Human ventricular refractoriness. Effects of cycle length, pacing site and atropine.

616

144

Background-A prolonged QT interval is associated with a risk for life-threatening events. However, little is known about prognostic implications of the reverse-a short QT interval. Several members of 2 different families were referred for syncope, palpitations, and resuscitated cardiac arrest in the presence of a positive family history for sudden cardiac death. Autopsy did not reveal any structural heart disease. All patients had a constantly and uniformly short QT interval at ECG. Methods and Results-Six patients from both families were submitted to extensive noninvasive and invasive work-up, including serial resting ECGs, echocardiogram, cardiac MRI, exercise testing, Holter ECG, and signal-averaged ECG. Four of 6 patients underwent electrophysiological evaluation including programmed ventricular stimulation. In all subjects, a structural heart disease was excluded. At baseline ECG, all patients exhibited a QT interval Յ280 ms (QTc Յ300 ms). During electrophysiological study, short atrial and ventricular refractory periods were documented in all and increased ventricular vulnerability to fibrillation in 3 of 4 patients. Conclusions-The short QT syndrome is characterized by familial sudden death, short refractory periods, and inducible ventricular fibrillation. It is important to recognize this ECG pattern because it is related to a high risk of sudden death in young, otherwise healthy subjects.

Section: Discussionsupporting

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Short QT Syndrome

Gaïta¹,

Giustetto²,

Bianchi³

et al. 2003

616

144

“…This protocol was repeated 4 minutes after the administration of i.v. propranolol, 0.1 mg/kg, over 30 …”

Section: Methodsmentioning

confidence: 99%

“…This protocol was repeated 4 minutes after the administration of i.v. propranolol, 0.1 mg/kg, over 30 seconds and again 5 minutes after i.v. atropine, 0.02 mg/kg, over 30 seconds.…”

Section: Methodsmentioning

confidence: 99%

Influence of heart rate and inhibition of autonomic tone on the QT interval.

Ahnve¹,

Vallin²

1982

276

108

SUMMARY To evaluate whether heart-rate-induced changes of the QT interval are dependent on autonomic tone, we studied 13 healthy subjects, mean age 67.5 years. The maximal uncorrected QT from leads I, II, V1 and V,, was determined during atrial pacing at 90 beats/min and 130 beats/min before and after i.v. administration of propranolol, 0.1 mg/kg, and atropine, 0.02 mg/kg.Significant reductions (p < 0.01) of QT were induced by the paced increases in heart rate before drugs (10%), after propranolol (10%) and after the combination of atropine and propranolol (9%). Propranolol caused no significant change in the QT interval when heart rate was held constant by pacing. In contrast, atropine produced rate-independent reductions of QT interval (5%) in subjects with ,3-adrenergic blockade (p < 0.05). Bazett's formula for heart-rate correction of the QT interval (QTc) was not applicable for atrial overdrive pacing, as it gave proportionately longer QTc values at higher heart rates.These results show that heart rate is a major determinant of the duration of the QT interval and that paced changes in heart rate induce QT-interval responses that are essentially uninfluenced by autonomic tone. The rate-independent effect of the QT interval produced by elimination of cholinergic tone suggests a direct influence of cholinergic activity on the repolarization of ventricular myocardium.INTEREST in obtaining clinical information from the QT interval of the ECG has recently increased. One reason for this is the reported association between prolonged QT intervals and serious ventricular arrhythmiasl'6 and the identification of QT prolongation as a prognostic factor for sudden death.' 7 8 Several factors influence the QT interval, including electrolyte disturbances" and drugs.9""' The effect of sympathetic nervous activity on the QT interval is well established.'2-'5 In addition, the autonomic nervous system affects the ventricular fibrillation threshold.'6, 17 Although cholinergic activity has been found to enhance ventricular electrical stability in dog experiments and the presence of cholinergic nerve fiber supplying the ventricular conducting system has been demonstrated in man,'8 an effect of cholinergic activity on the QT interval has not been reported before.Heart rate is a major determinant of the duration of the QT interval and this relation has been studied by many workers.9' [19][20][21][22] In those studies, data were collected and the QT interval was measured at the spontaneous heart rate of each subject. Consequently, the data probably include individual differences both in intrinsic properties of the ventricular myocardium and in the autonomic balance at the time of measurement and thus do not clarify whether QT is strictly ratedependent or whether it is also directly influenced by autonomic tone.We undertook the present study to determine the variation of the QT interval in the same subjects (1) spontaneous and atrially paced heart rates; (2) before and after inhibition of autonomic activity by propranolol and atropi...

