Mark M. Gallagher

Classification of atrial fibrillation

Atrial fibrillation (AF) is the subject of several overlapping schemes of classification in which the subgroups are often poorly defined. New methods of classification have been applied to accommodate new information and new concepts. These are often appropriate only in limited circumstances and may lead to confusion if applied out of context. We will describe the principal schemes used to classify AF and discuss the limitations of each.

Embolic complications of direct current cardioversion of atrial arrhythmias: Association with low intensity of anticoagulation at the time of cardioversion

OBJECTIVES The goal of this study was to identify the factors responsible for embolic complications of direct current (DC) cardioversion of atrial arrhythmias. BACKGROUND Direct current cardioversion of atrial fibrillation (AF) carries a risk of thromboembolism, which is reduced, but not eliminated, by anticoagulation. The risk of embolism after conversion of atrial flutter is believed to be lower. No series to date has included enough patients receiving anticoagulants or enough patients with atrial flutter to estimate the risk in these groups. METHODS We reviewed the case records of 1,950 patients who underwent 2,639 attempts at DC cardioversion. RESULTS Cardioversion was performed within two days of the apparent onset of the arrhythmia in 443 episodes, 352 without subsequent prolonged anticoagulation with one embolic complication. Cardioversion was preceded by warfarin therapy for > or = 3 weeks in 1,932 instances. No embolic complication occurred in 779 attempts performed with an international normalized ratio (INR) of > or = 2.5 (95% confidence limits 0% to 0.48%). Of 756 cases in which the INR was <2.5 or was not measured before conversion, nine were complicated by thromboembolism. Embolism was significantly more common at an INR of 1.5 to 2.4 than at an INR > or = 2.5 (0.93% vs. 0%, p = 0.012). The incidence of embolism after conversion of atrial flutter or tachycardia was similar to that after cardioversion of AF (0.72% vs. 0.46%, p = NS). CONCLUSIONS The INR should be > or = 2.5 at the time of cardioversion if the duration of AF is uncertain or >2 days. Cardioversion of atrial flutter presents similar risks and requires similar anticoagulation.

Classification of Atrial Fibrillation

Atrial fibrillation (AF) is the subject of several overlapping schemes of classification in which the subgroups are often poorly defined. New methods of classification have been applied to accommodate new information and new concepts. These are often appropriate only in limited circumstances and may lead to confusion if applied out of context. We will describe the principal schemes used to classify AF and discuss the limitations of each.

Comparison of Formulae for Heart Rate Correction of QT Interval in Exercise Electrocardiograms

The study investigated the differences in five different formulae for heart rate correction of the QT interval in serial electrocardiograms recorded in healthy subjects subjected to graded exercise. Twenty‐one healthy subjects (aged 37 ± 10 years, 15 male) were subjected to graded physical exercise on a braked bicycle ergometer until the heart rate reached 120 beats/min. Digital electrocardiograms (ECG) were recorded on baseline and every 30 seconds during the exercise. In each ECG, heart rate and QT interval were measured automatically (QT Guard package, Marquette Medical Systems, Milwaukee, WI, USA). Bazett, Fridericia, Hodges, Framingham, and nomogram formulae were used to obtain QTc interval values for each ECG. For each formula, the slope of the regression line between RR and QTc values was obtained in each subject. The mean values of the slopes were tested by a one‐sample t‐test and the comparison of the baseline and peak exercise QTc values was performed using paired t‐test. Bazett, Hodges, and nomogram formulae led to significant prolongation of QTc intervals with exercise, while the Framingham formula led to significant shortening of QTc intervals with exercise. The differences obtained with the Fridericia formula were not statistically significant. The study shows that the practical meaning of QTc interval measurements depends on the correction formula used. In studies investigating repolarization changes (e.g., due to a new drug), the use of an ad‐hoc selected heart rate correction formula is highly inappropriate because it may bias the results in either direction.

Initial energy setting, outcome and efficiency in direct current cardioversion of atrial fibrillation and flutter

OBJECTIVES The purpose of this study was to design a more efficient protocol for the electrical cardioversion of atrial arrhythmias. BACKGROUND Guidelines for electrical cardioversion of atrial arrhythmias recommend starting with low energy shocks, which are often ineffective. METHODS We recorded the sequence of shocks in 1,838 attempts at cardioversion for atrial fibrillation (AF) and 678 attempts at cardioversion for atrial flutter. These data were used to calculate the probability of success for each shock of a standard series and the probability of success with a single shock at each intensity. In 150 cases, a rhythm strip with the time of each shock allowed us to calculate the time expended on unsuccessful shocks. RESULTS We analyzed the effects of 5,152 shocks delivered to patients for AF and 1,238 shocks delivered to patients for atrial flutter. The probability of success on the first shock in AF of > 30 days duration was 5.5% at < 200 J, 35% at 200 J and 56% at 360 J. In atrial flutter, an initial 100 J shock worked in 68%. In AF of >30 days duration, shocks of < 200 J had a 6.1% probability of success; this fell to 2.2% with a duration >180 days. In those with AF for >180 days, the initial use of a 360 J shock was associated with the eventual use of less electrical energy than with an initial shock of < or =100 J (581 +/- 316 J vs. 758 +/- 433 J, p < 0.01, Mann-Whitney U test). CONCLUSIONS An initial energy setting of > or =360 J can achieve cardioversion of AF more efficiently in patients than traditional protocols, particularly with AF of longer duration.

