Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ventricular dilatation may have important prognostic implications for the survival of patients with left ventricular (LV) dysfunction. To determine the manner and extent to which the left ventricle of the rat remodels and dilates after myocardial infarction, we obtained the passive pressure-volume relationships, chamber stiffness constants, and mass during both the early and late phases. In moderate and large infarcts as inflammation and edema developed, LV weight increased then progressively decreased as a thin scar formed, returning to normal values as a result of compensatory hypertrophy of the residual myocardium. LV dilatation occurred in all rats with infarcts but to different extents depending on infarct size and duration. In the early postinfarction phase, pressure-volume relationship was relatively unchanged in all infarct-size groups, except for significant rightward shift in low pressure range for rats with moderate and large infarcts and significant leftward shift in high pressure range for rats with small infarcts. During resolution of the inflammatory response, LV dilatation occurred in all infarct groups in relation to infarct size. As scar formation became complete, LV enlargement did not progress in rats with small infarcts but did so in rats with moderate and large infarcts. LV chamber stiffness remained within the range of normal values during the early phase in all rats with infarcts but decreased significantly during the late phase in rats with moderate and large infarcts in association with the extent of ventricular enlargement. Alterations in the volume-to-mass ratio (V/Vwt) were most marked in the late postinfarction phase, wherein both volume (increased) and mass (decreased, then increased) changed dramatically and V/Vwt progressively increased in rats with large infarcts.
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PMID:Progressive ventricular remodeling in rat with myocardial infarction. 203 62

To elucidate the clinical characteristics associated with regional ventricular dilatation in the early phase of myocardial infarction (MI), 228 patients with acute Q-wave anterior MI were studied. Forty-nine patients (21 percent) had echocardiographically demonstrated regional ventricular dilatation (an abnormal bulge in the left ventricular contour during both systole and diastole) on the third hospital day. Careful auscultation revealed that a pericardial rub was present in 49 patients (21 patients with and 28 patients without regional ventricular dilatation) during the first three days after hospital admission. Multivariate analysis was performed to determine the relative importance of pericardial rub with six other clinical variables related to regional ventricular dilatation. Pericardial rub and cardiac output were the significant factors related to the presence of regional ventricular dilatation. Thus, a pericardial rub, in concert with impaired left ventricular function, is a physical sign associated with regional ventricular dilatation, and anatomically transmural infarction is the possible factor explaining their association.
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PMID:Clinical significance of pericardial rub with regional ventricular dilatation. 206 Mar 31

The overall cardiovascular mortality in patients with chronic renal failure is about 30 per cent of which 10 per cent is attributed to myocardial infarction. This prevalence led some workers to propose a hypothesis of "accelerated atherosclerosis" due to the hyperlipidaemia observed in 30 to 70 per cent of patients. However, the concept of accelerated atherosclerosis, which was based essentially on clinical studies, has been questioned. Pericardial effusion is a common complication of chronic renal failure and has been reported in over 62 per cent of patients in echocardiographic studies. There are many causes and symptoms are often mild; systematic echocardiographic examination of patients with renal failure undergoing haemodialysis has shown 32 per cent of pericardial effusions to be asymptomatic. There are two potential complications: cardiac tamponade and, lesser frequently, constrictive pericarditis. Cardiac failure is a common cause of death in patients undergoing long-term dialysis. The myocardial histological appearances are those of fibrosis, the etiology of which is not fully understood although the dialysis membranes and hypotensive episodes occurring during haemodialysis have been thought to play a role. Left ventricular hypertrophy and fibrosis may give rise to ventricular arrhythmias which could explain some of the cases of sudden death observed in patients with renal failure and often wrongly attributed to ischemic heart disease. Another form of myocardial disease which is observed later is characterised by an alteration of systolic function with left ventricular dilatation and hypokinesia and increased end diastolic pressures without an increase in left ventricular wall thickness. Valvular heart disease may also result from renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[So-called uremic heart diseases]. 210 35

