Influence of autonomic tone on QT interval duration

The autonomic tone has been shown to influence the duration of the QT interval, however the independent contribution of sympathetic and parasympathetic tone is not fully elucidated. The influence of autonomic tone on QT duration was studied in 10 young healthy volunteers by evaluating the changes in QT and RR duration induced by i.v. isoproterenol infusion and by standing before and after i.v. administration of propranolol or atropine. Furthermore, the relationship between RR interval and QT duration was evaluated during nocturnal sinus arrhythmia and submaximal exercise test. Low doses of isoproterenol reduced RR (p < 0.01) but not QT interval duration, while higher doses influenced both RR (p < 0.0001) and QT (p < 0.001) duration. Propranolol did not influence standing-induced shortening of RR and QT intervals; on the contrary, atropine administration abolished standing-induced QT interval shortening, without influencing RR changes. QT duration resulted significantly related to preceding RR interval at peak exercise (r = 0.87, p < 0.001) and during nocturnal sinus arrhythmia (r = 0.73, p < 0.0005), however, the regression lines showing the correlation between QT and preceding RR interval were different. Both sympathetic and parasympathetic tone appear to contribute to heart rate-independent changes in QT duration. In the basal state parasympathetic more than sympathetic tone influences the relation QT-heart rate. Major increases of sympathetic nervous system activity may change the relation QT-heart rate. Thus, in case of abrupt autonomic changes, any proposed formula for heart rate correction of QT may result inappropriate, also in the normal range of heart rate.     

QT dispersion, daily variations, QT interval adaptation and late potentials as risk markers for ventricular tachycardia

AIMS: The aim of the study was to determine the value and correlation between QT dispersion, daily variations in the QT interval and late potentials as risk markers for ventricular tachycardia. METHODS AND RESULTS: QT dispersion was defined as the difference between the longest and the shortest QT interval in 12 electrocardiographic leads, QTc variability as the difference between the maximal and minimal QTc interval during 24-h Holter monitoring and QT interval adaptation as the regression line between heart rate and the uncorrected QT interval. One hundred and forty-five patients, 3 months after myocardial infarction were included in the study. QT dispersion significantly increased with the severity of arrhythmia (modified Lown's classification; P< 0.001). The level of 80 ms was associated with ventricular tachycardia with a sensitivity of 72.7% and a specificity of 86.4%. The greater daily variability of the QTc interval in patients with ventricular tachycardia was insignificant (P > 0.05). QT interval adaptation did not discriminate between patients with ventricular tachycardia from those in other groups. Late potentials were associated with ventricular tachycardia with a sensitivity of 50% and a specificity of 90.3%. CONCLUSION: Large QT dispersion and late potentials were risk markers for ventricular tachycardia, but there was no correlation between QT dispersion, daily variations in the QT interval and late potentials in patients 3 months after myocardial infarction.     

The prognostic value of the QT interval and QT interval dispersion in all-cause and cardiac mortality and morbidity in a population of Danish citizens

AIMS: To evaluate the prognostic value of the QT interval and QT interval dispersion in total and in cardiovascular mortality, as well as in cardiac morbidity, in a general population. METHODS AND RESULTS: The QT interval was measured in all leads from a standard 12-lead ECG in a random sample of 1658 women and 1797 men aged 30-60 years. QT interval dispersion was calculated from the maximal difference between QT intervals in any two leads. All cause mortality over 13 years, and cardiovascular mortality as well as cardiac morbidity over 11 years, were the main outcome parameters. Subjects with a prolonged QT interval (430 ms or more) or prolonged QT interval dispersion (80 ms or more) were at higher risk of cardiovascular death and cardiac morbidity than subjects whose QT interval was less than 360 ms, or whose QT interval dispersion was less than 30 ms. Cardiovascular death relative risk ratios, adjusted for age, gender, myocardial infarct, angina pectoris, diabetes mellitus, arterial hypertension, smoking habits, serum cholesterol level, and heart rate were 2.9 for the QT interval (95% confidence interval 1.1-7.8) and 4.4 for QT interval dispersion (95% confidence interval 1.0-19-1). Fatal and non-fatal cardiac morbidity relative risk ratios were similar, at 2.7 (95% confidence interval 1.4-5.5) for the QT interval and 2.2 (95% confidence interval 1.1-4.0) for QT interval dispersion. CONCLUSION: Prolongation of the QT interval and QT interval dispersion independently affected the prognosis of cardiovascular mortality and cardiac fatal and non-fatal morbidity in a general population over 11 years.     