Circadian Variation of the QT Interval in Patients With Sudden Cardiac Death After Myocardial Infarction

To evaluate the potential prognostic value of the circadian variation of QT intervals in predicting sudden cardiac death (SCD) in patients after myocardial infarction (MI), 15 pairs of post-MI patients (15 died suddenly within 1 year after MI [SCD victims] and 15 remained event-free [MI survivors]) were studied (mean age 60 +/- 8 years; 24 men and 6 women). The pairs were matched for age, gender, infarct site, presence of Q wave, left ventricular ejection fraction, thrombolytic and beta-blocker therapy. Fourteen normal subjects served as controls (mean age 55 +/- 9 years; 12 men). A 24-hour Holter electrocardiographic (ECG) recording was obtained from each subject. All recordings were analyzed using a Holter ECG analyser. QT, RR, and heart rate-corrected QT intervals (QTc) were automatically calculated by the analyzer, and hourly and 24-hour mean values of each measurement were derived from each recording. There was a pronounced circadian variation in the QT interval in parallel with the trend in the RR interval in normal subjects and in MI survivors. Circadian variation in both indexes was blunted in SCD victims. The QT interval was significantly longer at night than during the day in normal subjects (388 +/- 28 vs 355 +/- 21 ms, p = 0.001) and in MI survivors (358 +/- 25 vs 346 +/- 15 ms, p = 0.008), but not in SCD victims (357 +/- 32 vs 350 +/- 31 ms, p = 0.6). The 24-hour mean value of the QT interval in SCD victims did not differ significantly from that in normal subjects or MI survivors. The QT interval at night was significantly shorter in SCD victims than in normal subjects (357 +/- 32 vs 388 +/- 28 ms, p = 0.02), but daytime values were similar. The QT interval in SCD victims did not differ significantly from that of MI survivors at any time. The QTc interval exhibited a small circadian variation in normal subjects. This variation was abolished in SCD victims and MI survivors. The 24-hour mean value of QTc was significantly longer in SCD victims than in normal subjects (424 +/- 25 vs 402 +/- 21 ms, p = 0.02), and in MI survivors (424 +/- 25 vs 404 +/- 32 ms, p < 0.05). The QTc interval of SCD victims differed from that of normal subjects during both the day (421 +/- 25 vs 400 +/- 17 ms, p = 0.02) and night (424 +/- 26 vs 403 +/- 23 ms, p = 0.03). Thus, blunted circadian variation in QT intervals, abolished circadian variation in QTc intervals, and prolonged QTc intervals may suggest an increased risk of SCD in patients after MI.

TACHYCARDIA-INDUCED ATRIAL MYOPATHY : AN IMPORTANT MECHANISM IN THE PATHOPHYSIOLOGY OF ATRIAL FIBRILLATION?

Tachycardia‐Induced Atrial Myopathy. The atrial myocardium of patients with chronic atrial fibrillation (AF) is often abnormal in its histologic features and in its electrophysiologic properties. These abnormalities have been interpreted in some cases as the cause of AF and in others as a consequence of AF. We believe that both are the case. We will review the features of this atrial myopathy and discuss the likely mechanisms and consequences of the process.

Prognostic value of blood pressure measured during hospitalization after acute myocardial infarction: an insight from survival trials.

Background The prognostic value of blood pressure measured during hospitalization after acute myocardial infarction (MI) has not been investigated, particularly with regard to arrhythmic death. Methods A total of 3311 placebo patients (2612 men, median age 64 years; range 23–92) from the EMIAT, CAMIAT, SWORD, TRACE and DIAMOND–MI studies with left ventricular ejection fraction less than 40% or asymptomatic ventricular arrhythmia surviving more than 45 days after MI were pooled. Systolic and diastolic blood pressures and pulse pressures were measured soon after MI (median 6 days, range 0–53 days). Mortality up to 2 years was examined using Cox regression. Results At the 2-year follow-up, after adjustment for age, sex, smoking, previous MI, hypertension, heart rate, New York Heart Association functional class, baseline treatments, study effect and diastolic blood pressure, reduced systolic blood pressure measured during hospitalization after acute MI significantly increased the risk of all-cause mortality [hazard ratio (HR) for 10% increase in systolic blood pressure 0.80, 95% confidence interval (CI) 0.71–0.90; P < 0.001] and arrhythmic mortality (HR 0.73, 95% CI 0.61–0.86; P = 0.001). Reduced diastolic blood pressure significantly increased the risk of all-cause mortality (HR 0.87, 95% CI 0.77–0.98; P = 0.02) and arrhythmic mortality (HR 0.80, 95% CI 0.68–0.93; P = 0.005). Conclusion In post-MI patients with left ventricular ejection fraction less than 40% or asymptomatic ventricular arrhythmia, reduced blood pressure measured during hospitalization after MI significantly predicts all-cause mortality and arrhythmic mortality, and can be reliably used to identify patients who are at risk of dying after MI.

