Background/aim: In patients with acute central retinal vein occlusion (CRVO), dynamic angiographymay reveal the presence of pulsatile flow (termed here pulsat ile venular outflow, PVO)-within first order veins (that i...Background/aim: In patients with acute central retinal vein occlusion (CRVO), dynamic angiographymay reveal the presence of pulsatile flow (termed here pulsat ile venular outflow, PVO)-within first order veins (that is, the large veins). The main goal of this study was to investigate the mechanism underlying PVO. Met hods: 10 patients with CRVO and PVO were included. Quantitative and qualitative analysis of venous flow on dynamic angiograms allowed the correlation, temporall y, of second and first order vein flow on the one hand, and venous flow and syst olic cycle on the other. Results: Analysis of the time-velocity curve showed th at (1) the onset of arterial systole preceded the onset of PVO by less than 0.08 seconds (n=5); (2) PVO onsetwas simultaneous to the time of onset of minimal fl ow (Vmin) in first order veins (n=10); (3) the time of onset of maximal flow (Vm ax) in first order veins occurred 0.20-0.44 seconds after the onset of PVO (n=6 ). Conclusions: During CRVO with severe reduction in blood flow, the presence of PVO is the result of the existence of a distinct haemodynamic regimen in first and second order veins. These data support the hypothesis that second order vein s flow is synchronous with the arterial flow, while the delayed peak flow in fir st order veins may reflect the consequences of the delayed IOP curve and/or of i ntermittent venous compression.展开更多
Background-Factors leading differentially to the development of isolated diastolic(IDH), systolic-diastolic(SDH), and isolated systolic(ISH) hypertension are poorly understood. We examined the relations of blood press...Background-Factors leading differentially to the development of isolated diastolic(IDH), systolic-diastolic(SDH), and isolated systolic(ISH) hypertension are poorly understood. We examined the relations of blood pressure(BP) and clinical risk factors to the new onset of the 3 forms of hypertension. Methods and Results-Participants in the Framingham Heart Study were included if they had undergone 2 biennial examinations between 1953 and 1957 and were free of antihypertensive therapy and cardiovascular disease. Compared with optimal BP(SBP< 120 and DBP< 80 mm Hg), the adjusted hazard ratios(HRs) for developing new-onset IDH over the ensuing 10 years were 2.75 for normal BP, 3.29 for high-normal BP(both P< 0.0001), 1.31(P=0.40) for SDH, and 0.61(P=0.36) for ISH. The HRs of developing new-onset SDH were 3.32, 7.96, 7.10, and 23.12 for the normal BP, high-normal BP, ISH, and IDH groups, respectively(all P< 0.0001). The HRs of developing ISH were 3.26 for normal and 4.82 for high-normal BP(both P< 0.0001), 1.39(P=0.24) for IDH, and 1.69(P< 0.01) for SDH. Increased body mass index(BMI) during follow-up predicted new-onset IDH and SDH. Other predictors of IDH were younger age,male sex, and BMI at baseline. Predictors of ISH included older age, female sex, and increased BMI during follow-up. Conclusion-Given the propensity for increased baseline BMI and weight gain to predict new-onset IDH and the high probability of IDH to transition to SDH, it is likely that IDH is not a benign condition. ISH arises more commonly from normal and high-normal BP than from “burned-out”diastolic hypertension.展开更多
文摘Background/aim: In patients with acute central retinal vein occlusion (CRVO), dynamic angiographymay reveal the presence of pulsatile flow (termed here pulsat ile venular outflow, PVO)-within first order veins (that is, the large veins). The main goal of this study was to investigate the mechanism underlying PVO. Met hods: 10 patients with CRVO and PVO were included. Quantitative and qualitative analysis of venous flow on dynamic angiograms allowed the correlation, temporall y, of second and first order vein flow on the one hand, and venous flow and syst olic cycle on the other. Results: Analysis of the time-velocity curve showed th at (1) the onset of arterial systole preceded the onset of PVO by less than 0.08 seconds (n=5); (2) PVO onsetwas simultaneous to the time of onset of minimal fl ow (Vmin) in first order veins (n=10); (3) the time of onset of maximal flow (Vm ax) in first order veins occurred 0.20-0.44 seconds after the onset of PVO (n=6 ). Conclusions: During CRVO with severe reduction in blood flow, the presence of PVO is the result of the existence of a distinct haemodynamic regimen in first and second order veins. These data support the hypothesis that second order vein s flow is synchronous with the arterial flow, while the delayed peak flow in fir st order veins may reflect the consequences of the delayed IOP curve and/or of i ntermittent venous compression.
文摘Background-Factors leading differentially to the development of isolated diastolic(IDH), systolic-diastolic(SDH), and isolated systolic(ISH) hypertension are poorly understood. We examined the relations of blood pressure(BP) and clinical risk factors to the new onset of the 3 forms of hypertension. Methods and Results-Participants in the Framingham Heart Study were included if they had undergone 2 biennial examinations between 1953 and 1957 and were free of antihypertensive therapy and cardiovascular disease. Compared with optimal BP(SBP< 120 and DBP< 80 mm Hg), the adjusted hazard ratios(HRs) for developing new-onset IDH over the ensuing 10 years were 2.75 for normal BP, 3.29 for high-normal BP(both P< 0.0001), 1.31(P=0.40) for SDH, and 0.61(P=0.36) for ISH. The HRs of developing new-onset SDH were 3.32, 7.96, 7.10, and 23.12 for the normal BP, high-normal BP, ISH, and IDH groups, respectively(all P< 0.0001). The HRs of developing ISH were 3.26 for normal and 4.82 for high-normal BP(both P< 0.0001), 1.39(P=0.24) for IDH, and 1.69(P< 0.01) for SDH. Increased body mass index(BMI) during follow-up predicted new-onset IDH and SDH. Other predictors of IDH were younger age,male sex, and BMI at baseline. Predictors of ISH included older age, female sex, and increased BMI during follow-up. Conclusion-Given the propensity for increased baseline BMI and weight gain to predict new-onset IDH and the high probability of IDH to transition to SDH, it is likely that IDH is not a benign condition. ISH arises more commonly from normal and high-normal BP than from “burned-out”diastolic hypertension.
