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.