“…PROGRAMMED ELECTRICAL STIMULA-TION has gained acceptance clinically as a means of initiating and terminating sustained tachyarrhythmias,'-8 studying arrhythmia mechanisms,7' 9-12 evaluating properties of excitability and refractoriness,5 [13][14][15][16][17] and determining the electrophysiologic effects of various pharmacologic and antiarrhythmic interventions. 4,6,7,13,[18][19][20][21][22] In clinical practice, bipolar pacing via a multipolar catheter is initiated at a rate faster than the patient's intrinsic rate, and the milliamperage of a 1-2-msec pulse is increased until consistent capture is evident.…”

mentioning

confidence: 99%

Strength-interval relations in a chronic canine model of myocardial infarction. Implications for the interpretation of electrophysiologic studies.

Michelson¹,

Spear²,

Moore³

1981

SUMMARY Fifteen adult mongrel dogs underwent two-stage occlusion of the mid-or distal left anterior descending coronary artery and then a reperfusion stage. The dogs were studied 3-30 days later to determine strength-interval relations in a canine model of chronic myocardial infarction. These dogs were susceptible to the initiation of sustained ventricular tachyarrhythmias with the introduction of one, two or three ventricular extrastimuli. Using unipolar cathodal stimuli with a pulse width of 2 msec, strength-interval curves were constructed from measurements made at multiple sites in the distribution of occluded and nonoccluded vessels during drive pacing at a cycle length of 300 msec. At 56 normal sites, ventricular refractory periods measured at twice-diastolic-excitability threshold approximated the relative refractory periods (mean absolute difference 3 msec), but were variably longer than effective refractory periods (mean difference 18 msec, range 4-29 msec). At 51 infarct sites, differences between ventricular refractory periods measured at twice-diastolic-excitability threshold and both relative refractory periods (mean difference 13 msec, range -60 to + 18 msec) and effective refractory periods (mean difference 28 msec, range 1-60 msec) were markedly disparate. These differences were further exaggerated after administration of i.v. procainamide. These findings suggest limitations in interpreting the results of programmed pacing studies performed using stimuli of twice-threshold intensity.PROGRAMMED ELECTRICAL STIMULA-TION has gained acceptance clinically as a means of initiating and terminating sustained tachyarrhythmias,'-8 studying arrhythmia mechanisms,7' 9-12 evaluating properties of excitability and refractoriness,5 13-17 and determining the electrophysiologic effects of various pharmacologic and antiarrhythmic interventions. 4,6,7,13,[18][19][20][21][22] In clinical practice, bipolar pacing via a multipolar catheter is initiated at a rate faster than the patient's intrinsic rate, and the milliamperage of a 1-2-msec pulse is increased until consistent capture is evident.The minimum milliamperage necessary for capture is then defined as the excitability threshold for that site.23 Routinely, clinical electrophysiologic studies have been performed at a milliamperage approximately twice the excitability threshold, and usually at less than 3 mA. 4' 7, 8, 24 Such methods have been considered adequate for obtaining necessary electrophysiologic information and safe enough to avoid inadvertent ventricular fibrillation.7 8,25 However, no specific data suggest that performing programmed electrical stimulation at twice-diastolic-threshold intensity is optimal. Even in the most experienced clin- Materials and Methods Studies were performed on 15 healthy adult mongrel dogs that weighed 8-16 kg. The dogs were anesthetized with i.v. sodium pentobarbital (30 mg/kg) and then ventilated with room air through a cuffed pharyngeotracheal tube using a volume-cycled positive-pressure respirator. Body temperature was ma...