老年人不同部位室性期前收缩与动态心电图判定心肌缺血的研究

目的对比研究老年人不同起源部位室性期前收缩合并心肌缺血状况。方法应用12导联同步动态心电图检测531例老年室性期前收缩患者,比较不同部位室性期前收缩合并心肌缺血发生率。结果左心室室性期前收缩合并心肌缺血发生率高于右心室室性期前收缩(P<0.05);左心室心尖部及前壁室性期前收缩合并心肌缺血发生率明显高于流出道和其他部位(P<0.05)。各部位室性期前收缩合并心肌缺血发生率均>50.0%。结论左心室室性期前收缩较右心室合并心肌缺血发生率高;左心室心尖部和前壁期前收缩合并心肌缺血发生率最高;老年人室性期前收缩半数以上合并心肌缺血。     

Modeling the Blood Pressure Response to a Ventricular Premature Complex with Special Reference to Heart Rate Turbulence

Ventricular premature beats have been used to characterize a risk factor for patients after myocardial infarction. This risk stratification has recently been improved by estimating the so-called heart rate turbulence, i.e., the acceleration and subsequent deceleration of the sinus beats following a ventricular premature beat. This response is triggered by oscillations in aortic blood pressure following a ventricular premature beat. In the following we report on a model to fit blood pressure oscillations due to ventricular premature beats in patients following myocardial infarction. The data on which this analysis is based were derived from 39 patients with varying degrees of left ventricular dysfunction following myocardial infarction. The recording included high-quality ECG and a noninvasive beat-to-beat recording of blood pressure from a finger artery. Records were chosen such that 5 to 30 ventricular premature beats occurred within a 30-min recording period. In a first step, we fed our data, i.e., a given series of coupling intervals, into two established cardiac models (Ten-Voorde and Mrovka et al.) and observed the blood pressure behavior. It turned out that both models were not able to reflect the full range of the observed blood pressure oscillations. For this reason we expanded the model of Mrovka et al. (Am J Physiol Regul Integr Comp Physiol 279: R1171–R1175, 2000), such that the desired pattern approximately appeared. This was achieved by introducing a more subtle left ventricular function curve and keeping track of the endsystolic volume in the left ventricle. After parameter fitting, a detailed picture of the hemodynamics appeared for each patient. It was found that left ventricular function and, in particular, post-extrasystolic potentiation was crucial for the prediction of the blood pressure response following a ventricular premature beat. Thus, in patients following myocardial infarction, not only impaired baroreceptor function but also altered left ventricular contraction behavior contributes to the phenomenon of heart rate turbulence.     

Alternating bundle branch block

Mechanisms postulated for alternating bundle branch block are incomplete-and cycle-length-dependent-block in both the right and left bundle branches. A patient with severe longstanding cardiac conduction disease who developed alternating bundle branch block during treatment for advanced ischemic heart disease and malignant ventricular arrhythmia is presented. In this patient alternation was induced by atrial premature beats as well as spontaneous and pacemaker induced premature ventricular beats. Right bundle branch block which followed a premature atrial beat resulted from the longer refractory period of the right bundle. The maintenance of right bundle branch block at long cycle lengths was presumed to be due to continuous retrograde reentry. This was terminated when a pause following a premature beat allowed functional recovery of the right bundle branch. This patient died suddenly at home with a functioning pacemaker, demonstrating the high risk of death from ventricular dysrhythmia in the post myocardial infarction patient with a new conduction defect.     

