Thrombin activatable fibrinolysis inhibitor : its role in slow coronary flow.

BACKGROUND: The slow coronary flow (SCF) phenomenon is characterized by slow progression of angiographic contrast medium in the coronary arteries in the absence of stenosis in the epicardial vessels. The pathophysiological mechanisms of SCF phenomenon remain uncertain. Several hypotheses, however, have been suggested for SCF phenomenon, including an early form of atherosclerosis, small vessel dysfunction, dilatation of coronary vessels, imbalance between vasoconstrictor and vasodilatory factors, platelet function disorder, and inflammation. Atherosclerosis and inflammation are the most accepted mechanisms for the pathogenesis of SCF. Thrombin activatable fibrinolysis inhibitor (TAFI) was described as a new inhibitor of fibrinolysis recently and plays an important role in coagulation and fibrinolysis. In previous studies, the role of TAFI was associated with inflammation and evolution of atherosclerosis in coronary artery disease. There are no data available about TAFI levels in patients with SCF phenomenon investigated by angiography. Our goal was to evaluate TAFI antigen (Ag) levels in patients with SCF and to determine the association of the TAFI Ag level with traditional cardiovascular risk factors in our study. METHODS: The study group constituted 41 patients with angiographically confirmed SCF and 46 patients with normal coronary flow as the control group. The TAFI Ag levels of each patient were determined. RESULTS: Between the control and study group, a statistical difference in the levels of TAFI Ag (p < 0.05) was observed. The TAFI Ag level was significantly higher in the SCF group than the control group (132.21 ± 21.14 versus 122.15 ± 21.59). CONCLUSION: We have demonstrated that TAFI might be a risk factor for the development of SCF independently of conventional cardiovascular risk factors. In addition, TAFI Ag levels were positively correlated with C-reactive protein (CRP) known as an acute phase reactant. Our findings support the reports of previous studies that increased TAFI levels may be associated with inflammation. Further large studies are required to evaluate the importance of TAFI antigen levels in relation to the development of SCF.

[P wave dispersion in hypertensive urgency].

BACKGROUND AND PURPOSE: P wave dispersion (PWD) has been accepted as a predictor for atrial fibrillation (AF) in hypertension and some other cardiac diseases. The aim of this study was to compare the P wave parameters between patients with mild-moderate hypertension and those with hypertensive crises. METHODS: A total of 48 patients, 24 of who presented to the emergency department with hypertensive urgency and 24 patients who were followed in the cardiology clinic with mild-moderate essential hypertension were included in this study. P wave durations were measured manually by two investigators blinded to data of patients. RESULTS: The maximal duration of P wave (P max) and the PWD were found to be significantly different between groups, being longer in patients with hypertensive urgency (p=0,05 and 0,02; respectively). CONCLUSIONS: PWD increases in hypertensive urgency states. Clinical implication of this finding should be addressed with further, prospective studies conducted on larger samples.

[Comparison of effects of nebivolol and atenolol on P-wave dispersion in patients with hypertension].

BACKGROUND: P-wave dispersion has been shown to be a noninvasive electrocardiographic predictor for development of atrial fibrillation . Thus it may be possible to attenuate atrial fibrillation risk through normalization of P-wave variables and improvement in P-wave dispersion may be an important goal in treatment of hypertension. OBJECTIVE: To compare the effects of nebivolol, a new b-blocker that have additional vasodilating activity via acting on endothelium and nitric oxide release, and atenolol on P-wave duration and dispersion in patients with mild-to-moderate hypertension. METHODS: A total of 34 newly-diagnosed hypertensive patients were enrolled in the study. The patients were randomly assigned to receive treatment with either nebivolol (5 mg) or atenolol (50 mg). P-wave durations (Pmin and Pmax) and P-wave dispersion were measured before and one month after treatment. RESULTS: While Pmin increased (50,6 +/- 11,2 ms to 54,7 +/- 9,1 ms, p=0,05), Pmax decreased (111,9 +/- 9,1 ms to 104,0 +/- 12,4 ms, p=0,003) and P-wave dispersion decreased (62,5 +/- 10,6 ms to 51,3 +/- 8,9 ms, p < 0,001) with nebivolol, Pmin increased (44,4 +/- 9,8 ms to 58,0 +/- 15,5 ms, p=0,02), Pmax didn t change (106,1 +/- 13,8 ms to 107,0 +/- 11,6 ms, p=NS) and P-wave dispersion decreased (61,7 +/- 15,0 ms to 49,0 +/- 13,7 ms, p < 0.001) with atenolol. However, there was no statistical difference between pre- and post-treatment values of two groups. CONCLUSIONS: Both nebivolol and atenolol are effective in improvement of P-wave dispersion in patients with hypertension and there s no significant difference between them.

