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Biomedical subjects

D Babuty

Publications and source records attributed to D Babuty.

At least 19 recordsLinked to original sources

[Risk stratification in atrial and ventricular arrhythmias].

Atrial fibrillation, the most frequent arrhythmia, has a growing incidence with increasing age and the most important complication of the disease is thromboembolic events that may be prevented by antivitamin K. They are the most efficient therapeutic class for the prevention of these events but they are associated with an increased haemorrhagic risk leading to a reduced prescription in general practice. Optimisation of the management should be based on an individual evaluation of the thromboembolic and haemorrhagic risks, taking into account age, the presence of an associated heart disease, hypertension, diabetes, history of cerebrovascular event, history of previous haemorrhagic event and the ability to achieve a stable target INR. The challenge in ventricular arrhythmias lies in identifying a high risk of sudden death, mainly related to ventricular fibrillation. In patients with structural heart disease, left ventricular dysfunction is the strongest predictor of sudden death. Non invasive markers such as non sustained ventricular tachycardia, late ventricular potentials, decreased heart rate variability and baroreflex sensitivity, and repolarization altemans are further elements to assess risk. However, most of these markers have a poor positive predictive value and a low specificity. In patients with normal hearts, genetic predisposition may in the future identify high risk patients. The electrophysiologic study with programmed ventricular stimulation remains a costly and invasive method and only has a strong positive predictive value in ischemic cardiomyopathy. More precise algorithms for risk stratification are thus needed that may help the strategy of therapy with prophylactic implantable cardioverter defibrillator in the future.

4-Hydroxycoumarins↗

[Indications for automatic implantable defibrillators in patients with the Brugada syndrome].

Brugada syndrome is a primary electrical cardiac disease characterized by an ST segment elevation in V1-V2 leads on surface ECG and an increased risk of polymorphic ventricular tachyarrhythmia (ventricular tachycardia and/or ventricular fibrillation). The objective of the treatment is to prevent sudden death and it therefore includes in some cases the implantation of an automatic implantable cardiac defibrillator (AICD). In secondary prevention (i.e. after a first episode of resuscitated ventricular fibrillation), the implantation of AICD is mandatory (indication of class 1 level A). In primary prevention (i.e. in patients without documented ventricular fibrillation), the guidelines are not definitively established. We may consider two different clinical situations. First, the patient complains from syncope and this justifies the implantation of an AICD. Second, the patient is asymptomatic and the physician has to discuss the implantation of an AICD. Two parameters should be analysed: the pattern of ECG and the result of right programmed ventricular stimulation. An evident ST segment elevation (>2 mm) is associated with a high risk of sudden death. Likewise, the inducibility of a ventricular tachycardia or fibrillation is considered at the present time as a factor linked to sudden death and justifies the implantation of an AICD. On the other hand, a normal resting ECG only associated with a provoked ST segment elevation by class I antiarrhythmic drug (flecainide) defines a group of patients with a low risk of sudden death, and these patients do not require the implantation of an AICD.

Death, Sudden, Cardiac↗

[Postmarketing surveillance in patients with cardiac pace-makers or automatic implantable defibrillators].

This article includes an overview of the actual French control and regulation system of the safety alerts involving pacemakers and implantable cardioverter-defibrillator and an evaluation of the general information and trends about the characteristics of the reported incidents obtained in the last years in that field. The national security agencies have the mission to collect the data on safety and efficacy of medical devices but manufacturers, physicians and patients also have a role to play. The technical appreciation of the necessity of a notification is not easy in some cases but the lack of notification of a severe incident may lead to heavy penal consequences. If doubtful cases, one should keep in mind the spirit of these safety systems: a collective insurance against the risks related to the use of medical devices. In the 10 last years, the annual advisory rate was increased. The pacemakers were recalled more frequently than implantable cardioverter-defibrillators in absolute value but less frequently in relative value (advisories per 100 person-years). This increase may be related to the growing number of device implants and expanding indications for device therapy, to the increasing sophistication of the devices and to the modifications in the regulation aspects of these problems with a closer attention of users and physicians to the several types of malfunctions.

Consumer Product Safety↗

[Evaluation after 20 years of a case of Takayasu's disease that presented with aortic regurgitation].

Takayasu's disease is a segmental multifocal affection of medium and large arteries. The diagnosis is based on the association of stenotic and aneurismal lesions of the aorta and its branches secondary to an inflammatory infiltration of the media and adventitia. Cases of aortic regurgitation associated with aneurismal dilatation of the ascending aorta as the presenting features of Takayasu's disease, as in this case, are rare. Histological examination of the aortic wall may help establish the diagnosis by showing signs of aortitis. The other usual arterial lesions are sometimes missing at the initial phase of the disease. A late histological diagnosis may be difficult as the inflammatory lesions tend to be progressively replaced by fibrotic lesions or a banal atheroma.

