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)

Of 1988 patients who underwent open-heart surgery from 1980 through 1988, 68 (3.4%) developed postoperative acute renal failure requiring dialysis (2.5% of adult and 8.3% of pediatric patients). Isolated aortocoronary bypass grafting was the operation with lowest incidence of this complication (0.6%). Acute renal failure usually appeared during the first 3 postoperative days. It carried a mortality rate of 63%, with half of the deaths occurring during the first few postoperative days, due to low cardiac output and progressive multiple organ failure. Logistic regression analysis in cases of aortic valve replacement demonstrated that significant independent preoperative risk factors for acute renal failure were renal insufficiency (serum creatinine greater than 110 mumol/l in greater than or equal to 2 samples) and increased cardiothoracic index/left ventricular end-diastolic dimension. Data from the literature indicated no time-related trend towards reduction of acute renal failure incidence or mortality. Prevention of low cardiac output is of major importance in these respects. Operative intervention before development of advanced disease with left ventricular dilatation and secondary kidney failure is advocated.
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PMID:Prognosis and risk factors in acute, dialysis-requiring renal failure after open-heart surgery. 178 Jul 30

Blood pressure, which ist the product of cardiac output and peripheral vascular resistance is regulated by a complex feedback mechanism involving the sympathetic and parasympathetic systems and hormones. An acute disturbance of regulation may lead to a life-threatening increase in blood pressure. Diagnosis is based upon a careful measurement of blood pressure, which must be performed under internationally standardized conditions. Hypertensive crisis refers to a rapid blood pressure increase greater than 30 mmHg above the age-related 95th percentile. The main causes of hypertension in childhood are renal diseases, which may be aggravated by additional conditions either by the clinician himself (e.g. cyclosporin, steroids) or by the patient (lack of compliance). Crisis affects the brain (hypertensive encephalopathy), the heart (left ventricular insufficiency), the retina (visual disturbances) and the mucous membranes (epistaxis). Hypertensive encephalopathy is induced by a break-through of the autoregulation of brain flow, leading to hyperperfusion and, thus to cerebral oedema. The clinical manifestations are characterized by restlessness, severe and diffuse headache, vomiting, nystagmus, impaired vision, dizziness, paraesthesia, seizures and palsies, which may lead - if untreated - to coma and death. The course is usually prolonged and reversible by adequate treatment. The morphological consequences are purpura cerebri, fresh retinal haemorrhages and papillary oedema, apart from left ventricular dilatation and hypertrophy. The diagnostic procedure rests on the quick realization of essential anamnestic (blood pressure, renal disease, drugs), clinical (oedema, cardiac action, central nervous system, fundus) and laboratory parameters (serum creatinine, electrolytes, glucose, blood count, urine). Treatment should start before the manifestation of clinical signs (hypertensive emergency) with rapidly acting antihypertensive drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The hypertensive crisis in childhood]. 305 87

The patient, 2 years and 9 months of age, was referred to our hospital with complaints of frequent vomiting, left hemiconvulsion and deep coma. The serum ammonia level was 251 micrograms/dl. Urine had a high orotate level (3,900 mumol/g creatinine). There was 7% residual of ornithine transcarbamylase (OTC) activity in the liver. Activities of other enzymes of the urea cycle were within normal limits. CT scanning on admission showed diffuse low density of both frontal lobes and of the right temporo-parietal lobe, narrowing of the right lateral ventricle and a shift of the mid-line to the left. The diffuse low density area was not enhanced after contrast medium injection. Follow-up CT scanning showed progressive bilateral ventricular dilatation and cerebral and cerebellar atrophy.
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PMID:A female case of ornithine transcarbamylase deficiency with marked computed tomographic abnormalities of the brain. 673 21

A 79-year-old female was admitted to our hospital because of a malignant pleural effusion following mastectomy 4 years ago. In the patient's history arterial hypertension and previous inferior myocardial infarction have been known. Two doses of 20 mg mitoxantrone were installed intrapleurally at an interval of 4 weeks. Six hours after the second mitoxantrone application and the patient had increasing dyspnea with consecutive left heart failure, pulmonary congestion, and a drop of blood pressure. The white-cell count was 14800/mm3. The levels of creatinine phosphokinase (CPK), lactate dehydrogenase (LDH) and serum aspartate aminotransferase (SGOT) were in the normal range. Transthoracic echocardiography showed concentric left ventricular hypertrophy and a markedly decreased fractional shortening, but no left ventricular dilatation. The electrocardiogram showed newly appeared down-sloping ST-segments and inverted T-waves. Clinical recovery was achieved after 6 days by application of oxygen, dobutamine and furosemide followed by angiotensin converting enzyme inhibition and digitalis. In the echocardiographic control examination 14 days later left ventricular function had normalized. The changes of electrocardiogram normalized 4 weeks later.
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PMID:[Mitoxantrone-induced acute left heart failure after intrapleural administration]. 937 56

