Holter Electrocardiographic Recordings Research Articles

Role of transtelephonic electrocardiographic monitoring in detecting short-term arrhythmia recurrences after radiofrequency ablation in patients with atrial fibrillation

The aim of our study was to determine the incidence of asymptomatic recurrences of atrial fibrillation (AF) by daily transtelephonic (TT) electrocardiographic (ECG) monitoring, as compared with standard ECG and 24-h Holter recording, in patients who underwent radiofrequency catheter ablation (RCA) of AF. The efficacy of RCA of AF is usually evaluated by means of patients' symptoms. Seventy-two patients with paroxysmal (n = 37) or persistent (n = 35) drug-refractory AF underwent circumferential RCA of the pulmonary vein (PV) ostia. Left isthmus ablation was performed in 57 patients, and cavotricuspid isthmus ablation was done in 69 patients. Patients were scheduled to obtain an ECG and Holter recordings one and four months after ablation, as well as a daily TT ECG, from 30 to 120 days after ablation or in the event of symptoms. A total of 5,585 TT ECGs were obtained (mean 77.5 per patient). In 20 patients (27.8%), AF recurrences were recorded during TT ECG, whereas ECG and Holter monitoring revealed AF recurrences in 10 patients (13.9%, p = 0.001). Ten patients had at least one asymptomatic AF recurrence, and eight were completely asymptomatic. The ECG recorded in the event of symptoms always showed AF. Transtelephonic ECG is better than standard ECG and 24-h Holter recordings in evaluating AF relapses after RCA, thus decreasing the short-term success of ablation from 86% to 72%. The absence of symptoms should not be interpreted as absence of AF, as 50% of patients were asymptomatic during at least one AF episode.

Sildenafil citrate does not alter ventricular repolarization properties: novel evidence from dynamic QT analysis.

Sildenafil citrate may have direct cardiac electrophysiological effects, and is possibly responsible for some cardiac events. The aim of our study was to investigate the effects of sildenafil citrate on QT dynamicity properties with a new QT analysis program showing even small changes in ventricular repolarization. Twenty-four-hour Holter electrocardiographic recordings were used to obtain the data in the predrug phase (1-hour rest position before drug administration), and in the postdrug phase (1-hour rest position, which began 60 minutes after 50 mg oral sildenafil citrate administration). With the special QT analysis program (Verda, Reynolds Medical Ltd., UK); mean values of RR, QT, QTo (corrected QT), J (the exponent of correction formula) and S (QT/RR plots slope) parameters together with QT variability indexes (QTVI) were calculated for study phases. Mean +/- SEM values for RR and QT were higher in postdrug phase than in predrug phase (RR: 845 +/- 42 ms vs 816 +/- 46 ms, P < 0.05; QT: 371 +/- 8 ms vs 361 +/- 9 ms, P < 0.05). However, sildenafil did not induce any significant change in mean +/- SEM values for QT(o), J, and S in postdrug phase compared with predrug phase (408 +/- 10 ms vs 406 +/- 8 ms, 0.474 +/- 0.030 vs 0.433 +/- 0.025, 0221 +/- 0.020 vs 0.198 +/- 0.017, respectively; P > 0.05). QTVIs were also not different in each phase (predrug: -0.874 +/- 0.071 vs postdrug: -0.997 +/- 0.067, P = 0.109). Fifty milligrams sildenafil does not affect QT dynamicity properties. The cardiac events associated with sildenafil could not be explained with ventricular arrhythmias.

Holter changes resulting from right-sided and bilateral infrastellate upper thoracic sympathectomy

Background We tested the hypothesis that no right-sided dominance exists after infrastellate surgical upper-thoracic sympathectomy. We aimed to confirm whether a significant bradycardia was constant and only dependent on the right side. Methods We performed 24-hour Holter electrocardiographic recordings in 12 patients referred for bilateral sympathectomy. Surgery was performed at two distinct times allowing for the study of the consequences of unilateral right and bilateral sympathectomy. Results Heart rate was 77 ± 8 beats per minute before surgery on the 24-hour recording and significantly decreased after bilateral (67.8 ± 6.5 beats per minute; p < 0.05) but not after unilateral right sympathectomy. Consistently spectral analysis variables significantly changed after bilateral surgery but showed no right-sided dominance. Little effect of sympathectomy was found on the QT interval, which tended to decrease after bilateral sympathectomy. Conclusions Patients should be informed of the bradycardia resulting from sympathectomy. No right-sided dominance can be found consistently with the random distribution of substellate cardiac fibers reported in anatomic studies.

