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PubMed2006

[Echocardiography and tissue Doppler imaging in assessment of haemodynamics in patients with idiopathic, premature ventricular complexes].

UNLABELLED: Premature ventricular complexes (PVC) in patients without organic heart disease may be associated with severe symptoms and haemodynamic disturbances. The aim of this study was to evaluate haemodynamics during PVC by echocardiography (ECHO) and tissue Doppler imaging (TDI). MATERIAL AND METHODS: 40 consecutive patients (mean age 55 +/- 15) with frequent, idiopathic PVC were included into analysis. Patients were included if they had at least 2500 PVC on 24 - hour Holter monitoring (mean: 12124 +/- 6851, range: 2560 - 28677). Parameters of blood flow at the inflow and outflow tracts of the right and left ventricle (LV) as well as TDI of mitral annulus were recorded during sinus rhythm (S), PVC and sinus rhythm following PVC (post-PVC). RESULTS: LV stroke volume (SV) in PVC correlated with PVC coupling interval (r = 0.65, p < 0.01). The absence of SV was observed in PVC with coupling interval below 400 ms. Significant differences in SV and duration of cardiac cycle periods between PVC, S and post-PVC were found. Peak systolic velocity (Sm) derived from TDI in PVC was significantly decreased (4.08 +/- 2.04 cm/s) compared to Sm in S (9.35 +/- 1.26 cm/s) and in post-PVC (9.58 +/- 1.26 cm/s) in all studied patients (p < 0.0001). CONCLUSIONS: In patients with frequent, symptomatic, idiopathic PVC severe haemodynamic disturbances may be recorded by ECHO. Dysfunction of LV systolic movement is revealed by TDI.

Adult↗
PubMed1994

Effects of diltiazem, metoprolol, enalapril and hydrochlorothiazide on frequency of ventricular premature complexes.

Ventricular arrhythmias occur frequently in patients with hypertensive left ventricular (LV) hypertrophy and have been associated with increased incidence of sudden death. In this study, the effect of various antihypertensive medications on ventricular arrhythmias was evaluated in 31 hypertensive patients with moderate to severe LV hypertrophy. Patients were assessed at baseline (after 3 weeks of placebo treatment) and after treatment with each of 4 monotherapies: diltiazem 120 or 240 mg/day, metoprolol 100 or 200 mg/day, enalapril 10 or 20 mg/day and hydrochlorothiazide 50 or 100 mg/day. Each drug therapy was administered for 4 weeks. The sequence of each treatment was determined at random. Echocardiographic measurements and electrocardiograms were obtained only at baseline. Biochemical measurements and 48-hour Holter monitoring were obtained at baseline and at the end of each treatment. All treatments resulted in a significant but similar decrease in blood pressure. In the group as a whole diltiazem decreased ventricular premature complexes (VPCs) by 65% (p < 0.05) and metoprolol by 52% (p = 0.07). Enalapril and hydrochlorothiazide had no effect. In 12 patients with > or = 5 VPCs/hour at baseline, diltiazem and metoprolol decreased VPCs by 66% (p < 0.05). It is concluded that in hypertensive patients with moderate to severe LV hypertrophy, both diltiazem and metoprolol significantly reduce VPCs.

Analysis of Variance↗
PubMed1981

Ventricular premature complexes and sudden death after myocardial infarction.

Among 1739 male survivors of myocardial infarction, mortality over 5 years was examined in relation to presence of complex ventricular premature complexes (R on T, runs of two or more, multiform or bigeminal complexes) identified during 1 hour of monitoring. Such arrhythmia was associated with excess risk of death over the entire period. Men with R on T or runs during the hour show a 5-year sudden coronary death rate of 25%, compared with 6% of men free of premature complexes. Men with complex ventricular premature complexes are also at relatively higher risk for nonsudden cardiac death than the other men (5-year mortality 15% and 7%, respectively), but no additional disadvantage was associated with the presence of R on T or runs. Multivariate survival analyses, controlling simultaneously for other important clinical factors, identify complex ventricular premature complexes as the strongest influence on risk of sudden coronary death and congestive heart failure as the strongest influence on risk of other cardiac death.

Actuarial Analysis↗
PubMed1992

Functional significance of premature ventricular complex morphology evaluated during treadmill exercise stress test in patients with coronary artery disease.

