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Objectives: Thoracoscopic sympathectomy at levels T2 or T2-T3 is a treatment for focal hyperhidrosis and facial blushing. These levels of the sympathetic trunk innervate the heart, and consequently, the procedure is reported to change the heart rate variability due to changes in efferent cardiac autonomic activity. Our objective was to investigate the effects of thoracoscopic sympathectomy on global autonomic control, including baroreceptor sensitivity., Methods: Eight patients (6 F, median age 28 years [range 20-58 years]) were exposed to the tilt-table test and cardiopulmonary exercise test before, and 3 months after, thoracoscopic sympathectomy. Eight healthy age-, gender- and BMI-matched controls were used as controls and underwent the same tests once. During tilt-table testing electrocardiogram, blood pressure, impedance cardiography and respiration were measured continuously, and efferent cardiac autonomic balance was estimated., Results: The heart rate measured during orthostatic stress test was lowered after thoracoscopic sympathectomy (between-group; P = 0.01) due to a change in autonomic tone, with increased vagal (high-frequency power n.u.; P = 0.001), and reduced sympathetic efferent cardiac activity (low-frequency power n.u.; P < 0.001). Baroreceptor sensitivity measured during rest was increased (26 ± 13 vs 44 ± 19 ms/mmHg; P = 0.01), and diastolic blood pressure reduced after surgery (P = 0.01). The increases in systolic blood pressure and the sympathetic marker CCV-LF in response to orthostatic stress were higher before sympathectomy, with almost no increases post-surgically (condition × group interaction; P = 0.01 and P = 0.001, respectively). We found no change in post-procedure exercise capacity, although patients had a lower peak VO2 and maximal cardiac index than controls., Conclusions: Thoracoscopic sympathectomy changes the autonomic tone towards increased vagal activity; this is potentially cardioprotective. To our knowledge, this is the first study to show increased baroreceptor sensitivity after thoracoscopic sympathectomy.

Aims: We compared the prevalence and prognostic implications of non-sustained ventricular tachycardia (nsVT) detected early after ST-segment elevation myocardial infarction (STEMI) in patients randomized to either fibrinolysis or primary angioplasty in the DANAMI-2 trial., Methods and Results: Holter recordings were available in 1017 patients (fibrinolysis: n=501; primary angioplasty: n=516). Primary endpoint was all-cause mortality. The prevalence of nsVT was 8.8% in fibrinolysis-treated, and 8.1% in primary angioplasty-treated patients (P=0.71). During 4519 patient-years of follow-up (median 4.3 years), 116 patients died [fibrinolysis vs. angioplasty: HR=1.1 (95% CI, 0.8-1.6), P=0.47]. In univariate analysis, nsVT patients treated with fibrinolysis, had significantly higher mortality when compared with those without nsVT (P<0.001). However, after adjustment for other relevant prespecified risk factors, the association between nsVT and mortality did not remain statistically significant. In patients treated with primary angioplasty, nsVT was not associated with mortality in either univariate or multivariate analyses., Conclusion: Immediate revascularization with primary angioplasty for STEMI does not affect the subsequent prevalence of nsVT when compared with fibrinolysis. After adjustment for other relevant risk factors, the prognostic value of nsVT detected early after STEMI is limited, regardless of the chosen reperfusion strategy.

Aim: To investigate the relationship between serum content of n-3 polyunsaturated fatty acids (PUFA) and the incidence of ventricular arrhythmias in patients with an implantable cardioverter defibrillator (ICD)., Methods: We included 98 patients with ischaemic heart disease and an ICD. The numbers of ventricular fibrillation (VF) and ventricular tachycardia (VT) events were assessed during a 12-month period and related to the concentration of n-3 PUFA in serum phospholipids., Results: Patients with more than one arrhythmic event had significantly lower n-3 PUFA levels compared with patients without arrhythmias (mean 7.1% vs 9.2%, P<0.01). Dividing the patients into quintiles according to their n-3 PUFA level those with the lowest content of n-3 PUFA had more ventricular arrhythmias than patients with the highest concentration of n-3 PUFA (mean 1.3 event vs 0.2 event, P<0.05)., Conclusion: Patients with a low content of n-3 PUFA in serum had a higher incidence of ventricular arrhythmias compared with patients with high serum levels of n-3 PUFA. The data suggest that the protection offered by n-3 PUFA against sudden cardiac death observed in previous studies is mediated by a direct antiarrhythmic effect of n-3 PUFA.

