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To evaluate the diagnostic performance of Fourier phase analysis of gated blood pool single-photon emission computed tomography (GBP SPECT) in arrhythmogenic right ventricular (RV) cardiomyopathy, 18 patients with confirmed arrhythmogenic RV cardiomyopathy underwent GBP SPECT and x-ray cineangiography. Results were compared with data obtained with GBP SPECT in 10 control subjects. This 3-dimensional method demonstrated good correlation with cineangiography for measurements of RV enlargement and extent of the disease; RV and left ventricular segments were analyzed with the same accuracy. Tomographic abnormalities were significant decreased RV ejection fraction, RV dilatation, nonsynchronized contraction of the ventricles, increased RV contraction dispersion, presence of segmental RV wall motion disorders and/or phase delays, and occasionally regional left ventricular abnormalities. RV-delayed phase areas were always present in our population. A scoring system with RV criteria was proposed to diagnose RV disease. Because Fourier analysis of GBP SPECT provides ventricular morphologic information for the right ventricle with the same accuracy as for the left ventricle, it may replace planar radionuclide studies. Therefore, this method is helpful in patients with a strong clinical suspicion of arrhythmogenic RV cardiomyopathy, and should be used as a screening method before right ventriculography. [ABSTRACT FROM AUTHOR]

Background: In idiopathic dilated cardiomyopathy (IDC), the predictive value of QT dispersion is still under debate., Aims: This study assessed the role of QT dispersion for the long-term risk of cardiac death and of major arrhythmic events in IDC., Methods and Results: In 162 patients with IDC (age 52+/-12 years), the QT interval on a 12-lead ECG was measured manually. QT dispersion was evaluated with QT range and QT standard deviation, for both QT and QTc (Bazett formula). With a follow-up of 53+/-41 months, QT dispersion was not a predictor of cardiac death in univariate or in multivariate analysis, and was of similar value for patients with or without bundle branch block. Using multivariate analysis, increased pulmonary capillary wedge pressure (p=0.003), decreased heart rate variability (Standard deviation of all NN intervals, p=0.01) and non-sustained ventricular tachycardia (NSVT) (p=0.03) were predictors of cardiac death. Sudden death and/or major arrhythmic events were independently predicted by NSVT (p=0.005), decreased heart rate variability (p=0.01) and late ventricular potentials on signal averaged ECG (p=0.02)., Conclusion: This study confirms the poor prognostic value of QT dispersion in patients with IDC. Other methods to assess repolarization abnormalities need to be evaluated in such patients.

There is considerable variability in segmental wall motion abnormalities and in the prognosis of idiopathic dilated cardiomyopathy (IDC). Radionuclide ventriculography with Fourier analysis was performed in 107 patients with angiographically proved IDC. Amplitude analysis located the wall motion abnormalities. Using phase analysis in the left and right ventricles, the interventricular delay between the mean phase of the right and left ventricles was used to assess interventricular dyssynchrony and SDs of the mean phase in each ventricle was used to assess intraventricular dyssynchrony. Hypokinesis was global in 56 patients (52%) and localized in the anteroseptal wall in 34 (32%), the inferior wall in 12 (11%), the anteroseptal and inferior walls in 2 (2%), and the lateral wall in 3 (3%). Patients with localized wall motion abnormalities had larger left ventricular (LV) end-diastolic diameters (70 +/- 9 vs 66 +/- 8 mm, p = 0.009) and lower LV ejection fractions (25 +/- 9% vs 31 +/- 12%, p = 0.005). Intraventricular dyssynchrony was lower in patients with global hypokinesis (SD of LV mean phase 67 +/- 35 vs 48 +/- 22 ms, p = 0.002). With a follow-up of 27 +/- 23 months, increased SD of the LV phase (p = 0.005), decreased right ventricular ejection fraction (p = 0.006), decreased LV ejection fraction (p = 0.04), and localized wall motion abnormality (p = 0.009) were independent predictors of cardiac death or worsening heart failure leading to heart transplantation. Thus, segmental wall motion abnormalities are frequent in IDC and are associated with severe systolic dysfunction and a worse prognosis.

Primary hypertrophic cardiomyopathy is a genetic disease causing sarcomere dysfunction. The structural and functional myocardial changes combine to produce cardiac arrhythmias related to reentry phenomena and to triggered automatic activity. The commonest arrhythmias are atrial fibrillation and ventricular arrhythmias; junctional tachycardias via the bundle of Kent are rare. Atrial fibrillation and the Wolff-Parkinson-White syndrome are more commonly associated with certain genetic mutations. Their treatment is mainly based on medication with amiodarone or on radiofrequency ablation in cases of junctional tachycardia. Ventricular arrhythmias are mainly isolated ventricular extrasystoles and non-sustained ventricular tachycardia. The prognostic significance of the latter has been subject of debate for many years but recent studies report a poor prognosis with non-sustained ventricular tachycardia especially in the young patients. Sustained ventricular tachycardia and ventricular fibrillation, though life-threatening complications of hypertrophic cardiomyopathy, are rarely documented and justify implantation of an automatic defibrillator as the risk of recurrence is high. The main objective of the cardiologist in cases of primary hypertrophic cardiomyopathy is to identify the patient at high risk of sudden death. This requires analysis of several parameters: clinical, anatomical, haemodynamic, rhythmic, functional and genetic. The presence of at least two risk factors for sudden death justifies preventive measures. The implantation of an automatic defibrillator is the most reliable form of treatment.

