Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intravenous nifedipine, a powerful calcium antagonist, had no obvious effect on atrioventricular conduction when administered to 11 patients during routine intracardiac electrophysiological studies. Verapamil on the other hand showed potent antiarrhythmic properties, depressing atrioventricular nodal conduction. Nifedipine thus appears safe in patients with angina pectoris who have disorders of atrioventricular nodal conduction, and in those receiving beta-adrenergic blocking drugs. There appear to be differential effects on the slow inward channels of cardiac cells with different 'calcium antagonists'.
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PMID:Effect of nifedipine on atrioventricular conduction as compared with verapamil. Intracardiac electrophysiological study. 48 72

A 60-year-old patient with coronary artery disease and antecedent (1976) myocardial infarction developed sinus standstill with nodal bradycardia of 41/min while on antiarrhythmic treatment with lidocain (2 mg/min drip infusion). Severe hypotension (70/50 mm Hg) occurred concomitantly. Withdrawal of lidocain and intravenous injection of 0.5 mg atropine restored sinus rhythm within 4 min, followed by a very sluggish, gradual increase in blood pressure over the next 45 minutes. Fortunately this episode did no harm to the patient. He was allowed to leave hospital 6 days later as there was no evidence of a second myocardial infarction and anginal pain was successfully controlled.
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PMID:[Sinus arrest after intravenous administration of lidocaine]. 53 35

Twenty four cases with myocardial rupture among 259 patients with autopsy after death due to myocardial infarction, were compared with patients with acute myocardial infarction and death secondary to other causes. Myocardial rupture occured during the first 72 hours in 58% of the patients and all cases within the first five days. Two thirds of the patients were males and 46% were 70 years of age. There were 24 myocardial ruptures (9.5%). Previous history of arterial hypertension and un-remittent anginal pain were predisposing factors for rupture (p=0.05). Other previously reported bad prognostic factors such as persistent hipertension after acute infarction, severe exercise before infarction and history of Diabetes Mellitus were not statistically significant in this study. Ruptured myocardium was not influenced by a previous history of myocardial infarction, hospitalization delay in the C.C.U., administration of anticoagulants, digitalis or pressor amines. There was no significant difference among the groups compared in enzyme curves or magnitude of leucocytosis. Electromechanic dissociation, sinus bradycardia, nodal rhythm followed by idioventricular rhythm and asystole, were observed following myocardial rupture.
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PMID:[Rupture of the free wall of the heart as cause of death in acute myocardial infarct]. 66 44

We conducted an intracardiac study of the electrophysiologic effects and kinetics of intravenous nicardipine (N) in 16 patients with or without impaired cardiac conduction, using a randomized, double-blind, crossover design versus placebo (P). N or P were infused intravenously over 5 min: the dose of N was 9.46 +/- 3.85 mg. Standard electrophysiologic parameters of atrioventricular (AV) conduction and sinus function were measured under basal conditions, between 10 and 25 min, and at 65 min, after beginning the first infusion of N or P, and between 10 and 25 min after beginning the second infusion of N or P. Treatment with N significantly reduced systolic (S) and diastolic (D) blood pressure (BP) at 10 min (35 +/- 19 and 25 +/- 17 mm Hg, respectively). N significantly shortened sinus cycle length (SCL), corrected sinus recovery time (CSNRT), AH interval, AV node (AVN) Wenckebach cycle length, and anterograde and retrograde effective (ERPs) and functional refractory periods (FRPs) of the AVN. Infranodal parameters were unaffected. Mean plasma N concentrations at 10 min were 18.5 +/- 7.7 ng/ml/kg and 5.3 +/- 3 ng/ml/kg at 60 min. Two patients experienced slight adverse effects (anginal pain and nausea); another with sick sinus syndrome developed a sinus pause. We conclude that intravenous N affects nodal, but not His conduction, and that it should be administered with care in the presence of SSS.
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PMID:Electrophysiologic effects of intravenous nicardipine on sinus node function and conduction in humans. 168 70

In this pilot study some cardiac effects of exogenous adenosine on the denervated heart were studied in a patient with transplanted heart since 3 years. He was instrumented with catheters into the left coronary artery, the coronary sinus and the right ventricle. Adenosine was given in increasing doses intracoronarily, into the aorta at the diaphragmal level and into a peripheral vein. When given into the aorta pain was provoked dose-dependently and not different from a reference group. When given intracoronarily no pain was provoked except at the highest dose when a slight discomfort of the chest was provoked. After intravenous injection no pain was provoked in the chest or in adjacent structures. Coronary sinus flow increased dose-dependently and not different from the reference group. No increased heart rate response occurred after intravenous or intracoronary injections. Extensive degrees of sinus and AV nodal blockade occurred. In conclusion, the results are in keeping with a role for adenosine as a messenger between myocardial ischaemia and angina pectoris and cardiac sympathetic pressure response. The importance of innervation for proper sinus and AV nodal function was also illustrated.
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PMID:Effects of exogenous adenosine in a patient with transplanted heart. Evidence for adenosine as a messenger in angina pectoris. 207 41

