The effects of chronic increase in aortic blood flow on arterial wall remodeling were investigated in vivo with the use of an aortocaval fistula (ACF) model in rats. Phasic hemodynamics and aortic wall structure upstream and downstream in 30 male Wistar rats with ACF and 30 sham-operated rats were compared immediately and 2 mo after the ACF was opened in anesthetized rats. Opening the ACF upstream acutely decreased aortic pressure (-30%, P < 0.001) and increased aortic blood velocity (x12, P < 0.001), blood flow (x9, P < 0.001), wall shear stress (x10, P < 0.001) and guanosine 3',5'-cyclic monophosphate (cGMP) wall content (+50%, P < 0.01). After 2 mo, aortic pressure decreased (-22%, P < 0.001) and aortic blood velocity, diameter, and blood flow increased (+114%, P < 0.001; +60%, P < 0.001; and +250%, P < 0.001; respectively) compared with the control group. Aortic wall shear stress and cGMP wall content dropped over time and tended to recover control values; aortic wall tensile stress was higher than in the control group (P < 0.05). Medial cross-sectional area and elastin and collagen contents increased (+38%, P < 0.01; +50%, P < 0.01; and +30%, P < 0.05, respectively) and were associated with smooth muscle cell hypertrophy) (+23%, P < 0.05), despite a decrease in arterial wall thickness (-13%, P < 0.01). Opening the ACF downstream acutely decreased aortic pressure (-30%, P < 0.001) without any change in aortic blood velocity, diameter, blood flow, shear stress, and cGMP wall content. After 2 mo, pressure, blood velocity, shear stress, and cGMP wall content decreased (-22%, P < 0.001; -31%, P < 0.01; -46%, P < 0.02; and -50%, P < 0.05; respectively) and diameter and blood flow were unchanged; smooth muscle cell hypertrophy and hypoplasia were the only observed changes in the aortic wall structure. These results suggest that both shear and tensile stresses are involved in the aortic wall remodeling. Increase in shear stress likely induces expansive remodeling in relation to flow-dependent vasodilation, whereas increase in tensile stress is responsible for medial hypertrophy and fibrosis.

In compensated HF induced by small myocardial infarction, hemodynamics, vascular wall function, and structure are altered in PA but preserved in TA. These results indicate that the pulmonary vascular bed is an early target of regional circulatory alterations in HF.

Background-After mechanical heart valve replacement (MHVR), long-term use of unfractionated heparin is sometimes required because vitamin K antagonists (VKA) are temporarily contraindicated or because the time to reach the target international normalized ratio is long. The aim of this study was to investigate the feasibility of low-molecular-weight heparin treatment in these patients. Methods and Results-This work was conducted as a prospective study. We selected all patients (nϭ695) who underwent MHVR and were transferred to a postoperative cardiac rehabilitation center between January 2000 and January 2005. The study focused on patients who had not yet started VKA therapy or who had a below-target international normalized ratio despite VKA therapy. Unfractionated heparin was replaced by enoxaparin (100 IU/kg BID) until VKA treatment was fully effective. Two hundred fifty patients (60Ϯ11 years old) were enrolled 16Ϯ11 days after surgery (aortic valve replacement, nϭ190; mitral valve replacement, nϭ34; double valve replacement, nϭ26). Of these, 50% had permanent or transient atrial fibrillation, 40% had hypertension, 13% had diabetes, and 19% had a history of cardiac surgery. The mean duration of low-molecular-weight heparin treatment was 8.3Ϯ6.0 days. Patients were followed for 90 days, during which there were two major and three minor bleeding episodes and one transient ischemic attack. There were no cases of valve thrombosis and no deaths. Conclusions-After MHVR, one third of patients leave the cardiac surgery unit before VKA treatment is fully effective.Bridging anticoagulation therapy with enoxaparin appears to be feasible during this high-risk period for thromboembolism and could shorten the length of hospital stay. (Circulation. 2006;113:564-569.)

The Karvonen formula underestimates the heart rate at the anaerobic threshold in beta-blocked patients, which may lead to undertraining of patients with coronary artery disease; we propose another formula more adapted to these patients.

No abstract

We investigated the alteration in flow-dependent-dilatation in the orthostatic intolerance occurring after bed-rest deconditioning. Eight men [aged mean (SEM) 32 (2) years] underwent two consecutive periods of 7 days of head-down-tilt (HDT, -6 degrees) during bed rest. A control age and sex matched group [n = 8, 30 (2) years], maintained its usual physical activity. Blood flow velocity (BFV) and diameter (Doppler and echotracking systems) were measured in the brachial artery, under basal conditions and during the post ischaemic hyperaemia following occlusion. The increase in BFV post-ischaemia did not change before, during and after HDT but the relative increase in the diameter was greater on the 7th day of the HDT period than before HDT [+8.8(1.6)% compared to +3.7(1.0)%, P < 0.001]. After HDT, 11 of 16 standing tests (comprising eight subjects in the two HDT periods) had to be stopped because of orthostatic intolerance. The flow-dependent-dilatation measured at the end of HDT was negatively correlated with the post-bed-rest duration of orthostatic tolerance (r = 0.78, P < 0.01). After the sublingual administration of glyceryl trinitrate, there was no change in the increase in diameter. No significant changes were observed in the control group. Bed-rest deconditioning enhances the flow-dependent vasodilatation of large arteries and might contribute to the orthostatic intolerance observed following bed-rest.

Exercise training performed in cardiac rehabilitation centres is an adjuvant therapy in chronic heart failure patients with left ventricular dysfunction; it decreases the deleterious consequences of chronic heart failure. Exercise training attenuates neurohormonal stimulation, the production of proinflammatory cytokines and natriuretic peptide overexpression. Trained patients showed a significant decrease in the peripheral organ injuries encountered in chronic heart failure, with a reduction in vascular resistance and improvements in endothelial dysfunction and the oxidative capacity of peripheral muscles, without a deleterious effect on left ventricular remodelling. Ultimately, exercise training leads to a notable improvement in ventilatory capacity. These beneficial effects are accompanied by improvements in symptoms at rest, exercise capacity and quality of life. Several training programmes are in current use: exercise training sessions always include endurance exercise performed either at a constant load intensity or with interval training, combining periods of exercise performed at high intensity with periods performed at low intensity. Most of the time, training programmes also include resistance training sessions, which improves large muscle strength. Exercise training programmes seem to have a favourable effect on prognosis, even if the results of Heart Failure: a Controlled Trial Investigating Outcomes of Exercise Training (HF-ACTION) remain controversial, emphasizing the difficulty in monitoring observance and the importance of compliance with a long-term exercise training programme. Patients who do not improve their exercise capacity significantly after an exercise training programme have a poorer prognosis.

Background-Exercise training is established as adjuvant therapy for chronic heart failure, but the prognostic value of improvement in exercise capacity after exercise training has never been evaluated.