"Normal" response of the QT interval and QT dispersion following intravenous injection of the sodium channel blocker disopyramide: methodological aspects

Measurement of the QT dispersion (the maximal interlead difference) on the surface electrocardiogram has been suggested for assessing the risk for ventricular arrhythmias and for examining drug effects and their proarrhythmic potential. The acute response of QT dispersion was assessed in 10 healthy subjects receiving disopyramide, which is known to delay repolarization and to prolong global measures thereof. The QRS, JT, and QT intervals and their dispersion were assessed at spontaneous rhythm and at atrial pacing at baseline and after an intravenous injection of disopyramide 2 mg/kg over 5 minutes. The short-term (within 30 minutes) and long-term (> or = 2 weeks) variabilities of the QT interval and the QT dispersion, expressed as the coefficient of variation, were also analyzed. At spontaneous rhythm the group average QT interval was between 369 and 375 msec, and the QT dispersion was between 33 and 37 msec; both were relatively stable over time. All subjects responded homogeneously to disopyramide with a significant QT prolongation (p < 0.001), but no consistent response of the QT dispersion was observed. This discrepancy reflects the significant difference in time-dependent variability with a coefficient of variation of spontaneous, paced, and heart rate-corrected QT dispersion between 25% and 42%, 8-42 times greater than the corresponding values of 1-4% for the QT intervals. The individual response of the QT dispersion to drug challenge should therefore be interpreted with caution. Furthermore and as a consequence, QT dispersion is less sensitive for assessing drug effects on ventricular depolarization and repolarization than the QT interval.     

Magnetocardiographic QT interval dispersion in postmyocardial infarction patients with sustained ventricular tachycardia: validation of automated QT measurements

QT dispersion is a measure of heterogeneity in ventricular repolarization. Increased ECG QT dispersion is associated with life-threatening ventricular arrhythmias. We studied if magnetocardiographic (MCG) measures of QT dispersion can separate postmyocardial infarction patients with and without susceptibility to sustained VT. Manual dispersion measurements were compared to a newly adapted automatic QT interval analysis method. Ten patients with a history of sustained VT (VT group) and eight patients without ventricular arrhythmias (Controls) were studied after a remote myocardial infarction. Single-channel MCGs were recorded from 42 locations over the frontal chest area and the signals were averaged. QT dispersion was defined as maximum-minimum or standard deviation of measured QT intervals. VT group showed significantly more QT and JT dispersion than Controls. QTapex dispersions were 127 +/- 26 versus 83 +/- 21 ms (P = 0.004) and QTend dispersions 130 +/- 37 versus 82 +/- 37 ms (P = 0.013), respectively. Automatic method gave comparable values. Their relative differences were 9% for QTapex and 27% for QTend dispersion on average. In conclusion, increased MCG QT interval dispersion seems to be associated with a susceptibility to VT in postmyocardial infarction patients. MCG mapping with automated QT interval analysis may provide a user independent method to detect nonhomogeneity in ventricular repolarization.     

