著者: Sana M Al-Khatib, William G Stevenson, Michael J Ackerman, William J Bryant, David J Callans, Anne B Curtis, Barbara J Deal, Timm Dickfeld, Michael E Field, Gregg C Fonarow, Anne M Gillis, Christopher B Granger, Stephen C Hammill, Mark A Hlatky, José A Joglar, G Neal Kay, Daniel D Matlock, Robert J Myerburg, Richard L Page
雑誌名: Circulation. 2018 Sep 25;138(13):e210-e271. doi: 10.1161/CIR.0000000000000548.
Abstract/Text
PMID
29084733 Circulation. 2018 Sep 25;138(13):e210-e271. doi: 10.116･･･
著者: Silvia G Priori, Carina Blomström-Lundqvist, Andrea Mazzanti, Nico Blom, Martin Borggrefe, John Camm, Perry Mark Elliott, Donna Fitzsimons, Robert Hatala, Gerhard Hindricks, Paulus Kirchhof, Keld Kjeldsen, Karl-Heinz Kuck, Antonio Hernandez-Madrid, Nikolaos Nikolaou, Tone M Norekvål, Christian Spaulding, Dirk J Van Veldhuisen
雑誌名: Eur Heart J. 2015 Nov 1;36(41):2793-867. doi: 10.1093/eurheartj/ehv316. Epub 2015 Aug 29.
Abstract/Text
PMID
26320108 Eur Heart J. 2015 Nov 1;36(41):2793-867. doi: 10.1093/e･･･
著者: Benjamin M Scirica, Eugene Braunwald, Luiz Belardinelli, Chester M Hedgepeth, Jindrich Spinar, Whedy Wang, Jie Qin, Ewa Karwatowska-Prokopczuk, Freek W A Verheugt, David A Morrow
雑誌名: Circulation. 2010 Aug 3;122(5):455-62. doi: 10.1161/CIRCULATIONAHA.110.937136. Epub 2010 Jul 19.
Abstract/Text
BACKGROUND: Most studies examining the relationship between ventricular tachycardia (VT) after acute coronary syndrome and sudden cardiac death (SCD) were performed before widespread use of reperfusion, revascularization, or contemporary medical therapy and were limited to ST-elevation myocardial infarction. The incidence and prognostic implications of VT in patients with non-ST-elevation acute coronary syndrome receiving contemporary care have not been examined.
METHODS AND RESULTS: The Metabolic Efficiency With Ranolazine for Less Ischemia in Non-ST-Elevation Acute Coronary Syndrome-Thrombolysis in Myocardial Infarction 36 (MERLIN-TIMI 36) trial randomized 6560 patients hospitalized with a non-ST-elevation acute coronary syndrome to ranolazine or placebo in addition to standard therapy. Continuous ECG recording was performed for the first 7 days after randomization and evaluated in a blinded core laboratory. SCD (n=121) was assessed over a median follow-up of 1 year. A total of 6345 patients (97%) had continuous ECG recordings evaluable for analysis. Compared with patients with no VT (n=2764), there was no increased risk of SCD in patients with only ventricular triplets (n=1978, 31.2%) (1.4% versus 1.2%); however, the risk of SCD was significantly greater in patients with VT lasting 4 to 7 beats (n=1172, 18.5%) (SCD, 2.9%; adjusted hazard ratio, 2.3; P<0.001) and in patients with VT lasting at least 8 beats (n=431, 6.8%) (SCD, 4.3%; adjusted hazard ratio, 2.8; P=0.001). This effect was independent of baseline characteristics and ejection fraction. VT occurring within the first 48 hours after admission was not associated with SCD.
CONCLUSIONS: Nonsustained VT is common after admission for non-ST-elevation acute coronary syndrome, and even short episodes of VT lasting 4 to 7 beats are independently associated with the risk of SCD over the subsequent year. Clinical Trial Registration- URL: http://www.clinicaltrials.gov. Unique identifier: NCT00099788.
PMID
20644019 Circulation. 2010 Aug 3;122(5):455-62. doi: 10.1161/CIR･･･
著者: J T Bigger, J L Fleiss, R Kleiger, J P Miller, L M Rolnitzky
雑誌名: Circulation. 1984 Feb;69(2):250-8.