The aim of the present study was to evaluate the vasomotion of the entire coronary tree in variant angina, particularly focusing the attention on the behaviour of the "non spastic" epicardial vessels, using a quantitative coronary technique. Two different groups of patients served as controls. The first group consisted of 10 patients with accessory nodal pathway but without any sign of myocardial ischemia (Group I). The second group included 8 patients with stable exertional angina pectoris and coronary artery disease (Group II). The third group (Group III) consisted of 16 patients presenting with variant angina and spontaneous or hyperventilation-induced (HV: 30 cycles/min for 5 min) ST segment elevation. All patients underwent coronary angiography before and 2 min after HV testing; the evaluation of the coronary diameters was performed on baseline and after HV. In Group III, the HV testing caused a 26 +/- 12% reduction of the "non spastic" coronary vessels, with the mean control diameter of 2.00 +/- 0.61 mm that decreased to 1.48 +/- 0.55 mm. The patients of Group I showed only a mild degree of vasoconstriction (9 +/- 6%) of the epicardial coronary vessels; the Group II patients, also, showed a moderate response to vasoactive stimulus (11 +/- 8%), with the mean control diameter of 2.36 +/- 0.69 mm that decreased to 2.09 +/- 0.65 mm. The greater amount of vasoconstriction showed by patients with variant angina was statistically significant compared to both control groups (p less than 0.001). A further analysis of the coronary vasomotion, in Group III patients, showed that the 6 patients with normal or near normal coronary angiograms exhibited a 34% reduction in the vessel diameter. The remaining 10 patients who presented with a diffuse atherosclerotic involvement of the epicardial vessels (organic stenosis greater than or equal to 50% at the site of spasm) showed a lesser (20%) but yet significant extent of vasoconstriction compared to both control groups (p less than 0.001). In conclusion, our data indicate that: patients with variant angina exhibit a marked and diffuse coronary narrowing of the coronary vessels during vasoconstrictor stimuli; focal spasm occurs more frequently at the level of atherosclerotic coronary segments, whether they are critical or not. An interaction between these 2 phenomena, ie atherosclerosis and abnormal vasoconstriction, is supposed to be a cause of the occurrence of focal coronary spasm in variant angina.
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PMID:[Variant angina which interacts with two phenomena: local hypersensitivity and abnormal response in the coronary tree to vasoconstrictor stimuli]. 226 56

After cytostatic treatment severe arrhythmias, the development of angina pectoris and even the development of acute myocardial infarction and sudden death were observed. Therefore we made in 42 patients with malignant haematological disease treated with cytostatics 96 Holter monitorings of the electrocardiographic signal. The monitoring was made during the administration of cytostatics as well as during the time interval between the administration of combinations of cytostatics. In both instances (during the administration and during the interval between administration) we recorded a surprisingly high, mean all-day as well as maximal, heart rate. In the group monitored during administration of chemotherapeutic drugs we observed 5-8 hours after administration of cytostatics serious ventricular arrhythmias [incl. ventricular tachycardia], denivelization of the ST segment, paroxysms of supraventricular tachycardia. In the group monitored during the interval between administration of cytostatics the sick-sinus syndrome was recorded, as well as a passive nodal rhythm, disorders of the intraventricular conduction. The described changes are explained by the release of vasoactive substances after administration of cytostatics, by a change of the transmembrane calcium transport leading to an increased excitability of the heart muscle and possibly to coronary spasms and direct irreversible damage of the conduction system.
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PMID:[Holter monitoring of patients treated with cytostatic agents]. 272 Jul 41

