The JT Interval as a Depolarization Independent Measurement of Repolarization: Lessons from Catheter Ablation of the Wolff-Parkinson-White Syndrome

In patients with Wolff-Parkinson-White syndrome (WPW), preexcitation precludes accurate assessment of the ventricular repolarization by the QT_C. In patients with long QT syndrome, it has been demonstrated that the JT_C does not change when depolarization abnormalities develop. We hypothesized that this phenomenon should also be applicable to WPW patients. To test this, we assessed the surface ECG of 29 patients (16 males, 13 females) with WPW pre- and postablation. The QRS, QT, and JT intervals were measured pre- and postablation at 50 mm/s paper speed in leads II and V₂. QT_C and JT_C were calculated according to Bazett's formula. The average age was 12.8 ± 4.9 years (range 1.5–21). All patients had no residual preexcitation on postablation ECG. Early and late follow-up ECGs were obtained at 32 ± 34 days and 388 ± 197 days postablation, respectively. Both the QRS and the QT_C intervals shortened significantly on the postablation versus preablation ECGs (QRS: 115 ± 23 ms vs 89 ± 15 ms, respectively; P < 0.0001), (QT_C: 454 ± 26 vs 423 ± 23, respectively; P < 0.0001). The preablation JT_C interval did not change, postablation (319 ± 21 vs 323 ± 23, respectively; P > 0.2). Also, the JT_C interval did not change between early and late follow- up, postablation. JT_C: is an independent measure of repolarization, not related to depolarization. JT_C may be a useful tool in assessing repolarization in patients with WPW and other depolarization abnormalities.     

Abnormal Response to Exercise, Face Immersion, and Isoproterenol in Children with the Long QT Syndrome

The present study was performed to observe the change of QT interval by sympathetic stimulations in patients with the long QT syndrome (LQTS). The study group consisted of 6 children with LQTS and 6 healthy children without QT prolongation. All LQTS patients had syncopal episodes. The QT_c and ΔQT_c% ([QT_C interval after examination - QT_c interval at rest]/QT_c interval at rest × 100) by treadmill testing, face immersion, and isoproterenol were examined. One minute after peak exercise of treadmill testing, the changes in the QT_r, interval were not significant in either group, but ΔQT_C% was larger in the LQTS group than in the control group (+ 11.0 ± 12.1% vs -2.6 ± 3.2%;P= 0.02). The QT_c interval at the shortest RR interval during face immersion was prolonged in the LQTS group (0.47 ± 0.01 s to 0.51 ± 0.04 s; P = 0.02), but there were no significant changes in the control group (0.40 ± 0.03 s to 0.41 ± 0.03 s; P = NS). ΔQT_C% was larger in the LQTS group than in the control group (+ 10.0 ± 7.3% vs +1.1 ± 5.5%; P = 0.04). In the LQTS group, the RR interval was shortened (P = 0.009) and QT_c interval was prolonged (P = 0.0008) after isoproterenol infusion. These sympathetic stimulations amplified the TU abnormality in the LQTS group. By observing the TU changes caused by face immersion, we hoped to find a possible new method with which to diagnose LQTS. The combination of these examinations may be helpful in screening the borderline cases of TU abnormalities.     

Relationship Between QT Interval Duration and Electrical Induction of Ventricular Tachycardia

The relation of inducible ventricular tachycardia (VT) to QT interval duration of ventricular paced rhythm has not been evaluated. To clarify this relation we measured corrected QT interval duration (QT_C) during sinus rhythm and QT interval duration during ventricular paced rhythm (QT-V) in patients with coronary artery disease without (non-VT group = group B) and with inducible VT (VT group = group A). Duration of QT-V was greater in the VT group (n = 20) compared with non-VT group (n = 20) during ventricular pacing at cycle lengths of 600 ms (424 ± 26 vs 396 ± 19 ms, P < 0.01), of 500 ms (407 ± 20 vs 383 ± 21 ms, P < 0.01), and of 400 ms (390 ± 21 vs 362 ± 17 ms, P < 0.001). During sinus rhythm the mean values of QT_C were similar in both groups (408 ± 25 vs 413 ± 20 ms, NSJ. During ventricular stimulation the percentage of patients with values of QT-V exceeding 380 ms was 35% in non-VT group and 95% in VT group (P <0.01) at cycle length of 500 ms and 5% versus 60%, respectively, (P < 0.01), at cycle length of 400 ms. Thus, a trend toward longer QT values of ventricular paced rhythm exists in patients with inducible VT.     

