Multiform Premature Ventricular Complexes Research Articles

Elevated premature ventricular complex counts on 24-hour electrocardiogram predict incident atrial fibrillation and heart failure-A prospective population-based cohort study.

BackgroundPremature ventricular complexes (PVCs) are known to predict heart failure (HF) and premature atrial contractions (PACs) are known to predict atrial fibrillation (AF) and stroke. PVCs and PACs share pathophysiological mechanisms; however, the combined effects of PVCs and PACs on HF, AF, and stroke risk have not been studied.ObjectivesTo study elevated PVC counts on 24-hour electrocardiogram monitoring (24hECG) in relation to incidence of AF, HF, and stroke, and whether this effect is altered by PAC frequency.MethodsThe prospective population-based Malmö Diet and Cancer study includes 24hECG registrations in 375 AF- and HF-free subjects (mean age 65 years, 55% women). During 17 years of follow-up there were 28 HF, 89 AF, and 28 stroke events. The hazard ratios (HR) of elevated PVC counts (defined as the top quartile, ≥77/24 hours) vs lower quartiles were assessed using multivariable adjusted Cox regression models.ResultsElevated PVC counts predicted incident AF (HR 1.9, 95% confidence interval [CI] 1.2–3.0) and HF (HR 3.1, 95% CI 1.4–7.0). Results were similar after adjustment for NT-proBNP and PACs. Multiform PVCs were associated with even higher risks (HR 2.8, 95% CI: 1.7–4.6 for AF; HR 5.0, 95% CI 2.2–11.7 for HF), as was the presence of both elevated PACs and PVCs (9% of the population, HR 4.1, 95% CI 2.4–6.8 for AF and HR 4.3, 95% CI 1.7–11.4 for HF). No significant association was found between elevated PVC counts and incident stroke.ConclusionElevated PVC counts predict incident AF and HF, particularly if PVCs are multiform or occur in combination with elevated PAC counts.

Long-term outcome of multiform premature ventricular complexes in structurally normal heart

BackgroundMultiform premature ventricular complexes (PVCs) are common electrocardiographic abnormalities in patients with structurally normal hearts. However, the prognostic value of these complexes remains unclear. This study aimed to clarify the role of PVC polymorphism in predicting adverse outcomes. Methods and resultWe examined the database for 24-hour electrocardiography monitoring between January 1, 2002 and December 31, 2004. We analyzed 3351 individuals with apparently normal hearts. Kaplan–Meier curves and multivariate Cox proportional hazards models were employed to estimate the effect of multiform PVC and uniform PVC on the number of incident adverse events. Average follow-up time was 10±1years. Patients with multiform PVC were older and had a higher prevalence of comorbidities. In multivariate analysis, patients with multiform PVC had an increased incidence of mortality (hazard ratio [HR]: 1.642, 95% confidence interval [CI]: 1.327–2.031), hospitalization (HR: 1.196, 95% CI: 1.059–1.350), cardiovascular hospitalization (HR: 1.289, 95% CI: 1.030–1.613), new-onset heart failure (HF; HR: 1.456, 95% CI: 1.062–1.997), transient ischemic accident (HR: 1.411, 95% CI 1.063–1.873), and new-onset atrial fibrillation (AF; HR: 1.546, 95% CI: 1.058–2.258) compared to the group without PVC. Patients with multiform PVC had a higher rate of mortality (HR: 1.231, 95% CI: 1.033–1.468) and all cause-hospitalization (HR: 1.147, 95% CI: 1.025–1.283) compared with patients with uniform PVC. ConclusionThe presence of multiform PVC was associated with a higher incidence of mortality, hospitalization, transient ischemic attack, new-onset AF, and new-onset HF independent of other clinical risk factors.

