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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We used intracellular microelectrodes to study the electrophysiological effects of combinations of components of ischemia and their relation to the occurrence of ventricular arrhythmias in the specialized conducting system of isolated canine right ventricles. The middle area of the free wall was exposed to various test solutions in the center compartment of a three-chambered bath; the base and apex of the preparation were superfused with normal Tyrode's solution in the outer control compartments. Hypoxia (Po2 40 mm Hg), lactic acidosis (pH 6.5), and orciprenaline (10(-6) M), either alone or combined, failed to affect the action potential amplitude or the conduction velocity of the subendocardial fibers, and no arrhythmias occurred. The action potential duration and the effective refractory period were markedly prolonged by lactic acidosis. Exposure of the test regions to 15 mM K+ plus orciprenaline resulted in marked decreases in action potential amplitude and conduction velocity. Abnormalities of impulse transmission through the depressed area included high degrees of rate-dependent block, one-way block, warming-up phenomenon, and the Wenckebach phenomenon. Such conditions regularly provoked the appearance of single, sustained, or concealed reentrant depolarizations. The combined effects of hypoxia, 15 mM K+, and orciprenaline resulted in further depression of the already depressed action potential in the depolarized fibers. Our results indicate that regional increases of extracellular K+ may be the predominant factor of the components of ischemia we studied which facilitates the initiation of reentrant arrhythmias.
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PMID:Effects of some components of ischemia on electrical activity and reentry in the canine ventricular conducting system. 42 79

This report described initiation of A-V nodal reentrant tachyycardia in a patient with acute inferior myocardial infarction. The onset of tachycardia was preceded by an abortive A-V nodal Wenckebach periodicity. A-V nodal ischemia with or without vagotonia was implicated as the cause of induction of critical functional dissociation between the two A-V nodal conduction pathways. Since the tachycardia manifested its rate between 95-110 beats/min during the evolutionary phase of acute inferior myocardial infarction, it simulated, electrocardiographically, an accelerated A-V junctional rhythm. Analysis of the onset of tachcardia was of diagnostic importance.
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PMID:A-V nodal reentrant tachycardia vs accelerated A-V junctional rhythm in acute inferior myocardial infarction. 73 96

A new nonexercise test to detect significant coronary disease was prospectively evaluated in 36 patients with chest pain syndrome and normal left ventricular contractility. Transesophageal atrial pacing was used to provoke ischemia during monitoring of left ventricular contractility by transesophageal echocardiography. A 12-lead ECG was recorded. A TSE was abnormal if new segmental wall motion abnormalities developed. On the basis of the TSE results, patients were separated into normal (group 1, n = 16) and abnormal response (group 2, n = 20). Arteriography revealed significant disease in 21 patients, 19 from group 2 and two from group 1. Sensitivity and specificity of TSE were 90% and 93%, respectively, and those for pacing ECG were 43% and 100%, respectively. In addition, TSE accurately predicted the coronary artery perfusion bed involved. In 10 patients, Wenckebach AV block developed during pacing and resolved immediately by the administration of atropine sulfate. No serious complications were seen. Thus TSE is a highly sensitive and specific novel technique to detect significant coronary disease in patients with chest pain syndrome and normal resting left ventricular contractility.
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PMID:Transesophageal stress echocardiography: detection of coronary artery disease in patients with normal resting left ventricular contractility. 195 Oct 11

Exogenous adenosine has been shown to have potent electrophysiologic effects and antiarrhythmic properties within the atrioventricular (AV) node. Endogenous adenosine, a nucleoside with an increased release signaled by ischemia and hypoxia, is not believed to exert significant effects during homeostatic conditions. Recent experimental evidence suggests, however, that under normoxic conditions, the amount of adenosine released may be sufficient to mediate some of its physiologic effects. This study was designed to test the hypothesis that in humans the electrophysiologic effects of endogenously released adenosine on AV nodal conduction can be demonstrated under normoxic conditions by inhibiting uptake and degradation of the nucleoside. In the first protocol, the effects of intravenous dipyridamole (0.56 mg/kg bolus i.v., 5 micrograms/kg/minute infusion), a nucleoside-transport blocker that elevates endogenous plasma levels of adenosine, on AV nodal conduction were evaluated in seven patients. At a constant atrial paced cycle length, dipyridamole increased the AH interval from 110 +/- 19 to 164 +/- 26 msec, p = 0.002 (+/- SEM). Aminophylline (5.6 mg/kg i.v.), a competitive antagonist of adenosine, completely reversed the effects of dipyridamole on AV nodal conduction. Similarly, dipyridamole increased the cycle length at which pacing-induced AV nodal Wenckebach occurred, from 348 +/- 31 (control) to 388 +/- 33 msec (dipyridamole) (p = 0.002). In a second protocol, the effects of intravenous dipyridamole were evaluated in another group of six patients who had supraventricular tachycardia (SVT) in which the AV node was part of the reentrant circuit.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Electrophysiologic effects of dipyridamole on atrioventricular nodal conduction and supraventricular tachycardia. Role of endogenous adenosine. 259 20

