The European Respiratory Society and European Society of Thoracic Surgeons clinical guidelines for evaluating fitness for radical treatment (surgery and chemoradiotherapy) in patients with lung cancer

The European Respiratory Society (ERS) and the European Society of Thoracic Surgeons (ESTS) established a joint task force with the purpose to develop clinical evidence-based guidelines on evaluation of fitness for radical therapy in patients with lung cancer. The following topics were discussed, and are summarized in the final report along with graded recommendations: Cardiologic evaluation before lung resection; lung function tests and exercise tests (limitations of ppoFEV1; DLCO: systematic or selective?; split function studies; exercise tests: systematic; low-tech exercise tests; cardiopulmonary (high tech) exercise tests); future trends in preoperative work-up; physiotherapy/rehabilitation and smoking cessation; scoring systems; advanced care management (ICU/HDU); quality of life in patients submitted to radical treatment; combined cancer surgery and lung volume reduction surgery; compromised parenchymal sparing resections and minimally invasive techniques: the balance between oncological radicality and functional reserve; neoadjuvant chemotherapy and complications; definitive chemo and radiotherapy: functional selection criteria and definition of risk; should surgical criteria be re-calibrated for radiotherapy?; the patient at prohibitive surgical risk: alternatives to surgery; who should treat thoracic patients and where these patients should be treated

Retentissement musculaire cardiaque et périphérique de l'hypertension artérielle pulmonaire induite par la monocrotaline chez le rat (dysfonction mitochondriale et effet de l'exercice excentrique)

Dans un premier temps, nous avons observé la chronologie des altérations de la biogenèse et de la fonction mitochondriale dans les ventricules droit (VD) et gauche (VG) et le muscle gastrocnémien (GAS) dans un modèle animal d hypertension artérielle pulmonaire (HTAP). Nous avons constaté une diminution précoce des facteurs impliqués dans la biogénèse mitochondriale du GAS. Plus tard, les mêmes anomalies apparaissaient dans le VD. Au stade décompensé de l insuffisance cardiaque droite s ajoutaient une diminution de la protéine PGC-1 , de l activité de la citrate-synthase et de la respiration mitochondriale. L expression des ARNm et la respiration mitochondriale du VG n étaient pas modifiées de façon significative.Dans un deuxième temps, nous avons étudié l effet de l entraînement en mode excentrique sur le même modèle d HTAP. La survie des rats entraînés n était pas différente de celle des rats sédentaires et la tolérance hémodynamique évaluée par échocardiographie et cathétérisme cardiaque a été bonne. Le bénéfice de l entraînement s est traduit par une augmentation de la vitesse maximale de course dans les deux groupes entraînés, malades et témoins.We assessed the time courses of mitochondrial biogenesis factors and respiration in the right ventricle (RV), gastrocnemius (GAS) and left ventricle (LV) in a model of pulmonary-hypertensive (PH) rats induced by monocrotaline (MT). The expression of the studied genes was decreased early in the MT GAS. At 4 weeks, the MT GAS and MT RV showed decreased mRNA levels whatever the stage of disease, but PGC-1 protein and citrate-synthase activity were significantly reduced only atthe decompensated stage. The functional result was a significant fall in mitochondrial respiration at the decompensated stage in the RV and GAS. The mRNA expression and mitochondrial respiration were not significantly modified in the MT LV. Secondly, we assessed the effects of eccentric exercise training (ECCt) in MT rats with PH. ECCt was initiated 2 weeks after MT injection for 4 weeks. The trained MT rats survival was not different from that of sedentary rats. ECCt was not detrimental on hemodynamic condition estimated by echocardiography and right heart catheterization. Maximal speed significantly increased in trained rats. The mRNA expression of mitochondrial biogenesis factors were not significantly modified in skeletal muscle and in RV.STRASBOURG-Bib.electronique 063 (674829902) / SudocSudocFranceF

LE SYSTEME RENINE-ANGIOTENSINE-ALDOSTERONE AU COURS DU CYCLE VEILLE-SOMMEIL

STRASBOURG-Sc. et Techniques (674822102) / SudocSudocFranceF

Lung segmentectomy: does it offer a real functional benefit over lobectomy?

Anatomical segmentectomy has been developed to offer better pulmonary function preservation than lobectomy, in stage IA lung cancer. Despite the retrospective nature of most of the studies and the lack of randomised studies, a substantial body of literature today allows us to evaluate to what extent lung function decreases after segmentectomy and whether segmentectomy offers a real functional benefit over lobectomy. From the available series, it emerges that the mean decrease in forced expiratory volume in 1 s (FEV1) is low, ranging from −9% to −24% of the initial value within 2 months and −3 to −13% 12 months after segmentectomy. This reduction in lung function is significantly lower than that induced by lobectomy, but saves only a few per cent of pre-operative FEV1. Moreover, the published results do not firmly establish the functional benefit of segmentectomy over lobectomy in patients with poor lung function. Some issues remain to be addressed, including whether video-assisted thoracic surgery (VATS) segmentectomy may preserve lung function better than VATS lobectomy in patients with poor lung function, especially within the early days after surgery, and whether this may translate to lowering the functional limit for surgery. Eventually, trials comparing stereotactic ablative body radiotherapy, radiofrequency ablation and segmentectomy functional consequences are warranted

Does functional evaluation before lung cancer surgery need reappraisal?

