Biomedical subjects

S Dinanian

Publications and source records attributed to S Dinanian.

11 recordsLinked to original sources

PubMed1999

Cardiac sympathetic denervation in familial amyloid polyneuropathy assessed by iodine-123 metaiodobenzylguanidine scintigraphy and heart rate variability.

Familial amyloid polyneuropathy (FAP) is a rare and severe hereditary form of amyloidosis, due to nervous deposits of a genetic variant transthyretin produced by the liver and characterized by both sensorimotor and autonomic neuropathy. Left ventricular systolic dysfunction is rare, but conduction disturbances and sudden deaths can occur. The neurological status of the heart has not been elucidated, and an alteration of the sympathetic nerves may be involved. We studied 17 patients (42+/-12 years) before liver transplantation by iodine-123 metaiodobenzylguanidine (MIBG) scintigraphy, heart rate variability analysis, coronary angiography, radionuclide ventriculography, rest thallium single-photon emission tomography (SPET) and echocardiography. Coronary arteries, left ventricular systolic function and rest thallium SPET were normal in all patients. Only mild evidence of amyloid infiltration was found at echocardiographic examination. Cardiac MIBG uptake was dramatically decreased in patients compared with age-matched control subjects (heart-to-mediastinum activity ratio at 4 h: 1.36+/-0.26 versus 1.98+/-0.35, P<0.001), while there was no difference in MIBG washout rate. Heart rate variability analysis showed a considerable scatter of values, with high values in four patients despite cardiac sympathetic denervation as assessed by MIBG imaging. The clinical severity of the polyneuropathy correlated with MIBG uptake at 4 h but not with the heart rate variability indices. Cardiac MIBG uptake and the heart rate variability indices did not differ according to the presence or absence of conduction disturbances. Patients with FAP have sympathetic cardiac denervation as assessed by MIBG imaging despite a preserved left ventricular systolic function and cardiac perfusion, without correlation with conduction disturbances. Results of the heart rate variability analysis were more variable and this technique does not seem to be the best way to evaluate the extent of cardiac sympathetic denervation in FAP patients.

3-Iodobenzylguanidine↗

PubMed1997

Primary culture of human atrial myocytes is associated with the appearance of structural and functional characteristics of immature myocardium.

We examined changes in the structural and physiological characteristics of human atrial myocytes during primary culture in the presence of serum. Action potentials and ionic currents were recorded in freshly dissociated (FM) and cultured (CM) whole-cell patch-clamped myocytes, alpha-smooth muscle actin, sarcomeric alpha-actinin and beta-myosin heavy chains (beta-MHC) were stained with monoclonal antibodies. From day 5 to day 21, myocytes lost their rod shape, spread and exhibited reorganized sarcomeres. These morphological changes were associated with a marked increase in membrane capacitance (+266%). Both beta-MHC and alpha-smooth muscle actin were expressed in CM but not in FM, indicating a dedifferentiation process. CM were characterized by a lower resting potential (-30 +/- 2 v -60 +/- 4 mV, P < 0.05) and, when repolarized, by a shorter action potential duration (APD) than FM (APD-60: 126.9 v 159.6 ms, P < 0.05). The inward rectifier K+ current was absent in CM, thus explaining the low resting potential. The density of the transient component of the voltage-activated K+ current Ito1 was not modified during culture, while that of the sustained component Isus was increased fourfold. The amplitude of ICa was increased, but its density was unchanged, indicating that CM maintained a normal density of functional calcium channels. Neither the voltage dependence nor the inactivation of ICa was modified in CM. The time constants of inactivation of ICa were unchanged, although the amplitude of the rapidly inactivating component of ICa was increased in CM compared to FM. Moreover, ICa was increased by the beta-adrenergic agonist isoproterenol (1 microM) throughout the culture period. Our results demonstrate that in long-term serum-supplemented culture, adaptation of human atrial myocytes to their new environment is associated with differential alterations of the main ionic currents and phenotypic changes characteristic of immature myocardium.

Action Potentials↗

PubMed1997

[Classification and pitfalls of atrioventricular blocks].

Atrioventricular blocks may be classified according to their degree, their site and their aetiology. Assessing the degree of block is not always easy when the P waves are poorly visible and/or masked by the ventricular complexes. Affirmation that a 2nd degree block is a Mobitz II block requires examination of the ECG to differentiate it from "false" Mobitz II due to variable PP intervals or concealed hisian extrasystoles. Complete atrioventricular block is easy to define on the ECG but not always synonymous with totally blocked conduction and should be interpreted taking into account the frequency of escape beats. Determining the site of block is important as it has therapeutic implications; the type of block evaluated from the surface ECG also provides useful but not always decisive information. The investigation of the aetiology of the block is valuable for differentiating acute, transient blocks from chronic (permanent or paroxysmal) blocks, the former sometimes requiring temporary but rarely permanent cardiac pacing.