Aortic Valve↗

[Conduction defects and arrhythmias in peripheral myopathies].

The association between peripheral myopathies and cardiac complications is well established. However, until recently, the clinical and genetic variability of these pathologies limited our ability to recognise individual risk of complications, particularly in the more rare pathologies. Advances have been made in the understanding of the progression, in the physiopathology of molecular deficits and cardiac complications of the different types of muscular dystrophy. This has partially helped to identify the risk of cardiac complications. The commonest condition, Steinert's disease, is associated with a high incidence of atrioventricular block and atrial arrhythmias. Prophylactic implantation of a dual chamber pacemaker with diagnostic functions may be envisaged when the HV interval is greater than 70 ms, on endocavitary electrophysiological investigations. In other patients, follow-up by standard ECG and/or amplified averaged ECG and Holter monitoring is essential. The natural history of Duchenne and Becker muscular dystrophies and the Emery Dreifuss dystrophy have been better described in the last few years. Recommendations have been proposed for the cardiological follow-up of these patients. Empiric recommendations of the same type have been proposed for patients with shoulder and girdle myopathies and propositions for their management have also been made, the pertinence of which is still being evaluated. Our understanding of the incidence, the type, the physiopathology and molecular biology of the various peripheral myopathies and their cardiac complications has advanced considerably in recent years. This has led to the elaboration of new recommendations for diagnostic and therapeutic strategies in these patients.

Arrhythmias, Cardiac↗

Comparative study of atrial vulnerability in patients with unexplained ischemic stroke or lone atrial paroxysmal fibrillation.

Strokes have a high prevalence, with a high rate of recurrence, and about 30-40% remain of unknown cause. Some patients might have asymptomatic paroxysmal atrial fibrillation (AF) which remains the main cause of embolic events. A latent atrial arrhythmogenic substrate may induce recurrent arrhythmias, including functional abnormalities such as nonuniform refractoriness and/or anatomic abnormalities such as atrial septum aneurysm (ASA) and patent foramen ovale (PFO). In 175 patients divided into three groups (Group I: 103 patients with unexplained ischemic stroke, Group II: 48 patients with paroxysmal AF and Group III or control group: 24 patients explored for another cause), such an atrial arrhythmogenic substrate was assessed by electrophysiological study. Groups I and II had a similar high rate of inducible atrial arrhythmias compared to control group III where no arrhythmia was induced. An induced atrial arrhythmia was observed in more than 50% of patients of Group I and in more than 70% of patients of Group II without any significant difference according to age. However, in 26 young patients of Group I who had a transesophageal echocardiography, both a high rate (46%) of ASA and/or PFO and a frequent latent atrial vulnerability (LAV) were observed, compared to older patients where an atrial septum abnormality was observed in only 21% of cases. Thus, among patients with stroke of unknown cause, a high percentage of them might have asymptomatic atrial paroxysmal arrhythmia. The predictive value of the electrophysiological study for spontaneous arrhythmias and recurrence of stroke remains to be demonstrated.

Atrial Fibrillation↗

[Conduction defects as the presenting feature of sarcoidosis or observed during the course of the disease: regression with corticoid steroid therapy].

Cardiac sarcoidosis is often unrecognised because of the absence of specific clinical and electrical signs. The consequences are serious, the main risk being sudden death due to conduction defects (24 to 31% of cases) or ventricular arrhythmias. Any conduction defect without an obvious cause in a young patient should suggest a possible diagnosis of sarcoidosis. The confirmation is histological when giant cell non-caseuting epithelioid granuloma is demonstrated but myocardial biopsies are only positive in 20% of cases. Therefore, biopsy of accessible organs such as salivary glands is recommended. Diagnostic strategy consists in searching for signs of systemic sarcoidosis, and, when the diagnosis has been established, perform a complete work-up with echocardiography, dipyridamole myocardial scintigraphy, cardiac MRI and 24 hour ambulatory ECG recordings (Holter). The only proven treatment is steroid therapy with occasional spectacular observations of reversibility of arrhythmias or conduction defects.

Adrenal Cortex Hormones↗

[Arrhythmias of primary hypertrophic cardiomyopathy].

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.

Arrhythmias, Cardiac↗

Heterogeneous changes of monophasic action potential induced by sustained stretch in atrium.