Effect of coronary angioplasty on precordial QT dispersion

Dispersion of the QT interval is a measure of inhomogeneity of ventricular repolarization. Because ischemia is associated with regional abnormalities of conduction and repolarization, we hypothesized that the surface electrocardiographic interval dispersion would increase in patients with symptomatic coronary artery disease in the absence of myocardial infarction and that successful revascularization would reduce QT interval dispersion. Thirty-seven consecutive patients with ischemia due to 1-vessel coronary artery disease without prior myocardial infarction who underwent percutaneous transluminal coronary angioplasty (PTCA) were evaluated. Standard 12-lead electrocardiograms were performed 24 hours before, 24 hours after, and late (>2 months) after PTCA. Precordial QT interval dispersions were determined from differences in the maximum and minimum corrected QT intervals. Mean QT interval dispersion before PTCA was 60 +/- 9 ms, immediately after PTCA 23 +/- 14 ms (p <0.001), and late after PTCA 29 +/- 18 ms (p <0.001 vs before PTCA). The shortest precordial QT interval increased immediately after PTCA (367 +/- 40 vs 391 +/- 39 ms; p <0.02) and then remained stable late after PTCA (376 +/- 36 ms, p = NS vs immediately after PTCA). Symptomatic recurrent ischemia in 8 patients with documented restenosis increased QT interval dispersion (56 +/- 15 ms [p <0.01] vs 25 +/- 14 ms immediately after PTCA), which decreased again after successful repeat PTCA (22 +/- 13 ms [p <0.01] vs before the second PTCA). QT interval dispersion decreases after successful coronary artery revascularization and increases with restenosis. Therefore, QT interval dispersion may be a marker of recurrent ischemia due to restenosis after PTCA.     

Dispersion of repolarization following double and triple programmed stimulation. A clinical study using the monophasic action potential recording technique

To study the dispersion of ventricular repolarization following double and triple programmed stimulation and its correlation with the inducibility of ventricular arrhythmias, monophasic action potentials were simultaneously recorded from the right ventricular apex and outflow tract during programmed stimulation in 12 patients with ventricular arrhythmias and a normal QT interval. The time difference between the ends of the two monophasic action potentials were used as a measure of the dispersion of ventricular repolarization, which consists of the activation time difference and the monophasic action potential duration difference. During double and triple programmed stimulation, the dispersion of ventricular repolarization increased significantly with the shortening of the coupling interval but decreased slightly with the shortening of the preceding interval. The induction of the ventricular arrhythmias in these patients was invariably associated with a marked increase in the dispersion of ventricular repolarization. The maximal dispersion of ventricular repolarization was significantly larger in the seven patients with polymorphic ventricular tachycardia and/or ventricular flutter/fibrillation induced than in the four patients with monomorphic ventricular tachycardia induced. Analysis of the two components of the dispersion of ventricular repolarization revealed that the increased dispersion of ventricular repolarization was mainly caused by an increase in the activation time difference in the monomorphic ventricular tachycardia subgroup, and by increases in both the activation time difference and monophasic action potential duration difference in the polymorphic ventricular tachycardia/fibrillation subgroup. These findings suggest that increased dispersion of ventricular repolarization is one of the underlying mechanisms accounting for the myocardial vulnerability to ventricular arrhythmias and that repolarization disturbance is important for the genesis of polymorphic ventricular tachycardia/fibrillation.     

Surgical relevance of diagnostic imaging of abdominal tumors--decision making in pancreatic tumor

1. An association has been reported between QT interval abnormalities and cardiovascular autonomic neuropathy in diabetic patients. The QT interval abnormalities reflect local inhomogeneities of ventricular recovery time and may be related to an imbalance in cardiac sympathetic innervation. Sympathetic innervation of the heart can be visualized and quantified by single-photon emission-computed tomography with m-[123I]iodobenzylguanidine. In this study we evaluated cardiac sympathetic integrity by m-[123I]iodobenzylguanidine imaging and the relationship between both QT interval prolongation and QT dispersion from standard 12-lead ECG variables and m-[123I]iodobenzylguanidine uptake in insulin-dependent diabetic patients. 2. Three patient groups were studied, comprising six healthy control subjects, nine diabetic patients without cardiovascular autonomic neuropathy (CAN-) and 12 diabetic patients with cardiovascular neuropathy (CAN+). Resting 12-lead ECG was recorded for measurement of maximal QT interval and QT dispersion. The QT interval was heart rate corrected using Bazett's formula (QTc) and the Karjalainen approach (QTk). Quantitative measurement (in counts/min per g) and visual defect pattern of m-[123I]iodobenzylguanidine uptake were performed using m-[123I]iodobenzylguanidine single-photo emission-computed tomography. 3. Global myocardial m-[123I]iodobenzylguanidine uptake was significantly reduced in both diabetic patient groups compared with control subjects. The visual defect score of m-[123I]iodobenzylguanidine uptake was significantly higher in CAN+ diabetic patients than in control subjects and in CAN- patients. This score was not significantly different between control subjects and CAN- patients. QTc interval and QT dispersion were significantly increased in CAN+ diabetic patients as compared with control subjects (QTc: 432 +/- 15 ms versus 404 +/- 19 ms, P < 0.05; QT dispersion: 42 +/- 10 versus 28 +/- 8 ms, P < 0.05). QT dispersion was also significantly longer in CAN- diabetic patients than in control subjects (41 +/- 9 ms versus 28 +/- 8 ms, P < 0.05). QTc interval was significantly related to global myocardial m-[123I]iodobenzylguanidine uptake and defect score in diabetic patients (r = -0.648, P < 0.01, and r = 0.527, P < 0.05, respectively). There was no correlation between QT dispersion and both m-[123I]iodobenzylguanidine uptake measures. 4. In conclusion, these findings suggest that m-[123I]iodobenzylguanidine imaging is a valuable tool for the detection of early alterations in myocardial sympathetic innervation in long-term diabetic patients without cardiovascular autonomic neuropathy. Insulin-dependent diabetic patients with cardiovascular autonomic neuropathy have a delayed cardiac repolarization and increased variability of ventricular refractoriness. The cardiac sympathetic nervous system seems to be one of the determinants of QT interval lengthening, but does not appear to be involved in dispersion of ventricular recovery time. It is assumed that QT dispersion is based on more complex electrophysiological mechanisms which remain to be elucidated.     