The Prognostic Significance of Frequency and Morphology of Premature Ventricular Complexes during Ambulatory Holter Monitoring

Multiform premature ventricular complexes (PVCs) are associated with an adverse prognosis in patients with structural heart disease. Very frequent PVCs are associated with ventricular dysfunction. Our hypothesis is that multiform PVCs confer an adverse prognosis in the general population. We performed a retrospective cohort study of patients ≥18 years old referred to our institution for 24-hour ambulatory Holter monitoring between July 1, 2008 and December 31, 2009. Holters without PVCs or with more frequent ectopy (couplets, triplets, or nonsustained ventricular tachycardia) were excluded. Clinical and adverse event (AE) data ("major adverse cardiovascular event" or new/worsening heart failure) were gathered from chart review. Data was analyzed by PVC frequency (rare, occasional, or frequent) and pattern (uniform or multiform). A total of 222 patients (43% male, mean age: 55 ± 16 years) were evaluated (median follow-up 2.3 years [IQR: 2.0-2.6]). Median frequency was 2 PVCs per hour (IQR: 1-13). Multiform PVCs were noted in 48%. Patients with multiform PVCs were older, and had a higher prevalence of comorbidities. Thirty-nine AE were noted. Patients with an AE were younger, had a higher prevalence of HTN, diabetes, CAD, CHF, and previous MI. The multiform group had a higher incidence of AE (28%) compared to the uniform group (8%) (P < 0.001). Increasing PVC frequency was associated with a higher incidence of AE (8% vs 24% vs 35%, respectively). In Cox regression analyses, the multiform pattern but not frequency predicted AE. Multiform PVCs were associated with a 4-fold increase in AE in patients referred for ambulatory Holter monitoring.

Characteristics of J Wave‐Associated Idiopathic Ventricular Fibrillation: Role of Drugs

A storm of J wave-associated idiopathic ventricular fibrillation (VF) was observed in a 49-year-old man. Multiform premature ventricular complexes initiated the episodes of VF. Intravenous isoproterenol attenuated the J wave and suppressed the VF storm. After the implantation of a cardioverter defibrillator, VF was induced by programmed electrical stimulation at baseline, and it was terminated by a 25-J shock after an unsuccessful 15-J shock. During oral treatment with quinidine sulfate, 600 mg daily, the J wave was attenuated and VF became noninducible by programmed electrical stimulation. VF induced by a shock delivered on the T wave was terminated by a single 10-J shock. Mean F-F interval and dominant frequency of the VF were 162 ms and 6.8 Hz at baseline, and 210 ms and 5.0 Hz during the quinidine sulfate treatment.

Characteristics of Premature Ventricular Complexes as Correlates of Reduced Left Ventricular Systolic Function: Study of the Burden, Duration, Coupling Interval, Morphology and Site of Origin of PVCs

Frequent premature ventricular complexes (PVCs) can cause a decline in left ventricular ejection fraction (LVEF). We investigated whether the site of origin and other PVC characteristics are associated with LVEF. We retrospectively studied 70 consecutive patients (mean age 42 ± 17 years, 40 [57%] female) with no other cause of cardiomyopathy undergoing ablation of PVCs. We analyzed the association of a reduced LVEF, defined by LVEF <50% on echocardiography, with features of PVCs obtained from electrocardiography, 24- or 48-hour Holter monitor and electrophysiology study. Patients with reduced LVEF (n = 17) as compared to normal LVEF (n = 53) had an increased burden of PVCs (29.3 ± 14.6% vs 16.7 ± 13.7%, P = 0.004), higher prevalence of nonsustained ventricular tachycardia (VT) [13 (76%) vs 21 (40%), P = 0.01], longer PVC duration (154.3 ± 22.9 vs 145.6 ± 20.8 ms, P = 0.03) and higher prevalence of multiform PVCs [15 (88%) vs 31 (58%), P = 0.04]. There was no significant difference in prevalence of sustained VT, QRS duration of normally conducted complexes, PVC coupling interval, or delay in PVC intrinsicoid deflection. Patients with fascicular PVCs (n = 5) had higher mean LVEF compared to others (66.2 ± 4.0% vs 53.0 ± 10.0%, P = 0.002). There was no association of LVEF with other PVC foci or with left-bundle versus right-bundle branch block morphologies. The threshold burden of PVCs associated with reduced LVEF was lower for right as compared to left ventricular PVCs. In addition to the PVC burden, other characteristics like a longer PVC duration, presence of nonsustained VT, multiform PVCs and right ventricular PVCs might be associated with cardiomyopathy.