Ca2+ channel antagonists are agents that interact with the voltage-dependent Ca2+ channel in a highly specific way. The prototype agents of cardiovascular importance are verapamil, nifedipine, and diltiazem, in historical order of appearance. These agents all have different molecular structures and bind separately with receptor sites located in or near the calcium channel, at molecular sites still to be fully identified. There are probably three distinct receptor sites (V, N, D) which stand in relation to the "gate" of the long-acting "L" calcium channel. There is probably overlap among the receptor sites, especially between the V and D sites to explain their common properties. All three agents inhibit the voltage-dependent calcium channel in vascular smooth muscle and also myocardial slow calcium channels. The ratio of the arterial to the myocardial effect is an index of the arterial selectivity, generally held to be a desirable property because the negative inotropic effect is usually a liability. The general clinical impression that nifedipine is the agent most active in vascular tissue in relation to the myocardial effect is supported by data on the relative potencies of these three agents on blood perfused dog preparations and by a comparison of the potency on rat vascular (portal vein) versus myocardial effects. Nonetheless all three agents are highly active in the inhibition of K(+)-induced vascular contractions (nifedipine 10(-9) M to 10(-8) M; verapamil 10(-7) M to 10(-6) M; and diltiazem 5 x 10(-7) M to 10(-6) M; concentrations for 50% inhibition of K(+)-induced vascular contractions in rat or rabbit aorta; comparative data for resistance vessels not available). The clinical impression that verapamil and diltiazem are more active on nodal tissue is also supported by a comparison of potencies on blood perfused dog nodal preparations in comparison with effects on coronary flow, with verapamil and diltiazem being approximately 10x more potent on the AV node than increasing coronary blood flow, so that the nodal effect is first detected. These basic pharmacological properties explain why all these three agents have clinical effects relevant to inhibition of vascular contraction (antihypertensive and antianginal effects) and only verapamil and diltiazem have clinically relevant inhibitory effects on the AV node (inhibition of supraventricular tachycardias). The comparative potencies of verapamil, diltiazem, and nifedipine in angina and hypertension will be examined in Parts II and III of this review.
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PMID:Calcium channel antagonists, Part I: Fundamental properties: mechanisms, classification, sites of action. 285 70

The chemistry, pharmacology, pharmacokinetics, clinical uses, and adverse effects of nicardipine, nitrendipine, and bepridil are reviewed. Nicardipine, nitrendipine, and bepridil are calcium antagonists under investigation for the treatment of cardiovascular disorders. Nicardipine and nitrendipine share a common dihydropyridine nucleus with the calcium antagonist nifedipine; bepridil is unrelated to other known calcium antagonists. Like nifedipine, nicardipine and nitrendipine produce peripheral vasodilation as their predominant in vivo effect. Bepridil has vascular, sinoatrial and atrioventricular nodal, and myocardial effects qualitatively similar to those of the calcium antagonist verapamil; it also interferes with the fast sodium channel and prolongs refractoriness in atrial and ventricular tissue. Nicardipine and nitrendipine undergo extensive first-pass hepatic extraction after oral administration; oral bioavailability of bepridil is about 60%. All three drugs are highly protein bound and have been reported to increase plasma digoxin concentrations. Both nicardipine and nitrendipine are effective antihypertensive agents used alone or combined with diuretics, beta blockers, or angiotensin-converting enzyme inhibitors. Nicardipine and bepridil effectively control angina, and preliminary studies indicate that nitrendipine has antianginal properties. Bepridil may be useful in the treatment of various cardiac arrhythmias; however, its tendency to cause or worsen cardiac arrhythmias and its association with torsade de pointes may limit its usefulness. Nicardipine and nitrendipine have similar adverse effect profiles, with vasodilation-related complaints being most common. Since nicardipine, nitrendipine, and nifedipine are similar in efficacy and safety, the eventual availability of sustained-release dosage forms may determine how these drugs are ultimately used. Bepridil is an effective antianginal drug, but, because of its proarrhythmic potential, it should probably not be used as a first-line agent.
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PMID:Nicardipine, nitrendipine, and bepridil: new calcium antagonists for cardiovascular disorders. 328 Feb 22

Atrial flutter is a supraventricular tachydysrhythmia believed to arise from electrophysiologic disturbances in the atria. It tends to be an unstable rhythm and is usually associated with intrinsic cardiac or pulmonary disease or adverse extrinsic influences on the heart. It is due to either a reentry mechanism or an increased atrial automaticity. Atrial depolarization is regular at a rate of 260 to 340 beats per minute. With a normal atrioventricular (AV) node there is usually a physiologic second-degree block with resultant 2:1 conduction. Higher degrees of AV block can occur in patients with AV nodal disease, increased vagal tone, or when certain drugs are in use. One-to-one conduction may occur in patients with accessory AV nodal pathways. In this situation, serious adverse effects are often seen, including palpitations, dizziness, syncope, angina, and dyspnea. Electrical cardioversion is the safest and most reliable way of terminating atrial flutter and its use should not be delayed in an unstable patient. In the nonemergent situation a variety of medications alone or in combination can be used to convert the rhythm or slow ventricular response.
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PMID:Atrial flutter. 328 16


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