Study on the relationship between myocardial ischemia assessed by 24-hour ambulatory electrocardiogram and ventricular premature beat originating from different positions in older adults

BackgroundMyocardial ischemia is a common reason of ventricular premature beat, and it plays an important role in arrhythmia in older adults. We could often see the report about the diagnosis and radiofrequency catheter ablation of ventricular arrhythmia from the right ventricular outflow tract, Haissaguerre et al. (2002) [1], Miyamoto et al. (2010) [2], Nakagawa et al. (2008) [3], Zhu et al. (1995) [4]. However, no study to date has examined the relation of myocardial ischemia and ventricular premature beat originating from different positions. In this article, we studied the incidences of myocardial ischemia of ventricular premature beats originating from different positions in older adults.MethodsWe located the original positions of ventricular premature beats according to the shape of the wide and malformed QRS waves in 12 leads synchronizing ECG. We used synchronism 12-lead ambulatory 24 hour electrocardiograms to examine 531 aged patients with ventricular premature beats, calculated the incidences of myocardial ischemia of the ventricular premature beats originating from different positions.ResultsThe incidence of myocardial ischemia of ventricular premature beats from the right ventricular outflow and the left ventricular outflow were 52.31% and 51.42% respectively. The incidence of myocardial ischemia of ventricular premature beat from the right ventricle anterior wall and the left ventricle anterior wall were 53.57% and 73.47% respectively. The incidence of myocardial ischemia of ventricular premature beat from the right ventricular apex and the left ventricular apex were 55.10% and 74.42% respectively. The total incidence of myocardial ischemia of right ventricular premature beats and left ventricular beats were 52.92% and 61.65% respectively.ConclusionsThe total incidence of myocardial ischemia of left ventricular premature beats was higher than that of right ventricular premature beats. The highest incidence of myocardial ischemia of ventricular premature beats was that from the left ventricular apex and anterior wall. The incidence of myocardial ischemia of ventricular premature beats was more than 50% in older adults.     

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。     

Relation of heart rate and blood pressure turbulence following premature ventricular complexes to baroreflex sensitivity in chronic congestive heart failure

Reduced heart rate variability (HRV) and attenuated baroreflex sensitivity (BS) after myocardial infarction and in patients with chronic congestive heart failure (CHF) are associated with poor prognosis. Recent studies have shown that a large proportion of the prognostic power from HRV measurements is localized in heart rate turbulence immediately after ventricular premature complexes. The mechanism of heart rate turbulence remains unknown. In the present study, we explore its relation to BS. In 45 patients with CHF and > or =3 ectopic beats in a 30-minute period, measurements of RR interval and continuous, noninvasive blood pressure (BP) were studied at rest. In response to an ectopic beat, average heart rate turbulence was 9.4 ms/beat (SD 6.1). Mean BP turbulence was 0.72 mm Hg/beat (SD 0.56). Using the ratio of heart rate and BP turbulence slopes to estimate BS showed good agreement (r = 0.67, p < 0.0001) with the alpha-index method (BSalpha). This relation was attributable to a marked correlation between heart rate turbulence and BSalpha (r = 0.70, p <0.0001); there was no correlation between BP turbulence and the BSalpha (r = 0.1, p = NS). Twenty-nine percent of patients had postectopic pulsus alternans, with a mean decay time of 1.4 beats (SD 0.5). The presence of pulsus alternans was associated with a significantly lower heart rate turbulence slope (6.3 [SEM 1.0] vs 10.7 [SEM 1.2] ms/beat, p = 0.03). Thus, heart rate turbulence is an effective measure of the baroreflex, correlating strongly with a standard measure. This is because it is the heart rate, rather than the BP, response to an ectopic beat that conveys the information relevant to BS measurement.     

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.     

Mechanisms involved in heart rate turbulence

Proper understanding of the mechanisms involved in heart rate turbulence (HRT) may offer anexplanation of why it is such a potent postinfarction risk stratifier. This article reviews the physiologicalbackground of ventriculophasic sinus arrhythmia—a phenomenon which shares some underlying physiologicalfeatures with HRT including cardiac autonomic regulation. It is now believed that HRT is principally triggeredby a transient loss of vagal efferent activity in response to the missed baroreflex afferent input due toventricular premature beat-induced haemodynamically inefficient ventricular contraction. Studies are summarizedwhich support more or less directly this hypothesis. The physiology of early acceleration and late decelerationof heart rate after a ventricular premature beat is discussed. Qualitatively different but otherwisequantitatively uniform postectopic dynamics of systolic blood pressure after ventricular premature beats isdemonstrated in subjects with normal and abnormal left ventricular function. It is concluded that the slope oflate deceleration of heart rate after ventricular premature beats can serve as a reasonable surrogate forbaroreflex sensitivity.     