Kinetic characterisation and solubilisation of gamma-hydroxybutyrate receptors from rat brain

The effects of single electrical shocks to myelinated A and unmyelinated C afferent fibers of perineal and limb somatic nerves on the reflex discharges in pelvic parasympathetic (L6/S1) efferent nerves to the bladder were examined in anesthetized central nervous system (CNS)-intact and acute spinal rats. When the bladder was empty, stimulation of perineal somatic inputs to the L6 and S1 segments from the perineo-femoral branch of a pudendal nerve produced excitatory A- and C-reflex discharge components in postganglionic parasympathetic efferent nerve branches on the bladder surface. When the bladder was expanded and pelvic efferent neurons were rhythmically active, additional inhibitory A- and C-reflex components could be seen. After acute spinal transection, the same stimuli elicited excitatory A- and C-reflex discharges of similar latency as those observed before the spinal transection, but were of larger amplitude and longer duration; resting activity in the pelvic nerve was low, and no evoked inhibitory reflex components could be observed. Electrical stimulation of afferents in the tibial nerve had no effect when the bladder pressure was low, but when the bladder was distended, early and late components of reflex inhibition and excitation of parasympathetic activity were visible in CNS-intact rats; these reflex responses were abolished following spinalization.     

Cardiac evaluation of liver transplant recipients: QT dispersion in electrocardiogram

Increased QT dispersion, the interlead variability of the QT interval length in the 12-lead electrocardiogram, reflects uneven ventricular repolarization as a sign of cardiomyopathy. We analyzed QT dispersion in the preoperative electrocardiogram of 100 adult liver transplant recipients and 20 healthy control subjects. In 12% of the liver recipients, QT dispersion was increased above 65 ms (mean + 3SD). Six of these patients had a liver storage disease (haemochromatosis, Wilson's disease or amyloidosis). Five had a history of cardiac disease. Severe intraoperative cardiac complications occurred in three patients with markedly increased QT dispersion (> or = 99 ms). In conclusion, in liver storage diseases the heart may be affected, leading to increased risk of cardiac complications, which might be predicted from increased QT dispersion. Analysis of QT dispersion, a noninvasive inexpensive technique, can be recommended to be included in the cardiac screening of liver transplant candidates.     