Effect of severity of myocardial failure on heart rate variability in Doberman pinschers with and without echocardiographic evidence of dilated cardiomyopathy.

To determine whether heart rate variability (HRV) is reduced in Doberman Pinschers with dilated cardiomyopathy. Case series. 62 overtly healthy Doberman pinschers. Heart rate variability was analyzed in time and frequency domains from data obtained during 24-hour ambulatory electrocardiographic Holter recordings in 41 overtly healthy Doberman pinschers with normal echocardiograms and 21 overtly healthy Doberman pinschers with abnormal echocardiograms. Heart rate variability usually was greater during night versus day, and 2 dogs with the most severe myocardial failure had reduced HRV. Reduced HRV was detected only in Doberman Pinschers with the most severe myocardial failure. Thus, HRV in less severely affected dogs is not reduced, or the normal sinus arrhythmia of dogs renders HRV relatively insensitive. Analysis of HRV did not provide additional information relative to the severity of left ventricular dysfunction or risk of sudden death from that which could be derived from echocardiography, analysis of Holter recordings, and signal-averaged electrocardiography.

Is Exercise Electrocardiography Useful for Risk Stratification before Noncardiac Surgery?

Is Exercise Electrocardiography Useful for Risk Stratification before Noncardiac Surgery?Gauss et al.(page 38)During a 2-yr period, Gauss et al. examined 204 patients who had coronary artery disease or were at risk for it before their scheduled noncardiac surgeries. Patients underwent exercise stress testing on a supine bicycle ergometer 1 day before surgery. A 12-lead electrocardiogram was recorded at rest, once per minute during exercise and during recovery until the electrocardiogram reverted to preexercise morphology. The exercise electrocardiogram was classified as abnormal if new horizontal or down-sloping ST-segment depressions of more than 0.1 mV were seen in three consecutive beats without baseline variation. Rest and exercise electrocardiograms were evaluated by two independent investigators blinded to patient identity and clinical outcome. A third investigator was consulted if the first two interpretations differed.Echocardiography was performed on each patient before surgery. Patients were monitored with a two-channel Holter electrocardiographic recorder from the evening before surgery until the morning of the second postoperative day. Twelve-lead electrocardiograms and creatine kinase, creatinine kinase MB, and troponin-T measurements were assessed until the sixth postoperative day. One of the study authors also performed a history and physical examination of each patient until the fifth postoperative day and on the day of discharge from the hospital. Telephone interviews with patients were conducted 30 days after surgery to obtain cardiac histories.Perioperative cardiac events (6 myocardial infarctions, 10 cases of minor myocardial cell injury) were observed in 16 of the 185 patients available for final examination. Despite the small sample size and the fact that physicians treating the patients were not blinded to preoperative resting and exercise electrocardiographic findings, the study showed that an ST-segment depression of 0.1 mV or more was an independent predictor of perioperative cardiac complications. An abnormal resting electrocardiogram was not an independent predictor of such complications. A combination of a clinical parameters, such as definite coronary artery disease and the type of surgery, with the results of the electrocardiographic exercise stress test, allowed sufficient risk stratification.

Electrocardiographic ST-segment changes during acute, severe isovolemic hemodilution in humans.

Controversy exists regarding the lowest blood hemoglobin concentration that can be safely tolerated. The authors studied healthy resting humans to test the hypothesis that acute isovolemic reduction of blood hemoglobin concentration to 5 g/dl would produce an imbalance in myocardial oxygen supply and demand, resulting in myocardial ischemia. Fifty-five conscious healthy human volunteers were studied. Isovolemic removal of aliquots of blood reduced blood hemoglobin concentration from 12.8 +/- 1.2 to 5.2 +/- 0.5 g/dl (mean +/- SD). Removed blood was replaced simultaneously with intravenous fluids to maintain constant isovolemia. Hemodynamics and arterial oxygen content (Cao2) were measured before and after removal of each aliquot of blood. Electrocardiographic (ECG) changes were monitored continuously using a Holter ECG recorder for detection of myocardial ischemia. During hemodilution, transient, reversible ST-segment depression developed in three subjects as seen on the electrocardiogram during hemodilution. These changes occurred at hemoglobin concentrations of 5-7 g/dl while the subjects were asymptomatic. Two of three subjects with ECG changes had significantly higher heart rates than those without ECG changes at the same hemoglobin concentrations. When evaluating the entire study period, the subjects who had ECG ST-segment changes had significantly higher maximum heart rates than those without ECG changes, despite having similar baseline values. With acute reduction of hemoglobin concentration to 5 g/dl, ECG ST-segment changes developed in 3 of 55 healthy conscious adults and were suggestive of, but not conclusive for, myocardial ischemia. The higher heart rates that developed during hemodilution may have contributed to the development of an imbalance between myocardial supply and demand resulting in ECG evidence of myocardial ischemia. However, these ECG changes appear to be benign because they were reversible and not accompanied by symptoms.

