[Brugada syndrome: a new clinical entity?].
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Biomedical subjects
Publications and source records attributed to E Aliot.
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BACKGROUND: Radiofrequency ablation of atrioventricular accessory pathway is widely used to cure patients with the Wolff-Parkinson-White syndrome. The site of successful ablation is determined using electrophysiological parameters, endocavitary bipolar electrogram measurements being the most commonly used. Interobserver reproducibility of these measurements may limit the reliability of ablation criteria based upon bipolar measurements only but, to our knowledge, this reproducibility has not been evaluated so far. Such was the aim of this study. METHODS: Three independent observers reviewed the bipolar electrograms recorded at sites were radiofrequency energy was delivered (successfully or not) in 28 consecutive patients with the Wolff-Parkinson-White syndrome. In each tracing, 4 intervals were measured: (1) A0V0 (onset of the atrial electrogram to onset of the ventricular electrogram), (2) AaVa (activation time of the atrial electrogram to activation time of the ventricular electrogram), (3) V0-QRS (onset of the ventricular electrogram to onset of delta wave on the surface ECG) and (4) Va-QRS (activation time of the ventricular electrogram to onset of delta wave on the surface ECG). RESULTS: The interobserver reproducibility was low since only 50% of A0V0 intervals were measured with an interobserver difference lower than 10 ms and up to 43% of Va-QRS intervals were measured with an interobserver difference greater than 30 ms. The reproducibility of interval measurement was graded from the highest to the lowest as follows: A0V0, AaVa, V0-QRS and Va-QRS (Chi-square statistic, chi 2 = 71.72, p < 0.0001). Kappa values were lower than 0.40, indicating a poor interobserver reproducibility. CONCLUSIONS: Our study suggests that interobserver reproducibility of only bipolar electrograms interval measurements at sites of radiofrequency ablation of atrioventricular accessory pathway is poor, which limits the reliability of bipolar criteria to predict a successful ablation site.
1. In patients with dilated cardiomyopathy, abnormal myocardial blood flow may contribute to poor myocardial function. 2. The aim of this study was to investigate the possible contribution of abnormal myocardial blood flow to the limitation of exercise capacity in patients with dilated cardiomyopathy. 3. Coronary flow reserve was assessed in 16 patients with dilated cardiomyopathy and 9 matched normal control individuals. All participants had angiographically normal coronary arteries. At rest and after dipyridamole infusion (0.56 mg/kg intravenously), peak systolic and diastolic coronary flow velocities were measured in the proximal left anterior descending coronary artery using transoesophageal pulsed Doppler echocardiography, guided by colour flow imaging. Coronary flow reserve was calculated as the ratio of hyperaemic to basal diastolic and systolic peak coronary flow reserve. 4. Baseline diastolic and systolic coronary flow velocities were significantly higher in patients (50 +/- 6 and 30 +/- 4 cm/s respectively) compared with control individuals (37 +/- 3 and 20 +/- 1 cm/s respectively) (mean +/- S.E.M.) (P < 0.05). Diastolic and systolic peak coronary flow reserve were significantly lower in patients (1.60 +/- 0.14 and 1.40 +/- 0.09 respectively) compared with control individuals (2.89 +/- 0.15 and 2.17 +/- 0.17 respectively) (P < 0.001). Although peak VO2 and exercise time were significantly lower in patients compared with control individuals, coronary flow reserve did not correlate to exercise capacity in patients with dilated cardiomyopathy. 5. These results confirm the abnormalities of coronary flow reserve previously observed in patients with dilated cardiomyopathy, but suggest that such abnormalities do not contribute to the limitation of exercise capacity in these patients.
