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

The antiarrhythmic activity of amitriptyline, a tricyclic antidepressant, was evaluated in anesthetized dogs 24 h after coronary occlusion, during the period of spontaneous ventricular arrhythmias. In all experiments amitriptyline was administered i.v. in incremental doses of 0.3 mg/kg at 1 min intervals until a conversion to normal sinus rhythm was evident. Amitriptyline administration resulted in conversion of the ventricular arrhythmia to a normal sinus rhythm in 100% of the animals tested at a mean dose of 1.3 +/- 0.1 mg/kg. Smaller doses also resulted in a dose-related decrease in non-sinus nodal pacemaker activity. Lidocaine, when administered to the same group of animals, produced a reduction of ectopic pacemaker activity, but did not eliminate it at a cumulative dose of 2 mg/kg. Antiarrhythmic doses of amitriptyline did not produce significant changes in arterial blood pressure, cardiac output or electrocardiographic parameters associated with atrioventricular or intraventricular conduction. The results of this study suggest that at very low doses amitriptyline may be an effective antiarrhythmic agent in ventricular arrhythmias associated with myocardial ischemia.
 ...
PMID:The antiarrhythmic action of amitriptyline on arrhythmias associated with myocardial infarction in dogs. 71 May

Accurate electrocardiographic diagnosis of myocardial ischemia or infarction is difficult in patients with the Wolff-Parkinson-White syndrome; however, myocardial ischemia may also have profound effects on the electrophysiologic characteristics of the bypass tract in these patients. Comparison of studies performed during and two months following an episode of significant myocardial ischemia demonstrated substantial prolongation of the refractoriness of the bypass tract during the period of ischemia. Bypass refractoriness was prolonged by 196 msec, yet atrioventricular nodal refractoriness was not significantly different from normal. These studies, therefore, suggest that, on occasion, the presence of acute myocardial ischemia may, in fact, obscure the electrocardiographic diagnosis of the Wolff-Parkinson-White syndrome.
 ...
PMID:Wolff-Parkinson-White syndrome. Alterations in electrophysiologic characteristics of the bypass tract secondary to ischemia. 88 79

R 56865 is an experimental compound that has been shown to ameliorate the effects of cardiac glycoside toxicity and myocardial ischemia. We evaluated the direct electrophysiological effects of R 56865 and its effects on the electrophysiological sequelae of ouabain toxicity in vivo and in vitro. In normal anesthetized dogs, R 56865 alone at doses of 0.04 to 0.16 mg/kg i.v. had no effect on atrial, AV nodal, or ventricular conduction times and refractoriness, but at doses of 0.64 to 2.5 mg/kg it tended to increase these parameters. In ouabain-pretreated dogs, R 56865 (0.08 to 0.32 mg/kg i.v.) dose-relatedly reduced ouabain-induced ventricular arrhythmias. In normal isolated canine Purkinje fibers, R 56865 (1-10 microM) reduced Vmax at short pacing cycle lengths and decreased the action potential duration at concentrations of 0.1 to 10 microM. R 56865 at concentrations through 10 microM had no significant effect on normal action potentials of canine ventricular muscle and slow response action potentials in guinea pig papillary muscles. In Purkinje fibers exposed to toxic concentrations of ouabain, R 56865 (1 microM) reduced the delayed after depolarization (DAD) amplitude and inhibited triggered activity. R 56865 had no effect on normal automaticity in canine Purkinje fibers at 1 microM, but 10 microM significantly slowed it. R 56865 at 10 microM did not affect isoproterenol-enhanced automaticity and only slightly reduced barium-induced abnormal automaticity that occurred at reduced membrane potentials. These results demonstrate that R 56865 reverses cardiac glycoside-induced arrhythmias in anesthetized dogs at doses that do not significantly affect conduction or refractoriness. Suppression of ouabain-induced DAD and triggered activity in isolated Purkinje fibers, at concentrations not affecting normal or abnormal automaticity, may be the mechanism of R 56865's antiarrhythmic actions in vivo. Suppression of DAD does not appear to be associated with blockade of voltage-dependent calcium channels, but R 56865 may prevent intracellular sodium overload by limiting excessive sodium entry during ouabain intoxication.
 ...
PMID:Investigation of electrophysiologic mechanisms for the antiarrhythmic actions of R 56865 in cardiac glycoside toxicity. 172 Aug 42