Cardiomyopathy is defined as primary myocardial dysfunction which is not due to hypertensive, valvular, congenital, coronary or pulmonary vascular disease. This term usually denotes a dismal prognosis short of cardiac transplantation. However, several organic diseases of the heart can result in right or left ventricular dysfunction resulting in congestive heart failure and prompting the physician to label them as cardiomyopathy; the etiological factor is overlooked as it produces very subtle features. Therefore, before labelling any child as cardiomyopathic, all possible causes of ventricular dysfunction must be excluded by clinical and investigative means. The causes of "treatable cardiomyopathy" include mechanical factors as critical aortic stenosis and pulmonic stenosis, severe coarctation of aorta in an infant and aortaarteritis is an older child. Some of the persistent arrhythmias like atrial tachycardia, fibrillation, paroxysmal junctional re-entrant tachycardia are also known for causing ventricular dysfunction producing tachycardiomyopathy. Treatment of arrhythmia improves the ventricular function. Myocardial ischemia as a result of congenital coronary anomaly (commonest being anomalous origin of left coronary artery from pulmonary artery) can also present with a cardiomyopathy like picture. Early surgical correction is very rewarding. Finally, some of the metabolic conditions like creatinine and thiamine deficiency can also produce ventricular dilatation and dysfunction. In conclusion, the so called cardiomyopathy like picture can be produced because of several reasons and an attempt must be made to identify them.
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PMID:Treatable cardiomyopathies. 1087 69

Cardiomyopathy is defined as primary myocardial dysfunction which is not due to hypertensive, valvular, congenital, coronary or pulmonary vascular disease. This term usually denotes a dismal prognosis short of cardiac transplantation. However, several organic diseases of the heart can result in right or left ventricular dysfunction resulting in congestive heart failure and prompting the physician to label them as cardiomyopathy; the etiological factor is overlooked as it produces very subtle features. Therefore, before labelling any child as cardiomyopathic, all possible causes of ventricular dysfunction must be excluded by clinical and investigative means. The causes of "treatable cardiomyopathy" include mechanical factors as critical aortic stenosis and pulmonic stenosis, severe coarctation of aorta in an infant and aortaarteritis is an older child. Some of the persistent arrhythmias like atrial tachycardia, fibrillation, paroxysmal junctional re-entrant tachycardia are also known for causing ventricular dysfunction producing tachycardiomyopathy. Treatment of arrhythmia improves the ventricular function. Myocardial ischemia as a result of congenital coronary anomaly (commonest being anomalous origin of left coronary artery from pulmonary artery) can also present with a cardiomyopathy like picture. Early surgical correction is very rewarding. Finally, some of the metabolic conditions like creatinine and thiamine deficiency can also produce ventricular dilatation and dysfunction. In conclusion, the so called cardiomyopathy like picture can be produced because of several reasons and an attempt must be made to identify them.
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PMID:Treatable cardiomyopathies. 1112 21

Patients with chronic renal failure have, as compared with age-matched controls with normal renal function, a markedly higher cardiovascular mortality. The reason is probably accelerated atherosclerosis and left ventricular hypertrophy as a result of accumulation of "classical" cardiovascular risk factors and the presence of some risk factors relatively specific for "uraemia" (e.g. anaemia, hyperhydratation, dyslipidaemia). It is assumed that the reversibility of left ventricular hypertrophy is limited in chronic renal failure due to more marked myocardial fibrosis ("uraemic cardiomyopathy"). Its regression can be achieved by treatment of hypertension with inhibitors of angiotensin converting enzyme with a positive effect on cardiovascular mortality. Regression of left ventricular hypertrophy occurs also in some patients after renal transplantation. Treatment of anaemia reduces the risk of progressive left ventricular dilatation. The cardiovascular risk increases probably already a relatively slight decline of glomerular filtration which need not lead to a significant rise of serum creatinine. The cardiovascular risk obviously increases further with progression of chronic renal insufficiency. Patients with a reduced renal function and chronic renal insufficiency have lower target blood pressure and should have also lower target values e.g. of serum cholesterol. Therapeutic procedures in these patients should not be focused only on a slower progression of chronic renal insufficiency but also on reduction of their high cardiovascular risk.
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PMID:[Cardiovascular complications in patients with chronic renal insufficiency and chronic kidney failure]. 1290 73