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Patients with Mahaim fibres form a distinct subgroup of the pre-excitation syndromes (less than 3%). They have episodes of a pre-excitation during sinus rhythm. Originally, Mahaim fibres have been classified into two main groups, nodoventricular and fasciculoventricular fibres. Recent evidence from both surgery and catheter ablation has shown that the substrate for tachycardia arises due to a slowly conducting fright atrioventricular (AV) accessory pathway (AP) with decremental properties. The pre-excited tachycardia (antidromic re-entrant tachycardia) is distinctive with a left bundle branch block (LBBB) pattern, long AV interval (due to the long conduction time over the AP) and short VA interval (over the AV node). The majority of these patients do not have episodes of narrow QRS complex, due to the absence of retrograde conduction of the AP. There are several ECG features that suggest Mahaim tachycardia as a cause of LBBB pattern tachycardia: QRS axis superior or between 0 degrees and 75 degrees, QRS duration of 0.15 s or less and precordial transition in lead V4 or after. Clinically, Ebstein's anomaly is relatively common and multiple APs are also observed with an increased frequency. Small studies and cases reports have demonstrated sensitivity to various classes of AA drugs. Class IA, IC and beta-blocker may be effective in preventing tachycardias. Small surgical series have reported excellent results in patients with accessory AV connections and Mahaim fibres tachycardia. However catheter ablation offers a definitive therapy in such patients with a high success rate and minimal morbidity.
Determinants of ventricular rate during atrial fibrillation (AF) are controversial. Concealed conduction, summation, rate and irregularity of atrial impulses, pacemaker activity of the AV node, and the electrophysiologic parameters of AV nodal function may all contribute. Findings from series of patients who underwent AV nodal modulation suggest that AV nodal conduction plays some role in the ventricular response to AF. The data are consistent with the presence of dual (or more) atrionodal inputs that play a role in determining AV nodal conduction properties. The data also strongly support the role of summation rather than simple prolongation of refractory periods as a mechanism of ventricular rate control.
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Prognostic studies after acute myocardial infarction (AMI) have mainly been performed in the prethrombolytic era. Despite the fact that modern management of AMI has reduced mortality rates, the occurrence of malignant ventricular arrhythmias in the late phase of AMI remains an important issue. We prospectively studied 244 consecutive patients (97 treated with thrombolytics) who survived a first AMI. All patients underwent time domain signal-averaged electrocardiography (vector magnitude: measurements of total QRS duration, terminal low [<40 microV] amplitude signal duration, and root-mean-square voltage of the last 40 ms of the QRS complex), Holter electrocardiographic monitoring, and cardiac catheterization. Late life-threatening ventricular arrhythmias were recorded. Eighteen arrhythmic events occurred during a mean follow-up period of 57 +/- 18 months. Three independent factors were associated with a higher risk of arrhythmic events: (1) left ventricular ejection fraction (odds ratio 1.9/0.10 decrease), (2) terminal low-amplitude signal duration (odds ratio 1.5/5 ms increase), and (3) absence of thrombolytic therapy (odds ratio 3.9). Low-amplitude signal duration sensitivity for sudden cardiac death was low (30%). Left ventricular ejection fraction had the highest positive predictive value for sudden cardiac death (10%). Thus, thrombolysis decreases both the incidence of ventricular tachycardia and sudden cardiac death with a higher reopening rate of the infarct-related vessel. Signal averaging predicts the occurrence of ventricular tachycardia and an impaired left ventricular ejection fraction predicts the occurrence of sudden cardiac death.
