Rasmussen V, Jensen G, Schnohr P, Hansen JF.
Premature ventricular beats in healthy adult subjects 20 to 79 years of age.
Eur Heart J. 1985 Apr;6(4):335-41. doi: 10.1093/oxfordjournals.eurheartj.a061860.
Abstract/Text
111 healthy subjects, 57 males and 54 females, 20-79 years of age, randomly selected among the participants of the Copenhagen City Heart Study were tested for ventricular ectopic activity using ambulatory 24-h ECG recording. One or more premature ventricular beats (PVBs) appeared in 68 subjects (61%), 35 males and 33 females (61% of each group). The prevalence of PVBs increased significantly with age: 31, 68 and 84% in the respective age groups: 20-39, 40-59 and 60-79 (P less than 0.05). The number of PVBs per 24 h was less than 24 in 88 (79%), less than 300 in 105 (95%), and less than 500 in 107 (96%). More than 1000 PVBs per 24 h appeared in 3 (2.7%), one of whom had 11 669. The number of PVBs per 24 h increased with age, but the increase was not statistically significant. The number of PVBs per 100 000 recorded QRS-complexes did not differ significantly from the number of PVBs per 24 h. The number of PVBs h-1 was highest in daytime, and apparently higher in males than in females. However, the difference between the two sexes was not statistically significant. Multiform PVBs appeared in 4 subjects, interpolated PVBs in 2, a run of 5 PVBs in 1, dropped beats in 3, two pauses of 1900 ms duration in 1, and several post-acceleration pauses of 1300 ms duration in 1.
Kennedy HL, Whitlock JA, Sprague MK, Kennedy LJ, Buckingham TA, Goldberg RJ.
Long-term follow-up of asymptomatic healthy subjects with frequent and complex ventricular ectopy.
N Engl J Med. 1985 Jan 24;312(4):193-7. doi: 10.1056/NEJM198501243120401.
Abstract/Text
From 1973 to 1983 we followed 73 asymptomatic healthy subjects who were discovered to have frequent and complex ventricular ectopy. Ventricular ectopy in these subjects was measured by 24-hour ambulatory electrocardiography, which showed a mean frequency of 566 ventricular ectopic beats per hour (range, 78 to 1994), with multiform ventricular ectopic beats in 63 per cent, ventricular couplets in 60 per cent, and ventricular tachycardia in 26 per cent. Asymptomatic healthy status was confirmed by extensive noninvasive cardiologic examination, although cardiac catheterization of a subsample of subjects disclosed serious coronary artery disease in 19 per cent. Follow-up for 3.0 to 9.5 years (mean, 6.5) was accomplished in 70 subjects (96 per cent) and documented one sudden death and one death from cancer. Calculation of a standardized mortality ratio (Monson's U.S. data, 8th revision) for 448 person-years of follow-up indicated that 7.4 deaths were expected, whereas 2 occurred (standardized mortality ratio, 27; P less than 0.05). A comparison of survival of the study cohort with that of persons without coronary artery disease or with mild disease, patients with moderate disease, and men with unrecognized myocardial infarction showed a favorable prognosis for the study cohort over 10 years. We conclude that the long-term prognosis in asymptomatic healthy subjects with frequent and complex ventricular ectopy is similar to that of the healthy U.S. population and suggests no increased risk of death.
Busby MJ, Shefrin EA, Fleg JL.
Prevalence and long-term significance of exercise-induced frequent or repetitive ventricular ectopic beats in apparently healthy volunteers.
J Am Coll Cardiol. 1989 Dec;14(7):1659-65. doi: 10.1016/0735-1097(89)90012-0.
Abstract/Text
Frequent or repetitive exercise-induced ventricular ectopic beats are often considered a marker for serious cardiac disease or sudden death, or both. However, the prognostic value of these arrhythmias in an unreferred asymptomatic community-dwelling population over a broad age range is unknown. Of 1,160 subjects aged 21 to 96 years who underwent maximal exercise treadmill testing an average of 2.4 times, 80 (6.9%) developed frequent (greater than or equal to 10% of beats in any 1 min) or repetitive (greater than or equal to 3 beats in a row) ventricular ectopic beats on at least one test. These 80 individuals were significantly older than the group without such arrhythmia (63.8 +/- 12.5 versus 50.0 +/- 16.1 years, p less than 0.0001). A striking age-related increase in the prevalence of frequent or repetitive exercise-induced ventricular ectopic beats was seen in men (p less than 0.0001) but not in women. The prevalence of electrocardiographic abnormalities at rest, exercise-induced ST segment depression and thallium perfusion defects, duration of treadmill exercise, maximal heart rate, systolic blood pressure and rate-pressure product did not differ between these 80 study subjects with frequent exercise-induced ventricular ectopic beats and a control group matched for age and gender. Furthermore, the incidence of cardiac events (angina pectoris, nonfatal myocardial infarction, cardiac syncope or cardiac death) (10% versus 12.5%) as well as noncardiac mortality (each 7.5%) was found to be similar for the study and control groups, respectively, over a mean follow-up period of 5.6 years. No study subjects required antiarrhythmic drugs over this time interval.(ABSTRACT TRUNCATED AT 250 WORDS)
Fleg JL, Kennedy HL.
Long-term prognostic significance of ambulatory electrocardiographic findings in apparently healthy subjects greater than or equal to 60 years of age.
Am J Cardiol. 1992 Sep 15;70(7):748-51. doi: 10.1016/0002-9149(92)90553-b.
Abstract/Text
To determine the long-term prognostic significance of frequent or complex ectopic beats and ST-segment changes on 24-hour ambulatory electrocardiogram (ECG) in apparently healthy older subjects, 98 volunteers were followed up from the Baltimore Longitudinal Study of Aging who were 60 to 85 years old and free of cardiac disease by history, physical examination and maximal treadmill testing at the time of ambulatory ECG between 1978 and 1980. Over a mean follow-up period of 10 years, coronary events developed in 14 subjects: angina pectoris in 7, nonfatal myocardial infarction in 3 and sudden cardiac death in 4. The incidence of coronary events did not differ significantly between subjects who developed the following arrhythmias and those who did not, respectively: greater than or equal to 30 supraventricular ectopic beats in any hour, 18 vs 13%; greater than or equal to 100 supraventricular ectopic beats in 24 hours, 20 vs 12%; paroxysmal atrial tachycardia, 15 vs 14%; greater than or equal to 30 ventricular ectopic complexes (VECs) in any hour, 17 vs 14%; greater than or equal to 100 VECs in 24 hours, 18 vs 14%; or repetitive VECs, 20 vs 13%. The mean 24-hour heart rate (75 +/- 8 vs 72 +/- 9 beats/min) as well as the maximal (116 +/- 20 vs 111 +/- 18 beats/min) and minimal (51 +/- 6 vs 53 +/- 7 beats/min) heart rate also did not differ between the coronary event and non-event groups.(ABSTRACT TRUNCATED AT 250 WORDS)
日本循環器学会編：循環器病の診断と治療に関するガイドライン（2008年度合同研究班報告） 不整脈薬物治療に関するガイドライン（2009年改訂版）、日本循環器学会、2009年.
