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Biomedical subjects

J P Darmon

Publications and source records attributed to J P Darmon.

7 recordsLinked to original sources
PubMed2005

[Arrhythmia and sport].

Sports arrhythmia has gained wide attention with the mediatization of the death of famous sports stars. Sport strongly modifies the structure of the heart with the development of left ventricular hypertrophy which may be difficult to differentiate from that due to doping. Intense training modifies also the resting electrocardiogram with appearance of signs of left ventricular hypertrophy whereas resting sinus bradycardia and atrioventricular conduction disturbances usually reverts upon exertion. Accordingly, arrhythmia may develop ranging from extrasystoles to atrial fibrillation and even sudden death. Recent data suggest that if benign arrhythmia may be the result of the sole intense training and are reversible, malignant ventricular arrhythmia and sudden death mostly occur in unknown structural heart disease. Hypertrophic cardiomyopathy is amongst the most frequent post mortem diagnosis in this situation. Doping is now present in many sports and further threatens the athlete in the safe practice of sport.

Arrhythmias, Cardiac↗
PubMed2004

[New concepts in the diagnosis and treatment of atrial flutter].

Atrial flutter may now be very frequently and definitely cured in a single session of radiofrequency ablation. However, the very name of atrial flutter gives rise to a certain confusion. Clinical experience from everyday activity in ablation laboratories, especially since the introduction of new mapping techniques, has shown that this entity is in fact multiple. Flutters may be classified by their electrocardiographic appearance and/or their electrophysiological mechanism with as many prognostic as therapeutic implications. This article reviews diagnostic features of typical and atypical flutter and the different treatments which may be proposed in different clinical situations.

Atrial Flutter↗
PubMed2004

[Sinus-like tachycardias].

Various tachycardias presenting with positive P waves in the standard leads are described in this article. Sinus tachycardia may occur as a normal adaptation reaction to the environment or in the setting of autonomic dysregulation. It may also be mimicked by various arrhythmias which share the earliest depolarisation in the sinus node area. The authors expose a review of these mechanisms.

Electrocardiography↗
PubMed1992

[Determination of the anaerobic threshold in chronic cardiac failure. Value and limitations].

Anaerobic threshold was studied in 35 patients with cardiac failure present for more than 6 months, of primary or ischemic origin and New York Heart Association Stage II or III. Each patient underwent an exercise test of ergometric bicycle (increments of 10 watts/1 minute) with analysis of expired gases respiratory cycle by respiratory cycle (oxygen consumption, carbon dioxide production, respiratory oxygen and carbon dioxide equivalent, respiratory quotient). Anaerobic threshold was determined indirectly following Wasserman's recommendations. It was possible to determine anaerobic threshold in 25 patients (83.3%). The test was well tolerated. The two best methods for detection of anaerobic threshold were divergence of the curve of production of carbon dioxide in relation to oxygen consumption and an increase in respiratory oxygen equivalent while the carbon dioxide equivalent remained constant. In addition, oxygen consumption at the anaerobic threshold was statistically correlated with functional class (p < 0.05) and with the Weber classification based upon peak oxygen consumption (p < 0.001). Finally, anaerobic threshold occurred on average at 5.4 +/- 1.8 min from the start of exercise with a heart rate of 119.7 +/- 18 bpm, an oxygen consumption of 10.5 +/- 2.3 ml/min/kg (i.e. 43.2 +/- 12.1% of maximum oxygen consumption and 70.5 +/- 19.3% of oxygen consumption limited by symptoms) and a respiratory quotient of 1.07 +/- 0.08. In conclusion, analysis of respiratory gases during exercise in cardiac failure patients enables, with sub-maximal exercise and noninvasively, the determination in the majority of cases of anaerobic threshold, which is statistically correlated with New York Heart Association stage and the Weber classification based upon oxygen consumption at peak effort.

Adult↗
PubMed1992

[Cardiac toxicity of fluoro-uracil. Typical and atypical aspects. Apropos of 8 cases].

The cardiac toxicity of 5 fluoro-uracil, an antimitotic agent widely used in various protocols, has been known for 16 years. Several cases have been reported in the literature, leading to the suggestion, without formal evidence, that the chief mechanism responsible for this cardiac toxicity is "classical" coronary spasm. However, certain clinical aspects already described may shed doubt on this theory. On the basis of 8 cases, the authors report different clinical pictures all caused by cardiac toxicity of 5FU. It is of interest to note that chest pain with the classically described electrocardiographic changes did not apply in the majority of cases. The commonest pattern was asymptomatic electrocardiographic abnormalities and/or arrhythmias without angina. Among the reported cases, one patient had pain with electrocardiographic abnormalities, recurrent after the withdrawal of 5FU and resistant to maximal medical treatment, despite the absence of any coronary disease or signs of spasm. One patient had a first myocardial infarction, later rechallenge with the drug resulting in failure. In another patient, with known coronary disease, 5FU probably cause cardiogenic shock. In total, some of our cases, as well as other features described in the literature, raise questions as to the pathophysiology of the cardiac toxicity of 5FU.

Adult↗
PubMed1991

[Prognostic factors of cardiac insufficiency: value of functional exercise capacity. Maximal oxygen consumption, anaerobic threshold].

This study concerned 43 patients with chronic cardiac failure. Twenty two patients had primary dilated cardiomyopathy and twenty one had ischaemic cardiomyopathy. Fifteen patients were in the NYHA functional Class II, 20 in Class III and 8 in Class IV. The parameters studied during a bicycle ergometric exercise stress test were the developed power (W), the duration (in seconds), the peak VO2 (in ml/kg/min), the anaerobic threshold (ml/kg/min) and pulse O2 (ml/beat). The ejection fraction and end systolic and end diastolic volumes were evaluated by M mode echocardiography. The results of the precited investigations were compared in survivors and patients who died. After 15 months, 7 patients had died and 36 survived, six of the patients who died were in NYHA Class IV. The peak VO2 was 10.1 ml/kg, the anaerobic threshold was 8.5 ml/kg and pulse 02 6.1 ml/beat in the patients who died compared to 17.6 ml/kg (p less than 0.001), 14.5 ml/kg (p less than 0.001) and 9 ml/beat (p less than 0.01) in the survivors. In addition, the ejection fraction was significantly lower in patients who died (24.7 +/- 8.3 versus 35.5 +/- 7.4%, p less than 0.001). Exercise capacity was therefore a predictive factor of mortality in cardiac failure. It is more discriminating than biological parameters such as natremia and serum adrenaline concentrations. However, these exercise stress parameters (VO2, anaerobic threshold) provide little complementary information with respect to the NYHA Classification in this study.

Adult↗