The radial artery compliance may be paradoxically increased in untreated arterial hypertension. However, the effect of blood pressure normalization on the radial artery compliance is not well known. We performed a cross-sectional study in order to investigate the effects of blood pressure control on the radial artery diameter and compliance (echotracking and digital photoplethysmography) by comparing these variables in a group of untreated hypertensive patients and in another group of adequately treated hypertensive patients as well as in a group of healthy normotensive subjects. All groups were sex- and age-matched. Radial artery internal diameter was increased in both untreated hypertensive patients and effectively treated hypertensive patients comparatively to controls. Cross-sectional compliance and volumic distensibility were not different between groups. As compared to controls (2.85 +/- 0.39 x 10(-3) mm2 x mm Hg(-1) and 0.42 +/- 0.05 x 10(-3) mm Hg(-1)), isobaric (100 mm Hg) compliance and distensibility were significantly increased in untreated hypertensive patients (4.46 +/- 0.44 and 0.65 +/- 0.07, P < .01) but not significantly different in treated hypertensive patients (3.19 +/- 0.33 and 0.45 +/- 0.04, P = NS). The results of this cross-sectional study suggest that compliance abnormalities of the radial artery, but not internal diameter changes may be reversed by effective therapeutic control of blood pressure in arterial hypertension.
The objective of this study was to assess the effects of radiofrequency energy application on implanted pacemaker functions. Radiofrequency (RF) catheter ablation may cause pacemaker dysfunction due to electromagnetic interferences. The effects of RF on pacemaker behavior were studied in a series of 38 pacemakers, implanted 18 +/- 26 months prior to a RF procedure using either a right ventricular approach (AV node ablation, n = 35) or a left ventricular approach (left concealed accessory pathway ablation, n = 1; VT ablation, n = 2). The 38 patients (mean age 65 +/- 9 years) included 20 men and 18 women. Before energy applications, the 23 different pacemaker models were programmed to the VVI mode at the lowest available rate. The continuous surface ECG was recorded throughout the procedure. Thorough testing of the devices was performed before and after each RF delivery. Unusual pacemaker responses occurred in 20 of the 38 cases studied (53%). The impact of RF delivery was unpredictable, and variable dysfunctions were observed at different times for a given patient or could vary for a given model. Unusual pacemaker responses included pacemaker inhibition (n = 8), untoggled backup mode (n = 3), electromagnetic interference noise mode (n = 3), temporary RF-induced pacemaker tachycardia (n = 2), erratic behavior (n = 1), oversensing of RF onset and offset (n = 8), and transient loss of ventricular capture, (n = 1). Postablation, most devices automatically toggled back to full functionality. The three devices in the untoggled backup mode had to be reprogrammed to obtain normal operations. At the end of the procedure, pacing thresholds remained unchanged in all but one patient, in whom the increase in ventricular threshold was due to a nicked lead. In conclusion, implanted pacemakers frequently exhibit transient, unpredictable responses to RF energy application. Although all pacemaker functions were restored postablation, some devices had to be reset manually. The anomalies observed during the RF application argue for the simultaneous use of an external pacemaker in pacing-dependent patients.
If the indications of coronary angiography are well chosen, the percentage of normal coronary angiographies should decrease. The authors analysed 7858 primary coronary angiographies performed between 1981 and 1990 in patients without valvular or congenital heart disease. The second 5 years were compared to the first. The percentage of primary coronary angiographies decreased (63% vs 75%; p < 0.01), the percentage of women increased (21.7% vs 18.4%; p < 0.001), and the mean age increased (58.5 +/- 0.3 vs 53.9 +/- 0.3; p < 10(-9)). The lesions were less extensive: 16.3% triple vessel disease versus 24.2% (p < 0.001); 31.3% double vessel disease versus 28.1% (p < 0.02); 49.1% single vessel disease versus 44.2% (p < 0.001). The percentage of normal coronary angiographies remained constant: 20.2% in the second five years versus 19.9% in the first. Over the 10 year period, there was no significant difference one year from another. The percentage of normal investigations remained the same in men (15.7%), decreased in women (34.7 vs 40.1%, p < 0.04), remained constant in patients under 60 years of age (24.5 vs 23.8%), but increased in the more elderly (14.9 vs 10.2%; p < 0.001). The percentage remained unchanged in stable angina (19.6 vs 19.8%) and in unstable angina (12.3 vs 11.2%): it increased in cases of atypical chest pain (72.2 vs 54.3%; p < 0.01). Although, globally, the number of normal coronary angiographies was unchanged at 20%, the indications of this investigation were more selective in the younger patients, especially women, in the second five years, but coronary angiography was more commonly performed in elderly patients because of the possibility of benefiting from coronary angioplasty.