Tight mechanism correlation between heart rate turbulence and baroreflex sensitivity: sequential autonomic blockade analysis

INTRODUCTION: Heart rate turbulence is a powerful de novo risk predictor for patients surviving acute myocardial infarction. However, little is known about its underlying physiologic mechanism. METHODS AND RESULTS: Hypothesizing that heart rate turbulence is barorceptor reflex related, we studied heart rate and blood pressure fluctuations at rest and after systematically introduced ventricular premature beats in 16 patients without structural heart disease (10 men and 6 women; mean age 45 +/- 17 years) before and after sequential sympathetic (esmolol 4-mg bolus followed by 120 microg/kg/min intravenously), parasympathetic (atropine 0.04 mg/kg intravenously), and combined autonomic blockade (esmolol plus atropine). Turbulence onset (%) and turbulence slope (msec/beat) were averaged from 10 respective ventricular premature beats. Spontaneous baroreflex sensitivity (msec/mmHg) was calculated from 5 minutes of sinus rhythm recording. The results showed that turbulence slope decreased after atropine (0.71 +/- 0.50 msec/beat vs 5.17 +/- 3.96 msec/beat at baseline; P < 0.01) and combined autonomic blockade (1.23 +/- 1.02 msec/beat; P < 0.01) but was unchanged after esmolol (4.53 +/- 3.30 msec/beat; P > 0.05). Turbulence onset increased after atropine (0.32% +/- 0.35% vs -0.45 +/- 0.94 at baseline; P < 0.05) and combined sympathetic and parasympathetic blockade (0.58% +/- 0.86%; P < 0.05) but was unchanged after esmolol (-0.62% +/- 1.33%; P > 0.05). Turbulence slope was positively correlated with baroreflex sensitivity at baseline (r = 0.78, P < 0.01) and after esmolol (r = 0.8, P < 0.01), but dissociated after atropine (r = 0.16, P > 0.05) and combined autonomic blockade (r = 0.31, P > 0.05). Turbulence onset was negatively correlated with baroreflex sensitivity at baseline (r = -0.61, P < 0.05), after esmolol (r = -0.80, P < 0.01), and after atropine (r = -0.53, P < 0.05). CONCLUSION: Heart rate turbulence of turbulence onset and turbulence slope is critically vagal dependent and highly correlated with spontaneous baroreflex sensitivity, which underscores its clinical importance in cardiovascular risk stratification.     

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.     

Enhanced left ventricular performance with phentolamine in acute myocardial infarction

The hemodynamic effects of phentolamine (Regitine) were evaluated in nine patients with increased left ventricular filling pressure and clinical left ventricular failure (Group A) and five patients with normal left ventricular filling pressure and an uncomplicated course (Group B) within 48 hours of an acute myocardial infarction. Decreased afterload was noted in both groups after administration of phentolamine. Improved left ventricular performance was noted only in Group A and was manifested by a decrease in left ventricular filling pressure (from 23.9 to 13.6 mm Hg), increase in cardiac index (from 2.1 to 2.9 liters/min per m²), increase in stroke volume index (from 22.5 to 29.3 cc/beat per m²), and little change in heart rate (from 94.2 to 99.8 beats/min). In contrast, a decrease in stroke volume index (32 to 26 cc/beat per m²) and a greater increase in heart rate (77 to 94 beats/min) were noted in Group B. Reduction of preload, which accompanies a reduction in afterload with administration of phentolamine, may have caused a greater decrease in end-diastolic volume in Group B, resulting in the reduced stroke volume index and compensatory increase in heart rate. Our findings suggest that afterload reduction induced by administration of phentolamine enhances depressed left ventricular function in patients with increased left ventricular filling pressure after myocardial infarction. Careful monitoring to prevent complications is required.     

