Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0018801 (heart failure)
72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Between 1961 and 1990, 52 patients with biopsy-proven familial amyloidosis born in North America were examined at the Mayo Clinic. At the time of diagnosis of familial amyloidosis, 83% of these patients had peripheral neuropathy, 33% had autonomic neuropathy, and 27% had cardiomyopathy. Renal disease was noted in fewer than 10%, and liver involvement was rare. The median age at diagnosis was 64 years. The sensitivity of various diagnostic biopsies was similar to that for primary amyloidosis: deposits of amyloid were found in 77 and 78% of the subcutaneous fat aspirates or rectal biopsy specimens, respectively, and in 41% of specimens of bone marrow. The median duration of survival of 5.8 years for patients with inherited amyloidosis was superior to that for patients with primary amyloidosis. When patients were stratified by organ involvement, the survival of patients with familial amyloidosis remained superior. The presence of cardiomyopathy and an interactive variable of age and the presence of autonomic neuropathy were powerful predictors of survival. Of the 52 patients, 22 died, 12 (55%) of cardiac failure or cardiac arrhythmia. Nine patients (41%) died of inanition in conjunction with progressive peripheral or autonomic neuropathy. Transthyretin was identified by immunohistochemical studies in 31 of the 34 tissue specimens tested. A transthyretin mutation was identified in 24 of the 31. A transthyretin mutation was found in five additional patients for whom tissue was unavailable for immunostaining.
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PMID:Familial amyloidosis: a study of 52 North American-born patients examined during a 30-year period. 140 68

In this study, independent contribution of age, HR, BMI, casual and ambulatory blood pressure, LVM and LVEF in evaluating diastolic filling have been investigated in 34 never-treated hypertensive patients and in 15 healthy normotensive subjects. All the subjects were free from coronary artery disease, valvular disease, heart failure, renal disease and psychiatric problems. All the hypertensive subjects (never treated) were subgrouped according to presence or absence of LVH. The PFR decreased significantly and tPFR increased significantly in hypertensive patients in comparison with normotensive subjects and they did not change in the presence vs absence of LVH. The PFR was inversely correlated with BMI, age, 24-h mean SBP and with 24-h DBP. In multiple regression analysis, PFR decreased with BMI, age, 24-h mean SBP and DBP but not with LVMI. These results suggest that BMI, age and 24-h mean blood pressure were the major determinants of PFR abnormalities in hypertensive patients.
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PMID:Rapid left ventricular filling in untreated hypertensive subjects with or without left ventricular hypertrophy. 142 72

A 28-year old male was admitted to our hospital because of heart failure, chronic renal failure and nephrotic syndrome. Light microscopic findings of his kidney biopsy showed proliferation of mesangial cell and marked narrowing the lumina of small arteries and arterioles. The changes of these small vessels were not those of typical vasculitis, when we considered his age and his past history. The diagnosis of dilated cardiomyopathy was made by the findings in echocardiography and cardiac catheterization. Since the heart failure and renal disease seemed to be simultaneous initiated, it was supposed that the diseases in two organs were caused by a common pathogenesis related to that of vasculitis. When steroid pulse therapy was adopted, both of cardiac and renal function responded to this treatment (ejection fraction from 26% to 52%, creatinine clearance from 48 to 62 ml/min). Increase of CD56 positive cells (natural killer cells) in peripheral blood was ameliorated after the treatment. These findings suggest that cellular immunity may be concerned with the pathogenesis of the combination of dilated cardiomyopathy and renal disease in this case.
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PMID:[Successful treatment with steroid pulse therapy in a case of dilated cardiomyopathy associated with mesangial proliferative glomerulonephritis]. 147 12

The risk for cardiovascular complications is already substantially increased in persons with borderline elevation of arterial pressure (141-159/90-94 mmHg and transiently below). It increases progressively with higher grades of hypertension. The main aim of treatment is thus a significant improvement in survival for the patient. Persons with raised blood pressure (BP) have often additional cardiovascular risk factors such as deranged carbohydrate metabolism, dyslipidemia, left ventricular hypertrophy, smoking and others. Treatment of hypertensive patients should thus not only normalize BP but should at the same time reduce associated risk factors or at least not increase them. Conventional antihypertensive treatment based on thiazides in high doses or beta-blocking agents led to marked reduction of strokes and heart failure, but did not satisfactorily reduce coronary heart disease or sudden cardiac death. It has been suspected that other cardiac risk factors are insufficiently influenced or eventually even deteriorated by conventional therapy, thus counteracting partly a beneficial effect of lowered BP. Beta-blockers however have at least a secondary preventive effect after myocardial infarction. Newer antihypertensive drugs such as ACE-inhibitors, calcium antagonists and alpha 1-blockers reduce left ventricular hypertrophy and are at least neutral with regard to metabolism of lipids and carbohydrates. The non-thiazide diuretic indapamide and the serotonin (S2-) blocker ketanserin likewise are neutral with regard to glucose and lipid metabolism. The efficacy of these new drugs regarding long term survival is as yet undetermined. Persisting borderline or established hypertension should as a rule always be approached with basic non-pharmacologic measures: loss of overweight, reduction of alcohol intake, exercise, avoidance of high salt foods, abstention from smoking and withdrawal of BP-raising drugs. If antihypertensive medication is indicated, potential first line drugs are ACE-inhibitors, calcium antagonists, beta-blockers, thiazides at low dose, indapamide, ketanserin, the alpha 1-blocker prazosin and others; initially as monotherapy, if needed in combinations of 2 or 3. Older patients or those will with additional disturbances such as diabetes, hypercholesterolemia, nephropathy, heart failure, ischemic heart disease, arrhythmias, claudication, asthma and others need problem-adjusted modifications of treatment.
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PMID:[Antihypertensive therapy in the nineties]. 153 54