Effect of aging on the incidence of digoxin toxicity.

To evaluate the relationship of the therapeutic serum digoxin concentration (SDC) range (0.5-2 ng/mL, as recommended in previous clinical studies) with the incidence of digoxin toxicity during digoxin maintenance therapy. Subjects included all inpatients (n = 462) and outpatients (n = 437) receiving digoxin oral maintenance therapy for heart failure and/or atrial fibrillation with tachycardia at Kosei Hospital, Anjo, Japan. SDC and blood chemistry analysis were determined, and a 24-hour Holter electrocardiographic recording was performed when the SDC was at the presumed steady-state concentration. Analysis of clinical data showed that there was an overlapping (toxic and nontoxic) range of SDCs in which the incidence of digoxin toxicity was patient-dependent (1.4-2.9 ng/mL). No patient exhibited signs or symptoms of digoxin toxicity when the SDC was <1.4 ng/mL; all patients had evidence of toxicity when the SDC was >3 ng/mL. Additionally, it was shown that the concentration range of this overlapping range tended to broaden and shift to lower concentrations with increasing age. Patients with signs of toxicity when their SDCs were in the overlapping range had normal serum creatinine, blood urea nitrogen, digoxin clearance, creatinine clearance, and potassium concentrations, except for a significantly higher mean age than patients without toxicity. The incidence of digoxin toxicity was dependent on increasing age in patients whose SDCs were within the recommended therapeutic range. Moreover, clinical evidence of digoxin toxicity in patients >71 years old was 26.5%, despite their SDCs falling between 1.4 and 2 ng/mL. Increased age is most likely associated with enhanced susceptibility to digoxin toxicity, possibly due to unknown pharmacodynamic changes. This raises the possibility that patients >71 years show clinical evidence of digoxin toxicity despite having SDCs within the recommended therapeutic range.

Effect of Aging on the Incidence of Digoxin Toxicity

OBJECTIVE:To evaluate the relationship of the therapeutic serum digoxin concentration (SDC) range (0.5–2 ng/mL, as recommended in previous clinical studies) with the incidence of digoxin toxicity during digoxin maintenance therapy.METHODS:Subjects included all inpatients (n = 462) and outpatients (n = 437) receiving digoxin oral maintenance therapy for heart failure and/or atrial fibrillation with tachycardia at Kosei Hospital, Anjo, Japan. SDC and blood chemistry analysis were determined, and a 24-hour Holter electrocardiographic recording was performed when the SDC was at the presumed steady-state concentration.RESULTS:Analysis of clinical data showed that there was an overlapping (toxic and nontoxic) range of SDCs in which the incidence of digoxin toxicity was patient-dependent (1.4–2.9 ng/mL). No patient exhibited signs or symptoms of digoxin toxicity when the SDC was <1.4 ng/mL; all patients had evidence of toxicity when the SDC was >3 ng/mL. Additionally, it was shown that the concentration range of this overlapping range tended to broaden and shift to lower concentrations with increasing age. Patients with signs of toxicity when their SDCs were in the overlapping range had normal serum creatinine, blood urea nitrogen, digoxin clearance, creatinine clearance, and potassium concentrations, except for a significantly higher mean age than patients without toxicity. The incidence of digoxin toxicity was dependent on increasing age in patients whose SDCs were within the recommended therapeutic range. Moreover, clinical evidence of digoxin toxicity in patients >71 years old was 26.5%, despite their SDCs falling between 1.4 and 2 ng/mL.CONCLUSIONS:Increased age is most likely associated with enhanced susceptibility to digoxin toxicity, possibly due to unknown pharmacodynamic changes. This raises the possibility that patients >71 years show clinical evidence of digoxin toxicity despite having SDCs within the recommended therapeutic range.

