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)

Nitrates exert their anti-anginal activity by a number of mechanisms. By reducing venous return and left ventricular end-diastolic pressure they lower myocardial oxygen demand and at the same time enhance blood flow to the sub-endocardium. They also directly increase myocardial oxygen supply by dilating the coronary artery stenoses and increasing collateral blood flow. These pharmacodynamic attributes are clinically efficacious in all the ischaemic myocardial syndromes. In stable angina pectoris, nitrates reduce myocardial ischaemia and ischaemic pain and increase exercise tolerance. In unstable angina, nitrates similarly reduce electrocardiographic evidence of myocardial ischaemia and relieve anginal pain. Following acute myocardial infarction, nitrates reduce ventricular dilatation and by so doing reduce pulmonary congestion and mitral regurgitation. The weak anti-aggregatory effect of nitrates on platelets may also play an adjuvant role in their anti-ischaemic activity. Early small-scale studies with both intravenous and oral nitrates demonstrated a trend to reduced mortality and reinfarction in survivors of acute myocardial infarction. However, the later and larger ISIS-4 and GISSI-3 trials have not confirmed this trend possibly due to the smaller doses of nitrates used and the diluting effect of the widespread use of open-label nitrates in the placebo group. In patients with congestive heart failure, including those of ischaemic aetiology, nitrates together with hydralazine have clearly demonstrated a significant reduction in the medium term mortality risk. Nitrates have the undoubted ability, probably greater than any other single anti-anginal drug, to rapidly and often completely relieve the pain and breathlessness associated with myocardial ischaemia. They are haemodynamically efficacious in reducing dilatation of the ischaemic left ventricle and enhancing coronary blood flow to ischaemic areas. Although their preventative impact in survivors of acute myocardial infarction awaits clarification, they have been shown in combination with hydralazine to extend survival in patients with congestive heart failure, including those of ischaemic origin.
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PMID:Secondary preventive potential of nitrates in ischaemic heart disease. 896 Apr 45

A 32-year-old obese female was hospitalized with dyspnea. Echocardiogram revealed left ventricular dilatation. Chest X-ray film showed enlarged heart size and prominent pulmonary congestion. Simple obesity with congestive heart failure (CHF) due to cardiomyopathy of obesity was diagnosed according to the absence of obvious disease that caused obesity or CHF. After diet therapy and medication, subjective symptoms disappeared and body weight was reduced from 137 kg to 85 kg. Although few reports of cardiomyopathy of obesity have been reported in Japan, we propose the possibility that similar cases will be on the increase because Japanese dietary habits are now becoming more similar to those of Caucasians.
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PMID:Simple obesity with cardiomyopathy of obesity. 896

Endocardial fibroelastosis is an uncommon congenital heart disease in dogs that may be manifested by signs of left-sided congestive heart failure. A three-month-old, male, Fila Brasileiro dog developed signs of generalised heart failure. Physical examination revealed normal temperature, ascites, and pale and cyanotic mucous membranes. The pup died just after radiography which revealed ascites, hepatomegaly, severe cardiac enlargement and pulmonary oedema. At necropsy, serosanguineous fluid in the thorax and abdomen, pulmonary oedema, right ventricular dilatation, hypertrophy and dilatation of the left ventricle, and mitral valve incompetence were observed. The histopathological examination demonstrated that the thickening of the endocardium of the left atrium and left ventricle was due to the presence of elastic and collagen fibres, although there were no signs of an inflammatory process.
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PMID:Endocardial fibroelastosis in a dog. 912 86

We evaluated the course of cardiac involvement in 27 previously reported patients with Becker muscular dystrophy (BMD) originating from nine kindreds. Since almost all affected individuals of each kindred were included, intrafamilial variability could be studied. We also attempted to identify associations between cardiac involvement, functional ability and mutations at DNA level. The mean follow-up period was 12.5 years. The number of patients with electrocardiographic abnormalities progressed from 44% to 71%. Dilated cardiomyopathy (DCM) with or without congestive heart failure was now present in 33% as compared with 15% in the previous study. In addition, 22% developed borderline echocardiographic abnormalities. Six patients (22%) became symptomatic and four patients died of congestive heart failure. In all families cardiac abnormalities were found. There was no association between DCM and mutation type. Despite equal functional motor ability, there was a considerable intrafamilial variation in cardiac involvement, even in brother pairs. We conclude that cardiac abnormalities are the rule and not the exception in BMD and are progressive over time. Left ventricular dilatation may begin at any moment in the course of BMD and the rate of progression is unpredictable. A substantial proportion of patients will develop an incapacitating and life-threatening DCM.
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PMID:Evolution of cardiac abnormalities in Becker muscular dystrophy over a 13-year period. 940 44