射频导管消融治疗顽固性频发室性早搏伴短阵室性心动过速的体会

报道 2 5例 (男 14例、女 11例 ,年龄 15～ 6 7岁 )顽固性频发室性早搏 (简称室早 )伴短阵室性心动过速 (简称室速 )接受RFCA的治疗结果。采用心室激动顺序与起搏标测法进行室早标测定位 ,标测到室早最早激动点较体表心电图QRS波提前 30ms以上或消融电极起搏心电图QRS波图形与室早图形完全一致时放电消融。结果 :2 5例患者室早起源分别为右室流出道 12例、右室心尖部 5例、左室游离壁 5例、左室近后间隔部 3例。 2 5例中 2 1例成功 (包括 1例频发室早伴短阵多形性室速患者 ) ,成功率为 84 % ,无并发症发生。结论 :RFCA治疗频发单形性室早伴短阵室速安全、有效。     

Role of early cycle ventricular extrasystoles in initiation of ventricular tachycardia and fibrillation: Evaluation of the R on T phenomenon during acute ischemia in a canine model

Eighteen open chest dogs anesthetized with pentobarbital sodium were studied to determine the role of early cycle premature ventricular beats in the initiation of ventricular tachycardia and fibrillation during the initial 30 minutes of acute myocardial ischemia. The coupling interval and prematurity index (R-R′/R-R) of every premature beat after a sinus beat were determined during both the “immediate” (2 to 12 minutes) and “delayed” (13 to 30 minutes) phases of ventricular arrhythmias that follow acute coronary ligatlon. During the immediate phase, characterized by marked fractionation of local electrograms and delayed intramyocardial conduction, early cycle beats were infrequent (8 percent of extrasystoles) and initiated only 3 (4 percent) of 75 episodes of ventricular tachycardia and fibrillation. However, during the delayed phase, characterized by less fractionation and more uniform conduction, early cycle beats were both more frequent (24 percent of extrasystoles, p < 0.001) and more successful (20 [34 percent] of 59 episodes, p < 0.001) in initiating ventricular tachycardia and fibrillation. Thus, the underlying electrophysiologic derangements appeared to be of primary importance in determining both the frequency and relative malignancy of early cycle beats during acute myocardial ischemia.     

七氟烷预处理改善离体大鼠心脏的再灌注心律失常

目的在Langendorff离体灌注模型研究七氟烷预处理对再灌注心律失常的影响。方法取SD大鼠心脏建立Langendorff灌注模型,随机分入以下三组：（1）对照组;（2）缺血再灌注组;（3）七氟烷预处理组（3％七氟烷预处理15分钟）。记录各组的血流动力学、心电图,测量冠脉流出液肌钙蛋白I水平,测定细胞内钙离子和活性氧水平。结果七氟烷预处理能显著增加缺血再灌注损伤后左室发展压,左室内压上升／下降速率和心率,降低左室舒张末期压力,减少冠脉流出液肌钙蛋白I水平（P均〈O．05）。在再灌注心律失常方面,与缺血再灌注组相比,七氟烷预处理能显著减少室性早搏个数[从182（133）次／分降至83（52）次／分],缩短室速[41（45）s降至20（22）s]和室颤[从22（43）s降至0（0）s]的发作时程,减少室颤发生率（从80％降至10％）,并降低再灌注心律失常评分[从4（0）降至2（O）]（P均〈0.05）。七氟烷预处理还能降低心肌细胞内钙离子和活性氧水平（P均〈0.05）。结论七氟烷预处理对缺血再灌注损伤心脏起保护作用,能改善离体大鼠心脏的再灌注心律失常。     

Influence of the point of origin on heart rate turbulence after stimulated ventricular and atrial premature beats

