Origins of heart rate variability. Inducibility and prevalence of a discrete, tachycardic event.
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BACKGROUND: We propose that heart period sequences are linearly organized, like sentences, and that there is a lexicon of recurrent, similarly shaped transient structures like words. Each word (or lexon) has a characteristic physiological basis. One potential lexon is the transient, reversible tachycardia that is induced by exercise initiation under laboratory conditions. We hypothesized that this lexon was inducible and observable on ambulatory ECGs of most or all subjects, was morphologically similar in both induced and detected bursts, and shared a plausible origin in both circumstances. METHODS AND RESULTS: Ten healthy subjects (mean age, 36 years) underwent a protocol in which subjects rolled themselves from supine to lateral decubitus positions and back. Transient tachycardias ("bursts") were seen in 36 of 40 rollovers. Bursts were characterized by an initial monoexponential heart period decay (K=0.39+/-0.23 s-1), a maximum heart period decrease of 277+/-109 ms after 10.8+/-4.5 seconds, and a subsequent return to baseline 23.3+/-10.8 seconds after roll initiation. The roll-induced bursts were detected with 97% sensitivity and 99% specificity with a search algorithm that incorporated morphological parameters. In 24-hour ambulatory ECGs of 10 healthy subjects (mean age, 38 years; range, 17 to 69 years), 117+/-59 bursts were detected. Induced and detected bursts were similar in most morphological parameters. Finally, many bursts occurred at night, when rolling over also occurs. CONCLUSIONS: Bursts are inducible, transient tachycardias that occur clinically and constitute a lexon with an understandable physiology. (+info)
Unsuitability of corrected QT dispersion as a marker for ventricular arrhythmias and cardiac sudden death after acute myocardial infarction.
(26/1346)
The present study investigated whether corrected QT (QTc) dispersion could play a role as a marker of ventricular arrhythmias and sudden cardiac death after acute myocardial infarction (MI). The study included 76 males and 24 females with a mean age of 60+/-11 years. Standard 12-lead ECGs were recorded during the recovery phase (15+/-9 days) after the onset of MI. The QTc was calculated according to Bazett's formula and QTc dispersion was calculated as the difference between the maximum and minimum QTc intervals. Patients were divided into 2 groups: 21 patients (group A) had a QTc dispersion of > or =80ms, and the other 79 patients (group B) had a QTc dispersion of <80ms in the recovery stage (15+/-9 days). Clinical, angiographical, and Holter monitoring data, and prognosis (mean follow-up period 29+/-18 months) were compared between these 2 groups. The frequencies of early coronary reperfusion and recanalization of infarct-related vessels during the recovery phase were significantly higher in group B than group A. The left ventricular ejection fraction was also higher in group B than group A (51+/-12 vs 43+/-12%, p=0.0029). There were no significant differences in the number of premature ventricular contractions, the percentage of patients with repetitive ventricular arrhythmias, or in the frequency of sudden cardiac death during the follow-up period between the 2 groups. In summary, QTc dispersion in the recovery stage is not a useful marker for ventricular arrhythmias or sudden cardiac death after acute MI, although increased QTc dispersion may correlate with an ineffective early coronary reperfusion and with the degree of depressed left ventricular function. (+info)
(123)I-metaiodobenzylguanidine myocardial scintigraphy in Parkinson's disease.
(27/1346)
OBJECTIVES: (123)I-metaiodobenzylguanidine (MIBG) myocardial scintigraphy is clinically used to estimate local myocardial sympathetic nerve damage in some forms of heart disease, autonomic nerve disturbance in diabetic neuropathy, and disturbance of the autonomic nervous system in neurodegenerative disease. In the present study, examinations were performed to clarify (1) the proportion of cardiac sympathetic nerve disturbance in Parkinson's disease, (2) the usefulness of (123)I-MIBG myocardial scintigraphy to detect sympathetic nerve disturbances compared with autonomic function tests, (3) cardiac function in patients who have a decreased MIBG uptake in (123)I-MIBG myocardial scintigraphy, (4) the usefulness of (123)I-MIBG myocardial scintigraphy to differentiate Parkinson's disease from the other neurological diseases mimicking it. METHODS: (123)I-MIBG myocardial scintigraphy was performed, together with autonomic function tests and cardiac examinations in 46 patients with Parkinson's disease and 25 patients with vascular parkinsonism, essential tremor, or multiple system atrophy. RESULTS: In an anterior image study, the average count per pixel in heart to mediastinum (H/M) ratio decreased in 80% of the patients with Parkinson's disease in the early phase and 84% in the late phase. The mean H/M ratio in Parkinson's disease was significantly lower than that in controls and the other diseases. The H/M ratio tended to decrease with the disease progression. In almost half of the patients in Hoehn and Yahr stage I, the H/M ratio was already decreased. The sympathetic skin response in upper and lower limbs, head up tilt test, and coefficient of variation of R-R interval were abnormal in 17%, 31%, 30%, and 17% of the patients, respectively. All the patients with abnormal autonomic functions were in Hoehn and Yahr stage III, IV, or V. Echocardiography showed normal left ventricular function. Twenty four hour Holter electrocardiography detected no serious arrhythmias except for one patient with non-sustained ventricular tachycardia. CONCLUSION: (123)I-MIBG myocardial scintigraphy might detect early disturbances of the sympathetic nervous system in Parkinson's disease and might give useful diagnostic information to differentiate vascular parkinsonism, essential tremor, and multiple system atrophy from Parkinson's disease. (+info)
An open label, randomised, crossover study comparing sotalol and atenolol in the treatment of symptomatic paroxysmal atrial fibrillation.
