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)

The aims of treatment in acute myocardial infarction are to limit evolving muscle necrosis, prevent heart failure, maintain electrical stability, and preserve the coronary circulation to avoid progressive or recurrent infarction. No single treatment achieves all these objectives. The rationale for the use of adrenoceptor blocking drugs is that they will oppose the effects of the increased sympathomimetic activity which follows acute infarction and which may adversely affect outcome. More is known of the clinical use of pure beta-blockade than of combined alpha- and beta-blockade with labetalol but in theory combined receptor blockade will produce additional beneficial effects over beta-blockade alone. beta-Adrenoceptor antagonists have a theoretical role in limiting infarct size. They may reduce the oxygen deficit of jeopardised though potentially viable tissue, limiting infarct size by their favourable effect on heart rate, systolic pressure, contractility, and metabolic pathways. That beta-blockade reduces myocardial damage has been confirmed in animal studies. Studies in man using enzyme release or R wave scoring as indicators of infarct size also suggest that oral or intravenous beta-blockers after infarction encourage myocardial salvage. Few studies have been reported in which the effects of combined alpha- and beta-blockade on infarct size have been determined. The actions of a dual blocking agent are more complex and the outcome less predictable than from beta-blockade alone: the advantages of the beta-blocking component will be retained while the alpha-blocking component may conceivably further diminish oxygen demand by reducing systolic pressure and heart size. Less favourably, coronary perfusion pressure may also fall. It is apparent that further clinical studies are needed. Adrenergic blockade may be used to prevent or treat ventricular arrhythmias which develop after infarction in the face of heightened sympathetic tone and continued ischaemia. Clinical and experimental evidence points to the efficacy of beta-blockade in ischaemia-related arrhythmias, but beta-blockade alone is probably ineffective against arrhythmias arising during reperfusion. In experimental studies, alpha-blockers are effective against both forms of arrhythmia although the doses required for reperfusion effects may produce unacceptable hypotension in clinical use. It is possible that combined alpha- and beta-blockade may have broader antiarrhythmic activity than beta-blockers alone but present clinical data on the value of labetalol in controlling postinfarction arrhythmias are sparse.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Combined receptor intervention and myocardial infarction. 615 93

Sympathomimetic amines are useful in the treatment of patients with ischemic heart disease complicated by heart failure and shock. These agents influence the cardiovascular system by action on alpha-adrenergic, beta-adrenergic, and dopamine receptors. Recent evidence has demonstrated the existence of subtypes of the classic adrenergic and dopamine receptors that mediate distinct physiologic effects. The relative actions of sympathomimetic amines on these receptors differ substantially, resulting in considerable variation in their cardiac and peripheral vascular effects. Two classes of sympathomimetic amines are being intensively investigated at present: (1) compounds acting predominantly on beta 1-adrenergic receptors (i.e., they increase cardiac contractile force with little or no peripheral vascular effects) and (2) compounds acting on both beta 1-adrenergic and dopamine receptors. Orally active compounds of these two classes have been synthesized recently and are now under study for the treatment of patients with heart failure. Results of preliminary studies with such components are briefly reviewed.
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PMID:Sympathomimetic amines: potential clinical applications in ischemic heart disease. 627 12

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

As the efficacy of oral long-acting sympathomimetic drugs is not yet well established, we investigated the hemodynamic effects of orally administered salbutamol in eight heart failure patients. Cardiac index, heart rate, blood pressure, and left ventricular filling pressure were monitored for 6 hours after a single oral administration of 4 to 8 mg salbutamol and placebo. In patients who had received salbutamol, a 40% increase in the cardiac index (+0.75 L/min/m2, p less than 0.01) was noted 1 hour post administration; a 44% increase (peak effect) occurred at 2 hours (+0.84 L/min/m2, p less than 0.05); and a significant increase persisted for 6 hours. Changes in heart rate showed a similar time course; however, the increase was less pronounced (+27% at 2 hours). The changes in blood pressure were slight and none of the eight patients developed ventricular arrhythmia or other complications. After placebo administration, no consistent changes in the hemodynamic parameters were noted. The present study suggests that, due to its sustained positive action on cardiac output, the oral administration of salbutamol may be efficacious in ambulatory patients with low cardiac output due to heart failure.
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PMID:Hemodynamic effects of salbutamol, an oral long-acting beta-stimulant, in patients with congestive heart failure. 675 47

