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 efficacy of muzolimine (BAY g 2821) in doses of 30 or 60 mg/day was studied over an observation period of 4 weeks in 48 patients with mild to moderate heart failure (NYHA stage 2 or 3) in a biometrically planned, multicentre study. Eleven of these patients were excluded from the evaluation of efficacy for various reasons. All 37 patients who remained (23 men and 14 women; mean age 59.6 years, mean body weight 73.8 kg) were treated throughout with one tablet per day (30 mg). A marked improvement of the symptoms of cardiac insufficiency was observed in these 37 evaluated cases in the course of the treatment period. At the end of the study body weight was reduced by 1.8 kg, heart rate fell from 84 to 75 beats/min and blood pressure decreased from 154/88 to 145/85 mm Hg on average. The laboratory parameters tested failed to show any clinically abnormal alterations. Twelve of 48 patients complained of side effects (dizziness, headaches, vomiting, nausea), these developing largely in the first 2 weeks and being transient in character. To summarize, it can be stated that patients with chronic heart failure (NYHA 2 and 3) can be effectively treated by muzolimine monotherapy.
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PMID:Muzolimine as monotherapy in the treatment of patients with congestive cardiac failure. 400

Over the last ten years the efficacy of lithium salts in cluster headache has been well demonstrated. Our patient, who had been suffering from cluster headache for approximately 30 years, had been in haemodialysis treatment for the last ten years for chronic renal failure. Moreover, he was affected by heart failure and peptic ulcer. The patient was currently under therapy with Digitalis, Isorbide dinitrate, and ranitidine and was dialyzed three times a week for a total of five hours each time. Neither prophylactic headache therapy nor high doses of analgesic drugs had proved effective. Although this patient was in haemodialysis, lithium treatment was indicated. The administration of lithium carbonate 300 mg during dialysis days and 150 mg during non-dialysis days improved the attacks. Complete recovery from the attacks was obtained when the serum levels of lithium reached the therapeutic range. No side effects were noted.
Cephalalgia 1985 Jun
PMID:Cluster headache: clinical efficacy of lithium salts in a haemodialysis treated patient. 401 22

Calcium channel blockers are assuming increasingly important roles in the practice of emergency medicine. Two cases and a review of the literature relating to treatment of hypertensive emergencies with nifedipine are presented. Nifedipine has a rapid onset of action (buccal, 10-15 minutes; oral, 30-45 minutes) and peak effect (buccal, 30 minutes, oral, 60 minutes). The duration of effects is four to six hours regardless of the route of administration, with a mean arterial pressure reduction of 21.6% (248/134 mm Hg to 165/87 mm Hg). In patients with severe hypertension and left ventricular failure, a consistent reduction in systemic vascular resistance (2,088 dynes/sec/cm-5 to 1242 dynes/sec/cm-5) and cardiac index (2.76 l/min/m2 to 3.77 l/min/m2) has been reported. The patients in this study had severe hypertension (systolic blood pressure greater than 180 mm Hg, diastolic blood pressure greater than 120 mm Hg) and end organ involvement (including heart failure, left ventricular strain, headache, confusion, dizziness, and shortness of breath). Nifedipine (10 mg) was administered buccally with prompt reduction of blood pressure and resolution of the patients' symptoms. Nifedipine appears to be a safe, effective agent for the management of hypertensive emergencies. Its pharmacokinetic profile and routes of administration make it particularly valuable in the practice of emergency medicine.
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PMID:Nifedipine in the management of hypertensive emergencies: report of two cases and review of the literature. 406 18

The action, efficient dosage and tolerance of a pure vasodilator, dihydralazine, used for the treatment of severe heart failure were studied in 30 children aged 1 month to 14 years. All of them presented with heart failure from various causes, not controlled by the usual medical treatment. Dihydralazine was administered orally, without interrupting the digoxin-diuretic treatment, with a dose of 34 to 140 mg/m2/day given in 4 equal doses. Clinical efficacy was considered null in 12 cases, low in 12 cases and good in 6 cases, without relationship with the original heart defect. Five of the 6 good results were obtained with doses greater than or equal to 100 mg/m2/day. In the group of 16 children who were given doses greater than or equal to 100 mg/m2/day, a significant improvement of the ECG indexes of left ventricular performance was obtained: decrease in systolic left ventricular internal dimension (p less than 0.05 at day 5), increase of the shortening fraction (p less than 0.05 since day 1) and of velocity of shortening (p less than 0.01 since day 1), while the diastolic left ventricular internal dimension remained unchanged. The only transitory undesirable effects observed were headache, vomiting and/or rash in 9 cases.
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PMID:[Dihydralazine treatment of cardiac insufficiency in children]. 407 3

