor of endothelium formation of prostaglandins, is successfully used as primary or secondary prophylaxis against myocardial infarction. Although prognosis may be improved, effects of long-term ASA treatment on wound healing and cardiac remodeling are not well understood. The aim of the present study was to mimic the clinical situation by inducing myocardial infarction in low-dose ASA (25 mg/kg/day, i.p.) pretreated rats, and to determine effects on plasma eicosanoid levels, cardiac hypertrophy and collagen deposition, and left ventricular function during continued ASA treatment. The effects of this dose were verified to selectively inhibit platelet thromboxane production, and lower plasma levels of thromboxane, but did not affect plasma levels of prostacyclin and prostaglandin E2 during the acute inflammatory stage following myocardial infarction. As measured by heart dry weight/body weight, cardiac hypertrophy was not affected by ASA treatment. However, interstitial fibrosis in the spared myocardium as well as perivascular fibrosis, associated with infarction-induced cardiac remodeling, were affected by ASA treatment. Replacement fibrosis in the infarct itself, considered as representing wound healing, was not significantly influenced by ASA treatment. Wall thinning following infarction was not aggravated, nor did treatment influence left ventricular cavity diameter in a relaxed state. Results from in vitro left ventricular function measurements showed no effects on left ventricular peak velocity of contraction or relaxation after ASA treatment. In conclusion, although low-dose ASA may not be expected to have anti-inflammatory action, it did influence post-infarct cardiac remodeling by affecting interstitial and perivascular fibrosis. ASA treatment did not have effects on in vitro left ventricular dysfunction.
 ...
PMID:Chronic aspirin treatment affects collagen deposition in non-infarcted myocardium during remodeling after coronary artery ligation in the rat. 859 99

In the normal myocardium matrix metalloproteinases (MMP) are present in the latent form. To examine whether MMP are activated following infarction or idiopathic dilated cardiomyopathy (DCM), we extracted and measured MMP activity in tissue derived from 7 explanted, failing human hearts due to either previous myocardial infarction (MI) or DCM. MMP activity in infarcted left ventricle (LV), noninfarcted LV and right ventricle (RV) from MI patients, as well as tissue from either ventricle of DCM patients, were compared to the activity of donor heart tissue. SDS-PAGE and dye-binding assays were used to determine total protein concentration, while collagenase activity was measured by SDS-PAGE type substrate gels embedded with type I gelatin (zymography). Accuracy of the zymographic technique was shown for tissue samples as small as 0.05 mg and was comparable to results obtained by a spectrophotometric method. After normalization for total protein concentration, we found 3 +/- 1% collagenase activity in normal atrial tissue which could be activated to 80-90% by trypsin or plasmin, indicating that collagenase is normally inactive or in a latent form in human heart. In endo- and epimyocardium of infarcted LV, on the other hand, collagenase activity was 85-95% and 10-20%, respectively, while 5-10% and 3-5%, respectively, in noninfarcted LV. In DCM, collagenolytic activity in the endo and epimyocardium was 75 +/- 5 and 35 +/- 5% in the LV and 35 +/- 7 and 20 +/- 5% in the RV, respectively. Thus, in dilated failing human hearts secondary to previous MI or DCM, MMP activity is increased. This is particularly the case within the endomyocardium of the infarcted and noninfarcted portions of either ventricle with MI and in both ventricles in DCM. This suggests that an activation of collagenase throughout the myocardium may contribute to its remodeling that includes ventricular dilatation and wall thinning.
 ...
PMID:Matrix metalloproteinase activity expression in infarcted, noninfarcted and dilated cardiomyopathic human hearts. 871 34

Rupture of the left-ventricular free wall may not always result in immediate irreversible hemodynamic collapse. We report a series of five patients (4 male, 1 female; age 59-79 years) successfully operated for postinfarction free-wall rupture with good long-term results. Two patients presented with syncopy and acute tamponade three days after an acute myocardial infarction. In two patients with atypical chest pain and congestive heart failure, a large pericardial effusion and an extreme localized thinning of a myocardial scar region was seen several weeks after an uncomplicated myocardial infarct. In one patient a pseudoaneurysm was detected, which developed asymptomatically within three weeks after a posterior myocardial infarct. In all cases myocardial rupture was suspected after an echocardiographic examination. At surgery a hemopericardium and a localized rupture site were found. The surgical procedure included closure of the defect by direct suture or patch, CABG in 3 cases, and mitral valve replacement in one patient. The postoperative course was uneventful, only one patient needed IABP for 24 hours. Three patients returned to NYHA functional class I, one patient to class II, and one patient to class III. The latter patient died of heart failure 17 months postoperatively, and the other patients are still alive 4,18,24, and 26 months postoperatively. Thus clinical representation of left-ventricular free-wall rupture after myocardial infarction can be highly variable. But close cooperation between experienced echocardiographers and surgeons may allow successful corrections with good long term-results.
 ...
PMID:Clinical presentation of rupture of the left-ventricular free wall after myocardial infarction: report of five cases with successful surgical repair. 878 31