Background Heart rate turbulence (HRT) is a new and auspicious parameter for risk stratification in patients suffering from structural heart disease. The HRT parameters onset (TO) and slope (TS) are derived from Holter ECGs. Only a few studies have evaluated physiologic properties like age or prematurity of the ventricular beat on HRT. Until now, to our knowledge, little is known about the influence of the point of origin of the premature beat on HRT. Therefore, we conducted a study consisting of 25 patients (pts) with premature beats generating from 2 different sites in the atrium and ventricle. Methods During an electrophysiologic study, premature extra beats were induced. The high right atrium (HRA) and the lateral part of the coronary sinus (CS) represented the atrial pacing sites, while the right ventricular apex (RVAP) and right ventricular outflow tract (RVOT) represented the ventricular pacing sites. Prematurity started at 450 ms and was decreased to the refractoriness of each site. TO and TS were computed and correlated to the site of origin and the coupling interval (CI). Results Atrial TO was positive in 9 pts (HRA) and 7 (CS) as well as ventricular TO in 2 pts, respectively. TO induced in CS correlated with the CI (r = –0.50, p < 0.05). TS was negative, independent of the site of origin. Atrial TS showed no correlation with the CI. TO generated from both ventricular sites was positive in 2 pts. TO from RVAP correlated with the CI (r = –0.81, p < 0.005), but not with RVOT. TS from both ventricular sites exhibited no correlation with the pacing site, but correlated with themselves (r = –0.69, p < 0.03). Conclusion The site of origin of the premature beat exhibits no influence on heart rate turbulence slope. The prematurity of the extra beat correlates with turbulence onset, but not with slope. Finally, the site of origin revealed no influence on HRT slope. Therefore, the calculation of heart rate turbulence derived from extra beats extracted from Holter ECG is reliable.     

Effect of procainamide and lidocaine on ventricular automaticity and reentry during acute coronary occlusion

A model was developed to study ventricular automaticity and reentry in the heart of open chest dogs during myocardlal ischemia. Atrioventricular (A-V) block and the resultant idioventricular rhythm were induced by surgical destruction of the His bundle, and acute myocardial ischemia was produced by ligation of the left anterior descending coronary artery. The ventricle was paced by basic stimuli, and one or two premature beats were introduced at various coupling Intervals after the 10th basic beat. Two different types of response to these premature beats could be observed: (1) rapidly repetitive beats or fibrillation due to reentry after early premature beats, and (2) the appearance of escape beats from idioventricular automatic fibers after late premature beats.With this model of ventricular reentry and automaticity, the effect of procainamide (group I antiarrhythmic agent) was studied in 12 dogs, and that of lidocaine (group II) in 13 dogs. Both procainamide and lidocaine were effective in decreasing automaticity since they significantly increased postextrasystolic escape intervals of idloventricular beats. Although procainamide failed to abolish the reentrant beats induced by early premature beats in all 12 dogs, lidocaine abolished these beats in 10 of 13 dogs. The results indicate that lidocaine is much more effective than procainamide in preventing ventricular reentrant activity induced by early premature beats.     

Electrocardiographic antecedents of primary ventricular fibrillation. Value of the R-on-T phenomenon in myocardial infarction.

Primary ventricular fibrillation was seen in 20 of 450 consecutive patients (4-4%) admitted within 24 hours after the onset of acute myocardial infarction. Compared with patients without primary ventricular fibrillation they showed a lower mean age group and a higher incidence of anterior infarction. Warning ventricular arrhythmias preceded primary ventricular fibrillation in 58% of cases. However, warning arrhythmias were also present in 55% of patients without primary ventricular fibrillation. The following mechanisms of initiation of primary ventricular fibrillation were seen. 1) In one patient, it was initiated by supraventricular premature beats showing aberrant intraventricular conduction. 2) In 2 patients, ventricular tachycardia degenerated into primary ventricular fibrillation. 3) In 17 patients, it was initiated by a ventricular premature beat; in 10 of these, the premature beat showed early coupling (RR/QT less than 1--the R-on-T phenomenon). However, ventricular premature beats showing the R-on-T phenomenon were also observed in 49% of patients without primary ventricular fibrillation. In 7, primary ventricular fibrillation was initiated by a late-coupled ventricular premature beat (RR/QT greater than 1); in 2, the very late coupling resulted in a ventricular fusion beat. The study suggests that warning arrhythmias and the R-on-T phenomenon are poor predictors of primary ventricular fibrillation in acute myocardial infarction. The observation that 41% of primary ventricular fibrillation was initiated by a late-coupled ventricular premature beat suggests that ventricular vulnerability during acute myocardial infarction may extend throughout most of the cardiac cycle and is not necessarily confined to the QT interval.     

