On line (real time) quantitative measurement of premature ventricular beats

A real time system for graphically displaying premature ventricular beat trends is described. The system consists of analog detector circuits coupled to a Fortran based software program for premature ventricular beat processing. The software program runs four independent channels and has three available analysis modes: a "counting" mode which provides a running total of counts to date; an "averaging" mode which displays average number of events over time, and a "ratio" mode which provides an output reflecting changes in the ratio of premature ventricular beats to all beats. Various scale factors can be applied to accommodate differing background states. The system's strengths lie in its simplicity, accuracy, and simultaneous analog display of both the original ECG signal as well as the derived quantitative data.     

全方向M型超声评价右心室流出道起源室性期前收缩患者左心室运动同步性

目的 探讨全方向M型超声心动图评价右心室流出道（RVOT）起源室性期前收缩（PVB）患者左心室心肌径向运动同步性的临床价值。方法 对30例右心室流出道起源PVB患者（PVB组）和30例健康志愿者（对照组）,应用全方向M型超声系统测量左心室短轴乳头肌水平6个节段收缩期速度达峰时间(Ts)及舒张早期速度达峰时间(Td),计算6个节段的标准时间差(Ts-6-SD, Td-6-SD),以评价PVB对左心室运动同步性的影响。结果 在所有节段中, PVB组正常窦性心律时Ts、Td与对照组比较,差异无统计学意义(P＞0.05),而Ts-6-SD、Td-6-SD均大于对照组(P＜0.05), PVB组PVB时的Ts、Td、Ts-6-SD、Td-6-SD均大于正常窦性心律时(P＜0.01）。结论 右心室流出道起源PVB患者在窦性心律及PVB时左心室收缩与舒张均存在失同步,全方向M型超声能够为评价左心室心肌径向运动同步性提供一定的参考价值。     

扩张型心肌病患儿室性早搏与心率变异性相关性研究

目的探讨扩张型心肌病（DCM）患儿室性早搏与心率变异性的关系。方法采用TLC3000A十二导动态心电仪,对30例正常儿童和65例DCM患儿进行动态心电分析。DCM组分为室早组和非室早组,室性早搏组按室早发生频率不同分为A组（偶发）、B组（频发）、C组（联律.多形.成对.室速）,对各组进行心率变异（HRV）分析。结果DCM患儿室早各组和非室早组HRV与对照组比较差异有显著性（P〈0.01）;非室早组和室早A组HRV值差异无显著性（P〉0.05）;室早B组及C组与非室早组比较HRV明显下降,差异有显著性,且室早各组HRV依次下降,各指标组间均有显著性差异（P〈0.05）。结论DCM患儿HRV值与室性早搏的严重程度有一定相关性,HRV值对DCM患儿并发室性心律失常的诊断有一定价值,也可作为预测DCM预后的一项指标。     

胺碘酮与慢心律联合治疗顽固性室性早搏的疗效观察

目的 :观察胺碘酮与慢心律联合治疗顽固性室性早搏的疗效和安全性。方法 :17例顽固性室性早搏病人给予胺碘酮口服负荷量后加维持量 ,同时联合口服慢心律。结果 :15例 (88% )得到有效控制 ,未见严重毒副作用。结论 :胺碘酮与慢心律联合治疗顽固性室性早搏有良好的临床疗效及安全性     

Multiple premature beats triggered ventricular arrhythmias during pilsicainide infusion in a patient with inferior ST-segment elevation

A 17-year-old man was referred to our hospital for treatment of common paroxysmal atrial flutter. His electrocardiogram at rest showed subtle ST-segment elevation in leads II, III, and aV(F). Intravenous pilsicainide caused further ST-segment elevation in the inferior leads, new ST-segment depression in leads V2-V6, two distinct forms of premature ventricular complexes (PVCs) triggering short runs of polymorphic ventricular tachycardia (VT). An infusion of isoproterenol suppressed these arrhythmias and normalized the ST-segment. Pilsicainide may induce PVCs and polymorphic VT in atypical Brugada syndrome.     

急性冠脉综合征患者室性期前收缩发生部位的研究

目的 对比研究急性冠脉综合征(ACS)患者与健康人室性期前收缩发生部位的差异.方法 选择12导联同步动态心电图检测的186例室性期前收缩患者,其中ACS患者91例、健康体检者95 例,计算不同起源部位室性期前收缩发生率,进行对比分析.结果 ACS患者左心室前壁及心尖部期前收缩发生率、左心室期前收缩总发生率显著高于健康体检者(P＜0.05);健康体检者右心室流出道期前收缩发生率、右心室期前收缩总发生率显著高于ACS患者(P＜0.05).结论 判定室性期前收缩的临床意义要结合期前收缩发生的部位.ACS患者出现室性期前收缩,则应及时监测电生理活动,同时要采取积极有效的治疗措施预防或处理威胁生命的恶性室性心律失常.     

Failure of right atrial premature beats to reset atriofascicular tachycardia

A patient with a right atriofascicular (Mahaim) tachycardia was found to have inducible antidromic supraventricular tachycardia, but atrial premature beats from the right atrial free wall failed to reset the tachycardia. An interesting transition from AV nodal reentry tachycardia to Mahaim tachycardia is also presented.     

Behavior of postextrasystolic His-Purkinje system refractoriness after multiple premature beats

Although the steady-state refractoriness of the human His-Purkinje system has been shown to be directly related to the cycle length of pacing, the effect that a varying number of premature beats would have on His-Purkinje system refractoriness of the first postextrasystolic beat has not been described. These effects were systematically investigated in 10 patients with normal intraventricular conduction. The His-Purkinje system relative refractory period (HPS-RRP) of the postextrasystolic beat and that of a comparable constant cycle length ventricular drive were measured by the ventricular extrastimulus technique. Results were as follows: the HPS-RRP of the postextrasystolic beat after one premature beat was longer than the HPS-RRP during a comparable constant ventricular drive. However, with the addition of each successive premature beat, the HPS-RRP of the postextrasystolic beat alternated between lower and higher values, in a manner dependent on whether there was an odd or even number of premature beats. In contrast, ventricular refractoriness of the postextrasystolic beats behaved in a cumulative manner, decreasing progressively with the addition of each premature beat.     