Body Surface Potential Mapping↗

PubMed1996

Initial and long-term evaluation of escape rhythm after radiofrequency ablation of the AV junction in 50 patients.

Between 1986 and 1994, 50 patients (mean age 63 +/- 13 years), 25 of whom had organic heart disease and presenting with atrial arrhythmias refractory to 5.6 +/- 1.6 antiarrhythmic drugs, underwent radiofrequency ablation (5 +/- 3 pulses by procedure; duration of pulses 50.5 +/- 32 s) of the proximal AV junction to create complete and permanent AV block. The escape rhythm was studied immediately after the procedure and during long-term follow-up. Immediately after the procedure, an escape rhythm was observed in 80% of the patients (junctional in 92%). Over a mean follow-up of 36 +/- 16 months in 47 patients (2 patients died before assessment of escape rhythm and 1 was lost to follow-up), an escape rhythm was present in 39 patients (83%) and absent in the remaining 8 (17%). The only significant difference between the two groups was the initial presence of an escape rhythm (P = 0.008). However, three patients with an initial escape rhythm had none during long-term follow-up. The initial presence of an escape rhythm as a predictive factor of its presence during follow-up had a sensitivity of 87%, specificity of 63%, positive predictive value of 92%, and negative predictive value of 50%. Thus, the absence of an escape rhythm during long-term follow-up causing pacemaker dependency was noted in 1 of 6 patients. This represents a limitation to this palliative treatment, which should be reserved for patients suffering from supraventricular tachycardias refractory to other treatments.

Adult↗

PubMed1995

[Electrocardiographic aspects of atrial fibrillations].

The electrocardiographic analysis of atrial fibrillation is usually easy. However, some cases may be difficult to interpret: the organisation and voltage of the fibrillation waves can be very variable leading to appearances of atypical flutter in cases with large "f" waves or, conversely, in cases with low voltage fibrillation, to those of sinus mode dysfunction. The ventricular response may be slow: the conduction is usually delayed in the atrioventricular node where concealed conduction plays an important role in determining the ventricular response. Regular ventriculogrammes correspond to a junctional or ventricular escape rhythms. Aberrant conduction in the His-Purkinje system may sometimes be observed after long diastoles (phase 4 block) but often terminates short, preceded by long cycles (phase 3 block). It is usually easy to differentiate them from ventricular ectopics or preexcitation by careful examination and application of classical diagnostic criteria.

Atrial Fibrillation↗

PubMed1995

[Double responses].

Double response is a rare electrocardiographic phenomenon requiring two atrioventricular conduction pathways with very different electrophysiological properties. Double ventricular responses are the usual manifestation: an atrial depolarisation (spontaneous or provoked, anticipated or not) is followed by a first ventricular response dependent on an accessory pathway or a rapid nodal pathway and then a second response resulting from sufficiently delayed transmission through a nodal pathway for the ventricles to have recovered their excitability when the second wave of activation reaches them. A simple curiosity when isolated and occurring under unusual conditions, particularly during electrophysiological investigation of the Wolff-Parkinson-White syndrome, the double response may initiate symptomatic non-reentrant junctional tachycardia when associated with nodal duality and repeating from atria in sinus rhythm. The functional incapacity and resistance to antiarrhythmic therapy may require referral for ablation of the slow pathway.

Atrioventricular Node↗

PubMed1994

[Electrophysiological mechanisms of ventricular arrhythmia in myocardial infarction].

In experimental models of coronary occlusion, the physiopathology of ventricular arrhythmias varies with its timing, there being three main phases: early, late and chronic. The early phase covers the first 30 minutes and is dominated by tachycardias and fibrillations resulting from multiple micro-reentry circuits which are the consequence of major changes in conduction and excitability created by acute ischaemia. These arrhythmias may be triggered by extrasystoles which have a different mechanism related to the injury current generated in the border zone between ischaemic and healthy cells. The late phase lasts about 72 hours: it is characterised by polymorphic ventricular extrasystoles and bursts of relatively slow ventricular tachycardia. Much more rapid tachycardia can be induced by stimulation. The origin of these arrhythmias is usually in the surviving Purkinje fibres of the subendocardium. The mechanisms are variable: abnormal automaticity, reentry or activity triggered by delayed after depolarisations. During the chronic phase, reentrant tachycardia is possible but only when induced by stimulation. Delayed conduction is the consequence of non-uniform antisotropism related to the disorientation of the myocardial fibres caused by fibrosis. In the clinical situation, most research has been centered on sustained monomorphic ventricular tachycardias of the chronic phase. Their mechanism is almost exclusively reentry (the circuits usually being located in the subendocardium) as suggested by the triggering and interruption of clinical tachycardias by stimulation, the recording of fragmented activation or prepotentials at the site of emergence of the tachycardia and the phenomena of pacing.