Fifteen cases of chronic heart block were studied. Eight of them could be designated as idiopathic or primary heart block; the others were associated with hypertension, diabetes and ischaemic heart disease, either singly or in various combinations. In six cases, the whole heart was available for histopathological study of the conduction system. In the other 9 cases, only a portion of the heart muscle was available for examination. A V nodal fibrosis extending upto the proximal bundle of His was seen in all the six whole heart autopsy materials. Fibrosis of the adjacent myocardium was seen in five cases. In three cases, conducting system fibrosis was associated with atherosclerotic (1 case) or diabetic changes (3 cases) of the intramural vessels. In the 9 partial autopsy studies, myocardial fibrosis was seen in two cases, diabetic microangiopathy in one and atherosclerotic changes in two including an old thrombus in one. Thus, diabetic microangiopathy was seen in total four cases. These changes may be responsible for the cardiomegaly and cardiac failure associated with conduction defects observed in diabetes. In the idiopathic group also, heart block could be considered as a significant facet of a primary myocardial degenerative process.
 ...
PMID:Cardiac changes implicated in chronic heart block. 181 5

The diagnosis of the origin of a broad complex tachycardia may be difficult, especially in the absence of a 12-lead electrocardiogram of the tachycardia. This study investigates the value of signal averaging in the differential diagnosis of broad complex tachycardia. Signal averaging during sinus rhythm was performed in 102 consecutive patients who presented with broad complex tachycardia (QRS width greater than 110 ms), in whom a definitive electrophysiological diagnosis was made. The presence of late potentials was determined on the basis of two definitions, the second including total QRS duration. The patients studied included 75 with ventricular tachycardia; 33 of these patients had suffered previous myocardial infarction, five had dilated cardiomyopathy, and 37 had a 'normal' heart. Of the 27 patients with supraventricular tachycardia, 22 had an atrioventricular accessory pathway (seven with a delta wave in sinus rhythm), three had atrioventricular nodal tachycardia and two had atrial tachycardia. The sensitivity of late potentials for the diagnosis of ventricular tachycardia was low utilizing both definitions (28% and 45%) although specificity was high (96% and 95%). The sensitivity for the diagnosis of ventricular tachycardia was higher for patients with ischaemic heart disease (43% and 70%) but very low for patients with ventricular tachycardia and a normal heart (16% and 22%). In conclusion, signal averaging in the remote diagnosis of broad complex tachycardia is specific but not sensitive for ventricular tachycardia, which limits its usefulness in selecting patients for electrophysiological study.
 ...
PMID:Signal averaging of the electrocardiogram in the remote differential diagnosis of broad complex tachycardias. 188 42

Hemodynamic and electrophysiologic studies were performed in 30 survivors of sudden cardiac arrest with hypertrophic cardiomyopathy (HC) to determine responsible factors. Electrophysiologic abnormalities alone were present in 27 patients (90%): sinus node dysfunction in 14 (47%), delayed atrio-ventricular nodal conduction in 1 (3%), abnormal His-Purkinje conduction in 7 (23%), an inducible atrial tachycardia in 7 (23%), and inducible sustained ventricular arrhythmia in 21 (70%). Sustained ventricular arrhythmia was polymorphic ventricular tachycardia (VT) in 18 patients (86%), monomorphic VT in 2 patients (7%) and ventricular fibrillation in 1 patient (3%). In 1 patient the arrhythmia recorded during an episode of cardiac arrest and induced at electrophysiologic study was polymorphic VT. VT was induced with less than or equal to 2 extra-stimuli in only 1 patient (3%) but with less than or equal to 3 extra-stimuli in 20 patients (97%). Potential causes of sudden cardiac arrest were found in all patients and were multiple in 13 patients (43%). These were (1) ventricular electrical instability in 21 patients (70%), (2) severe left ventricular outflow tract obstruction in 8 patients (27%), (3) bradycardia in 5 patients (17%), (4) myocardial ischemia associated with hypotension in 5 patients (17%), and (5) atrial tachycardia resulting in hypotension in 4 patients (13%). Of the 21 patients with inducible sustained ventricular arrhythmia, 17 received an implantable defibrillator device and 4 were treated with antiarrhythmic drugs. Seven patients underwent left ventricular septal myectomy.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Hemodynamic and electrophysiologic evaluation of patients with hypertrophic cardiomyopathy surviving cardiac arrest. 199 Jul 92

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.
 ...
PMID:[Variant angina which interacts with two phenomena: local hypersensitivity and abnormal response in the coronary tree to vasoconstrictor stimuli]. 226 56