We have attempted to define a normal range for blood urea and creatinine for elderly inpatients and to determine the relative importance of pre-renal, renal and post-renal pathology in those with renal impairment. A total of 118 admissions to an acute geriatric unit and 67 separate post mortems in patients over 67 years of age were studied prospectively. Up to 123 items of data were coded and analysed including blood urea and creatinine, clinical or pathological changes associated with renal disease, clinical outcome and post mortem findings. We determined our own 'normal' hospital ranges for urea (1.4-13.2 mmol/l) and creatinine (48-141 mumol/l) from plasma values in 76 patients with no evidence of renal impairment, either on admission or in the past. Using these values 41% of post mortem cases and 25% of clinical admissions had a raised blood urea. Pre-renal conditions such as cardiac failure, dehydration and gastrointestinal haemorrhage, either alone or in combination, were present in 56% of these patients. Urea and creatinine values were substantially higher in patients who died in hospital as opposed to those who were discharged or transferred. Creatinine values were greater in those with intrinsic renal disease or post-renal obstruction as compared to patients with pre-renal causes of renal impairment. Patients with histological evidence of extensive glomerulosclerosis or nephrosclerosis had higher urea and creatinine levels than those with only minor ageing changes.
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PMID:Raised blood urea in the elderly: a clinical and pathological study. 158 74

Diabetic patients have an increased mortality following myocardial infarction (MI) due to left ventricular failure rather than larger infarcts or dysrhythmias. As this may be due to diabetic microangiopathy affecting the myocardium, we have examined the case records of diabetic clinic patients admitted to the Coronary Care Unit (CCU) with proven MI and compared the hospital outcome of those with and without retinopathy or nephropathy, i.e. markers for generalised microangiopathy. Sixty four consecutive records were traced, for the period when diabetic treatment policy was standardised in CCU, 24 patients had retinopathy (7 proteinuria). When compared to non-retinopathy patients they had similar ages 67 +/- 12 yr [+/- SD] v 63 +/- 9yr) but were of longer duration of diabetes p less than 0.05). There were no differences between the groups in size or site of infarct, previous infarct or hypertension history, blood glucose on admission or diabetic treatment before or after admission. Death occurred in 29% of retinopathy patients compared to 3% of non-retinopathy patients (p less than 0.01). Cardiac failure complicated 75% of retinopathy patients and 25% of non-retinopathy patients (p less than 0.001). Dysrhythmia occurred in 50% and 33% of patients respectively (P = NS). Nine patients had clinical peripheral vascular disease and five of these died. This study, of a selected group of diabetic clinic attenders admitted to CCU with acute MI, demonstrates that microangiopathy and peripheral vascular disease are important prognostic factors in determining hospital outcome as these patients are at increased risk of cardiac failure and death.
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PMID:Microangiopathy as a prognostic indicator in diabetic patients suffering from acute myocardial infarction. 160 65

All hyponatremic states have in common elevation of vasopressin. Without this the loss of salt would be followed by appropriate diuresis and normonatremia. If hyponatremia is triggered by a volume change as in heart failure or portal cirrhosis not only is ADH released but the mechanisms that control salt retention create an essentially sodium free urine, always less than 20 mEq/L. If the initial event is inappropriate ADH secretion whether it be cerebral disease, neoplasm, a pulmonary lesion or a growing list of drugs; there is no related signal for salt retention and urine sodium and tonicity are high, the latter usually higher than that of plasma. If salt loss is due to intrinsic renal disease, diuretics, osmotic or otherwise, or adrenal failure urinary sodium is variable depending upon the magnitude of the response to volume of salt retaining factors. Because hyponatremia is often present with major illness and because more than one factor may be involved in its genesis, the establishment of its origin and appropriate treatment remain a diagnostic and therapeutic challenge.
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PMID:Hyponatremia: manifestations and treatment. 162 51

