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A Leenhardt

Publications and source records attributed to A Leenhardt.

87 records · Page 5Linked to original sources
PubMed1988

[Characteristics and prognosis of ventricular arrhythmia in arrhythmogenic right ventricular dysplasia].

The authors report their findings in 47 cases of ventricular arrhythmias due to arrhythmogenic dysplasia. The 47 patients were selected on the presence of ventricular tachycardia or fibrillation associated with dysplasia affecting selectively (44/47) or predominantly (3/47) the right ventricle at angiography. In this series males were predominant (38/47, 81 p. 100), familial incidence was high (13/47, 28 p. 100) and ECG abnormalities were constant. Most of the dysrhythmias (40/47) consisted of sustained ventricular tachycardia (VT) with left bundle branch block pattern (96 p. 100), occurring at the rate of 1.6 per patient on average and seldom with extreme axial deviation, as seen in post-infarction VT or VT associated with cardiomyopathy. The QRS complex was slightly prolonged (151 +/- 28 ms) and of high amplitude (2.5 +/- 1 mV on a VR, a VL and a VF leads), these values being intermediate between those of mild VT bursts and those of post-infarction or cardiomyopathy-related VT. The tachycardia was easily tippered by EP study, Intercritical Holter recordings showed frequent ventricular extrasystoles in the vast majority of cases; these were usually polymorphous and grouped into short bursts in one-half of the patients. On an 8.3 +/- 7 years' follow-up starting with the first attack of VT, it was found that only during the initial phase the spontaneous onset of VT was mediated by the adrenergic system (triggered by sports). Only 3 patients died during the follow-up period: one of ventricular fibrillation, 2 of right heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Arrhythmias as predictors of sudden death.

Two methods are available for exploring arrhythmias in cardiac patients who are at risk of sudden death: Holter monitoring and invasive electrophysiology. Despite numerous studies, the predictive value of these techniques, in terms of prognosis, remains poor for many reasons. Neither technique considered individually can give reliable prognostic indications simply because each technique addresses different issues which are only partially involved in the mechanism of sudden death. Invasive electrophysiology, by artificially provoking an arrhythmia, detects the potential substrate which may ultimately lead to lethal arrhythmias. Although this is an important technique it is insufficient because merely identifying the substrate for an arrhythmia does not necessarily mean that arrhythmia will occur. On the other hand, ambulatory ECG allows monitoring of spontaneous arrhythmias which may be considered as potential initiating factors in arrhythmias. However, even if initiating factors and potential substrates are present, they are not sufficient conditions to cause lethal arrhythmias to occur. When there is an opportunity to scrutinize the mechanism of arrhythmias which are indeed lethal, as in sudden death, it appears that the lethal event results from the intervention of a new factor which was either absent or not considered during preceding investigations. In coronary patients, curiously, ischemia more often provokes cardiac arrest or an electromechanical dissociation rather than a ventricular tachycardia or fibrillation. Sudden death is not infrequently of iatrogenic origin, because of the arrhythmogenic effect of powerful antiarrhythmic drugs. More important, ventricular fibrillation often occurs in the setting of a progressively increased sympathetic tone, which explains either the particular seriousness of a previously known arrhythmia or the occurrence of an arrhythmia which was never before observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1987

[Value of beta blockers in the treatment of recurrent ventricular tachycardia in cardiac insufficiency].

Beta-blockers were used to treat 20 patients (mean age 55 +/- 12 years) presenting with severe ventricular arrhythmia on chronic heart failure (NYHA stages II to IV; mean ejection fraction 29.7 +/- 7.8%) due to coronary disease (18 cases) or to cardiomyopathy (2 cases). Ventricular tachycardia sustained (7.6 +/- 6.3 attacks/patient) in 19 patients, unsustained in 18, monomorphous in 8 and polymorphous in 12, had been present for 12.4 +/- 18 months. In all but one hitherto untreated patient, the condition had failed to respond to amiodarone combined with a type Ia (19 patients) and type Ic (16 patients) antiarrhythmic drug. Short-term results were: 17 successes, 2 failures and 1 death due to cardiogenic shock. Fifteen patients were followed up for 14 +/- 6.7 months. Thirteen of them benefited from smaller doses of a formerly ineffective treatment; there was one failure, and one patient in whom the attacks of tachycardia, but not the numerous and polymorphous extrasystoles, were controlled by the beta-blockers suddenly died at night. The actuarial mortality rate was 11.4% as against an expected figure of 30% in such a high risk group. Although no significant changes in ejection fraction were observed, heart failure became worse in 8 patients, but it was compensated by diuretics and/or vasodilators. The effects of beta-blockers in resistant ventricular arrhythmia on heart failure suggest that an adrenergic factor is involved in the mechanism of arrhythmia. Provided treatment is progressive and its haemodynamic consequences carefully monitored, beta-blockade is well tolerated. Its effectiveness on severe arrhythmia and on mortality rate seems to confirm that it prevents sudden death by an anti-arrhythmic mechanism.