Yarlagadda RK, Iwai S, Stein KM, Markowitz SM, Shah BK, Cheung JW, Tan V, Lerman BB, Mittal S.
Reversal of cardiomyopathy in patients with repetitive monomorphic ventricular ectopy originating from the right ventricular outflow tract.
Circulation. 2005 Aug 23;112(8):1092-7. doi: 10.1161/CIRCULATIONAHA.105.546432. Epub 2005 Aug 15.
Abstract/Text
BACKGROUND: Tachycardia-induced cardiomyopathy caused by ventricular tachycardia is a well-defined clinical entity. Less well appreciated is whether simple ventricular ectopy can result in cardiomyopathy. We sought to examine a potential causal relationship between repetitive monomorphic ventricular ectopy originating from the right ventricular outflow tract and cardiomyopathy and the role of ablation in reversing this process.
METHODS AND RESULTS: The study consisted of 27 patients (11 men; age, 47+/-15 years) with repetitive monomorphic ventricular ectopy, including 8 patients (30%) with depressed ventricular function (ejection fraction < or =45%). All patients underwent assessment of cardiac structure and function. The burden of ectopy was quantified through 24-hour Holter monitoring. Patients then underwent ablation guided by 3D mapping. After ablation, patients underwent repeated Holter monitoring and reassessment of cardiac function. Patients with depressed ventricular function were more likely to be older than patients with normal function (58+/-14 versus 42+/-18 years; P=0.013). However, the burden of ventricular ectopy was similar in patients with (17,859+/-13,488 ectopic beats per 24 hours) and without (17,541+/-11,479 ectopic beats per 24 hours; P=0.800) preserved ventricular function. Successful ablation was performed in 23 patients (85%), including 7 of 8 patients with depressed ventricular function. In this latter group, ventricular function improved in all patients (from 39+/-6% to 62+/-6%; P=0.017).
CONCLUSIONS: Repetitive monomorphic ventricular ectopy (in the absence of sustained ventricular tachycardia) originating from the right ventricular outflow tract is an underappreciated cause of unexplained cardiomyopathy. Successful ablation of the focal source of ventricular ectopy results in normalization of left ventricular function. Patients with ectopy-induced cardiomyopathy are significantly older than patients with preserved ventricular function, which suggests either that older patients are more susceptible to the development of a cardiomyopathy or that the cardiomyopathy has had a longer period of time in which to evolve.
Takemoto M, Yoshimura H, Ohba Y, Matsumoto Y, Yamamoto U, Mohri M, Yamamoto H, Origuchi H.
Radiofrequency catheter ablation of premature ventricular complexes from right ventricular outflow tract improves left ventricular dilation and clinical status in patients without structural heart disease.
J Am Coll Cardiol. 2005 Apr 19;45(8):1259-65. doi: 10.1016/j.jacc.2004.12.073.
Abstract/Text
OBJECTIVES: The present study evaluated clinical benefits of radiofrequency catheter ablation (RFA) for premature ventricular complexes from right ventricular outflow tract (RVOT-PVC) in patients without structural heart disease.
BACKGROUND: It is unknown whether PVC causes left ventricular (LV) dilation, which is a well-recognized precursor of LV dysfunction and heart failure, and whether eliminating PVC by RFA produces clinical benefits in patients with RVOT-PVC.
METHODS: Frequency of PVC per total heart beats by 24-h Holter monitoring, left ventricular ejection fraction (LVEF), left ventricular end-diastolic internal dimension (LVDd), mitral regurgitation (MR) by echocardiogram, cardiothoracic ratio (CTR) by chest radiogram, and New York Heart Association (NYHA) functional class of 40 patients with RVOT-PVC without structural heart disease were evaluated before and 6 to 12 months after RFA.
RESULTS: Before RFA, a subgroup of patients with frequent (>20%) PVC demonstrated significantly enlarged LVDd and CTR, reduced LVEF, increased MR, and deteriorated NYHA functional class as compared to the subgroup with rare (<20%) PVC (54 +/- 1 mm vs. 45 +/- 1 mm, 52 +/- 2% vs. 46 +/- 1%, 66 +/- 2% vs. 73 +/- 2%, 1.2 +/- 0.2 degree vs. 0.4 +/- 0.1 degree, and 1.8 +/- 0.2 vs. 1.3 +/- 0.1, respectively; p < 0.05). Furthermore, ablating RVOT-PVC readily produced the improvement of all these abnormalities (47 +/- 1 mm, 41 +/- 1%, 72 +/- 2%, 0.3 +/- 0.1 degree, and 1.0 +/- 0.0, respectively; p < 0.05 compared with before RFA).
CONCLUSIONS: These findings suggest that frequent (>20%) RVOT-PVC may be a possible cause of LV dysfunction and/or heart failure, and RFA produces clinical benefits in these patients.
Bogun F, Crawford T, Reich S, Koelling TM, Armstrong W, Good E, Jongnarangsin K, Marine JE, Chugh A, Pelosi F, Oral H, Morady F.
Radiofrequency ablation of frequent, idiopathic premature ventricular complexes: comparison with a control group without intervention.
Heart Rhythm. 2007 Jul;4(7):863-7. doi: 10.1016/j.hrthm.2007.03.003. Epub 2007 Mar 12.
Abstract/Text
BACKGROUND: Idiopathic premature ventricular complexes (PVCs) usually are considered benign, even when frequent. However, case reports have demonstrated a possible link between frequent PVCs and left ventricular (LV) dysfunction. In addition, frequent PVCs recently were demonstrated to be associated with increased LV dimensions and cardiomyopathy.
METHODS: Among 60 consecutive patients with idiopathic, frequent PVCs (>10/hour), a reduced LV ejection fraction (EF; mean 34% +/- 13%) was present in 22 (37%) patients. Patients with decreased LV function had a greater PVC burden on a 24-hour Holter monitor than patients with normal EF (37% +/- 13% vs. 11% +/- 10% of all QRS complexes; P <.0001). There was a significant inverse correlation between the PVC burden and the EF before ablation (r = 0.73, P <.0001).
