Short‐Term Variability of the QT Interval Can be Used for the Prediction of Imminent Ventricular Arrhythmias in Patients With Primary Prophylactic Implantable Cardioverter Defibrillators

Background Short‐term variability of the QT interval (STV QT ) has been proposed as a novel electrophysiological marker for the prediction of imminent ventricular arrhythmias in animal models. Our aim is to study whether STV QT can predict imminent ventricular arrhythmias in patients. Methods and Results In 2331 patients with primary prophylactic implantable cardioverter defibrillators, 24‐hour ECG Holter recordings were obtained as part of the EU‐CERT‐ICD (European Comparative Effectiveness Research to Assess the Use of Primary Prophylactic Implantable Cardioverter Defibrillators) study. ECG Holter recordings showing ventricular arrhythmias of >4 consecutive complexes were selected for the arrhythmic groups (n=170), whereas a control group was randomly selected from the remaining Holter recordings (n=37). STV QT was determined from 31 beats with fiducial segment averaging and calculated as , where D n represents the QT interval. STV QT was determined before the ventricular arrhythmia or 8:00 am in the control group and between 1:30 and 4:30 am as baseline. STV QT at baseline was 0.84±0.47 ms and increased to 1.18±0.74 ms ( P <0.05) before the ventricular arrhythmia, whereas the STV QT in the control group remained unchanged. The arrhythmic patients were divided into three groups based on the severity of the arrhythmia: (1) nonsustained ventricular arrhythmia (n=32), (2) nonsustained ventricular tachycardia (n=134), (3) sustained ventricular tachycardia (n=4). STV QT increased before nonsustained ventricular arrhythmia, nonsustained ventricular tachycardia, and sustained ventricular tachycardia from 0.80±0.43 ms to 1.18±0.78 ms ( P <0.05), from 0.90±0.49 ms to 1.14±0.70 ms ( P <0.05), and from 1.05±0.22 ms to 2.33±1.25 ms ( P <0.05). This rise in STV QT was significantly higher in sustained ventricular tachycardia compared with nonsustained ventricular arrhythmia (+1.28±1.05 ms versus +0.24±0.57 ms [ P <0.05]) and compared with nonsustained ventricular arrhythmia (+0.34±0.87 ms [ P <0.05]). Conclusions STV QT increases before imminent ventricular arrhythmias in patients, and the extent of the increase is associated with the severity of the ventricular arrhythmia.

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Relationship between myocardial amiodarone concentration and antiarrhythmic effect in dogs with myocardial infarction and electrically induced ventricular arrhythmias

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y91-122 ◽

1991 ◽

Vol 69 (6) ◽

pp. 812-817 ◽

Cited By ~ 3

Author(s):

Hoshiar Abdollah ◽

F. James Brennan ◽

Sandra Jimmo ◽

James F. Brien

Keyword(s):

Ventricular Tachycardia ◽

Ventricular Fibrillation ◽

Ventricular Arrhythmias ◽

Dose Group ◽

Low Dose ◽

Antiarrhythmic Effect ◽

Baseline Data ◽

Sustained Ventricular Tachycardia ◽

Control Group ◽

High Dose

The relationship between the antiarrhythmic effect of amiodarone and its myocardial concentration was studied in dogs with 1-week-old myocardial infarction and reproducibly inducible sustained ventricular tachycardia or ventricular fibrillation. Three groups of animals (n = 10/group) received amiodarone, 40 mg∙kg−1∙day−1 (low-dose amiodarone), amiodarone 60 mg∙kg−1∙day−1 (high-dose amiodarone), or no amiodarone (control group). After 1 week of treatment, programmed electrical stimulation was repeated, and plasma and myocardial amiodarone and desethylamiodarone concentrations were measured. In the control group, sustained ventricular tachycardia or ventricular fibrillation was induced in six dogs (p = NS) when compared with baseline data. In the low-dose amiodarone group, sustained ventricular tachycardia or ventricular fibrillation was induced only in two dogs after 1 week of treatment (p < 0.01 vs. baseline data). Sustained ventricular tachycardia or ventricular fibrillation was induced in seven dogs after treatment with high-dose amiodarone (p = NS vs. baseline data). Plasma amiodarone concentration in the low-dose amiodarone group (2.54 ± 1.9 μg/mL) was significantly less (p < 0.01) than that in the high-dose amiodarone group (4.64 ± 1.66 μg/mL). Similarly, the plasma desethylamiodarone in the low-dose amiodarone group (0.32 ± 0.16 μg/mL) was significantly less (p < 0.001) than that in the high-amiodarone dose group (0.56 ± 0.23 μg/mL). The myocardial amiodarone concentration in the low-dose amiodarone group (49.7 ± 23.1 μg/g) was significantly lower (p < 0.001) than that in the high-dose group (98.4 ± 32.1 μg/g). There was no significant difference in the myocardial desethylamiodarone concentrations between the two treatment groups (25.1 ± 12.2 μg/g in the low-dose amiodarione group vs. 37.4 ± 16.4 μg/g in the high-dose amiodarone group). These data show that the high-dose amiodarone regimen, which produced high myocardial amiodarone concentration, didn't suppress sustained ventricular arrhythmias.Key words: amiodarone, ventricular arrhythmias, plasma and myocardial drug concentrations.

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