ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb01089.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Antiadrenergic Interventions and Prevention of Sudden Death after MI.Introduction:Growing evidence points to sympathetic hyperactivity as one critical trigger for life‐threatening arrhythmias among postmyocardial infarction patients.Methods and Results:We have evaluated, in a placebo‐controlled multicenter study, the efficacy of a β‐adrenergic blocking agent (oxprenolol 160 mg) and of a selective left cardiac sympathetic denervation in preventing sudden death in patients with a first and anterior myocardial infarction. Two patient groups were studied. The high‐risk group included 144 patients who survived a myocardial infarction complicated by either ventricular tachycardia or fibrillation. The relatively low‐risk group included 869 patients whose myocardial infarction did not have these complications; they were allocated only to placebo or oxprenolol. Randomization took place 30 days postmyocardial infarction; mean follow‐up was 22 months. In the high‐risk group the sudden cardiac death (crude rate) in the placebo subgroup was indeed high (21.3%), and was strikingly reduced to 2.7% and to 3.6% by oxprenolol and by left cardiac sympathetic denervation, respectively (P<0.05). In the low‐risk group the sudden cardiac death (crude rate) in the placebo subgroup was 5.2% and was still reduced by oxprenolol to 1.6% (P<0.05). The results for total mortality were quite similar to those for sudden death iu both groups.Conclusion:This study, unique for the populations studied and for one of the treatments used, demonstrates that pharmacologic and surgical antiadrenergic interventions significantly reduce sudden cardiac death in postmyocardial infarction patients at high and at low risk. With due consideration to the relatively small size of the high‐risk group, it seems reasonable to suggest that left cardiac sympathetic denervation may be considered as a possible alternative for high‐risk patients with contraindications to beta blockers. (J Cardiovasc Electrophysiol, Vol 3, pp.

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb01090.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Frequency‐Dependent Effects of Verapamil.Introduction:The purpose of this study was to examine the frequency‐dependent effects of verapamil on refractoriness and development of conduction block in the human atrioventricular (AV) node.Methods and Results:To more closely simulate conditions thai would be found when the drug is used clinically, the drug was assessed in the absence of autonomic blockade. Antegrade refractory periods were determined in nine patients before and during the administration of verapamil by constant intravenous infusion. In addition, continuous recordings were made during 30‐second sequences of atrial pacing at a long cycle length alternating with sequences at shorter pacing cycle lengths. Mean verapamil levels were constant throughout the study and averaged 111.6 ± 70.7 ng/mL. In the majority of patients, refractoriness in the atrium prevented determination of the effective refractory period of the AV node in the control state. Therefore, although the effective refractory period of the AV node lengthened with decrease in pacing cycle length in the presence of verapamil, the relative contribution of the change in cycle length itself compared to the effect of verapamil could not be determined. A frequency‐ and time‐dependent change in A‐H interval was found with verapamil during atrial pacing. Kinetic analysis of drug effect on AV nodal function was possible in only three patients; in these three patients the mean time constant for onset of block was 2.9 seconds (range 1.9–4.0 sec). In one patient at a pacing cycle length that did not result in second‐degree AV block, transient periods of alternation between short and long A‐H intervals occurred in the presence of verapamil.Conclusion:Verapamil causes frequency‐dependent block of conduction through the AV node. Since changes in autonomic tone will vary from patient to patient, the actual magnitude of the effects of verapamil will vary as well. This may account for some of the interpatient variability seen with clinical use of this drug, despite comparable blood levels. (J Cardiovasc Electrophysiol, Vol. 3, pp.

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb01092.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Magnetic Field Interference.Introduction:High‐resolution electrocardiography, with or without signal averaging, requires extremely low levels of extraneous noise pickup. A significant amount of such interference is transmitted to the patient electrode wires as a magnetic (as opposed to electric) field, which is unresponsive to many commonly used shielding methods.Methods and Results:To investigate the source and quantify the strengths of magnetic fields, we used a battery‐powered device of our own design and performed magnetic field measurements in various locations in two hospitals. We found that significant sources of magnetic interference were cathode ray tube defiection coils, electric motors, and power transformers on wall‐mounted ophthalmoscopes or on the electrocardiographic equipment itself. The lowest noise level could be produced by running the patient electrode wires twisted closely together and by distancing the magnetic field sources, including electrocardiographic equipment.Conclusion:We conclude that magnetic fields at typical locations in modern hospitals are usually of such strength as to cause significant interference in high‐resolution electrocardiography. To reduce such an interference, the patient electrode wires should be twisted together and all suspected magnetic field sources, including the signal‐averaging equipment itself, should be placed as remotely from the patient as possible. (J Cardiovasc Electrophysiol. Vol. 3. pp. 34–39, Fe