First-day thallium-201 myocardial perfusion scans and technetium-99m RBC gated scintiangiography were performed during the initial clinical and prognostic evaluation of 69 patients with suspected acute myocardial infarction. Patients were monitored for clinical course, diagnosis confirmation, and use of specialty services (cardiac catheterization, percutaneous balloon angioplasty, and cardiac surgery) during hospitalization. Myocardial infarction, confirmed in 20 patients, was associated with significantly more left ventricular dilatation, lower ejection fractions, lower peak left ventricular filling rates, wall motion abnormalities, and thallium-201 perfusion defects than nonmyocardial infarction patients. Among all patients, left ventricular dilatation carried a relative risk of myocardial infarction of 5.8; low ejection fraction and right ventricular dilatation were strongly associated with myocardial infarction. A logistic model for congestive heart failure included: left ventricular dilation, lower mean left ventricular filling rates and time to peak filling rates, and abnormal thallium-201 lung:heart uptakes. Among nonmyocardial infarction patients, subsequent cardiac catheterization was predicted by the presence of anterior thallium-201 perfusion defects, Killip functional class II-III, and ischemia on ECG. These findings suggest that early detection of myocardial perfusion defects and cardiac dysfunction by radionuclide scans enhances initial evaluation of suspected acute myocardial infarction patients. Additional studies are needed to confirm these findings.
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PMID:Early radionuclide scans for risk assessment in suspected acute myocardial infarction. 943 58

Activation of the renin-angiotensin-aldosterone system (RAAS) in left ventricular systolic dysfunction is a critically important determinant in the pathophysiologic processes that lead to progression of heart failure and sudden death. Angiotensin II, acting at the specific angiotensin receptor (AT1-R), activates a series of intracellular signaling sequences which are ultimately expressed within the cardiovascular system as vasoconstriction and associated vascular hypertrophy and remodeling. Angiotensin converting enzyme (ACE) inhibition leads to increases in the vasodilatory peptides bradykinin and substance P and at least an initial reduction in angiotensin II concentrations. AT1-R blocking drugs prevent access of angiotensin II to the AT1-R and thus prevent cellular activation. ACE inhibitors have clearly been demonstrated through a large number of clinical trials to increase survival in congestive heart failure, primarily by reducing the rate of progression of left ventricular dilatation and decompensation. However, this beneficial effect diminishes over time. Preliminary short-term clinical studies evaluating the efficacy of AT1-R blocking drugs in the treatment of heart failure have suggested that they elicit similar hemodynamic and neuroendocrine effects as do the ACE inhibitors. The combination ACE inhibitors and AT1-R blocking drugs offer the theoretical advantage of increasing bradykinin while blocking the actions of angiotensin II, and thus possibly show a synergistic effect. Again, preliminary studies have yielded encouraging results that are difficult to interpret because neither ACE inhibitor nor the AT1-R blocking drug doses were titrated to tolerance. Pharmacological manipulation of the RAAS has led to better understanding of its role in heart failure and improved clinical outcomes.
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PMID:Angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists in the treatment of heart failure caused by left ventricular systolic dysfunction. 1036 49

Records of previous electrocardiographic (ECG) and echocardiographic examinations of 39 Irish wolfhounds with cardiac failure, obtained during a 10-year survey, were examined to establish whether previously detected abnormalities might be prognostic indicators for the development of congestive heart failure (CHF) due to dilated cardiomyopathy (DCM) in later life. Eighteen dogs (46 per cent) had had atrial fibrillation (AF) at their first examination. Other ECG abnormalities detected at previous examinations were ventricular and supraventricular premature contractions, first and second degree atrioventricular block, P mitrale and left anterior fascicular and right bundle branch blocks. All 39 dogs had developed AF by the time of onset of CHF. The mean age at which CHF was diagnosed was 77 months in males and 86 months in females. The mean age at which AF was first detected was 45 months in males and 59 months in females, and the mean time from the first detection of AF to CHF was 27 months in males and 24 months in females. Previous echocardiographic examinations in eight dogs, over a period of up to five years, revealed progressive left atrial and left ventricular dilatation. Fractional shortening was reduced to below the normal range at the onset of CHF compared with previous examinations in three cases but increased in five. It appears, therefore, that certain ECG abnormalities, especially AF, and/or progressive ventricular and atrial dilatation, may be indicators of 'occult' DCM in wolfhounds.
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PMID:Observations on the development of congestive heart failure in Irish wolfhounds with dilated cardiomyopathy. 1047 24