Adrenergic beta-Antagonists↗
PubMed1985

[Transesophageal stimulation in the treatment of atrial flutter and tachysystole].

Transoesophageal left atrial pacing was used to reduce 102 episodes of ectopic atrial rhythms (79 common flutters and 23 ectopic tachycardias) in 83 patients (64 men, 19 women) aged 33 to 85 years (average 61 years). Overdrive pacing, at a faster rate than that of the spontaneous rhythm, was delivered via a bipolar pacing catheter introduced nasally and positioned behind the atrium under fluoroscopic and/or electrocardiographic control. Long pulse durations (up to 20 ms) were used to capture the atria with intensities of less than 20 mA for better tolerance. The overall results were: a) conversion to sinus rhythm in 60.8 p. 100 of cases (47 p. 100 directly and 13.8 p. 100 after transient atrial fibrillation), b) atrial fibrillation lasting over 24 hours in 7.8 p. 100 of cases, c) failure (31.4 p. 100) due to non-capture or intolerance (20.6 p. 100) or recurrence of the arrhythmia after transient atrial fibrillation (10.8 p. 100). Atrial flutter is more accessible to pacing than tachycardia (restoration of sinus rhythm in 63.3 p. 100 and 52.2 p. 100, respectively). Arrhythmias in the postoperative period of cardiac surgery, and isolated and recent arrhythmias were more easily converted. Prior antiarrhythmic therapy did not seem to improve results. Fifty per cent of failures of oesophageal pacing were converted to sinus rhythm by endocavitary pacing. These results show that atrial flutter or tachycardia may be successfully treated by oesophageal pacing in over 50 p. 100 of cases without having to use other forms of electrotherapy (endocavitary pacing or cardioversion).

Adult↗
PubMed1984

Therapeutic use of adenosine for terminating spontaneous paroxysmal supraventricular tachycardia.

Intravenous adenosine proved effective in eight out of ten episodes of acute spontaneous supraventricular tachycardia. AV node blockade induced by adenosine occurred 20 s after injection, and disappeared very quickly. Side-effects were transient and never serious. Therefore, it is thought that adenosine can be proposed safely for the short-term treatment of supraventricular tachycardia. Because of the different mechanisms of action, the specific side-effects observed after ATP administration are unlikely to be encountered.

Adenosine↗
PubMed1984

[Arterial hypertension in periarteritis nodosa. 37 case reports].

Hypertension in periarteritis nodosa poses the problem of aetiology, prognostic significance and treatment. Thirty seven cases of periarteritis noda with hypertension were analysed with à follow-up of over 10 years. These cases were taken from a series of 91 patients with polyarteritis nodosa admitted to the Department of Internal Medecine at the Pitié Hospital, between 1960 and 1980. Hypertension was observed on admission in 40% of the patients and developed during the first year of the disease in another 40%. The prognosis of patients with polyarteritis nodosa and hypertension is not significantly different from those without hypertension during the first six years. The overall prognosis depends mainly on the degree of renal involvement. The hypertension is renovascular in a number of cases due to ischaemia of the renal cortex. This was demonstrated by renal arteriography or by evaluating plasma renin activity in the renal veins. In some cases, especially those in which the hypertension preceded the periarteritis nodosa, the hypertension seemed to progress independently. In some cases, however, it was not possible to determine the relationship between the periarteritis nodosa and the hypertension or confirm that this association was coincidental. The use of angiotensin I converting enzyme inhibitors is an important advance in the treatment of the hypertension of periarteritis nodosa with high plasma renin activity as it counteracts the exact mechanism of the hypertension. Their use is justified in high plasma renin activity hypertension of periarteritis nodosa; patients who fail to respond may be treated with betablockers or other antihypertensive drugs.

Adolescent↗
PubMed1982

[The renin-angiotensin system in hypertensive patients with scleroderma and polyarteritis nodosa (author's transl)].

The renin-angiotensin system was studied in 14 normotensive and hypertensive patients with scleroderma and polyarteritis nodosa (PAN). The variations in blood pressure, plasma renin activity (PRA) and serum aldosterone were compared after the Captopril test. Mean arterial pressure fell 15,7 +/- 2,6 p. 100 (p less than 0,01) in hypertensive patients, but no change was observed in normotensive subjects. PRA and serum aldosterone did not change significantly in hypertensives with scleroderma. Large variations in blood pressure, PRA and serum aldosterone were observed in 2 out of 3 patients with PAN, the third one presenting a fall in blood pressure without significant changes in PRA or serum aldosterone. These results suggest that other mechanisms are responsible for hypertension in these patients and that the Captopril acted on other factors than the renin-angiotensin system.