There is an increasing use and variety of beta-adrenoceptor blocking agents (beta-blockers) available for the treatment of hyperthyroidism. Recent comparative studies suggest that atenolol (200mg daily), metoprolol (200mg daily); acebutolol (400mg daily), oxprenolol ( 160mg daily), nadolol ( 80mg daily) and timolol (20mg daily) produce a beneficial clinical response equal to that seen with propranolol ( 160mg daily). Most beta-blockers reduce resting heart rate by approximately 25 to 30 beats/min, although a lesser reduction is seen with those possessing intrinsic sympathomimetic activity such as oxprenolol and pindolol. While earlier studies employing large doses of intravenous propranolol concluded that beta-blockade reduced myocardial contractility, more recent non-invasive studies suggest that the predominant cardiac effect is on heart rate. In patients with cardiac failure, beta-blockers may, however, produce a profound fall in cardiac output. Nevertheless, in combination with digoxin they may be useful in controlling the atrial fibrillation of thyrocardiac disease. beta-Blockers improve nervousness and tremor (although to a lesser extent with cardioselective agents) and severe myopathy, and they also reduce the frequency of paralysis in patients with thyrotoxic periodic paralysis. There is often subjective improvement in sweating but usually no major effect on eye signs. Recent studies show a 10% reduction in oxygen consumption/basal metabolic rate with long term oral use of selective or nonselective beta-blockers. In addition, many agents (propranolol, metoprolol, nadolol and sotalol but not acebutolol, atenolol or oxprenolol) reduce circulating tri-iodothyronine (T3) concentration by between 10 and 40%, although the clinical significance of this effect (if any) is not established. beta-Blockers may also have endocrinological effects on gastrin, cyclic AMP, catecholamines and other hormone levels. Given in adequate dosage, propranolol has been shown to control thyrotoxic hypercalcaemia. Minor side effects (nausea, headaches, tiredness, etc.) are quite common but overall beta-blockers are well tolerated by the thyrotoxic patient. The major use of these drugs is in symptomatic control while awaiting definitive diagnosis or treatment. As an adjunct to antithyroid drugs or radioactive iodine, beta-blockers will produce a satisfactory clinical response in the weeks to months before these forms of therapy produce a euthyroid state. beta-Blockers are more convenient than antithyroid drugs in the control of patients receiving therapeutic radioiodine, in that continuous therapy and assessment of biochemical response is possible.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Use of beta-adrenoceptor blocking drugs in hyperthyroidism. 614 1

Trichloroethylene is an industrial solvent used primarily in degreasing operations with some use as an anesthetic agent as well. The primary route of exposure is inhalation and the central nervous system effects consist of headache, nausea, sleepiness, burning of the eyes. Human cases of intoxication have been associated with trigeminal neuropathy, however this is probably caused by a breakdown product dichloroacetylene. Fatal exposures may be the result of cardiac failure. Chronic exposure in industrial settings may cause alterations in a variety of behavioral parameters such as reduced memory and intellectual functioning. Experimental human exposures reveal fatigue and sleepiness effects and possible alterations in reaction time, but no deterioration in performance on manual dexterity tasks up to 300 ppm exposures. Animal experiments using acute exposures generally fail to reveal behavioral effects at concentrations below 1000 ppm, with a range of 75-2000 ppm. Cessation of exposure results in rapid behavioral recovery with no residual behavioral deficits. Exposure of dogs to 3000 ppm chronically results in severe cerebellar pathology, with no trigeminal nerve damage. No neurochemical effects of exposure have been documented. The neurobehavioral literature on the toxic effects of trichloroethylene is fragmented and poorly documented suggesting that more and better quality work is needed to understand the potential toxicity of this compound.
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PMID:The neurobehavioral toxicity of trichloroethylene. 627 43