In ischemic heart disease, the left ventricle has been considered the main target of an imbalance between myocardial oxygen supply and demand. Accordingly, the approach to ischemia has been directed at the evaluation of the left ventricle. The aim of this study was to assess the relative involvement of the left and right ventricle in patients with isolated right coronary artery stenosis. We studied 20 patients with a clinical history of effort angina (15 male, 5 female, mean age 54.1 +/- 6.2) using radionuclide angiography and atrial pacing. Findings were compared with those of 6 normal subjects that were paced at the maximal heart rate of 150 beats/min. Atrial pacing was interrupted because of diagnostic ST segment depression in 8 patients, Wenckebach type atrioventricular block in 1, chest pain without electrocardiographic changes in 4 and the achievement of the maximal prefixed heart rate of 150 beats/minute in 7. With respect to control conditions, during atrial pacing right ventricular ejection fraction declined from 46.8 +/- 6.8% to 37.4 +/- 8.1% (p less than 0.001), while no significant change was observed in left ventricular ejection fraction values (55.2 +/- 4.5% and 51.1 +/- 10.2% respectively). During atrial pacing, left ventricular peak filling rate increased from 1.77 +/- 0.53 to 4.71 +/- 1.8 end-diastolic volumes/second (p less than 0.0001). Qualitative analysis of regional wall motion showed a right ventricular dysfunction in 19/20 patients; this was prevalent in 9 and involving also the left ventricle in 10; an isolated impairment of the left ventricle was observed in 1 patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Right ventricular dysfunction in demand-induced ischemia in patients with isolated right coronary artery disease: a radioisotope study]. 325 39

Atrioventricular-nodal-conduction abnormalities following cardiac surgery have been attributed to the potassium ion in cardioplegic solutions. To clarify the etiology of these rhythm problems, 15 dogs were subjected to (I) 60 min 4 degrees C potassium cardioplegic arrest; (II) 30 min normothermic ischemic arrest; or (III) cardiac hypothermia without ischemia. In sinus rhythm and during atrial pacing, A-H and H-V intervals, Wenckebach cycle length (WCL), atrial- and AV-nodal refractory periods (ARP and NRP) were measured at 37 degrees C before and 30 min after arrest (groups I and II) and at various myocardial temperatures (group III). Following cardioplegic arrest and reperfusion, all AV-nodal-conduction properties were unchanged from preischemic values. In contrast, unprotected ischemia significantly prolonged AV-nodal-conduction time (P less than 0.01) and myocardial hypothermia resulted in prolonged WCL (P less than 0.01), prolonged functional NRP (P less than 0.05), in addition to delayed A-H interval (P less than 0.05). The data suggest that properties of AV-nodal conduction are preserved following potassium cardioplegic arrest, but impaired by ischemic injury or persistent local cardiac hypothermia.
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PMID:Etiology of atrioventricular-conduction abnormalities following cardiac surgery. 670 Feb 9

Electrophysiologic features of spontaneous, ischemia-induced ventricular fibrillation were studied in 17 dogs using multiple endocardial bipoles positioned in normal and ischemic zones and at the border of ischemic myocardium. All dogs showed ventricular tachyarrhythmias prior to the initiation of ventricular fibrillation. The heart rate prior to the fatal arrhythmia in the ventricular fibrillation dogs was significantly faster than that of nonventricular fibrillation dogs. There was no difference in the coupling intervals of the initial premature complex between episodic and sustained ventricular arrhythmia in most dogs. However, shorter coupling intervals initiated sustained arrhythmia in some dogs. Sites of initiation of arrhythmia were mostly in the ischemic zone. Furthermore, diastolic electrical activity was consistently observed in the ischemic zone during fatal arrhythmia in dogs showing diastolic activity. Cycle length during the fatal arrhythmia prior to ventricular fibrillation gradually shortened, whereas cycle length of episodic ventricular tachycardia remained approximately 200 msec followed by lengthening prior to restoration of sinus rhythm. The disparity of local activation (time differences between the earliest and latest onset of the activation in the five recording sites) increased during the fatal arrhythmia. Examples of progressive intraventricular block (Wenckebach-like) between the border and the center of ischemic myocardium leading to ventricular fibrillation are resynchronization of this disparity leading to the termination of ventricular tachycardia are shown. The recording of continuous electrical activity using bipolar electrodes with an interelectrode distance of 1 mm suggests a smaller reentrant pathway during fatal arrhythmia. Our observations confirm the importance of endocardial recordings within ischemic myocardium, and adds new insight into the events leading to both episodic and sustained ventricular tachycardia.
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PMID:Electrophysiologic observations during the spontaneous initiation of ischemia-induced ventricular fibrillation. 682 98