Echocardiography has established an important role in the surveillance of patients with myocardial infarction. Segmental wall motion abnormalities are easily identified and their extension reflects the size of the infarct. Global left ventricular function may be assessed and left ventricular dilatation documented. This information is useful in evaluating the long-term prognosis. In addition, Doppler echocardiography is valuable for detecting complications persisting or occurring after the acute phase such as pericardial effusion, mural thrombus, aneurysm or mitral regurgitation. The indications of Doppler echocardiography should be guided by the symptomatology and the results of clinical examination.
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PMID:[Doppler echocardiography in myocardial infarction and its complications]. 211 35

Angiotensin-converting enzyme inhibitors have had a significant impact on the treatment of congestive heart failure (CHF). Hemodynamic and clinical improvements in patients with severe CHF fostered the use of angiotensin-converting enzyme inhibitors in mild to moderate CHF. Angiotensin-converting enzyme inhibitors produce acute and sustained improvements in ventricular hemodynamics and quality of life. Captopril plus diuretic therapy is an effective alternative to digoxin in patients with mild to moderate CHF. Enalapril maleate and lisinopril have been shown to be effective in moderate to severe CHF when combined with digoxin and diuretics. Captopril and enalapril also improve survival in selected patients; captopril attenuates left ventricular dilatation after myocardial infarction. Although all angiotensin-converting enzyme inhibitors are similar in mechanism of action, pharmacokinetic differences impact their clinical use. Prolonged symptomatic hypotension compromising systemic perfusion and organ function has been reported with longer-acting agents; hypotension is usually short-lived and rarely compromises organ function with shorter-acting agents.
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PMID:Angiotensin-converting enzyme inhibitors in congestive heart failure. 187 77

Sequential alterations of left ventricular volumes and haemodynamics were studied in 29 patients between 4 days and 4 weeks after myocardial infarction. Left ventricular volume was determined by single photon emission computerized tomography (SPECT), infarct size by creatine kinase (CK) analysis, angiography and thallium201 SPECT. Left ventricular volume index (ml m-2) decreased in patients with small infarcts (74.5 +/- 4.9 vs 62.5 +/- 3.0, P less than 0.005), but increased significantly in patients with moderate (74.6 +/- 4.7 vs 83.6 +/- 5.0, P less than 0.0001) and large (71.7 +/- 4.8 vs 90.2 +/- 6.5, P less than 0.0001) infarctions between 4 days and 4 weeks after acute myocardial infarction. The latter groups contained almost two-thirds of our patients. This dilation occurred without significant changes in filling pressures (Swan-Ganz catheter) and resulted in significant augmentation and finally, normalization of stroke volume at 4 weeks (33.2 +/- 3.3 vs 42.6 +/- 2.9), despite persistently depressed ejection fraction (conventional radionuclide ventriculography). It is concluded that left ventricular dilatation post-myocardial infarction is structural (unchanged filling pressure) and compensatory (increased stroke volume) during the interval observed in this study.
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PMID:Early remodelling of the left ventricle in patients with myocardial infarction. 214 80

Progressive asymptomatic ventricular dilatation can occur following myocardial infarction and severe ventricular dysfunction is often present by the time clinical congestive heart failure occurs. In a randomized, double-blind trial, the effects of captopril 25 mg tid, frusemide 40 mg daily and placebo were studied in 90 patients with asymptomatic left ventricular dysfunction (ejection fraction less than 45%) 1 week following Q wave myocardial infarction. Left ventricular volumes and function were assessed at intervals during the subsequent year using two-dimensional echocardiography. The frusemide and placebo groups showed significant increases in ventricular volumes with stroke volume index unchanged and ejection fraction slightly reduced, whereas the captopril group showed a significant reduction in left ventricular end-systolic volume index with stroke volume index and ejection fraction increased. At 12 months the difference in the change in ejection fraction from baseline between the captopril and frusemide groups was 10.5% and captopril and placebo groups 9.6% (both P less than 0.0001). There was a significant difference in occurrence of clinical heart failure in the placebo group compared with the other groups (P less than 0.05). Blood pressure increased significantly within the normal range in the placebo and frusemide groups whereas there was essentially no change from baseline in the captopril group. There was no significant correlation between baseline left ventricular volumes and function and subsequent change, and anterior and inferior infarct subgroups showed similar responses within the treatment groups. In conclusion, captopril improves asymptomatic ventricular dysfunction and prevents clinical heart failure during the year following myocardial infarction. Frusemide may also prevent clinical heart failure but not progressive ventricular dilatation.
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PMID:Preventive treatment of asymptomatic left ventricular dysfunction following myocardial infarction. 214 81

