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)

Six hundred and twenty-five patients with diabetes mellitus were studied by standardised clinical methods, resting and exercise electrocardiography (ECG) and digitised echocardiography to determine the prevalence of coronary and non-coronary heart disease. Clinical evidence of coronary artery disease (angina and infarction) was present in 110 (18 per cent) normotensive patients. Hypertension (blood pressure greater than 165/95 mmHg) was present in 172 (27 per cent) of whom 32 had cardiac symptoms. Heart failure or left ventricular dilatation was seen in 18 of whom 11 had either hypertension or coronary artery disease and six asymptomatic patients had unexplained ventricular hypertrophy. Echocardiograms in 245 of 290 asymptomatic patients with normal ECG showed that relaxation was prolonged (p less than 0.001) and mitral valve opening delayed (p less than 0.001) from normal especially in those with severe microangiopathy (proliferative retinopathy and/or heavy proteinuria). The peak rates of cavity dimension increase and posterior wall thinning were reduced from normal (both p less than 0.001) and patients with severe microangiopathy had the most marked changes. Redivision of these 245 diabetics by abnormalities of left ventricular function showed that 147 had normal function in whom only one of 23 (random 15 per cent sample) had a positive exercise ECG. Prolonged relaxation or delayed mitral valve opening alone (a nonspecific abnormality) was present in 41 and only three of 28 had a positive exercise ECG. Thirty-one had delayed mitral valve opening with inco-ordinate relaxation (abnormalities very suggestive of coronary artery disease) of whom 20 of 29 had a positive exercise ECG. Twenty-six had delayed mitral valve opening with slow cavity dimension increase or wall thinning (without hypertrophy) of whom 21 of 25 had a negative exercise ECG. This is a relatively specific abnormality similar to that found in left ventricular hypertrophy. Coronary artery disease is common in symptomatic and asymptomatic forms in diabetes mellitus. Non-coronary left ventricular diseases, such as dilation and hypertrophy, are probably no more common in diabetics than non-diabetics. A small number of diabetics with severe microangiopathy had abnormal relaxation and reduced peak rate of dimension increase or wall thinning which may represent left ventricular disease due to microangiopathy.
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PMID:A prospective study of heart disease in diabetes mellitus. 670 23

To determine the effects of chronic constriction of the left coronary artery on the function and structure of the heart, coronary artery narrowing was surgically induced in rats and ventricular pump performance, extent and distribution of myocardial damage, and the hypertrophic and hyperplastic response of myocytes were examined. Alterations in cardiac hemodynamics were found in all rats, but the characteristics of the physiological properties of the heart allowed a separation of the animals into two groups which exhibited left ventricular dysfunction and failure, respectively. Left ventricular hypertrophy occurred in both groups and was characterized by ventricular dilatation and wall thinning which were more severe in the failing animals. Multiple foci of myocardial damage across the wall were seen in all animals but tissue injury was more prominent in the endomyocardium and in failing rats. The anatomical and hemodynamic changes resulted in a significant increase in diastolic wall stress which paralleled the depression in ventricular performance. Myocyte cell loss and myocyte cellular hypertrophy were more severe with ventricular failure than with dysfunction. Finally, diastolic overload appeared to be coupled with activation of the DNA synthetic machinery of myocytes and nuclear mitotic division. In conclusion, a fixed lesion of the left coronary artery leads to abnormalities in cardiac dynamics with marked increases in diastolic wall stress and extensive ventricular remodeling in spite of compensatory myocyte cellular hypertrophy and hyperplasia in the remaining viable tissue.
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PMID:Ventricular remodeling in global ischemia. 757 15

Patients with morbid obesity have high rates of sudden, unexpected cardiac death. The mechanism of death in these patients is uncertain. Twenty-eight patients with morbid obesity (22 sudden cardiac deaths, 6 unnatural deaths) were compared to 11 age-matched nonobese patients with traumatic deaths. Heart weight, left ventricular cavity diameter, left and right ventricular wall thickness, ventricular septal thickness, epicardial fat thickness, and extent of coronary artery atherosclerosis were determined; myocyte size, nuclear size, and degree of interstitial fibrosis were calculated morphometrically. Mean heart weights in the patients with morbid obesity were increased but remained constant as a percentage of body weight. Of the gross parameters, only heart weight and left ventricular cavity size were independent predictors of obesity. Of microscopic parameters, only nuclear area was an independent predictor of obesity. Of 22 patients with morbid obesity, dilated cardiomyopathy was the most frequent cause of sudden cardiac death in (10 patients), followed by severe coronary atherosclerosis (6), concentric left ventricular hypertrophy without left ventricular dilatation (4), pulmonary embolism (1), and hypoplastic coronary arteries (1). The cardiomyopathy of morbid obesity is characterized by cardiomegaly, left ventricular dilatation, and myocyte hypertrophy in the absence of interstitial fibrosis. It is the most common cause of sudden cardiac death in these patients.
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PMID:Sudden death as a result of heart disease in morbid obesity. 763 12