Randomized double‐blind study of intravenous tocainide versus lidocaine for suppression of ventricular arrhythmias after cardiac surgery

To compare the therapeutic efficacy and safety of intravenous tocainide with that of intravenous lidocaine in patients with ventricular arrhythmias after cardiac surgery, 25 patients were randomized to either agent in a double-blind manner. Tocainide was given in 16 patients as a 250 mg bolus followed by a loading infusion of 500 mg over 15 minutes and a maintenance infusion of 33.3 mg/min. Lidocaine was administered in 9 patients as a 100 mg bolus followed by a loading infusion of 60 mg over 15 minutes and a maintenance infusion of 1.4 mg/min. Therapy was continued for 24 hours in initially responding patients. With analysis of 24-h taped electrocardiograms it was found that single premature ventricular complexes (PVCs) were suppressed by tocainide by more than 80% in 94% of patients and by lidocaine in 75% of patients (p = NS). Couplets and ventricular tachycardia events were eliminated in all patients by either drug. Multiform PVCs were abolished in 94% of the patients after tocainide and in 75% after lidocaine (p = NS). Average overall success over the 24 hours with more than 80% suppression of single PVCs and simultaneous elimination of higher forms of arrhythmia was 71% with tocainide and 59% with lidocaine (p = NS). Adverse effects were negligible, with only one patient in the lidocaine group developing diaphoresis without necessitating termination of therapy. Treatment rapidly produced and then maintained blood levels of 4-10 mg/l for tocainide and 1-4 mg/l for lidocaine. We conclude that intravenous tocainide is well tolerated and has comparable efficacy to lidocaine in the acute therapy of postcardiac surgery ventricular arrhythmias.

Multiform ventricular complexes: A transitional arrhythmia form?

This study was undertaken to better characterize the role of multiform premature ventricular complexes in the classification of ventricular arrhythmias based on form and frequency. Twenty impatients with organic heart disease and multiform ventricular complexes underwent continuous electrocardiographic monitoring with full disclosure analysis of the number and morphology of single premature ventricular complexes, of repetitive forms of ≥2 premature ventricular complexes, and of the variability of coupling intervals (≥40 msec). Multiform premature ventricular complexes were of 3 ± 1.4 (mean ± S.D.) different QRS morphologies. Nineteen patients (95%) had repetitive forms of ≥2 premature ventricular complexes; 18 patients (90%) showed variable coupling (125 ± 29 msec). Repetitive forms or variable coupling were present in each (100%) of the 20 patients studied. These data suggest that multiform premature ventricular complexes may be a transitional arrhythmia, since repetitive forms almost always coexist. Variability in coupling, rather than just form and frequency, may be an electrocardiographic characteristic linking single and repetitive forms.

QRS morphology-dependent, concordant frequency distribution of single and repetitive forms of ventricular ectopic activity

We tested the relationship between the frequency of single premature ventricular complexes (PVCs) of specific QRS morphologies and repetitive forms (RF) of ≥ 2 PVCs. Fourteen patients with multiform PVCs and RFs underwent 8-hour, two-channel continuous electrocardiographic monitoring. After a 2-hour baseline, procainamide was administered intravenously at 25 mg/min until PVC suppression or 1000 mg. Multiple regression analysis was used to relate the frequencies of repetitive forms initiated by PVCs of the most frequent QRS morphology (M 1) and the second most frequent QRS morphology (M 2) to the frequency of M 1 and M 2 single PVCs. Parallel changes in the frequency of M 1 RFs and M 1 PVCs occurred in 9 of 14 patients and parallel changes in the frequency of M 2 RFs and M 2 PVCs occurred in 7 of 14 patients (i.e., the relationships were concordant). In two patients, M 1 RFs related to M 2 PVC frequency; in three patients, M 2 RFs related to M 1 PVC frequency (i.e., the relationships were discordant). Thus concordant frequency distributions were present in 16 or 28 (57%) comparisons, while a discordant relationship occurred in only 5 of 28 (18%) comparisons ( p < 0.005). In conclusion, there is frequent concordance in the frequency distribution of single multiform PVCs and of RFs initiated by PVCs of the same QRS morphology during a pharmacologic intervention. This relationship was demonstrable for PVCs of at least one specific QRS morphology in 13 of the 14 patients studied. Concordance was independent of the absolute frequency of the initiating PVC, suggesting one mechanism whereby RF suppression may become independent of total PVC suppression.