Ectopic Ventricular Beats Originating in Ischemically-Injured Left Ventricular Epicardium, 24 Hours Following Coronary Artery Occlusion in the Dog

Epicardial Ectopics. Introduction: Ventricular ectopic beats demonstrating: (1) depolarization in ischemically-injured anterior epicardium preceding His-Purkinje activation by more than 25 msec; (2) initial delta waves on the anterior chest leads of the surface ECG coincident with presystolic epicardial activation; and (3) a left bundle branch block morphology were observed in 46 of 256 anesthetized dogs evaluated 18–24 hours following anterior descending coronary artery occlusion. Methods and Results: In 18 experiments, endocardial and epicardial recordings, and signal-averaged recordings from the left ventricle were used to determine the earliest activation time/site for epicardial ectopic beats. In these ventricular ectopic beats, early epicardial activation was coupled to the preceding beat by a constant, fixed coupling interval. Electrical activity during the interectopic interval was not detected with composite or multiple bipolar recordings, or with signal averaging from the heart. The mean coupling interval was prolonged by lidocaine from 385 ± 24to 409 ± 45 msec (P < 0.01), and was decreased by epinephrine (364 ± 7 msec) and D-600 (324 ± 32 msec)(P < 0.05). Spontaneous ventricular beats of epicardial origin could be reversibly suppressed by epicardial lidocaine administration or permanently suppressed with intracoronary latex injection, eliminating presystolic potentials. Histologic examination of the epicardium revealed surviving tissue bands (0.5–2.0 mm) distributed throughout transmural infarcted epicardium. Conclusion: The present experiments demonstrate constant-coupled ectopic ventricular beats of epicardial origin, 18–24 hours following myocardial infarction. The ventricular ectopic beats may result from abnormal automaticity or electrotonic excitation from an initiating beat across an unexcitable gap with slow conduction from the “site of origin’ to reactivate the left ventricle. (JCardiovasc Electrophysiol, Vol. 3, pp. 315–333, August 1992)     

Heart Rate Turbulence: A New Predictor for Risk of Sudden Cardiac Death

Initial acceleration and a subsequent deceleration of sinus rhythm following a ventricular ectopic beat with a compensatory pause has been termed heart rate turbulence (HRT). The changes in sinus rhythm are thought to be mediated by a baroreflex response to the lower stroke volume of the ectopic beat. HRT is vagally mediated and abolished by atropine, whereas β‐blockers have no effect. HRT has been shown to be an independent and powerful predictor of mortality after myocardial infarction. In patients on β‐blockers, it scores better than left ventricular ejection fraction (LVEF) in its predictive value. Two common measures of HRT are turbulence onset and turbulence slope. When both these measures are abnormal, it is as powerful a predictor of mortality as LVEF. HRT correlates with other indices of cardiac autonomic functions like baroreflex sensitivity and heart rate variability. A composite autonomic index including all these three has been shown to be a powerful predictor of mortality. In patients undergoing direct percutaneous intervention for myocardial infarction, HRT improves in those attaining successful reperfusion. Abnormal values for HRT have been noted in patients with dilated cardiomyopathy and Chagas disease. Diabetic and elderly individuals are more likely to have blunted HRT. HRT cannot be measured in patients lacking ventricular ectopic beats and in patients presenting with atrial fibrillation.     

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.     

Effects of xamoterol in acute myocardial infarction: blood pressure, heart rate, arrhythmias and early clinical course.

Xamoterol is a novel partial agonist of beta 1 adrenoceptors that reduces myocardial ischaemia and improves ventricular function in patients with mild to moderate heart failure. In a double blind, randomised, placebo controlled study, the effects of xamoterol given in a dose of 200 mg twice daily were studied in 51 consecutive patients with acute myocardial infarction, including 17 receiving diuretics for left ventricular failure. Treatment was started on the third day of admission and continued for 7 days. Blood pressure was recorded at 0900 daily, and 24 hour ambulatory electrocardiogram monitoring was commenced at this time on days 1 (pre-treatment), 4, 6 and 9 of admission. Additional drug therapy was recorded daily throughout the study. One patient died prior to randomisation and three were withdrawn (1 placebo, 2 xamoterol) with ventricular arrhythmias and/or disturbances of conduction. Compared to placebo, xamoterol had no effect on the rate of ventricular premature beats or ventricular tachycardia. Xamoterol increased nocturnal heart rate (0000-0600 hrs 79 +/- 2; placebo 72 +/- beats/min; P less than 0.03) but did not change blood pressure. Three patients receiving xamoterol, and 7 on placebo, required new (after randomisation) antianginal therapy. One patient treated with placebo developed new heart failure. These results show that xamoterol can be administered safely to selected patients following myocardial infarction, including those treated for mild heart failure.     