Ｄｉｇｏｘｉｎ中毒の発生率および臨床効果に及ぼす新しい目標治療Ｄｉｇｏｘｉｎ血清中濃度域の影響

Our previous study suggested that maintaining the serum digoxin concentration (SDC) in a lower target range (0.5-1.4 ng/ml) than the generally recommended range (0.5-2.0 ng/ml) may be useful to avoid the occurrence of digoxin toxicity in elderly patients (over 71 years old). Thus, the present prospective clinical study was carried out to evaluate the significance of the new target therapeutic SDC range in decreasing the incidence of digoxin toxicity during digoxin maintenance therapy in elderly patients.Study subjects who received oral maintenance therapy with digoxin for heart failure and/or atrial fibrillation with tachycardia included 899 patients and 946 patients in 1995 and 1997, respectively at Kosei Hospital. In all study subjects, measurements of SDC, blood chemistry analysis, and 24-hour Holter electrocardiographic recording were performed when the SDC was at a presumed steady state.After treatment of patients with a lower SDC range, the incidence (1.8%) of digoxin toxicity in 1997 was significantly less than that (7.3%) in 1995. In addition, the incidence (2.6%) of adverse reactions of patients over 71 years old in 1997 was also markedly lower than that (16.4%) in 1995. In 83 elderly patients, no significant difference in heart rate under conditions of resting and exercise was observed between patients with SDCs over 1.4 ng/ml (mean SDC 1.79 ng/ml) and patients with SDCs less than 1 .4 ng/ml (mean SDC 1.26 ng/ml).These results indicate that the treatment of elderly patients with the new therapeutic SDC range reduces the incidence of digoxin toxicity with an equivalent therapeutic efficacy to that obtained with the generally recommended range.

Metoprolol CR/XL in patients with heart failure: A pilot study examining the tolerability, safety, and effect on left ventricular ejection fraction

Background This study was designed to investigate the tolerability, safety, and effect on left ventricular function of a new long-acting preparation of metoprolol, metoprolol succinate (CR/XL). Methods and Results Sixty patients were randomly assigned with a 2:1 ratio, drug versus placebo, administered with a gradually increasing dose of 12.5 to 150 mg of blinded medication during an 8-week period and continued for 6 months. The average peak dose achieved was 99 mg and 132 mg in the metoprolol succinate and placebo groups, respectively. The drug was well tolerated and there was no significant difference in drug withdrawals, New York Heart Association class, or quality of life assessment. The increase in left ventricular ejection fraction measure at baseline and 6 months measured by radioisotopic ventriculography was greater in the metoprolol succinate group (27.5% to 36.3%) than in the placebo group (26% to 27.9%) (P < .015). Examination of serial Holter electrocardiographic recordings indicate that metoprolol succinate therapy was associated with a significant ( P < .05) decrease in total ventricular ectopy at 8 weeks of therapy and a decrease in ventricular couplets and nonsustained ventricular tachycardia at 8 through 26 weeks of therapy. No changes were observed in plasma norepinephrine during therapy except a transitory significant ( P < .05) increase in N terminal proatrial natriuretic factor at 8 weeks in the metoprolol succinate group. Conclusions This study indicates that treatment with metoprolol succinate for a 6-month period is safe and well tolerated and is associated with an increase in left ventricular ejection fraction and a decrease in ventricular ectopic beats. (Am Heart J 1999;138:1158-65.)

Effects of short-acting and long-acting loop diuretics on heart rate variability in patients with chronic compensated congestive heart failure

Background We investigated the effects of a short-acting loop diuretic (furosemide) and a long-acting loop diuretic (azosemide) on heart rate variability, fluid balance, and neurohormonal responses in patients with mild to moderate chronic congestive heart failure. Methods Nineteen patients with mild to moderate chronic congestive heart failure received furosemide (40 to 60 mg/day) or azosemide (60 to 90 mg/day) for 5 days in a crossover manner. We performed time-domain and frequency-domain analyses of 24-hour Holter electrocardiographic recordings to assess heart rate variability. Results The 24-hour urinary sodium excretion was similar during the furosemide and azosemide treatment periods but was significantly greater in the first 2 hours after drug administration during furosemide treatment. Plasma renin activity and the hematocrit level increased and high-frequency power significantly decreased 2 hours after the administration of furosemide only. The standard deviation of all normal R-R intervals and the root mean square of successive differences in the R-R interval were lower with furosemide than with azosemide ( P < .05). Conclusions Furosemide, a short-acting loop diuretic, has a greater influence on heart rate variability and fluid balance than azosemide, a long-acting loop diuretic, in patients with mild to moderate chronic congestive heart failure. (Am Heart J 1999;137:543-8.)

