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)

The purpose of this study was to investigate, if besides the hypocontractility, which is the main finding in Primary Cardiomyopathy (PDC) there was some other mechanism in the development of heart failure and if this fact could influence in it's prognosis. We studied 13 patients with PDC in the hemodynamic cardiac laboratory from January 1982 to January 1988, these with systemic arterial hypertension. Coronary heart disease, myocarditis, primary valvular lesion, infiltrative disease, nephropathy, congenital heart disease, diabetes and alcoholism, were excluded. The control group was formed by 12 healthy subjects, which were studied for another purpose. We analyzed nine variables, including ejection fraction, peripheral vascular resistance, systolic and diastolic circumferential stress, left ventricular mass, left ventricular end diastolic and systolic volumes as well as force-velocity and force-fiber length relationship. The patients were followed up from 8 to 60 months (average 39 months). The cases with PDC were divided in two groups, "compensated" and "decompensated". The last ones with low ejection fraction and significantly increases systolic stress. We investigated which was the mechanism of compensation and decompensation through the force-velocity and force-fiber length relation. We found that compensation is associated with great increase of the after-load forces, the more end systolic volume at the end of the systole is not only controlled by the "force", but the decompensation is developed when the hypocontractility is added to the incompetence to compensate the after load. We found that the three deaths in this study had these hemodynamic characteristics, being the cause of death: the presence of heart failure in two patients and ventricular fibrillation in one.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prognostic indexes in primary dilated cardiomyopathy]. 234 26

A 37-year-old woman presented with hypocalcemic heart failure complicating end-stage renal disease. Heart failure persisted despite conventional therapy but improved after correction of hypocalcemia. Continuous monitoring of left ventricular function by radionuclide study during calcium replacement showed dramatic improvement. Our case showed that hypocalcemia could be a rare but reversible cause of frank heart failure in uremic patients.
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PMID:Hypocalcemic heart failure in end-stage renal disease. 234 61

In order to determine the relationships between allograft function and the recipient's plasma concentrations of atrial natriuretic factor (ANF), plasma ANF was measured by radioimmunoassay for 14 days after cadaveric renal transplantation in 9 patients aged 19-64 years. All received immunosuppression with prednisolone, azathioprine, and cyclosporine. No patient was in heart failure. During the study period, six grafts functioned, and three were nonfunctioning--two due to rejection and one to acute tubular necrosis. Plasma ANF concentration at the time of transplantation was 48 +/- 16 pmol/L (mean +/- SEM) range 15-145 pmol/L. In the six patients with functioning grafts, ANF declined in parallel with the fall in serum creatinine (658 +/- 35 to 210 +/- 34 mumol/L). In the three with nonfunctioning grafts, serum creatinine and plasma ANF concentration both increased. There was overall a significant linear relation between serum creatinine and plasma ANF (r = 0.527, P less than 0.001). The changes in plasma ANF after renal transplantation bore no relationship to changes in body weight or blood pressure. However, plasma ANF concentration was related to allograft fractional sodium excretion (r = 0.687, p less than 0.001). We conclude that elevated plasma ANF concentrations in end-stage renal disease are restored to normal by successful renal transplantation, implying that renal function is a determinant of plasma ANF concentration. Circulating plasma ANF may also have a direct effect on allograft sodium excretion.
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PMID:Plasma atrial natriuretic factor and graft function in renal transplant recipients. 253 Jun 66

The safety of 738 high-risk patients treated with enalapril under various clinical programs was evaluated. High risk was defined as the presence of a collagen vascular disease; a renal disease, including renovascular hypertension; or either hypertension or refractory cardiac failure with serum creatinine greater than or equal to 1.7 mg/dl at baseline. Essential hypertension was the primary diagnosis in most of these patients. Treatment with enalapril in these patients usually continued without interruption for the length of the particular protocol. The incidence of adverse reactions resulting in discontinuation of treatment was comparable to that observed with other standard antihypertensive therapies in patients with milder forms of disease. No enalapril-related neutropenia, proteinuria, dysgeusia or ageusia were reported in these high-risk patients. The incidence of discontinuation due to rash was less than 0.5%. Resolution and/or improvement of captopril-related adverse effects was observed in many patients crossed over to treatment with enalapril. In patients with collagen vascular diseases and those with severe impairment of renal function (serum creatinine greater than or equal to 3.0 mg/dl), the incidence of discontinuation due to adverse experiences or death as well as the profile of reported adverse experiences was similar to those for the total group of high-risk patients. The data suggest that enalapril is efficacious and well tolerated by the high-risk patients.
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PMID:High-risk patients treated with enalapril maleate: safety considerations. 253 44

1. The population pharmacokinetics of lisinopril were investigated using data collected from two multicentre trials of lisinopril in the treatment of hypertension in elderly patients (n = 40) and patients with renal disease (n = 20). 2. Lisinopril was started at doses of 2.5-5 mg daily and increased at 2-4 weekly intervals as required for control of blood pressure. Steady-state concentration-time profiles were measured after at least 2 weeks at a constant dose. 3. All concentration-time data were analysed simultaneously using the program NONMEM and the influence of clinical factors on clearance/F and volume of distribution/F was tested. 4. Clearance was significantly influenced by creatinine concentration, age, weight and cardiac failure. No clinical features tested were found to influence volume of distribution. 5. The influence of renal function and cardiac failure on lisinopril clearance has been confirmed using a population pharmacokinetic analysis technique.
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PMID:Lisinopril population pharmacokinetics in elderly and renal disease patients with hypertension. 253 50