Cardiovascular diseases are a leading cause of death in end-stage renal disease (ESRD) largely as a result of the progressively increasing age of ESRD patients and the broad constellation of uremia-associated factors that can adversely affect cardiac function. Hypertension, one of the leading causes of renal failure, is a major culprit in this process, causing left ventricular hypertrophy, cardiac chamber dilation, increased left ventricular wall stress, redistribution of coronary blood flow, reduced coronary artery vasodilator reserve, ischemia, myocardial fibrosis, heart failure, and arrhythmias. In addition to impairing the coronary microcirculation, hypertension may contribute to the development of atherosclerotic coronary artery disease, particularly in the presence of the many lipid abnormalities observed in ESRD. These patients have reduced high-density lipoprotein cholesterol and increased plasma triglyceride concentrations, and there is a defect in cholesterol transport. Other abnormalities that may contribute to atherosclerotic coronary artery disease in ESRD are reduced high-density lipoprotein cholesterol synthesis and reduced activity of the reverse cholesterol pathway. Treatment with fibric acids, nicotinic acids, and lovastatin may be useful in lowering cholesterol and triglyceride concentrations in some of these patients. The incidence of coronary artery disease in ESRD populations is difficult to determine. About 25 to 30% of ESRD patients with angina have no evidence of significant coronary artery disease, and an undetermined number have silent coronary disease. The presence of resting electrocardiographic abnormalities caused by hypertension or conduction defects makes it difficult to accurately diagnosis coronary artery disease in ESRD populations by noninvasive methods, including exercise testing and thallium scintigraphy with or without the use of dipyridamole. Hypotension is a frequent complication of the dialytic process. Many factors have been implicated, including autonomic neuropathy. There is no consensus on the function of the efferent limb of the sympathetic nervous system. The afferent limb (arterial baroreflex function) is felt to be impaired. Further, there may be defects in the ability of the cardiovascular system to respond to sympathetic nerve activity. Most studies of autonomic function have used indirect measurements. Studies are underway that use techniques to assess sympathetic function directly. Such experiments with microneuropathy suggest greater skeletal sympathetic muscle discharge in uremic patients than in normal patients.
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PMID:Cardiovascular complications in renal failure. 177 85

Atrial natriuretic peptide (ANP) and plasma renin activity (PRA) were studied in 19 patients with end-stage renal disease (ESRD) under haemodialysis (HD). On the basis of clinical findings, patients were divided into three groups: group A, 6 patients, of mean age 41 +/- 15 years, without heart failure and in need of ultrafiltration (658 +/- 282 ml h-1); group B, 6 patients, of mean age 54 +/- 15 years, without heart failure under isovolaemic HD; group C, 7 patients, of mean age 60 +/- 3 years, with heart failure (NYHA III-IV) and in need of ultrafiltration (607 +/- 120 ml h-1). The highest predialysis ANP levels were found in group C (1534 +/- 471 pg ml-1) followed by group A (476 +/- 168 pg ml-1) and group B (236 +/- 138 pg ml-1) (normal range 62 +/- 27 pg ml-1). Systolic and diastolic blood pressure and heart rate did not correlate with ANP levels in either of the groups. However, iso-osmotic reduction of the body weight by ultrafiltration was correlated with decreasing ANP levels during HD (for groups A and C, r = 0.88 and 0.98, respectively). Isovolaemic HD did not alter ANP concentrations (group B). All patients received a volume bolus at the end of HD, and they responded with an instant increase in ANP concentration, which was most pronounced in patients with concomitant heart failure. PRA was not significantly correlated with ANP levels during HD. In conclusion, the results of this study indicate that there is a sensitive response of ANP levels to changes in body fluid status in ESRD.
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PMID:Atrial natriuretic peptide in dialysis patients under various conditions of volume homeostasis. 182 25

Recent studies indicate that endothelin (ET), a potent endogenous systemic and renal vasoconstrictor peptide, may mediate decreases in GFR in models of acute renal dysfunction. Moreover, in an animal model of radiocontrast-induced nephropathy (RCIN), it was recently demonstrated that early renal hemodynamic responses to radiocontrast are attenuated by intra-arterial atrial natriuretic factor (ANF), which prevents subsequent RCIN. The studies presented here were therefore designed to determine whether i.v. infusion of radiocontrast produces increases in endogenous plasma and urinary ET and whether these responses are modulated by intra-arterial ANF in an animal model of RCIN. In these studies, dogs with pacing-induced heart failure received i.v. radiocontrast in the presence and absence of an intra-aortic infusion of ANF. Significant increases in both plasma and urinary ET were observed during and after radiocontrast. Although coadministration of ANF did not prevent increases in plasma and urinary ET, ANF preserved renal function acutely in this model of RCIN by increasing GFR above baseline levels.
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PMID:Radiocontrast increases plasma and urinary endothelin. 183 65


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