Silent myocardial ischemia after myocardial infarction: severity of coronary artery disease, impact on left ventricular systolic and diastolic functions and prognosis.

The aim of the present study was assessment of the relationship of silent myocardial ischemia with clinical, coronary angiography findings, and left ventricular systolic and diastolic function, and its prognostic significance in patients early after myocardial infarction. One hundred nineteen male patients (mean age 48.2+/-1.2 years) with first Q wave myocardial infarction entered the study. Routine coronary angiography, 24-hour Holter electrocardiographic recordings, and two-dimensional and Doppler echocardiography with assessment of left ventricular systolic and diastolic function were performed in all the patients. Prospective follow-up was done during 1 year. Patients with signs of silent myocardial ischemia early after myocardial infarction had more severe coronary artery disease, pronounced disturbances of left ventricular systolic and diastolic performance, and adverse prognosis than those without ischemia appearance during Holter recordings.

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 β-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.

Role of autonomic tone in facilitating spontaneous onset of typical atrial flutter.

This study sought to study the change in autonomic tone that precedes the initiation of paroxysmal atrial flutter. An abrupt change in the autonomic tone of the heart is an important initiating factor in the pathogenesis of ventricular tachyarrhythmias and paroxysmal atrial fibrillation. Whether the autonomic tone has a role in the initiation of paroxysmal atrial flutter has not been reported. Holter electrocardiographic recording was used to investigate the changes in heart rate variability before the onset of paroxysmal atrial flutter. A total of 12 patients with paroxysmal atrial flutter were analyzed. An increase in the normalized value of the low frequency (LF) component and the LF/high frequency (HF) ratio and a decrease in the normalized value of the HF component began at 6 min before the onset of episodes of paroxysmal atrial flutter, which indicated that sympathovagal balance had shifted to more sympathetic predominance. An increase in sympathetic modulation or vagal withdrawal, or both, may facilitate the initiation of atrial flutter.

T wave spectral variance: A new method to determine inhomogeneous repolarization by T wave beat-to-beat variability in patients prone to ventricular arrhythmias

Inhomogeneous repolarization is considered to be associated with increased risk of ventricular arrhythmias, but exact determination of the end of the T wave is difficult, and a single measurement of the QTc interval may be insufficient for risk stratification. A new algorithm was therefore developed to determine the beat-to-beat variability of the T wave in Holter electrocardiographic recordings. This algorithm, termed T Wave Spectral Variance (TWSV) uses the two-dimensional fast Fourier transform to determine the beat-to-beat variability of the T wave in Holter ECG recordings. The two-dimensional fast Fourier transform was calculated by use of a data matrix with 1,024 consecutive single beats (first dimension) and a 200-ms segment centered on the T wave (second dimension). The power spectra of the 2D-FFT revealed the frequency content of the T wave in the first dimension and the periodicity of these frequencies in cycles per beat in the second dimension. A TWSV index of periodicity was calculated by dividing total spectral energy by spectral energy at 0 cycles per beat. A TWSV index of 0 means a constant T wave from beat to beat; a TWSV index of 1 means a completely irregular T wave. Of the 200 patients investigated, all of whom had had myocardial infarctions, 50 had documented sustained ventricular tachycardia (VT) (<230 beats/min) (group 1), 50 had ventricular fibrillation (VF) (group 2), and 100 were without VT or VF (group 3); 10 normal subjects were also investigated. The visually determined QTc was 442 ± 62 ms in group 1, 402 ± 13 ms in group 2, 411 ± 26 ms in group 3, and 398 ± 43 ms in normal subjects (differences not significant). The TWSV index was 0.95 ± 0.14 in group 1, 0.90 ± 0.16 in group 2, and 0.64 ± 0.24 in group 3; it showed a highly constant T wave in normal subjects (0.52 ± 0.23). Differences between patients with VT and VF as against patients without VT or VF were significant ( P < .05), whereas no statistical differences between patients with VT and VF could be found. Thus, TWSV, a new method to assess beat-to-beat variability of the T wave, revealed increased heterogeneity of repolarization in patients prone to both VT and VF after myocardial infarction, whereas a single QTc interval measurement showed no significant differences.