Effects of morphine on left ventricular dimensions and function in patients with previous myocardial infarction

To assess the effects of morphine sulfate on left ventricular function and dimensions we administered 15 mg of this agent to 11 stable patients with previous transmural myocardial infarction. All studies were carried out in the supine position. Before morphine administration an echocardiogram was obtained, and this procedure was repeated at 15, 30, 60, 120, and 240 min after morphine. Heart rate decreased from a control value of 69 +/- 4 to 62 +/- 5 beats/min 2 h after morphine (p less than 0.01, analysis of variance); this slower heart rate persisted for 4 h after morphine. Serial measurements of blood pressure, echocardiographic ejection fraction, percent of fractional shortening, and mean normalized velocity of circumferential fiber shortening also showed no significant alterations after morphine. We conclude that in stable patients with chronic ischemic heart disease studied in the supine position, 1) morphine exerts no effect on left ventricular dimensions, an observation which does not support the concept that this agent acts in humans by producing a 'pharmacologic phlebotomy'; and 2) morphine does not alter left ventricular function at rest. Whether different results will be found in patients with increased sympathetic activity, such as occurs in the setting of an acute myocardial infarction or during an episode of acute pulmonary edema, remains to be investigated.     

Short-term heart rate turbulence analysis versus variability and baroreceptor sensitivity in patients with dilated cardiomyopathy

New methods for the analysis of arrhythmias and their hemodynamic consequences have been applied in risk stratification, particularly to patients after myocardial infarction. This study investigates the suitability of shortterm heart rate turbulence (HRT) in comparison to heart rate and blood pressure variability as well as baroreceptor sensitivity analyses to characterize the regulatory differences in patients with dilated cardiomyopathy (DCM) and healthy controls. In this study, 30 minutes data from noninvasive continuous blood pressure and ECG of 37 DCM patients and 167 controls under standard resting conditions were analyzed. The results showed highly significant differences between DCM patients and controls in heart rate and blood pressure variability as well as baroreceptor sensitivity parameters. Applying a combined heart rate-blood pressure trigger, in 24.3% (9) of the DCM patients and in 11.3% (19) of the controls ventricular premature beats were detected. This fact demonstrates the constricted applicability of short-term HRT analyses. However, the HRT parameters showed significant differences in this subgroup with ventricular premature beats (Turbulence Onset: DCM: 1.80+/-2.72, Controls: -4.34+/-3.10, p<0.001; Turbulence Slope: DCM: 6.75+/-5.50, Controls: 21.30+/-17.72, p = 0.021). Considering all (including HRT) parameters in the subgroup with ventricular beats, a discrimination rate between DCM patients and controls of 88.0% was obtained (max. 6 parameters). In comparison, in the total group this rate was 86.3% (without HRT parameters). The comparable classification rates and the high correlations between heart rate turbulence and variability and baroreflex parameters point to a more universal applicability of the last-mentioned methods.     

比索洛尔对早期急性心肌梗死患者心率振荡的影响

目的:观察早期使用比索洛尔对急性心肌梗死(AMI)患者心率振荡现象的影响.方法:将我院2007-08-2008-08期间住院的AMI患者100例,相应分为比索洛尔组和对照组;利用24 h动态心电分析系统获得其室性期前收缩,分别计算2组治疗前及治疗2周后的振荡初始(TO)和振荡斜率(TS)2个指标.结果:治疗前2组TO值和TS值均异常,但组间差异无统计学意义(P>0.05),治疗后与同组治疗前比较,TO值和TS值差异均有统计学意义(P<0.05),与对照组比较,治疗后比索洛尔组TO值显著降低,TS值显著升高(均P<0.01).结论:早期使用比索洛尔可以有效改善AMI患者心率振荡现象,降低猝死风险.     

Noninvasive beat to beat monitoring of left ventricular function by a nonimaging nuclear detector during premature ventricular contractions

A specially designed cardiac probe was used to evaluate beat to beat changes in left ventricular performance caused by premature ventricular contractions in four open chest dogs and 15 patients with various cardiac disorders. After intravenous injection of 15 to 20 mCi of technetium-99m serum albumin, left ventricular time-activity curves were obtained by positioning the probe over the left ventricular area in a 40 ° lateral anterior oblique projection with a 10 to 20 ° caudad tilt. Correct positioning was found by maximizing both the stroke counts and the end-diastolic counts. In the animal experiments, data generated by the probe were displayed side by side with left ventricular pressure, aortic pressure and aortic flow. Increases or decreases in stroke volume measured with the flowmeter correlated well with those measured with the cardiac probe. In the patients, the relative standard deviation of filling volumes, stroke volumes and ejection fractions of the sinus beats was 16 ± 5 percent, 14 ± 5 percent and 12 ± 5 percent, respectively. The premature ventricular contractions manifested end-systolic volume greater than, equal to or less than that of sinus beats. The filling volume, stroke volume and ejection fraction of these contractions were 51 ± 21 percent, 57 ± 17 percent and 45 ± 19 percent lower, respectively, than those of the sinus beats. In the compensatory sinus beats stroke volume and ejection fraction were 20 ± 27 percent and 26 ± 12 percent higher, respectively, than those in the sinus beats; however, the filling volume of these beats was essentially equal to that of the sinus beats.     