Timolol, a nonselective beta-adrenoreceptor blocking agent without intrinsic sympathomimetic or membrane stabilizing activity, has been shown effective in the treatment of angina and hypertension. It is particularly useful in patients with stable angina pectoris and patients with mild to moderate hypertension. In both of these conditions, timolol appears to be comparable to propranolol. A recent study has suggested that timolol reduces mortality and reinfarction rate in patients who have recently had a myocardial infarction. When given topically timolol reduces intraocular pressure in patients with open-angle glaucoma; the drug may be used as the primary agent or as an adjunct to standard therapy. Careful selection of patients will reduce the frequency of adverse effects due to beta-receptor inhibition. Thus, timolol should not be used in patients who are predisposed to asthmatic bronchitis or cardiac failure, and it should be used with caution in patients with peripheral vascular disease or diabetes mellitus.
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PMID:Pharmacokinetics, mechanisms of action, indications, and adverse effects of timolol maleate, a nonselective beta-adrenoreceptor blocking agent. 676 88

The complications of myocardial infarction after transfer from the Coronary Care Unit on the 6th day were analysed bu a retrospective study of 3,460 computerised case reports (1973-1980). The mortality rate was 6% (1/3 of hospital deaths) in the period from the 7th day to discharge from hospital (14th to 30th day). Cardiac arrest as not uncommon (20% of all cardiac arrests) but the prognosis was better thn during the initial phase (p less than 0.05) as the mechanism was more commonly ventricular fibrillation or tachycardia (p less than 0.05). This series was compared with a similar population from 1970-1973; an improvement was observed in global hospital mortality (27% previously compared to 17%, in the study series, p less than 0.001). As the population were comparable, this phenomenon seems to be related to better treatment of shock and cardiac failure and the advances in cardiac surgery during the initial phase of infarction. Thd commonest mechanical complication was ventricular aneurysm; its occurrence does not influence the vital prognosis during this period. The incidence of cardiac arrest and death due to cardiac failure is not negligible after the first week of myocardial infarction. Therefore, we do not believe that the hospital period should be reduced after myocardial infarction. Special training of the nursing staff is essential for the successful treatment of these complications. The global prognosis could be improved by the rehabilitation of digitalis therapy and the introduction of new sympathomimetic amines in the acute phase of myocardial infarction.
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PMID:[Complications of myocardial infarction between the 2d and 4th week]. 681 81

A 60-year-old man under digitalis treatment for hypertensive heart tried to commit suicide by absorbing a 15 mg dose of digitoxin. Severe intestinal bleeding occurred 12 hours later, followed by pseudo-occlusive syndrome and ischaemia of the distal lower limbs. On abdominal incision the whole gut was found to be invaded by haemorrhagic necrosis and perforated on three points. The patients subsequently died of peritonitis. The responsibility of digitoxin in these events was demonstrated by the absence of any other cause of ischaemia, such as heart failure, shock, arrhythmia, consumption coagulopathy or use of sympathomimetic drugs. This case shows that the vasoconstrictor effect of digitalis, experimentally demonstrated but clinically controversial, is a reality, and that digitalis compounds are contra-indicated in patients with haemorrhagic necrosis of the digestive tract.
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PMID:[Haemorrhagic necrosis of the digestive tract consecutive to massive digitalis intoxication (author's transl)]. 697 39