Electrocardiographic antecedents of primary ventricular fibrillation. Value of the R-on-T phenomenon in myocardial infarction.

Primary ventricular fibrillation was seen in 20 of 450 consecutive patients (4-4%) admitted within 24 hours after the onset of acute myocardial infarction. Compared with patients without primary ventricular fibrillation they showed a lower mean age group and a higher incidence of anterior infarction. Warning ventricular arrhythmias preceded primary ventricular fibrillation in 58% of cases. However, warning arrhythmias were also present in 55% of patients without primary ventricular fibrillation. The following mechanisms of initiation of primary ventricular fibrillation were seen. 1) In one patient, it was initiated by supraventricular premature beats showing aberrant intraventricular conduction. 2) In 2 patients, ventricular tachycardia degenerated into primary ventricular fibrillation. 3) In 17 patients, it was initiated by a ventricular premature beat; in 10 of these, the premature beat showed early coupling (RR/QT less than 1--the R-on-T phenomenon). However, ventricular premature beats showing the R-on-T phenomenon were also observed in 49% of patients without primary ventricular fibrillation. In 7, primary ventricular fibrillation was initiated by a late-coupled ventricular premature beat (RR/QT greater than 1); in 2, the very late coupling resulted in a ventricular fusion beat. The study suggests that warning arrhythmias and the R-on-T phenomenon are poor predictors of primary ventricular fibrillation in acute myocardial infarction. The observation that 41% of primary ventricular fibrillation was initiated by a late-coupled ventricular premature beat suggests that ventricular vulnerability during acute myocardial infarction may extend throughout most of the cardiac cycle and is not necessarily confined to the QT interval.     

右室流出道室性早搏的射频消融治疗

目的探讨射频消融治疗右室流出道室性早搏的方法和疗效。方法选择52例右室流出道室性早搏患者进行射频消融法治疗,男28例,女24例,年龄15~67岁,平均45.1岁;病史3~14年,平均6.8年均有明显症状,但无器质性心脏病的证据。多种抗心律药物治疗无效,心电图显示室性早搏均呈左束支阻滞图形,Ⅱ、Ⅲ、AVF导联为高大的R波。采用起搏标测。结果即刻成功率94%(49/52)。术前与术后1周24h动态心电图检查室性早搏为(11250~37460)次/24h和(0~1120)次/24h,两者间差异(P<0.01)。随访2~32个月,无复发。结论无器质性心脏病顽固性右室流出道室早的导管射频消融是一种安全可靠的方法。     

Effect of mexiletine on monophasic action potentials recorded from the right ventricle in man.

The effect of mexiletine, a new antiarrhythmic agent, on ventricular refractoriness and monophasic action potentials recorded from the right ventricle was studied in nine subjects. The effective refractory period of the right ventricle was determined by the extra stimulus technique using a pacing electrode situated at the right ventricular apex. Following this determination the right ventricular apex was paced at a constant cycle length and premature stimuli were introduced starting at a coupling interval of 2 ms greater than the ventricular refractory period and then at progressively increasing coupling intervals of 5 ms increments. Simultaneous recordings of monophasic action potentials of both the regular paced beats and the induced premature beats were made using a specially designed suction electrode catheter. The monophasic action potential durations were measured at 50% and 90% repolarisation. All these control measurements were repeated after an intravenous dose of 2 mg.kg-1 body wt. of mexiletine. The results showed that mexiletine did not significantly change the effective ventricular refractory period nor did it alter the monophasic action potential duration of the regular paced beat. The drug did, however, significantly prolong the monophasic action potential duration of the early induced premature beats and it is possible that this property of the drug may be related to its antiarrhythmic activity.     