Magnetocardiographic QT Interval Dispersion in Postmyocardial Infarction Patients with Sustained Ventricular Tachycardia: Validation of Automated QT Measurements

T 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. QT_apex dispersions were 127 ± 26 versus 83 ± 21 ms (P = 0.004) and QT_end dispersions 130 ± 37 versus 82 ± 37 ms (P = 0.013), respectively. Automatic method gave comparable values. Their relative differences were 9% for QT_apex and 27% for QT_end 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.     

Prolonged QRS duration increases QT dispersion but does not relate to arrhythmias in survivors of acute myocardial infarction

QT dispersion has been suggested and disputed as a risk marker for ventricular arrhythmias after myocardial infarction. Delayed ventricular activation after myocardial infarction may affect arrhythmic risk and QT intervals. This study determined if delayed activation as assessed by (1) QRS duration in the 12-lead ECG and by (2) late potentials in the signal-averaged ECG affects QT dispersion and its ability to assess arrhythmic risk after myocardial infarction. QT duration, JT duration, QT dispersion, and JT dispersion were compared to QRS duration in the 12-lead ECG and to late potentials in the signal-averaged ECG recorded in 724 patients 2-3 weeks after myocardial infarction. Prolonged QRS duration (> 110 ms) and high QRS dispersion increased QT and JT dispersion by 12%-15% (P < 0.05). Presence of late potentials, in contrast, did not change QT dispersion. Only the presence of late potentials (n = 113) was related to arrhythmic events during 6-month follow-up. QT dispersion, JT dispersion, QRS duration, and QRS dispersion were equal in patients with (n = 29) and without arrhythmic events (QT disp 80 +/- 7 vs 78 +/- 1 ms, JT disp 80 +/- 6 vs 79 +/- 2 ms, mean +/- SEM, P > 0.2). In conclusion, prolonged QRS duration increases QT dispersion irrespective of arrhythmic events in survivors of myocardial infarction. Presence of late potentials, in contrast, relates to arrhythmic events but does not affect QT dispersion. Therefore, QT dispersion may not be an adequate parameter to assess arrhythmic risk in survivors of myocardial infarction.     

Heart Rate Variability and Major Arrhythmic Events in Patients with Idiopathic Dilated Cardiomyopathy

This prospective study of 71 patients with idiopathic dilated cardiomyopathy (IDC) and preserved sinus rhythm was designed to evaluate the relation between heart rate variability (HRV) and subsequent major arrhythmic events. Standard time- and frequency-domain HRV parameters were obtained from analysis of 24-hour Holter ECG recordings. During a mean follow-up of 15 ± 5 months, major arrhythmic events including sustained ventricular tachycardia, ventricular fibrillation, and sudden cardiac death occurred in 10 of the 71 study patients (14%). Neither time- nor frequency-domain indices of HRV differed significantly between patients with and patients without subsequent major arrhythmic events. However, there was a trend toward a lower standard deviation of the average normal RR interval for all 5-minute segments of the 24-hour recording (68 ± 17 ms vs 80 ± 31 ms; P = 0.06) in patients with major arrhythmic events. In addition, the percentage of adjacent normal RR intervals differing > 50 ms over the recording period tended to be lower in patients with major arrhythmic events (6%± 3% vs 9%± 6%; P = 0.08). Our results indicate a tendency toward attenuated parasympathetic activity in IDC patients with subsequent major arrhythmic events compared to arrhythmia-free patients. Larger studies with longer follow-up periods are necessary to clarify the role of HRV measurements for arrhythmia risk prediction in patients with IDC.     

Value of Time- and Frequency-Domain Analysis of Signal-Averaged Electrocardiography for Arrhythmia Risk Prediction in Idiopathic Dilated Cardiomyopathy

Signal-averaged electrocardiography (SAECG) was performed in 120 consecutive patients with idiopathic dilated cardiomyopathy (IDC), and in 60 healthy controls. Time-domain analysis of SAECGs revealed ventricular late potentials in 27 of 120 patients with IDC (23%) compared to 2 of 60 controls (3%; P < 0.05). Frequency-domain analysis of SAECGs showed ventricular late potentials in 9 of 120 patients with IDC (8%) compared to none of the 60 controls (0%, P < 0.05). During a prospective follow-up of 15 ± 7 months, serious arrhythmic events, defined as sustained ventricular tachyarrhythmias or sudden death, occurred in 17 of 120 patients with IDC (14%). The sensitivity, specificity, and positive and negative predictive values of ventricular late potentials for serious arrhythmic events were 35%, 80%, 22%, and 88% for the time-domain analysis, and 18%, 94%, 33%, and 87% for the frequency-domain analysis of SAECG, respectively. Thus, neither the time- nor the frequency-domain analysis of SAECG appears to be useful for risk stratification in the setting of IDC in view of their low sensitivity and low positive predictive value for serious arrhythmic events during follow-up.     

