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)

Echocardiographic findings in patients with ischemic heart disease are described; their correlations with clinical, hemodynamic and angiographic data are presented and discussed. Regional abnormalities of left ventricular wall motion and/or thickening during systole are detected in 84 per cent of patients with acute myocardial infarction and in a high percentage of patients with larger than or equal to 75 per cent narrowing of a major coronary artery. These abnormalities may occur with stress and may be reversible. Left ventricular wall thinning during systole indicates acute ischemia or infarction and thin, dense myocardial echoes indicate scar. Echocardiographic evidence of left ventricular dysfunction is useful in predicting heart failure and mortality in patients with acute myocardial infarction and in predicting surgical mortality for patients undergoing aneurysmectomy and/or coronary artery bypass surgery. Echocardiography has not proved useful in determining graft patency following coronary artery bypass surgery. Technical difficulties and limitations of echocardiography in patients with coronary artery disease are discussed.
 ...
PMID:Echocardiography in ischemic heart disease. 32 1

Echocardiographic septal and posterior wall thicknesses and the percent change with systole were measured in 146 patients with the following diagnoses: acute myocardial infarction (40), chronic coronary artery disease (49), congestive cardiomyopathy (8), atrial septal defect (20), and no cardiac disease (29). Mean diastolic thicknesses for the groups of patients with coronary artery disease and congestive cardiomyopathy were not significantly different from normal although there were abnormal values for individual patients within each group. Mean diastolic thickness of the septum was greater than normal for the group with atrial septal defect (P less than 0.02). Wall thinning with systole was associated with acute infarction or ischemia (P less than 0.0001); decreased thickening (less than normal) commonly occurred in patients with acute myocardial infarction, chronic coronary artery disease, and congestive cardiomyopathy. Patients with atrial septal defect had normal thickening with abnormal motion. Results of this study show that 1) systolic thinning is indicative of an acute event; 2) abnormal changes in systolic wall thickening occur commonly in patients with coronary artery disease or congestive cardiomyopathy; and 3) abnormal wall motion may occur without abnormal wall thickening, as the echoes of patients with atrial septal defect indicate.
 ...
PMID:Systolic thickening and thinning of the septum and posterior wall in patients with coronary artery disease, congestive cardiomyopathy, and atrial septal defect. 83 Jan 97

Apart from their ability to relieve myocardial ischemia, nitrates have an important role to play on preservation of left ventricular (LV) geometry and function after acute myocardial infarction (MI). In the first 48 hours after acute MI, intravenous nitroglycerin infusion titrated to a low-dose regimen produces multiple benefits, including smaller infarct size, better regional and global LV function, less remodeling, fewer in-hospital complications, and fewer deaths in-hospital and up to 1 year. This regimen might be an effective adjunct during reperfusion therapy for salvaging ischemic myocardium, LV geometry, and function. Recent studies indicate that prolonged therapy with nitrates during the healing phase after acute MI can effectively further limit progressive LV remodeling (less LV dilation, expansion, thinning, and aneurysm formation) and preserve LV function. Tolerance with chronic therapy is avoided by an eccentric dose regimen to provide a nitrate-free interval.
 ...
PMID:Role of nitrates after acute myocardial infarction. 152 30

The primary goal of the current study was to assess in situ, using magnetic resonance imaging, the effect of a new angiotensin-converting enzyme inhibitor, cilazapril, in reducing left ventricular remodeling after acute myocardial infarction. Three groups of animals were investigated: (1) sham-operated rats (n = 19); (2) infarcted rats receiving no treatment (n = 23); and (3) infarcted rats receiving cilazapril (100 mg/L drinking water, n = 20). Treatment with cilazapril began on the third day postocclusion and continued for 3 to 4 months. Myocardial infarction was produced by ligation of the left coronary artery, and electrocardiographic (ECG)-gated short-axis images were acquired 3 to 4 months later. Sham-operated animals were subjected to the same procedure but the left coronary artery was not ligated. From the image acquired in the middle of the left ventricle (equatorial slice), left ventricular wall thicknesses, chamber diameters, and surface area measurements of the cavities were determined. At autopsy examination, infarct size and tissue water content were determined. The results demonstrate that magnetic resonance imaging has the potential to assess in situ the alterations of left ventricular dimensions and mass after acute myocardial infarction and can be used to document the influence of therapeutic interventions. Cilazapril provided protection against the deleterious remodeling changes such as ventricular dilation and wall thinning consequent to acute myocardial infarction.
 ...
PMID:Effect of cilazapril on regional left ventricular wall thickness and chamber dimension following acute myocardial infarction: in vivo assessment using MRI. 153 34