Using Fourier phase analysis of equilibrium radionuclide angiography in both ventricles, inter- and intraventricular delays were correlated with QRS morphology and duration in 103 patients with idiopathic dilated cardiomyopathy. We found that left bundle branch block on the left axis may reflect a high intra-left ventricular dyssynchrony. A precise evaluation of the dyssynchrony appears useful because a high proportion of patients with incomplete bundle branch block, left anterior hemiblock, or "normal" QRS exhibit a marked intra-LV dyssynchrony and may respond to cardiac resynchronization therapy.

Biventricular pacing is a new form of treatment for patients with dilated cardiomyopathy and ventricular dyssynchrony. Limited information is available regarding the relationship between ventricular dyssynchrony and risk markers of ventricular arrhythmias in idiopathic dilated cardiomyopathy (IDC). In 103 patients with IDC, Fourier phase analysis of both ventricles was performed from equilibrium radionuclide angiography (ERNA). The difference between the mean phase of the LV and RV was a measure of interventricular dyssynchrony, and the standard deviations of the mean phases in each ventricle measured intraventricular dyssynchrony. There were no significant differences in inter- and intraventricular dyssynchrony between patients with versus without histories of sustained VT or VF, nonsustained VT, abnormal signal-averaged ECG, or induced sustained monomorphic VT. Dyssynchrony was not related to decreased heart rate variability (HRV). LV and interventricular dyssynchrony were weakly related to QT duration and QT dispersion. During a follow-up of 27 +/- 23 months, 21 patients had major adverse cardiac events (MACE), including 7 cardiac deaths, 11 progression of heart failure leading to cardiac transplantation, and 3 sustained VT/VF. The only independent predictors of MACE were an increased standard deviation of LV mean phase (P = 0.003), a decreased HRV (standard deviation of normal-to-normal intervals, P = 0.004), and histories of previous VT/VF (P = 0.03) or nonsustained VT (P = 0.04). In conclusion, left intraventricular dyssynchrony evaluated with ERNA was an independent predictor of MACE in IDC and was not related to usual risk markers of ventricular arrhythmias. This may have implications for resynchronization therapy and/or the use of implantable cardioverter defibrillators in IDC.

Objectives: The study evaluated the prognostic value of interventricular and intraventricular dyssynchrony in idiopathic dilated cardiomyopathy (IDC)., Background: Biventricular pacing is an emerging treatment for patients with dilated cardiomyopathy and ventricular dyssynchrony. The prognostic values of interventricular and intraventricular dyssynchrony have not been previously compared., Methods: A total of 103 patients with IDC were studied. Left bundle branch block was present in 25% of patients. Equilibrium radionuclide angiography was performed and Fourier phase analyses were examined in both ventricles. Difference between the mean phase of left ventricle (LV) and right ventricle (RV) assessed interventricular dyssynchrony, and standard deviations (SDs) of the mean phase in each ventricle assessed intraventricular dyssynchrony., Results: The QRS duration was related to both interventricular and intraventricular dyssynchrony. A degradation of the hemodynamic status was associated with an increase in intraventricular dyssynchrony but not in interventricular dyssynchrony. With a follow-up of 27 +/- 23 months, 18 patients had a major cardiac event (7 cardiac deaths; 11 worsening, leading to heart transplantation). The SDs of the LV and RV mean phase and QRS duration were predictors of cardiac event (all p < 0.0001), but interventricular dyssynchrony was not. Among 13 univariate predictors of cardiac event, the only independent predictors were an increased SD of LV mean phase (p = 0.0004) and an increased pulmonary capillary wedge pressure (p = 0.009)., Conclusions: Intraventricular dyssynchrony evaluated with phase analysis of radionuclide angiography is an independent predictor of cardiac event in IDC. The prognosis is related to intraventricular rather than to interventricular dyssynchrony in IDC.

Some of the classical concepts of mitral valve prolapse (MVP) should be reviewed in the light of recent publications. It is a condition, according to strict echocardiographic criteria excluding near physiological abnormalities, which affects 2 to 3% of the adult population in the industrialised world. Only repetitive atrial arrhythmias and complex ventricular arrhythmias are more common in this condition than in control groups, the differences being more pronounced in cases of mitral regurgitation. The risk of syncope or sudden death is 0.1% per year, hardly any different to that of the rest of the general adult population (0.2%). However, this risk may attain 0.9 to 2% in cases with mitral regurgitation. The causes of sudden death are unclear (haemodynamic, neurohumoral, arrhythmic, etc...), although there is evidence in favour of malignant ventricular arrhythmias. Detailed clinical, electrophysiological, isotopic and anatomopathological studies have raised doubts as to the direct responsibility of the vascular malformation (or its eventual consequences on the atrial and ventricular chambers) in this mode of fatal outcome. On the other hand, localised or diffuse myocardial disease is often observed, usually a- or pauci-symptomatic, associated with MVP, the responsibility of which is more plausible. Therefore, the physician should adopt a flexible attitude towards these patients, reassuring those with benign symptoms at low risk and following up or actively treating the rarer malignant forms (especially familial, syncopal with mitral regurgitation and/or severe arrhythmias).