Long Runs of Non-Sustained Ventricular Tachycardia on 24-Hour Ambulatory Electrocardiogram Predict Major Arrhythmic Events in Patients with Idiopathic Dilated Cardiomyopathy

This study examined the prognostic significance of the rate and length of non-sustained (NS) ventricular tachycardia (VT) on 24-hour ambulatory electrocardiograms (ECG) recorded in 343 patients with idiopathic dilated cardiomyopathy (IDC) in the prospective Marburg Cardiomyopathy study. NSVT was defined as ≥3 consecutive ventricular premature beats at >120 bpm. During 52 ± 21 months of follow-up, major arrhythmic events defined as sustained VT, VF, or sudden cardiac death occurred in 46 of 343 patients (13%). Patients with 3–4 beat runs of NSVT had a similar arrhythmia-free survival as patients without NSVT on baseline 24-hour ambulatory ECG. The incidence of major arrhythmic events during follow-up increased significantly from 2% per year in patients without NSVT, to 5% per year in patients with 5–9 beat runs of NSVT, to 10% per year in patients with ≥10 beat runs of NSVT (P < 0.05). Unlike the length, the rate of NSVT was similar in patients with versus without subsequent major arrhythmic events (163 ± 23 vs 160 ± 24 bpm). Thus, the length but not the rate of NSVT on 24-hour ambulatory ECG was a predictor of major arrhythmic events in patients with IDC. The presence of NSVT with ≥10 beat runs on ambulatory ECG was associated with a particularly high risk of major arrhythmic events.     

Arrhythmia Risk Prediction in Idiopathic Dilated Cardiomyopathy Based on Heart Rate Variability and Baroreflex Sensitivity

This study examined the relation between heart rate variability (HRV) and baroreflex sensitivity (BRS) and subsequent major arrhythmic events (MAE), defined as sustained VT, VF or sudden death, in 263 patients with idiopathic dilated cardiomyopathy (IDC) in sinus rhythm. The predefined measure of HRV was the standard deviation of all normal-to-normal RR intervals (SDNN) on baseline 24-hour ambulatory ECG. BRS was determined by the phenylephrine method. Over 52 ± 21 months of follow-up, MAE occurred in 38 patients (14%). SDNN at baseline 24-hour ambulatory ECG (106 ± 46 vs 109 ± 45, ns) and BRS (7.9 ± 5.5 vs 7.7 ± 5.3 ms/mmHg, ns) were both similar in patients with versus without MAE during follow-up. In contrast, left ventricular ejection fraction was significantly lower in patients with versus without MAE (24%± 7% vs 31%± 10%, P < 0.019. Conclusions: Neither HRV nor BRS predicted MAE in patients with IDC.     

Predictive Value of High-Sensitivity C-Reactive Protein in Patients with Idiopathic Dilated Cardiomyopathy

We analyzed the serum concentrations of high-sensitivity C-reactive protein (hsCRP) at the time of diagnostic cardiac catheterization in 198 patients with idiopathic dilated cardiomyopathy (IDC) to evaluate its prognostic value. Patients were dichotomized according to a median value of hsCRP of 2 mg/dL. Predefined study endpoints over 69 ± 33 months of follow-up included major arrhythmic events and transplant-free survival. Major arrhythmic events during follow-up occurred in 20 of 98 patients (20%) with low, compared to 22 of 100 patients (22%) with high hsCRP (ns). By multivariate analysis, a depressed left ventricular ejection fraction (LVEF) was the only significant predictor of arrhythmic risk. Death or cardiac transplantation was observed in 36% of patients with high, versus 22% of patients with low hsCRP (P < 0.05). By multivariate analysis, hsCRP and LVEF were independent predictors of transplant-free survival. Thus, in this patient population with IDC, hsCRP had independent prognostic value with regard to transplant-free survival, but did not contribute in the stratification with regard to arrhythmic risk.     