Frequency of left atrial thrombus and spontaneous echocardiographic contrast in acute myocardial infarction.

Left ventricular systolic dysfunction may precipitate blood stasis as well as thrombus formation in the left atrial appendage of patients with acute myocardial infarction, even in the presence of sinus rhythm. Thus, left atrial thrombi may be an alternative source for systemic embolism in acute myocardial infarction.

A case of arrhythmogenic right ventricular cardiomyopathy in sinus rhythm associated with thrombus in the right atrium.

We describe a patient with arrhythmogenic right ventricular cardiomyopathy (ARCV) in sinus rhythm associated with thrombus in the right atrium. The occurrence of a right heart thrombus in ARCV is extremely rare and, to our knowledge, has been previously reported only in the right ventricle. In our case, ARCV most probably led to right atrial spontaneous echo contrast, and later, right atrial thrombus formation by blood stasis caused by right ventricular systolic dysfunction. In conclusion, our case suggests that right atrial thrombus may occur in ARCV, even in sinus rhythm.

A case of left atrial appendage thrombus with embolic stroke in association with aortic stenosis in sinus rhythm.

Although left atrial appendage (LAA) thrombus formation in the presence of sinus rhythm may potentially be the source for embolic events in various types of heart disease, no cases of LAA thrombus with embolic stroke in association with aortic stenosis in sinus rhythm have been reported. We present a case of valvular aortic stenosis with cerebral embolism in a person who was in sinus rhythm and had an LAA thrombus diagnosed by transesophageal echocardiography.

Does acute-phase beta blockade reduce left atrial appendage function in patients with chronic nonvalvular atrial fibrillation?

To investigate whether acute-phase beta-blocker therapy has a harmful effect on left atrial appendage (LAA) function in patients with chronic nonvalvular atrial fibrillation by transesophageal echocardiography (TEE), we evaluated 21 patients with normal left ventricular systolic function and a poorly controlled ventricular rate, despite the use of digoxin. Baseline parameters that were obtained included heart rate, blood pressure, LAA emptying velocities, and left atrial spontaneous echo contrast intensity. Then, each patient was given a bolus dose of 5 mg metoprolol. Ten minutes later, a second set of assessments was performed. After the first TEE studies, each patient began treatment with metoprolol (50 mg orally twice daily for 1 week). A second TEE study was performed after 1 week of continuous oral metoprolol therapy at maintenance dose, and values were again determined. The average resting apical heart rate was 91 +/- 7 bpm. As expected, beta-blocker therapy showed a marked decrease in heart rate at 10 minutes (79 +/- 6 bpm, P <.001) and at 1 week (71 +/- 4 bpm, P <.001). Beta-blocker therapy caused a significant reduction in systolic and diastolic blood pressures (144 +/- 16 / 93 +/- 6 mm Hg at baseline, 137 +/- 16 / 87 +/- 9 mm Hg at 10 minutes, and 135 +/- 12 / 86 +/- 8 mm Hg at 1 week, P <.001). With the beta-blocker therapy, the baseline transesophageal Doppler parameter of LAA emptying velocities (at baseline 24 +/- 7 cm/s) fell significantly at 10 minutes (19 +/- 7 cm/s, P <.001) and at 1 week (17 +/- 6 cm/s, P <.001) after initiation of beta-blocker therapy. After a bolus of metoprolol, spontaneous echo contrast intensity did not change in any patients, but 1 week later, it increased in 1 patient. In 2 patients who had not been found to have an LAA thrombus at baseline TEE study, the second TEE examination demonstrated new thrombi in the LAA. In conclusion, our findings suggest that in patients with chronic nonvalvular atrial fibrillation who have normal left ventricular systolic function and a poorly controlled ventricular rate despite the use of digoxin, acute-phase beta blockade may have a harmful effect on LAA function.

Transesophageal echocardiography assessment of left atrial appendage function in untreated systemic hypertensive patients in sinus rhythm.