Left ventricular hypertrophy is an adaptive response to long standing hypertension. However, the influence of left ventricular hypertrophy with hypertension on extent of infarct expansion has not been studied. We compared the effects of left ventricular hypertrophy with hypertension on infarct expansion in spontaneously hypertensive rats (SHR, n = 76), Wistar-Kyoto rats (WKY; n = 46) and spontaneously hypertensive rats treated with delapril, an angiotensin converting enzyme (ACE) inhibitor (SHRD; n = 39). The survival rates at 7 days after myocardial infarction were 41%, 24%, and 46% for WKY, SHR, and SHRD. The survival rate of SHR was significantly lower than those of both SHRD and WKY (P < .05). In the surviving rats (18 SHR, 19 WKY, 18 SHRD), both left ventricular cavity area (LCVA) and the infarct segment length per the noninfarct segment length (FW/IVS), measured as indices of left ventricular dilation, were significantly less in SHR and SHRD than in WKY, and the thickness of the left ventricular free wall (Wth), used as an index of left ventricular thinning, was significantly higher in both SHR and SHRD than in WKY (P < .01). However, there was no significant difference in FW/IVS, LCVA, and Wth between SHR and SHRD. Hemodynamic findings 1 week after coronary occlusion demonstrated that all rats were in heart failure, and there were no significant differences in hemodynamics among the three groups. In conclusion, our findings showed that hypertrophy with hypertension reduced infarct expansion, but that reduction of blood pressure by ACE inhibitor did not reduce infarct expansion more than hypertrophy did. However, this finding suggest that an ACE inhibitor may improve the rate of survival of patients with left ventricular hypertrophy with hypertension.
 ...
PMID:Effects of chronic hypertension and left ventricular hypertrophy on the extent of infarct expansion in rats. 886 21

Progressive changes typically occur in left ventricular (LV) architecture following moderate- to large-sized myocardial infarction (MI). These changes include early expansion and thinning of the infarct zone and subsequent increase in myocardial mass within the non-infarcted zone, with LV dilatation and loss of the normal elliptical configuration of the LV cavity. These changes are accompanied by impaired myocyte function and advancing clinical expression of heart failure. Numerous animal and human studies have documented inhibition of LV remodeling post-MI by angiotensin converting enzyme (ACE) inhibitors. Although the ideal timing for initiating treatment remains uncertain, evidence exists that benefit persists long after the time of initial injury. Mechanisms for the effects of ACE inhibitors on LV remodelling may be dependent on changes in myocardial load, may be load independent, or both. These effects are likely to be mediated by reductions in circulating and local tissue concentrations of angiotensin II and in bradykinin degradation. Regardless of the exact mechanism or mechanisms by which ACE inhibitors exert their favourable influence on LV remodelling, it is likely that this effect is a key mediator of the documented clinical benefits afforded by treatment with this class of agents.
 ...
PMID:Role of angiotensin converting enzyme inhibitors in preventing left ventricular remodelling following myocardial infarction. 886 35

Extracellular structural remodeling is the compensatory response of the tissue following pathological stage. Myocardial infarction, which leads to adverse remodeling, thinning of the ventricle wall, dilatation and heart failure, is one of the leading causes of death. Remodeling implies an alteration in the extracellular matrix and in the spatial orientation of cells and intracellular components. The extracellular matrix is responsible for cardiac cell alignment and myocardial structural integrity. Substances that break down the extracellular matrix, specialized proteinases as well as inhibitors of proteinases, appear to be normally balanced in maintaining the integrity of the myocardium. Myocardial infarction leads to an imbalance in proteinase/antiproteinase activities causing alterations in the stability and integrity of the extracellular matrix and adverse tissue remodeling. To explore mechanisms involved in this process and, in particular, to focus on matrix metalloproteinases, their inhibitors, and activators, an understanding of proteinase and antiproteinase is needed. This review represents new and significant information regarding the role of activated matrix proteinases antiproteinases in remodeling. Such information will have a significant impact both on the understanding of the basic cell biology of extracellular matrix turnover, as well as on potential avenues for pharmacological approaches to the treatment of ischemic heart disease and failure.
 ...
PMID:Proteinases and myocardial extracellular matrix turnover. 906 88