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Comment optimiser le bilan d'opérabilité

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The Endocrine Function of the Heart: Physiology and Involvements of Natriuretic Peptides and Cyclic Nucleotide Phosphodiesterases in Heart Failure

Besides pumping, the heart participates in hydro-sodium homeostasis and systemic blood pressure regulation through its endocrine function mainly represented by the large family of natriuretic peptides (NPs), including essentially atrial natriuretic (ANP) and brain natriuretic peptides (BNP). Under normal conditions, these peptides are synthesized in response to atrial cardiomyocyte stretch, increase natriuresis, diuresis, and vascular permeability through binding of the second intracellular messenger’s guanosine 3′,5′-cyclic monophosphate (cGMP) to specific receptors. During heart failure (HF), the beneficial effects of the enhanced cardiac hormones secretion are reduced, in connection with renal resistance to NP. In addition, there is a BNP paradox characterized by a physiological inefficiency of the BNP forms assayed by current methods. In this context, it appears interesting to improve the efficiency of the cardiac natriuretic system by inhibiting cyclic nucleotide phosphodiesterases, responsible for the degradation of cGMP. Recent data support such a therapeutic approach which can improve the quality of life and the prognosis of patients with HF

Maximal aerobic capacity in ageing subjects: actual measurements versus predicted values

We evaluated the impact of selection of reference values on the categorisation of measured maximal oxygen consumption (V′O2peak) as “normal” or “abnormal” in an ageing population. We compared measured V′O2peak with predicted values and the lower limit of normal (LLN) calculated with five equations. 99 (58 males and 41 females) disease-free subjects aged ≥70 years completed an incremental maximal exercise test on a cycle ergometer. Mean V′O2peak was 1.88 L·min−1 in men and 1.26 L·min−1 in women. V′O2peak ranged from 89% to 108% of predicted in men, and from 88% to 164% of predicted in women, depending on the reference equation used. The proportion of subjects below the LLN ranged from 5% to 14% in men and 0–22% in women, depending on the reference equation. The LLN was lacking in one study, and was unsuitable for women in another. Most LLNs ranged between 53% and 73% of predicted. Therefore, choosing an 80% cut-off leads to overestimation of the proportion of “abnormal” subjects. To conclude, the proportion of subjects aged ≥70 years with a “low” V′O2peak differs markedly according to the chosen reference equations. In clinical practice, it is still relevant to test a sample of healthy volunteers and select the reference equations that better characterise this sample

Targeting Mitochondrial Dynamics during Lower-Limb Ischemia Reperfusion in Young and Old Mice: Effect of Mitochondrial Fission Inhibitor-1 (mDivi-1)

Peripheral arterial disease (PAD) strikes more than 200 million people worldwide and has a severe prognosis by potentially leading to limb amputation and/or death, particularly in older patients. Skeletal muscle mitochondrial dysfunctions and oxidative stress play major roles in this disease in relation with ischemia-reperfusion (IR) cycles. Mitochondrial dynamics through impairment of fission–fusion balance may contribute to skeletal muscle pathophysiology, but no data were reported in the setting of lower-limb IR despite the need for new therapeutic options. We, therefore, investigated the potential protective effect of mitochondrial division inhibitor-1 (mDivi-1; 50 mg/kg) in young (23 weeks) and old (83 weeks) mice submitted to two-hour ischemia followed by two-hour reperfusion on systemic lactate, muscle mitochondrial respiration and calcium retention capacity, and on transcripts specific for oxidative stress and mitochondrial dynamics. At the systemic levels, an IR-related increase in circulating lactate was still major despite mDivi-1 use (+305.9% p p p p p p = 0.09, respectively) were not corrected by mDivi-1 preconditioning, whatever the age. Further, mDivi-1 treatment did not oppose superoxide anion production (+71.4% p p < 0.05, respectively). At the transcript level, markers of antioxidant enzymes (SOD 1, SOD 2, catalase, and GPx) and fission markers (Drp1, Fis) remained unchanged or tended to be decreased in the ischemic leg. Fusion markers such as mitofusin 1 or 2 decreased significantly after IR in both groups. In conclusion, aging enhanced the deleterious effects or IR on muscle mitochondrial respiration, and in this setting of lower-limb IR, mDivi-1 failed to protect the skeletal muscle both in young and old mice