Absolute left ventricular volumes, normalized to body surface area, were determined by a count-based radionuclide technique in 189 patients with myocardial infarction (MI). All examinations were performed in the second week after MI. Fifty-three percent of the patients had an increased end-diastolic volume index (EDVI) and 72% an increased end-systolic volume index (ESVI). Patients with anterior MI had the same median EDVI as patients with inferoposterior MI, but significantly higher median ESVI and significantly lower median stroke volume index (SVI). SVI was subnormal in 19% of the 189 patients and left ventricular ejection fraction (LVEF) was subnormal in 67%. A non-linear, inverse relationship was present between EDVI and LVEF and between ESVI and LVEF, but LVEF varied greatly for any degree of ventricular dilatation. During a 1-year follow-up period, death from cardiac causes occurred in 29 patients. A strong relationship was present between the degree of ventricular dilatation and 1-year mortality, as well as between the degree of SVI or LVEF reduction and 1-year mortality but, next to clinical heart failure, LVEF was the single most powerful predictor of cardiac death, and various combinations of EDVI, ESVI and SVI did not add more prognostic information to that obtained by heart failure than did LVEF.
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PMID:Left ventricular volumes in the recovery phase after myocardial infarction: relation to infarct location, left ventricular function and one-year cardiac mortality. 182 33

An important antecedent to the development of late congestive heart failure is left ventricular dilatation and remodeling following myocardial infarction, which occurs in 30-40% of acute anterior transmural infarcts. Dilatation and remodeling commence within the first 24 hours following myocardial infarction and may be steadily progressive over months to years. Both the infarcted and uninfarcted regions of the myocardium are equally involved in the process. The remodeling process comprises left ventricular wall thinning (mainly due to cell slippage), chamber dilatation, and compensatory hypertrophy of the uninfarcted segment of the myocardium. The hypertrophy may initially be physiologic but may ultimately become a pathologic process, and thereby contribute to pump dysfunction. The possible reasons why the ventricular hypertrophy may ultimately be dysfunctional include alterations in local architecture and their sequelae alone or in concert with local changes in the beta-adrenergic, alpha-adrenergic, or renin angiotensin systems. At the present time, there are encouraging data to suggest that nitroglycerin, or the angiotensin converting enzyme inhibitor captopril, may ameliorate this process.
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PMID:Left ventricular dilatation and failure post-myocardial infarction: pathophysiology and possible pharmacologic interventions. 214 59

Cardiac function in myocardial infarction (MI) depends on the extent of damage in ischemic myocardium and the compensatory response of residual myocardium. Because thrombolytic therapy is performed in many patients, reperfusion of ischemic myocardium may take place at various stages of progression of the ischemic insult. If perfusion is reestablished before necrosis occurs, myocardium may recover immediately or after hours to weeks ("stunned myocardium"). If coronary occlusion persists, necrosis develops in the subendocardium, propagates transmurally and forms a scar after the healing phase. Residual myocardium responds to loss of contractile tissue and material properties of the ischemic zone by hypertrophy and dilatation. This study shows that left ventricular dilatation is accompanied by an increase in stroke volume from 4 days to 4 weeks; however, left ventricular dilatation progresses while stroke volume remains constant from 4 weeks to 6 months, suggestive of noncompensatory left ventricular dilatation. Angiotensin-converting enzyme (ACE) inhibitors have been shown to reduce lactate production after 60 seconds, and infarct size after 6 hours of coronary occlusion in dogs. Stunned myocardium recovers faster in animal experiments and pacing-induced myocardial ischemia may be prevented by ACE inhibitors. Left ventricular dilatation and mortality is reduced by ACE inhibitors in rats after MI. Several potential mechanisms are discussed to establish a favorable action of ACE inhibitors at various stages of MI. Clinical evidence is still pending; however, large studies are ongoing to clarify potential indications of ACE inhibitors in ischemic heart disease in humans.
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PMID:Influence of angiotensin-converting enzyme inhibition on cardiac function in myocardial infarction. 218 51


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