Alterations in cardiovascular function may be an aetiological factor for the development of microalbuminuria in patients with insulin-dependent diabetes mellitus. We studied cardiac function with echocardiography in relation to the degree of albuminuria in 27 insulin-dependent diabetes mellitus patients and 13 healthy subjects. Patients were grouped according to urinary albumin excretion: <20 microg x min(-1) (normoalbuminuric), and 20 to 200 microg x min(-1) (microalbuminuric). None were or had been treated with cardiovascular drugs. The normoalbuminuric patients had a higher heart rate, mean velocity of circumferential shortening, stroke velocity index (a measure of contractility), and aortic peak velocity than controls. No difference in diastolic function was present. In the microalbuminuric group, the stroke velocity index was comparable to values observed in healthy subjects. The increased systolic performance (heart rate and contractility) may contribute to the renal hyperperfusion and glomerular hyperfiltration observed in insulin-dependent diabetes mellitus patients before the development of micro- and in turn macroalbuminuria. The possible cause effect mechanisms should be further studied, as preventive medical treatment of the hypercontractile heart is possible. In conclusion, cardiac contractility is increased in insulin-dependent diabetes mellitus patients with normoalbuminuria and returns to levels observed in healthy subjects when microalbuminuria develops.

Late potentials are detected at various noise levels in clinical studies. The aim of this study was, in a case-control design, to assess the effect of residual noise level on the identification of patients with sustained monomorphic ventricular tachycardia after myocardial infarction. Electrocardiograms from 16 patients with prior myocardial infarction and documented sustained monomorphic ventricular tachycardia and 41 patients with prior myocardial infarction and without ventricular tachycardia, were analysed by two signal averaging procedures to noise level 0.2 and 0.4 muV. Standard time domain parameters were measured. Two definitions of late potential were analysed: (1) if any two of the following criteria were present (signal-averaged QRS duration > 120 ms, late potential duration > 40 ms, and root-mean-square voltage of the terminal 40 ms of the filtered QRS < 25 muV); or (2) if the signal-averaged QRS duration > or = 120 ms. Overall the signal-averaged electrocardiogram performed better at noise level 0.4 muV compared to noise level 0.2 muV with respect to identification of patients with or without ventricular tachycardia after myocardial infarction. Reducing noise level from 0.4 to 0.2 muV increased the sensitivity, but the consequence was a substantial decrease in specificity. Our data indicate that when a high sensitivity is the goal, the definition based only on signal-averaged QRS duration > or = 120 ms should be applied; sensitivity was 88% and specificity 59% at noise level 0.4 muV. If a high specificity is the goal, the definition should be based on the definition with two abnormal parameters; sensitivity was 69% and specificity 68% at noise level 0.4 muV.

The pathophysiology of angina pectoris in patients with a normal coronary angiogram is not clear. Furthermore, the pathophysiological impact of ST changes in syndrome X is controversial. The purpose of this study was to investigate cardiac autonomic function, by measuring 24 h heart rate variability, in patients with and without electrocardiographic evidence of ischaemia during exercise. Thirty-two patients with angina pectoris, a normal coronary angiogram, echocardiogram, hyperventilation test and gastro-oesophageal investigation were studied. Fourteen healthy subjects served as controls. Fifteen patients had significant ST segment depression during stress testing, whereas 17 had no electrocardiographic signs of ischaemia. Heart rate variability was calculated as (1) mean RR = mean of all normal RR intervals, (2) the difference in mean RR level between when awake and when asleep (mean RR wake-sleep)-a tentative index of sympathetic activation, (3) the standard deviation (SD)-a broad band measure of autonomic balance, and (4) a percentage of successive RR interval differences > or = 6% (pNN6%)-an index of vagal modulation. The coronary vascular resistance was measured at rest and during pacing. Mean RR and autonomic indexes did not differ between patients with a positive exercise test and controls (831/884 ms; 24 h SD 125/134 ms; pNN6% 6.715.4%, respectively). Patients with a normal exercise test had shorter mean RR (758 ms vs 844 ms; P < 0.05) and significantly reduced 24-h SD (103 ms vs 134 ms; P < 0.05) than controls, whereas values for vagal index (6.5% vs 5.4%) did not differ from healthy controls. Mean RR wake-sleep also tended to be lower in patients with a normal exercise test (-125 ms vs -173 ms) compared to controls (P < 0.1). Patients with a positive exercise test had a significantly attenuated reduction in coronary vascular resistance during pacing in comparison to patients with a normal exercise test (-0.131 -0.26 mmHg x min. ml-1; P < 0.05). The findings suggest the occurrence of general elevated sympathetic activation in angina patients with a normal exercise test. Patients with a positive exercise test exhibited no signs of autonomic dysfunction although these patients had altered coronary vascular resistance indicating microvascular angina. This supports the suggestion that patients with a normal exercise test constitute an independent pathophysiological entity.

To investigate the impact of pre-operative autonomic balance and atrial ectopic activity on the risk of atrial fibrillation or flutter after aorto-coronary artery bypass surgery 24-h Holter monitoring was analysed in 102 patients before coronary artery bypass grafting. Index for vagal tone was calculated as % successive RR interval differences > 6%. Twenty-nine (28%) of the 102 patients developed atrial fibrillation or flutter. Independent predictors (90% confidence interval) of postoperative atrial fibrillation or flutter were identified by logistic regression analysis: the independent predictors were older age, relative risk 1.07.year-1 (1.02-1.12), vagal index < 10%, relative risk 4.50 (1.40-14.5), > or = 10 ectopic supraventricular beats . 24 h-1, relative risk 3.03 (1.05-8.72), and one or more events of non-sustained supraventricular tachycardia, relative risk 3.02 (1.11-8.22). Thus, age of the patient, attenuated pre-operative cardiac vagal modulation, ectopic supraventricular beats, and paroxysmal non-sustained supraventricular tachycardia are independent risk factors for the development of atrial fibrillation or flutter after coronary artery bypass surgery.

Cardiac neural control can be estimated by frequency domain characterization of RR interval variations. This technique may become a clinical tool, as autonomic dysfunction is involved in the pathophysiology of sudden cardiac death. The study was designed to investigate 24-h cardiac autonomic control in 104 healthy subjects aged 40-77 years and to evaluate the impact of gender, age, smoking and physical training level. The sympathovagal balance was evaluated by spectral analysis of RR interval oscillations. The square-root of power of the high- (HF; 0.15-0.40) and low-frequency (LF; 0.04-0.15 Hz) bands were considered indexes of the vagal function and of the sympathovagal interaction, respectively. In addition, the precise centre frequency of the LF and HF oscillations was determined. The vagal mediated respiratory-dependent HF oscillation exhibited a clear circadian variation, and obtained the highest power values during sleep. The centre frequency was significantly lower during sleep (0.26 Hz vs 0.28 Hz), probably due to a slower respiratory frequency at night. Values for vagal tone were higher in physically trained subjects throughout the 24-h, and decreased by 13% for every 10-year increase in age; it was also reduced in smokers. The amplitude of the LF oscillation exhibited no clear diurnal variation. The mean LF/HF ratio was 3.1. LF power was much higher in males, was reduced by 15% per 10 year increase in age, and was lower in sedentary and smoking subjects, throughout the 24-h. The mean centre frequency of this component was reduced with advancing age (0.08 to 0.06 Hz from age 40 to 80 years). LF and HF power correlated positively, (r = 0.68), and 46% and 16% of the interindividual variation in LF and HF power, respectively, was explained by the four factors (gender, age, smoking, physical activity). Thus gender, age smoking and physical training level have a significant impact on the power and centre frequency of the HF and LF components. These effects must be addressed in investigations on autonomic balance.

This report describes the fate of two young men wrongly treated with thrombolysis for suspected myocardial infarction. Both had electrocardiographic changes upon admission. Correct diagnosis of aortic dissection and haemorrhagic pericarditis was obtained within a few hours, but due to the prolonged disturbance of haemostasis, appropriate therapy could not be instituted, and outcome was fatal for both patients. These cases underline the importance of rigid ST criteria, and procedures for neutralization of thrombolysis are proposed.

Heart rate variability (HRV) in 24-h Holter recordings is normally determined using commercially available Holter equipment. However, short-term speed variations in tape-based Holter systems have not been thoroughly investigated and recommendations for speed control are vague. In this study, overall accuracy and precision of RR interval measurement was assessed for two types of tape recorder replayed on the same Reynolds Pathfinder II system. Artificial QRS complexes spaced at exact intervals were recorded simultaneously by the two recorders. In addition, records of 118 healthy subjects were evaluated for false-positive normal-normal intervals. During replay, digital output from the pathfinder was processed by a locally developed personal computer-based HRV system. Using the recorded crystal generated timing track (TT) for speed control and the TT dependent speed surveyor (SS), set to allow speed errors up to +/- 3.1%, mean RR per 5 min.h-1.24 h-1, for test tapes, corresponded exactly to true RR, for both recorders. Beat-to-beat variation, for 1000 ms test intervals, calculated as standard deviation (SD) and root mean square of successive differences (RMSSD) was 3 ms, 3 ms versus 5 ms, and 8 ms for Oxford and Tracker tapes respectively. No difference between sequential intervals exceeded +/- 10 ms versus +/- 20 ms for Oxford and Tracker respectively. Reproducibility of mean RR and HRV parameters for patient records, expressed as a coefficient of variation, was 0.1-1.7%. False positive normal-normal intervals greater than 2.3 s, due to artifacts, were found in 99 of 118 records, and these increased mean SD and RMSSD values significantly, whereas percent successive RR interval differences greater than 50 ms were unaffected. A crystal generated TT (60/16 Hz) and an SS allowing a maximum error of +/- 3.1%, together correct speed during recording and replay to a degree that is acceptable for HRV analysis. A simple estimate of HRV counts of successive RR interval differences greater than 50 ms is a reliable parameter as it is relatively insensitive to artifact.

A 24-h Holter monitoring (HM) record was obtained on two occasions 8 years apart in 183 healthy subjects (120 male and 63 female), aged 40-85 years. The purpose of the study was to determine the minimal mean heart rate (HR-min) and longest pauses in heart rhythm, and to examine possible changes in these parameters over a longer period of time. (HR-min was calculated from a 1-min sample period.) HR-min was influenced by physical activity level and smoking habit, but was independent of age. Females had higher HR-min than males. In the male group mean HR-min was 54 beats min-1 and 53 beats min-1 on the two recordings (P greater than 0.05) (range 36-75 beats min-1 and 38-69 beats min-1). HR-min less than 40 beats min-1 was seen in 2.5% of the males. In the female group, the lowest recorded HR was 42 beats min-1 and mean HR-min on the two recordings was 58 beats min-1 and 56 beats min-1 (P less than 0.001). The paired HR-min observations were highly correlated. In all subjects, pauses greater than or equal to 1.75 s were registered in 6% and 6.5% on the two recordings. The occurrence of pauses was related to low HR-min. Above the age of 60 years sinus arrest was the type of pause most often seen.(ABSTRACT TRUNCATED AT 250 WORDS)