RESULTS: The PVCs originated in the right ventricular outflow tract in 31 (52%) of 60 patients, the LV outflow tract in 9 (15%) of 60 patients, and in other sites in 13 (22%) of 60 patients. The site of PVC origin could not be determined in seven patients. Ablation was completely successful in 48 (80%) patients. In patients with an abnormal EF before ablation, LV function normalized in 18 (82%) of 22 patients from a baseline of 34% to 59% +/- 7% (P <.0001) within 6 months. In the four patients in whom ablation was ineffective, the EF further declined from 34% +/- 10% to 25% +/- 7% (P = .06) during follow-up. In a control group of 11 patients with a similar PVC burden (30% +/- 8%) and a reduced EF (28% +/- 13%) who did not undergo ablation, the EF remained unchanged in 10/11 patients over 19 +/- 17 months of follow-up and one patient underwent heart transplantation.
CONCLUSION: LV dysfunction in the setting of frequent, idiopathic PVCs may represent a form of cardiomyopathy that can be reversed by catheter ablation of the PVCs.
Baman TS, Lange DC, Ilg KJ, Gupta SK, Liu TY, Alguire C, Armstrong W, Good E, Chugh A, Jongnarangsin K, Pelosi F Jr, Crawford T, Ebinger M, Oral H, Morady F, Bogun F.
Relationship between burden of premature ventricular complexes and left ventricular function.
Heart Rhythm. 2010 Jul;7(7):865-9. doi: 10.1016/j.hrthm.2010.03.036. Epub 2010 Mar 27.
Abstract/Text
BACKGROUND: Frequent idiopathic premature ventricular complexes (PVCs) can result in a reversible form of left ventricular dysfunction. The factors resulting in impaired left ventricular function are unclear. Whether a critical burden of PVCs can result in cardiomyopathy has not been determined.
OBJECTIVE: The objective of this study was to determine a cutoff PVC burden that can result in PVC-induced cardiomyopathy.
METHODS: In a consecutive group of 174 patients referred for ablation of frequent idiopathic PVCs, the PVC burden was determined by 24-hour Holter monitoring, and transthoracic echocardiograms were used to assess left ventricular function. Receiver-operator characteristic curves were constructed based on the PVC burden and on the presence or absence of reversible left ventricular dysfunction to determine a cutoff PVC burden that is associated with left ventricular dysfunction.
RESULTS: A reduced left ventricular ejection fraction (mean 0.37 +/- 0.10) was present in 57 of 174 patients (33%). Patients with a decreased ejection fraction had a mean PVC burden of 33% +/- 13% as compared with those with normal left ventricular function 13% +/- 12% (P <.0001). A PVC burden of >24% best separated the patient population with impaired as compared with preserved left ventricular function (sensitivity 79%, specificity 78%, area under curve 0.89) The lowest PVC burden resulting in a reversible cardiomyopathy was 10%. In multivariate analysis, PVC burden (hazard ratio 1.12, 95% confidence interval 1.08 to 1.16; P <.01) was independently associated with PVC-induced cardiomyopathy.
CONCLUSION: A PVC burden of >24% was independently associated with PVC-induced cardiomyopathy.
Copyright 2010 Heart Rhythm Society. All rights reserved.
Pitzalis MV, Mastropasqua F, Massari F, Totaro P, Di Maggio M, Rizzon P.
Holter-guided identification of premature ventricular contractions susceptible to suppression by beta-blockers.
Am Heart J. 1996 Mar;131(3):508-15. doi: 10.1016/s0002-8703(96)90529-3.
Abstract/Text
To evaluate whether the identification of the different types of relations between premature ventricular contractions (PVCs) and the preceding sinus cycle length is capable of predicting the effect of beta-blockers on the PVCs themselves, 55 patients (43 men, 12 women, mean age 52.6 +/- 15.6 years) with different cardiac diseases, and >30 PVCs/hr characterized by stability and the same relation at two Holter monitoring periods were studied. The relation was tachycardia enhanced (the shorter the preceding cycle length, the higher the incidence of PVCs) in 23 patients (group 1); indifferent (no correlation between the preceding cycle length and PVC incidence) in 21 (group 2); and bradycardia enhanced (the longer the preceding cycle length, the higher the incidence of PVCs) in 11 (group 3). A third Holter monitoring was performed 6 days after nadolol administration (80 mg/day) to evaluate its effect on the three types of PVCs. Incidence in all patients (-88;p<0.001). In group 2, it caused a reduction in the majority of patients (-60%;p<0.05) but an increase in five. In group 3, it caused a reduction in only half of the patients (-45%) and a 91% increase in the remainder. The difference in the effect of nadolol in the three groups was highly significant (X2=27.5;p<0.0001). The relation between the incidence of PVCs and the preceding cycle length is a useful means of identifying subsets of patients with PVCs who will benefit from beta-blockers.
Morganroth J, Duchin KL.
Effectiveness of low-dose nadolol for ventricular arrhythmias.
Am J Cardiol. 1986 Aug 1;58(3):273-8. doi: 10.1016/0002-9149(86)90061-5.
Abstract/Text
To determine the minimal effective dose of nadolol to suppress frequent ventricular premature complexes (VPCs), 23 patients with at least 30 VPCs/hour on 2 baseline 24-hour Holter recordings were studied. The initial dose of nadolol was 10 mg/day orally, and this dose was doubled at weekly intervals until arrhythmia suppression was achieved, adverse effects appeared, or a maximal dose of 160 mg/day was reached. After each dose level a 24-hour ambulatory Holter monitor was recorded. A pharmacokinetic trial was conducted in patients who responded to nadolol treatment. Frequent VPCs were suppressed at least 75% by nadolol in 11 of 23 patients (48%) and the minimal effective dose was 10 mg/day in 3 patients, 20 mg/day in 4, 40 mg/day in 3 and 80 mg/day in 1 patient. At these doses, minimal steady-state levels of nadolol in serum (Cmin) ranged from 3.9 to 47.0 ng/ml, and these serum concentrations were proportional to the oral dose of nadolol (r = 0.753, p less than 0.001). No relation, however, was observed between Cmin levels and percent reduction of VPCs. Cmin and heart rate changes were comparable between responders and nonresponders, suggesting that the degree of beta blockade was similar between these 2 groups. Adverse reactions were noted in 6 patients, and 2 had an asymptomatic increase in the frequency of VPCs and 1 patient an increase in beats of ventricular tachycardia. This study details the importance of selecting an individualized dose for nadolol for control of ventricular arrhythmias; in more than half of the patients doses of 20 mg/day or less were effective.
Pitzalis MV, Mastropasqua F, Massari F, Totaro P, Scrutinio D, Rizzon P.