A 5-year-old, 29-kg, female Labrador retriever developed tachypnea, tachycardia, and ataxia following ingestion of approximately 48 mg/kg of phenylpropanolamine. Initial diagnostic tests showed multiform ventricular tachycardia, left ventricular dilatation with a focal dyskinetic region in the dorsal interventricular septum, and elevations in creatinine kinase and cardiac troponin I. All abnormalities resolved within 6 months. The transient electrocardiographic, echocardiographic, and biochemical abnormalities were consistent with myocardial necrosis from infarction or direct catecholamine-induced myocardial toxicity.
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PMID:Cardiac toxicity from phenylpropanolamine overdose in a dog. 1626 67

We assessed prognostic value of clinical-laboratory and instrumental parameters in 100 patients with acute decompensation of chronic heart failure (CHF) in relation to hospital mortality. Independent predictors of lethal outcome in patients with acute decompensation of CHF were low systolic arterial pressure at admission (odds ratio [OR] 1.03, 95% confidence interval [CI] 1.01 to 1.05 per each 1 mm Hg of blood pressure lowering), elevation of urea content (OR 1.29, 95%CI 1.11 to 1.47 per each 1 mmol/L of elevation), potassium (OR 2.09, 95%CI 1.08 to 4.38 per 1 mmol/L of elevation) and creatinine (OR 1.01, 95%CI 1.01 to 1.03 per 1 mmol/L of elevation), lowering of glomerular filtration rate (OR 1.29, 95%CI 1.18 to 1.41 per 1 ml/min/1,73 m2 of lowering), left ventricular dilatation (OR 9.53, 95%CI 1.44 to 38.17; =0.043), pulmonary hypertension according to echocardiography data (=0.007), scarry changes according to electrocardiography data (OR 3.00, 95%CI 1.00 to 10.58; p=0.05), lack of therapy with acetylsalicylic acid (OR 6.21, 95%CI 1.62 to 22.73; =0.009) and -adrenoblockers (OR 6.99, 95%CI 1.39 to 14.49; =0,005) at ambulatory stage.
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PMID:[Prognosis of hospital mortality in patients with acute decompensation of chronic heart failure]. 2354 86

Left ventricular remodeling commonly complicates end-stage renal disease following chronic kidney disease (CKD). This study investigated the therapeutic efficacy of resveratrol (RSV), a polyphenolic compound, on left ventricular remodeling in subtotal nephrectomy rats and sought to uncover the underlying molecular mechanisms. Subtotal nephrectomy caused renal dysfunction, such as gradual increases in serum creatinine and blood urea nitrogen, glomerular sclerosis, and tubulointerstitial fibrosis. In addition, subtotal nephrectomy also resulted in significant increases in myocyte cross-sectional area, interstitial and perivascular fibrosis, and left ventricular dilatation. All these detrimental effects were alleviated in the presence of RSV. Mechanistically, RSV treatment led to the upregulation of manganese-containing superoxide dismutase (MnSOD) in the heart. Coimmunoprecipitation studies showed that silent information regulator 1 (Sirt1) bound forkhead box protein O1 (FoxO1) and thus reduced acetylated FoxO1. RSV strengthened this interaction between Sirt1 and FoxO1. Loss of one allele of Sirt1 aggravated renal damage, myocyte hypertrophy, and interstitial fibrosis in nephrectomized mice. Taken together, our data show that Sirt1 is an important mediator for the protective roles of RSV on renal and heart damage in CKD rodent model, and FoxO1 and MnSOD are likely downstream targets of Sirt1. Therefore, Sirt1 might be a potential therapeutic target for the treatment of left ventricular remodeling caused by CKD.
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PMID:Resveratrol improves left ventricular remodeling in chronic kidney disease via Sirt1-mediated regulation of FoxO1 activity and MnSOD expression. 3168 99


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