This study examined the impact of transcatheter fulguration on creatine kinase-MB release in 21 patients (age range 17-71 years). Arrhythmia diagnoses were ventricular tachycardia 9, atrial fibrillation with a rapid ventricular response 7, atrioventricular nodal reentry 2, and reciprocating tachycardia utilizing a posteroseptal accessory pathway 3. Seven patients had apparently normal hearts while 8 had ischemic heart disease and 6 cardiomyopathy. Timing of initial elevated creatine kinase-MB activity (mean 1.34 +/- 0.69 SD hours) and peak creatine kinase-MB activity (mean 3.73 +/- 0.89 SD hours) was relatively uniform in all patients. Time to peak creatine kinase-MB activity was unrelated to either underlying cardiac disease (normal: 3.9 +/- 1.0 hours; ischemic heart disease: 3.5 +/- 0.9 hours; cardiomyopathy: 3.8 +/- 0.9 hours), or fulguration site (His bundle (n = 9): 4.2 +/- 0.9 hours, proximal coronary sinus (n = 3): 3.3 +/- 0.3 hours, ventricle (n = 9): 3.4 +/- 0.8 hours). The magnitude of peak serum creatine kinase-MB activity was independent of myocardial diagnosis or fulguration site, but was linearly related to total energy delivered (r = 0.5, P less than 0.022). The latter correlation was particularly strong within cardiac diagnosis subgroups (normal: r = 0.92, P less than 0.002; ischemic heart disease: 0.73, P less than 0.04; non-ischemic cardiomyopathy: r = 0.57, P = NS). Thus, serum creatine kinase-MB activity following transcatheter fulguration is linearly related to the magnitude of delivered energy, and is similar to that observed after transient coronary artery occlusion and reperfusion.
 ...
PMID:Timing and magnitude of serum creatine kinase-MB after transcatheter cardiac tissue fulguration in man. 229 21

Esmolol is an ultra-short-acting beta-adrenergic blocking agent that possesses minimal partial agonist activity or direct membrane depressant activity. The short duration of action of esmolol is attributable to rapid enzymatic hydrolysis by red blood cell esterases, forming ASL-8123 and methanol. Experiments in the constant-flow-perfused isolated canine hindlimb indicate that therapeutic (beta blocking) doses of esmolol lack direct vascular effects and alpha-adrenergic blocking activity and that therapeutic doses do not interfere with vascoconstrictor effects of peripheral sympathetic nerve stimulation. Esmolol produces cardiac electrophysiologic and hemodynamic effects consistent with those of beta blockade. Specifically, esmolol decreases heart rate, depresses atrioventricular nodal conduction, and decreases determinants of myocardial oxygen demand. The beneficial antiarrhythmic and infarct-size limiting effects of esmolol have been demonstrated in several experimental models. Whereas beta blockers in general are effective in settings of supraventricular arrhythmias, sinus tachycardia, and myocardial ischemia, esmolol provides the added dimension of "titratability." Thus, the short duration of action of esmolol allows for very rapid titration to a preferred steady-state level of beta blockade; rapid adjustment to different steady-state levels of beta blockade, as may be required by changing status of the patient, and rapid disappearance of beta blockade following discontinuation of esmolol infusion, should this be necessary in the event of deleterious cardiac hemodynamic effects. Thus, esmolol is ideally suited for use in the treatment of patients in whom beta blockade is desirable, but in whom level of beta blockade must be very carefully modulated.
 ...
PMID:Pharmacology and pharmacokinetics of esmolol. 287 84

Sinus node and atriventricular (A-V) nodal functions were evaluated by right atrial pacing in 220 consecutive patients recovering from acute myocardial infarction (AMI), 10-28 days after the infarct (mean = 14 days). In the 188 patients in whom a pacing rate of 120 beats/min could be achieved, sinus node recovery time, corrected sinus node recovery time (CSNRT) and total recovery time were correlated to infarct site and the presence or absence of myocardial ischemia. Sinus node recovery time and total recovery time were significantly longer in patients with inferior (1,153 + 28 and 3,129 + 179 ms, respectively) or non-Q-wave infarct (1,112 + 28 and 3,730 + 266 ms, respectively), than in patients with anterior infarct (1,044 + 20 and 1,153 + 28 ms, respectively). The parameters were within the reported normal range. When corrected for heart rate (CSNRT), these differences were no longer present. The presence or site of residual ischemia during right atrial pacing did not affect the sinus nodes parameters. A-V nodal function, studied in all 220 patients, was assessed by the appearance of second-degree A-V block at pacing rates below 120 beats/min and by measuring the shortest atrially paced cycle length with 1:1 A-V conduction. Second-degree A-V block appeared at a similar frequency in different AMI locations. Thus, sinus and A-V node functional status in patients recovering from AMI are not affected by infarct site or by the presence or absence of residual myocardial ischemia.
 ...
PMID:Sinus node and atrioventricular nodal function in 220 patients recovering from acute myocardial infarction. 316 17


1 2 3 Next >>