To assess left atrial appendage (LAA) function in hypertensive patients without treatment, transesophageal echocardiography (TEE) was performed in 46 hypertensive patients in sinus rhythm, aged 40 to 55 years, and in 16 control subjects (group I) without cardiovascular disease, aged 41 to 54 years. The hypertensive patients were divided into 2 groups according to left ventricular (LV) systolic function: group II, the group with normal LV systolic function (ejection fraction 0.63 +/- 0.08), and group III, the group with LV systolic dysfunction (ejection fraction 0.39 +/- 0.05). The LAA late emptying velocities (EVs) were significantly reduced in the hypertensive subgroups compared with the control group (P <.001), but no significant difference in the LAAEV was found between groups II and III. The LAAEV in the hypertensive patients had a significant negative correlation with diastolic blood pressure, systolic blood pressure, and left atrial (LA) diameter. The maximal LAA areas were significantly larger in the hypertensive subgroups than in the control group (P <.05). No significant difference in LAA maximal area existed between groups II and III. The maximal LAA area in the hypertensive patients had a significant positive correlation with diastolic blood pressure, systolic blood pressure, and LA diameter, but a significant negative correlation with LV ejection fraction. With TEE, LA spontaneous echocardiographic contrast (SEC) was present in 6 (43%) of 14 patients in group III (P <.01) and in 7 (22%) of 32 patients in group II (P <.05). No significant difference in the occurrence of LASEC was found between groups II and III. Left atrial appendage thrombi by TEE were observed in 4 (29%) of 14 patients in group III (P <.05) and in 4 (13%) of 32 patients in group II (P = not significant). No significant difference in the occurrence of LAA thrombus existed between groups II and III. In conclusion, in patients with untreated hypertension, marked elevation of afterload imposed on the left atrium may involve both the left atrium and the LAA, resulting in impairment of LAA function. This condition may worsen with subsequent occurrence of SEC and later, thrombus formation. Therefore assessment of LAA function may be important even in the hypertensive patient in sinus rhythm.

Biatrial thrombosis after acute inferior wall myocardial infarction--a case report.

The authors describe a case of biatrial thrombosis after acute inferior wall myocardial infarction (MI) with sinus rhythm. The presence of atrial thrombosis in patients with acute MI has recently been recognized with the aid of echocardiography. However, to the author's knowledge, a case of biatrial thrombosis after acute MI has not been reported previously. In this case, blood stasis, resulting from both left ventricular and right ventricular systolic dysfunction, was the most likely cause of the biatrial thrombi formation. In summary, this case suggests that biatrial thrombosis may occur in acute MI, even in the presence of sinus rhythm.

Effect of blood pressure reduction on abnormal left atrial appendage function in untreated systemic hypertensive patients with sinus rhythm.

To investigate whether reduction in blood pressure has a beneficial effect on left atrial appendage (LAA) function, the authors evaluated 24 untreated systemic hypertensive patients with normal left ventricular systolic function in sinus rhythm at baseline and at 3 months after initiation of antihypertensive therapy. They performed transthoracic and transesophageal echocardiographic examinations in hypertensive patients before and after treatment of hypertension. Three of the 24 patients had blood pressure that failed to respond to the regimen of antihypertensive therapy and were removed from the analysis. Of the remaining 21 patients, mean systolic and diastolic blood pressures at baseline were 170 +/- 18 and 104 +/- 6 mm Hg, respectively, and fell significantly at 3 months to 141 +/- 10 and 90 +/- 5 mm Hg, respectively, (p<0.001) after initiation of antihypertensive therapy. There was no significant change in heart rate with treatment (baseline 81 +/- 8 and at 3 months 84 +/- 9 beats/min). There was no significant change in left ventricular end-diastolic diameter, left ventricular ejection fraction, left ventricular wall thickness, or left atrial diameter from baseline (49 +/- 4 mm, 58 +/- 5%, 12 +/- 1 mm, and 41 +/- 4 mm, respectively) at 3 months (48 +/- 5 mm, 59 +/- 4%, 12 +/- 1 mm, and 40 +/- 3 mm). The treatment caused a significant reduction in maximal LAA areas (6.3 +/- 1.3 cm2 at baseline, 4.6 +/- 0.7 cm2 at 3 months, p<0.001), with a concomitant increase in LAA emptying velocity (44 +/- 7 cm/sec at baseline, 60 +/- 9 cm/sec at 3 months, p<0.001). In conclusion, these findings suggest that reduction in blood pressure with antihypertensive therapy could improve LAA function in hypertensive patients with normal left ventricular systolic function in sinus rhythm.

