UMLS:C0018801 - FACTA Search

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

Both circulating and local renin-angiotensin systems (RAS) may contribute to cardiovascular homeostasis under normal and pathophysiologic conditions. They may also play a role in the effects of angiotensin-converting enzyme (ACE) inhibitors. In the present study, we compared systemic and regional hemodynamic effects of nonhypotensive doses of captopril and enalaprilate in normal rats, spontaneously hypertensive rats (SHR), and rats with heart failure due to myocardial infarction (MI). Enalaprilate (0.1 mg/kg) or captopril (3 mg/kg) was injected intravenously (i.v.) in conscious rats equipped with miniature Doppler flow probes on renal and mesenteric artery and abdominal aorta or an electromagnetic flow probe on the ascending aorta to measure cardiac output (CO). This resulted in a shift of the angiotensin-I (ANG I) dose-pressor curve (ED50 of ANG I after saline 0.21 +/- 0.33 micrograms, enalaprilate 1.45 +/- 0.26 micrograms, captopril 2.38 +/- 0.73 micrograms; mean +/- SEM; n = 6-12). In the systemic hemodynamic groups, no significant changes in mean arterial pressure (MAP), CO, or total peripheral resistance (TPR) were observed. In the regional hemodynamic groups, enalaprilate caused a slight (-8 +/- 1 mm Hg) reduction in MAP in normal rats. Resistance in the hindquarters was not affected by ACE inhibitors, whereas only enalaprilate reduced mesenteric resistance in MI rats. In contrast, renal resistance was reduced and renal blood flow (RBF) increased after captopril in normal and MI rats and after enalaprilate in MI rats. Effects were greatest in MI rats (RBF: saline -0.05 +/- 1.9%, enalaprilate 10.3 +/- 2.4%, captopril 10.1 +/- 2.0%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal hemodynamic effects of nonhypotensive doses of angiotensin-converting enzyme inhibitors in hypertension and heart failure rats. 137 83

Severe tissue carnitine deficiency impairs fatty acid oxidation. In explanted hearts from patients with end stage heart failure a 57% carnitine decrease was found in comparison with healthy donor hearts (p less than 0.05). The reduction of myocardial carnitine levels affected all areas of the explanted hearts to a comparable extent. Carnitine decreases in patients with dilated cardiomyopathy or coronary artery disease were similar. Endomyocardial biopsies from patients with less severe heart failure due to cardiomyopathy (n = 28) or other myocardial diseases (n = 8) showed a 42% decrease of total myocardial carnitine (in nmol/mg non-collagen protein) in comparison with biopsies from patients with normal cardiac function (controls) (heart failure: 5.7, confidence interval 4.2-7.0; controls 9.3, confidence interval 7.6-12.0, p less than 0.005). Free myocardial carnitine in heart failure was also different from controls (heart failure: 4.2, confidence interval 3.7-5.3; controls 10.3, confidence interval 7.5-12.2, p less than 0.001). The decrease of free and total myocardial carnitine was comparable in dilated cardiomyopathy and heart failure due to other diseases. Alterations in myocardial carnitine content represent therefore non-specific biochemical markers in heart failure with yet unknown consequences for myocardial function.
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PMID:Metabolic alterations in end-stage and less severe heart failure--myocardial carnitine decrease. 229 80

The chronic reserve for the secretion of atrial natriuretic factor (ANF) was studied in conscious dogs with an arteriovenous (a-v) fistula, a model of high-output heart failure. After the first 7 days of marked sodium retention after creation of the a-v fistula, the animals regained sodium balance for the subsequent 3 wk. This compensatory natriuresis occurred in the presence of significant increases in right atrial pressure and was associated with marked and sustained elevations in plasma ANF and with the return of plasma renin and aldosterone to base-line values. The cardiac reserve for ANF secretion was further evaluated in these dogs with compensated high-output heart failure during additional progressive elevations in cardiac filling pressures induced by 3 wk of deoxycorticosterone acetate (DOCA) administration. During the DOCA regimen, plasma ANF increased an additional twofold from its high base line. Arterial blood pressure increased by 6-12 mmHg, and plasma renin activity was suppressed. However, the animals consistently retained sodium, and the high plasma levels of ANF were unable to counterbalance the sodium-retaining actions of DOCA. After termination of DOCA, the dogs exhibited a marked natriuresis, and all the hemodynamic and hormonal parameters returned to pre-DOCA control levels. This longitudinal study demonstrates that the cardiac reserve for chronic ANF secretion is well maintained in dogs with an a-v fistula during progressive cardiac volume overload. The present results suggest that the ANF endocrine system may represent one chronic compensatory mechanism to achieve sodium balance in heart failure when there is concomitant normalization of the renin-aldosterone system.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:DOCA administration and atrial natriuretic factor in dogs with chronic heart failure. 252 18