Role of sympathovagal balance in the initiation of idiopathic ventricular tachycardia originating from right ventricular outflow tract.

VT originating from the right ventricular outflow tract (RVOT) is prone to occur when sympathetic nervous activity is increased. beta-Blockade is, therefore, effective in suppressing this VT. The purpose of this study was to determine the role of sympathovagal balance assessed by heart rate variability (HRV) in the spontaneous initiation of repetitive premature ventricular contractions (PVCs) and VT (five or more consecutive PVCs) arising from RVOT in seven patients without structural heart diseases. Frequency-domain measures of HRV were determined by analyzing 24-hour Holter electrocardiographic recording with the maximum entropy method over a 1,280-second period immediately before the onset of 35 single PVCs, 26 episodes of 2-4 consecutive PVCs, and 21 episodes of VT. High frequency component (HF: 0.15-0.40 Hz) was used as an index of parasympathetic activity, and the ratio of low frequency component (LF: 0.04-0.15 Hz) to HF (LF/HF ratio), as an index of sympathovagal balance. NN50(%), a time-domain variable of parasympathetic activity, was also determined. Mean RR interval and any measures of HRV did not change significantly before single PVCs. Mean RR interval shortened and HF decreased prior to repetitive PVCs and VT. The LF/HF ratio, however, increased only before the onset of VT. NN50(%) tended to decrease before repetitive PVCs and decreased significantly before VT. With propranolol (30-60 mg/day), frequency of repetitive PVCs was suppressed from 2,048 +/- 1,201 to 746 +/- 658/day and VT was totally abolished, but frequency of single PVCs did not change significantly. In conclusion, sympathetic predominance plays an important role in the initiation of repetitive PVCs and VT originating from RVOT in patients without structural heart diseases.

Factors influencing heart rate variability in patients with severe aortic valve disease.

Heart rate variability (HRV) is an accepted tool for the assessment of cardiovascular autonomic tone. There are no sufficient data concerning its application to patients with severe aortic valve disease (AVD) requiring cardiac surgery. It was the aim of this study to examine HRV and its physiologic correlates in patients with severe aortic valve disease requiring cardiac surgery. The correlates of time domain indices of HRV obtained from 24-h Holter electrocardiographic recordings were analyzed in 36 consecutive patients (23 men and 13 women, mean age 62 +/- 11 years) with AVD prior to cardiac surgery (aortic stenosis: 17 patients, aortic valve regurgitation: 3 patients, combined aortic valve disease: 16 patients). Low values of HRV were found in the entire study group: SDNN 96.8 +/- 30.9 ms, SDNNI 39.3 +/- 14.4 ms, SDANN 86 +/- 28.9 ms, and RMSSD 30 +/- 18.1 ms. In a univariate analysis, there was no significant correlation between the time domain measures of HRV and age, gender, medication, left ventricular ejection fraction, peak aortic pressure gradient, fraction of aortic valve regurgitation, and left ventricular mass assessed by echocardiography. Patients in advanced functional classes of heart failure [New York Heart Association (NYHA) III or IV] had significantly lower values for SDNN (83.8 +/- 33.6 vs. 107.3 +/- 24.7 ms; p < 0.05) and SDANN (72.7 +/- 29.4 vs. 96.6 +/- 24.3 ms; p < 0.05) than patients in NYHA class I or II. Reassessment of HRV 1 week after aortic valve replacement was performed in 17 patients and showed a significant further decrease of SDNN (102.4 +/- 29.7 vs. 61.5 +/- 23.5 ms; p < 0.001), SDNNI (40.7 +/- 13.6 vs. 23.4 +/- 12.4 ms; p < 0.001) and SDANN (91.8 +/- 29.2 vs. 54.2 +/- 22.8 ms; p < 0.001). Patients with AVD requiring cardiac surgery reveal reduced time domain indices of HRV. This observation is pronounced in patients with a progressed clinical class of heart failure, whereas hemodynamic and echocardiographic parameters seem to have no significant influence on HRV parameters in this population. In addition, there is evidence of a further reduction of HRV time domain indices 1 week after uncomplicated aortic valve replacement.