QT Dispersion Does Not Predict Early Ventricular Fibrillation After Acute Myocardial Infarction

Ventricular arrhythmias may be associated with increased QT dispersion (difference between maximum and minimum QT on standard 12-lead ECG). We performed a case control study to determine if QT dispersion on the admission ECG could predict early VF after acute myocardial infarction. The cases were 24 patients with acute myocardial infarction (14 inferior, 8 anterior, and 2 lateral) with VF within 12 hours of admission. There were 24 control patients without VF matched for site of infarction and ST segment score (sum of ST segment elevation). VF occurred a median of 153 minutes (interquartile range 93–245) after onset of chest pain and 33 minutes (range 7–104) after initial ECG. QT (399 ± 37 and 394 ± 37), QT corrected (440 ± 38 and 429 ± 29), and QT dispersion (68± 20 and 66 ± 27) were similar in patients and controls. By design, ST score was similar (11 ± 9 vs 9 ± 5 mV), although a good match could not be obtained for three patients with extreme ST elevation. Patients with VF presented to the hospital earlier after the onset of chest pain (median 95 min [range 65–188] compared to 150 min [range 80–270], P= 0.05) and had a lower serum sodium (138 ± 2.4 vs 140 ± 2.5, P = 0.05) than controls. Thus, QT interval and QT dispersion, measured on the presenting ECG, did not predict early VF after myocardial infarction.     

Noninvasive Arrhythmia Risk Stratification in Idiopathic Dilated Cardiomyopathy: Design and First Results of the Marburg Cardiomyopathy Study

The Marburg Cardiomyopathy Study (MACAS) is a prospective, observational study designed to determine the value of the following potential noninvasive arrhythmia risk predictors in at least 200 patients with idiopathic dilated Cardiomyopathy (IDC) over a 5-year follow-up period: NYHA-class, left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter, left bundle branch block and atrial fibrillation on ECG, QT/JT dispersion on 12-lead ECG, signal-averaged ECG, ventricular arrhythmias and heart rate variability (HRV) on 24-hour Hotter ECG, baroreflex sensitivity, and microvolt T wave alternans during exercise. This article describes the findings among the first 159 patients with IDCs enrolled in MACAS until May 1998 (40 women, 119 men;age:49 ± 12 years; LVEF: 32 ± 10%). Twenty-nine patients (18%) had atrial fibrillation and 130 patients (82%) were in sinus rhythm. Patients with sinus rhythm were further stratified according to LVEF < 30% (n = 54) versus LVEF ≥ 50% (n = 76). Compared to patients with LVEF ≥ 30%, patients with LVEF < 30% more often had left bundle branch block (43% vs 25%, P < 0.05), nonsustained VT (44% vs 22%, P < 0.05), decreased HRV (SDNN: 95 ± 39 vs 128 ± 42 ms, P < 0.01), decreased baroreflex sensitivity (5.6 ± 4 vs 8.3 ± 6 ms/mmHg, P < 0.01), and T wave alternans (59% vs 37%, P < 0.05). The prognostic significance of these findings will be determined by multivariate Cox analysis at the end of a 5-year follow-up. Primary endpoints in MACAS are overall mortality and arrhythmic events (i.e., sustained VT or VF, or sudden cardiac death).     

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.     

QT Interval Variability and Adaptation to Heart Rate Changes in Patients with Long QT Syndrome

Background: Increased QT variability (QTV) has been reported in conditions associated with ventricular arrhythmias. Data on QTV in patients with congenital long QT syndrome (LQTS) are limited.
Methods: Ambulatory electrocardiogram recordings were analyzed in 23 genotyped LQTS patients and in 16 healthy subjects (C). Short-term QTV was compared between C and LQTS. The dependence of QT duration on heart rate was evaluated with three different linear models, based either on the RR interval preceding the QT interval (RR₀), the RR interval preceding RR₀ (RR_-1), or the average RR interval in the 60-second period before QT interval (mRR).
Results: Short-term QTV was significantly higher in LQTS than in C subjects (14.94 ± 9.33 vs 7.31 ± 1.29 ms; P < 0.001). It was also higher in the non-LQT1 than in LQT1 patients (23.00 ± 9.05 vs 8.74 ± 1.56 ms; P < 0.001) and correlated positively with QTc in LQTS (r = 0.623, P < 0.002). In the C subjects, the linear model based on mRR predicted QT duration significantly better than models based on RR₀ and RR_-1. It also provided better fit than any nonlinear model based on RR₀. This was also true for LQT1 patients. For non-LQT1 patients, all models provided poor prediction of QT interval.
Conclusions: QTV is elevated in LQTS patients and is correlated with QTc in LQTS. Significant differences with respect to QTV exist among different genotypes. QT interval duration is strongly affected by noninstantaneous heart rate in both C and LQT1 subjects. These findings could improve formulas for QT interval correction and provide insight on cellular mechanisms of QT adaptation.     

