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)

Serum levels endothelin-1,2 aldosterone, renin activity were performed in 52 patients with chronic congestive heart failure during captopril therapy. The investigations were done before therapy, after 10-15 days therapy and after disappearance symptoms of heart failure. The levels endotelin-1,2,aldosterone and renin activity were determined using radioimmunologic methods. Fraction ejection and peripheral vascular resistance were determined by echocardiography technics. It was found that serum endothelin levels in patients with chronic congestive heart failure were increased proportionally to functional class of heart failure and decreased after disappearance symptoms of heart failure. An increase in plasma endothelin concentration has not correlated with ejection fraction, aldosterone concentration and renin activity. These studies have demonstrated that in patients with congestive heart failure on captopril therapy endothelin serum levels positively correlates with peripheral vascular resistance. No correlation was found between ejection fraction and activity renin-angiotensin-aldosterone system. These findings indicated that captopril therapy decreases endothelin production.
Pol Merkur Lekarski 1997 Sep
PMID:[Does captopril decrease endothelial production of endothelin?]. 946 3

Pharmacologic management of patients with ventricular arrhythmias remains in a state of considerable flux. New findings from controlled clinical trials, suggest that use of the principles of risk stratification permits identification of patients at very high risk for developing sustained ventricular tachyarrhythmias or ventricular fibrillation. Available data suggest that patients with sustained ventricular tachyarrhythmias require treatment. Patients with frequent ventricular ectopy or nonsustained ventricular tachycardia in the absence structural heart disease do not require treatment except when relief of symptoms is warranted. The indication for treatment of patients with underlying structural heart disease, particularly coronary artery disease and a previous myocardial infarction, who manifest frequent ventricular ectopy or more particular nonsustained ventricular tachycardia remain uncertain. From meta-analytic studies, it has become clear that beta-blockers reduce sudden death and total cardiac mortality. Data also suggest that amiodarone appears to be the safest antiarrhythmic drug for treatment sustained and nonsustained arrhythmias, and improved survival in patients with advanced heart failure.
Pol Merkur Lekarski 1997 Aug
PMID:[Pharmacologic treatment for ventricular arrhythmias]. 948 Jan 72

The patients with chronic congestive heart failure and acute deterioration of heart failure (pulmonary oedema, significant reduction of blood pressure) have decrease liver's perfusion with signs of acute damage of liver's cells--ischemic hepatitis. Aspat, AIAT and LDH in blood rich very high level. The level of bilirubin, alkaline phosphatase and glucose increase slightly. Hepatotoxic viruses are never observed. The authors described a case of 34 years old man, who two years earlier had large myocardial infarction with aneurysm of heart and congestive heart failure. He was admitted to hospital in shock. The shock was caused probably by overdose of nitroglycerin. In ECG and Echo examinations he had no signs of acute myocardial infarction, but we observed serious damage of liver's cells with very high levels of AspAT, AIAT and LDH. Based on clinical and biochemical examinations we diagnosed ischemic hepatitis. The patient's clinical and biochemical tests were normalized after improvement of heart failure. Biopsy of liver was normal at that time. Prognosis in ischemic hepatitis depends on course of heart failure.
Pol Merkur Lekarski 1997 Dec
PMID:[Ischemic hepatitis]. 952 68

Angiotensin-converting enzyme (ACE) inhibitors are now established drugs in the treatment of hypertension and heart failure. The renin-angiotensin-aldosterone system is complex and acts as a circulating hormonal system, a local endogenous tissue system and neuromodular. Current experimental evidence suggests that ACE inhibitors reduce the risk associated with atherosclerotic cardiovascular disease. The antiatherogenic action of ACE inhibitors is related to complex effects mediated by these agent, including an antiproliferative and antimitotic action, beneficial effects on endothelial function, plaque-stabilizing effects and the action of these agents on the sympathetic nervous system. The role of ACE inhibitors in preventing the clinical sequale of atherosclerotic cardiac disease has been evaluated in various patient populations. Several small trial assess the effects of ACE inhibitors in severity of angina pectoris have reported conflicting results, with benefit is some patients and no benefit or even exacerbation of angina in others, indicating that ACE inhibitors do not have consistent antianginal effects in short-term study. ACE inhibitors have the theoretical potential to prevent restenosis after PTCA but they do not prevent restenosis and has no effect on overall clinical outcome. New data suggest that ACE inhibitors may be effective therapy fir patients following acute myocardial infarction. The renin-angiotensin system, is activated during new myocardial infarction and has an impact on the process of remodeling of the left ventricle which causes ist dysfunction and heart failure. In most of the large mortality trials the rationale for early treatment with ACE inhibitors after myocardial infarction was stated. ACE inhibitors have a positive effect in preventing the ventricular dilatation and they reduce the rate of reinfarctions and the mortality rate.
Pol Merkur Lekarski 1998 Jan
PMID:[The significance of converting enzyme inhibitor angiotensin I to angiotensin II in treatment of patients with coronary disease]. 955 7