OBJECTIVES: To evaluate the relation between premature ventricular complexes morphology and left ventricular myocardial systolic function in patients with proved coronary artery disease. SETTING: Department of Cardiology at General Hospital. METHODS: From 112 patients (pts) with proved coronary artery disease, thirty-three pts with premature ventricular complexes (PVC) detected during treadmill exercise stress test were selected. Two groups of pts were considered: group I-20 pts with regular contour or with a narrow notching (< 40 ms; type I PVC) and group II-13 patients with wide notching (> 40 ms; type II PVC). In each group the following parameters were studied: ejection fraction, QRS duration, duration of exercise, number of metabolic units and the prevalence of ventricular aneurysm and mitral regurgitation. RESULTS: Statistical significant differences were found between group I and II concerning the mean ejection fraction (59.2% vs 48.6%; p < 0.05). The prevalence of ventricular aneurysm and mitral regurgitation was higher in patients with type II ventricular premature complexes (10% vs 30%). CONCLUSION: Particular characteristics of premature ventricular complexes detected during treadmill exercise stress test, in patients with proved coronary artery disease, suggest the presence of left ventricular myocardial systolic dysfunction.

Coronary Disease↗
PubMed1992

Dynorphin A (1-13) in the brain suppresses epinephrine-induced ventricular premature complexes and ventricular tachyarrhythmias.

The objectives of this study were to test the hypothesis that dynorphin in the central nervous system modulates epinephrine-induced cardiac arrhythmias and that central cholinergic mechanisms are operative in this action of dynorphin. Cardiac arrhythmias were produced by continuous intravenous infusion of epinephrine, in Wistar rats, previously instrumented with catheters in the lateral cerebral ventricle, femoral vein and femoral artery. Epinephrine produced ventricular premature complexes and later the development of fatal ventricular fibrillation. Dynorphin A (1-13), 5 or 20 micrograms (3 or 12 nM) administered into the lateral cerebral ventricle (ICV), significantly (P less than 0.05) increased the threshold for development of cardiac arrhythmias. Dynorphin A (1-13), 20 micrograms, increased the epinephrine dose at the occurrence of ventricular premature beats to 171 +/- 8 (mean +/- 1 S.E.M.) compared to 120 +/- 5 micrograms epinephrine/kg in the control group and increased the dose at the onset of fatal arrhythmias to 186 +/- 8 compared to 141 +/- 10 micrograms epinephrine/kg in the control group. The action of dynorphin was significantly (P less than 0.05) antagonized by the kappa opioid antagonist MR2266. Atropine sulfate, administered ICV or intravenously, produced a dose dependent antagonism of this action of dynorphin A (1-13). This was not due to the peripheral effects of atropine, as atropine methylnitrate, which does not cross the blood brain barrier, did not oppose the effects of dynorphin A (1-13). These data indicate (i) dynorphin A (1-13) increases the threshold for or suppresses the manifestations of epinephrine-induced ventricular arrhythmias, (ii) dynorphin's action on cardiac arrhythmias is mediated through central cholinergic rather than peripheral parasympathetic mechanisms (iii) dynorphin may play a role as an endogenous opioid within the brain that modulates cardiac arrhythmias in circumstances of elevated circulating epinephrine concentration.

Animals↗
PubMed1991

Prevalence, characteristics and significance of ventricular premature complexes and ventricular tachycardia detected by 24-hour continuous electrocardiographic recording in the Cardiac Arrhythmia Suppression Trial. CAST Investigators.

The prevalence, characteristics and significance of ventricular arrhythmias detected by ambulatory electrocardiography were evaluated in 1,498 patients who were randomized to encainide, flecainide or placebo in the Cardiac Arrhythmia Suppression Trial. The mean ventricular premature complex (VPC) frequency at baseline was 133 +/- 257 VPCs/hour. Nonsustained ventricular tachycardia (VT) (rate greater than or equal to 120 beats/min) was present in 22% of patients. Accelerated idioventricular rhythm (rate less than 120 beats/min) occurred in 22% of subjects. There were 63 deaths/resuscitated cardiac arrests in the active treatment (encainide/flecainide) group and 26 in the placebo group. In the treatment group mortality increased with increasing VPC frequency, (p = 0.006), whereas in the placebo group such a relation was not present. Mortality/resuscitated cardiac arrest increased in patients with greater than or equal to 2 VT episodes than in those with less than or equal to 1 episode in the active treatment group (p = 0.04). There was no significant association between VT and mortality/resuscitated cardiac arrest in the placebo group. The presence of accelerated idioventricular rhythm was not associated with increased mortality/resuscitated cardiac arrest in either the active treatment or placebo groups. However, mortality was lower in patients with accelerated idioventricular rhythm rates less than 100 beats/min than in those with rates greater than or equal to 100 beats/min (p = 0.05). Thus, in the Cardiac Arrhythmia Suppression Trial the previously described association between mortality/resuscitated cardiac arrest and ventricular arrhythmias (VPC and VT) were only observed in the active treatment group. In addition, based on the results obtained in this highly selected population, it is suggested that the definition of accelerated idioventricular rhythm should be a rate less than 100 beats/min, and at a rate greater than or equal to 100 beats/min it should be categorized as VT.