Effects of Ischemia and Reperfusion on QT Dispersion During Coronary Angioplasty

The effects of ischemia and reperfusion on QT interval dispersion (QTD: QT_max-QT_min in the 12-lead ECG) were analyzed in 15 patients (12 males, 57 ± 13 years) undergoing coronary angiopiasty (PTCA). AH patients had single-vessel coronary artery disease (only one ≥ 85% stenosis in a major coronary artery) and normal left ventricular function. AH were in sinus rhythm with normal atrioventricular and intraventricular conduction on the surface ECG. No patient was on therapy that could affect the QT interval. The ECG was recorded (all 12 leads simultaneously) at 50 mm/s speed before the first balloon inflation, at the end of the first inflation during PTCA, and at 30" and 60" during reperfusion following the first inflation. In order to avoid ischemic preconditioning, only recordings of the first inflation were used. In each tracing QT_max and QT_min were evaluated. All values were rate corrected using a simple linear equation (QT linear corrected = QT + 0.154 [1-RR]). QTD increased significantly during both ischemia and reperfusion. QT_max was not changed by ischemia and was increased by reperfusion. QT_min was reduced by ischemia and increased by reperfusion. These results indicate that both ischemia and reperfusion alter ventricular repolarization, inducing a less homogeneous ventricular recovery pattern.     

QT Duration and Dispersion in Patients with Anomalous Origins of Coronary Arteries

Background: Coronary artery anomalies have been reported to show various symptoms ranging from chest pain and dyspnea to cardio-respiratory arrest and sudden death. In this study, we attempted to assess the changes in QT interval duration and dispersion in anomalous origins of coronary arteries (AOCA).
Methods: Nineteen AOCA patients (mean age: 52 ± 11 years) and 30 healthy control subjects (mean age: 50 ± 12 years) were included in the study. Minimum and maximum corrected QT intervals, and corrected QT dispersion were calculated. The two groups were compared in terms of QT dispersion and QT duration.
Results: There was no difference between the two groups in terms of baseline demographic characteristics. Maximum corrected QT intervals (QTc max), minimum corrected QT intervals (QTc min), and corrected QT dispersion were higher in AOCA patients than controls (452 ± 38 vs 411 ± 25 ms [P = 0.0001], 402 ± 31 vs 383 ± 28 ms [P = 0.048], and 51 ± 30 vs 28 ± 12 ms [P = 0.001], respectively).
Conclusion: In the patients with anomalous origins of coronary arteries, QT dispersion that is an indicator of sudden cardiac death and arrhythmias frequency increased. QTc max, QTc min, and corrected QT dispersion are higher in patients with anomalous origin of the coronary artery than in control subjects.     

Effects of Postmyocardial Infarction Scar Size, Cardiac Function, and Severity of Coronary Artery Disease on QT Interval Dispersion as a Risk Factor for Complex Ventricular Arrhythmia

The aim of the study was to determine the relation between QT dispersion and ventricular arrhythmia after myocardial infarction, as well as the effects of postinfarction scar size, cardiac function, and severity of coronary artery disease on QT dispersion. Three hundred three patients, 3 months after myocardial infarction, and a group of 21 healthy subjects were evaluated. QT dispersion was the difference between maximal and minimal QT interval in 12-ECG leads. Postinfarction scar size was determined by Selvester's QRS scoring system. Cardiac function was evaluated by echocardiography and exercise stress test, and the severity of coronary artery disease by the number and degree of coronary artery stenoses. QT dispersion increased significantly in relation to the severity of arrhythmia (< 50 premature ventricular complexes vs ventricular tachycardia; 61.6 [± 12.3] vs 84.8 [± 16.4] ms, P < 0. 001). QT dispersion > 80 ms was associated with ventricular tachycardia with the sensitivity of 68% and specificity of 88%. QT dispersion also increased significantly, dependent on the postinfarction scar size (0% vs ± 33% of left ventricular myocardium; 61.8 [± 16.4] vs 74.7 [± 16] ms, P < 0. 001), as well as in the case of significantly impaired cardiac function. Although QT dispersion increased with the number of diseased vessels and the degree of stenoses, the differences were not significant (P > 0. 05). In conclusion, QT dispersion is a risk marker of complex ventricular arrhythmia in the chronic stage of myocardial infarction. Multiple regression analysis indicates that only the postinfarction scar size has an independent effect on QT dispersion (R²= 0. 39, P < 0. 05).     