Nosocomial infection following cardiovascular surgery: comparison of two periods, 1987 vs. 1992

BACKGROUND: QT dispersion has been proposed as a simple, noninvasive measure for identifying patients at risk of postinfarction arrhythmia. It is assumed to reflect nonuniform ventricular repolarization, which, in turn, may result from regional differences in repolarization time as well as from localized activation delay. The aim of this study was to examine the relation between QT dispersion and intraventricular conduction abnormalities in patients with acute anterior wall myocardial infarction. METHODS AND RESULTS: Standard 12-lead electrocardiographic and 12-lead signal-averaged electrocardiographic recordings were performed in 25 patients with a first Q-wave anterior wall myocardial infarction. Measures calculated by using the 6 precordial (V1 through V6) leads for QT dispersion were (1) difference between maximum and minimum QT and QTc intervals and (2) standard deviation of QT and QTc intervals. Measures calculated from the signal-averaged electrocardiogram were (1) maximum filtered QRS duration; (2) mean; and (3) standard deviation of filtered QRS duration. No relation was found between any measure of filtered QRS duration and that of QT dispersion by using linear correlation analysis. Similarly, no significant association was demonstrated between the filtered QRS duration and corresponding QT interval measurements (total 131 leads). CONCLUSIONS: The lack of correlation between signal-averaged electrocardiogram indexes of slow intraventricular conduction and electrocardiogram variables of QT dispersion suggests an independent predictive value for the 2 methods in identifying patients at risk of postinfarction arrhythmia. This suggestion is further supported by the finding that altered activation sequence is an unlikely mechanism of QT dispersion in patients with acute myocardial infarction, as indicated by the lack of association between the filtered QRS duration and corresponding QT interval measurements.     

Electrocardiographic and clinical predictors of torsades de pointes induced by almokalant infusion in patients with chronic atrial fibrillation or flutter: a prospective study

The aim of this study was to identify predictors of torsades de pointes (TdP) in patients with atrial fibrillation (AF) or flutter exposed to the Class III antiarrhythmic drug almokalant. TdP can be caused by drugs that prolong myocardial repolarization. One hundred patients received almokalant infusion during AF (infusion 1) and 62 of the patients during sinus rhythm (SR) on the following day (infusion 2). Thirty-two patients converted to SR. Six patients developed TdP. During AF, T wave alternans was more common prior to infusion (baseline) in patients developing TdP (50% vs 4%, P < 0.01). After 30 minutes of infusion 1, the TdP patients exhibited a longer QT interval (493 +/- 114 vs 443 +/- 54 ms [mean +/- SD], P < 0.01), a larger precordial QT dispersion (50 +/- 74 vs 27 +/- 26 ms, P < 0.05), and a lower T wave amplitude (0.12 +/- 0.21 vs 0.24 +/- 0.16 mV, P < 0.01). After 30 minutes of infusion 2, they exhibited a longer QT interval (672 +/- 26 vs 489 +/- 74 ms, P < 0.001), a larger QT dispersion in precordial (82 +/- 7 vs 54 +/- 52 ms, P < 0.01) and extremity leads (163 +/- 0 vs 40 +/- 34 ms, P < 0.001), and T wave alternans was more common (100% vs 0%, P < 0.001). Risk factors for development of TdP were at baseline: female gender, ventricular extrasystoles, and treatment with diuretics; and, after 30 minutes of infusion: sequential bilateral bundle branch block, ventricular extrasystoles in bigeminy, and a biphasic T wave. Patients developing TdP exhibited early during almokalant infusion a pronounced QT prolongation, increased QT dispersion, and marked morphological T wave changes.     

Electrophysiological basis of arrhythmogenicity of QT/T alternans in the long-QT syndrome: tridimensional analysis of the kinetics of cardiac repolarization