Prognostic Significance of Serial P Wave Signal‐Averaged Electrocardiograms Following External Electrical Cardioversion for Persistent Atrial Fibrillation: A Prospective Study

GUO, X.H., et al.: Prognostic Significance of Serial P Wave Signal‐Averaged Electrocardiograms Following External Electrical Cardioversion for Persistent Atrial Fibrillation: A Prospective Study. The authors hypothesized that the persistence of abnormal atrial conduction detected by serial P wave signal‐averaged electrocardiograms (P‐SAECGs) can identify patients who are at high risk of recurrent atrial fibrillation (R‐AF) following electrical cardioversion (ECV). P‐SAECGs were recorded in 60 consecutive patients after ECV (53 men, age 66 ± 10 years) and repeated in those who had remained in sinus rhythm (SR) 1 week, and 1, 3, and 6 months later. Filtered P wave duration (PD), root mean square (RMS) voltage of the terminal 40, 30, 20 ms (RMS‐40, RMS‐30, RMS‐20) of the filtered P wave, RMS voltage of the entire filtered P wave (RMS‐p), and the integral of the voltages in the entire P wave (integral‐p) were analyzed. Thirty‐one (52%) patients returned to AF within 1 week, an additional 11 (18%) by 1 month, and a further 2 (3.3%) at each subsequent assessment (3 and 6 months). The patients with R‐AF had longer PD (157 ± 24 vs 143 ± 17 ms, P < 0.0001) and lower RMS‐40, RMS‐30, RMS‐20 ( 5.3 ± 2.0 vs 6.1 ± 3.4 μV, P = 0.007; 4.3 ± 1.5 vs 5.7 ± 3.2 μV, P < 0.0001; 3.6 ± 1.4 vs 5.2 ± 3.0 μV, P < 0.0001 , respectively) than those who remained in SR. These measurements did not change significantly in either group. RMS‐p increased in SR patients (P = 0.009) but decreased in those who subsequently reverted to AF (P = 0.032) with a significant difference between the slopes of the RMS‐p change (P = 0.006) . Integral‐p decreased from the time of ECV in the R‐AF group only (P = 0.0028) and created a significant difference between the two slopes (P = 0.0004) . The evolution of P‐SAECG parameters after ECV differs in patients whose AF recurs versus patients who remain in SR. (PACE 2003; 26[Pt. II]:299–304)

Optimising the dichotomy limit for left ventricular ejection fraction in selecting patients for defibrillator therapy after myocardial infarction

Background: The selection of patients for prophylactic implantable cardioverter-defibrilator (ICD) treatment after myocardial infarction (MI) remains controversial. Aim: To determine the optimum left ventricular ejection fraction (LVEF) dichotomy limit for ICD treatment in patients with a history of MI. Methods and results: Data from the placebo arms of four randomised trials were pooled to create a cohort of 2828 patients (2206 men, mean (SD) age 65 (11) years) with reduced left ventricular function after MI. The median LVEF was 33% (range 6–40%). LVEF significantly predicted mortality. Each 10% reduction in LVEF <40% conferred a 42% increase in all-cause mortality, a 39% increase in arrhythmic cardiac mortality and a 49% increase in non-arrhythmic cardiac mortality over the 2-year period of follow-up (p<0.001 for all modes of mortality). As the LVEF progressively decreased from ⩽40% to ⩽10%, the data show a U-shaped relationship between the dichotomy limit for LVEF used and the number of patients who must be treated to prevent one arrhythmic death in 2 years. At an LVEF of 16–20%, more patients are likely to die from arrhythmic than non-arrhythmic cardiac deaths, whereas in those with LVEF ⩽10% all deaths were non-arrhythmic. However, the total number of deaths substantially decreased with lower LVEF. Conclusion: A trade-off exists between the sensitivity and positive predictive accuracy across a range of LVEF, and no single dichotomy limit is completely satisfactory. In patients with LVEF ⩽10% ICD treatment was not beneficial as all patients in this subgroup died from non-arrhythmic causes. The use of a single dichotomy limit for LVEF alone is not sufficient in selecting patients for ICD treatment in the primary prevention of cardiac arrest.