We investigated the relationship between exercise capacity and the level of neurohormonal activation at rest and during exercise in patients with various degrees of severity of chronic heart failure. We performed exercise testing with measurements of peak oxygen consumption (pVo2) and blood sampling at rest and at peak exercise in eight patients with moderate heart failure (pVo2 = 17 +/- 0.4 ml/kg/min) (mean +/- S.E.M.) and eight patients with severe CHF (pVo2 = 9 +/- 1 ml/kg/min). None of the patients was taking angiotensin converting enzyme inhibitors or beta-blockers. Plasma levels of atrial natriuretic peptide, cGMP, arginine-vasopressin, renin, angiotensin II, epinephrine and norepinephrine increased significantly (P < 0.01), from rest to peak exercise, in all patients. Among all the studied neurohormonal factors, only atrial natriuretic peptide levels at rest as well as at peak exercise, in patients with severe heart failure were correlated significantly to pVo2 (r = -0.77, P = 0.04; r = -0.85, P = 0.01, respectively) and to exercise duration (r = -0.72, P = 0.05; r = -0.79; P = 0.03, respectively). The relationship between plasma levels of atrial natriuretic peptide and of cGMP was shifted downward in the more severe patients suggesting the loss of biological activity of atrial natriuretic peptide.
The viscoelastic, muscular and endothelial components of the vessel wall may be altered in patients with congestive heart failure (CHF). In order to investigate the relative contribution of each of these components to the peripheral vascular mechanisms of the disease, we have studied post-ischemic (endothelial-dependent) and post-nitroglycerin (endothelial-independent) vasodilatation as well as the response to cold pressure test and the geometry and compliance of the radial artery using a non-invasive echotracking method coupled to digital photoplethysmography. Thirty-nine patients with congestive heart failure (ejection fraction = 28 +/- 2%) were compared to age- and sex-matched healthy controls. Baseline therapy was unchanged during the study. In congestive heart failure patients, cross-sectional compliance and volumic distensibility were greater (P < 0.05) but isobaric compliance which is independent of blood pressure value was unchanged. Post-ischemic and post-nitroglycerin vasodilatation were lower (7 +/- 1 vs. 11 +/- 1%, P < 0.01 and 6 +/- 1 vs. 14 +/- 2%, P < 0.001, respectively) and both of the arterial diameter and pressure responses to cold pressor test were blunted (-5 +/- 1 vs. -8 +/- 1%, P = 0.058 and 6 +/- 3 mmHg vs. 13 +/- 2 mmHg, P < 0.01, respectively) in congestive heart failure. These changes were similar in primary and ischemic congestive heart failure, suggesting that they are more likely related to common neuro-hormonal factors rather than to an atherosclerotic process.
