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Biomedical subjects

D Lamaison

Publications and source records attributed to D Lamaison.

At least 19 recordsLinked to original sources
PubMed1993

[Antiarrhythmic treatments of permanent atrial fibrillation].

The treatment of chronic atrial fibrillation has 3 different objectives: the control of the ventricular rate, the attempts to restore sinus rhythm, and the prevention of arrhythmia recurrences. Digitalis compounds, beta-adrenergic antagonists and calcium-channel blocking agents can be used to achieve reduction of the ventricular response, in recent-onset arrhythmia with rapid heart rate, and for long-term rate control in patients who cannot be converted to sinus rhythm. In some of them, a combination of 2 of these drugs is needed to slow the ventricular rate, at rest and on exertion. Sinus rhythm can be restored by direct-current cardioversion or by using various regimens of amiodarone, a type III antiarrhythmic drug, given orally or intravenously. Cardioversion might also be accomplished by type IA and IC antiarrhythmic drugs, including quinidine, flecainide and propafenone. However, proarrhythmic effects and haemodynamic deterioration are a major concern with these compounds. On the other hand the best indication of type IA and IC antiarrhythmic drugs is the control of arrhythmia recurrences; beta-blocking agents are highly effective in patients with a high sympathetic tone or hypertrophic cardiomyopathy. Finally the widespread use of amiodarone should be limited by its non-cardiac toxicity. Whatever the drug employed in the treatment of atrial fibrillation, monitoring the inotropic effect of the drug and the effect on cardiac conduction is mandatory.

Anti-Arrhythmia Agents↗
PubMed1991

Collective human food poisonings by clenbuterol residues in veal liver.

Twenty-two patients were reported to complain of tremor, headaches, tachycardia and dizziness 1-3 h after eating veal liver. As clinical symptoms were not suggestive of an infectious cause, the presence of veterinary drug residues was suspected. Clenbuterol, a beta 2-agonist, was being illegally used in cattle because of its anabolizing properties and may explain the observed effects. Assays of clenbuterol in samples of veal liver showed concentrations of 0.375 and 0.500 micrograms/g. To our knowledge, this is one of the first reports of clinical symptoms in humans associated with the consumption of veterinary drug residue-containing food.

Animals↗
PubMed1990

[General physiopathology of chronic left ventricular insufficiency].

The failing heart is unable to provide some organs, notably the brain and the myocardium, with the amount of blood flow they require. To this myocardial inadequacy and resulting "circulatory insufficient" the body reacts by setting in action compensatory mechanisms which are "intracardiac" first (Starling's heterometric regulation, ventricular hypertrophy), then neurohormonal, with the activation of vasoconstrictor systems (noradrenergic system, renin-angiotensin-aldosterone system, arginine-vasopressin system) counterbalanced by the activation of vasodilator systems (vasodilator prostaglandins, atrial natriuretic factor and kinins). However, the vasoconstrictor systems outweigh the vasodilator systems. They create an excessive arterial and venous vasoconstriction, together with water-and-salt retention, which leads to an increase of left ventricular work during both systole and diastole and to a gradual worsening of the heart failure. The present-day treatment of heart failure aims at reducing the water-and-salt retention and at restoring the balance between the vasoconstrictor and vasodilator systems.

Cardiomegaly↗
PubMed1990

[Potassium cyanide poisoning treated with hydroxocobalamin].

A fifteen-year-old girl, with a clean medical history, was admitted to the intensive care unit 90 minutes after ingestion of 2.5 g potassium cyanide. She had typical signs of severe cyanide poisoning including deep coma, circulatory failure, and major metabolic acidosis. Gastric lavage and antidotal treatment with 4 g hydroxocobalamin and 8 g sodium hyposulfite was administered without delay together with supportive treatment consisting of mechanical ventilation with FIO2, blood alkalinisation and administration of beta-stimulants. These measures led to a rapid clinical improvement. The ventilatory support was discontinued after 24 hours and the patient left the intensive care unit on the fourth day with only slightly impaired mental status. She survived despite a very high blood cyanide concentration (494 mumol.l-1 on admission) probably because of the rapid symptomatic and antidotal treatment.

Acidosis↗
PubMed1990

Endless-loop tachycardias: description and first clinical results of a new fully automatic protection algorithm.