The incidence and the nature of medium-term complications of automatic implantable cardiac defibrillators (AICD) were studied. Seventy-nine AICD were implanted in 50 consecutive patients (42 men, aged 54.5 +/- 13.7 years). Forty-six patients had spontaneous ventricular arrhythmia. These arrhythmias were resistant to treatment (N = 9), reproducible with treatment (N = 28). In 4 patients, the indication was prophylactic, in 2 a Brugada syndrome, in 2 syncope with reinducible ventricular tachycardia and in 1 patient, torsades with a short coupling interval. Forty-six patients had underlying cardiac disease (ischaemic, N = 28, primary dilated cardiomyopathy, N = 10, others, N = 8). The ejection fraction was > 40% in 32 patients. The average follow-up was 41.3 +/- 34.9 months. Eight patients died, 2 from cardiac failure. Twenty-one patients (42%) had 1 or more complications related to their AICD. These occurred: in the operative period (N = 3): 1 post-shock atrioventricular block, 1 ruptured electrode and 1 increased threshold with amiodarone; in the postoperative period (N = 6): infection in 3 cases, cerebrovascular accident in 1 case, deep venous thrombosis of the left arm in 1 case, pneumothorax in 1 case. In the medium-term, the complications were mainly inappropriate electrical shocks observed in 14 patients related to atrial arrhythmias in 7 cases, sinus tachycardia in 1 case, over-detection of myopotentials in 2 cases and electrode dysfunction in 4 cases. In addition, the authors observed complications related to the material: AICD failure in 1 case, electrode displacement in 1 case, and electrode rupture in 3 cases. The authors conclude that AICD are effective for the treatment of malignant ventricular arrhythmias which justify strict specialist follow-up given the incidence and diversity of their complications.

Background: Ventricular premature beats are common in patients with mitral valve prolapse (MVP). The purpose of this study was to determine whether symptomatic patients with MVP had certain functional characteristics and if ventricular arrhythmia (VA) could be explained by functional extravalvular abnormalities. Single photon emission computed tomography equilibrium radionuclide angiography with Fourier phase analysis was preferred to the planar radionuclide method. Only patients without significant mitral regurgitation were studied., Methods and Results: A total of 23 symptomatic patients with MVP (13 men, 10 women, mean age, 47+/-14 years) without mitral regurgitation underwent single photon emission computed tomography equilibrium radionuclide angiography. Symptoms were present in 20 patients, and VA was present in 14 patients. Ejection fraction, regional wall motion, and Fourier phase analysis were examined in both ventricles and compared with results for normal subjects. Ventricular abnormalities were observed in 20 (87%) patients: decreased left ventricular and right ventricular ejection fractions, increased standard deviations of the mean phase and focal wall motion, and/or delayed phase abnormalities. Abnormalities were less frequent but more marked in the right ventricular free wall, the infundibulum, or the septum compared with left ventricular delayed abnormalities, which were more frequent but limited. In 12 of 14 patients with VA, phase-delayed areas were observed in the ventricle where the origin of ventricular premature beats was suspected on the basis of their electrocardiographic morphologic features. A relation was found between late potentials and delayed-phase areas (right ventricle or septum) and left bundle branch block morphologic features of VA., Conclusions: Symptomatic patients with MVP frequently have ventricular dysfunction in 1 or both ventricles, sometimes limited but more marked in the presence of severe VA even without significant mitral regurgitation, suggesting structural modification. The use of a sensitive, accurate, and 3-dimensional method such as single photon emission computed tomography equilibrium radionuclide angiography may be of interest for a noninvasive investigation, especially in young symptomatic patients with MVP and VA.

In the prospective Data from an Epidemiological Study on the Insulin Resistance Syndrome, 2,894 healthy subjects aged 30 to 64 years had determinations of fasting glucose, insulin, serum lipid and fibrinogen concentrations, blood pressures, body mass index, and waist-hip ratio, as well as tobacco and alcohol consumptions and physical activity. A 12-lead electrocardiogram with automatic measurement of the QT interval was recorded and the formula used for heart rate correction was based on the best-fit regression between QT and heart rate. The QT duration was influenced by glucose homeostasis in both sexes, and increased in men with physical activity; there was a dose-effect relation for men who smoked.