The aim of the study was to estimate the influence of long-term treatment with molsidomine on structure, systolic function and neurohormonal parameters in patients with chronic heart failure (CHF). Investigations were carried out in 30 patients (mean age 63.0 +/- 10.9) in NYHA class III and IV. The cause of CHF was: coronary artery disease in 60% of patients, hypertension in 20% and dilated cardiomyopathy in 20% of patients. Molsidomine was administrated in dose of 2 mg tid for 3 months. During the study the previous treatment with ACEI, diuretics and digitalis was maintained. Using echocardiographic method left atrial dimension (LA), left ventricular end diastolic (LVEDD) and end systolic diameter (LVESD), interventricular septum (IVSDD) and posterior wall end diastolic diameter (LVPWDD), ejection fraction (LVEF) and fraction of shortening (LVFS) were measured. Plasma level of atrial natriuretic peptide, endotelin, neuropeptide Y and aldosterone and plasma renin activity were estimated radioimmunologically. All echocardiographic and neurohormonal measures were performed 4 times: before therapy, after 3 days, 2 weeks and 3 months of treatment with molsidomine. We observed significant increase in LVEF, which at baseline was 33.8% and after 3 months 44.8% (p < 0.05). None of the other echocardiographic parameters nor any of neurohormonal factors changed significantly during the 3-months treatment with molsidomine.
Pol Merkur Lekarski 1998 Jun
PMID:[The influence of 3-month treatment with molsidomine on structure, function and some neurohormonal parameters in patients with chronic heart failure treated with digoxin, diuretic and angiotensin converting enzyme inhibitors]. 977 Oct 14

The aim of the study was to assess the relation between urinary excretion of epinephrine and norepinephrine, and stroke severity, prognosis and standard biochemical investigations in acute phase of ischaemic stroke. The study was done on the material of 36 patients (17 women and 19 men, aged 41-89 years, mean: 69 +/- 13 years) admitted to the stroke unit of the Neurology Department within 24 hours (mean: 7.7 hours), after the first ever ischaemic stroke affecting the territory of the internal carotid artery circulation, confirmed by CT. Patients with the history of diabetes mellitus, cardiac insufficiency and infection on admission were excluded from the study. The 24-hour urine collection for catecholamines (epinephrine and norepinephrine) was done on the first and third day of hospitalization. An even single increased daily excretion of epinephrine (> 10 micrograms/24 hr) was found in 21 and norepinephrine (> 50 micrograms/24 hr) in 10 of 36 patients. No correlation between daily excretion of epinephrine and norepinephrine was found. Statistical analysis revealed a significant relation between norepinephrine, but not epinephrine, and neurological deficit, prognosis and some biochemical parameters of investigated patients. Patients with increased daily excretion of norepinephrine showed worse neurological deficit (p < 0.01), greater mortality assessed on the 30-th and 90-th day of stroke (p < 0.05) and increased plasma glucose, sedimentation rate, white blood cells count, creatinine kinase activity as well as microalbuminuria and decreased plasma kalium concentration.
Neurol Neurochir Pol
PMID:[Daily excretion of epinephrine and norepinephrine in acute phase of cerebral ischemia]. 986 6

The circadian heart rate course was assessed in 3 groups of patients with left ventricular ejection fraction (LVEF) 10-15%, 20-25% and 30-35%. The study comprised 36 persons. In 9 patients heart failure was due to MI and in 17--to dilated cardiomyopathy. Those with atrial fibrillation, ventricular tachycardia, supraventricular tachycardia, diabetes, valvular heart diseases and with central system disorders were excluded from the study. Left ventricular ejection fraction was evaluated by echocardiography. Heart rate, calculated as a mean value every 5 minutes, was taken in patients during 24 hour recordings. For each patient separately, mean value of all measurement was calculated. Then a ratio of each actual value to the mean value was calculated. This ratio was defined as relative heart rate; [formula: see text] Circadian heart rate courses were approximated by Fourier row: [formula: see text]. The 24 harmonics were analyzed. Statistically significant differences in circadian courses were closed to amplitudes of 1st, 12th, 13th, 14th, 16th, 18th harmonics. Using test of variance homogeneity it has been demonstrated that variability of amplitudes of 12th and 17th harmonics as well as phase of 5th harmonic depend on left ventricular ejection fraction.
Pol Arch Med Wewn 1998 Jun
PMID:[Use of fourier row as a method for analyzing the course of circadian heart rate in patients with left ventricular ejection fraction impairment]. 1008 2