Acute ECG changes and chest pain induced by neck motion in patients with cervical hernia--a case report.

We report two cases of acute cervical angina and ECG changes induced by anteflexion of the head. Cervical angina is defined as chest pain that resembles true cardiac angina but originates from cervical discopathy with nerve root compression. In these patients, Prinzmetal's angina, valvular heart disease, congenital heart disease, left ventricular aneurysm, and cardiomyopathy were excluded. After all, the patient's chest pain was reproduced by anteflexion of head, at this time, their ECGs showed nonspecific ST-T changes in the inferior and anterior leads different from the basal ECG. ECG changes returned to normal when the patient's neck moved to the neutral position. To our knowledge, these are the first cases of cervical angina associated with acute ECG changes by neck motion.

Brachial artery blood flow velocity pattern in patients with congestive heart failure: duplex Doppler ultrasonographic assessment.

The purpose of this study was to determine whether there are abnormalities in blood flow velocity pattern of the brachial artery in patients with congestive heart failure (CHF). Brachial artery blood flow velocities were measured with duplex Doppler ultrasonography in 12 normal subjects, 31 patients with congestive heart failure (CHF), and 26 patients with coronary artery disease (CAD). None of the patients had clinical evidence of arterial disorders at upper extremities. In both patient groups, the presence of hypertension was correlated with the peak systolic velocity (r=0.48, p<0.05). Patients with heart failure had significantly larger (p<0.0001) peak reverse velocity (20 +/- 6 m/sec) than healthy subjects (5 +/- 4 m/sec) and patients with CAD (7 +/- 3 m/sec). Peak reverse velocity did not differ significantly between normal subjects and CAD group. These data indicate that the blood flow velocity pattern at brachial artery is abnormal in CHF. The simple measurement of brachial artery flow velocity suggests changes in peripheral vasculature related to CHF.

Wolff-Parkinson-White syndrome mimicking acute anterior myocardial infarction in a young male patient--a case report.

A young male with Wolff-Parkinson-White syndrome whose electrocardiographic pattern was suggestive of acute anterior myocardial infarction is described. A 21-year-old male with a history of ventricular fibrillation after being successfully resuscitated was admitted to the coronary care unit. His electrocardiogram showed ST elevation in the precordial leads (V1-V6). This condition was erroneously interpreted as an acute myocardial infarction. At the fourth day, while ST elevations returned to baseline, short PR interval and delta waves were observed on the ECG. Myocardial infarction was excluded by biochemical tests, echocardiography, and coronary angiography. Electrophysiologic study confirmed Wolff-Parkinson-White syndrome with two accessory pathways.

Cardiac troponin I levels in patients with left heart failure and cor pulmonale.

Cardiac troponin levels are regarded as the most specific of currently available biochemical markers of myocardial damage. Elevated levels of troponin have been previously reported in patients with left heart failure, reflecting small areas of undetected myocardial cell death. The aim of this study was to compare the levels of the cardiac troponin I (cTnI) in patients with left- and right-sided heart failure. Cardiac troponin I levels were studied with immunochemical methods in patients with right heart failure (n = 17) resulting from chronic obstructive pulmonary disease, ischemic left heart failure (n = 23), and nonischemic left heart failure (n = 18) who were admitted to departments of cardiology and chest diseases. Also, cTnI levels were measured in 32 healthy subjects as control group. Protein markers of myocardial injury (cTnI and myoglobin) in patients with left and right heart failure were collected approximately 12 to 36 hours after onset of obvious symptoms. Serum creatine kinase MB band was determined on admission and thereafter twice a day during the first 3 days. Elevated levels of serum cTnI were found in patients with nonischemic (0.83 +/- 0.6 ng/mL, p<0.01) and ischemic left heart failure (0.9 +/- 0.5 ng/mL, p<0.01) when compared to healthy subjects, whereas serum cTnI levels in patients with right heart failure due to chronic obstructive pulmonary disease were not significantly different from those of control subjects (0.22 +/- 0.1 vs 0.16 +/- 0.1 ng/mL, p>0.05). In addition, creatine kinase MB band and myoglobin levels were not significantly different between patient and healthy groups. The mean of cTnI levels in ischemic and even nonischemic left heart failure were increased compared to the mean of values in healthy individuals but without significant creatine kinase MB band and myoglobin elevations. But cTnI levels were not increased in patients with right heart failure due to chronic obstructive pulmonary disease. These data indicate that the cTnI levels are abnormal in left heart failure but not in cor pulmonale.