Proarrhythmia related to a kinetic and dynamic interaction of mexiletine and theophylline

Mexiletine is a group lb antiarrhythmic agent used to control ventricular dysrhythmias. Drug-mexiletine interactions have been reported,‘-4 including inhibition of caffeine metabolism5 and a report of increased theophylline levels with gastrointestinal symptoms.6 We recently observed a patient with a potentially important mexiletine-theophylline interaction. A 55year-old man with diet-controlled diabetes mellitus, mild hypertension, and a history of smoking, had two acute anterior wall myocardial infarctions in 1971 and two-vessel coronary artery bypass grafting, left ventricular aneurysmectomy, and encircling subendocardial resection in 1980 for drug-resistant, symptomatic ventricular tachycardia (VT). Eight months prior to admission, mild congestive heart failure was noted. One week prior to admission, he had witnessed ventricular fibrillation unassociated with an acute myocardial infarction. The ECG showed sinus rhythm, left atria1 abnormality, old anterolateral myocardial infarction, and nonspecific ST-T wave abnormalities. A multiple gated acquisition scan (MUGA) ejection fraction was 23%. Rhythm monitoring in the Coronary Care Unit (with summaries every 8 hours of recorded memory events) revealed multiform premature ventricular complexes (PVCs) at a frequency of <lO/hr, and couplets or triplets of fewer than 1 event per hour (Fig. 1, upper panel). On electrophysiologic testing, the patient was induced by double extrastimuli into a rapid sustained monomorphic VT (R-R interval = 250 msec) with hypotension and loss of consciousness that required external cardioversion. Procainamide did not prevent reinduction of symptomatic VT. After seven doses of mexiletine (200 mg, thrice daily; level-O.9 H/ml), recurrent episodes of spontanteous nonsustained VT (10 to 29 beats) were noted for the first time (Fig. 1, middle panel). The patient was emotionally labile, and his theophylline level was 31 rg/ml. Stable theophylline dosing of 400 mg, three times daily for 11 days, with levels of 12.5 to 15.3 Kg/ml, had been documented (Table I). The nonsustained VT responded to lidocaine; both mexiletine and theophyl-

Prevalence of ventricular tachycardia in patients with different underlying heart diseases: A study by Holter ECG monitoring

Twenty-four-hour Holter ECGs were recorded in 1089 patients. Ventricular tachycardia (VT) was observed in 184 tapes obtained from 81 patients (73 men and 8 women). Underlying heart diseases were present in 72 patients and no organic heart diseases were found in nine patients. The analysis of continuous 1-hour rhythm strips immediately before VT revealed that, in ischemic heart disease and hypertrophic cardiomyopathy, there was no correlation between the incidence of VT and the number or complexity of premature ventricular complexes (PVCs) within 1 hour before VT. In contrast, frequent or multiform PVCs were often observed during the pre-VT period in the patients with rheumatic heart disease or dilated cardiomyopathy. These findings suggest that the mechanism of VT may be different among the various underlying heart diseases. In addition, the mode of initiation of VT was evaluated. Only few episodes of VT occurred with the prematurity index value smaller than 1.0 or the vulnerability index value greater than 1.1. The correlation between the rate of VT and the preceding sinus rate was not significant, and the correlation between the rate of VT and the coupling interval of VT was weak. These facts suggest that the malignancy of VT, represented by the rate of VT, cannot be predicted by the preceding sinus rate or by the coupling interval of VT.

Complex ventricular arrhythmias in patients with Q wave versus non-Q wave myocardial infarction.

