Chemoreflexsensitivity in patients with survived sudden cardiac arrest and prior myocardial infarction.
For evaluation of patients with an increased risk of sudden cardiac death, the analyses of ventricular late potentials, heart rate variability, and baroreflexsensitivity are helpful. But so far, the prediction of a malignant arrhythmic event is not possible with sufficient accuracy. For a better risk stratification other methods are necessary. In this study the importance of the ChRS for the identification of patients at risk for ventricular tachyarrhythmic events should be investigated. Of 41 patients included in the study, 26 were survivors of sudden cardiac arrest. Fifteen patients were not resuscitated, of whom 6 patients had documented monomorphic ventricular tachycardia and 9 had no ventricular tachyarrhythmias in their prior history. All patients had a history of an old myocardial infarction (> 1 year ago). For determination of the ChRS the ratio between the difference of the RR intervals in the ECG and the venous pO2 before and after a 5-minute oxygen inhalation via a nose mask was measured (ms/mmHg). The 26 patients with survived sudden cardiac death showed a significantly decreased ChRS compared to those patients without a tachyarrhythmic event (1.74 +/- 1.02 vs 6.97 +/- 7.14 ms/mmHg, P < 0.0001). The sensitivity concerning a survived sudden cardiac death amounted to 88% for a ChRS below 3.0 ms/mmHg. During a 12-month follow-up period, the ChRS was significantly different between patients with and without an arrhythmic event (1.64 +/- 1.06 vs 4.82 +/- 5.83 ms/mmHg, P < 0.01). As a further method for evaluation of patients with increased risk of sudden cardiac death after myocardial infarction the analysis of ChRS seems to be suitable and predicts arrhythmias possibly more sensitive than other tests of neurovegetative imbalance. The predictive importance has to be examined by prospective investigations in larger patient populations.
Hennersdorf
M G
MG
Department of Cardiology, Pneumology and Angiology, Heinrich-Heine-University, Duesseldorf, Germany. hennersd@uni-duesseldorf.de
Perings
C
C
Niebch
V
V
Hillebrand
S
S
Vester
E G
EG
Strauer
B E
BE
D000368:Aged; D001341:Autonomic Nervous System / Q000503:physiopathology*; D002628:Chemoreceptor Cells / Q000503:physiopathology*; D002940:Circadian Rhythm / Q000502:physiology; D016757:Death, Sudden, Cardiac; D004562:Electrocardiography; D005260:Female; D006323:Heart Arrest / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D006339:Heart Rate / Q000502:physiology; D006352:Heart Ventricles / Q000294:innervation / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications / Q000503:physiopathology*; D010102:Oxygen Inhalation Therapy; D011379:Prognosis; D012018:Reflex / Q000502:physiology*; D012151:Resuscitation; D017180:Tachycardia, Ventricular / Q000209:etiology / Q000503:physiopathology