Biomedical subjects

P Cosnay

Publications and source records attributed to P Cosnay.

At least 55 records · Page 3Linked to original sources

PubMed1997

Heart rate variability in idiopathic dilated cardiomyopathy: characteristics and prognostic value.

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.

Adult↗

PubMed1997

[Value of tomoscintigraphy with Fourier analysis in the diagnosis of arrhythmogenic right ventricular cardiomyopathy].

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.

Adolescent↗

PubMed1996

[Arteriovenous fistula with cardiac insufficiency disclosing kidney cancer].

A 66 year-old woman free of any coronary and valvular heart disease presented to our hospital with acute and severe congestive heart failure associated with increased blood flow-angiography showed an intraparenchymatous arteriovenous fistula of the left kidney and a kidney cancer. The patient was discharged after nephrectomy and complete heart recovery as assessed from the normality of the hemodynamic exploration of the right ventricle.

Aged↗

PubMed1996

Time-domain signal-averaged electrocardiogram in nonischemic ventricular tachycardia.

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.

Death, Sudden, Cardiac↗

PubMed1996

[Contact dermatitis following cardiac pacemaker implantation].

The authors report a case illustrating the causality between the appearance of contact eczema and the implantation of a cardiac pacemaker. To the authors' knowledge, only 11 cases of eczema secondary to the implantation of a pacemaker have been previously reported, all in dermatological journals. In 60% of caes, the lesions were observed over the pacemaker implantation and the appearance of the rash varied from 2 days to 24 months. The causal allergens were mainly the metallic and plastic components. The physiopathological mechanisms, though not completely understood, are related to cellular immunity and therefore, to delayed hypersensitivity reactions. From the therapeutic point of view, locak steroid applications to limited excema lesions have been suggested but recurrence is common. The only effective treatment is removal of the allergen.

Aged↗

PubMed1996

[Precapillary pulmonary arterial hypertension disclosing systemic lupus erythematosus].

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.

Adult↗

PubMed1996

[Idiopathic monomorphic ventricular tachycardia].

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.

Action Potentials↗

PubMed1996

[A study of 36 cases of mitral valve prolapse by isotopic ventricular tomography].

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.

Adult↗

PubMed1996

Detection of acute cardiac allograft rejection with high resolution electrocardiography: experimental study in rats.

BACKGROUND AND METHODS: To diagnose early acute cardiac rejection, we evaluated high-resolution electrocardiography in rats. Heterotopic heart transplantations were performed in allogeneic animals, either treated with cyclosporine or untreated, and in syngeneic animals. High-amplification electrocardiograms were recorded daily, under anesthesia, with two intra-abdominal leads. After amplification (x 5000 to 20,000), the electrocardiographic signal was acquired and analyzed with P-Clamp software. We measured the amplitude (millivolts) and duration (milliseconds) of the auriculogram (P wave) and the ventriculogram (QRS wave), the duration of auriculoventricular conduction (milliseconds; PQ interval) and the heart rate. Twenty-five grafted hearts were fully studied in recipients not treated with cyclosporine (allogeneic n = 16, syngeneic n = 9). RESULTS: In the allogeneic group, acute cardiac rejection was always accompanied by an early and progressive increase in P wave duration and PQ interval, whereas an increase in QRS duration was subsequently recorded. No significant change in P wave, PQ interval, or QRS wave duration was recorded in the syngeneic group, which showed no histologic rejection lesions. A decrease in P wave and QRS wave amplitude was recorded in both groups of animals. In the allogeneic group treated with cyclosporine (n = 21), grafted hearts were removed early (4.5 +/- 0.5 days): 10 cardiac grafts were rejected and 11 were not. An increase in P wave duration > or = 20% was associated with mild rejection in most cases. The sensitivity and specificity of this electrocardiographic sign were excellent (100%). The auricular (right and left atria) and the ventricular (right and left ventricles) tissues were evaluated histologically. In the allogeneic groups (n = 26), the histologic lesions during acute rejection were greater in the auricular myocardium than in the ventricular myocardium. Rejection in the atrial and ventricular myocardium was most often differentiated by one degree according to the Billingham classification. CONCLUSIONS: We concluded that acute cardiac rejection in rats is associated with early conduction disturbances in the atrial myocardium which can be shown by high-resolution electrocardiography.

Abdomen↗

PubMed1995

[Anti-arrhythmic therapy and cardiac failure].