The authors report a long term success of bipulmonary transplantation in a 15 year old girl with cystic fibrosis and respiratory failure complicated by severe right heart failure. The operation did not cause any particular problems. After transplantation, the clinical signs of right ventricular failure and echocardiographic right ventricular dilatation regressed in less than one week. The right ventricular hypertrophy also regressed. Echocardiography shows no abnormality after 5 years' follow-up.
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PMID:[Favorable outcome of severe right cardiac insufficiency after bipulmonary transplantation]. 770 41

The effect on myocardial function and structure of long-term administration of quinapril (10-20 mg daily), an angiotensin-converting-enzyme (ACE) inhibitor, was investigated in 24 patients (18 men, 6 women; mean age 48 [20-65] years) with chronic isolated asymptomatic aortic or mitral regurgitation. Coronary heart disease had been excluded angiographically. After one year's treatment the regurgitation fraction, compared with the pretreatment value, had decreased by 27% in those patients with aortic regurgitation (AR) and 42% in those with mitral regurgitation (MR) (P = 0.0001). The mean left ventricular enddiastolic volume was reduced from 150 +/- 33 to 128 +/- 30 ml/m2 in patients with AR, from 146 +/- 26 to 109 +/- 24 ml/m2 in those with MR (P = 0.0001). The mean endsystolic volume fell from 55 +/- 27 to 44 +/- 28 ml/m2 in patients with AR and from 63 +/- 43 to 47 +/- 29 ml/m2 in those with MR (P = 0.002). The mean left ventricular ejection fraction at rest and on exercise rose slightly in patients with AR, remaining unchanged in those with MR. The left ventricular mass, as measured by echocardiography, was reduced by 35% in patients with AR, and the left ventricular hypertrophy, demonstrated in all patients, regressed. In patients with MR the left ventricular mass decreased by 15% and septal thickness became normal (borderline hypertrophy). These data indicate that, after one year's treatment with quinapril, left ventricular dilatation, mass and hypertrophy regressed and left ventricular function improved in patients with AR or MR.
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PMID:[Long-term treatment with quinapril in chronic aortic and mitral insufficiency]. 771 32

End-stage renal disease (ESRD) patients have a high cardiovascular mortality rate. Precise estimates of the prevalence, risk factors and prognosis of different manifestations of cardiac disease are unavailable. In this study a prospective cohort of 433 ESRD patients was followed from the start of ESRD therapy for a mean of 41 months. Baseline clinical assessment and echocardiography were performed on all patients. The major outcome measure was death while on dialysis therapy. Clinical manifestations of cardiovascular disease were highly prevalent at the start of ESRD therapy: 14% had coronary artery disease, 19% angina pectoris, 31% cardiac failure, 7% dysrhythmia and 8% peripheral vascular disease. On echocardiography 15% had systolic dysfunction, 32% left ventricular dilatation and 74% left ventricular hypertrophy. The overall median survival time was 50 months. Age, diabetes mellitus, cardiac failure, peripheral vascular disease and systolic dysfunction independently predicted death in all time frames. Coronary artery disease was associated with a worse prognosis in patients with cardiac failure at baseline. High left ventricular cavity volume and mass index were independently associated with death after two years. The independent associations of the different echocardiographic abnormalities were: systolic dysfunction-older age and coronary artery disease; left ventricular dilatation-male gender, anemia, hypocalcemia and hyperphosphatemia; left ventricular hypertrophy-older age, female gender, wide arterial pulse pressure, low blood urea and hypoalbuminemia. We conclude that clinical and echocardiographic cardiovascular disease are already present in a very high proportion of patients starting ESRD therapy and are independent mortality factors.
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PMID:Clinical and echocardiographic disease in patients starting end-stage renal disease therapy. 773 Nov 45