The aim of this study was to evaluate the long-term prognostic value of signal-averaged electrocardiography (SAECG) in idiopathic dilated cardiomyopathy (IDC). Time domain analysis of SAECG was assessed in 131 patients with angiographically confirmed IDC (age 52+/-12 years; 108 men; left ventricular ejection fraction 33+/-12%) using specific criteria in 44 patients with bundle branch block. Late potentials (LP) on SAECG were present in 27% of the patients. Patients with LP had a similar left ventricular ejection fraction and a similar left ventricular end-diastolic diameter than patients with a normal SAECG. With a follow-up of 54+/-41 months, 24 patients suffered cardiac death and 19 had major arrhythmic events (sudden death, resuscitated ventricular fibrillation, or sustained ventricular tachycardia). Patients with LP had an increased risk of all-cause cardiac death (RR 3.3, 95% confidence interval 1.5 to 7.5, p = 0.004) and of arrhythmic events (RR 7.2, 95% confidence interval 2.6 to 19.4, p = 0.0001). Using multivariate analysis, only LP on SAECG (p = 0.001), reduced SD of all normal-to-normal intervals (SDNN) (p = 0.002), increased pulmonary capillary wedge pressure (p = 0.005), and history of sustained ventricular tachyarrhythmia (p = 0.02) predicted cardiac death. A history of previous sustained ventricular tachyarrhythmia (p = 0.0001), reduced SDNN (p = 0.003), and LP on SAECG (p = 0.006) were the only independent predictors of major arrhythmic events. Results were not altered when considering separately patients with or without bundle branch block, or after exclusion of patients with a history of sustained ventricular tachyarrhythmia. This study is one of the first to suggest that LP on SAECG is an independent predictor of all-cause cardiac death and is of high interest for arrhythmia risk stratification in IDC.

Cardiovascular mortality, the principal cause of early death in diabetics, is multifactorial. A prospective study was undertaken to analyse the different factors of excess cardiac complications in 40 patients with type 2 diabetes, whatever the symptomatology, by making an inventory of the cardiac abnormalities (systolic and diastolic left ventricular function, left ventricular hypertrophy, abnormalities of myocardial perfusion, heart rate variability and arrhythmias). Patients underwent 24 hour Holter monitoring, high amplification signal averaged electrocardiography, echocardiography, Thallium scintigraphy with a dipyridamole test followed by coronary angiography when positive. Patients were aged 60 +/- 8 years, diabetics for 11.8 +/- 6.8 years, and had associated cardiovascular risk factors: 85% were obese, 75% were hypertensive, 62.5% had hypercholesterolaemia and 60% were smokers. The HbA1C was 9.2 +/- 19%. An increased left ventricular mass was observed in 34.2% of patients. The left ventricular ejection fraction was normal (59.1 +/- 6.8%); 69.7% of patients had left ventricular diastolic dysfunction. Reduced heart rate variability was observed in 51.8% of cases. Late ventricular potentials were recorded on high amplification signal averaging in 39.5% of patients; 25.6% had significant ventricular extrasystoles and 52.2% had atrial extrasystoles. Twelve patients (45%) underwent Thallium myocardial scintigraphy with a positive dipyridamole test, 8 of whom had coronary lesions on angiography. The excess cardiac complications of diabetes is mainly due to ischaemic heart disease aggravated by autonomic neuropathy, left ventricular diastolic dysfunction, arrhythmias and left ventricular hypertrophy. In future, larger series are required to demonstrate that this detection can guide therapeutic intervention and reduce cardiac morbidity and mortality of diabetics.

Aims: The outcome of alcoholic cardiomyopathy is thought to be better than idiopathic dilated cardiomyopathy if patients abstain from alcohol. The aim of this study was to compare the long-term clinical outcome of alcoholic and idiopathic dilated cardiomyopathy., Methods and Results: Of 134 patients with dilated cardiomyopathy and normal coronary angiography, 50 had alcoholic cardiomyopathy; they were compared serially to 84 patients with idiopathic dilated cardiomyopathy. Left ventricular end-diastolic diameter, left ventricular ejection fraction and cardiac index, severity of ventricular arrhythmias, measurement of heart rate variability and results of signal-averaged ECG were similar in both groups. Although alcohol withdrawal was strongly recommended but observed in only 70% of patients with alcoholic cardiomyopathy, both groups had similar outcome in terms of cardiac death after follow-up treatment of 47+/-40 months. Multivariate analysis in the entire cohort demonstrated that increased pulmonary capillary wedge pressure (P=0. 003), alcoholism and lack of abstinence during follow-up (P=0.006) and decreased standard deviation of all normal-to-normal RR intervals (P=0.02) were independent predictors of cardiac death., Conclusion: In contrast with previous studies, patients with alcoholic cardiomyopathy did not have a better outcome than patients with idiopathic dilated cardiomyopathy. Alcoholism without abstinence was a strong predictor of cardiac death. This suggests that a more aggressive approach to alcohol cessation is needed in these patients., (Copyright 2000 The European Society of Cardiology.)

In 39 patients with myotonic dystrophy, we found a high percentage of infrahissian cardiac conduction abnormalities (51%) and late potentials (46%), whereas spontaneous and inducible ventricular arrhythmias were rare. These results suggest that the prolongation of QRSD and the duration of the low-amplitude signal on the signal-averaged electrocardiogram were related to delayed activation of the His and Purkinje tissue rather than true late potentials.