Late systolic wave on brachial artery blood flow velocity pattern in patients with coronary artery disease and its relation to vascular stiffness.

Duplex-Doppler study typically exhibits triphasic brachial artery blood flow velocity pattern in subjects classified as normal without clinically evident atherosclerotic complications, heart disease, hypertension, or diabetes mellitus. In this study, the authors described the late systolic wave on the brachial artery blood flow velocity pattern in patients with coronary artery disease and investigated the relation between late systolic wave and vascular stiffness. Blood flow profile and velocity of the brachial artery were determined noninvasively by ultrasound pulsed-Doppler technique under the guidance of a B-mode ultrasound image in 96 patients with coronary artery disease (CAD). The control group consisted of 23 healthy subjects with no or maximally 2 risk factors (only among age, cigarette smoking, obesity, and gender) for vascular disease. None of the patients and controls had clinical evidence of arterial disorders at upper extremities. In 32 patients (33%) with CAD, a late systolic wave was observed in the brachial artery Doppler study. On the other hand, no late systolic wave was observed in the healthy subjects. In addition, multivessel disease, hypertension, advanced age, diabetes, and smoking were significantly more frequent in patients with the late systolic wave. In conclusion, peripheral arterial abnormalities induced by vascular stiffness may produce alterations in regional wave reflections, and the normal triphasic pattern of the brachial artery blood flow may change by the appearance of the late systolic wave.

Recurrent pulmonary emboli and thrombus attached to a permanently implanted pacemaker wire in pregnancy.

We present a case of pacer wire thrombus and recurrent pulmonary emboli in pregnancy associated with a permanent pacemaker. Transthoracic echocardiography demonstrated a thrombus attached to the pacer wire at the point where it crossed the tricuspid valve. After the uncomplicated vaginal delivery, thrombolytic therapy was given. This thrombus persisted despite thrombolytic therapy. Consequently, the patient was referred for cardiac surgery. The suspected cause was confirmed during the surgery.

The effect of autonomic nervous system activity on exaggerated blood pressure response to exercise: evaluation by heart rate variability.

OBJECTIVE: We investigated the effect of autonomic nervous system activity on exaggerated systolic blood pressure (SBP) response to exercise in healthy subjects using heart rate variability (HRV) analysis. METHOD AND RESULTS: We studied 53 healthy volunteer subjects with exercise treadmill test according to the Bruce protocol. Time domain and frequency domain of HRV were measured for each 5-minute segment before (rest) and after exercise (recovery) and during the total exercise period. The mean change in SBP (delta SBP) was 39 +/- 18 mm Hg. The delta SBP above the value of mean (> or = 40 mm Hg) was defined as an exaggerated delta SBP. According to the delta SBP, subjects were classified into two groups. Group I consisted of 32 patients who showed a normal delta SBP, group II consisted of 21 patients who showed exaggerated delta SBP. There were no significant differences in baseline clinical characteristics and exercise duration between the two groups. There were no significant differences in the mean RR intervals, SDNN (standard deviation of all RR intervals), RMSSD (the square root of the mean of the sum of the squares of differences between adjacent RR intervals), and HF (high-frequency power, 0.15 to 0.40 Hz) at rest between the two groups. However, LF (low-frequency power, 0.04 to 0.15 Hz) and LF/HF ratio at rest were significantly higher at rest in group II than in group I. There were no significant differences in the mean RR intervals and HF at exercise between the groups. However, SDNN and RMSSD were significantly lower, LF and the LF/HF ratio were significantly higher at exercise in group II than in group I. No differences in these parameters were observed at recovery between the two groups. CONCLUSIONS: The sympathetic activity was higher at rest and during the total exercise period, parasympathetic activity was lower during the total exercise period in healthy subjects with exaggerated SBP response to exercise than in those with normal SBP response.

The effect of electroconvulsive therapy on QT dispersion.