The contention that female gender is an independent factor that affects survival after acute myocardial infarction (AMI) is still controversial. The aim of this retrospective study was to assess whether or not early and late mortality after AMI is greater in women than in men. Data of 464 consecutive patients (130 women and 334 men) who had a documented acute myocardial infarction in our Department of Cardiology between 1990 and 1993 were eligible for the study. We excluded 48 patients from the study for the following reasons: the location of infarct could not be determined in 18 patients: 16 patients refused to take part in the study and we were not able to contact 14 patients. The remaining 416 patients were analyzed in the study. The mean follow-up period was 36 months (from 1 to 72 months). Women were significantly older than men (62.1 +/- 11.2 vs 58.1 +/- 11.6; p < 0.001), especially those who died in hospital (70.7 +/- 9.3 vs 64.4 +/- 8.7; p < 0.01). In hospital died 26 women (20%) and 39 men (11.7%)--p < 0.05. However, age-adjusted in-hospital mortality did not differ between women and men (p = 0.256). We did not find any significant difference in 3-year survival after AMI between women and men (22% vs 20.7%; NS). Total mortality was also similar (38% vs 30.2%; NS). QMI was diagnosed in 85 women and 234 men (73% vs 78%; NS), NQMI in 31 women and 66 men (27% vs 22%; NS). The rate complications of acute phase of AMI (acute heart failure and/or rhythm disturbances) was similar in women and men. Fibrinolytic treatment was introduced in 27.2% of women and in 26.4% of men. Hypercholesterolemia and hypertension were more often associated with female gender. In multivariate analysis we found that age, acute heart failure, previous MI, hypercholesterolemia and diabetes mellitus were significant factors which affects survival after AMI. Of these only age and diabetes mellitus appeared to be significant in women.
Pol Arch Med Wewn 1998 Jul
PMID:[Survival of women and men after myocardial infarction does not differ. Results of several years' observation]. 1008 14

Sudden cardiac death due to ventricular arrhythmias remains a significant problem. In most studies about 50% of all death related to coronary artery disease and heart failure are sudden and unexpected and are caused by acute fatal ventricular tachycardia and fibrillation. Most of the patients suffering sudden cardiac death have some kind of structural heart disease but 80% of SCD events are associated with coronary artery disease, 10-15% with dilated and hypertrophic cardiomyopathy, and only small fraction with the less common disorders as valvular heart disease, ventricular dysplasia and cardiac involvement in sarcoidosis or amyloidosis. In some patients the anomaly responsible for sudden cardiac death is not structural but mainly electrical as in patients with the long QT syndrome, WPW syndrome or in patients with a proarrhythmic effect from antiarrhythmic drugs. In this review, data from clinical trials and other studies on on antiarrhythmic therapies have been evaluated in order to determine effective strategies for the prevention sudden cardiac death in high risk patients. Taken together with the mortality data routine prophylactic use of class I antiarrhythmic drugs in the patients survivors of acute myocardial infarction and patients with heart failure is associated with increased risk of death. Conversely beta-blockers are associated with significant reduction in nonfatal cardiac arrest in the short term trials and sudden cardiac death in long term trials. These benefits are likely due to relief ischemia, reduction of heart rate and maintenance favourable autonomic nervous system balance. Overall trial data on amiodarone suggests that this agent is effective in reducing the risk of death in survivors of cardiac arrest, post infarction patients, and patients with heart failure but the routine prophylactic use of amiodarone remains of uncertain efficacy. The physician who considers the use of antiarrhythmic medications in patients with ventricular arrhythmias must be aware of which arrhythmias are malignant or potentially malignant and which are benign and the decision to initiate antiarrhythmic therapy should be based on consideration of the patients absolute mortality risk.
Pol Merkur Lekarski 1999 Mar
PMID:[Antiarrhythmic agents in the prevention of sudden cardiac death]. 1036 92

The discovery of opioid receptors and endogenous substances capable of specific binding to these receptors, i.e. endorphin and enkephalin, is one of the most spectacular indications suggesting that the presence of a receptor for a certain drug in the organism authenticates searching for an endogenous substances with high affinity at this receptor. Later, further studies were undertaken to detect other endogenous drug-like factors. Some experiments led to the discovery of digoxin-like factor in blood which could bind to a specific receptor on Na+, K(+)-ATPase subunit, showing also the affinity for cardiac glucosides. Digoxin-like factor was detected in blood of healthy people who did not receive any drug treatments. It has been estimated to be present in 15% of the population but in some diseases this value is much higher, e.g. digoxin-like factor was detected in 90% of patients with IDDM, and it can be used as a risk factor of the occurrence of vascular complications. In cases with NIDDM, the digoxin-like factor was detected in patients with insulin-resistance. The presence of digoxin-like factor was ascertained in patients with heart failure who did not take digitalis preparations. Endogenous digoxin-like factor can contribute to the detection of falsely increased digoxin blood concentrations during the monitoring of drug level in the course of the therapy. In our studies we ascertained the presence of the quinidine-, cyclosporin-, theophylline- and phenytoin-like substances in the blood of the healthy people who did not receive any drugs. It seems that these endogenous substances resembling drugs are synthesized in human organism when they are needed for maintaining the physiological equilibrium. We can suggest that stimulation of the production of drug-like factors in the organism can be used in the future in the therapy of some diseases.
Pol J Pharmacol
PMID:Endogenous drug-like factors. 1038 21


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