Infarct expansion can be defined pathologically as a distortion of ventricular topography produced by thinning and disproportionate dilation of the infarct segment. Large transmural infarcts tend to be associated with greater propensity for infarct expansion. Two-dimensional echocardiography has made it feasible to detect these acute alterations in cardiac topography by serial examination of patients with acute myocardial infarction. A practical approach to the echocardiographic quantification of expansion involves analysis of end-diastolic cross-sectional echo views at the papillary muscle level, which can be used as fixed internal landmarks to divide the left ventricle into 2 segments, anterior and posterior. An off-line computer system can be used to track relative lengths of these segments as well as their thicknesses over time. In the initial clinical study, one third of patients with acute anterior transmural infarcts showed an average 50% increase in the infarct segment length beginning within the first 3 days of infarction, characterized by disproportionate progressive dilation and transmural thinning of this zone. These patients demonstrated a significantly higher mortality than those without expansion. Later studies demonstrated not only continuing dilation of the infarcted anterior wall, but also progressive dilation of the noninfarcted posterior wall, underscoring the importance of continuing long-term noninvasive follow-up. Not only is expansion associated with a poor clinical outcome; it has also been shown experimentally and clinically to be modifiable or even preventable by various therapeutic maneuvers, which may well improve survival. Because of the limitations of the echocardiographic window, it is often possible to obtain only a single cross-sectional view of high quality, and even then technical quality may not be sufficiently high to enable detailed quantitative analysis.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Myocardial infarct expansion: recognition, significance and pathology. 183 95

Low-dose intravenous nitroglycerin infusion can be safely administered during acute myocardial infarction to unload the left ventricle and salvage ischemic myocardium and left ventricular geometry and function. In an experimental conscious dog model, low-dose infusion titrated to decrease mean blood pressure by 10% over the first 6 hours after coronary artery ligation resulted in 51% decrease in infarct size, 54% decrease in preload, and more than 50% increase in collateral blood flow. The same benefits were seen when methoxamine was given to counteract that 10% decrease in blood pressure. Similar short-term nitroglycerin infusion also limited remodeling in the dog model. More important, no myocardial salvage was seen with excessive nitroglycerin-induced hypotension to levels less than 80 mm Hg. Clinically, prolonged low-dose nitroglycerin infusion was evaluated in a prospective, randomized, single-blinded, placebo-controlled study of 310 patients with acute infarction: 154 received nitroglycerin and 156 received placebo. Nitroglycerin was titrated to reduce mean blood pressure by 10% in normotensive patients and up to 30% in hypertensive (blood pressure greater than 140/90 mm Hg) patients, but not to less than 80 mm Hg. Nitroglycerin produced several benefits compared with placebo: (1) smaller creatine kinase infarct size; (2) less regional left ventricular dysfunction, better global ejection fraction, and less infarct expansion and thinning; (3) better clinical functional status and hemodynamics; (4) fewer inhospital complications such as acute left ventricular failure and dilation due to marked infarct expansion, left ventricular thrombus, cardiogenic shock, and infarct extension; and (5) fewer deaths up to 1 year in patients with anterior Q-wave infarction.
 ...
PMID:Intravenous nitroglycerin unloading in acute myocardial infarction. 183 97

An acute myocardial infarction, particularly one that is large and transmural, can produce expansion and alterations in the topography of both the infarcted and non-infarcted regions or the ventricle. This remodelling can importantly affect the function of the ventricle and the prognosis. Side-to-side slippage of myocytes in the myocardium occurring in association with ventricular dilatation is responsible for wall thinning. The increased internal load that is sustained through the cardiac cycle is thought to promote further stress, dilatation and hypertrophy of the non-infarcted area. The collagen network has been showed to be high responsible for the remodelling of the interstitium and therefore for the scar formation involved in the expansion. The process for ventricular enlargement can be influenced by infarct size, healing end ventricular wall stresses. The process of scarification can be interfered with during the acute infarct period by the administration of glucorticosteroids and non-steroidal anti-inflammatory agents, which results in thinner infarct and further expansion. A most effective way to prevent or minimize the increase in ventricular size is to limit the initial insult. Acute thrombolytic reperfusion therapy may work in this way. Finally early and long-term therapy with an angiotensin converting enzyme inhibitor can favorably alter the loading conditions of the left ventricle, reducing progressive enlargement with a prolongation in survival.
 ...
PMID:[Left ventricular remodelling]. 184