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OBJECTIVE: To compare sotalol and atenolol in the treatment of symptomatic paroxysmal atrial fibrillation. DESIGN: Prospective, randomised, open label, crossover study. SETTING: University hospital. PATIENTS: 47 subjects aged over 50 years were recruited from the hospital outpatient department following ECG documentation of paroxysmal atrial fibrillation that coincided with symptoms. Six patients withdrew and 41 completed the trial. INTERVENTIONS: Patients were randomised to one month's treatment with sotalol 80 mg twice daily or atenolol 50 mg once daily. Treatment arms were then crossed over. Patients underwent 72 hour Holter monitoring before randomisation and repeat studies were carried out at the end of both treatment periods. Symptom assessments were completed using linear analogue scales and the Nottingham health profile. MAIN OUTCOME MEASURE: Frequency of paroxysmal atrial fibrillation; secondary outcome measures included average and total duration of paroxysmal atrial fibrillation, total ectopic count, and symptom assessments. RESULTS: A reduction in the number and duration of episodes of paroxysmal atrial fibrillation was noted following treatment with sotalol and atenolol. There was no difference in frequency of paroxysmal atrial fibrillation during treatment with sotalol or atenolol (median difference 0; 95% confidence interval (CI) 0 to 1; p = 0.47). There was no difference in total duration of paroxysmal atrial fibrillation (median difference 0 min; 95% CI -1 to 2; p = 0. 51) or in average duration (median difference 0 min; 95% CI 0 to 1; p = 0.31). No difference was found in total ectopic count between sotalol and atenolol (median difference -123; 95% CI -362 to 135; p = 0.14). Treatments were equally tolerated with no difference in linear analogue scores for symptoms of paroxysmal atrial fibrillation (median difference -5; 95% CI -20 to 5; p = 0.26) or in all categories of the Nottingham health profile. CONCLUSIONS: No difference was found in terms of ECG or symptomatic control of paroxysmal atrial fibrillation between prescribing sotalol 80 mg twice daily and atenolol 50 mg once daily. There was an improvement in paroxysmal atrial fibrillation from baseline following treatment with either sotalol or atenolol. (+info)
A new physiological method for heart rate correction of the QT interval.
(29/1346)
AIM: To reassess QT interval rate correction. BACKGROUND: The QT interval is strongly and inversely related to heart rate. To compare QT intervals between different subjects with different heart rates requires the application of a QT interval rate correction formula. To date these formulae have inappropriately assumed a fixed relation between QT interval and heart rate. An alternative method of QT interval rate correction that makes no assumptions about the QT interval-heart rate relation is needed. PROPOSAL: A QT heart rate correction method should maintain or accentuate biological QT interval variability, should totally remove the dependence of the rate corrected QT interval on heart rate, and should be applicable over a wide range of conditions with a wide range of differing autonomic states. METHODS: QT intervals were obtained at rest and during exercise from subjects expected to have different QT intervals and different QT interval-heart rate relations. A linear regression line was obtained from the exercise test data, and the QT interval at a notional heart rate of 60 and 0 beats/min, termed the QT(60) interval, and the QT y intercept obtained by back calculation. RESULTS: QT(60) and QT y intercept values were prolonged in heart failure compared with either left ventricular hypertrophy or controls. There was no relation between heart rate and either QT(60) or QT y intercept CONCLUSIONS: This new physiologically based method of correcting QT interval for heart rate removes the dependence of the corrected QT interval on heart rate, and maintains biological differences. (+info)
Cyclic bursts of ventricular premature contractions of more than one minute intervals.