Anti-Arrhythmia Agents↗
PubMed1984

The timing of ventricular premature complexes initiating chronic ventricular tachycardia.

Prematurity index (PI), defined as the ratio of the coupling to QT intervals of isolated ventricular premature complexes (VPC) and those initiating ventricular tachycardia (VT) on 24-hour ambulatory ECG recording, was examined in 496 episodes of VT occurring in 122 patients. The PI of VPC initiating VT was less than 1 in only 62 (13%) of the VT episodes and occurred in 14 patients. Although the range of PI was similar for isolated VPC and those initiating VT, for individual patients the PI of VPC initiating VT was significantly longer than the PI of isolated VPC (P less than 0.01). This relationship was not affected by age, sex, presence of absence of heart disease, or drug therapy. The coupling interval of the first VT complex was longer than the first interectopic interval of the VT (VT1-VT2) in 88 (72%) patients; and, the VT1-VT2 interval correlated strongly with the average R-R during VT (r = 0.75), (p less than 0.001). The VT was irregular in 48 patients with 300 episodes of VT. Irregularity of the VT was significantly associated with shorter duration of VT (p less than 0.05). These results show that, for individual patients, the PI of VPC initiating VT tends to be longer than that of isolated VPC, and that the rate of VT is usually predictable from the duration of the first interectopic interval of the VT. These results may have mechanistic implications.

Adolescent↗
PubMed2006

[Idiopathic premature ventricular complexes--catheter ablation as a therapeutic alternative].

UNLABELLED: Frequent isolated ventricular premature complexes (VPCs) in patients without major structural heart disease are generally associated with benign prognosis, however can lead to serious symptoms and also to the development of left ventricular dysfunction. Purpose of this study is to present mapping findings and immediate results of catheter ablation of frequent idiopathic VPCs, and evaluation of long-term clinical outcome and the role of catheter ablation in clinical practice. METHODS: Twenty-seven patients, aged 48 +/- 14 years without major structural heart disease, presenting with frequent VPCs, were investigated electrophysiologically in 28 procedures. Twenty-five patients underwent catheter ablation. RESULTS: In 19 patients, the ectopic focus was found in the right ventricular outflow tract (RVOT) and could be reached from the endocardial approach. In these patients, VPCs were successfully eliminated by the ablation. Comparison of 24-hour Holter ECG recordings showed complete elimination of the target VPCs in all the cases [18,483 +/- 12,790 (2,152-48,820)/17 +/- 10 (3-42) % VPCs before ablation vs. 94 +/- 219 (0-763)/0.01 +/- 0.2 (0-0.7) % VPCs after ablation]. In 5 patients, mapping revealed epicardial localization of the ectopic focus in the OT. Ablation endocardially from the RVOT failed in 2 of the patients, cryoablation epicardially from the venous system was partially successful in 1 patient, and no ablation was attempted in 2 patients. In another 3 patients, ectopic foci were found in other parts of the ventricles and ablation was completely successful in one case. During the 14 +/- 9 (1-34) month follow-up period, full elimination of the target VPCs and elimination or significant reduction of symptoms was achieved in 20 (74%) patients. The procedures were accomplished without complications and with fluoroscopy time of 8,2 +/- 5,9 minutes. CONCLUSION: Catheter ablation of frequent idiopathic VPCs was performed effectively and safely, particularly, if the ectopic focus was localized on the endocardial aspect of the RVOT. Efficacy of catheter ablation ofVPCs arising from the epicardium of ventricular OT or other atypical sites is limited by inaccessibility or proximity to the conduction system. Indication to more aggressive mapping and ablation methods like intrapericardial approach or ablation from inside the venous system should be always critically considered with regard to the symptoms or other clinical risk factors.