Tachycardia-dependent QT/T alternans occurs in patients with the congenital or idiopathic form of long-QT syndrome (LQTS) and may presage the onset of polymorphic ventricular tachyarrhythmias. To examine the electrophysiological basis of arrhythmogenicity of QT/T alternans in LQTS, the tridimensional repolarization pattern of QT/T alternans was studied in the anthopleurin-A model of LQTS, a surrogate for LQT3. In 11 anesthetized mongrel puppies, tridimensional repolarization and activation patterns were analyzed from 256 to 384 unipolar electrograms. Cardiac repolarization was evaluated as the activation-recovery interval (ARI) of local electrograms. To induce QT/T alternans, the pacing cycle length (CL) was abruptly shortened in steps of 50 ms from a basic drive of 1000 ms. ARIs were calculated at epicardial (Epi), midmyocardial (Mid), and endocardial (End) sites. ARI restitution at each site was assessed by using a single premature stimulation delivered after the basic drive. ARI alternans occurred at longer CLs at Mid sites compared with End and Epi sites, and the magnitude of alternans at Mid sites was greater. Two factors contributed to the modulation of ARI during QT/T alternans: (1) differences in restitution kinetics at Mid sites, characterized by larger DeltaARI and a slower time constant (tau), and (2) differences in diastolic intervals resulting in different input to restitution at the same constant CL. These 2 factors could explain not only the onset of alternans at Mid sites at longer CLs but also the critical observation that ARI dispersion between Epi and Mid sites during alternans was greater than during the slower basic CL. Marked ARI alternans could be present in local electrograms without manifest alternation of the QT/T segment in the surface ECG. The latter was seen at critically short CLs associated with reversal of the gradient of ARI between Epi and Mid sites, with a consequent reversal of polarity of the intramyocardial QT wave in alternate cycles. The arrhythmogenicity of QT/T alternans was primarily due to the greater degree of spatial dispersion of repolarization during alternans than during slower rates not associated with alternans. This could result in functional conduction block and reentrant ventricular tachyarrhythmias during the fixed drive associated with alternans.     

The practice of medical and surgical synovectomy: a UK survey

BACKGROUND: QT dispersion (QTd = QTmax-QTmin) measured as interlead variability of QT interval reflects the spatial inhomogeneity of ventricular repolarization times, and increased QTd may provide a substrate for malignant ventricular arrhythmias. Ischemia is associated with regional abnormalities of conduction and repolarization. HYPOTHESIS: This study aimed to investigate the effect of acute ischemia on QTd during successful percutaneous transluminal coronary angioplasty (PTCA). METHODS: Forty-three patients (10 women, 33 men, mean age 56 years) were enrolled in the study. Electrocardiogram (ECG) recordings were taken before PTCA and during balloon inflation period. QT maximum (QTmax), QT minimum (QTmin), and QTd (QTmax-QTmin) values were calculated from the surface ECG. RESULTS: There was no difference among QTmax values (p = 0.6). Mean QTmin during balloon inflation was lower than before PTCA (368 +/- 45 vs. 380 +/- 41 ms, p = 0.002). The difference between QTd values before and during balloon inflation was statistically important (65 +/- 9 vs. 76 +/- 10 ms, p = 0.001). This difference is caused by a decrease in QTmin during balloon inflation. CONCLUSION: Acute reversible myocardial ischemia induced by balloon inflation causes an increase in QTd value, and this increment is the result of a decrease in QTmin interval. Therefore, QTd may be a marker of reversible myocardial ischemia.     

The effects of a left bundle-branch block on ventricular repolarization dispersion

Patients with left bundle-branch block (LBBB) often present electrocardiographic abnormalities and, therefore, are excluded from studies concerning electrocardiographic evaluation of ventricular repolarization. The aim of the study was to assess whether LBBB could influence dispersion of ventricular repolarization. Surface electrocardiograms of 16 patients (9 males and 7 females, mean age 58 +/- 14 years) with episodes of intermittent LBBB were analyzed. Six patients were affected by coronary artery disease, 6 by hypertensive cardiomyopathy and 4 by dilated cardiomyopathy. Maximal QT and JT corrected intervals, QT and JT dispersion, and QT and JT dispersion corrected for heart rate, were obtained before and after LBBB. We observed a significant prolongation of maximal QT (412 +/- 29 vs 433 +/- 25 ms; p < 0.05), and of maximal corrected QT (457 +/- 37 vs 497 +/- 56 ms; p < 0.05) after LBBB. Maximal JT interval, also corrected for heart rate, did not show any significant modification after LBBB. Moreover, we did not observe any significant difference in electrocardiographic parameters of dispersion of repolarization. Our results seem to indicate that LBBB did not alter significantly dispersion of ventricular repolarization. QT dispersion is considered an important marker of risk for incidence of ventricular arrhythmias. If our results will be confirmed in larger groups of patients, analysis of QT dispersion could be extended even to patients with LBBB.     

Increased QTc dispersion predicts lethal ventricular arrhythmias complicating coronary angioplasty

This study found that increased QT dispersion just before angioplasty is an useful marker to predict the risk for lethal ventricular arrhythmias during angioplasty. The fact that successful coronary revascularization decreased QT dispersion suggested that a part of increased QT dispersion is related to myocardial ischemia.     