动态心电图判断室性早搏起源部位的分析

目的探讨12导联同步动态心电图（AECG）对室性早搏起源部位的定位价值。方法选择我院经12导联同步AECG检查明确诊断有频发单源室性早搏的患者90例,分析12导联AECG及该患者常规12导联心电图上室性早搏QRS波群形态的差异,对其起源部位分别进行初步定位,并与心内电生理检查结果进行对照分析。结果室性早搏起源于右室共65例,其中起源于右室流出道55例（占61．11％）、右室心底部5例（占5．56％）、右束支2例（占2．22％）、其他3例（占3．33％）,起源于左室流出道20例（占22．22％）、左室心底部3例（占3．33％）、左束支2例（占2．22％）。结论根据12导联同步AECG的室性早搏QRS波群的形态可以初步判断其起源部位,指导室性早搏射频消融治疗方式的选择。     

Characterization of left ventricular mechanical function during arrhythmias by two-dimensional echocardiography. II. Location of the site of onset of premature ventricular systoles

Two-dimensional echocardiography was applied experimentally in a closed chest dog model with intact pericardium to determine the location, magnitude and extent of contractile response during pacing from discrete ventricular sites. Midventricular short-axis tomographic images obtained during regular sinus rhythm and subsequent premature ventricular beats provided comparative measurements of global and segmental systolic changes of cross-sectional luminal areas and myocardial wall thickness. Computer-assisted standardized analysis of segmental systolic fractional area change and wall thickening was used to map left ventricular contraction during normal rhythm and premature beats of 70% coupling interval, induced alternately from anterior and lateral aspects of the mid-left ventricular short-axis cross-sectional plane. A characteristic pattern consisting of early systolic contraction and wall thickening was followed by paradoxical motion and wall thinning in late systole in segments corresponding to the region of direct electrical stimulation. Statistical analysis of segment by segment function indicated a maximal amount of premature beat contractile derangement at the site of the stimuli. Pacing from a right ventricular wall site in the midventricular plane caused a similar premature beat response at the anterior aspect of the interventricular septum. It is concluded that two-dimensional echographic analysis of segmental ventricular function can identify the location of electrical stimuli, and thus might noninvasively characterize regional patterns of contraction associated with ectopic foci during arrhythmias.     

Increased R-wave amplitude induced by acute myocardial ischemia in the dog: A predictor of malignant ventricular arrhythmias

The ability of an increase of 25 % or greater in the sum of R-wave amplitudes in leads X, Y, Z, L₂, and V₅ to predict the occurrence of malignant ventricular arrhythmias (10 or more ventricular premature beats/min, ventricular tachycardia [5 or more consecutive premature beats], and/or fibrillation) was evaluated in 17 dogs during experimental acute myocardial ischemia. Each dog underwent a 15 minute ligation of the left anterior descending coronary artery followed by reperfusion and after recovery, 2 hours later, a 15 minute ligation of the circumflex coronary artery. During ligation of the left anterior descending coronary artery, 12 of 17 dogs (71%) showed no R-wave increase and no arrhythmias (true-negative response). In 5 (29%) of 17 dogs malignant ventricular arrhythmias developed: 2 of 5 (40%) dogs with arrhythmias had a concomitant R-wave increase (true-positive response), and 3 of 5 (60%) with arrhythmias had a less than 25% increase in R-wave amplitude (false-negative results). During circumflex coronary artery ligation, 13 of 17 (76%) dogs showed both R-wave increases and arrhythmias (true-positive response). Four (24%) of 17 dogs had no arrhythmias: 3 of 4 (75%) with no arrhythmias also had a less than 25% increase in R-wave amplitude (true-negative response), whereas 1 of 4 (25%) dogs with no arrhythmias had an increase in R-wave amplitude (false-positive response). In dogs with both arrhythmias and R-wave increases, R-wave changes preceded the onset of arrhythmias by a mean (± standard deviation) of 1 minute 27 seconds (± 43 seconds). Overall, R-wave increases were highly sensitive (83%), specific (94%), and predictive (94%) for the occurrence of malignant ventricular arrhythmias during experimental acute myocardial ischemia.     

Energy metabolism and contractile function after 15 beats of moderate myocardial ischemia.