Multisite pacing for the treatment of heart failure has added a new dimension to the electrocardiographic evaluation of device function. During left ventricular (LV) pacing from the appropriate site in the coronary venous system, a correctly positioned lead V1 registers a right bundle branch block pattern with few exceptions. During biventricular stimulation associated with right ventricular (RV) apical pacing, the QRS is often positive in lead V1. The frontal plane QRS axis is usually in the right superior quadrant and occasionally in the left superior quadrant. Barring incorrect placement of lead V1 (too high on the chest), lack of LV capture, LV lead displacement or marked latency (exit block or delay from the stimulation site), ventricular fusion with the spontaneous QRS complex, a negative QRS complex in lead V1 during biventricular pacing involving the RV apex probably reflects different activation of an heterogeneous biventricular substrate (ischemia, scar, His-Purkinje participation in view of the varying patterns of LV activation in spontaneous left bundle branch block) and does not necessarily indicate a poor (electrical or mechanical) contribution from LV stimulation. In this situation, it is imperative to rule out the presence of coronary venous pacing via the middle cardiac vein or even unintended placement of two leads in the RV. During biventricular pacing with the RV lead in the outflow tract, the paced QRS in lead V1 is often negative and the frontal plane paced QRS axis is often directed to the right inferior quadrant (right axis deviation). In patients with sinus rhythm and a relatively short PR interval, ventricular fusion with competing native conduction during biventricular pacing may cause misinterpretation of the ECG because narrowing of the paced QRS complex simulates appropriate biventricular capture. This represents a common pitfall in device follow-up. Elimination of ventricular fusion by shortening the AV delay, is often associated with clinical improvement. Anodal stimulation may complicate threshold testing and should not be misinterpreted as pacemaker malfunction. One must be cognizant of the various disturbances that can disrupt 1:1 atrial tracking and cause loss of ventricular resynchronization. (1) Upper rate response. The upper rate response of biventricular pacemakers differs from the traditional Wenckebach upper rate response of conventional antibradycardia pacemakers because heart failure patients generally do not have sinus bradycardia or AV junctional conduction delay. The programmed upper rate should be sufficiently fast to avoid loss of resynchronization in situations associated with sinus tachycardia. (2) Below the programmed upper rate. This may be caused by a variety of events (especially ventricular premature complexes and favored by the presence of first-degree AV block) that alter the timing of sensed and paced events. In such cases, atrial events become trapped into the postventricular atrial refractory period at atrial rates below the programmed upper rate in the presence of spontaneous AV conduction. Algorithms are available to restore resynchronization by automatic temporary abbreviation of the postventricular atrial refractory period.
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PMID:Electrocardiographic follow-up of biventricular pacemakers. 1584 37

Resveratrol (trans-3, 4', 5-trihydroxystilbene), a natural antioxidant derived from grapes, has beneficial effects against coronary heart disease. Its electrophysiological characteristics for antiarrhythmic efficacy are largely unknown; thus, this study aims to explore the resveratrol's antiarrhythmic effects and conduction system in isolated hearts as well as its electrophysiological effects on cardiac myocytes. In the experiment, resveratrol suppressed the ischemia/reperfusion-induced ventricular arrhythmias in Langendorff-perfused rat hearts. In the current clamp study of the experiment, resveratrol prolonged the action potential duration (APD(50) and APD(90)) and suppressed the upstroke velocity of the action potential (V(max)). In the voltage clamp study, resveratrol inhibited sodium inward current (I(Na)) in a concentration-dependent manner and negative-shifted the voltage-dependent inactivation curve. Resveratrol also reduced the calcium inward current (I(Ca), 51.2+/-13.3% at 100 microM). Furthermore, the transient (I(to)) and sustained (I(ss)) outward potassium currents were decreased 60.2+/-5.7% and 42.3+/-5.2% after exposure to resveratrol (100 microM), respectively. The inward rectifier potassium current (I(K1)) was also reduced 24.2+/-7.0% in the presence of resveratrol (100 microM). In the isolated heart perfusion model, resveratrol (100 microM) prolonged AV nodal refractory period, the Wenckebach cycle length and the conduction through AV node and His-Purkinje system. In conclusion, resveratrol increased the cardiac effective refractory period mainly through inhibiting the ionic channels including I(Na), I(to) and I(ss) which could contribute to the conversion of ischemia/reperfusion-induced lethal arrhythmias.
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PMID:In vitro electrophysiological mechanisms for antiarrhythmic efficacy of resveratrol, a red wine antioxidant. 1710 72