Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 18 patients with documented ischaemic heart disease the cardiovascular effects of ketamine (1.5 mg/kg iv) were studied under three different conditions: 1. in awake premedicated patients (n = 6); 2. after the previous administration of flunitrazepam (0.015 mg/kg iv, n = 6) and 3. under conditions of neuroleptanalgesia and muscle relaxation (n = 6). Flunitrazepam prevented or at least attenuated the increases in heart rate (30%), mean arterial pressure (37%), mean pulmonary artery pressure (165%), left ventricular filling pressure (230%), total peripheral resistance (50%), pulmonary vascular resistance (100%) and in the rate-pressure product (66%) which were associated with the use of ketamine as the sole anaesthetic agent. In addition, the flunitrazepam-pretreatment abolished the fall in cardiac index and stroke index which occured in patients given ketamine alone. Flunitrazepam therefore appears to be a promising drug to prevent adverse cardiovascular reactions, when ketamine should be chosen for induction of anaesthesia. Neuroleptanalgesia and muscle relaxation also proved effective in controlling the sympathomimetic actions of ketamine. The response of the mean pulmonary artery pressure and of the ventricular filling pressures to ketamine in this group was even more damped than in the patients pretreated with flunitrazepam alone.
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PMID:[Flunitrazepam-pretreatment for prevention of adverse cardiovascular effects following ketamine]. 4 95

Bretylium tosylate (Bretylol) has recently been approved for parenteral use against resistant ventricular arrhythmias. The pharmacologic action of bretylium is complex, and its antiarrhythmic action differs significantly from other drugs. Bretylium is an adrenergic neuronal blocking agent taken up selectively at peripheral adrenergic nerve terminals, where it initially releases norepinephrine (sympathomimetic effect) and then produces adrenergic neuronal blockade. It has direct cardiac membrane effect to prolong action potential duration and effective refractory period but, unlike other membrane active antiarrhythmic agents, does not depress conduction velocity or automaticity. Bretylium increases ventricular fibrillation threshold and prevents the decrease in ventricular fibrillation threshold associated with myocardial ischemia. It does not depress myocardial contractility. Clinical studies have shown parenteral bretylium to be effective in suppressing ventricular arrhythmias, particularly recurrent, drug resistant ventricular tachycardia or ventricular fibrillation.
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PMID:Bretylium tosylate: a newly available antiarrhythmic drug for ventricular arrhythmias. 38 Apr 36

Anticholinergics (in particular, ipratropium bromide [Atrovent]) are first-line therapy in patients with chronic obstructive pulmonary disease (COPD). Although more studies are needed to support the use of combination therapy, adding an inhaled beta agonist to the therapeutic regimen is reasonable in patients who remain symptomatic and need quick relief. Patients frequently receive inadequate amounts of drug with standard doses delivered by metered-dose inhalers, often as the result of improper technique, so symptomatic patients may require higher doses. Caution is recommended when the dose of inhaled sympathomimetics is increased in COPD patients with ischemic heart disease or tachyarrhythmias. The addition of an oral sympathomimetic is seldom necessary. Theophylline may be considered in outpatients who remain symptomatic despite their use of inhaled bronchodilators, but heart disease, seizure disorders, and gastroesophageal reflux are contraindications. Corticosteroid therapy remains controversial but can be helpful in patients who still have severe disease despite maximum bronchodilator therapy. Antibiotics can be of benefit in COPD patients undergoing an exacerbation who have increasing dyspnea, cough, and phlegm production.
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PMID:Drug treatment of COPD. Controversies about agents and how to deliver them. 134 54

In principle, all forms of treatment applied in patients with symptomatic coronary heart disease may likewise be used in silent myocardial ischemia. Based on Bayes' theorem, therapeutic measures may only be applied in patients with a positive exercise ECG with a high likelihood of coronary heart disease, and/or with myocardial ischemia revealed by another, ECG-independent method, such as, for example, thallium-scintigraphy. As symptomatic improvement cannot be expected in patients with silent myocardial ischemia, therapeutic efficacy can only be documented by an improvement in prognosis. Results of controlled randomized trials are not available in silent myocardial ischemia; therapeutic recommendations can, therefore, only be based on analogous results obtained in patients with symptomatic forms of the disease. Apart from reduction of the known risk factors of coronary heart disease, aspirin may be given to all patients at risk. Among the antiischemic antianginal drugs, beta-receptor blocking agents without intrinsic-sympathomimetic activity may be expected to improve prognosis. In asymptomatic patients with left-stem stenosis and three-vessel disease with impaired left-ventricular function (also, in two-vessel disease with a stenotic dominant LAD) aorto-coronary bypass surgery may be considered in order to improve prognosis.
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PMID:[Therapeutic possibilities, respective implications in silent ischemia]. 135 29