Endless-loop tachycardia (ELT) is one of the most common pacemaker mediated tachycardia. An innovative ELT protection algorithm has proven to be clinically effective. A new improved version that will eliminate the need to program any parameter is now under clinical evaluation. Nine patients entered the study: six men and three women, aged 52 +/- 22 years. This automatic algorithm needs only 10 cycles to detect and confirm an ELT. Three hundred thirty-three ELTs lasting more than 9 cycles have been induced and analyzed. The total results are the following: mean duration: 6.7 sec +/- 3.1; mean ELT rate: 137 +/- 21.9 bpm, mean programmed upper rate limit (URL): 142.5 +/- 26.5 bpm (Only 70% of ELTs presented rates equal to programmed URL). (1) ELTs reduced by postventricular atrial refractory period (PVARP) extension on one cycle: 291 ELTs (87%). ELT rate: 128.5 +/- 18.2 bpm. (2) Retrograde block: algorithm operation may induce a retrograde block due to a short atrioventricular delay (AVD) applied during the confirmation phase to discriminate an ELT from a stable sinus rhythm. Thirty-two ELTs (10%) have been reduced and detected on a retrograde block occurrence. (3) Algorithm failure due to an unstable ventriculoatrial conduction time (VACT) even at fixed rate or to a retrograde Wenckebach behavior on AVD reduction during the confirmation phase. A total of 10 algorithms failed to detect or confirm an ELT have been recorded (3%). Mean duration: 8.2 +/- 4.2 sec, mean ELT rate: 148.9 +/- 14.3 bpm. This new fully automatic algorithm has reduced 97% of ELTs, including high rate episodes (100-175 bpm).(ABSTRACT TRUNCATED AT 250 WORDS)

Algorithms↗
PubMed1990

Improved dual chamber pacing mode in paroxysmal atrioventricular conduction disorders.

Dual chamber pacing may sometimes be directly indicated for carotid sinus hypersensitivity, vasovagal syndrome, and certain cases of sinoatrial block and intermittent atrioventricular (AV) block, although AV conduction is dominantly normal. At times of normal AV conduction, competition between ventricular pacing and spontaneous ventricular depolarization may occur, with its adverse hemodynamic effects on ventricular function and unnecessary drainage of pacemaker battery energy. A new mode of stimulation is described, called automatic DDD mode, which functions in 'pseudo-AAI' mode during normal AV conduction and reverts to classical DDD function during episodes of AV blocks. Furthermore, during pseudo-AAI function, the pacemaker measures certain physiological parameters that serve to automatically program certain parameters used in DDD mode. Preliminary clinical evaluation has shown that this new mode functions satisfactorily.

Atrioventricular Node↗
PubMed1988

A new algorithm for a high level of protection against pacemaker-mediated tachycardia.

Pacemaker-mediated tachycardia (PMT) is a well-known complication of DDD pacing. PMT needs a permeable V-A conduction and is usually initiated by a premature ventricular or atrial systole, artifact sensing, or misprogramming (long AV delay [AVD]). Today, protection against PMT is expected from pacemaker multiprogrammability. Unfortunately, this prevention is often ineffective; postventricular atrial refractory period (PVARP) must be prolonged, which limits the upper tracking rate and the patient capacity. The new Chorus ELA Medical DDD pacemaker provides classic protection against PMT (PVARP prolongation after premature V or A complex, magnet application, noise sensing), but also automatically reduces an eventual PMT and adjusts AVD or PVARP for a high level of protection. The process is divided in four steps: (1) a sensing step for 16 cycles, with V-P conduction analysis; (2) confirmation of the presence of the PMT and analysis of V-A conduction time; (3) a termination step, by extending the PVARP after the following ventricular heart beat; and (4) in case of immediate recurrence of the tachycardia, reprogramming of the AVD and eventually of the PVARP. By first reducing AVD, before reprogramming PVARP, the pacemaker preserves point 2:1, providing a higher exercise capacity. This algorithm was successfully tested in three patients who had a permeable V-A conduction, without any adverse effect.

Algorithms↗
PubMed1986

Intracardiac ectopic thyroid.

The case of a patient with an intracardiac ectopic thyroid is reported. A lesion was found in a 25-year-old man and was diagnosed by two-dimensional echocardiography as a right intraventricular tumor. An operation was performed. Histologic and ultrastructural studies showed that the tumor was a thyroid mass. The origin of intracardiac ectopic thyroids is probably to be found in disturbances occurring early in embryogenesis.

Adult↗
PubMed1985

[Fatal poisoning by alcohol-free aniseed aperitif].