Difficulties in studying myocardial metabolism with adequate time resolution have led to contradictory conclusions regarding the mechanisms causing contractile abnormalities during the early stages of ischemia. In acutely instrumented swine, we investigated whether abnormalities in subendocardial ATP, phosphocreatine, or lactate content develop rapidly enough during the first few heart beats after onset of partial myocardial ischemia to contribute to contractile failure. Within the first 15 beats of a 40-50% reduction in left anterior descending coronary artery blood flow, regional myocardial function was significantly reduced but continuing to deteriorate. Rapidly frozen transmural left ventricular biopsies obtained on the 15th heart beat (+/- 1.5 beats) after the onset of ischemia revealed significant decrements in subendocardial phosphocreatine and ATP levels to 77% (p less than 0.05) and 84% (p less than 0.005) of control values, respectively, but minimal change in lactate content. Metabolic effects as assessed by transmural averages took longer to become detectable; thus, there was a tendency to underestimate the importance of subendocardial metabolic effects on myocardial function. When left ventricular preload was assessed during this early time period, left ventricular end-diastolic wall thickness only decreased by 3%, and left ventricular end-diastolic pressure did not change significantly despite a large fall in coronary perfusion pressure. Thus, in an in vivo pig model with techniques optimized to detect subendocardial metabolic changes within the period of very early moderate myocardial ischemia, abnormalities in high energy phosphate compounds occurred rapidly enough to contribute to developing myocardial dysfunction, whereas preload-mediated mechanisms related to vascular distending pressure could not explain the functional deterioration under these conditions.     

Statistical analysis of the different factors which could affect postextrasystolic potentiation in the human heart.

The effect of different coupling indices and intervals that could theoretically affect postextrasystolic potentiation has been investigated. A total of 150 ventricular premature beats corresponding to 20 patients submitted to routine cardiac catheterization were studied. Only single ventricular premature contractions following at least four regular sinus beats were considered. Percentage changes in left ventricular systolic pressure, end-diastolic pressure, and max dp/dt were correlated against seven indices and intervals. Index 2 (coupling interval/coupling interval + postextrasystolic pause) gave the better correlations. Besides, this Index includes two intervals that were demonstrated to have statistical significance when individually considered. It has been proved that in the first postextrasystolic beat the highest values of max dt/dt, or left ventricular systolic pressure occurred in early ventricular premature beats, giving a negative regression with Index 2, while in the second postextrasystolic beat the highest values of max dp/dt and left ventricular systolic pressure corresponded to late prematuring beats, giving therefore positive regressions with Index 2 (slope inversion phenomenon). The third and fourth postextrasystolic beats had similar positive regressions but with progressively smaller slopes. Correlations between left ventricular end-diastolic pressure and Index 2 were very poor. It is suggested that variations in baroreceptor activity could account for the different forms of potentiation observed in early and late extrasystoles. In five cases, there were no consistent differences in potentiation when premature beats were elicited from either right or left ventricles.     

Comparison in the same patient of two programmed ventricular stimulation protocols to induce ventricular tachycardia

In 24 consecutive patients with documented ventricular tachycardia (VT) (22 patients) or fibrillation (VF) (2 patients), results of 2 programmed ventricular stimulation protocols to initiate VT/VF were prospectively studied. Seventeen patients had VT/VF after a healed myocardial infarction (MI) and 7 patients had idiopathic VT. In both protocols (designated 1 and 2), the right ventricular (RV) apex was paced at 100 beats/min, using a maximum of 2 ventricular premature complexes (VPCs) given at twice diastolic threshold. This protocol had a sensitivity of 25%. In protocol 1, the pacing site was changed to the RV outflow tract and the previous steps were repeated; in protocol 2, the pacing rate was increased to 120 and 140 beats/min at the RV apex, also using a maximum of 2 VPCs. The next step in protocol 1 consisted of increase of current strength to 20 mA and repeating previous steps at the RV apex and RV outflow tract, with a maximum of 2 VPCs; in the next step in protocol 2, three VPCs were used during sinus rhythm and pacing was performed at rates of 100, 120 and 140 beats/min. In protocol 1, therefore, only stimulation site and current strength were changed, while in protocol 2 only pacing rate and number of VPCs were modified. Protocol 1 had a sensitivity of 54% and protocol 2 a sensitivity of 83%. The sensitivity of protocol 2 was statistically higher than that of protocol 1 (p less than 0.05). In the group of patients with VT after MI, the sensitivity was 66% for protocol 1 and 93% for protocol 2.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ryanodine and caffeine prevent ventricular arrhythmias during acute myocardial ischemia and reperfusion in rat heart