Adult↗
PubMed1993

Antiarrhythmic and pharmacokinetic evaluation of intravenous recainam in patients with frequent ventricular premature complexes and unsustained ventricular tachycardia.

The pharmacokinetics, antiarrhythmic activity and safety of intravenously administered recainam were evaluated in 15 men and 3 women. All patients had frequent (> 30/hour) ventricular premature complexes (VPCs) and unsustained ventricular tachycardia. Recainam was administered at a loading dose of 4.5 mg/kg/hour over 40 minutes, followed by a maintenance infusion of 0.9 mg/kg/hour for 23 hours and 20 minutes. Sixteen patients had satisfactory efficacy data. The mean frequency of total VPCs decreased by 92.6% and the mean frequency of runs decreased by 99.9% during the maintenance infusion. Suppressions of > or = 70% of total VPCs and > or = 90% of runs were maintained over the 23-hour, 20-minute maintenance infusion period in 16 of the 18 patients. During the maintenance infusion, hourly group plasma recainam concentrations ranged from mean +/- SD 2.6 +/- 0.7 to 3.4 +/- 0.9 micrograms/ml. Patients were observed for 24 hours after termination of the infusion. Periodic blood samples were obtained during and after termination of the infusion to determine recainam concentration. Urine specimens were collected over scheduled intervals to determine urinary excretion of recainam. A 2-compartment pharmacokinetic model was used to analyze the data. The following pharmacokinetic parameters were obtained: terminal elimination half-life, 5.0 +/- 0.8 hours; systemic clearance, 0.27 +/- 0.08 liter/hour/kg; and central and steady-state volume of distribution, 0.32 +/- 0.11 and 1.4 +/- 0.4 liter/kg, respectively. Adverse experiences were reported in 4 of the 18 patients, possibly drug-related in 2; none was considered severe or required discontinuation of recainam.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Suppressant effects of conventional beta blockers and sotalol on complex and repetitive ventricular premature complexes.

Beta-blocking drugs have been shown to reduce the overall mortality and risk of sudden cardiac death in survivors of acute myocardial infarction. It is not known whether such an effect is mediated by suppression of ventricular premature complexes (VPCs). The circadian rhythmicity of ventricular arrhythmia can also be suppressed by beta-blocking drugs, and this may help reduce the risk of sudden cardiac death during the morning hours. Recent studies have also shown that beta blockers can provide a safe and effective combination with class IA antiarrhythmic agents when arrhythmias cannot be controlled with class IA agents alone. Sotalol, a nonselective beta antagonist, has unique electrophysiologic properties, and several studies have shown it to be more effective than conventional beta blockers in suppressing ventricular arrhythmias. However, direct comparative studies of the suppression of VPCs are lacking. In a recent double-blind, placebo-controlled, parallel study, the antiarrhythmic effects of sotalol and propranolol were compared in 172 patients with greater than 30 VPCs/hour. After the initial 1-week washout and 1-week placebo period, patients were randomly assigned to either 160 mg of sotalol administered twice daily (76 patients) or 40 mg of propranolol administered 3 times daily (91 patients). Those responding to therapy (decreases greater than 75% VPCs) continued to take these doses, but nonresponders were given higher doses, 320 mg of sotalol twice daily or 80 mg of propranolol 3 times daily, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed2001

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.

Autonomic Nervous System↗
PubMed1976

Comparative study of exercise-induced ventricular arrhythmias in normal subjects and patients with documented coronary artery disease.