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb01093.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Effect of DC Shock Ablation on Myocardial Blood Flow.Introduction:High energy direct current ablative shocks delivered through endocardial electrode catheters have been used as a treatment for various cardiac arrhythmias including ventricular tachycardia. Frequently, these shocks result in depression of myocardial function, at least transiently.Methods and Results:This study assessed the effect of a 200‐joule direct current shock delivered endocardially to the apex of the heart in ten adult mongrel dogs. Arterial blood pressures were monitored continuously. Myocardial contraction was monitored via two‐dimensional echocardiography. Regional myocardial blood flows were measured using radionuclide labeled microspheres before delivery of the shock, 30 seconds after delivery of the shock, and at 5 and 10 minutes after the shock. The results of the study demonstrated that there was a marked drop in arterial blood pressure immediately after the shock that gradually recovered over a 20‐minute period. Regional myocardial blood flow at the site of catheter ablation was severely depressed immediately after the shock. The degree of myocardial blood flow depression was inversely related to the distance from the site of ablation. At 5–10 minutes after ablation there was a marked hyperemic response in areas that suffered from depressed flow immediately after the shock. Two‐ dimensional echocardiography demonstrated depressed contractile function immediately after the shock with gradual recovery over a 10‐ to 20‐minute period. The catheter shock also generated prominent echo densities within the myocardium surrounding the ablative site. In contrast to the intracavitary echo densities that cleared quickly, the intramyocardial densities cleared much more slowly.Conclusion:The results of the study confirm the clinical observation that human left ventricular function is depressed acutely following a high‐energy ablative shock delivered to the left ventricular endocardium. Our results also demonstrated for the flrst time the effect of such ablative shocks on regional myocardial blood flow. Such depressions of blood flow may help explain the sudden drop in contractile function of the heart. The persistent intramyocardial echoes seen after the shock probably represented generation of intramyocardial bubbles that could obstruct arterial flow as well as disrupt cellular function. (J Cardiovasc Electrophysiol, Vol. 3, pp. 40–

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb01094.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

ATP‐Sensitive Potassium Channels in Human Heart.Introduction:The purpose of this study was to examine the electrophysiologic derangements that underlie contractile failure in single human heart muscle cells exposed to metabolic inhibition.Methods and Results:Single myocytes were isolated from right atrial appendage specimens obtained intraoperatively from patients undergoing routine cardiac surgery. On exposure to lO‐mM 2‐deoxyglucose (to inhibit glycolysis) and 2‐mM cyanide (to inhibit oxidative phosphorylation), twitch shortening decreased to undetectable levels over 5–6 minutes. The action potential duration declined in parallel with the contractile failure. Using voltage clamp depolarizations of a fixed duration the twitch was maintained in metabolic blockade until the development of maintained (rigor) contracture. At this time a large increase in K+conductance, which can be attributed to the activation of ATP‐sensitive K+channels (KATPchannels), was measured. In isolated inside‐out membrane patches, the ATP dependence of KaTPchannel activity was described by a sigmoid curve with Ki,ATP(ATP concentration required for half‐maximal inhibition of KATPchannel activity) = 8 μM and Hill coefficient (nH) = 1.2. The single channel current‐voltage relationship reversed close to the K+equilibrium potential and the conductance was approximately linear (g = 29 pS) over the voltage range included in the action potential (‐60 m V to +20 mV).Conclusion:In human atrial cardiac myocytes subjected to complete metabolic inhibition, contractile failure is caused by action potential shortening resulting from an increase in K + conductance presumably through the activation of KATPchannels. (J Cardiovasc Electrophysiol, Vol. 3, pp.

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb01096.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Impulse Propagation in Ischemia. The disturbances in impulse propagation in the heart with regional ischemia and the heart with chronic infarction, which underlie the initiation and perpetuation of arrhythmias, are briefly reviewed. Evidence is presented that reentry is responsible for ventricular tachycardia in both conditions. During acute ischemia, reentrant excitation is characterized by unstable functional reentrant circuits, the properties of which are determined by the changes in transmembrane action potential. Tachycardia is caused by a single unstable reentrant circuit. Fibrillation ensues when a single circuit is broken up into many independent reentrant wavelets. In contrast, ventricular excitation during sustained monomorphic tachycardia in hearts with a healed infarct is characterized by stable reentrant circuits determined by the architecture of surviving myocardial cell bundles within the infarct. In acutely ischemic myocardium, conduction velocity is reduced to about half of the value in normal myocardium, due to the reduced action potential amplitude and upstroke velocity. After about 5–10 minutes ischemic cells become inexcitable at resting membrane potentials of ‐50 to ‐60 mV. An important characteristic of ischemic cells is the dependence of the action potential upstroke on cycle length mainly because of the markedly prolonged recovery from inactivation of the fast Na+current in partially depolarized cells. Changes in transmembrane potentials do not occur homogeneously throughout the ischemic zone, and small differences in resting potential (associated with small differences in local K+accumulation) of depolarized cells result in large local differences in refractory periods. The time dependence of refractoriness explains why an increase in sinus rate, or a single premature beat, may produce conduction block at certain sites, and allow conduction in adjacent areas, thus setting the stage for reentry. A decrease in electrical cell‐to‐cell coupling, which also is a factor in decreasing conduction velocity, only occurs after 15–20 minutes of ischemia. Its role in the type 1B arrhythmias, which coincide with the period when uncoupling begins, remains to be elucidated. The cellular electrophysiology of myocardial cells surviving in the subendocardium of infarcts in human hearts is close to normal. Conduction slowing may be caused by “zigzag” conduction along small bundles that are separated by fibrous tissue, and that merge and divide over small distances. (J Cardiovasc Electrophysiol, Vol. 3, pp. 77–

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb01098.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb01099.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY