title: Heart rate variability in patients suffering from structural heart disease and decreased AV-nodal conduction capacity. Insights into the formation of heart rate variability.
abstract: METHODS
  Time and frequency domain analysis were conducted during a period of 600 s each. We performed a special protocol consisting of five different "pacing" periods: 1) recording of normal sinus rhythm (SR1); 2) atrial pacing with a rate 15% higher than the intrinsic heart rate; 3) ventricular pacing triggered by atrial activation (VAT, with a short AV-delay of 80 ms); 4) AV-sequential pacing with an atrial rate 15% higher than the intrinsic heart rate and a very short AV delay of 80 ms (DDD); 5) normal sinus rhythm (SR2). Only patients with normal AV-nodal conduction or with AV-block I degrees were included. The influence of a structural heart disease as well as a non-sustained VT on Holter ECG and a depressed EF on HRV parameters were analyzed using a multivariate analysis. All patients were lying in a supine position. Blood pressure was measured continuously and the frequency of breathing was controlled.
  
  
  RESULTS
  No differences in HRV between the two sinus rhythm periods SR1 versus SR2 could be detected. Neither SR1 vs VAT showed a significant difference for SDNN and r-MSSD. In contrast, HRV during SR1 compared to AAI, and HRV during VAT compared to AAI were significantly different (p < 0.001). When comparing HRV during DDD, which should be zero, and AAI, we found a significantly lower SDNN and r-MSSD (1.2 ms vs 4 ms, p < 0.04). The presence of structural heart disease, a non-sustained ventricular tachycardia, a depressed ejection fraction of less than 0.50 did not reveal a significant influence on the HRV parameters (multivariate analysis). The mean Wenckebach in patients with structural heart disease tended to be greater (437 ms vs 350 ms, p = 0.05); an increase in the Wenckebach was not correlated to a change in HRV parameters (p = ns).
  
  
  CONCLUSIONS
  Heart rate variability derived from consecutive RR-intervals is predominantly caused by periodicity in sinus-node impulse formation. A conduction variability of the AV-node exists, but is very low. The presence of a structural heart disease, a non-sustained ventricular tachycardia on Holter ECG, as well as a depressed ejection fraction of less than 0.50 showed no significant influence on the HRV parameters. Therefore, one can apply the calculation of heart rate variability for risk stratification in patients suffering from structural heart disease and moderate AV-nodal conduction disturbances. Attenuation of the oscillation of the heart rate, i. e. heart rate variability (HRV), is associated with an increased risk for mortality in patients with structural heart disease. Many of these patients also suffer from conduction disturbances, e. g. AV-nodal conduction delays. Whether the calculation of HRV in those patients is recommendable has not been investigated yet. Therefore, we conducted a study consisting of 20 consecutive patients in order to determine the formation of HRV, the influence of structural heart disease, the presence of a nonsustained ventricular tachycardia (VT), and a reduced ejection fraction (EF) on the HRV parameters during an elective electrophysiologic study.
authors.affiliation: Department of Medicine-Cardiology, University of Bonn, Sigmund-Freud-Str. 25, 53105 Bonn, Germany. joerg.schwab@ukb.uni-bonn.de
authors.forename: J O
authors.initials: JO
authors.lastname: Schwab
authors.forename: G
authors.initials: G
authors.lastname: Eichner
authors.forename: H
authors.initials: H
authors.lastname: Schmitt
authors.forename: J
authors.initials: J
authors.lastname: Schrickel
authors.forename: A
authors.initials: A
authors.lastname: Yang
authors.forename: O
authors.initials: O
authors.lastname: Balta
authors.forename: B
authors.initials: B
authors.lastname: Lüderitz
authors.forename: T
authors.initials: T
authors.lastname: Lewalter
mesh_terms: D000328:Adult; D000368:Aged; D001283:Atrioventricular Node / Q000503:physiopathology*; D002304:Cardiac Pacing, Artificial; D002311:Cardiomyopathy, Dilated / Q000175:diagnosis / Q000503:physiopathology; D003327:Coronary Disease / Q000175:diagnosis / Q000503:physiopathology; D004562:Electrocardiography; D015716:Electrocardiography, Ambulatory; D005260:Female; D006325:Heart Atria / Q000503:physiopathology; D006327:Heart Block / Q000175:diagnosis / Q000503:physiopathology; D006331:Heart Diseases / Q000175:diagnosis* / Q000503:physiopathology; D006339:Heart Rate / Q000502:physiology*; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D012815:Signal Processing, Computer-Assisted; D012849:Sinoatrial Node / Q000503:physiopathology; D013318:Stroke Volume / Q000502:physiology; D013617:Tachycardia, Supraventricular / Q000175:diagnosis* / Q000503:physiopathology; D017180:Tachycardia, Ventricular / Q000175:diagnosis / Q000503:physiopathology; D016277:Ventricular Function, Left / Q000502:physiology