The incidence, types and patterns of emergence of treadmill exercise induced ventricular arrhythmias were studied in 482 subjects with and without coronary heart disease. All subjects were free of premature ventricular complexes at rest and were classified into groups on the basis of their clinical status. In Group 1A were 141 patients with chest pain and normal coronary arteriograms and in Group IB 144 age-matched subjects free of clinical evidence of heart disease. Group II consisted of 197 patients with chest pain and arteriographically documented coronary artery disease. Patients in Group IA and II exercised to at least 85% of their predicted maximal heart rate or until chest pain occurred. Subjects in Group IB underwent maximal exercise testing. The total incidence of exercise-induced ventricular arrhythmias was 16% in Group IA, 44% in Group IB and 29% in Group II. However, when exercise heart rate at the time of appearance of ventricular arrhythmias was taken into account the incidence of exercise-induced ventricular arrhythmias up to a heart rate of 130/min was 27% in the patients with documented coronary artery disease (Group II) compared with rates of 9 and 6%, respectively, for Groups IA and IB (P less than 0.001). The incidence rates of multifocal ventricular premature complexes, ventricular tachycardia and ventricular premature complexes at a rate of more than 10/min were also significantly greater at submaximal heart rates in the patients with coronary disease. Patients with three vessel coronary artery disease and abnormal left ventricular wall motion had a significantly greater incidence of exercise-induced ventricular arrhythmias. The incidence of exercise-induced ventricular arrhythmias in patients with coronary disease and a positive S-T segment response was not significantly increased.

Adult↗
PubMed1989

[Estimation of myocardial viability in left ventricular regions with akinetic wall motion by postextrasystolic potentiation using list-mode radionuclide ventriculography in an interesting case with silent ischemia and with premature ventricular complexes (quadrigeminy)].

For determining an indication of percutaneous transluminal angioplasty (PTCA), a 73-year-old-man with silent ischemia and with ventricular premature complexes (quadrigeminy) were performed cardiac nuclear studies. This case had 99% stenosis in LCX (#11) and 90% stenosis in RCA (#1), and demonstrated akinetic wall motion in left ventricular (LV) inferior and posterior regions. Exercise-redistribution Tl-201 studies indicated myocardial viability in a portion of the inferior wall but not in the posterior wall. To estimate the potential contractile function in the regions with akinesis, from the list-mode data of radionuclide ventriculography, those of postsinus beats and postextrasystolic beats were separately selected and were analyzed for investigating LV wall motion and LV ejection fraction (EF). With the post-extrasystolic potentiation, LVEF increased from 36% to 45% and the systolic wall motion was augmented in the inferior wall but not in the posterior wall. From these findings we recognized the existence of myocardial viability in a portion of the inferior wall. After PTCA for the RCA lesion, improvements of the myocardial Tl-201 distribution and LV wall motion in the inferior wall were definitely observed and hence LVEF increased by 16% to contribute to an increase in exercise performance. Thus, this case indicates that the postextrasystolic potentiation is useful for determining an indication of PTCA in patients with LV asynergy, demonstrating the myocardial viability and the potential LV function.

Aged↗
PubMed1987

Spontaneous variability in the frequency of ventricular premature complexes over prolonged intervals and implications for antiarrhythmic treatment.

Spontaneous variability in the frequency of premature ventricular complexes (VPCs) during ambulatory electrocardiography was examined over short (2- to 14-day) and long (6- to 12-month) periods in 20 patients. The coefficient of variation of the mean daily VPC frequency was significantly lower in the short-term periods than the long-term periods. The 95% confidence limit for spontaneous variation in mean daily arrhythmia frequencies was estimated with a linear regression method comparing two 1-day electrocardiographic recordings. The relative reduction in VPCs reaching the confidence limit calculated from the short-term periods was 69% at the beginning and 73% at the end of the 6- to 12-month follow-up. Corresponding values for repetitive VPCs were 78% and 77%. In comparing 2 recordings separated by the long interval, the reductions required were 98 to 100% for all VPCs, and even a 100% reduction was not significant for repetitive VPCs. The number of VPCs fell spontaneously below the initial confidence limit in 8 of 20 patients in later assessments. Thus, apparently positive individual responses are achieved in long-term treatment studies if stringent efficacy criteria are not followed. The variability between recordings over short periods remains fairly constant when reassessed after a long interval, even if the frequency of arrhythmias changes over the long interval. This permits application of conventional percentage limits in evaluation of therapeutic effects if the natural extent of the arrhythmias is periodically reassessed.

Anti-Arrhythmia Agents↗
PubMed1989

Cifenline in the short-term treatment of patients with ventricular premature complexes: a double-blind placebo-controlled study.