Heart failure is common in patients aged over 65 years, and is the fourth leading cause of hospitalization in the United States. Treatment of congestive heart failure involves remodeling the cardiac chamber with ventricular dilatation. New approaches to resolve this problem include medical therapies (digoxin, diuretics, ACE inhibitors, beta-blockers and phosphodiesterase inhibitors) to stabilize patients, followed by chamber remodeling. As yet, surgical intervention in advanced heart failure has been contraindicated, but newly evolving strategies show significant promise. It appears possible that patients can receive surgical therapy to improve cardiac function, followed by state-of-the-art medical therapy for congestive heart failure. This combined medical/surgical approach has led to the evolution of a new subspecialty within cardiology that deals with the management of heart failure.
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PMID:New surgical options for the failing heart. 1051 85

Hypertension is an important risk factor for cardiovascular morbidity and mortality. Hypertension is associated with the development of congestive heart failure by way of left ventricular hypertrophy, with left ventricular dilatation and through myocardial ischemia and left ventricular damage. Reports on the natural history of untreated hypertension indicate that at least 50% of affected subjects develop congestive heart failure. Hypertension is an important precursor of heart failure, and still the most common risk factor for congestive heart failure in the population. In clinical trials, particularly in elderly patients, a reduction in the incidence of congestive heart failure has been observed. Despite increments in the use of antihypertensive drugs, mortality from congestive heart failure among the elderly is increasing. Moreover, several patients with hypertension are unaware, untreated and uncontrolled for the most important risk factor for congestive heart failure. For the primary prevention of heart failure, improvements in blood pressure control are of vast importance.
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PMID:Hypertension: an important precursor of heart failure. 1080 84

The clinical diagnosis of heart failure is based upon history and physical examination. Careful questioning and examination requires understanding of the pathophysiology of this systemic disorder. Symptoms and signs of congestive heart failure need to be differentiated from the manifestations of the underlying cardiovascular disorder. Only then will the specific signs and symptoms be unraveled. Symptoms arise from pulmonary congestion and peripheral or organ-underperfusion. Findings related to congestion can be found over the lungs (rales, pleural effusion), or at the jugular veins displaying either frank central venous pressure elevation or paradoxic inspiratory venous pressure rise (Kussmaul sign), or the more discrete sign of right, left of biventricular failure, the hepatojugular reflux. Dilatation and hypertrophy of the cardiac chambers can clinically easily and reliably be assessed by careful palpation. Galopprhythm, right and/or left ventricular in origin, is a particularly reliable sign of a failing ventricle. While a presystolic, atrial sound indicates merely elevated resistance to ventricular filling, i.e. the presence diastolic dysfunction or increased chamber filling, is the ventricular diastolic galopp a reliable sign of ventricular failure. Especially the appearance of a quadruple rhythm or a summation galopp can be considered both highly specific as well as prognostically dubious. Relative mitral and/or tricuspid insufficiency as a sign of ventricular dilatation needs to be differentiated from organic valve disease. This requires often echocardiography. Oedema of cardiac origin is symmetric and more pronounced in the evening. It arises both from left and from right ventricular failure. History and physical examination are both reliable tools in the initial diagnosis, as well as during follow-up and for control of therapeutic measures. Technical methods, such as chest x-ray, echocardiography or else are used for quantification and documentation. Properly applied and utilized they allow the physician to sharpen his clinical acumen, thus allowing for both a reliable diagnosis and a semi-quantitative estimation of ventricular size, enddiastolic and atrial, as well as pulmonary pressures and valve function.
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PMID:[Clinical diagnosis of heart failure]. 1085 88


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