Cardiac function is regulated by four parameters: heart rate, preload, contractility and after-load. In the treatment of heart failure cardiac function is influenced by way of these parameters. The longterm pacemaker can normalize heart rate in patients with bradycardia; diuretics and volume load influence the filling pressure of the heart, while glycosides and sympathomimetic drugs increase contractility. If these mechanisms fail, peripases cardiac work. Vasodilators reduce this peripheral constriction was well as the elevated preload, and can therefore improve cardiac performance. The use and limitations of these pharmacological agents are discussed.
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PMID:[New aspects in the treatment of cardiac insufficiency]. 739 2

In animals, intermittent sympathomimetic stimulation with dobutamine produces benefits analogous to those of physical conditioning. Longer intermittent or continuous beta-stimulant therapies have not, however, been successful in managing patients with chronic heart failure. We have investigated the role of beta-receptor stimulants in patients with severe chronic heart failure by changing the method of administration to intermittent, very short-duration pulsed intrope therapy (PIT). We studied 10 patients (mean age 64 [SE 2] years) with stable moderate to severe chronic heart failure (ejection fraction 23 [3]%) who received PIT, and 10 control patients matched for age and severity. We infused sufficient dobutamine to raise heart rate to 70-80% maximum for 30 min per day, 4 days per week for 3 weeks. PIT increased exercise tolerance (from 10.4 [1.2] min at baseline to 13.0 [1.5] min at 3 weeks; p < 0.001, 95% CI for difference 1.6 to 3.9) and lowered peripheral vascular resistance (19.8 [3.1] to 17.7 [2.4] mm Hg.min.L-1; p < 0.05, -4.1 to -0.1). PIT produced significant increases in lymphocyte beta-receptor density (502 [110] to 1200 [219] per cell, p < 0.02, 258 to 1138) and chronotropic responsiveness to exercise (change in heart rest to peak exercise 51.0 [3.2] to 57.5 [3.9] beats per min; p < 0.01, 2.9-10.1). Plasma noradrenaline concentrations (2.39 [0.28] to 1.65 [0.19] nmol/L, p < 0.05) were reduced. The patients' symptoms were also improved. By contrast, no change in autonomic function or exercise capacity was seen in the control group. Short-duration PIT induces pharmacological conditioning with improved symptoms, autonomic balance, exercise tolerance, beta-receptor up-regulation, and enhanced chronotropic responsiveness in chronic heart failure.
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PMID:Effects of pulsed beta-stimulant therapy on beta-adrenoceptors and chronotropic responsiveness in chronic heart failure. 770 39

The essential goal of medical treatment following myocardial infarction with left ventricular dysfunction must be the prevention of secondary cardiac failure. The existence of left ventricular dysfunction, in particular when it is not accompanied by clinical cardiac failure, is a virtually formal indication for beta-blocker treatment after an infarction. Beta-blockers with intrinsic sympathomimetic activity (ISA) are possibly better tolerated in this context. However, experience shows that cardiologists and general practitioners often remain reluctant to prescribe beta-blockers whenever left ventricular function is impaired. Converting enzyme inhibitors decrease the risk of onset of secondary cardiac failure, reduce sudden deaths by ventricular arrhythmias, reduce recurrences of myocardial infarction or unstable coronary insufficiency, and more generally reduce overall and cardiovascular mortality. This is a class effect. While there is no urgency to prescribe them during the acute phase, it is generally considered that it is extremely useful to give them fairly quickly, i.e. during the first 72 hours. At the end of the hospital phase, around two weeks, it is desirable, whenever possible, to prescribe a dose of the order of 75 mg/day of captopril or 2.5 mg/day of ramipril. The administration of aspirin can be considered virtually routine. Oral anticoagulants are desirable in the presence of a large akinetic pocket, a frequent starting point of thrombosis and/or systemic emboli, or in the presence of atrial fibrillation. Digitalis/diuretic treatment does not appear to be indicated at this stage. Other types of anti-ischemic treatment are not theoretically indicated as a matter of principle at this stage in the absence of residual ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[What is the appropriate treatment for myocardial infarction with left ventricular dysfunction?]. 786 55


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