Clinical and echocardiographic manifestations of cardiac disease are frequently present in patients starting end-stage renal disease therapy. Congestive heart failure, ischemic heart disease, systolic dysfunction, concentric left ventricular hypertrophy, and left ventricular dilatation are significant, adverse prognostic indicators, independent of age, diabetes mellitus, and smoking. Risk factors related to the uremic state, which are potentially reversible, include inadequate dialysis, anemia, hypoalbuminemia and hypocalcemia. Hypertension predisposes patients to congestive heart failure, following the development of which hypotension becomes an independent predictor of mortality.
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PMID:Risk factors for cardiac morbidity and mortality in dialysis patients. 788 84

A 71 years old man, ex-smoker, moderate drinker, with a history of diabetes mellitus (type II), moderate arterial hypertension, mild aortic stenosis and moderate uniform left ventricular hypertrophy echographically documented, developed a non Hodgkin low malignancy cavum lymphoma. He has underwent chemotherapy for two years (adriamycin and other chemotherapy drugs) at moderate dosages. A complete remission of the lymphoma followed the treatment, but an initial deterioration of left ventricular function, with heart dilatation and congestive heart failure, was found. The patient improved by medical treatment, returning to the previously stable clinical condition. However a ventricular dilatation reoccurred and a paroxysmal complete atrio-ventricular block developed, necessitating the implantation of a pace maker. The patient died suddenly, during sleep, at home. This is a unique case, because of the numerous cardiac factors associated (chemotherapy and clinical findings). More probably the combination of these multiple factors and their interrelationship could explain the unique non-linear evolution of the left ventricular hypertrophy. In conclusion in these patients a very strict clinical and pharmacological follow up with serial echocardiographical examinations is fundamental and highly recommended.
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PMID:[Normalization of left ventricular function and subsequent recurrence of dilatation and pump failure in a patient with hypertensive heart disease in dilated phase after treatment with anthracycline]. 792 84

Congestive heart failure is often preceded by a latent or preclinical phase in which patients are relatively asymptomatic. During this period, there is neuroendocrine activation, left ventricular dysfunction, and remodeling of the heart. The extent to which these activities are interrelated is unclear, but it appears from experimental studies that myocardial damage is associated with chronic sympathetic nervous system activation, left ventricular hypertrophy, and a subsequent increase in left ventricular volume. The nondamaged myocardial tissue demonstrates enhanced messenger RNA for angiotensinogen and angiotensin converting enzyme activity. Angiotensin II along with other trophic signals may prime the cell for "growth." Alteration of left ventricular function may produce unusual loading conditions on the myocardium. Stretch of membrane-bound ion channels may impart mechanical signals that may be transduced and expressed as cellular hypertrophy. Interstitial collagenase may be activated, leading to disruption of the collagen-supporting network. Elongated cells (eccentric hypertrophy), cell slippage, and cell dropout may contribute to the dilatative process. The end product is cardiac dilatation, inefficient left ventricular performance, and congestive heart failure. We have observed that an increase in left ventricular mass is the initial morphological response to acute myocardial damage in a canine model. This occurs at 1 week and is followed by progressive activation of the sympathetic nervous system, left ventricular dilatation, and modest left ventricular dysfunction, a condition that mimics preclinical heart failure in patients. The remodeling process in the canine model, including the increase in mass and volume, may be blocked by angiotensin converting enzyme inhibitor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neurohumoral activation in preclinical heart failure. Remodeling and the potential for intervention. 809 70

The boy was first admitted to the Department of Pediatric Cardiology at the age of 4 1/2 because of cardiac murmur diagnosed on the third day of life. A diastolic murmur of a grade 4/6, left ventricular hypertrophy as well as left aortal and ventricular dilatation were discovered. The findings showed a tendency of increase with time, but the patient had no symptoms. X-ray in the long axis view revealed a defect within the upper part of the interventricular septum immediately below the aorta, and dilated right coronary sinus. An invasive diagnostic method was undertaken, as well. The operative procedure was done with a total cardio-pulmonary bypass and hypothermia (29 degrees C). A tunnel from the anterior aortal wall through the outflow tract of the right ventricle to the left side of the heart was established intraoperatively. The defect was solved by a "sandwich" technique (two patch technique). Postoperative period was uneventful. A Doppler echocardiogram demonstrated the normal hemodynamic status of the patient without the left-to-right or right-to-left shunt and aortal insufficiency.
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PMID:[Aortico-left ventricular tunnel]. 813 66


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