Sleep suppression of ventricular arrhythmias: a predictor of beta-blocker efficacy.
Eur Heart J. 1996 Jun;17(6):917-25. doi: 10.1093/oxfordjournals.eurheartj.a014974.
Abstract/Text
It has been reported that the frequency of premature ventricular contractions in some patients tend to decrease during the hours of sleep when modifications in autonomic tone and bradycardia occur. The aim of this study was to evaluate whether the phenomenon of sleep suppression may be a sensitive and specific parameter for predicting the antiarrhythmic effect of beta-blockers on premature ventricular contractions. The presence of sleep suppression was evaluated in 45 patients (mean age 50 +/- 17 years) with frequent premature ventricular contractions at two baseline Holter recordings. Sleep suppression was defined as > 50% reduction in the number of nighttime as opposed to day-time premature ventricular contractions. Three groups of patients were identified: those with sleep suppression at both Holter recordings (group 1); those with sleep suppression at only one Holter recording (group 2); and those without sleep suppression at either Holter recording (group 3). A third Holter was performed 5 days after nadolol administration. In group 1, nadolol led to a mean reduction in the number of premature ventricular contractions of 90% (> 70% in 21/23 patients). In group 2, the mean reduction was 76% (> 70% in three out of six patients). In group 3, there was a mean increase in the number of premature ventricular contractions of 33%. The positive predictive accuracy of sleep suppression in relation to the antiarrhythmic efficacy of nadolol is very high (88%) when sleep suppression is present during two baseline Holter recordings. Sleep suppression is a sensitive parameter for identifying the premature ventricular contractions likely to benefit from beta-blocker administration.
Gill JS, Mehta D, Ward DE, Camm AJ.
Efficacy of flecainide, sotalol, and verapamil in the treatment of right ventricular tachycardia in patients without overt cardiac abnormality.
Br Heart J. 1992 Oct;68(4):392-7. doi: 10.1136/hrt.68.10.392.
Abstract/Text
OBJECTIVE: A comparison of the efficacy of verapamil, sotalol, and flecainide to suppress right ventricular tachycardia (VT) in patients with a clinically normal heart.
DESIGN: Patients underwent treatment serially with verapamil (360 mg daily), sotalol (240 or 320 mg daily), and flecainide (200 or 300 mg daily), (the larger dose was for patients heavier than 80 kg) to suppress tachycardia. Each drug was given orally for five half lives before testing.
PATIENTS: 23 patients with right VT associated with a clinically normal heart were studied.
OUTCOME MEASURES: The effects of drug treatment were examined by the number of ventricular events on 24 hour Holter monitoring, and the ability of tachycardia to be induced by treadmill exercise testing (Bruce protocol) and programmed ventricular stimulation (Wellens protocol), compared with drug free baseline tests.
SETTING: Patients were studied in a tertiary referral centre.
RESULTS: All three drugs suppressed ventricular salvos (> 3, < 5 consecutive ventricular premature contractions) (p < 0.01) and VT (p < 0.05) on Holter monitoring and did not differ statistically in effect. Exercise induced VT was also suppressed by all three drugs (p < 0.01), and of these sotalol was the most effective although this was not statistically significant (14/23 inducible when drug free, 4/23 on flecainide, 2/23 on sotalol, 5/23 on verapamil). Sustained and non-sustained VT induced by programmed stimulation was also suppressed by the three drugs (p < 0.01) and again sotalol was the best of these though the differences did not achieve statistical significance (17/23 inducible when drug free, 4/17 on flecainide, 2/17 on sotalol, and 6/17 on verapamil). Proarrhythmic effects of drugs were found in a few patients. There was no difference in the efficacy of the drugs in patients with histological abnormalities of the myocardium when compared with those of normal histology.
CONCLUSIONS: Ventricular tachycardia associated with a clinically normal heart can be suppressed by flecainide, sotalol, or verapamil. In individual patients sotalol was the most frequently effective drug (effective in > 89% of patients) and is a suitable choice for first line treatment.
Gill JS, Blaszyk K, Ward DE, Camm AJ.
Verapamil for the suppression of idiopathic ventricular tachycardia of left bundle branch block-like morphology.
Am Heart J. 1993 Nov;126(5):1126-33. doi: 10.1016/0002-8703(93)90664-u.
Abstract/Text
This study examines the efficacy of verapamil for the suppression of idiopathic ventricular tachycardia (VT) of left bundle branch block LBBB-like morphology. Forty-two patients (mean age 36.2 +/- 12.1 years; 20 men and 22 women) with VT and without any underlying cardiac abnormality on clinical examination and noninvasive investigation were studied. The inducibility of clinical VT was examined by treadmill exercise testing and programmed ventricular stimulation (PVS). In 29 patients VT was inducible by exercise testing, in 24 by PVS, and in 23 there was evidence of VT on Holter monitoring. After baseline testing, patients were treated with verapamil 120 mg thrice daily for at least 5 half-lives for the drug to load before evaluation. With Holter monitoring, 74% of patients with evidence of VT at baseline testing demonstrated a change of status from nonsustained VT to no VT or from sustained VT to nonsustained VT. Four patients had nonsustained VT during verapamil treatment but no VT at baseline. There was a significant reduction in the number of ventricular ectopic beats over 24 hours (baseline: 15,541 +/- 17,599 vs verapamil treatment: 8892 +/- 15,582, p < 0.01). Exercise-induced VT was suppressed in 56% of patients with VT during baseline testing, but no effect of verapamil on the tachycardia was observed in 26%. The remaining patients demonstrated a partial response to verapamil; the rate of VT was unchanged, although the duration of the runs was reduced. Sustained monomorphic VT was inducible in only 5 patients, of whom 4 were rendered noninducible; 1 patient remained inducible.(ABSTRACT TRUNCATED AT 250 WORDS)
Lee KL, Lauer MR, Young C, Lai WT, Tai YT, Chun H, Liem LB, Sung RJ.
Spectrum of electrophysiologic and electropharmacologic characteristics of verapamil-sensitive ventricular tachycardia in patients without structural heart disease.
Am J Cardiol. 1996 May 1;77(11):967-73. doi: 10.1016/s0002-9149(96)00011-2.