To study the efficacy and safety of cifenline (cibenzoline), a new antiarrhythmic agent, we enrolled 46 patients with greater than 700 premature ventricular complexes (VPCs)/24 h in an ambulatory electrocardiography study. During an open-label titration phase, 25 patients showed greater than 75% VPC suppression while receiving 130 mg (15 patients) or 160 mg (10 patients) cifenline twice daily. During a double-blind placebo-controlled phase in 23 of these patients, cifenline was more effective than placebo in controlling VPCs (p less than 0.0001) and VPC pairs (p less than 0.025). A small (0.01 s) increase in QRS duration was observed (p less than 0.05) during cifenline treatment. Adverse experiences included gastrointestinal complaints and dizziness as well as two instances of hypotension and one instance of symptomatic ventricular tachycardia. Cifenline appears to be effective and well tolerated in the treatment of VPCs.

Adult↗
PubMed2005

Mean frequency of premature ventricular complexes as predictor of malignant ventricular arrhythmias.

AIM: The aim was to test the hypothesis that mean frequency of premature ventricular complexes (PVCs) correlates with vulnerability to malignant arrhythmias such as ventricular tachycardia and/or ventricular fibrillation (VT/VF). METHODS: Patients with an implantable cardioverter defibrillator (ICD) device for underlying ischemic or non-ischemic cardiac pathology were selected from a database. Availability of total count of single (s) PVCs and runs (r) of PVCs was the only inclusion criterion. Forty-four subjects (6 females and 38 males) aged 18-74 years (mean 547.1 years), were eligible. All had a European Pacemaker Identification Card (EPIC) documenting left ventricular ejection fraction (LVEF). The frequency of recorded episodes of VT and VF was obtained from ICD memory. RESULTS: Among patients with ischemic heart disease (IHD) and those with IHD and an LVEF of less than 30%, the mean frequency of PVCs was significantly higher in those with subsequent episodes of VT/VF compared to those without subsequent episodes (p < 0.05 for sPVCs and rPVCs in both groups). CONCLUSION: Among patients with IHD, mean frequency of PVCs is a useful marker of vulnerability to potentially fatal arrhythmias and may be a useful tool for the risk stratification of patients.

Adult↗
PubMed2002

Concealed ventricular extrasystoles. A family of premature ventricular complexes with high spontaneous variability.

BACKGROUND: The term concealed ventricular extrasystoles defines a phenomenon in which premature beats have a cyclical distribution and manifest after a predictable number of intervening sinus beats. The extent of its spontaneous variability as well as the stability of its orderly distribution, however, have not been defined yet. The aim of this study was to assess whether there is any difference between the variability of concealed ventricular extrasystoles and their allorhythmic patterns. METHODS: The distribution of premature ventricular complexes (PVCs) was evaluated in 39 patients with frequent monomorphic PVCs (> 1000/die) during a baseline 24-hour ambulatory monitoring electrocardiogram. Patients were divided into two groups: group A had evidence of concealed ventricular extrasystoles, while in group B PVCs were randomly distributed. All patients underwent a second ambulatory monitoring electrocardiogram within 30-360 days. RESULTS: The overall number of PVCs did not differ between the groups. Patients of group A showed a very high spontaneous variability (p = 0.006) between the first and the second ambulatory monitoring electrocardiogram, whereas significant differences were not observed among patients of group B. CONCLUSIONS: Concealed ventricular extrasystoles are not casual and transient, but should be regarded as a marker of a "family" of PVCs that have the tendency either to maintain their orderly distribution for long periods or to disappear suddenly.

Adolescent↗
PubMed2000

Relation between spatial distribution of late potentials and location of origin of premature ventricular complexes on body surface map in patients with postinfarction ventricular tachycardia.

We studied the relationship between the spatial distribution of late potentials (LPs) and the origin of premature ventricular complexes (PVCs) using body surface maps in 55 patients with postinfarction sustained ventricular tachycardia (VT). Body surface maps were recorded from 87 leads to construct departure maps during sinus rhythm and signal-averaged ECGs were recorded from 32 unipolar leads to construct a LP map. The root-mean-square values during 40 ms intervals behind the QRS end were computed as LPs. The PVC map was recorded simultaneously in 14 patients presenting PVC with similar morphology to VT during LP detection. The origin of PVC was localized at the site of isopotential minimum when the potential exceeded -0.5 mV during the early QRS period. The LP area and the departure area showed a similar distribution. However, the PVC origin was closer to the site of LP maximum than the departure minimum in 11 (79%) patients, and the spatial correlation between the LP maximum and the PVC origin was good in 12 (86%) patients. LP and PVC mapping from the body surface is feasible and of worth to predict noninvasively the site of origin of ventricular arrhythmias in patients with remote myocardial infarction and sustained VT.

Adult↗