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)

The method of monophasic action potential (MAP) recording has experienced a significant surge in interest since the introduction of the contact electrode, which in contrast to the suction electrode, allows the safe and simple use of this technique in the clinical electrophysiology laboratory. MAP recording not only provide for a more precise determination of local activation, but most importantly, permit direct measurement of myocardial repolarization and action potential duration (APD), respectively. This had led to new insights into the cycle-length-dependence of the human APD, both in response to single extrastimuli and to steady-state heart rate changes. An advancement of the contact electrode catheter design now permits simultaneous pacing and MAP recording, and thereby, simultaneous determinations of APD and effective refractory periods (EPP) at the same endocardial site in the human heart. MAP recordings have demonstrated significant usefulness in the direct monitoring of antiarrhythmic drug effects, both in terms of dosage control and in the direct measurement of antiarrhythmic drug effects on the relationship between ERP and APD (ERP/ARD-ratio). Because MAP recordings reflect the local cellular electrophysiology, they also provide a more sensitive and precise index of myocardial ischemia than conventional ECG recordings. This can be utilized to assess the success of revascularizing procedures directly during or after the intervention. Recently, MAP recordings helped to discover early after-depolarizations in patients with "torsade de pointes", providing a possible explanation for the mechanism of polymorphous ventricular tachycardia in man.
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PMID:[Clinical value of monophasic action potentials]. 186 64

Pharmacologic action of antiarrhythmic agents in hypoxia was studied with the microelectrode using the guinea pig papillary muscle. Tyrode solution saturated with 95% O2 and 5% CO2 provided normoxic condition and that with 95% N2 and 5% O2 hypoxic condition. The parameters measured were as follows: 1) Vmax: the maximum rate of rise of the action potential, 2) ERP: effective refractory period, 3) ERP/APD90%: the ratio of effective refractory period to action potential duration at 90% repolarization. [1] When the papillary muscle was perfused more than 15 minutes with the hypoxic solution, irreversible changes ensued inevitably. Accordingly, a perfusion with the hypoxic solution for 15 minutes was succeeded by that with the normoxic solution for 30 minutes. This was then followed by another perfusion with the hypoxic solution. [2] Flecainide was examined in 7 cases. The rate of the depression of Vmax by flecainide was significantly (p less than 0.01) increased in hypoxia (16.3 +/- 4.2%) than in normoxia (7.4 +/- 2.0%). There were no significantly differences in the rate of the change of ERP between both conditions. The rate of ERP/APD90% was significantly (p less than 0.01) increased by flecainide during hypoxia (2.2 +/- 0.8%) than during normoxia (0.1 +/- 2.1%). [3] The depression of Vmax and the increase of ERP/APD90% by flecainide occurred in a dose-dependent manner in normoxia. it was concluded that the depression of Vmax by flecainide over the concentration of 2 micrograms/dl were ascribed to its inhibitory effect on the fast Na channel and that its depressive effects were enhanced during hypoxic condition. This inhibitory action was regarded as the main antiarrhythmic action of flecainide. From the above results, it is expected that flecainide could be effective in the treatment of ventricular arrhythmias in the ischemic heart disease.
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PMID:[A design of the electrophysiological model on the action of antiarrhythmic agent in hypoxic condition and the electrophysiological study of flecainide]. 190 36

In our earlier experiments administration of the stable PGI2 analogue: 7-oxo-PGI2-ephedrine salt to dogs resulted in a late appearing and long-lasting protection from coronary ligation induced ischemia and subsequent postocclusion and reperfusion arrhythmias. Objective of the present study was to evaluate the extent and duration of antiischemic and antiarrhythmic action induced by a single dose 50 micrograms/kg i.m. 7-oxo-PGI2 in dogs subjected to myocardial ischemia evoked by left anterior descending coronary (LAD) ligation at different intervals (2, 6, 24, 48, 72 hours and 2 weeks) after treatment. In the 2 weeks prolonged treatment group treatment started with 50 micrograms/kg i.m. dose, followed every third day by administration of 25 micrograms/kg 7-oxo-PGI2. After anesthesia and thoracotomy the electrophysiological parameters (SCL, CSNRT, AFRP, VFRP and A-V ERP) were determined by means of computer controlled programmed electrical stimulation. Then the animals were subjected to LAD occlusion for 25 min and subsequent reperfusion. 7-oxo-PGI2 pretreatment considerably protected against myocardial ischemia, i.e. there was a marked reduction in ST-segment elevation, the number of ES and the incidence of VF. The maximal antiischemic action and the most striking reduction in ventricular arrhythmias could be observed 48 hours after a single dose of 7-oxo-PGI2 and also after prolonged treatment of two weeks. In this latter group CSNRT showed the most expressed prolongation, however, AFRP and to lesser degree VFRP was also prolonged.
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PMID:7-oxo-PGI2 induced late protective action from arrhythmias due to local myocardial ischemia. 202 55