In cardiac failure, continuous ambulatory electrocardiographic recording for 24 hours (Holter system) enables detection of 60 to 80% of complex ventricular arrhythmias, 15 to 40% of atrial arrhythmias and sudden death accounts for about 40% of fatalities but its causes are multiple and sometimes unrelated to arrhythmias. Abnormalities of cardiac structure, metabolic and neuro-hormonal changes and some drug therapies are implicated in the genesis of these arrhythmias, the management of which is discussed in two different situations with respect to the functional incapacity: in paucisymptomatic ventricular arrhythmias in patients with cardiac failure, class I antiarrhythmics and d-sotalol should be avoided and betablockers prescribed with caution; the indications of amiodarone have not yet been determined. When the arrhythmia is symptomatic (sustained ventricular tachycardia or ventricular fibrillation), class I antiarrhythmics are not effective enough in the prevention of sudden death; betablockers and amiodarone may give good results but should be compared with implantable defibrillators in the future. The multiplicity and complexity of the mechanisms of arrhythmias in cardiac failure, and the inadequate results obtained with classical antiarrhythmics necessitate the development of new antiarrhythmics based on blockade of non-selective channels probably activated in cardiac failure by the stretching of myocardial fibres.

Adrenergic beta-Antagonists↗

PubMed1994

Ventricular arrhythmia factors in mitral valve prolapse.

To assess the prevalence of ventricular arrhythmias and late potentials (LPs) in mitral valve prolapse (MVP) and to identify clinical, ECG, and echocardiographic markers of spontaneous ventricular arrhythmias, we studied 58 consecutive patients (mean age 46.6 +/- 17.8 years; 29 males, 29 females) with MVP diagnosed by echocardiography. Patients underwent ambulatory ECG recording (n = 58), exercise stress test (n = 56), signal-averaged ECG (n = 58), and programmed ventricular stimulation (n = 52). Ten patients (17.2%) had spontaneous nonsustained ventricular tachycardia (NSVT), 26 patients (44.8%) had premature ventricular contractions (PVCs), Lown grade > or = 3 during 24-hour ECG, and 19 had Lown grade > or = 3 PVCs during exercise stress test; 13 patients had LPs (22.4%). We provoked sustained VT in one case and NSVT in ten cases. Patients with complex ventricular arrhythmias during 24-hour ECG and exercise stress test were older and more often had mitral regurgitation. There was a statistical correlation between the presence of LPs and spontaneous VT (46.1% vs 8.9%; P < 0.005) and induced ventricular arrhythmias (50% vs 12.8%; P < 0.005). No correlation was found between spontaneous ventricular arrhythmias and thickness or posterior displacement of the mitral valve. In conclusion, complex ventricular arrhythmia (especially VT) and LPs are frequent in MVP. Patient age and mitral regurgitation seem to be determinant factors of complex ventricular arrhythmias in MVP. On signal-averaged ECG, absence of LPs seems to be a good additional marker to identify MVP patients without spontaneous VT. On the other hand, programmed ventricular stimulation does not appear valuable in determining a MVP subgroup with a high risk of ventricular arrhythmias.

Adult↗

PubMed1994

Electrocardiographic and electrophysiologic properties of cardiac allografts.

The increasing number of heart transplant patients requires that physicians be able to recognize the electrocardiographic (ECG) and electrophysiologic properties of cardiac allografts. Cardiac allografts are characterized by modifications of resting ECGs and frequent arrhythmias in the postoperative period, and the loss of autonomic nervous control illustrated by permanent tachycardia and loss of heart rate variability during 24-hour ambulatory ECG recording. Some clinical and experimental observations suggest a mid-term reinnervation of the cardiac allograft, but this requires histologic confirmation. The electrophysiologic characteristics of the denervated myocardium are similar to those of the innervated myocardium at rest. However, supersensitivity to circulating catecholamines has been observed in cardiac allografts as in experimentally denervated hearts, which is responsible for a progressive increase in heart rate during exercise and a slow decrease during recovery. Supersensitivity of the denervated heart to acetylcholine may explain the high prevalence of donor sinus dysfunction due to impairment of its automaticity. More often, the sinus node dysfunction is transient and can be treated with an adenosine antagonist, such as theophylline, before permanent implantation of a pacemaker. In the case of pacemaker implantation, synchronization of the donor atria with the recipient atria is desirable, and an endocardial lead implantation is preferred. Several electrophysiologic changes have been observed during acute cardiac allograft rejection. From experimental studies, the most important of these are the disturbance of conduction in the atria and the atrioventricular node and a decrease in the amplitude of the ventricular potential. Initial studies on isolated myocytes show profound changes in membrane conductance during experimental cardiac rejection. The development of new noninvasive detection methods of cardiac allograft rejection, such as intramyocardial voltage electrogram monitoring and high-resolution ECG, could help early diagnosis.

Animals↗

PubMed1994

[Surgical treatment of atrial fibrillation].