INTRODUCTION: Chronic enlargement of atrium is common in atrial fibrillation, and the effects of stretch on atrial action potentials seem inconsistent. As atrial muscle is heterogeneous, we suggest that atrial stretch induces a variable electrophysiologic response and that the effects of stretch are only partially mediated by stretch-activated channels. METHODS AND RESULTS: Sixteen guinea pig hearts were perfused by the Langendorff method using Kreb's solution with and without 80 microM streptomycin, which is a stretch-activated channel blocker. Suction electrodes were used to record monophasic action potentials (MAPs) of the left atrium. Left auricular pressure was monitored by a balloon. We determined the MAP duration at 50% and 90% repolarization (MAPD50 and MAPD90) in basal conditions and after a slow onset but sustained stretch of the atrium in the absence and presence of streptomycin. Stretch induced no overall consistent or significant change in mean MAPD50 and MAPD90. The individual responses were markedly variable. The most frequent response (about 50%) was a decrease in MAPD50 and MAPD90. In 25% of cases, there was no change, and in 25% we observed increases in MAPD50 and MAPD90. Streptomycin did not affect MAPD50 and MAPD90, but it dramatically modified the distribution of MAPD changes induced by stretch. In particular, streptomycin removed stretch-induced shortening of MAPD50 and MAPD90, whereas it did not affect stretch-induced lengthening. CONCLUSION: Sustained stretch of atrium induces variable modifications of MAPD that are only partially inhibited by streptomycin. This suggests the participation of ionic channels other than specific stretch-activated channels in the response of atrial myocardium to sustained stretch.

Action Potentials↗

Long-term prognostic value of time domain analysis of signal-averaged electrocardiography in idiopathic dilated cardiomyopathy.

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.

Arrhythmias, Cardiac↗

[Pericardial extravasation as an indicator of congestive heart failure due to thiamine deficiency in a young adult].

INTRODUCTION: Thiamine (B1) deficiency is one of the classical causes of congestive heart failure. Although in the western world and in other developed regions this disorder is generally associated with chronic alcoholism, it may also only occur as a result of a deficient diet. EXEGESIS: A young patient was admitted for electrocardiographic examination, and pericardial extravasation was recorded. The etiological assessment showed a case of congestive heart failure due to thiamine (B1) deficiency. A hemodynamic examination and investigation of thiamine blood levels confirmed this diagnosis. The patient's health status improved following thiamine administration, with complete and rapid regression of symptoms of congestive heart failure. CONCLUSION: Although cardiomyopathic beriberi is infrequent, it should systematically be taken into account in the etiology of congestive heart failure. The present study also notes that a dietary thiamine deficiency is uncommon, but should nevertheless be considered when other symptoms of denutrition are present.

Adult↗

Analysis of the distribution of histologic myocardial lesions during acute cardiac rejection. Experimental study in rodents.

BACKGROUND AND METHOD: Asymmetric distribution of histologic lesions have been reported in grafted hearts that could hamper the interpretation of right ventricular endomyocardial biopsy. Heterotopic heart transplantations were performed in rats (n=59) and guinea pigs (n=20). Grafted hearts were examined by a pathologist who established the degree of cardiac rejection in the four cardiac cavities. RESULTS: Forty cardiac rejections were diagnosed in rats and ten in guinea pigs. An asymmetric distribution of histologic lesions was observed in 34 (68%) rejected hearts with greater lesions in the auricular myocardium than in the ventricular myocardium (n=25, 50%). One (n=18) or two degrees (n=7) differentiated the severity of rejection between atria and ventricles. Cardiac rejection score was significantly greater in atria than in ventricles (3.12+/-0.18 vs. 2.6+/-0.2 (P<0.01) in rats and 2.35+/-0.37 vs. 1.6+/-0.47 (P<0.001) in guinea pigs. There were histologic lesions of rejection in the auricular myocardium in seven cases, although the ventricular myocardium was completely normal. In nine (18 %) other grafted hearts the degree of rejection was equal in the auricular myocardium and ventricular septum but was greater than the degree of rejection noted in the right and left ventricular free walls. CONCLUSION: The distribution of histologic lesions of acute cardiac rejection in rodents was heterogeneous in grafted hearts which exhibited greater lesions in the atria than in ventricles. This should be taken into consideration in the evaluation of new methods of detection of cardiac rejection and in the diagnosis of acute cardiac rejection in humans.

Animals↗

Comparison of long-term outcome of alcoholic and idiopathic dilated cardiomyopathy.

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.

Adult↗