Cardiac remodeling following myocardial infarction denotes changes of left ventricular shape, chamber size and wall thickness. It involves both the infarcted and the noninfarcted segments. This process begins at the time of acute myocardial infarction, progresses by stages, and can lead to congestive heart failure. The major determinants of lest ventricular remodeling are infarct size and transmural, adequacy of the healing process, mechanical deformation forces, and progressive ventricular dilation. Infarct expansion is a relatively frequent, early occurring alteration of the ventricular shape. It denotes thinning and lengthening of the infarct segment. The progressive ventricular remodeling can be halted by reactive hypertrophy of the viable myocytes, on condition that it is appropriate. The left ventricular increase results from myocytes hypertrophy, partly their hyperplasia, and increase of fibrosis. Major ways of action in order to limit the cardiac remodeling after myocardial infarction are: reperfusion of the infarct-related vessel by thrombolysis, nitrate therapy, and angiotensin-converting enzyme inhibitors administration. Maximum benefit is when therapy is begun very early.
 ...
PMID:[Remodeling of the left ventricle after myocardial infarction]. 915 27

Coronary artery diseases may categorized into asymptomatic disease, angina pectoris, myocardial infarction, chronic heart failure, and sudden coronary death. Unstable angina, acute myocardial infarction, and sudden cardiac death are known as the acute coronary syndromes. Coronary atheroma is unstable in the patients with acute coronary syndromes. Stable plaques will be unstable when dynamic alterations occur. The alterations are plaque rupture, plaque hemorrhage, coronary thrombosis and vasospasm. They act each other. We analysed the histopathology of coronary arteries who died of acute myocardial infarction in 85 cases. It showed that the risk factors of plaque rupture are clusters of form cells, eccentric plaque with soft lipid rich core, and thinning of fibrous cap in atheroma. Most of these cases ruptured at edge of the atheroma.
 ...
PMID:[Pathogenesis of acute coronary syndromes]. 978 Jul 33

Coronary atherosclerosis is by far the most frequent cause of ischemic heart disease and plaque disruption with superimposed thrombosis is the main cause of the acute coronary syndromes of unstable angina, myocardial infarction, and sudden coronary death. Therefore, for event-free survival, the vital question is not why atherosclerosis develops but rather why, after years of indolent growth, it suddenly becomes complicated by life-threatening thrombosis. Therefore, we have to focus on plaque composition and vulnerability to rupture and plaque thrombogenicity rather than on plaque size and stenosis severity. The risk for plaque disruption depends more on plaque vulnerability (plaque type) than on degree of stenosis (plaque size). Lipid-rich and soft plaques are more vulnerable and prone to rupture than collagen-rich and hard plaques. They are also highly thrombogenic after disruption because of high content of tissue factor. There seems to be three major determinants of a plaque's vulnerability to rupture: 1) the size and consistency of the lipid-rich atheromatous core, 2) the thickness of the fibrous cap covering the core, and 3) ongoing inflammation and repair processes within the fibrous cap. Lipid accumulation, cap thinning, lack of smooth muscle cells (smc), and macrophage-related inflammation destabilize plaques, making them vulnerable to rupture. In contrast, smc-related healing and repair processes stabilize plaques, protecting them against disruption. Plaque size or stenosis severity tell nothing about a plaque's vulnerability. Many vulnerable plaques are invisible angiographically due to their small size and compensatory vascular remodeling.
 ...
PMID:Plaque pathology and coronary thrombosis in the pathogenesis of acute coronary syndromes. 1038 96

A 63-year-old woman with abnormal Q waves in leads II, III, aVF developed ventricular tachycardia after an operation for thyroid carcinoma. Coronary arteriography revealed no organic stenosis, but acetylcholine induced total occlusion of the right coronary artery and severe narrowing of the left coronary artery. Left ventriculography showed inferoposterior and septal akinesis, and echocardiography revealed slight thinning of these affected walls. She had old myocardial infarction due to spasm. One year later, she developed bilateral uveitis and recurrence of tachycardia. Cardiac sarcoidosis was diagnosed by endomyocardial biopsy. In our patient with cardiac sarcoidosis, the presence of multivessel coronary spasm made the diagnosis difficult and may have contributed to cardiac dysfunction. Coronary arteries are rarely involved, but the development of coronary spasm may be linked to sarcoidosis.
 ...
PMID:[Cardiac sarcoidosis complicated by multivessel coronary spasm: a case report]. 1046 90


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>