Abstract/Text
Verapamil-sensitive ventricular tachycardia (VT) is a well-recognized clinical entity that some authorities believe may result from triggered activity. Despite its uniform response to verapamil, however, there is evidence that this uncommon form of VT may not be as homogeneous as first believed. Standard intracardiac electrophysiologic techniques were used to study verapamil-sensitive VT in 32 patients (aged 38 years +/- 20 years) without evidence of structural heart disease. More than half of these patients (69%) exhibited VT with a right bundle branch block-type QRS pattern, with the remainder (31%) displaying VT with a left bundle branch block pattern. In 31% of the patients the VT could be induced by fixed-cycle length atrial pacing, whereas in 59% of patients fixed-cycle length ventricular pacing was necessary. A critical range of cycle lengths for VT induction was required in 66% of the patients. Ventricular tachycardia was initiated with single atrial premature extrastimuli in 16% of patients, single ventricular extrastimuli in 50% of patients, and double ventricular premature extrastimuli in 9% of patients. Ventricular tachycardia displaying cycle-length alternans was observed in 28% of patients. In only 19% of patients was it possible to entrain VT during pacing from the right ventricular apex. Isoproterenol infusion was required for tachycardia induction in 50% of patients, 44% of whom had VT with a left bundle branch block QRS pattern, with the remaining 56% exhibiting VT with a right bundle branch block pattern. Beta-adrenergic blockers suppressed 53% of verapamil-sensitive VT in patients tested, whereas adenosine terminated VT in 50% of patients, with 81% of these patients exhibiting either a left bundle branch block QRS pattern or isoproterenol dependence. Ventricular tachycardia exhibiting a left bundle branch block pattern was more likely to be isoproterenol dependent (p <0.05) and adenosine sensitive (p <0.001). However, verapamil-sensitive, catecholamine-dependent VT was no more likely to be adenosine sensitive than the catecholamine-independent form of the arrhythmia (p >0.5). Verapamil-sensitive VT exhibits properties expected of both a reentrant and triggered arrhythmia, and it is inconsistently dependent on both exogenous catecholamines for induction and intravenous adenosine for termination. Verapamil-sensitive VT encompasses a heterogeneous group of tachycardias that may result from multiple cellular electrophysiologic mechanisms.
Echt DS, Liebson PR, Mitchell LB, Peters RW, Obias-Manno D, Barker AH, Arensberg D, Baker A, Friedman L, Greene HL.
Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial.
N Engl J Med. 1991 Mar 21;324(12):781-8. doi: 10.1056/NEJM199103213241201.
Abstract/Text
BACKGROUND AND METHODS: In the Cardiac Arrhythmia Suppression Trial, designed to test the hypothesis that suppression of ventricular ectopy after a myocardial infarction reduces the incidence of sudden death, patients in whom ventricular ectopy could be suppressed with encainide, flecainide, or moricizine were randomly assigned to receive either active drug or placebo. The use of encainide and flecainide was discontinued because of excess mortality. We examined the mortality and morbidity after randomization to encainide or flecainide or their respective placebo.
RESULTS: Of 1498 patients, 857 were assigned to receive encainide or its placebo (432 to active drug and 425 to placebo) and 641 were assigned to receive flecainide or its placebo (323 to active drug and 318 to placebo). After a mean follow-up of 10 months, 89 patients had died: 59 of arrhythmia (43 receiving drug vs. 16 receiving placebo; P = 0.0004), 22 of nonarrhythmic cardiac causes (17 receiving drug vs. 5 receiving placebo; P = 0.01), and 8 of noncardiac causes (3 receiving drug vs. 5 receiving placebo). Almost all cardiac deaths not due to arrhythmia were attributed to acute myocardial infarction with shock (11 patients receiving drug and 3 receiving placebo) or to chronic congestive heart failure (4 receiving drug and 2 receiving placebo). There were no differences between the patients receiving active drug and those receiving placebo in the incidence of nonlethal disqualifying ventricular tachycardia, proarrhythmia, syncope, need for a permanent pacemaker, congestive heart failure, recurrent myocardial infarction, angina, or need for coronary-artery bypass grafting or angioplasty.
CONCLUSIONS: There was an excess of deaths due to arrhythmia and deaths due to shock after acute recurrent myocardial infarction in patients treated with encainide or flecainide. Nonlethal events, however, were equally distributed between the active-drug and placebo groups. The mechanisms underlying the excess mortality during treatment with encainide or flecainide remain unknown.
Cardiac Arrhythmia Suppression Trial II Investigators.
Effect of the antiarrhythmic agent moricizine on survival after myocardial infarction.
N Engl J Med. 1992 Jul 23;327(4):227-33. doi: 10.1056/NEJM199207233270403.
Abstract/Text
BACKGROUND: The Cardiac Arrhythmia Suppression Trial (CAST) tested the hypothesis that the suppression of asymptomatic or mildly symptomatic ventricular premature depolarizations in survivors of myocardial infarction would decrease the number of deaths from ventricular arrhythmias and improve overall survival. The second CAST study (CAST-II) tested this hypothesis with a comparison of moricizine and placebo.
METHODS: CAST-II was divided into two blinded, randomized phases: an early, 14-day exposure phase that evaluated the risk of starting treatment with moricizine after myocardial infarction (1325 patients), and a long-term phase that evaluated the effect of moricizine on survival after myocardial infarction in patients whose ventricular premature depolarizations were either adequately suppressed by moricizine (1155 patients) or only partially suppressed (219 patients).
RESULTS: CAST-II was stopped early because the first 14-day period of treatment with moricizine after a myocardial infarction was associated with excess mortality (17 of 665 patients died or had cardiac arrests), as compared with no treatment or placebo (3 of 660 patients died or had cardiac arrests); and estimates of conditional power indicated that it was highly unlikely (less than 8 percent chance) that a survival benefit from moricizine could be observed if the trial were completed. At the completion of the long-term phase, there were 49 deaths or cardiac arrests due to arrhythmias in patients assigned to moricizine, and 42 in patients assigned to placebo (adjusted P = 0.40).
CONCLUSIONS: As with the antiarrhythmic agents used in CAST-I (flecainide and encainide), the use of moricizine in CAST-II to suppress asymptomatic or mildly symptomatic ventricular premature depolarizations to try to reduce mortality after myocardial infarction is not only ineffective but also harmful.
Teo KK, Yusuf S, Furberg CD.
Effects of prophylactic antiarrhythmic drug therapy in acute myocardial infarction. An overview of results from randomized controlled trials.
JAMA. 1993 Oct 6;270(13):1589-95.
Abstract/Text
OBJECTIVE: To investigate the effects of prophylactic therapy with antiarrhythmic agents on mortality in patients with myocardial infarction.
DATA SOURCES AND STUDY SELECTION: Data were obtained from all completed, published or unpublished, randomized, parallel controlled trials of antiarrhythmic agents, regardless of sample size. Investigators were contacted for data on patients excluded after randomization.
DATA EXTRACTION: Data on mortality were extracted by one author and confirmed where necessary by the others.