To assess the cardiac and extracardiac safety and efficacy of flecainide versus propafenone in patients suffering from episodes of paroxysmal atrial fibrillation (AF) or atrial flutter, 97 patients were enrolled in a randomized, open-label, long-term, parallel, comparative multicenter study. The diagnosis of paroxysmal AF or atrial flutter had to be fully documented prior to inclusion in the study. Of the 97 patients enrolled in the study, 48 patients (25 men, 23 women, mean age 62.4 +/- 12.3 years) received flecainide; 49 patients (26 men, 23 women, mean age 63.6 +/- 12.2 years) received propafenone. The initial dose of flecainide was 50 mg twice daily, and this could be increased in steps of 50 mg twice daily every 4 days to a maximum of 300 mg/day. The initial dose of propafenone was 300 mg twice daily and this could be increased in steps of 300 mg every 4 days to a maximum of 1200 mg/day. At each visit, medical events, vital sign measurements (blood pressure, pulse rate), concomitant medications, adverse experiences, and study drug dosage changes were evaluated. Routine clinical laboratory tests were evaluated at the month 6 visit, and a 24-hr Holter recording was obtained at the month 1 visit. Almost half (45) of the patients were discontinued from the study before completing 1 year of therapy. The probability of successful treatment versus time--i.e., the proportion of patients who remained on therapy over the course of 1 year therapy--was 0.619 for the flecainide group and 0.469 for the propafenone group (p = 0.079; difference not significant). The difference is largely attributed to the higher proportion of patients in the propafenone group (9) than in the flecainide group (2) who experienced side effects important enough to stop the treatment. (The incidence of side effects was not statistically different between treatment groups, although it was higher in the propafenone group.) The proportion of patients who discontinued treatment due to inadequate response was similar in the 2 groups: 11 patients (22.9%) in the flecainide group and 12 patients (24.4%) in the propafenone group withdrew from the study, primarily because of an inadequate response, i.e., they experienced an increase in duration, frequency, and severity of attacks of AF or atrial flutter. Neurologic signs, central and peripheral, were mostly encountered in the flecainide group (8.5%), and, gastrointestinal effects were more often reported in the propafenone group (16.7%). In paroxysmal AF and paroxysmal atrial flutter, flecainide and propafenone are equally effective. However, in this study the probability of a patient's staying on flecainide after 1 year had a tendency to be higher than the probability of staying on propafenone, due to a greater proportion of secondary effects with propafenone.
OBJECTIVES: This study sought to determine whether the reopening of the infarct-related vessel is related to clinical characteristics or cardiovascular risk factors, or both. BACKGROUND: In acute myocardial infarction, thrombolytic therapy reduces mortality by restoring the patency of the infarct-related vessel. However, despite the use of thrombolytic agents, the infarct-related vessel remains occluded in up to 40% of patients. METHODS: We studied 295 consecutive patients with an acute myocardial infarction who underwent coronary angiography within 15 days (mean [+/- SD] 6.7 +/- 3.2 days) of the onset of symptoms. Infarct-related artery patency was defined by Thrombolysis in Myocardial Infarction trial flow grade > or = 2. Four cardiovascular risk factors--smoking, hypertension, hypercholesterolemia and diabetes mellitus--and eight different variables-age, gender, in-hospital death, history of previous myocardial infarction, location of current myocardial infarction, use of thrombolytic agents, time interval between onset of symptoms, thrombolytic therapy and coronary angiography--were recorded in all patients. RESULTS: Thrombolysis in current smokers and anterior infard location on admission were the three independent factors highly correlated with the patency of the infarct-related vessel (odds ratios 3.2, 3.0 and 1.9, respectively). In smokers, thrombolytic therapy was associated with a higher reopening rate of the infard vessel, from 35% to 77% (p < 0.001). Nonsmokers did not benefit from thrombolytic therapy, regardless of infarct location. CONCLUSIONS: These observational data, if replicated, suggest that in patients with acute myocardial infarction, thrombolytic therapy may be most effective in current smokers, whereas nonsmokers and ex-smokers may require other management strategies, such as emergency percutaneous transluminal coronary angioplasty.
The aim of our study was to investigate the contribution of physical deconditioning in skeletal muscle metabolic abnormalities in patients with chronic heart failure (CHF). Phosphate metabolism was studied in the leg muscle at rest and during exercise by using phosphate 31 nuclear magnetic resonance spectroscopy in a group of 14 patients with New York Heart Association class II and III CHF and left ventricular ejection fraction <40% and in two groups of age-matched healthy volunteers: one group of 7 sedentary and another of 7 trained subjects. Phosphocreatine depletion rate, intracellular pH, and adenosine diphosphate levels in the muscle during exercise were not statistically different in the CHF patients and in the sedentary healthy subjects, but both groups were statistically different from the trained healthy subjects, who had slower phosphocreatine depletion rates, as well as less intracellular acidosis and lower adenosine diphosphate levels during exercise (p = 0.02; analysis of variance). Our results suggest that metabolic changes occurring in the skeletal muscle of patients with CHF may contribute to the limitation of exercise capacity and are most likely to be a consequence of physical deconditioning because they are very similar to what is observed in sedentary and otherwise healthy subjects as compared with trained subjects.