Recovery of renal function was observed in 10 out of 300 patients (3.3%) treated by CAPD. These 10 patients presented the following primary renal diseases: 4 nephroangiosclerosis, 4 interstitial nephropathies, 1 diabetic nephropathy, 1 unknown nephropathy, and were treated by CAPD for a mean period of 10.2 +/- 5.5 months. CAPD was discontinued when residual renal function reached 12 ml/min. After recovery 8 patients were still alive, including 1 patient who returned to dialysis. 2 patients died. When risk factors such as uncontrolled hypertension, cardiac failure, severe nephrotic syndrome, rapidly progressive renal failure, analgesics or non steroidal anti-inflammatory drug treatments or abuses, chronic urinary obstruction, cholesterol emboli were associated with end stage renal failure, CAPD should be the dialysis treatment of choice, expecting the preservation of the kidney capacities and further a recovery of renal function.
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PMID:Recovery of renal function in patients treated by CAPD. 257 29

We measured cardiac functions by means of mechanocardiogram and echo-cardiogram in 93 patients with diabetes mellitus, excluding those who had apparent cardiac diseases, such as angina pectoris and cardiac failure. We used pre-ejection-period/ejection time (PEP/ET) as the index of the left ventricular systolic function and isovolumic relaxation time (IRT) as that of the left ventricular diastolic function. We compared the diabetic cases without complications to those with complications such as retinopathy, nephropathy, neuropathy and autonomic disorder. Conclusions obtained were as follows; An abnormal IRT was noted in the early stage of diabetic complications. The IRT was not normal among the subjects even when those with cardiac hypertrophy or ST-depression on the ECG were excluded. On the contrary, the PEP/ET did not show any abnormality in the early stage of diabetic complications until they advanced into, eg. renal failure or severe neuropathy. Our findings suggest that the disorder of the left ventricular diastolic function precedes that of the left ventricular systolic function, indicating the association of microangiopathy and autonomic disorder.
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PMID:[Left ventricular function in patient with diabetes mellitus--Evaluated by mechanocardiogram and echocardiogram]. 261 9

Renin plays a major role in the control of blood pressure and water and electrolyte metabolism and it is clear that blocking of this system is particularly effective in the treatment of essential hypertension and heart failure. A large number of converting enzyme inhibitors have been synthesized. Converting enzyme inhibitors are remarkably active in heart failure and they reduce microalbuminuria and possibly maintain glomerular function. Blocking of the renin-angiotensin system by converting enzyme inhibitors is not accompanied by hypotension or reflex stimulation of the sympathetic nervous system. Converting enzyme inhibitors represent a major therapeutic advance in the field of cardiovascular and renal disease but the long-term effects of decreased angiotensin II levels are unknown. There are other ways to inhibit the renin-angiotensin system. The recent discovery of orally-active non-peptide angiotensin II antagonists opens a range of fascinating prospects. Another approach consists in inhibiting the reaction of renin on angiotensinogen, which is remarkably selective. Although it is too early to know whether these new approaches will be less active, more active or as active as current converting enzyme inhibitors, they may constitute a progress in relation to currently available treatments.
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PMID:New therapeutic prospects of renin-angiotensin system inhibition. 269 Nov 25

To test the hypothesis that race is a predictor of hypertensive renal disease, we examined a general medicine clinic population of 6,880 hypertensive patients who were treated for at least 1 year (mean, 5.2 years). Their mean age was 55.8 years; 70% were women, 72% were black, and 41% were diabetic (95% type II). Many were already under treatment at the time of enrollment. Their mean blood pressure at entry was 150/92 mmHg; during treatment it was 142/86 mmHg. Decreased renal function, defined as a serum creatinine greater than or equal to 2 mg/dL, developed in 18.1%. A multivariable logistic regression analysis identified diabetes, glucose control, systolic blood pressure levels, heart failure, and male gender as indicators of decreased renal function. These data suggested that glucose and blood pressure control may decrease the frequency of impaired renal function. However, when these variables were controlled, blacks still had almost twice the risk for renal dysfunction (91% greater risk) than whites (P less than 0.0001). With increasing creatinine values, the percentage of black patients increased progressively. The data draw attention to and elucidate the exceptionally high incidence of renal dysfunction in blacks with or without diabetes. Further, they may explain the inordinate numbers of blacks with hypertension requiring dialysis. Finally, these retrospective data suggest that prospective trials to test the effect of blood pressure and glucose control on the course of renal disease in hypertensive and/or type II diabetic patients are warranted.
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PMID:Renal disease in hypertensive adults: effect of race and type II diabetes mellitus. 272 68

We report the cases of four patients with end-stage renal disease and New York Heart Association class III or IV heart failure of nonischemic origin as documented by coronary angiography. Because of left ventricular dysfunction (left ventricular end-diastolic pressure, 23 to 30 mm Hg; ejection fraction, 20% to 35%), all four patients were initially considered poor surgical candidates for renal transplantation. These same four patients became asymptomatic, however, with markedly improved cardiac function (ejection fraction, 43% to 69%) detected as early as 6 and 14 days after renal engraftment. Therefore, there exists a subset of patients with end-stage renal disease in whom congestive heart failure should not be considered a contraindication to renal transplantation. We conclude that some dialysis-dependent patients who manifest symptomatic heart failure of nonischemic origin have a reversible cardiomyopathy and should not be denied renal transplantation.
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PMID:Reversal of left ventricular dysfunction after renal transplantation. 280 18


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