Labetalol is a combined alpha- and beta-adrenoceptor blocking agent for oral and intravenous use in the treatment of hypertension. It is a nonselective antagonist at beta-adrenoceptors and a competitive antagonist of postsynaptic alpha 1-adrenoceptors. Labetalol is more potent at beta that at alpha 1 adrenoceptors in man; the ratio of beta-alpha antagonism is 3:1 after oral and 6.9:1 after intravenous administration. Labetalol is readily absorbed in man after oral administration, but the drug, which is lipid soluble, undergoes considerable hepatic first-pass metabolism and has an absolute bioavailability of approximately 25%. There are no active metabolites, and the elimination half-life of the drug is approximately 6 hours. Unlike conventional beta-adrenoceptor blocking drugs without intrinsic sympathomimetic activity, labetalol, when given acutely, produces a decrease in peripheral vascular resistance and blood pressure with little alteration in heart rate or cardiac output. However, like conventional beta-blockers, labetalol may influence the renin-angiotensin-aldosterone system and respiratory function. Clinical studies have shown that the antihypertensive efficacy of labetalol is superior to placebo and to diuretic therapy and is at least comparable to that of conventional beta-blockers, methyldopa, clonidine and various adrenergic neuronal blockers. Labetalol administered alone or with a diuretic is often effective when other antihypertensive regimens have failed. Studies have shown that labetalol is effective in the treatment of essential hypertension, renal hypertension, pheochromocytoma, pregnancy hypertension and hypertensive emergencies. In addition, preliminary studies indicate that labetalol may be of value in the management of ischemic heart disease. The most troublesome side effect of labetalol therapy is posture-related dizziness. Other reported side effects of the drug include gastrointestinal disturbances, tiredness, headache, scalp tingling, skin rashes, urinary retention and impotence. Side effects related to the beta-adrenoceptor blocking effect of labetalol, including asthma, heart failure and Raynaud's phenomenon, have been reported in rare instances.
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PMID:Labetalol: a review of its pharmacology, pharmacokinetics, clinical uses and adverse effects. 631 May 29

Antihypertensive vasodilators share the capability of producing vasodilation of arterioles. In addition, two of them, i.e. nitroprussiate and prazosine, also produce vasodilation of veinulae. Both of these agents cause a simultaneous decrease in pre-load and post-load, and may be used in heart failure. The effectiveness of vasodilators is offset by regulatory cardiac and/or renal mechanisms, and the association with a sympatholytic agent and/or a diuretic is generally needed. Consequently, vasodilators are usually the third step in the course of managing a hypertensive patient. Association with a betablocking agent is especially necessary in patients with coronary insufficiency, in order to prevent an increase in myocardial oxygen requirements and worsening of angina pectoris. Vasodilators are active within a fairly wide dosage range, making individualized dosages requisite. In treating hypertension by the oral route, daily doses above 200 mg for dihydralazine, 60 mg for minoxidil and 10 mg for prazosine are only exceptionnaly useful. In emergency treatment of hypertension, diazoxide and nitroprussiate can be used only in patients under continuous cardiovascular monitoring. Nitroprussiate must, in addition, be given through a controlled infusion device, but ensures more flexible and safer control of blood pressure. Dihydralazine may produce headache. This side effect occurs very early and is hardly compatible with continuation of treatment. Long term side effects are very uncommon or strictly biological for dosages below 200 mg/day. With currently used dosages (20 to 60 mg per day) minoxidil consistently produces hypertrichosis, outruling its protacted use in women.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Antihypertensive vasodilators]. 631 28

Tolerance and cross-tolerance to nitrates has been known since 1900 but the actual clinical importance of this phenomenon is unclear. Vasodilator treatment of congestive heart failure has provided an important new role for long-acting nitrates. The advent of high-dose nitrate regimens for both angina and heart failure raises the possibility that nitrate tolerance could be a potential detriment to therapy. A number of older studies have documented the development of tolerance and cross-tolerance to blood pressure and heart rate responses to nitrates as well as the rapid onset of tolerance to nitrate headaches in subjects given nitrates on a regular basis. Animal experiments also confirm the ready appearance of nitrate tachyphylaxis. Needleman has proposed a cellular mechanism for nitrate tolerance based on a chemical alteration of nitrate receptors in the vascular wall. In spite of these studies, there is considerable evidence that clinically relevant tolerance to nitrates is rare. Several recent investigations designed to look at this problem using high-dose isosorbide dinitrate (ISD) failed to demonstrate tachyphylaxis to the anti-anginal or hemodynamic effect of ISD. However, very recent work in patients with angina suggests that tolerance to high dose ISD does occur and may reduce the duration of action of long-acting nitrates. Overall, the bulk of current evidence does not support tolerance to be a major problem in nitrate treatment of cardiac diseases, although attenuated vasodilator responses may occur after several weeks of nitrate therapy.
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PMID:Nitrate tolerance and dependence. A critical assessment. 677 5

We gave intravenous amrinone to 40 patients in heart failure, and oral amrinone to 18 patients. Acute intravenous administration caused a significant reduction in mean blood pressure and this was severe enough to require correction by plasma infusion in five patients. Oral amrinone was accompanied by thrombocytopenia in 10 patients but no complications were associated with the low platelet count. Other potentially serious adverse effects were: abdominal pain (two patients), nausea and vomiting (three patients), jaundice (one patient), myositis (one patient), pulmonary infiltrates (two patients), and polyserositis (one patient). Less serious adverse effects observed were: splenomegaly, eosinophilia, fever, headache, reduced tear secretion, dry skin, and nail discoloration. The potentially severe adverse reactions with amrinone need to be weighed carefully against its benefits in the treatment of heart failure.
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PMID:Side effects of amrinone therapy. 683 32


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