The difference between the end of monophasic action potentials recorded in the outflow tract of right ventricle and the T-wave on the surface electrocardiogram was measured as an estimate for disparity of termination of repolarisation. It was measured during right ventricular pacing at three basic cycle lengths 500, 600 and 700 msec and programmed stimulation with single extra stimuli in 15 patients with coronary arterial disease. The disparity of termination of repolarisation was rate dependent, showing increased values when stimulated at cycle length of 700 ms compared to 600 msec (P less than 0.005) and 500 ms (P less than 0.001). Premature stimulation revealed three different modes in changes of dispersion: in six patients the premature dispersion was increased at the shortest coupling intervals from the effective refractory period. It was unchanged compared to basic values in four, and in the rest of the patients the premature dispersion was reduced at the shortest coupling intervals. These results show that the dispersion of recovery of repolarisation increases at the lower stimulation frequencies. Premature dispersion is not always increased in the closest proximity to V-ERP during programmed ventricular stimulation in patients with ischemic heart disease.
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PMID:Rate-dependent change in dispersion of repolarisation during ventricular pacing in man. 272 86

An integrative approach is suggested to track symbolically simulated work environment stressors, as an act to burden higher cortical function in the exposed groups. ERP would be made together with measurement of end organ stress responses as well as measurements of perceived conditions. Field studies would be the necessary complement. The following conclusions are culled from the reviewed literature: among the pilots, cardiovascular problems are the most important cause of loss of licence in Europe and North America. Interactions with coworkers for air traffic controllers have been associated with cardiovascular disability. Comparing various degrees of heart disease severity among professional drivers, the IHD drivers showed the smallest N2 amplitudes and the greatest diastolic blood pressure reactivity. P300 target amplitude showed an inverse correlation with number of work hours behind the wheel. The IHD drivers were envisioned in a phase of disturbance of the selective attentional process. An interrelation has been found between Event-Related Slow Potential ERSP and midinterval heart rate acceleration associated with displeasure and arousal. A positive correlation has been found between the amplitude of the ERSP and ventricular arrhythmia rate in cardiac patients. Lowering of arrhythmia rate in response to antiarrhythmic agents was associated with a significant attenuation of the ERSP. Either acceleration or deceleration is associated with the appearance of the late CNV to the aversive noise burst. There might be a "common generator behind both anticipatory heart rate responses and cortical events." CNV might be related to frontally mediated stress mechanisms.
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PMID:Cardiovascular dysfunction related to threat, avoidance, and vigilant work: application of event-related potential and critique. 932 11

We investigated the response of refractory periods and blood flow to blockade of alpha 1- and beta-adrenoceptors alone, or in combination on endocardium and epicardium, during myocardial ischemia. Dogs were anesthetized with alpha-chloralose and divided into bunazosin (an alpha 1-blocking agent)-treated (0.1-0.2 mg/kg, i.v., n = 14), propranolol-treated (0.2 mg/kg, i.v., n = 12), and vehicle-control (n = 10) groups. The diagonal branches of the left anterior descending artery were ligated. The refractory period (ERP) and blood flow (RMBF) were determined by an S1-S2 extrastimulus method and a nonradioactive microsphere technique, respectively. The duration of regional electrograms (DRE) was measured in the endocardial and epicardial sites. Bunazosin alone reversed the ischemia-related shortening of ERPs at both the endocardial and epicardial sites, with a greater effect seen epicardially (P < .05). Subsequent administration of propranolol further prolonged ERPs in both sites, although the effect was greater in the epicardial surface (P < .05). Bunazosin reduced RMBF to a greater degree at the endocardial site than at the epicardial site in the ischemic zone (P < .01 and P < .05, respectively), but the magnitude of the reduction in RMBF and the difference in RMBF between sites were similar to the control group (P < .01). Propranolol alone and subsequent administration of bunazosin prolonged the ERP more at the epicardial site (P < .01) than at the endocardial sites in the ischemic zone. Propranolol produced no significant difference in RMBF between both sites. DREs in animals treated with bunazosin and propranolol alone, or in combination, were similar to those in animals treated with vehicle. These results suggest that differences in ERPs between endocardium and epicardium with blockade of alpha 1- and/or beta-adrenoceptor are not due to concomitant alterations in RMBF, but to differences in electrophysiological properties of the endocardial and epicardial cells during the acute phase of myocardial ischemia.
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PMID:Disproportional response between refractory period and blood flow to alpha 1- and beta-adrenoceptor blockade in canine ischemic myocardium. 1041 Aug 26