Influence of physical activity upon bone mineralization of school age children of both sexes]

The effect of topical lignocaine applied to the eye muscles, on the incidence of the oculocardiac reflex during squint surgery of the medial rectus was investigated in 56 healthy children aged between 3-14 years. Three groups were studied. One (n = 16): stimulation of the reflex without lignocaine; 2 (n = 10): stimulation of the reflex after topical administration of 1 mg kg-1 lignocaine 2% to the medial part of the eye after induction of anaesthesia; 3 (n = 30): stimulation of the oculocardiac reflex without, and after a 5 min interval under the influence of lignocaine. Topical administered lignocaine significantly attenuated the OCR (105 vs. 68 bpm group II vs. group 1:82 vs. 63 bpm in group III). Severe bradycardiac rhythm disturbances, in particular cardiac stand-still, were not observed after lignocaine had been applied. Systemic side effects of lignocaine were not seen.     

The effects of irritation at various levels of the airway upon tracheal mucus secretion in the cat

1. Sulphated glycoprotein output from the trachea, isolated in situ, has been measured in anaesthetized cats by a radio-isotopic method. The effects of irritation of various parts of the airway on this mucus output were studied. 2. Mechanical stimulation of the nose and nasopharynx increased tracheal mucus output by reflexes which involved parasympathetic and probably also sympathetic motor pathways. 3. Laryngeal stimulation had a similar through the same motor pathways. 4. Inhalation of ammonia vapour into the lower airways reflexly increased mucus output from the isolated trachea. The efferent pathway for this reflex was mainly or entirely parasympathetic. It is argued that the afferent pathway involved cough receptors. 5. Lung inflation, inhalation of histamine aerosol and intravenous injection of phenyl diguanide (which excite mainly lung stretch receptors, lung 'irritant' receptors and alveolar 'J-receptors' respectively) had no consistent effect on tracheal mucus secretion. 6. The afferent and efferent pathways of these reflexes are discussed.     

Probucol-induced QT prolongation and syncope

We report a patient who experienced a reversible prolongation of the QT interval and episodes of syncope while receiving probucol. A 64-year-old woman experienced syncopal attacks 8 and 11 weeks after beginning probucol treatment (500 mg twice daily). The pre-treatment ECG showed a slight prolongation of the corrected QT interval (QTc) (0.46 sec). Her QTc increased to 0.62 sec 12 weeks after beginning probucol treatment and decreased to about the baseline value (0.48 sec) 6 weeks after treatment was discontinued. Probucol is known to prolong the QT interval. A long QT interval has been linked to an increased risk of ventricular arrhythmias, syncope or sudden death. However, clinical reports which causally relate probucol treatment to syncope are very rare. Although an ECG during the episodes of syncope was not available, this patient's syncope might be due to ventricular tachyarrhythmia associated with probucol-induced QT prolongation. This case emphasizes the need for careful evaluation of the QT interval before and during probucol treatment.     

Duration of QT interval in clinically normal dogs

The QT interval is the period from onset of the QRS complex to the end of the T wave. The QT interval is useful for monitoring drug (eg, quinidine) and electrolyte (eg, calcium) effects on the heart. It depends principally on heart rate (HR), and the relationship between QT interval and HR has been expressed for human beings and for dogs. The purpose of the study reported here was to quantify that relationship for dogs and to assess whether body weight also influenced QT interval. The ECG was recorded from 17 dogs, ranging in weight between 7 and 25 kg. Dogs were anesthetized with fentanyl/droperidol/ketamine, and HR was accelerated by administration of graded doses of atropine. A significant relationship was not found between QT interval and body weight. Despite changes in HR during sinus arrhythmia, a significant relationship was not found between QT and RR intervals. The QT interval vs HR accelerated by atropine was analyzed for all dogs and for small (7 to 10 kg, n = 5), medium (10 to 20 kg, n = 7), and large dogs (20 to 25 kg, n = 5). Equations relating QT interval to mean HR were calculated for each group. Our data may serve as a baseline with which to compare QT intervals from dogs with heart disease and/or electrolyte imbalance.