Role of hypotension in heart rate turbulence physiology.

BACKGROUND: Heart rate turbulence is a recently described cardiac prognostic marker that may be mediated by arterial baroreceptor sensitivity, suggesting it is induced by a brief initial hypotension. OBJECTIVES: The purpose of this study was to assess whether heart rate turbulence could be noninvasively induced through a previously implanted defibrillator and whether hypotension modulates turbulence physiology. METHODS: Premature ventricular paced beats was delivered during continuous ECG and blood pressure monitoring in patients with implanted defibrillators. Heart rate turbulence parameters from paced beats were compared with those from spontaneous premature ventricular beats. Subsequently, turbulence hemodynamic parameters were compared in 11 subjects with turbulence induced by pacing trains of 1, 3, 5, and 8 beats at a cycle length of 400 ms. RESULTS: Heart rate turbulence was very similar whether it followed a spontaneous premature ventricular complex or a paced beat. Induced and spontaneous turbulence slopes correlated well (R(s) = 0.917, P = .001). With increasing pacing train length, the magnitude of hypotension, cumulative hypotension time from the last sinus beat, turbulence tachycardia magnitude, magnitude of hypertension in recovery, and turbulence onset (but not turbulence slope) all increased. The cumulative hypotension time, but not the magnitude of hypotension, was tightly correlated with the magnitude of tachycardia (R2 = 0.999, P = .003) and turbulence onset (R2 = 0.975, P = .01). CONCLUSION: Heart rate turbulence can be induced noninvasively through an implanted device. Turbulence parameters are physiologically modulated by the duration of the initial hypotension, suggesting a possible important role for arterial baroreceptors.     

Atrial contribution to ventricular filling in patients with coronary artery disease as assessed by cardiac pacing

Analysis of beat to beat changes in left ventricular (LV) ejection time during cardiac pacing was utilized to assess the atrial contribution to ventricular filling in coronary artery disease. The recordings of aortic pressure were made during atrial and ventricular pacing at a rate of 5 to 10 beats/min above sinus rhythm. During ventricular pacing, LV ejection time became maximum when an atrial contraction preceded a ventricular contraction by a physiologic interval and was similar to that obtained during atrial pacing (max ET). When the atrial systole occurred with or followed the paced ventricular contraction, LV ejection time became minimum (min ET). The atrial contribution was calculated as (max ET--min ET)/max ET X 100(%). Patients with coronary artery disease had a significantly large atrial contribution. In patients without myocardial infarction, the atrial contribution was increased to compensate for impaired early diastolic filling. In patients with myocardial infarction, the atrial contribution was reduced when LV end-diastolic pressure was markedly high. The atrial contribution generally plays an important role in increasing stroke volume, but it had less effect despite the forceful atrial contraction as LV filling pressure became more elevated.     

Influence of post-extrasystolic potentiation on left ventricular function estimated by means of systolic time intervals.

Systolic time intervals were measured in 50 patients with frequent premature ventricular beats. The patients were divided into two groups: group I included those which showed in the beat that preceded an extrasystole a pre-ejection period/left ventricular ejection time (PEP/LVET) ratio greater than or equal to 0.43, and group II with PEP/LVET ratio greater than 0.44. Systolic time intervals recorded during post-extrasystolic potentiation were compared with those measured in the preextrasystolic complex. Also the measured intervals were tested against the hourly rate of premature beats obtained by electrocardiographic telemetric monitoring. The results confirmed the following results of previous reports: a) ventricular premature beats are followed by sinus-potentiated contractions inversely related to the coupling interval and dependent on adequate compensatory pauses; b) potentiated contractions are greater in patients with ventricular dysfunction. No relationship was found between left ventricular performance and the rate of premature beats. It is concluded that the effect of an antiarrhythmic intervention on the left ventricular function might be adequately evaluated by means of systolic time intervals and provoked post-extrasystolic potentiation, with the advantage of using totally non-invasive procedures.