DATA SYNTHESIS: Mortality data from 138 trials on 98,000 patients were combined by the Yusuf-Peto adaptation of the Mantel-Haenszel method. There were 660 deaths among 11,712 patients allocated to receive class I agents and 571 deaths among 11,517 corresponding control patients (51 trials: odds ratio [OR], 1.14; 95% confidence interval [CI], 1.01 to 1.28; P = .03). Of 26,973 patients allocated to receive beta-blockers (class II agents), 1464 died compared with 1727 deaths among 26,295 control patients (55 trials: OR, 0.81; 95% CI, 0.75 to 0.87; P = .00001). Of 778 patients allocated to receive amiodarone (a class III agent), 77 died compared with 101 deaths in 779 control patients (eight trials: OR, 0.71; 95% CI, 0.51 to 0.97; P = .03). There were 982 deaths in 10,154 patients allocated to receive a class IV agent (calcium channel blockers) and 949 deaths in 10,188 control patients (24 trials: OR, 1.04; 95% CI, 0.95 to 1.14; P = .41).
CONCLUSIONS: The routine use of class I antiarrhythmic agents after myocardial infarction is associated with increased mortality. beta-Blockers have been conclusively demonstrated to reduce mortality. The limited data on amiodarone appear promising. Data on calcium channel blockers remain unpromising.
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Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure (MERIT-HF).
Lancet. 1999 Jun 12;353(9169):2001-7.
Abstract/Text
BACKGROUND: Metoprolol can improve haemodynamics in chronic heart failure, but survival benefit has not been proven. We investigated whether metoprolol controlled release/extended release (CR/XL) once daily, in addition to standard therapy, would lower mortality in patients with decreased ejection fraction and symptoms of heart failure.
METHODS: We enrolled 3991 patients with chronic heart failure in New York Heart Association (NYHA) functional class II-IV and with ejection fraction of 0.40 or less, stabilised with optimum standard therapy, in a double-blind randomised controlled study. Randomisation was preceded by a 2-week single-blind placebo run-in period. 1990 patients were randomly assigned metoprolol CR/XL 12.5 mg (NYHA III-IV) or 25.0 mg once daily (NYHA II) and 2001 were assigned placebo. The target dose was 200 mg once daily and doses were up-titrated over 8 weeks. Our primary endpoint was all-cause mortality, analysed by intention to treat.
FINDINGS: The study was stopped early on the recommendation of the independent safety committee. Mean follow-up time was 1 year. All-cause mortality was lower in the metoprolol CR/XL group than in the placebo group (145 [7.2%, per patient-year of follow-up]) vs 217 deaths [11.0%], relative risk 0.66 [95% CI 0.53-0.81]; p=0.00009 or adjusted for interim analyses p=0.0062). There were fewer sudden deaths in the metoprolol CR/XL group than in the placebo group (79 vs 132, 0.59 [0.45-0.78]; p=0.0002) and deaths from worsening heart failure (30 vs 58, 0.51 [0.33-0.79]; p=0.0023).
INTERPRETATION: Metoprolol CR/XL once daily in addition to optimum standard therapy improved survival. The drug was well tolerated.
Freemantle N, Cleland J, Young P, Mason J, Harrison J.
beta Blockade after myocardial infarction: systematic review and meta regression analysis.
BMJ. 1999 Jun 26;318(7200):1730-7. doi: 10.1136/bmj.318.7200.1730.
Abstract/Text
OBJECTIVES: To assess the effectiveness of beta blockers in short term treatment for acute myocardial infarction and in longer term secondary prevention; to examine predictive factors that may influence outcome and therefore choice of drug; and to examine the clinical importance of the results in the light of current treatment.
DESIGN: Systematic review of randomised controlled trials.
SETTING: Randomised controlled trials.
SUBJECTS: Patients with acute or past myocardial infarction.
INTERVENTION: beta Blockers compared with control.
MAIN OUTCOME MEASURES: All cause mortality and non-fatal reinfarction.
RESULTS: Overall, 5477 of 54 234 patients (10.1%) randomised to beta blockers or control died. We identified a 23% reduction in the odds of death in long term trials (95% confidence interval 15% to 31%), but only a 4% reduction in the odds of death in short term trials (-8% to 15%). Meta regression in long term trials did not identify a significant reduction in effectiveness in drugs with cardioselectivity but did identify a near significant trend towards decreased benefit in drugs with intrinsic sympathomimetic activity. Most evidence is available for propranolol, timolol, and metoprolol. In long term trials, the number needed to treat for 2 years to avoid a death is 42, which compares favourably with other treatments for patients with acute or past myocardial infarction.
CONCLUSIONS: beta Blockers are effective in long term secondary prevention after myocardial infarction, but they are underused in such cases and lead to avoidable mortality and morbidity.
Brophy JM, Joseph L, Rouleau JL.
Beta-blockers in congestive heart failure. A Bayesian meta-analysis.
Ann Intern Med. 2001 Apr 3;134(7):550-60. doi: 10.7326/0003-4819-134-7-200104030-00008.
Abstract/Text
PURPOSE: Congestive heart failure is an important cause of patient morbidity and mortality. Although several randomized clinical trials have compared beta-blockers with placebo for treatment of congestive heart failure, a meta-analysis quantifying the effect on mortality and morbidity has not been performed recently.
DATA SOURCES: The MEDLINE, Cochrane, and Web of Science electronic databases were searched from 1966 to July 2000. References were also identified from bibliographies of pertinent articles.
STUDY SELECTION: All randomized clinical trials of beta-blockers versus placebo in chronic stable congestive heart failure were included.
DATA EXTRACTION: A specified protocol was followed to extract data on patient characteristics, beta-blocker used, overall mortality, hospitalizations for congestive heart failure, and study quality.
DATA SYNTHESIS: A hierarchical random-effects model was used to synthesize the results. A total of 22 trials involving 10 135 patients were identified. There were 624 deaths among 4862 patients randomly assigned to placebo and 444 deaths among 5273 patients assigned to beta-blocker therapy. In these groups, 754 and 540 patients, respectively, required hospitalization for congestive heart failure. The probability that beta-blocker therapy reduced total mortality and hospitalizations for congestive heart failure was almost 100%. The best estimates of these advantages are 3.8 lives saved and 4 fewer hospitalizations per 100 patients treated in the first year after therapy. The probability that these benefits are clinically significant (>2 lives saved or >2 fewer hospitalizations per 100 patients treated) is 99%. Both selective and nonselective agents produced these salutary effects. The results are robust to any reasonable publication bias.
CONCLUSIONS: beta-Blocker therapy is associated with clinically meaningful reductions in mortality and morbidity in patients with stable congestive heart failure and should be routinely offered to all patients similar to those included in trials.