We examined whether or not subsets of patients with complex ventricular arrhythmias after myocardial infarction are at high risk with respect to 1 year mortality after hospital discharge. Based on previous studies showing increased risk for those with non-Q wave infarcts, we hypothesized that complex PVCs (premature ventricular complexes) in this group might be associated with a poorer prognosis than complex PVCs in patients with Q wave infarcts. Seven hundred seventy-seven patients entering our study with acute infarction were followed prospectively for 1 year after undergoing a predischarge 24 hr ambulatory electrocardiographic examination. Patients were classified by electrocardiographic criteria into the following groups: Non-Q wave (n = 191), Q wave anterior (n = 261), and Q wave inferior infarction (n = 325). The following arrhythmias were classified as complex: multiform PVCs, couplets, and ventricular tachycardia. Sixty-two percent of patients with non-Q wave infarcts who did not survive 1 year had complex PVCs, compared with 32% of survivors (p less than .01). No differences were seen in the Q wave subgroup. The survival for patients with Q wave and non-Q wave infarction without complex PVCs were nearly identical at 1 year (93% and 90%), whereas in patients with complex PVCs survival for those with Q wave and non-Q wave infarction was 92% and 76%, respectively (p less than .001). Of those with non-Q wave infarction, only 4% of nonsurvivors were free of any PVCs, as compared with 28% of nonsurvivors in the Q wave group (p less than .02).(ABSTRACT TRUNCATED AT 250 WORDS)

Coupling interval and types of ventricular ectopic activity associated with ventricular runs

Repetitive 10-hour ECG recordings of 289 patients obtained within a year after myocardial infarction were analyzed for the presence of ventricular runs, and their association with various types of ventricular ectopic activity (VEA), average rate of premature ventricular complexes (PVCs), and coupling interval of PVCs initiating the runs. Tapes which contained complex VEA (bigeminy, multiform PVCs, couplets, or runs), early PVCs (coupling interval < 400 msec), or late PVCs (coupling interval > 600 msec) had a substantially higher average PVC rate than those without them. The occurrence of ventricular runs was significantly more likely in tapes having other complex VEA or late PVCs than in those without them, and when tapes were stratified by PVC rates the presence of these dysrhythmias appeared to have an independent predictive value for the occurrence of runs. In contrast, the influence of early PVCs on the occurrence of runs was rather minimal, and this seemed to be related to their common association with the PVC rate. Furthermore, a larger percentage of isolated PVCs had coupling intervals between 400 msec and 600 msec, and most couplets (77%) and runs (67.8%) were initiated by PVCs with coupling intervals in this range. However, the proportion of either short (< 400 msec) or long (> 600 msec) coupling interval PVCs initiating couplets or runs was significantly higher than those with intermediate coupling intervals (between 400 and 600 msec).

Premature ventricular complexes in the absence of identifiable heart disease.

To define the prevalence, frequency and characteristics of premature ventricular complexes (PVCs) in adults free of recognizable heart disease, we performed 24-hour ambulatory electrocardiography on 101 subjects (51 men and 50 women, mean age 48.8 years) in whom physical examination, chest x-ray, ECG, echocardiogram, maximal exercise stress test, right- and left-heart catheterization and coronary arteriography were normal. Thirty-nine subjects had at least 1 PVC/24 hours, but only four had more than 100 PVCs/24 hours and fewer than five had more than five PVCs in any given hour. The probability of having at least 1 PVC/24 hours increased with age (chi square = 11.789, p = 0.019). The number of PVCs/24 hours was also positively associated with age (4 = 0.33, p = 0.001). These was no consistent relationship between the presence or number of PVCs/24 hours and sex, blood pressure, weight, height, body mass index, serum potassium or calcium, cholesterol and triglyceride, hemoglobin, the ingestion of coffee, tea or alcohol, and cigarette smoking. Four subjects had multiform PVCs, two of whom had early PVCs.

Cardiac arrhythmias in end-stage renal disease.

In 16 patients with end-stage renal disease (ESRD), 24-hour electrocardiographic recordings showed an incidence of supraventricular and ventricular arrhythmias similar to that in patients who had had myocardial infarction and in low-risk subjects. Eight patients (50%) with ESRD had supraventricular complexes. This incidence was significantly higher than that after myocardial infarction (P < .001). Fifteen ESRD patients (94%) had premature ventricular complexes (PVCs), including nine (56%) with complex PVCs (multiform PVCs, couplets, or runs). The incidence of PVCs as well as complex PVCs in patients with ESRD was comparable to that of the patients who had had myocardial infarction but was significantly higher than that found in low-risk subjects (P less than .005 for PVCs and P less than .05 for complex PVCs). The high incidence of complex PVCs in patients with ESRD may predispose them to increased cardiovascular death, and further investigation of this finding is indicated.