Electroconvulsive therapy (ECT) is used frequently in psychiatric practice and various electrocardiographic (ECG) changes have been described during ECT. QT dispersion (defined as maximal QT interval minus minimal QT interval) as assessed on the surface electrocardiogram has been demonstrated to reflect regional inhomogeneity of ventricular repolarization. The aim of this study is to examine the effect of electroconvulsive therapy on QT dispersion. We studied 27 patients (age range 24-42 y, mean age 34 y, 11 men) without heart disease who were treated with ECT. Structural heart disease was eliminated with routine clinical examination and laboratory tests, echocardiography, and exercise treadmill test. QT interval and corrected QT (QTc) dispersion was measured on a 12-lead ECG before and just after ECT. QTc dispersion increased from 28.9 +/- 7.4 ms at baseline to 81.4 +/- 12.8 ms after the procedure (P < 0.0001). This result demonstrated that QTc dispersion increased significantly during ECT. This finding may explain that increased inhomogeneity of ventricular repolarization is associated with enhanced vulnerability to arrhythmias during ECT.

Effects of cigarette smoking on the circadian rhythm of heart rate variability.

BACKGROUND: The effects of cigarette smoking on the circadian rhythm of heart rate variability (HRV) are not known. METHODS: We studied the effects of cigarette smoking on the circadian rhythm of HRV in 24 smoking and 21 non-smoking healthy subjects. Twenty-four hour ambulatory electrocardiograms were recorded and time domain parameters of HRV (SDNN [standard deviation of all R-R intervals], SDANN [standard deviation of the averages of R-R intervals in all 5-minute segments of the entire recording], RMSSD [the square root of the mean of the sum of the squares of differences between adjacent R-R intervals]) were determined for the entire 24-hour period and for each 3-hour period. RESULTS: In total, SDNN and SDANN were significantly lower in smokers than non-smokers (116 +/- 26 vs 136 +/- 27, p < 0.05 for SDNN, 109 +/- 25 vs 121 +/- 24, p < 0.05 for SDANN). However, there were no statistical differences between smokers and non-smokers in heart rate (81 +/- 9 vs 76 +/- 10, p > 0.05) and RMSSD (32 +/- 12 vs 37 +/- 18, p > 0.05). These HRV parameters showed a circadian variation: they increased at night and decreased during the day in both groups. The parameters were lower in smokers than non-smokers during daytime (especially, between 8-14 hours). However, no differences were detected during night-time. CONCLUSIONS: Time domain parameters of HRV (SDNN, SDANN and RMSSD) in both smoking and non-smoking healthy subjects have a circadian rhythm. SDNN and SDANN were lower in smokers than non-smokers during daytime.

The effects of halothane and sevoflurane on QT dispersion.

QT dispersion is defined as the difference between QT (max) and QT (min) in the 12-lead surface ECG. It has been shown to reflect regional variations in ventricular repolarization and is significantly greater in patients with arrhythmic events than in those without them. The aim of this study was to examine the effects of halothane and sevoflurane on QT and QTc dispersion during inhalational induction of anaesthesia. The effects on QT and QTc dispersion of halothane and sevoflurane have been investigated during induction of anaesthesia. Forty-six ASA (American Society of Anaesthesiologists) physical status I-II patients, aged 16-50 years, undergoing general anaesthesia were randomly allocated to receive either halothane or sevoflurane. The mean baseline values for QT and QTc dispersion were not significantly different between the two groups (P > 0.05). QT dispersion was increased with halothane compared with baseline values (50 +/- 16 ms vs. 29 +/- 9 ms, P < 0.01) and after sevoflurane compared with baseline (48 +/- 15 vs. 33 +/- 8 ms, P < 0.01). Also, QTc dispersion was increased with halothane compared with baseline values (48 +/- 13 ms vs. 31 +/- 9 ms, P < 0.001) and after sevoflurane compared with baseline (50 +/- 14 vs. 40 +/- 11 ms, P < 0.01). The QTc interval did not change by both sevoflurane (443 +/- 7 vs. 431 +/- 21 ms, P > 0.05) and halothane (419 +/- 33 vs. 431 +/- 19 ms, P > 0.05) compared with baseline. Both halothane and sevoflurane cause myocardial repolarisation abnormalities in man in terms of increased QTc dispersion. This may be relevant in the aetiology of arrhythmias in patients during anaesthesia with halothane or sevoflurane.