BACKGROUND: DDD pacing has been advocated as an effective treatment for drug refractory obstructive hypertrophic cardiomyopathy. This study reports the outcome of pacing in 56 patients with refractory symptoms referred to four tertiary centres. METHODS: Core data on symptoms, drug burden, and left ventricular outflow tract gradient were recorded. Patients underwent a temporary pacing study with optimisation of the atrioventricular (AV) delay for greatest gradient reduction without haemodynamic compromise. Patients were assessed after implantation in terms of changes in symptoms, drug load, and outflow tract gradient. RESULTS: 56 patients underwent pacing assessment. The mean (SD) left ventricular outflow tract gradient before pacing was 78 (31) mm Hg. At temporary study the mean (SD) left ventricular outflow tract gradient was 38 (24) mm Hg with a median (range) optimised sensed AV delay of 65 (25-125) ms. Fifty three patients were implanted and followed up for a mean (SD) of 11 (11) months. The median (range) programmed sensed AV delay was 60 (31-200) ms. Left ventricular outflow tract gradient at follow up was 36 (25) mm Hg. Forty four patients had improved functional class. Although a correlation (r = 0.69) was shown between acute and chronic left ventricular outflow tract gradient reduction, there was no correlation between magnitude of gradient reduction and functional improvement, and no appreciable change in pharmacological burden. CONCLUSION: This series confirms symptomatic improvement after DDD pacing in hypertrophic cardiomyopathy. There remains, however, a discrepancy between perceived symptomatic benefit and modest objective improvement. Furthermore, the optimal outcome has been achieved only with continued pharmacological treatment. Current methods of temporary evaluation do not predict functional outcome which seems to be independent of the magnitude of gradient reduction.
PURPOSE: The aim of this phase-III clinical trial was prospectively to evaluate the clinical safety and diagnostic efficacy as well as the effects on laboratory and electrocardiographic parameters of new iodinated, nonionic, low-osmolality contrast medium, iobitridol(Xenetix 350) during coronary angiography in adults in comparison to an iodinated, nonionic, low-osmolality reference product, iohexol (Omnipaque). MATERIALS AND METHODS: This 2-center, comparative, randomized, double-blind trial involved 90 patients, 46 receiving iobitridol and 44 iohexol. Clinical safety was evaluated by recording the adverse events observed during investigation and by the patient's assessments. Electrocardiographic effects on laboratory parameters were evaluated as well as diagnostic efficacy. RESULTS: The age, sex, presence of risk factors and clinical picture ( unstable angina, postinfarction) were not significantly different between the 2 treatment groups. The incidence of significant coronary lesions (stenosis 50%) was also not significantly different between the 2 treatment groups. Clinical safety was good in both groups. Four patients experienced an adverse event, 2 in each group. In the iobitridol group, one patient had an episode of hypertension, followed by hypertension and prolonged chest pain was observed and one patient had sinus tachycardia. In the iohexel group, chest pain was observed in one patient and nausea in another. ECG safety was good in both groups. Transient excitability disorders were observed in 10 and 6 patients, respectively. Moderate conduction abnormalities were noted in one patient in each group and repolarization abnormalities in 10 and 8 cases, respectively. Safety in laboratory parameters was good with no significant changes in either. Diagnostic efficacy was good to excellent in all patients. CONCLUSION: Diagnostic efficacy and safety of iobitridol 350 in terms of effects on clinical, laboratory and electrocardiographic parameters were comparable to those of the nonionic reference product.