QT Variability Before and After Episodes of Nonsustained Ventricular Tachycardia in Patients with Hypertrophic Cardiomyopathy

This study examined the changes in QT dynamics occurring during 5-minute intervals sampled immediately before and 1 hour after episodes of nonsustained ventricular tachycardia (VT) in patients with hypertrophic cardiomyopathy (HCM). Twenty-four hour Holter recordings were performed in 10 patients with HCM in the absence of antiarrhythmic medications and processed by the ELA Medical QT analysis software. All sinus complexes were averaged over 30-second segments and 2,880 templates were created. For each template, a mean corrected QT_ec (time interval between the onset of QRS and the end of the T wave) and QT_ac (time interval between the onset of the QRS and the peak of the T wave) were calculated, with their standard deviations (SDQT_e and SDQT_a) taken as indices of QT variability. The slopes of the regression line for the QT_e and QT_a against the corresponding RR also were calculated. Forty 5-minute segments were analyzed immediately before (sample A) and 1 hour after (sample B) 20 episodes of nonsustained VT. QT_ac was significantly longer in group A than in group R (321 ± 20 vs 312 ± 22, P < 0.0001) and SDQT_a was significantly lower (2.8 ± 1.2 vs 4.7 ± 3.7, P < 0.03). There were no significant differences in QT_ec, SDQT_e, QTe/RR and QT_a/RR before and after the episodes. Our data indicate that in patients with HCM, the averaged QT_ac is significantly longer and the QT_a variability significantly lower before episodes of nonsustained VT.     

Serotonin receptor adaptation in patients with analgesic-induced headache

Analgesic abuse has recently been recognized as a cause of deterioration in primary headache patients. Although the pathogenesis of this headache transformation is still obscure, alteration of serotonin receptor function is one possible mechanism. To assess the plasticity of 5HT₂ serotonin receptors in this condition, we investigated receptor binding by the platelet membrane in patients with analgesic-induced headache (AIH), migraine and non-headache controls. The technique involved radioligand binding with (phenyl-4-³H)spiperone and ketanserin. A greater density of receptor numbers (B_max) was found in patients with AIH and in non-headache controls (96.47±10.2 and 92.01±13.15 fmol/mg protein), as compared to migraine patients (49.52±5.14 fmol/mg protein). The value of dissociation equilibrium constant (K_D) remained unchanged (3.07±0.49, 2.24±0.24 and 2.9±0.42 nM for patients with AIH, migraine and non-headache controls, respectively). Based on these findings, we suggest that up-regulation of 5HT₂ serotonin receptors may be a possible mechanism of headache transformation in patients with AIH.     

The Effect of DDD Pacing on Ergospirometric Parameters and Neurohormonal Activity in Patients with Hypertrophic Obstructive Cardiomyopathy

This study examined the acute and long-term effects of DDD pacing on ergospirometric parameters and neurohormonal activity in patients with hypertrophic obstructive Cardiomyopathy (HOCM). We studied eight patients (five males), aged 56 ± 7 years, with HOCM refractory to drugs. In all patients a DDD pacemaker was implanted and programmed with an atrioventricular (AV) delay that insured full ventricular activation. The patients underwent echocardiographic examination and exercise stress testing before and 3 days, 3 months, and 12 months after pacemaker implantation. Oxygen consumption was measured at the anaerobic threshold (VO_2AT) and peak exercise (pVO₂). Atrial natriuretic peptide (ANP) and cyclic adenosine monophosphate (c-AMP) levels were measured concomitantly. Left ventricular outflow tract (LVOT) pressure gradient decreased significantly from 70 ± 18 to 25 ± 12 mmHg (P < 0.05) 3 days after pacing and remained unchanged at 3 and 12 months. pVO₂ and VO_2AT increased significantly, from 20.1 ± 3 to 23.4 ± 3 mL/kg/min and from 16 ± 3 to 17.8 ± 2 mL/kg/min, respectively (P < 0.05). This improvement continued up to 3 months, and then remained stable until the end of the 12-month follow-up period. ANP levels decreased at 3 days from 85.4 ± 5.7 to 75.4 ± 7.3 fmol/mL (P < 0.05), and remained unchanged over the 12 months. c-AMP levels did not change significantly after the onset of pacing. DDD pacing in patients with HOCM not only reduces the LVOT pressure gradient but also causes a significant early and long-term improvement in exercise capacity and neurohormonal profile.