Objective: To identify intracardiac conduction abnormalities in patients with myotonic dystrophy from their clinical, ECG, and genetic features., Methods: 39 consecutive patients (mean (SD) age 42. 9 (12.1) years; 16 female, 23 male) underwent clinical examination, genetic studies, resting and 24 hour ambulatory ECG, signal averaged ECG, and electrophysiological studies., Results: 23 patients suffered from cardiac symptoms, 23 had one or more cardiac conduction abnormality on resting ECG, one had sinus deficiency, and 21 (53.8%) had prolonged HV intervals. No correlation was found between the severity of the neurological symptoms, onset of disease, cardiac conduction abnormalities on ECG, and the intracardiac conduction abnormalities on electrophysiological study. The size of the DNA mutation was longer in the abnormal HV interval group than in the normal HV interval group (3.5 (1.8) v 2.2 (1.0) kb, p < 0.02). Signal averaged ECG parameters (total QRS duration (QRSD) and duration of low amplitude signals /= 100 ms with LAS 40 >/= 36 ms identified patients with an abnormal HV interval with good sensitivity (80%) and specificity (83. 3%)., Conclusions: Infrahissian conduction abnormalities are common in myotonic dystrophy and can be identified using signal averaged electrocardiography.

Objective: This study was designed to evaluate the prognostic value of heart rate variability for sudden death, resuscitated ventricular fibrillation or sustained ventricular tachycardia in patients with idiopathic dilated cardiomyopathy., Background: Previous studies have shown that heart rate variability could predict arrhythmic events and sudden death in postinfarction patients, but the prognostic value of heart rate variability for arrhythmic events or sudden death in patients with idiopathic dilated cardiomyopathy has not been established., Methods: Time and frequency domain analysis of heart rate variability on 24-h electrocardiographic (ECG) recording was assessed in 116 patients with idiopathic dilated cardiomyopathy (91 men, aged 51+/-12 years, left ventricular ejection fraction 34+/-12%)., Results: Mean follow-up (+/-SD) was 53+/-39 months. Sixteen patients reached one of the defined study end-points (sudden death, resuscitated ventricular fibrillation or sustained ventricular tachycardia) during follow-up. Using multivariate analysis, only reduced standard deviation of all normal-to-normal intervals (SDNN) (p = 0.02) and ventricular tachycardia during 24-h ECG recording (p = 0.02) predicted sudden death and/or arrhythmic events. For SDNN, a cutoff level of 100 ms seemed the best for the risk stratification., Conclusions: Decrease in heart rate variability is an independent predictor of arrhythmic events and sudden death in idiopathic dilated cardiomyopathy, whether the mechanism of sudden death is ventricular tachyarrhythmia or not.

Using measurements of QT/RR slopes with a computerized Holter system, QT interval dynamicity was evaluated in 19 patients with normal structural heart before and 2 months after oral treatment with verapamil prescribed for paroxysmal atrioventricular nodal reentrant tachycardia. Verapamil significantly shortened QT at low heart rates, mainly in the diurnal period, and this characteristic may explain, in part, the previously reported protective effect of verapamil against torsades de pointes.

Heart rate variability is a noninvasive indicator of autonomic nervous system activity. The role of the autonomic nervous system in the genesis of atrial or ventricular arrhythmias is now well established. Little is known about the effects of flecainide on heart rate variability in patients with normal heart structure, the main population receiving flecainide. This study was designed to evaluate the effects of flecainide on heart rate variability in patients without coronary artery disease or congestive heart failure. Time and frequency domain analysis of heart rate variability on 24-hour electrocardiogram recording were assessed in 40 patients with normal echocardiography and without evidence of coronary artery disease before and after 2 months of oral treatment with flecainide (321 +/- 57 mg/day) prescribed for Wolff Parkinson White syndrome with circus movement tachycardia. Flecainide significantly decreased all parameters of heart rate variability in the time domain (median delta% -10% to -25%) and in the frequency domain (median delta% -27% to -38%), including the markers of vagal activity. There was no correlation between plasma concentrations of flecainide and reduction in heart rate variability. It was concluded that in subjects without coronary artery disease or congestive heart failure, flecainide decreases all the measurements of heart rate variability and this decrease is not related to plasma concentrations of flecainide.

Introduction: Alteration of cardiac action potential and its adaptation to heart rate could contribute to cardiac dysfunction and arrhythmias during acute cardiac rejection., Methods and Results: Heterotopic heart transplantation was performed in allogeneic and syngeneic rats in which the action potentials of right and left ventricles were measured at 1, 2.5, 3.3, and 5.7 Hz successively using standard microelectrode techniques and compared with nontransplanted hearts. For each frequency, we measured action potential amplitude, action potential duration, transmembrane resting potential, and Vmax. In the right ventricle, at 1 Hz in the presence of rejection (n = 40), a significant increase was observed in action potential duration at 20%, 50%, and 70% repolarization (82.5%, 75.6%, and 70.8%, respectively) and in action potential amplitude (+17.9 mV), and the resting potential was decreased (-5.3 mV). A lack of adaptation of action potential duration to the driving frequency was observed in the rejecting heart group in contrast to controls (n = 20) and nonrejecting hearts (n = 13). Similar results were observed in the left ventricle and surprisingly in the native hearts (n = 11) of recipients with allografted rejecting hearts in the abdominal position., Conclusion: Action potential and its adaptation to the driving frequency is considerably altered during acute rejection. A humoral factor could contribute to cardiac dysfunction.