Stress-induced ventricular arrhythmia after repair of tetralogy of fallot

The combination of ventricular arrhythmias found on routine electrocardiography at rest and elevated right ventricular pressures may be associated with sudden death in patients after repair of tetralogy of Fallot. In this study data were reviewed from 104 patients who underwent treadmill exercise testing with a modified Bruce protocol at a mean age of 13.8 years, an average of 7 years after repair of tetralogy of Fallot. The frequency and form of ventricular arrhythmias as manifested in an electrocardiogram at rest as well as before, during and after treadmill exercise tests were tabulated for each patient. Cardiac catheterizatlon was performed within 1 week of the treadmill test in 82 of the 104 patients and the right ventricular systolic pressure, right ventricular end-diastolic pressure, pulmonary arterial systolic pressure and pulmonary to systemic flow ( Qp Qs ) ratio were compared in patients with and without ventricular arrhythmias. In 15 (14 percent) of the 104 patients, ventricular arrhythmia was evident in the electrocardiogram at rest and in 31 (30 percent) it was induced by treadmill exercise; 5 of the 15 with arrhythmia at rest had no arrhythmia during exercise. Compared with the remaining 73 patients, the 31 patients who had ventricular arrhythmias during treadmill testing (1) were older (16.2 versus 12.8 years, p < 0.01, t test) and were tested at a longer interval after repair of tetralogy of Fallot, (2) had greater right ventricular systolic pressure (52.7 versus 41.3 mm Hg, p < 0.005), (3) had greater right ventricular end-diastolic pressure (8.0 versus 6.1 mm Hg, p < 0.001), and (4) had no difference in pulmonary arterial systolic pressure or Qp Qs ratio. Uniform premature ventricular complexes were found in 28 patients, multiform premature ventricular complexes in two and ventricular tachycardia in one. Patients whose ventricular arrhythmia appeared with exercise had similar hemodynamic findings to-those whose arrhythmia disappeared with exercise. Two patients, each with elevated right ventricular systolic pressure and multiform premature ventricular complexes, had cardiac arrest at home. It is concluded that (1) treadmill exercise testing is a sensitive method for detecting ventricular arrhythmia in patients after repair of tetralogy of Fallot; (2) ventricular arrhythmia during treadmill exercise is related to abnormal hemodynamic status; (3) multiform premature ventricular complexes, couplets or ventricular tachycardia with exercise testing are highly associated with abnormal hemodynamic status and sudden death; (4) suppression of ventricular arrhythmia with exercise is neither the characteristic nor necessarily the benign response in these patients; and (5) ventricular arrhythmia may be a late developing phenomenon and may increase with longer postoperative intervals. Patients after repair of tetralogy of Fallot should be treated for ventricular arrhythmia detected in the electrocardiogram at rest or during treadmill exercise testing.

A myocardial syndrome: With particular reference to the occurrence of sudden death and of premature systoles interrupting antecedent T waves ∗

Eighty cases of a well defined myocardial syndrome, an important feature of which is the interruption of T waves by premature QRS complexes, are reported. Other features of the syndrome include myocardial damage and sudden death, multiform premature ventricular complexes, aberration in the form of ventricular complexes of supraventricular origin, variation in the interval between successive ectopic complexes and the preceding sinus complex and ectopic complexes in runs of two or more. Post-extrasystolic T wave changes are sometimes observed. The R on T phenomenon is by no means uncommon when looked for, and it may be seen in a wide variety of pathologic states involving the heart, such as myocardial infarction, ischemic heart disease, hypertensive heart disease and several distinct myocardiopathies. It may also be seen during cardiac surgery and during diagnostic procedures such as cardiac catheterization, angiocardiography and ventricular puncture. The phenomenon may be suspected clinically when very premature beats are noted on auscultation, and it is frequently found in electrocardiograms recording such arrhythmias as multiform ventricular systoles, ventricular tachycardia, flutter and fibrillation, auricular paroxysmal ftachycardia and auricular fibrillation. The incomplete syndrome without T wave interruption is very common and, frequently, further observation and electrocardiography will reveal the missing features. The syndrome is frequently associated with sudden death and prophylactic administration of quinidine is recommended as a therapeutic measure.