This study investigates the possible role of oscillatory release of calcium from sarcoplasmic reticulum in the genesis of ventricular arrhythmias during acute myocardial ischemia and reperfusion in isolated rat hearts. We used ryanodine and caffeine, which are known to modulate the oscillatory release of calcium from sarcoplasmic reticulum. During 30 minutes of left main coronary artery ligation, all 13 control hearts developed ventricular premature beats (number of beats, 225 +/- 51) and ventricular tachycardia (duration, 123 +/- 21 seconds); five hearts developed ventricular fibrillation. In a separate series of experiments, reperfusion after 15 minutes of coronary artery ligation caused ventricular fibrillation to occur within 15 seconds in all 12 hearts. Ryanodine (10(-9) to 10(-7) M) abolished ventricular arrhythmias during coronary artery ligation and prevented reperfusion ventricular fibrillation. Ryanodine (10(-9), 10(-8), and 10(-7) M) caused 15%, 23%, and 74% decreases in the maximal rate of rise of left ventricular pressure development and 20%, 32%, and 85% decreases in the maximal rate of fall of left ventricular pressure development, respectively, prior to coronary artery ligation. During acute myocardial ischemia, ryanodine 10(-9) M maintained and 10(-8) M impaired left ventricular function; 10(-7) M caused left ventricular failure. Coronary perfusion rate did not increase during ischemia. Antiarrhythmic activity occurred independent of preservation of high energy phosphates, reduction in tissue lactate, or tissue cyclic adenosine monophosphate in the ischemic myocardium. Caffeine 10(2) M decreased the incidence of ventricular arrhythmias during ischemia and upon reperfusion; protection occurred coincident with development of diastolic contracture. Caffeine increased ischemic tissue cyclic adenosine monophosphate content and worsened tissue energy status.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrophysiologic and anatomic characteristics of ventricular tachycardia induced at the right ventricular outflow tract but not at the apex.

The site of ventricular stimulation is an important variable in the initiation of ventricular tachycardia (VT) by programmed ventricular stimulation. Among 169 patients studied consecutively, 17 (10%) had ventricular tachycardia induced by programmed electrical stimulation from the right ventricular outflow tract but not from the apex. Fourteen of these 17 patients had had prior myocardial infarction (12 had inferior, and two had both inferior and anterior myocardial infarction), two had a dilated cardiomyopathy, and one had a localized cardiomyopathy. Fourteen patients had echocardiograms suitable for analysis. Of these, 12 had posterior/inferior ventricular wall motion abnormalities located at the base of the heart. The ventricular effective refractory periods from the right ventricular outflow tract and right ventricular apex were 237 +/- 4 and 244 +/- 5 msec, respectively (p less than 0.05, mean +/- SEM). Induced VT had a cycle length of 229 +/- 4 msec and had the morphology of right bundle branch block in 12 patients, of left bundle branch block in three patients, and had both morphologies in two patients. In 14 patients the axis was superior. VT was initiated with two extrastimuli in 15 patients and with burst right ventricular pacing in two patients. Similar pacing techniques with identical pacing intervals did not induce VT at the right ventricular apex in 14 of these 17 patients. Further, among the 15 patients whose VT was induced at the right ventricular outflow tract with two extrastimuli, neither burst pacing (n = 13) nor two extrastimuli introduced at faster paced rates (n = 12) induced VT at the right ventricular apex.(ABSTRACT TRUNCATED AT 250 WORDS)