The present-day optimal treatment of patients with acute myocardial infarction (AMI) is reviewed. The prehospital phase should be as brief as possible. Emergency observation and treatment in hospital should be initiated without delay. Schematic stages for mobilization have been discarded and free mobilization is recommended. Routine acute intervention with thrombolysis is recommended for patients in whom symptoms have been present for 6-12 hours and treatment with Aspirin is recommended. Beta-blocking agents are recommended for patients with increased risk after discharge. Treatment of ventricular and supraventricular arrhythmias, block and cardiac failure are reviewed in detail. Patients without complications should be monitored for three to five days and may be discharged after seven to ten days. Exercise ECG should be carried out at discharge to assess the working capacity, ischaemia and subjective reaction. The importance of good patient information is emphasized. Cessation of smoking, control of lipids and blood pressure are important as secondary interventions. As far as possible, outpatient control should be offered after discharge. The criteria for referral to specialized cardiological departments are established both for emergency and elective referral. Patients under the age of 70 years with high risk for repeated AMI or death after discharge (with residual ischaemia) should possibly be referred for coronary arteriography.
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PMID:[Treatment of acute myocardial infarction--an elucidative report]. 256 43

An important consideration in the choice of initial treatment is race. In a Veterans Administration study nadolol reduced blood pressure more in whites than in blacks, while the reverse was true with hydrochlorothiazide. Combining both drugs enhanced antihypertensive effectiveness and abolished the racial difference. The results of this and other studies suggest that for first drug selection, beta-blockers are indicated in whites and diuretics in blacks. Beta-blockers are also indicated in all patients with prior myocardial infarction or with tachycardia. Thiazides are also used in combination with other antihypertensive drugs and in patients with heart failure. Reluctance to use thiazide diuretics stems from the possibility of hypokalemia-induced arrhythmias and long-term elevations of serum cholesterol. However, a causal relationship between hypokalemia and the incidence of arrhythmias is not well supported by physiologic or clinical evidence. Elevation of cholesterol appears to be transient, reverting back to pretreatment levels after 6-12 months of treatment. An alternative regimen which is both highly effective and well tolerated is the combination of small doses of both a thiazide diuretic and captopril. Perhaps less well tolerated, but useful where cost is the major consideration, is a thiazide followed by small doses of reserpine, if needed; this is an effective, low-cost treatment. Calcium channel blockers appear promising but require further evaluation.
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PMID:Angiotensin converting enzyme inhibition in clinical practice. Choice of initial treatment. 258 Jan 62

Results of early studies support the concept that steroid treatment may reduce mortality from acute myocardial infarction. This double-blind, randomized, 1118-patient study was performed to determine if methylprednisolone sodium succinate (MPSS, Solu-Medrol Sterile Powder, The Upjohn Company) reduced 28-day mortality following myocardial infarction complicated by cardiac failure. Treatment with 30 mg/kg intravenous MPSS (maximum dose, 3 g) resulted in 28-day mortality rates of 11.7% with MPSS and 9.9% with placebo when treatment was initiated within six hours of the onset of chest pain (Group 1). Mortality rates at 28 days were 10.4% with MPSS and 14.7% with placebo when the treatment was initiated 6-12 hours after onset of chest pain (Group 2). In the late-treatment group, six-month mortality rates were 13.7% with MPSS and 20.3% with placebo (p = 0.08). Analysis of data by life table methods showed similar survival rates between MPSS- and placebo-treated patients in Group 1. In Group 2, survival rates were increased in MPSS-treated patients in the intervals from 48 hours through seven days (p = 0.04) and from three months through six months (p = 0.03). A Cox regression analysis showed that the relative risk of death for Group 1 patients was similar, regardless of treatment; Group 2 patients on MPSS had a significantly decreased relative risk of death (p less than 0.01). MPSS treatment was not associated with increased incidence of myocardial rupture, cardiac aneurysm, early malignant ventricular arrhythmias, or other adverse cardiac events.
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PMID:Methylprednisolone as an intervention following myocardial infarction. The Solu-Medrol Sterile Powder AMI Studies Group. 287 3

It is difficult to maintain the long-term patency after conventional anastomosis especially for the small caliber vessels. Since 15 years we have performed aortocoronary bypass with suture materials for the patients with ischemic heart disease. There are some problems in maintaining the long-term patency of the bypass grafts. Low energy CO2 laser was utilized to make vascular anastomosis with a few stay sutures. Vascular anastomoses (side-to-side, end-to-end, end-to-side) were carefully made by CO2 laser in the regions of the femoral arteries and veins, the carotid arteries and jugular veins in dog. A-C bypass was also successfully carried out between the internal mammary artery and the left anterior descending artery under the beating heart in experiment. Outputs of 20-40 mW and irradiation times of 6-12 sec/mm were optimal conditions for anastomosis of the small caliber vessels. There were no problems in the intensity and the healing of the anastomotic sites in comparison with the conventional suture method. On the basis of these excellent experimental results a low energy CO2 laser was employed clinically for vascular anastomosis of the peripheral vessels in 28 patients with angina pectoris or chronic renal failure and cardiac failure. There were no complications such as bleeding and suture line aneurysm after surgery. In conclusion, vascular anastomosis by laser might be recommended in performing with safety and rapidity for small caliber vessels.
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PMID:[A new method of vascular anastomosis by CO2 laser: experimental and clinical study]. 349 23