A case of chronic poisoning with alcohol-free "pastis" leading to the death of a 32 year old alcoholic patient is reported. The mean daily amount of ingested glycyrrhizinic acid was 0.35 g. "Torsades de pointes" secondary to severe hypokalemia were observed and prolonged cardiac arrest occurred. There was evidence of chronic hypokalemic myopathy and of rhabdomyolysis with acute renal failure. Furthermore, the origin of an associated cardiomyopathy is discussed.

Adult↗
PubMed1982

[Intravenous isosorbide dinitrate in acute cardiac failure (author's transl)].

Isosorbide dinitrate (ISDN) was used by intravenous infusion in 7 patients with acute cardiac failure consecutive to acute (5) or chronic (1) myocardial infarction or to non-obstructive cardiomyopathy (1). Pulmonary artery pressure (PAP), pulmonary capillary pressure (PCP), right atrial pressure (RAP) and cardiac output were measured (PCP), right atrial pressure (RAP) and cardiac output were measured by intracardiac catheterization. The initial dosage of 2.5 mg/hour was increased until PCP was reduced to 15 mmHg or less or until troublesome side-effects developed. Control was achieved in 3 patients with doses of 2.5 to 7 mg/hour and, to a lesser extent, in one patient with up to 20 mg/hour. Three patients failed to respond even to higher doses and needed furosemide i.v. or furosemide + dobutamine. One patient died of cardiogenic shock. No changes in cardiac output, heart rate and blood pressure and no clinical side-effects were recorded. Thus, in acute cardiac failure ISDN may be effective in doses slightly superior to those of nitroglycerin, but increasing the dosage above 7 or 8 mg/hour does not bring additional benefits. The drug is remarkably well tolerated.

Acute Disease↗
PubMed1982

[Hemodynamic effects of intravenous isosorbide dinitrate in chronic heart failure (author's transl)].

During cardiac catheterization, isosorbite dinitrate (ISDN) was given intravenously to ten patients with confirmed left ventricular failure (10 NOMC, 1 ischemic cardiopathy, 1 valvular disease). When the left ventricular filling pressure was above 15 mmHg and the systemic systolic pressure exceeded 100 mmHg, a 500 gamma (first half of patients) or 800 gamma (second half of patients) bolus of ISDN was given intravenously, followed by an infusion of 2.5, 5 or 10 mg ISDN per hour. In all patients, the functional tolerance was excellent ; the heart rate remained unchanged and the systolic systemic pressure decreased only slightly (10 %). Left ventricular filling pressures returned to normal in four patients, decreased significantly in three, and remained unchanged in three. The cardiac output increased significantly in four patients. The poor initial hemodynamic conditions and the doses given, subsequently considered insufficient especially during the first part of the study, probably explain why ISDN was only partly effective.

Cardiac Catheterization↗
PubMed1982

[Myocobacterium tuberculosis endomyocarditis. Apropos of a case in a patient with a mitral valve prosthesis].

A case of lethal cardiac tuberculosis with myocardial and endocardial involvement is reported in a 46 year old man with a Starr-Edwards mitral valve prosthesis inserted two years previously for severe mitral regurgitation, secondary to ruptured chordae of the posterior mitral leaflet. Apart from tuberculous pericarditis, cardiac involvement is extremely rare; it occurs in "tuberculous septicemia" whose characteristic features--tuberculinic anergy, hematological abnormalities especially pancytopenia,--lead to delay in diagnosis, which is usually fatal. The case presented is an example.

Diagnosis, Differential↗
PubMedDate not supplied

[Combination of slow-release diltiazem and a beta-blocker in arterial hypertension. 2 cases of cardiogenic shock with severe bradycardia].

Patient 1 received carteolol and captopril for hypertension. Three days after a slow-release diltiazem preparation (300 mg) had been introduced, he developed cardiogenic shock and sinus bradycardia (heart rate: 30/mn) with acidosis and severe hyperkaliemia. He was successfully treated by temporary pacing and dobutamine. Patient 2 had received sotalol and captopril for several years. Twelve hours after slow release diltiazem had been added, he was found in cardiogenic shock and extreme bradycardia with wide QRS, acidosis and hyperkaliemia. He died one hour later despite intensive emergency treatment. Concomitant use of beta-blockers and calcium channel blockers has been reported in patients suffering of severe coronary heart disease. However, several adverse reactions similar to our cases have been described. Slow-release diltiazem should be avoided in hypertensive patients taking beta-blockers.

Adrenergic beta-Antagonists↗