Unlabelled: Frequency-domain analysis of heart rate variability provides information about influences of autonomic nervous system on the heart and can be measured on short-term or long-term electrocardiogram recording. We compared heart rate variability on 24 h electrocardiogram recording with measurements of heart rate variability over shorter periods of 1 h and 12 h in order to determine the influence of duration and hour of recording on the heart rate variability parameters in the frequency domain. Heart rate variability was analyzed in 24 subjects with normal heart, with measurement of total power (Tot P), ULF, VLF, LF, HF and LF/HF ratio. Reference measurements over 24 h were compared with measurements over 4 periods of 1 h (2 AM-3 AM, 8 AM-9 AM, 2 PM-3 PM, 8 PM-9 PM) and over 4 periods of 12 h (2 AM-2 PM, 8 AM-8 PM, 2 PM-2 AM, 8 PM-8 AM). The correlations with measurements over 24 h were lower for the measurements over 1 h than for the measurements over 12 h. ULF had the lowest mean of correlation coefficients for measurements over 1 h and 12 h, whereas the other frequency bands had high correlations with measurements over 24 h. When using Bland and Altman method, only measurements over 2 AM-2 PM and 2 PM-2 AM periods were a reliable estimation of heart rate variability over 24 h., Conclusion: Spectral measurements of heart rate variability over 12 h have high correlations with measurements on 24 h. ULF is the parameter the most affected by the duration of the recording. Spectral measurements over 2 AM-2 PM and 2 PM-2 AM periods are reliable appreciations of heart rate variability over 24 h.

Temporal and spectral analysis of heart rate variability over 24 hours (HRV) was undertaken in 89 patients with primary dilated cardiomyopathy (DCM) confirmed by left ventriculography with normal coronary angiography and compared with 60 control subjects. The left ventricular ejection fraction was 35 +/- 12% in the DCM patients (71 men and 18 women: age 51 +/- 11 years). Clinical signs of cardiac failure were observed in 66% of patients, requiring medication in 62% of patients (diuretics: 47%, digitalis: 45% and ACE inhibitors: 33%). The HRV was significantly lower in the DCM patients than in the control group, even in the absence of clinical signs of cardiac failure. The global HRV was correlated to left ventricular fractional shortening (r = 0.5, p < 0.001) and peak oxygen consumption on exercise (r = 0.56, p < 0.01), but was independent of the degree of left ventricular dilatation, pulmonary capillary pressure and cardiac index. It was not significantly different in cases of sustained or non-sustained ventricular tachycardia on Holter ECG or in cases with late ventricular potentials on signal averaging of the surface ECG. During follow-up of 51 +/- 35 months, patients with decreased HRV on the global indices and those reflecting sympathetic activity had a much higher risk of cardiovascular death and of cardiac transplantation (p < 0.01). The authors conclude that HRV is decreased in DCM. This is mainly related to the degree of left ventricular dysfunction and is independent of the ventricular arrhythmogenic substrate. The HRV may also identify subgroups of patients with DCM at high risk of cardiovascular death or of haemodynamic decompensation requiring cardiac transplantation.

Heart rate variability on 24-hour electrocardiographic recording was assessed in 23 patients without structural heart disease before and after 2 months of oral treatment with verapamil prescribed for paroxysmal atrioventricular nodal reentrant tachycardia. Verapamil had no significant effect on overall heart rate variability in the frequency domain, but it increased ultra low frequency power and decreased the low-frequency/high-frequency ratio, deemed to be a marker of sympathetic activity.

Objectives: This study was designed to evaluate heart rate variability (HRV) in patients with idiopathic dilated cardiomyopathy (IDC), to determine its correlation with hemodynamic variables and ventricular arrhythmias and to evaluate its prognostic value in IDC., Background: Previous studies have shown that HRV could predict arrhythmic events in patients after infarction, but the characteristics of HRV in IDC have not been fully established., Methods: Time domain analysis of HRV on 24-h electrocardiographic (ECG) recording was performed in 93 patients with IDC, and results were compared with those in 63 control subjects., Results: Patients with IDC, even those without congestive heart failure, had significantly lower values for HRV than those of control subjects. HRV was related to left ventricular shortening fraction (R = 0.5, p = 0.0001) and to peak oxygen uptake (R = 0.53, p = 0.01). HRV was not different in patients with runs of ventricular tachycardia or in patients with late potentials on the signal-averaged ECG. During a mean follow-up period (+/-SD) of 49.5 +/- 35.6 months, patients with reduced HRV had an increased risk of cardiac death or heart transplantation (p = 0.006). On multivariate analysis, cardiac events were predicted by increased left ventricular end-diastolic diameter (p = 0.0001), reduced standard deviation of all normal to normal RR intervals (p = 0.02) and increased pulmonary capillary wedge pressure (p = 0.04)., Conclusions: Decreased HRV in patients with IDC is related to left ventricular dysfunction and not to ventricular arrhythmias. Analysis of HRV can identify patients with IDC who have an increased risk of cardiac death or heart transplantation.