Burkart F, Pfisterer M, Kiowski W, Follath F, Burckhardt D.
Effect of antiarrhythmic therapy on mortality in survivors of myocardial infarction with asymptomatic complex ventricular arrhythmias: Basel Antiarrhythmic Study of Infarct Survival (BASIS).
J Am Coll Cardiol. 1990 Dec;16(7):1711-8. doi: 10.1016/0735-1097(90)90324-i.
Abstract/Text
In view of the high risk of sudden cardiac death and the prognostic importance of complex ventricular ectopic activity, the effects of prophylactic antiarrhythmic treatment were investigated prospectively in patients with persisting asymptomatic complex arrhythmias after myocardial infarction. End points were total mortality and arrhythmic events (sudden death, sustained ventricular tachycardia and ventricular fibrillation). Of 1,220 consecutively screened survivors of myocardial infarction, 312 had Lown class 3 or 4b arrhythmia on 24 h electrocardiographic recordings before hospital discharge and consented to the study. They were randomized to individualized antiarrhythmic treatment (Group 1, n = 100), treatment with low dose amiodarone, 200 mg/day (Group 2, n = 98) or no antiarrhythmic therapy (Group 3 [control group], n = 114). During the 1 year follow-up period, 10 patients in Group 1 died, as did 5 in Group 2 and 15 in Group 3. On the basis of an intention to treat analysis, the probability of survival of patients given amiodarone was significantly greater than that of control patients (p less than 0.05). In addition, arrhythmic events were significantly reduced by amiodarone (p less than 0.01). These effects were less marked and not significant for individually treated patients (Group 1). These findings suggest that low dose amiodarone decreases mortality in the 1st year after myocardial infarction in patients at high risk of sudden death.
Singh SN, Fletcher RD, Fisher SG, Singh BN, Lewis HD, Deedwania PC, Massie BM, Colling C, Lazzeri D.
Amiodarone in patients with congestive heart failure and asymptomatic ventricular arrhythmia. Survival Trial of Antiarrhythmic Therapy in Congestive Heart Failure.
N Engl J Med. 1995 Jul 13;333(2):77-82. doi: 10.1056/NEJM199507133330201.
Abstract/Text
BACKGROUND: Asymptomatic ventricular arrhythmias in patients with congestive heart failure are associated with increased rates of overall mortality and sudden death. Amiodarone is now used widely to prevent ventricular tachycardia and fibrillation. We conducted a trial to determine whether amiodarone can reduce overall mortality in patients with congestive heart failure and asymptomatic ventricular arrhythmias.
METHODS: We used a double-blind, placebo-controlled protocol in which 674 patients with symptoms of congestive heart failure, cardiac enlargement, 10 or more premature ventricular contractions per hour, and a left ventricular ejection fraction of 40 percent or less were randomly assigned to receive amiodarone (336 patients) or placebo (338 patients). The primary end point was overall mortality, and the median follow-up was 45 months (range, 0 to 54).
RESULTS: There was no significant difference in overall mortality between the two treatment groups (P = 0.6). The two-year actuarial survival rate was 69.4 percent (95 percent confidence interval, 64.2 to 74.6) for the patients in the amiodarone group and 70.8 percent (95 percent confidence interval, 65.7 to 75.9) for those in the placebo group. At two years, the rate of sudden death was 15 percent in the amiodarone group and 19 percent in the placebo group (P = 0.43). There was a trend toward a reduction in overall mortality among the patients with nonischemic cardiomyopathy who received amiodarone (P = 0.07). Amiodarone was significantly more effective in suppressing ventricular arrhythmias and increased the left ventricular ejection fraction by 42 percent at two years.
CONCLUSIONS: Although amiodarone was effective in suppressing ventricular arrhythmias and improving ventricular function, it did not reduce the incidence of sudden death or prolong survival among patients with heart failure, except for a trend toward reduced mortality among those with nonischemic cardiomyopathy.
Julian DG, Camm AJ, Frangin G, Janse MJ, Munoz A, Schwartz PJ, Simon P.
Randomised trial of effect of amiodarone on mortality in patients with left-ventricular dysfunction after recent myocardial infarction: EMIAT. European Myocardial Infarct Amiodarone Trial Investigators.
Lancet. 1997 Mar 8;349(9053):667-74. doi: 10.1016/s0140-6736(96)09145-3.
Abstract/Text
BACKGROUND: Ventricular arrhythmias are a major cause of death after myocardial infarction, especially in patients with poor left-ventricular function. Previous attempts to identify and suppress arrhythmias with various antiarrhythmic drugs failed to reduce or actually increase mortality. Amiodarone is a powerful antiarrhythmic drug with several potentially beneficial actions, and has shown benefit in several small-scale studies. We postulated that this drug might reduce mortality in patients at high risk of death after myocardial infarction because of impaired ventricular function, irrespective of whether they had ventricular arrhythmias.
METHODS: The European Myocardial Infarct Amiodarone Trial (EMIAT) was a randomised double-blind placebo-controlled trial to assess whether amiodarone reduced all-cause mortality (primary endpoint) and cardiac mortality and arrhythmic death (secondary endpoints) in survivors of myocardial infarction with a left-ventricular ejection fraction (LVEF) of 40% or less. Intention-to-treat and on-treatment analyses were done.
FINDINGS: EMIAT enrolled 1486 patients (743 in the amiodarone group, 743 in the placebo group). Median follow-up was 21 months. All-cause mortality (103 deaths in the amiodarone group, 102 in the placebo group) and cardiac mortality did not differ between the two groups. However, in the amiodarone group, there was a 35% risk reduction (95% CI 0-58, p = 0.05) in arrhythmic deaths.
INTERPRETATION: Our findings do not support the systematic prophylactic use of amiodarone in all patients with depressed left-ventricular function after myocardial infarction. However, the lack of proarrhythmia and the reduction in arrhythmic death support the use of amiodarone in patients for whom antiarrhythmic therapy is indicated.
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Effect of prophylactic amiodarone on mortality after acute myocardial infarction and in congestive heart failure: meta-analysis of individual data from 6500 patients in randomised trials. Amiodarone Trials Meta-Analysis Investigators.
Lancet. 1997 Nov 15;350(9089):1417-24.
Abstract/Text
BACKGROUND: There have been 13 randomised controlled trials of prophylactic amiodarone in patients with recent myocardial infarction (MI) or congestive heart failure (CHF). None of these was powered to detect a mortality reduction of about 20%. We undertook a meta-analysis, based on data from individual patients, to provide a more sensitive and accurate assessment of the benefits and risks of prophylactic amiodarone.