Bucindolol is a new beta blocker with marked vasodilatory properties and intrinsic sympathomimetic activity. We tested its potential effect against ventricular fibrillation (VF), in a pig model of acute myocardial ischemia. Bucindolol 6 mg/kg IV was administered in two equally divided doses, the first 30 minutes prior to, and the second 10 minutes after, ligation of the anterior descending coronary artery (CAL) in anesthetized open-chest pigs. Bucindolol decreased the incidence of VF to 1/11 versus 14/16 in the control group (p less than 0.005). Bucindolol also decreased the duration of ventricular tachycardia, 15 +/- 8 seconds versus 104 +/- 32 seconds in the control group (p less than 0.01). Bucindolol maintained LVmaxdP/dt at predrug and pre-CAL values, whereas LVmaxdP/dt was decreased by CAL in the control group. Bucindolol decreased arterial pressure and heart rate. Bucindolol increased blood flow in the peripheral ischemic zone (24.6 +/- 1.8% versus 16.2 +/- 1.7% (percent of pre-CAL value) in controls, p less than 0.002), as well as in the nonischemic zones (periischemic zone: 126.4 +/- 6.1% versus 96.7 +/- 4.8% in the control group, p less than 0.0005; remote nonischemic zone: 126.6 +/- 7.1% versus 87.1 +/- 4.3% of pre-CAL value in the control group, p less than 0.0001). Bucindolol had marked antiarrhythmic effects that were associated with beneficial effects on the mechanical function of the left ventricle and on blood flow to the ischemic myocardium.
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PMID:Bucindolol, a beta blocker, decreased ventricular fibrillation and maintained mechanical function in a pig model of acute myocardial ischemia. 135 66

Cocaine exerts a myriad of adverse cardiovascular effects which are dependent on the dose, rate of administration, and duration of use. The drug has two primary pharmacologic actions: it is a powerful sympathomimetic agent and a local anesthetic. The drug blocks the presynaptic reuptake of catecholamines resulting in the marked hormonal increase at the postsynaptic receptor sites. These effects, in turn, lower the threshold for coronary vasoconstriction and vasospasm, myocardial ischemia and infarction. In addition, the drug's multiple pharmacologic and electrophysiologic cardiovascular actions can promote arrhythmias, myocarditis, cardiomyopathy, as well as unmasking subclinical diseases. Long-term cocaine use can cause autonomic disturbances and alter catecholamine homeostasis: chronic cocaine addicts face serious cardiovascular sequelae from the drug's multiple adverse effects. It is important to assess the prevalence of cocaine-related cardiovascular diseases, to understand how the drug affects the autonomic nervous system, and to determine its long-term effects on the cardiovascular system.
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PMID:Cardiovascular effects and toxicities of cocaine. 148 95

We review the pharmacology, pharmacokinetics, and relative costs of beta-blockers, as well as indications for and therapeutic controversies surrounding their use. It is hoped that this discussion will assist clinicians in making informed decisions when choosing a drug for a hospital formulary or a particular patient. Beta-blockers are indicated for a variety of noncardiovascular and cardiovascular conditions, including hypertension, ischemic heart disease, arrhythmias, and prophylaxis of myocardial infarction (MI). These agents compete with catecholamines at beta-adrenoreceptors. They have different ancillary properties, including intrinsic sympathomimetic activity (ISA), cardioselectivity, and membrane stabilizing-activity, and vary in their duration of action, route of elimination, and lipophilicity. Beta-blocking agents decrease oxygen demand by exerting a negative inotropic and chronotropic effect. They also reduce blood pressure and possess antiarrhythmic effects. Beta-blockers penetrate the central nervous system (CNS) to different degrees and can cause a wide variety of CNS adverse effects. Nonselective beta-blockers have been noted to slightly reduce renal blood flow. Nadolol is an exception in that either no change, or even a small increase in renal blood flow, is observed upon initiation of therapy. Beta-blockers also act on the pulmonary bed by preventing beta 2-mediated bronchodilation, thereby exacerbating bronchospastic disease in some patients. Beta-adrenergic blocking agents can potentiate both hypoglycemia and hyperglycemia in diabetic patients. Their effects on total peripheral resistance (TPR) are controversial. Initially it appears that beta-blockade increases TPR. After chronic therapy, however, TPR decreases to or below baseline values. These agents appear to be equally efficacious in the treatment of hypertension, arrhythmias, and ischemic heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Around the beta-blockers, one more time. 168 78

