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As an independent risk factor, UCMS reproduced the endothelial alterations observed in depression but was not sufficient to provoke morphological alterations.

A case of bilateral progressive stenosis of both external auditory canals with resultant conductive hearing loss is presented. The stenosis revealed multifocal erosive and synechiant lichen planus. To our knowledge, this is the first reported case of lichen planus involvement of the external ear.

-We aimed to assess the accuracy of Doppler tissue imaging (DTI) in detecting right ventricle (RV) dysfunction and electromechanical coupling alteration following pulmonary hypertension (PHT) in rat. PHT was induced by chronic hypoxia exposure (hypoxic PHT) or monocrotaline treatment (monocrotaline PHT). In both PHT models, we observed transparietal RV pressure increase and remodeling, including hypertrophy and dilation. Conventional echocardiography provided evidence for pulmonary outflow impairment with midsystolic notch and acceleration time decrease in PHT groups (21.7 Ϯ 1.6 and 13.2 Ϯ 2.9 ms in hypoxic and monocrotaline PHT groups vs. 28.1 Ϯ 1.0 ms in control). RV shortening fraction was decreased in the monocrotaline PHT group compared with the hypoxic PHT and control groups. Combining conventional Doppler and DTI was more helpful to detect RV diastolic dysfunction in the monocrotaline PHT group (E/Ea ratio ϭ 17.0 Ϯ 1.4) compared with the hypoxic PHT and control groups (11.5 Ϯ 0.7 and 10.2 Ϯ 0.4, respectively). Tei index measured using DTI highlighted global RV dysfunction in the monocrotaline PHT group (1.36 Ϯ 0.24 vs. 0.92 Ϯ 0.05 and 0.86 Ϯ 0.05 in the hypoxic PHT and control groups, respectively). Q-S m time measured from the onset of Q wave to the onset of DTI S m wave was increased in both PHT groups. PHT-induced electromechanical coupling alteration was confirmed by in vitro activation-contraction delay measurements on isolated RV papillary muscle, and both Q-S m time and activation-contraction delay were correlated with PHT severity. We demonstrated that Q-Sm time measured in DTI was an easily and convenient index to detect early RV electromechanical coupling alteration in both moderate and severe PHT. echocardiography; hypertrophy; right ventricular remodeling CHRONIC ALVEOLAR HYPOXIA, which often occurs in patients suffering from chronic obstructive pulmonary diseases, secondarily induces a sustained increase in pulmonary artery resistance. The subsequent pulmonary artery hypertension (PHT) leads to right ventricle (RV) pressure overload and hypertrophy (22).Conventional transthoracic echocardiography is widely used to detect PHT in humans and animal models (14, 18). The standard parameters are the RV free wall thickening recorded in time-motion (TM) mode, the presence of mild-systolic notch, and the acceleration time decrease in the pulmonary outflow spectrum recorded in pulsed-Doppler mode. Nevertheless, a more extensive assessment of PHT-induced RV dysfunction remains difficult using conventional echocardiography. Indeed, accuracy of RV systolic and diastolic functions assessment is limited by complex anatomy and geometry of the ventricle.The Tei index, which combines both systolic and diastolic parameters, was suggested to determine global myocardial performance (27). It has been used in the assessment of RV dysfunction, especially in PHT (26). In conventional pulsed Doppler, the Tei index derives from both isovolumic contraction and relaxation times (IVCT and IVRT) as well as ejection time of...

Exercise training and hypertension induced cardiac hypertrophy but modulate differently left ventricle (LV) function. This study set out to evaluate cardiac adaptations induced by moderate exercise training in normotensive and untreated severe hypertensive rats. Four groups of animals were studied: normotensive (Ctl) and severe hypertensive (HT) Wistar rats were assigned to be sedentary (Sed) or perform a moderate exercise training (Ex) over a 10-wk period. Severe hypertension was induced in rat by a two-kidney, one-clip model. At the end of the training period, hemodynamic parameters and LV morphology and function were assessed using catheterism and conventional pulsed Doppler echocardiography. LV histology was performed to study fibrosis infiltrations. Severe hypertension increased systolic blood pressure to 202 +/- 9 mmHg and induced pathological hypertrophy (LV hypertrophy index was 0.34 +/- 0.02 vs. 0.44 +/- 0.02 in Ctl-Sed and HT-Sed groups, respectively) with LV relaxation alteration (early-to-atrial wave ratio = 2.02 +/- 0.11 vs. 1.63 +/- 0.12). Blood pressure was not altered by exercise training, but arterial stiffness was reduced in trained hypertensive rats (pulse pressure was 75 +/- 7 vs. 62 +/- 3 mmHg in HT-Sed and HT-Ex groups, respectively). Exercise training induced eccentric hypertrophy in both Ex groups by increasing LV cavity without alteration of LV systolic function. However, LV hypertrophy index was significantly decreased in normotensive rats only (0.34 +/- 0.02 vs. 0.30 +/- 0.02 in Ctl-Sed and Ctl-Ex groups, respectively). Moreover, exercise training improved LV passive filling in Ctl-Ex rats but not in Ht-Ex rats. In this study, exercise training did not reduce blood pressure and induced an additional physiological hypertrophy in untreated HT rats, which was slightly blunted when compared with Ctl rats. However, cardiac function was not worsened by exercise training.