METHODS: Individual data from the studies were abstracted according to a predefined protocol. The summary odds ratios were calculated according to standard methods.
FINDINGS: There were eight post-MI and five CHF trials; nine trials were double-blind and placebo-controlled, and four compared amiodarone with usual care. 6553 patients were randomly assigned treatment, of which 78% were in post-MI trials and 22% in CHF trials. 89% had had previous MI. The mean left-ventricular ejection fraction was 31%, and median frequency of ventricular premature depolarisation 18 per h. Total mortality was reduced by 13% (odds ratio 0.87 [95% CI 0.78-0.99], p = 0.030) based on classic fixed-effects meta-analysis and by 15% (0.85 [0.71-1.02], p = 0.081) with the more conservative random-effects approach. Arrhythmic/sudden death was reduced by 29% (0.71 [0.59-0.85], p = 0.0003). There was no effect on non-arrhythmic deaths (1.02 [0.87-1.19], p = 0.84). There was no difference in treatment effect between post-MI and CHF studies. The risk of arrhythmic/sudden death in control-group patients was higher in CHF than in post-MI studies (10.7 vs 4.1%), and the best single predictor of risk of arrhythmic/sudden death among all patients was symptomatic CHF. The excess (amiodarone minus control) risk of pulmonary toxicity was 1% per year.
INTERPRETATION: Prophylactic amiodarone reduces the rate of arrhythmic/sudden death in high-risk patients with recent MI or CHF and this effect results in an overall reduction of 13% in total mortality.
Morady F, Kadish AH, DiCarlo L, Kou WH, Winston S, deBuitlier M, Calkins H, Rosenheck S, Sousa J.
Long-term results of catheter ablation of idiopathic right ventricular tachycardia.
Circulation. 1990 Dec;82(6):2093-9. doi: 10.1161/01.cir.82.6.2093.
Abstract/Text
Ten consecutive patients with recurrent episodes of symptomatic, idiopathic, sustained monomorphic ventricular tachycardia (VT) originating in the right ventricle underwent an attempt at catheter ablation of the ventricular tachycardia. There were seven women and three men, with a mean age of 39 +/- 14 years (+/- SD). None of the patients had any evidence of structural heart disease. The VT had a left bundle branch block configuration and an inferior axis in each patient, and the mean cycle length was 313 +/- 75 msec. Based on the methods of induction of the VT and the response of the VT to verapamil, the VT mechanism was presumed to be reentry in six patients, triggered activity in three patients, and catecholamine-sensitive automaticity in one patient. Sites for ablation were guided by pace mapping, and an appropriate target site was identified in the right ventricular outflow tract in each patient. From one to three shocks of 100-360 J (mean total, 336 +/- 195 J) were delivered from a defibrillator between the tip of the ablation catheter (cathode) and a patch electrode on the anterior chest (anode). An electrophysiology test 7-9 days after ablation demonstrated that VT was still inducible in only one patient, who was treated with amiodarone. One other patient had a recurrence of VT 3 weeks after ablation and was treated with verapamil. Eight of 10 patients were not treated with antiarrhythmic medications and have had no episodes of symptomatic VT during 15-68 months of follow-up (mean follow-up, 33 +/- 18 months). There were no acute or long-term complications.(ABSTRACT TRUNCATED AT 250 WORDS)
European Heart Rhythm Association; Heart Rhythm Society; Zipes DP, Camm AJ, Borggrefe M, Buxton AE, Chaitman B, Fromer M, Gregoratos G, Klein G, Moss AJ, Myerburg RJ, Priori SG, Quinones MA, Roden DM, Silka MJ, Tracy C, Smith SC Jr, Jacobs AK, Adams CD, Antman EM, Anderson JL, Hunt SA, Halperin JL, Nishimura R, Ornato JP, Page RL, Riegel B, Priori SG, Blanc JJ, Budaj A, Camm AJ, Dean V, Deckers JW, Despres C, Dickstein K, Lekakis J, McGregor K, Metra M, Morais J, Osterspey A, Tamargo JL, Zamorano JL; American College of Cardiology; American Heart Association Task Force; European Society of Cardiology Committee for Practice Guidelines.
ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death).
J Am Coll Cardiol. 2006 Sep 5;48(5):e247-346. doi: 10.1016/j.jacc.2006.07.010.
Abstract/Text
Tanaka Y, Tada H, Ito S, Naito S, Higuchi K, Kumagai K, Hachiya H, Hirao K, Oshima S, Taniguchi K, Aonuma K, Isobe M.
Gender and age differences in candidates for radiofrequency catheter ablation of idiopathic ventricular arrhythmias.
Circ J. 2011;75(7):1585-91. doi: 10.1253/circj.cj-10-0941. Epub 2011 May 12.
Abstract/Text
BACKGROUND: The prevalence, gender- and age-related differences, ablation success rate and inter-relationship between the origins of the idiopathic ventricular arrhythmias (I-VA) have not been clarified.
METHODS AND RESULTS: A total of 625 consecutive patients with symptomatic, drug resistant I-VA (315 males and 310 females; mean age, 54 ± 17 years; 218 ventricular tachycardias, 407 premature ventricular contractions) who underwent catheter ablation were studied. The patients were divided into 5 groups based on the VA origin: (1) outflow tract (OT)-VA, consisting of right ventricular (RV) OT-VA and left ventricular (LV) OT-VA; (2) inflow tract (IT)-VA, consisting of tricuspid annulus (TA)-free wall (FW)-VA, IT-septum-VA, and mitral (MA)-FW-VA; (3) LV-inferoseptum-VA; (4) LV-other-VA; and (5) RV-other-VA. RVOT-VA in women were 1.5 times more frequent than in men, while LVOT-VA were more frequent in men. The prevalence of LVOT origin I-VA increased with age compared to that for the RVOT. The mean age of MA-FW-VA patients (62 ± 14 years) was higher than that of TA-FW-VA patients (51 ± 18 years; P = 0.03). The ablation success rate for RVOT-VA (88%) was higher than that for LVOT-VA (58%; P<0.0001). A multivariate analysis revealed that the patient age was one of the valuable predictors of a successful ablation (odds ratio=0.97; 95% confidence interval: 0.95-0.99; P=0.007).
CONCLUSIONS: Distinct gender and age differences were found in the incidence of I-VA according to their site of origin.
日本循環器学会他編：日本循環器学会/日本不整脈心電学会合同ガイドライン 不整脈非薬物治療ガイドライン（2018年改訂版） https://www.j-circ.or.jp/cms/wp-content/uploads/2018/07/JCS2018_kurita_nogami191120.pdf（2020年3月閲覧） 班長：栗田隆志、野上昭彦、p.104 表72.