ECG gated blood pool tomography has been performed in sixteen patients with right ventricular arrhythmias in whom the diagnosis of arrhythmogenic right ventricular cardiomyopathy was made based on the finding of abnormalities on contrast angiography. They were compared both to control subjects and to patients with primary dilated cardiomyopathy. Thick slices of ventricles were obtained throughout the cardiac cycle in three orthogonal planes: horizontal long axis and short axis thick slices for analysis of right and left ventricular regional wall motion abnormalities and analysis of the spread of the contraction by means of Fourier phase imaging, vertical long axis slices (one for each ventricle) for ejection fractions, because of easy and reproducible determination of valvular planes and analysis of all right ventricular segments, especially the pulmonary infundibulum. Five typical right ventricular abnormalities were seen: decreased ejection fraction (32 +/- 15% vs 55 +/- 3% in control; p < 0.001), increased diameter (ratio of right to left diameters = 1.2 +/- 0.3 vs 0.9 +/- 0.1; p < 0.01), global delayed contraction versus that of the left ventricle (22 +/- 20 degrees vs -2 +/- 6%; p < 0.01), increased dispersion of contraction (32 +/- 16 degrees vs 13 +/- 4 degrees; p < 0.01) and presence of segments with decreased and/or delayed contraction. Right ventricular disease was observed in all the patients: localized form (56%), diffused form (44%). This method provides accurate functional data for diagnosis and follow-up of patients. In future, this wall motion evaluation method may replace planar nuclear angiography as myocardial SPECT have replaced myocardial planar scintigraphy.

Although paroxysmal atrial arrhythmias are the commonest form of arrhythmia, their therapeutic management still remains controversial. Seventy one patients were included in a multicentre, randomized double-blind, double-placebo study, in parallel groups (37 in group C and 34 in group F) to compare the efficacy of cibenzoline (C) and flecainide (F), administered orally, in the prevention of recurrent atrial arrhythmia. The arrhythmia usually consisted of atrial fibrillation (n = 65), while 6 patients presented with paroxysmal atrial flutter. The mean daily dosages were 221 +/- 60 mg (C) and 165 +/- 49 mg (F). The mean age was 63 +/- 12 years in group C and 63 +/- 16 years in group F. In this trial, atrial arrhythmia was idiopathic in almost two-thirds of cases. The duration of follow-up of this study was 6 months, during which recurrences of arrhythmia were evaluated in terms of the symptoms experienced and in terms of ECG and Holter examinations repeated at the 3rd and 6th months. Supplementary ECG and Holter examinations were also performed in the presence of a clinical suspicion of recurrent symptoms. Comparison of the percentages of patients not developing a documented recurrence and who tolerated treatment, by Kaplan-Meler curves, showed a significant difference between cibenzoline (58%) and flecainide (56%). In the not-responders, the mean time to recurrence was 75 +/- 48 days in group C and 75 +/- 62 days in group F(NS). Six patients dropped out of the trial because of adverse events, including 3 cardiac adverse events (2 case of ventricular proarrhythmic activity). Four extracardiac adverse events led to discontinuation of treatment in group C. In conclusion, the efficacy of cibenzoline and flecainlde in the secondary prevention of atrial arrhythmia was found to be comparable, with 58% and 58% of patients in sinus rhythm, respectively, with a follow-up of 6 months.

Left and right ventricular wall motion was studied in mitral valve prolapse with or without ventricular arrhythmias. Regional and global ventricular wall motion was evaluated by isotopic methods, based in ejection fraction and Fourier phase analysis representing the progression of wall contraction. The synchronisation of the ventricles was characterized by the difference of the mean phase of each ventricle. The heterogeneity of contraction of each ventricle was defined by the dispersion around the mean (standard deviations of the phases). Fifteen of the 36 patients had complex ventricular arrhythmias (Lown grade > or = III). 12 had LVP and 16 had mitral regurgitation. In mitral valve prolapse, the RV EF was decreased compared with normal controls (30 +/- 9% vs 40 +/- 10% ; p < 0.001), especially in patients with mitral regurgitation (26 +/- 7% vs 30 +/- 10%; p = NS) and complex ventricular arrhythmias (26 +/- 7% vs 32 +/- 10%; p < 0.01). The SDP of the LV was greater than those of controls (18 +/- 11 degrees vs 11 +/- 5 degrees ; p = NS) whereas the SDP of the RV was greater (27 +/- 17 degrees vs 12 +/- 5 degrees ; p < 0.05) especially in those with complex ventricular arrhythmias (36 +/- 21 degrees vs 21 +/- 10 degrees : p < 0.01). The SDP of LV and RV were greater in patients with mitral regurgitation: 20 +/- 11 degrees versus 17 +/- 10 degrees (NS) and 35 +/- 21 degrees versus 20 +/- 8 degrees (p < 0.01). Heterogenous ventricular contraction, more marked in the right ventricle in mitral valve prolapse suggests severe myocardial disruption in this valvular disease, reflected by the high incidence of LVP and complex ventricular arrhythmias.