The persistence of atrial fibrillation with a controlled ventricular response with medical treatment or ablation of the His bundle, suppresses troublesome palpitations but leaves potential haemodynamic problems and the risk of thromboembolism. Surgical treatment of this arrhythmia, by leaving an anatomic bridge between the sinus and atrioventricular nodes, aims to allow acceleration of the ventricular rhythm on exercise whilst preventing by partial, total or selective exclusion of atrial tissues, the multiple intra-atrial reentries responsible for atrial flutter or fibrillation. The first method proposed was isolation of the left atrium (Cox, 1980) which allows acceleration of the ventricular rhythm during exercise, leaving little or no haemodynamic disturbance, but, in theory, the same risk of embolism. The second method, the "corridor" operation (Guiraudon, 1985) consists in isolating both atria, but significantly alters the haemodynamic efficacy without reducing the embolic risk, and hardly offers any advantage over ablation of the nodo-hisian pathway completed by implantation of a ventricular, rate responsive, pacemaker. The recently described "maze" procedure (Cox and Boineau, 1991) would seem to be more promising with judiciously chosen incisions (at the base of the atria, around the pulmonary veins, between the vena cavae, along the interatrial septum, etc.) and points of cryoablation in the region of the coronary sinus, allowing modulation of the ventricular response with activation of sufficient atrial tissue to prevent reentry and recurrence of atrial fibrillation without affecting haemodynamic efficacy. The results of this technique are encouraging in the hands of its inventors but require confirmation in larger series of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗

PubMed1994

[Late ventricular potentials and mitral valve prolapse].

In order to determine the predictive value for ventricular arrhythmias of ventricular late potentials (LP) in mitral valve prolapse (MVP) the authors performed high amplification signal-averaging ECG (SA) and 24 hours ambulatory ECG (Holter) monitoring in 68 consecutive patients (34 men, 34 women, average age 48 +/- 17.7 years) with echocardiographically diagnosed MVP. Patients with bundle branch block or associated cardiac disease were excluded. Echocardiography showed 26 patients to have floppy mitral valves (38.2%), 50 patients to have posterior deplacement > or = 5 mm of the mitral valves in systole (73.5%) and 35 patients to have mitral regurgitation (51.4%). Holter monitoring showed 17 patients without ventricular extrasystoles (VES), 15 had Lown Grade I, 6 had Lown Grade II, 3 had Lown Grade III, 15 had Lown Grade IV A and 12 had Lown Grade IV B ventricular arrhythmias. Therefore, 30 patients had complex ventricular arrhythmias (> or = Lown Grade III) and 13 patients had spontaneous non-sustained ventricular tachycardia (NSVT) (one patient had NSVT on resting ECG but not on Holter monitoring). Eighteen patients had LP (26.5%). The incidence of complex ventricular arrhythmias was higher in patients with mitral regurgitation (62.8% versus 27.7%; p < 0.005) whereas the incidence of NSVT was not significantly different (25.7% versus 17.1%; p = 0.15). On the other hand, the frequency of complex ventricular arrhythmias was not significantly different in the presence or absence of LP (61.1% versus 40%: NS) whereas the incidence of NSVT was higher in patients with LP (44.4% versus 10%; p < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed1994

[Isotopic study of myocardial perfusion and innervation in 28 patients with primary hypertrophic cardiomyopathy: relation to ventricular arrhythmia].

Ventricular arrhythmias are frequent, sometimes complex and severe, in primary hypertrophic cardiomyopathy. They carry a poor prognosis. Some workers have reported that these arrhythmias are more common in patients with abnormal myocardial perfusion. Other groups have underlined the important role of the sympathetic nervous system in the development of ventricular hypertrophy and the genesis of ventricular arrhythmias. Therefore, a population of 28 patients with primary hypertrophic cardiomyopathy (PHCM) were studied by thallium 201 myocardial scintigraphy and sympathetic innervation was assessed using a structural analogue of noradrenaline, meta-iodobenzyl-guanidine (MIBG). Then, perfusion and innervation were correlated with ventricular arrhythmias observed on 24 hours holter monitoring electrocardiogram. Perfusion abnormalities were observed in 60% of patients: stable in mild left ventricular hypertrophy, labile in severe left ventricular hypertrophy. They were not related to the presence of muscular bridges and systolic compression of septal arteries demonstrated by coronary angiography. These perfusion abnormalities were closely correlated to ventricular extrasystoles observed on Holter monitoring. In this series, and compared to controls, the fixation of MIBG as determined by the Heart/Mediastinum (H/M) ratio was significantly decreased (2.27 +/- 0.31 versus 2.57 +/- 0.33 in controls). Uniform myocardial uptake of MIBG with no defect or significant global hypofixation was observed in 32% of PHCM. Regional and occasionally global hypofixation was observed in 68% of patients. In moderate hypertrophy, reduced uptake was not uniform, the lateral wall and apex being the most abnormal. Uptake of MIBG was significantly correlated to septal wall thickness and to left ventricular mass index. These defects were related to abnormal neuronal uptake of MIBG.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Iodobenzylguanidine↗

PubMed1994

[Injectable and oral cibenzoline in the treatment of supraventricular tachycardia related to intranodal reentry or accessory atrioventricular conduction pathway].