Differential effects of glyburide on premature beats and ventricular tachycardia in an isolated tissue model of ischemia and reperfusion.

Possible anti- and proarrhythmic effects of glyburide, an ATP-sensitive K+ channel blocker, were assessed in an isolated tissue model of reperfusion. Transmembrane electrical activity was recorded from endo- and epicardium of isolated segments of guinea pig right ventricular free walls, or two sites on papillary muscles with microelectrodes. An electrocardiogram was recorded by two electrodes placed at opposite ends of the tissue bath. Regular stimulation was delivered to endocardium. Tissues were exposed to simulated ischemia for 15 min and then were reperfused with normal Tyrode's solution. Rapid sustained or nonsustained ventricular tachycardia, bigeminy or trigeminy with characteristics of transmural re-entry occurred early in reperfusion in 50% of free walls. Triggered arrhythmias with characteristics of oscillatory afterpotentials (delayed afterdepolarizations) occurred in 20%. Arrhythmias were accompanied by prolongation of transmural conduction times and abbreviation of endocardial effective refractory periods and action potential durations. Glyburide (3 or 30 microM) significantly attenuated abbreviation of action potential durations and effective refractory periods during ischemic conditions and early reperfusion. Neither endocardial nor transmural conduction times were modified by glyburide; however, glyburide significantly decreased the incidence of transmural conduction block during ischemic conditions. Glyburide abolished reperfusion arrhythmias with characteristics of re-entry, but potentiated oscillatory afterpotentials in papillary muscles and triggered arrhythmias with characteristics of oscillatory afterpotentials in free walls. Identical effects were seen with glyburide present in ischemic solution, or in both ischemic and reperfusion solutions, but no effect was observed with glyburide present only in reperfusion. Our study demonstrates possible cellular mechanisms underlying simultaneous pro- and antiarrhythmic drug effects exerted on late premature beats and rapid arrhythmias and closely coupled premature beats.     

Effect of beta-blockade on the premature ventricular beats/heart rate relation and heart rate variability in patients with coronary heart disease and severe ventricular arrhythmias

We examined the effects of beta-blockers on the associations between heart rate and number of premature ventricular beats (PVBs) and on heart rate variability and myocardial ischemia in patients with coronary heart disease. After 2 weeks of run-in placebo treatment, 18 patients with coronary artery disease were randomized to a 7-day treatment with either propranolol (40 mg) three times a day or placebo. During run-in and after 7 days of treatment, patients underwent 24-hour Holter monitoring and exercise tests. We analyzed the 24-hour Holter recordings with customized software that computes the correlation between heart rate and occurrence of PVBs. We also computed spectral measures of heart rate variability on the same recordings. Propranolol caused a significant decrease in the log-transformed total number of PVBs recorded over 24 hours and during the day. The number of PVBs was much lower during the night than during the day both after placebo and after propranolol. There were no differences between the two treatments. During the day, there was a positive correlation between heart rate and the number of PVBs in all 18 patients. The mean correlation coefficients between heart rate and number of PVBs increased significantly after propranolol treatment both during the 24-hour monitoring (p < 0.05) and during the day (p < 0.05). The night-recorded correlation coefficients between heart rate and number of PVBs were not significantly different in the placebo versus propranolol group. Propranolol significantly increased the total power during the day. Placebo caused a significant decrease in the low-frequency band (LF) and a significant increase in the high-frequency band (HF) during the night compared with the day. During the day, propranolol significantly reduced LF power and increased HF power, with respect to placebo. After propranolol treatment, the values of LF and HF power during the day were comparable to those recorded at night. The LF/HF ratio decreased significantly after propranolol treatment with respect to placebo in the day and became similar to that recorded during sleep. Propranolol significantly reduced heart rate and systolic blood pressure at rest and at peak exercise and reduced signs of myocardial ischemia. Propranolol administration reduces PVBs in patients with coronary artery disease and severe ventricular arrhythmias possibly through an improvement of cardiac autonomic regulation and through anti-ischemic effects, antiarrhythmic effects, or both.     

Premature ventricular beats in the athlete: management considerations

Introduction: Premature ventricular beats (PVBs) in competitive athletes are incidentally found during pre-participation ECG screening. Their clinical significance remains debatable with several studies suggesting they are a benign reflection of athlete’s heart, and others proposing they may indicate underlying structural heart disease and heightened risk for sudden cardiac death (SCD).

Areas covered: Effective management of athletes with PVBs may best be accomplished using an algorithmic approach for risk stratification with a goal of differentiating benign PVBs from those reflective of underlying cardiomyopathies. Current AHA/ACC consensus recommendations provide a platform for determining optimal medical and invasive therapeutic strategies for symptom control and management of long-term complications without erroneously restricting an athlete’s ability to play. Utilizing a shared decision-making model is an optimal method for managing expectations and guiding exercise recommendations.

Expert commentary: Though pre-participation ECG screening as the standard of care for competitive athletes remains controversial in the United States, a 12-lead ECG is often the first indication of underlying structural heart disease in athletes with PVBs and can therefore identify athletes at greater risk of SCD. Advancements in non-invasive imaging continue to improve in diagnostic potential and prognostication. Invasive therapies provide a curative strategy for refractory PVBs and PVB-induced cardiomyopathy.