Short- and long-term assessment of heart rate variability for risk stratification after acute myocardial infarction

Depressed heart rate variability (HRV) has been shown to be a powerful and independent risk factor in patients following acute myocardial infarction (AMI). A detailed comparison of the predictive values between short- and long-term HRV has not been made. The predictive value of short-term HRV for 1-year total cardiac mortality was studied in 700 consecutive patients after AMI. All patients underwent 24-hour Holler monitoring before discharge from the hospital (5 to 8 days after AMI) and were followed up for 1 year. Short-term HRV was computed as the standard deviation of all normal RR intervals (SDNN) from a 5-minute stationary period selected from 24-hour Holter electrocardiographic recordings. Long-term HRV was computed as an HRV index over the entire 24 hours. There was a significant but relatively poor correlation between SDNN and HRV index (r = 0.51, p < 0.001). The positive predictive accuracy of SDNN for 1-year mortality (13% to 18%) was lower than the HRV index (17% to 43%) over a range of sensitivity of 25% to 75%. Assessment of HRV index in ≥35% of the patients preselected by the lowest SDNN was able to achieve predictive power similar to that of HRV index assessed in all the patients. These data suggest that lower predischarge short-term HRV is associated with increased 1-year total cardiac mortality in patients after AMI. Analysis of long-term HRV for postinfarction risk stratification can safely be limited to patients preselected by depressed short-term HRV measures.

Effect of long-term digoxin therapy on autonomic function in patients with chronic heart failure

Objectives.This study was conducted to determine the effect of long-term digoxin therapy on autonomic function in patients with mild to moderate chronic heart failure.Background.Chronic heart failure is characterized by increased sympathetic activity and decreased parasympathetic activity. Intravenous digitalis has been found to reduce sympathetic activity immediately in these patients, but whether short-term neurohormonal effects are sustained during long-term oral therapy has not been assessed.Methods.We determined sympathetic activity in 26 patients with heart failure by measuring plasma norepinephrine levels and parasympathetic activity from variables of heart period variability derived from 24-h ambulatory electrocardiographic Holter recordings obtained before and after 4 to 8 weeks of digoxin therapy.Results.After digoxin therapy, plasma norepinephrine decreased significantly from a mean ± SEM of 552 ± 80 to 390 ± 37 ng/ml. In addition, the RR interval increaed significantly from 719 ± 19 to 771 ± 20 ms. High frequency power increased from 84 ± 24 to 212 ± 72ms2, and the root mean square of successive differences in RR interval increased from 203 ± 1.8 to 27.0 ± 3.4 ms, indicating a substantial increase in parasympathetic activity. Low frequency power, an index of baroreflex activity, was also significantly increased (239 ± 80 to 482 ± 144 ms2) by digoxin therapy.Conclusions.These results indicate 1) that long-term therapy with digoxin acts to ameliorate the autonomic dysfunction of patients with heart failure, and 2) that the short-term neurohormonal effects of digoxin are sustained during prolonged treatment with the drug.

Antiarrhytmic effect of converting enzyme inhibitors in congestive heart failure

In this study 24-h Holter electrocardiographic recordings were used to measure the effects of an angiotensin converting enzyme inhibitor, enalapril given for 4 weeks, on the frequency of cardiac arrhythmias in 24 patients (14 patients had enalapril, 30 patients had placebo) with congestive heart failure (New York Heart Association Functional Class 3) receiving maintenance therapy with digoxin and furosemide. Although the placebo group had no change in the frequence of arrhythmias, enalapril-treated patients showed significant decrease in the frequency of premature ventricular complexes couplet, bigemine VPS and ventricular tachycardia. Moreover, it was observed that six cases of atrial fibrillation returned to sinus rhythm. During enalapril treatment, some, patients experienced increased serum potassium levels, but there was no change in serum digoxin levels. We also observed echocardiographic improvement in left ventricular function as well as clinical symptoms of congestive heart failure. Finally we observed that there was an antiarrhythmic effect of enalapril in congestive heart failure. We thought that the antiarrhythmic effect of enalapril in congestive heart failure was probably due to hemodynamic improvement.