Cibenzoline, a Vaughan-Williams Class I antiarrhythmic agent, was studied in 26 patients with orthodromic supraventricular tachycardia (SVT) by nodal reentry (n = 10) or an accessory pathway (AP) (n = 16). IV cibenzoline accelerated sinus rhythm, prolonged PR, AH, HV and QT, widened QRS and depressed or blocked anterograde and retrograde conduction in the accessory pathway, significantly, without significantly modifying conduction capacity in the AV node, nor atrial, nodal or ventricular refractory periods. It converted 6/10 of nodal reentries and 9/16 of reentries due to an AP, by a mean dose of 1 mg/kg, in 2 to 3 minutes, in 12 cases out of 16 by blocking retrograde conduction in the reentry circuit. It prevented reinduction of 12 of the 26 cases of SVT, significantly slowing the cycle of induced SVT in other patients. Oral cibenzoline (260 to 390 mg/day) prevented induced SVT in 11 cases out of 25 and spontaneous SVT in 14 cases out of 26, with a follow-up of 11 +/- 4 months (6 to 16), and this regardless of the reentry mechanisms. Intravenous cibenzoline was not associated with any clinical or hemodynamic intolerance but there was facilitation of episodes of SVT in one patient. Oral administration caused only one case of digestive intolerance, leading to lowering of the dose. Plasma levels showed no significant differences between successes and failures, for both the injection and oral formulations of cibenzoline, whether in terms of the conversion or prevention of episodes. Electrophysiological investigations had a 60% positive and 50% negative predictive value, a sensitivity of 64% and a specificity of 50%. Cibenzoline thus appears to be useful for the conversion and prevention of episodes, SVT, regardless of the reentry circuit, and seems justified, in view of its good safety/acceptability, as first line treatment in this diagnostic indication, measurement of plasma levels and electrophysiological investigations being of little apparent value in terms of guiding treatment and predicting its results.

Administration, Oral↗

PubMed1993

[Non-invasive exploration methods of supraventricular arrhythmia in current practice].

In patients with supraventricular rhythm disorders ambulatory electro-cardiographic recording (Holter system) is an indispensable examination as it detects attacks that pass unrecorded by conventional ECG, being asymptomatic, too brief or too rare. It confirms the diagnosis, defines the factors triggering the attacks, detects the association of rhythm and conduction disorders, guides the treatment and monitors its effectiveness. Sequential ambulatory recording lends itself particularly well to this last objective. Biochemical examinations explain the cause of certain relapses (potassium depletion, high alcohol blood level) or detect the origin, clinically more or less obvious, of these disorders of rhythm (essays of thyroid hormones). Measuring blood levels of therapeutic drugs makes the handling of these various drugs safer. Finally, echocardiography detects an underlying heart disease, evaluates the size of the left atrium (a factor of relapse when it is dilated and of embolism when it harbours thrombi) and assesses the left ventricular function before administration of antiarrhythmics which, to varying extents, are all negative inotropic drugs.

Arrhythmias, Cardiac↗

PubMed1993

[Drug-induced ventricular tachycardia].

Certain drugs can induce ventricular tachycardia (VT) by creating reentry, ventricular after potentials or exaggerating the slope of phase 4. These may or may not be symptomatic, sustained or non-sustained and have variable ECG appearances: monomorphic or polymorphic, bidirectional, torsades de pointes. They risk degenerating into ventricular flutter of fibrillation and have been held responsible for the increased mortality observed unexpectedly in some long-term treatments. The drugs responsible are mainly those used in cardiology, probably due to predisposing circumstances (cardiomegaly, cardiac failure, previous severe ventricular arrhythmias, therapeutic associations, metabolic abnormalities). These include primarily the antiarrhythmic drugs (IA, IC, sotalol and bepridil), digitalis, sympathomimetics and phosphodiesterase inhibitors. These complications may be toxic or idiosyncratic, in patients with or without cardiac disease, and may also occur with other drugs: vasodilators and anti-anginal drugs (lidoflazine, vincamine, fenoxedil), psychotropic agents (phenothiazine and imipramine), antimitotics, antimalarials (chloroquine) or antibiotics (erythromycin, pentamidine). The prognosis is severe and the treatment is often difficult which makes prevention, helped by repeated surface ECG (or Holter monitoring), very important with careful assessment of patients at risk.

Anti-Arrhythmia Agents↗