Idiopathic monomorphic ventricular tachycardia (IVT) represents 10% of all cases of VT and is usually observed in young subjects. The origin of the VT may be right ventricular, especially in the infundibulum, giving rise to runs of VT with inter-critical ventricular extrasystoles of the same morphology, or to paroxysmal sustained exercise-induced VT; they usually show left bundle branch block with right axis deviation: the triggering mechanism is probably a parasystole incompletely protected from the sinus rhythm (for the runs of VT) whereas the mechanism of maintenance is probably that of triggered repetitive activity (for the runs and paroxysmal forms of VT). When the origin is in the left ventricle, the VT shows right bundle branch block and left axis deviation and is typically paroxysmal and sustained, triggered by coupled atrial stimulation and followed by a post-tachycardial syndrome; these forms are probably due to reentry into or near to the left posterior hemibranch. These forms of IVT are unique by: 1) their triggering by acceleration of the heart rate, especially during the day, on effort or during an emotion; 2) the usual absence of late ventricular potentials on surface recordings; 3) their capricious outcome, usually good with 92% survival at 10 years; 4) their response to drugs (verapamil, betablockers and/or adenosine) which are relatively ineffective against other forms of VT; 5) their tendency to recur often leading to radiofrequency ablation procedures (80% success rate). The exclusion of underlying inapparent cardiac disease (especially arrhythmogenic right ventricular dysplasia) is an essential part of diagnosis.

Transient reproducible complete infrahisian atrioventricular block occurred after endocavitary cardioversion of ventricular tachycardia and ventricular fibrillation by an automatic implantable cardiac defibrillator in a patient with left bundle branch block and baseline borderline H-V interval. Six months later, a permanent complete atrioventricular block occurred after repetitive endocavitary shocks. Several hypothetical mechanisms may explain this infrahisian atrioventricular block a "fatigue" phenomenon of the His-Purkinje system, vagally mediated atrioventricular block, and/or ablation of the His conduction system. The last seems to be the most probable, which would justify implantation of an automatic implantable cardiac defibrillator with backup pacing in all patients, especially in the presence of bundle branch block.

Precapillary pulmonary hypertension was diagnosed in a 29 year old woman who became progressively more breathless (NYHA Class III) after her pregnancy, two years previously: systolic pulmonary artery pressure was 120 mmHg with an arterio-capillary pressure gradient of 30 mmHg. She had anti-nuclear autoantibodies detectable at 1/1000 and anti-DNA autoantibodies at 1/800 without any other manifestation of lupus. Treatment with prednisone (2 mg/kg/day) resulted in regression of her dyspnoea with a decrease of systolic pulmonary artery pressure to 65 mmHg, and of the arterio-capillary gradient to 15 mmHg; the lupus serology became negative with a clinical follow-up of 37 months. This observation shows that systemic lupus erythematosus may present with precapillary pulmonary hypertension, the conventional treatment of which may be successfully completed by steroid therapy.

The prevalence of late ventricular potentials (LVPs) detected by signal averaged ECG (SAECG) is variable in nonischemic heart diseases. In idiopathic dilated cardiomyopathy, the prevalence increases from about 25% to 70%-90% in cases of spontaneous sustained ventricular tachycardia (VT), is not significantly correlated with hemodynamic and Holter data, and has a good positive predictive value for induced and spontaneous sustained VT. However, its predictive value for cardiac death has not been established. In primary hypertrophic cardiomyopathy, LVPs are rare (about 10%), not correlated to hemodynamic data, enhanced in cases of spontaneous sustained VT (up to 77%), and have a good predictive value of induced VT. LVP-SAECG are frequent in arrhythmogenic right ventricular dysplasia (ARVD) (70%-80%). They can identify patients with VT and an unapparent or limited form of this disease, or ARVD with few ventricular arrhythmias. The prevalence (26%-37%) of LVPs in mitral valve prolapse is clearly higher than in normal individuals or in other valvular diseases and is enhanced in cases of spontaneous and induced VT. Its significance remains speculative. After surgical repair of tetralogy of Fallot, LVPs can identify a group of patients with higher probability of induced and spontaneous risk of VT. The usefulness and significance of LVPs in other nonischemic cardiac diseases have not to date been established. In "true" idiopathic VT, without proved structural cardiac disease, the prevalence of LVPs does not exceed that observed in normal individuals (0%-5%), but in "apparent" idiopathic VT the prevalence of LVPs rises to 20%-40%. In these latter cases more invasive techniques must be used to discover a limited form of myocardiopathy.