Patients who have sustained greater than or equal to 1 myocardial infarcts are at high risk for sudden death or reinfarction; the risk is highest for those with lowest ventricular ejection fraction, continuing myocardial ischemia and asymptomatic high-density and complex premature ventricular contractions. At present, beta blockers when given prophylactically are the only agents that reduce the incidence of sudden death and reinfarction in survivors of myocardial infarction (MI) in the first 2 years. The beneficial effect was shown to correlate with a reduction in heart rate, the effect being absent or deleterious with beta blockers with marked sympathomimetic activity. The effects of beta blockers on ventricular fibrillation appeared to be dissociated from those on premature ventricular contractions. Trials with calcium antagonists indicate that these drugs had no effect or increased the mortality rate. The divergent effect of beta blockers and calcium antagonists is unexplained but may be due in part to a lack of bradycardiac effect of calcium antagonists; there were no differences in effect among different calcium antagonists. Data from trials involving class I antiarrhythmic agents indicate that agents acting by depression of cardiac conduction are either devoid of effect or produce a modest increase in mortality. Results of the Cardiac Arrhythmia Suppression Trial, employing the newer class I agents flecainide and encainide, were used to determine whether the suppression of premature ventricular contractions in the survivors of acute MI reduces mortality. Flecainide and encainide suppressed premature ventricular contractions greater than 80%, but resulted in an increased mortality rate undoubtedly due to a marked proarrhythmic effect. Whether these data can be extrapolated to all class I agents is uncertain. Preliminary data with class III antiarrhythmic agents suggest that these agents, especially amiodarone, similarly to beta blockers, have the potential to reduce mortality in survivors of MI. Evolving data suggest that in the secondary prevention of morbid events in the survivors of acute MI, the focus must shift away from antiarrhythmic agents that delay conduction and toward beta blockers and antifibrillatory actions resulting from a prolongation of refractoriness.
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PMID:Advantages of beta blockers versus antiarrhythmic agents and calcium antagonists in secondary prevention after myocardial infarction. 169

Beta-adrenoceptor antagonists (BB) demonstrate a competitive antagonism with endogenous catecholamines. Beta-1 receptor blockade mediates the depressive action on contractility, heart rate and atrio-ventricular conduction. Beta-2 receptor blockade mediates vascular, bronchial and uterine smooth muscle constriction. BB with beta-1 selective and intrinsec sympathomimetic activity do not increase systemic vascular resistance. BB are mostly used to treat ischaemic heart disease, hypertension and arrhythmias. Bradycardia, hypotension and bronchospasm are the main hazards in BB treated patients undergoing anaesthesia. However giving BB with premedication to patients taking usely this treatment allows better perioperative haemodynamic stability and avoids rebound effect. Experimentally, oxprenolol reverses regional dysfunction in ischaemic myocardium under halothane anaesthesia. During and after anaesthesia, intravenous (i.v.) BB must be used with caution to treat hypertension associated with tachycardia. In controlled hypotension, i.v. BB potentialise other agents. In phaechromocytoma surgery, alpha-blocking drugs are essential but additional BB can control tachycardia successfully. In coronary artery bypass surgery, giving BB prior to induction decreases cardiac enzymes serum levels. Esmolol, a new ultra-short-acting BB, would control perioperative tachycardia and hypertension without risk of prolonged cardiac depression.
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PMID:[Beta blockers and anesthesia]. 197 29

Beta adrenoceptor blocking drugs are all competitive inhibitors of the beta receptor although they may or may not possess, beta 1-(cardio)selectivity, intrinsic sympathomimetic activity (ISA) or partial agonist activity, alpha-blocking properties, while membrane stabilizing activity is now thought not to be important. Drugs with ISA give less of a reduction in resting and maximal exercising heart rate and consequently in cardiac output, than those without ISA. The possession of alpha-blocking activity also leads to less fall in cardiac output. Overall evidence suggests that peripheral resistance and peripheral blood flow is less reduced by ISA drugs. Post-beta blockade hypersensitivity which may be important in patients with ischemic heart disease if beta blocking drugs are suddenly stopped, is absent after beta-blocking drugs with ISA as they result in down regulation of beta receptors. Beta 1-selective drugs may result in less of a rise in blood pressure in response to isometric exercise, insulin hypoglycemia or smoking. There do not appear to be important differences in the effect on coronary flow. While presently available drugs can produce asthma in susceptible subjects there seems little doubt that beta 1 selective agents have less effect than other beta-blocking drugs, and give less inhibition of sympathomimetic bronchodilators. Nonselective, non ISA, beta-blocking drugs elevate triglycerides, cardioselective drugs possibly less so. Those with ISA may elevate HDL unlike those beta-blocking agents without this property. Beta adrenergic blocking drugs without ISA do not lower resting plasma noradrenaline, evidence suggests an increase; whereas those agents with marked ISA, suggests an increase; whereas those agents with marked ISA, e.g., pindolol, reduce it. Renin levels are lowered, but less so with ISA possessing agents. Some agents, e.g. atenolol, nadolol, sotalol, are hydrophilic, show poor brain penetration, are long-acting, are not liver metabolized, but are excreted by the kidneys unchanged. Others are lipophilic, e.g., metoprolol, propranolol, penetrate the brain, and are liver metabolized. Pindolol is metabolized about 50% by each route. Similarities between beta blocking drugs are dominant but differences are often clinically relevant.
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PMID:The additional properties of beta adrenoceptor blocking drugs. 242 33


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