Abstract/Text
We examined the relationships among ventricular arrhythmias, left ventricular dysfunction, and mortality after the occurrence of myocardial infarction in 766 patients who enrolled in a nine-hospital study and underwent two special tests. Frequency and repetitiveness of ventricular premature depolarizations (VPDs) were determined by computer analysis of predischarge 24 hr electrocardiographic recordings. The left ventricular ejection fraction (LVEF) was determined by radionuclide ventriculography and dichotomized at its optimal value of 30%. Frequency of VPDs was divided into three categories: (1) less than one per hour, (2) one to 2.9 per hour, and (3) three or more per hour. Repetitiveness of VPDs was also divided into three categories: (1) no repetitive VPDs, (2) paired VPDs, and (3) VPD runs. These variables were related, one at a time and jointly, to total mortality and to deaths caused by arrhythmias. The hazard ratios for dying in the higher or highest risk stratum vs the lower or lowest stratum for each variable (adjusted for the effects of the others) were: LVEF below 30%, 3.5; VPD runs, 1.9; and VPD frequency of three or more per hour, 2.0. There were no significant interactions among the three variables with respect to effects on the risk of mortality. There was a suggestion of an interaction between each risk variable and time after infarction. LVEF below 30% was a better predictor of early mortality (less than 6 months) and the presence of ventricular arrhythmias was a better predictor of late mortality (after 6 months).(ABSTRACT TRUNCATED AT 250 WORDS)
PMID
6690098 Circulation. 1984 Feb;69(2):250-8.
著者: H C Doval, D R Nul, H O Grancelli, S D Varini, S Soifer, G Corrado, S Dubner, O Scapin, S V Perrone
雑誌名: Circulation. 1996 Dec 15;94(12):3198-203.
Abstract/Text
BACKGROUND: The goal of the study was to determine the prognostic value of nonsustained ventricular tachycardia (NSVT) in total mortality in severe congestive heart failure (CHF) and in death modes. NSVT is associated with an increased mortality in CHF. However, the predictive value of NSVT as a marker for sudden death or death due to progressive heart failure has not been determined.
METHODS AND RESULTS: Five hundred sixteen patients from the GESICA trial (33.4% with NSVT) were initially studied with the results of 24-hour Holter and 2 years of follow-up. Within 2 years, 87 of 173 patients (50.3%) with NSVT and 106 of 343 patients (30.9%) without NSVT died. Relative risk (RR) was 1.69 (95% confidence interval [CI], 1.27 to 2.24; P < .0002), and Cox proportional hazard analysis was 1.62 (95% CI, 1.22 to 2.16; P < .001). Sudden death increased from 8.7% (30 of 343) to 23.7% (41 of 173) in patients with NSVT (RR, 2.77; 95% CI, 1.78 to 4.44; P < .001). Progressive heart failure death was also increased from 17.5% (60 of 343) to 20.8% (36 of 173) (P = .22). Quantitative analysis of 24-hour Holter (first 295 patients) demonstrated that couplets had a similar RR to that of NSVT for both total mortality (RR, 1.81; 95% CI, 1.22 to 2.66; P < .002) and sudden death (RR, 3.37; 95% CI, 1.57 to 7.25; P < .0005). Couplets and/or NSVT (ventricular repetitive beats) were even more predictive for sudden death (RR, 10.1; 95% CI, 1.91 to 52.7; P < .01).
CONCLUSIONS: In patients with CHF, NSVT is an independent marker for increased overall mortality rate and sudden death. The absence of NSVT and ventricular repetitive beats in a 24-hour Holter indicates a low probability of sudden death.
PMID
8989129 Circulation. 1996 Dec 15;94(12):3198-203.
著者: J A Cairns, S J Connolly, R Roberts, M Gent
雑誌名: Lancet. 1997 Mar 8;349(9053):675-82.