Thinning and dilatation (expansion) of the infarct region and complete rupture of the ventricular wall are significant complications of acute transmural myocardial infarction associated with increased morbidity and mortality. The pathogenesis of these related events is unknown. Recent studies of myocardial connective tissue have delineated an extensive array of intercellular and pericellular structures which serve as a skeletal framework and which may modulate contractile activity. We have employed a modified silver impregnation method to visualize the connective tissue components by light microscopy. To explore whether the skeletal framework is altered in acute myocardial infarction with and without ventricular rupture, we studied 9 human hearts at autopsy, and 4 canine infarcts of known duration. The human infarctions included 4 nonruptured cases with infarcts 1-5 days old, and 5 ruptured cases with infarcts 3-10 days old. Sections from normal, lateral, and central infarct or ventricular rupture sites were stained with silver. The normal tissue from each heart served as a control. Silver staining was moderately decreased in the lateral infarct zones, and markedly decreased in the central non-ruptured infarct zones. In the 5 ventricular rupture cases, the rupture site had no silver staining. A similar pattern was observed in the 4 canine infarcts. Thus, we conclude that the skeletal framework is markedly altered in the central zone of acute myocardial infarction. The acute changes of silver stained connective tissue may contribute significantly to the development of infarct expansion or ventricular wall rupture.
 ...
PMID:Alterations of the myocardial skeletal framework in acute myocardial infarction with and without ventricular rupture. A preliminary report. 245 17

To determine whether decreasing preload and afterload by prolonged nitroglycerin therapy (NTG) after acute myocardial infarction (AMI) might improve left ventricular (LV) geometry and function, 43 patients with a first anterior transmural AMI (ATAMI) were given low-dose intravenous NTG infusion for the first 48 h and then randomized to buccal NTG (1-3 mg t.i.d., five hourly with an eight-h washout period to avoid vascular tolerance; dose titrated as for i.v. NTG for 10% decrease in blood pressure but not below 80 mm Hg) or placebo for six weeks. All patients had serial two-dimensional echocardiography for 12 weeks for regional LV function and topography: Expansion index = asynergic/non-asynergic endocardial segment length; Thinning ratio = asynergic/normal wall thickness. Asynergy was defined as akinesis + dyskinesis. Between initial and 12-week studies, expansion index did not change in the buccal NTG group (2.09 vs 2.28, N.S.; n = 23) but increased in the placebo group (2.10 vs 2.89, p less than 0.05; n = 20). Over the same period, thinning ratio was unchanged with buccal NTG (0.82 vs 0.77, N.S.) but increased with placebo (0.78 vs 0.66 p less than 0.05). Both expansion and thinning at 12 weeks were greater with placebo than buccal NTG (p less than 0.01). The results indicate that prolonged NTG therapy decreased infarct expansion and infarct thinning. Compared to placebo, the NTG group also showed improved hemodynamics, decreased LV volume and asynergy, and increased ejection fraction. Thus, prolonged NTG therapy after ATAMI preserves LV function and topography. The beneficial early and late remodeling with prolonged NTG therapy might prevent aneurysm formation.
 ...
PMID:Improved left ventricular function and topography by prolonged nitroglycerin therapy after acute myocardial infarction. 251 85

The enlarged heart has long been recognized as an important sign of systolic dysfunction of many different etiologies. Regardless of etiology, cardiac enlargement is associated with decreased survival. Cardiac enlargement after acute myocardial infarction (AMI) may be a progressive process. Early after AMI, the process of infarct expansion, or thinning and stretching of the infarct region leads to early volume enlargement detectable within 3 days of the infarct. During the next 2 weeks, volume enlargement takes place which includes lengthening of both the infarcted and the non-infarcted regions. Finally, additional left ventricular enlargement occurs during the next year after the infarction. Both experimental and clinical studies have demonstrated that such progressive LV enlargement may be halted by angiotensin converting enzyme inhibition with captopril. A large scale randomized trial is currently under way to determine whether captopril improves survival after infarction (Survival and Ventricular Enlargement, SAVE).
 ...
PMID:Left ventricular dilatation following myocardial infarction: clinical course and potential for therapy. 252 55


1 2 3 4 5 6 7 Next >>