title: [Chemoreflex and baroreflex sensitivity in patients with survived sudden cardiac death].
abstract: BACKGROUND
  To evaluate patients with an increased risk of sudden cardiac death the analysis of ventricular late potentials, heart rate variability and baroreflexsensitivity is helpful. However, the prediction of malignant arrhythmic events cannot be performed with sufficient accuracy. For a better identification of high risk patients other methods are necessary. In this study the impact of the chemoreflexsensitivity for the prediction of ventricular tachyarrhythmias was investigated.
  
  
  METHODS
  Out of 44 patients included in the study, 23 were survivors of sudden cardiac death (SCD). Seven patients suffered from sustained monomorphic ventricular tachycardias, 14 had no arrhythmic events in their prior history. For the investigation of the baroreflexsensitivity (BRS) systolic blood pressure was augmented by Norfenefrin (Novadral) and the resulting increase of RR-intervals was measured in the surface-ECG. For determination of the chemoreflexsensitivity (ChRS) the ratio of the RR-interval-shift and the blood pressure shift during a 5-min inhalation of oxygen with a nose mask was formed.
  
  
  RESULTS
  Patients with aborted SCD showed significantly decreased values for the ChRS compared to those patients without an arrhythmic event in their prior history (2.49 +/- 1.86 vs. 6.75 +/- 6.79 mm Hg, p < 0.001). In contrast, for the BRS no significant differences could be found (5.23 +/- 3.95 vs. 5.34 +/- 3.10 mm Hg, p = n.s.). Patients with aborted sudden cardiac death and inducible tachyarrhythmias during the electrophysiologic study showed significantly lower values of BRS and ChRS compared to patients without inducibility.
  
  
  CONCLUSIONS
  As a new method for identification of patients with an increased risk of sudden cardiac death the analysis of chemoreflexsensitivity seems feasible and indicates an increased arrhythmic risk with a high sensitivity. The predictive impact has to be corroborated in larger patient collectives by prospect studies.
authors.affiliation: Abteilung für Kardiologie, Pneumologie und Angiologie, Heinrich-Heine-Universität, Düsseldorf.
authors.forename: M
authors.initials: M
authors.lastname: Hennersdorf
authors.forename: C
authors.initials: C
authors.lastname: Perings
authors.forename: M
authors.initials: M
authors.lastname: Kristovic
authors.forename: H
authors.initials: H
authors.lastname: Dees
authors.forename: S
authors.initials: S
authors.lastname: Hillebrand
authors.forename: B
authors.initials: B
authors.lastname: Holz
authors.forename: E G
authors.initials: EG
authors.lastname: Vester
authors.forename: B E
authors.initials: BE
authors.lastname: Strauer
mesh_terms: D001341:Autonomic Nervous System / Q000503:physiopathology; D001794:Blood Pressure / Q000502:physiology; D016887:Cardiopulmonary Resuscitation; D002628:Chemoreceptor Cells / Q000503:physiopathology*; D016757:Death, Sudden, Cardiac / Q000209:etiology* / Q000517:prevention & control; D004562:Electrocardiography / Q000187:drug effects; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009655:Octopamine / Q000031:analogs & derivatives; D011311:Pressoreceptors / Q000503:physiopathology*; D012021:Reflex, Abnormal / Q000502:physiology*; D012307:Risk Factors; D013318:Stroke Volume / Q000502:physiology; D017180:Tachycardia, Ventricular / Q000503:physiopathology; D016277:Ventricular Function, Left / Q000502:physiology
chemical_list: D009655:Octopamine; C005310:norfenefrine