Paediatric cardiac transplantation (pHTX) has gained widespread acceptance as a therapy in end-stage myocardial failure and some forms of congenital heart disease, particularly hypoplastic left heart syndrome (HLHS). The major problems to the anaesthesiologist in these patients are induction of anaesthesia in infants with HLHS and treatment of pulmonary hypertension in the early post-bypass period. PATIENTS AND METHODS. Anaesthesia for pHTX was performed in 15 children < 1 year of age (4-237 days); 12 suffered from HLHS, 2 from endocardial fibroelastosis, and 1 from dilatative cardiomyopathy. Induction of anaesthesia in patients with HLHS IS a challenge to the anaesthesiologist, as he has to maintain the delicate balance between pulmonary and systemic blood flow. Anaesthesia was induced with fentanyl (10-15 micrograms/kg) and pancuronium (0.2-0.4 mg/kg) and maintained with fentanyl (total dosage 70-100 micrograms/kg). Modification of ventilatory parameters such as FiO2, PaCO2, and airway pressure (PEEP, I:E ratio) was used to influence systemic and pulmonary blood distribution in the pre-bypass period according to changes in haemodynamics (target: O2 saturation approximately 75%-80%, PaCO2 45-50 mmHg). Treatment of pulmonary hypertension in the weaning and early post-bypass period consisted of respiratory (PaCO2 < 30 mmHg) and metabolic alkalinisation (pH 7.45-7.55, BE > +3 mmol/l), the use of prostaglandin E1 (3-6-12 micrograms/kg.h), and the phosphodiesterase inhibitor enoximone (10-15 micrograms/kg.min). Additional positive inotropic support was achieved with dobutamine (5-10 micrograms/kg.min), adrenaline (0.1-0.5 micrograms/kg.min), and/or orciprenaline (0.1-0.2 micrograms/kg.min) and calcium chloride (25-100 mg/kg). RESULTS. Two children died intraoperatively and 1 on the 1st postoperative day from overwhelming pulmonary vascular resistance and right ventricular failure. Three children died between 3 and 4 weeks postoperatively, 1 from cytomegalovirus infection, 1 from sepsis, and 1 from acute rejection. Nine patients survived and are well up to 5.5 years after transplantation. CONCLUSION. Pulmonary hypertension in the weaning and early post-bypass period is the main anaesthesiological problem of pHTX, particularly in children with HLHS. A polypragmatic approach to this problem consisting of alkalinisation, pulmonary vasodilatation, and inotropic support is presented and seems to be effective. Further improvements in concepts of pHTX are limited by the lack of donor organs. Though the experience with pHTX in neonates and infants is growing slowly, it might be a routine procedure from the anaesthesiological point of view within a few years in some selected centres.
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PMID:[Anesthesia for heart transplantation in newborn and suckling infants. Special aspects of the hypoplastic left heart syndrome]. 778 53

Rabbit Coronavirus (RbCV) infection was divided into two phases based upon day of death and pathologic findings. During the acute phase (days 2-5) heart weights (HW) and heart weight-to-body weight (HW/BW) ratios were increased with striking dilation of the right ventricle. These changes as well as increased dilation of the left ventricle were especially pronounced during the subacute phase (days 6-12). Myocytolysis, pulmonary edema, and degeneration and necrosis of myocytes, were seen during both phases. Myocarditis, pleural effusion, calcification of myocytes, and congestion in the liver and lungs were seen in the subacute phase. Electrocardiograms (ECGs) exhibited low voltage, nonspecific ST-T wave changes, sinus tachycardia, occasional ventricular and supraventricular premature complexes and 2(0) AV block consistent with myocarditis and heart failure. Forty-one percent of the survivors exhibited increased HW and HW/BW ratios, biventricular dilation, interstitial and replacement fibrosis, myocyte hypertrophy and myocarditis. ECGs exhibited nonspecific ST-T wave changes, sinus arrhythmia, occasional ventricular and supraventricular premature complexes and 2(0) AV block. These data suggest that RbCV infection may result in viral myocarditis and heart failure with a proportion of survivors progressing into DCM.
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PMID:Electrocardiographic changes following rabbit coronavirus-induced myocarditis and dilated cardiomyopathy. 820 55

The literature concerning the importance of coenzyme Q10 in health and disease has been reviewed. Usual dietary intake together with normal in vivo synthesis seems to fulfil the demands for Q10 in healthy individuals. The importance of Q10 supplementation for general health has not been investigated in controlled experiments. The literature allows no firm conclusions about the significance of Q10 in physical activity. In different cardiovascular diseases, including cardiomyopathy, relatively low levels of Q10 in myocardial tissue have been reported. Positive clinical and haemodynamic effects of oral Q10 supplementation have been observed in double-blind trials, especially in chronic heart failure. These effects should be further examined. No important adverse effects have been reported from experiments using daily supplements of up to 200 mg Q10 for 6-12 months and 100 mg daily for up to 6 y.
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PMID:Coenzyme Q10 in health and disease. 1055 81

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