Arrhythmias, Cardiac↗

PubMed1993

[Diagnosis of ventricular tachycardia by electrocardiography].

In monomorphic wide QRS complex tachycardia, it is important to differentiate ventricular tachycardia from supraventricular tachycardia with aberration or preexcitation both from the prognostic and therapeutic view points. Atrioventricular dissociation with fusion complexes allows diagnosis of ventricular tachycardia but the negative predictive value of these criteria is low. Extreme QRS axis deviation, concordant morphological criteria in leads V1-V2 and V6 and analysis of the RS complexes in the precordial leads, nearly always enable supraventricular tachycardia with aberration. The distinction with other causes of wide QRS complex tachycardias (supraventricular tachycardia with preexcitation or with non-systematized intraventricular conduction defects) is much more difficult in the absence of a reference recording and depends more on the clinical context than ECG analysis.

Diagnosis, Differential↗

PubMed1992

[Drug treatment of chronic ventricular arrhythmia].

The treatment of chronic ventricular arrhythmias depends on the severity and tolerance of the arrhythmia. Extrasystoles, even repetitive, in the healthy heart, are usually respected when asymptomatic or treated with betablockers in first intention when symptomatic. These drugs should also be proposed for patients with ischemic heart disease and non-sustained ventricular tachycardia, a situation in which Class I antiarrhythmics should be avoided. The prevention of sustained ventricular tachycardial may be empirical, with betablockers and/or amiodarone, or guided by the results of pharmacological tests during endocavitary electrophysiological studies.

Adrenergic beta-Antagonists↗

PubMed1992

[How to evaluate the arrhythmogenic risk after myocardial infarction?].

The risk of sudden arrhythmic death after myocardial infarction is high, especially during the first months. The evaluation of this risk should be performed before hospital discharge in the same way as residual ischaemia and left ventricular function, which are independent risk factors for arrhythmia, are assessed. Holter monitoring provides information not only about ventricular hyperexcitability (especially the detection of unsustained ventricular tachycardia) but also about the activity of the autonomic nervous system by analysis of variations of the sinus rhythm, the decrease of which carries a poor prognosis. The search for an arrhythmogenic substrate requires signal averaged electrocardiography, but although the absence of late potentials carries a good prognosis, the positive predictive value of this investigation is very low. The association of non-invasive indices of poor prognosis greatly increases the probability of a major arrhythmic event; this may require consideration of programmed ventricular pacing, another method of substrate and risk assessment, which has the added advantage of sometimes indicating the most appropriate therapy.

Arrhythmias, Cardiac↗

PubMed1992

[Double-blind clinical and echocardiographic study of oral enoximone versus placebo in severe cardiac insufficiency].

The effect of enoximone was assessed by a randomised double blind trial versus placebo. The clinical status of the patients was evaluated by the NYHA classification and quality of life score. Inotropic state was estimated from the maximum acceleration of aortic and pulmonary blood flow recorded by Doppler echocardiography. Thirty patients with severe cardiac failure, aged 66.4 +/- 14 years, symptomatic despite maximal therapy associating diuretics, digitalis, nitrate derivatives and angiotensin converting enzyme inhibitors, were included. Fifteen patients were given enoximone 100 mg three times a day orally (Group E) and the other 15 were given a placebo (Group P). The NYHA class and quality of life scores were assessed at D0, D4 and D31. Doppler echocardiography and Holter recordings were performed on D0 and D31. The two groups were comparable at D0. Ten patients abandoned the trial, 3 from Group E (including 1 death) and 7 from Group P (including 3 deaths). At D4, 13 patients from Group E and 8 from Group P were clinically improved (p < 0.05). At D31, the clinical state was stable or improved in 10 of the 12 patients in Group E and 6 of the 8 patients in Group P (NS). No secondary effects were severe enough to warrant the withdrawal of treatment: the frequency of ventricular extrasystoles was comparable in the two groups at D0 and D31. At D31 the maximal aortic acceleration had increased by 20% compared with D0 (p < 0.05) and the maximal pulmonary acceleration by 31% (p < 0.05) in Group E. The same parameters showed no significant change in Group P (-6% and +5% respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