Blood Pressure↗
PubMed1981

[Efficacy of captopril in periarteritis nodosa with arterial hypertension and renal failure (author's transl)].

In a patient with periarteritis nodosa failure of antihypertensive treatment with beta-blockers and diuretics encouraged the authors to use captopril in doses of 150 mg per day. Blood pressure rapidly returned to normal levels. The hypotensive effect of captopril is ascribable to its action on the renin-angiotensin system, since plasma renin activity was particularly high in this patients.

Angiotensin I↗
PubMedDate not supplied

Heterozygous mutation in the pore of potassium channel gene KvLQT1 causes an apparently normal phenotype in long QT syndrome.

Mutations in KvLQT1, a gene encoding a potassium channel, cause both the recessive Jervell and Lange-Nielsen (JLN) syndrome and the dominant Romano-Ward (RW) syndrome. These diseases are characterised by a prolonged QT interval on the ECG, syncopes and sudden death due to cardiac arrhythmias. The JLN syndrome is also associated with a congenital bilateral deafness. We report here a novel missense mutation, W305S, in the pore region of KvLQT1 identified by PCR-SSCP analysis in two consanguineous JLN families. In contrast to several missense mutations found in the same region of KvLQT1 in RW patients which are associated with severe cardiac phenotypes, the W305S mutation is responsible for an apparently normal phenotype in heterozygous JLN carriers.

Consanguinity↗
PubMedDate not supplied

[The surgical section of the bundle of Kent as an operative treatment of the Wolff-Parkinson-White syndrome: apropos a series of 82 operated cases].

Eighty two patients diagnosed of the Wolff-Parkinson-White syndrome (WPW) underwent operation for the surgical section of the Kent-His bundle. In these cases, posteroseptal localization (PS) occurred in 32, left lateral (LL) in 25, right lateral (RL) in six, anteroseptal (AS) in one, posteroseptal and left lateral in 14, right and left posteroseptal in two, anteroseptal and left lateral in one, and left lateral and right and left posteroseptal in one. All of the patients presented an invalidating clinical of palpitations and/or loss of consciousness, and episodes of atrial fibrillation and/or reciprocal rhythm were registered in all cases. The mean anterograde refractory period in the accessory pathways was 244 +/- 60 msec, and the shortest RR in atrial fibrillation was 190 +/- 36 msec. A mitral commissurotomy was carried out in 3 patients during surgery, mitral prostheses were implanted in two, a double aorto-coronary bypass was made in three and an interventricular communication was closed in one. After a follow-up of 36 +/- 18 months, the surgical section of the Kent bundle was found to be effective in 77 out 82 patients (94%). (In 70 out of 77 cases, both anterograde and retrograde conduction were totally abolished and in seven out of 77 obtunded. All patients were asymptomatic during the follow-up period). In 5 out of 82 patients, surgical treatment was ineffective all five showed a PS Kent-His and two presented a second Kent-His fascicle (LL).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

[Prognostic factors for success in catheter ablation of the right Kent bundle: report of 27 patients].

In 27 patients with atrial fibrillation and/or reciprocating tachycardia, ablation of right-sided Kent bundles (23 in the right posterior paraseptal region and four of the right free wall) was performed. The anterograde refractory period of the accessory pathways was 253 +/- 70 msec and the shortest R-R interval during atrial fibrillation 211 +/- 47 msec. Cumulative energies of 589 +/- 396 J per patient were used, with 3 +/- 2 shocks and 195 +/- 312 J per shock. Accessory pathway ablation was effective in 16/27 patients (59%) during an 11 +/- 8 months of follow-up (in 15/16 pre-excitation disappeared; in nine of them the anterograde and retrograde conductions were abolished and in the other six the anterograde and retrograde conductions were severely altered; ablation was partially ineffective in 1/16 patients who remained asymptomatic on medical treatment and without inducible reciprocal rhythm). Ablation was ineffective in 11/27 patients. Three hours after ablation a patient died from electromechanical dissociation; during ablation a 200 J shock cancelled preexcitation, not being possible to produce reciprocal rhythm. The emergency echocardiography only showed a minimum posterior pericardial effusion. Ablation was effective in 15/23 patients (65%) right posterior paraseptal. Overall success in 1989 (10/27 patients) was 70% (7/10 patients). The success in 1989 was 70% (6/8 patients) right posterior paraseptal. The shortest RP' interval (was 82 +/- 19 msec) during the reciprocal rhythm, where the ablation was performed, was 82 +/- 19 msec (74 +/- 17 msec with success and 99 +/- 19 msec with failure).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

[Phonomechanography].

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Carotid Arteries↗