(30/1346)
Ventricular premature contractions (VPCs) occasionally appear successively in the form of bigeminy, trigeminy or quadrigeminy associated with quiescent periods. However, details of these rhythmic VPC bursts have not been well documented. We analyzed the incidence, periodicity and interval of VPC bursts exhibiting bigeminy or trigeminy using ambulatory ECG monitoring and computer analysis. We defined VPC bursts as more than 5 successive groups of VPCs each containing more than 20 VPCs in the form of bigeminy or trigeminy that were interrupted by normal sinus rhythm lasting for more than 60 seconds. Bursts thus defined were observed transiently or continuously in 78 out of 500 consecutive patients showing > 3000 VPCs a day. Their age ranged from 14 to 76 years (mean 48). Forty patients were men and 38 were women. We could discriminate between two types of bursts on the instantaneous heart rate tachograms. Dome type bursts (n = 48) showed gradual shortening of the VPC coupling intervals whereas horizontal type bursts (n = 30) demonstrated fixed coupling intervals during the bursts. Cycle length of the dome type burst was 185 +/- 40 seconds and regular, whereas it was 210 +/- 63 seconds and irregular in the horizontal type (NS). Duration of the VPC bursts was 101 +/- 31 seconds in the dome type and 98 +/- 41 seconds in the horizontal type. Both burst types were associated with transient increases in sinus rate and abbreviated VPC-VPC intervals. We suspect ventricular parasystole to be the mechanism of these bursts especially in the dome type. Recognition of these two burst types from heart rate tachograms may be of value in the suppression of VPCs. (+info)
Cardiac assessment of veteran endurance athletes: a 12 year follow up study.
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OBJECTIVES: Sustained aerobic dynamic exercise is beneficial in preventing cardiovascular disease. The effect of lifelong endurance exercise on cardiac structure and function is less well documented, however. A 12 year follow up of 20 veteran athletes was performed, as longitudinal studies in such cohorts are rare. METHODS: Routine echocardiography was repeated as was resting, exercise, and 24 hour electrocardiography. RESULTS: Nineteen returned for screening. Mean (SD) age was 67 (6.2) years (range 56-83). Two individuals had had permanent pacemakers implanted (one for symptomatic atrial fibrillation with complete heart block, the other for asystole lasting up to 15 seconds). Only two athletes had asystolic pauses in excess of two seconds compared with seven athletes in 1985. Of these seven, five had no asystole on follow up. Two of these five had reduced their average running distance by about 15-20 miles a week. One athlete sustained an acute myocardial infarction during a competitive race in 1988. Three athletes had undergone coronary arteriography during the 12 years of follow up but none had obstructive coronary artery disease. Ten of 19 (53%) had echo evidence of left ventricular hypertrophy in 1997 but only two (11%) had left ventricular dilatation. Ten athletes had ventricular couplets on follow up compared with only two in 1985. CONCLUSIONS: Although the benefits of moderate regular exercise are undisputed, high intensity lifelong endurance exercise may be associated with altered cardiac structure and function. These adaptations to more extreme forms of exercise merit caution in the interpretation of standard cardiac investigations in the older athletic population. On rare occasions, these changes may be deleterious. (+info)
Kinetics of 123I-MIBG after acute myocardial infarction and reperfusion therapy.
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Metaiodobenzylguanidine (MIBG) washout from the myocardium has been thought to reflect sympathetic nerve tone. After acute myocardial infarction, however, little is known about this parameter. The aim of this study was to determine the significance of cardiac washout after myocardial infarction and early reperfusion by investigating MIBG kinetics and correlating those kinetics to clinical parameters. METHODS: Sixty patients with acute myocardial infarction underwent planar MIBG and thallium imaging within 14 d of early reperfusion therapy. Global uptake and washout in myocardium, lungs and liver were calculated from early and delayed images. A regional analysis of myocardial kinetics in normal and infarcted myocardium and in an infarct border zone was also performed. Scintigraphic data were correlated with heart-rate variability as an electrophysiologic marker for autonomic tone and prevalence of arrhythmia in 52 patients. Heart-rate variability was described by time-domain indices from long-term electrocardiogram recordings. An age-matched normal control group for MIBG consisted of 10 individuals without heart disease. RESULTS: The infarct patients had preserved left-ventricular ejection fraction (LVEF) (56% +/- 17%). Although late myocardial uptake was expectedly lower in infarct patients compared with healthy volunteers (2.36 +/- 0.66 versus 2.80 +/- 0.55; P = 0.04), global myocardial MIBG washout was faster (11.6% +/- 7.9% versus 0.2% +/- 10.2%, respectively; P = 0.002). Lung and liver kinetics did not differ in patients and healthy volunteers. Global MIBG washout showed a weak but significant positive correlation with the baseline heart rate (r = 0.28, P = 0.03) and an inverse correlation with LVEF (r = -0.28, P = 0.04). Washout was faster in a subgroup of 8 patients with reduced heart-rate variability (16.5% +/- 9.9% versus 10.3% +/- 8.3%; P = 0.04). Regional analysis revealed similar degrees of enhanced MIBG washout for infarcted (low perfusion, low MIBG uptake) and remote myocardium (normal perfusion, high MIBG uptake), whereas the border zone (normal perfusion, low MIBG uptake) showed a nonsignificant trend toward higher washout. CONCLUSION: After myocardial infarction, changes in MIBG kinetics occur specifically in the myocardium, whereas kinetics in lung and liver remain unchanged. Even in patients with left-ventricular function preserved by reperfusion therapy, MIBG washout is abnormal and globally increased. Enhanced washout may reflect increased sympathetic nerve tone and represent increased catecholamine turnover or impaired reuptake in the subacute phase of myocardial infarction. (+info)