Abstract/Text
BACKGROUND: Survivors of acute myocardial infarction with frequent or repetitive ventricular premature depolarisations (VPDs) have higher mortality 1-2 years after the event than those without VPDs. Although there is no therapy of proven efficacy for such patients, previous studies of amiodarone have been encouraging. CAMIAT was a randomised double-blind placebo-controlled trial designed to assess the effect of amiodarone on the risk of resuscitated ventricular fibrillation or arrhythmic death among survivors of myocardial infarction with frequent or repetitive VPDs (> or = 10 VPDs per h or > or = 1 run of ventricular tachycardia).
METHODS: Patients from 36 Canadian hospitals were randomly assigned amiodarone or placebo; a loading dose of 10 mg/kg daily for 2 weeks, a maintenance dose of 300-400 mg daily for 3.5 months, 200-300 mg daily for 4 months, and 200 mg for 5-7 days per week for 16 months. Patients were followed up for 2 years. The primary outcome was the composite of resuscitated ventricular fibrillation or arrhythmic death.
FINDINGS: We recruited 1202 patients (606 in the amiodarone group and 596 in the placebo group). The mean follow-up was 1.79 years (SD 0.44). In the efficacy analysis, resuscitated ventricular fibrillation or arrhythmic death occurred in 39 (6.9%) [corrected] patients in the placebo group and in 25 (4.5%) [corrected] in the amiodarone group (relative-risk reduction 48.5% [95% CI 4.5 to 72.2], p = 0.016). In the intention-to-treat analysis, primary outcome events occurred in 24 (6.9%) patients in the placebo group and in 15 (4.5%) in the amiodarone group (38.2% [95% CI -2.1 to 62.6], p = 0.029). The absolute-risk reductions were greatest among patients with congestive heart failure or a history of myocardial infarction.
INTERPRETATION: Amiodarone reduces the incidence of ventricular fibrillation or arrhythmic death among survivors of acute myocardial infarction with frequent or repetitive VPDs. Treatment decisions for individual survivors should require an assessment of their baseline risk factors and judgments based on the synthesis of our findings with those of related trials.
PMID
9078198 Lancet. 1997 Mar 8;349(9053):675-82.
著者:
雑誌名: N Engl J Med. 1989 Aug 10;321(6):406-12. doi: 10.1056/NEJM198908103210629.
Abstract/Text
The occurrence of ventricular premature depolarizations in survivors of myocardial infarction is a risk factor for subsequent sudden death, but whether antiarrhythmic therapy reduces the risk is not known. The Cardiac Arrhythmia Suppression Trial (CAST) is evaluating the effect of antiarrhythmic therapy (encainide, flecainide, or moricizine) in patients with asymptomatic or mildly symptomatic ventricular arrhythmia (six or more ventricular premature beats per hour) after myocardial infarction. As of March 30, 1989, 2309 patients had been recruited for the initial drug-titration phase of the study: 1727 (75 percent) had initial suppression of their arrhythmia (as assessed by Holter recording) through the use of one of the three study drugs and had been randomly assigned to receive active drug or placebo. During an average of 10 months of follow-up, the patients treated with active drug had a higher rate of death from arrhythmia than the patients assigned to placebo. Encainide and flecainide accounted for the excess of deaths from arrhythmia and nonfatal cardiac arrests (33 of 730 patients taking encainide or flecainide [4.5 percent]; 9 of 725 taking placebo [1.2 percent]; relative risk, 3.6; 95 percent confidence interval, 1.7 to 8.5). They also accounted for the higher total mortality (56 of 730 [7.7 percent] and 22 of 725 [3.0 percent], respectively; relative risk, 2.5; 95 percent confidence interval, 1.6 to 4.5). Because of these results, the part of the trial involving encainide and flecainide has been discontinued. We conclude that neither encainide nor flecainide should be used in the treatment of patients with asymptomatic or minimally symptomatic ventricular arrhythmia after myocardial infarction, even though these drugs may be effective initially in suppressing ventricular arrhythmia. Whether these results apply to other patients who might be candidates for antiarrhythmic therapy is unknown.
PMID
2473403 N Engl J Med. 1989 Aug 10;321(6):406-12. doi: 10.1056/N･･･
著者:
雑誌名: 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.
PMID
1377359 N Engl J Med. 1992 Jul 23;327(4):227-33. doi: 10.1056/N･･･
