It is controversial whether specific tension (the ratio between muscle strength and size) declines with aging. Therefore, contractile muscle volume was estimated separately from the intramuscular noncontractile tissue by magnetic resonance imaging, and maximum isometric torque was measured in the knee extensors and flexors of 10 young (22.8 +/- 5.7 years) and 10 older (69.5 +/- 2.4 years) healthy active women. Specific tension was lower in the older women both in the extensors (93.1 +/- 20.1 kN x m(-2) vs. 112.1 +/- 12.3 kN x m(-2); P < 0.05) and in the flexors (100 +/- 31 kN x m(-2) vs. 142.7 +/- 23.9 kN x m(-2); P < 0.01). This was accompanied by an increase in the percentage coactivation of the knee flexors during knee extension. These data suggest that the lower level of muscle torque in the older women can be explained not only by smaller contractile muscle mass but also by increased coactivation of the antagonist muscles during knee extension.
Magnetic resonance imaging (MRI) can provide accurate anatomical measurements of the cardiac ventricles. This study investigated whether a calculated ventricular mass index (VMI) would provide an accurate means of estimating pulmonary artery pressure noninvasively, and compared the results with conventional Doppler echocardiography and invasive measurement.A total of 26 subjects referred for investigation of pulmonary hypertension were studied by MRI and echocardiography within 2 weeks of cardiac catheterisation. The correlations for mean pulmonary artery pressure were as follows: VMI (ratio of right ventricular mass over left ventricular mass) r=0.81; pulmonary artery systolic pressure (echocardiography) r=0.77. The confidence intervals for the VMI were narrower than for echocardiography. Sensitivity and specificity for pulmonary hypertension were 84 and 71% respectively for the VMI compared with 89 and 57% for echocardiography.The calculated ventricular mass index provides an accurate and practical means of estimating pulmonary artery pressure noninvasively in pulmonary hypertension and may provide a more accurate estimate than Doppler echocardiography. This may be because it reflects the right ventricular response to sustained pulmonary hypertension over a long period and is not influenced by short-term physiological variables affecting echocardiography, such as heart rate, posture, hydration status and oxygen supplementation. Pulmonary arterial hypertension (PAHT) is a rare disorder characterised by high pulmonary vascular resistance. Prognosis is related to mean pulmonary artery pressure (MPAP) measured at right heart catheterisation (RHC) [1], and repeated measurements are often necessary to assess disease progression and the response to treatment. The most widely used noninvasive technique, Doppler echocardiography (ECHO) [2] is safe and widely available, but has several limitations. Firstly, it cannot measure MPAP and only provides an estimate of pulmonary artery systolic pressure (PASP). Secondly, it depends upon the presence of detectable tricuspid regurgitation and has a significant failure rate in some patient groups [3]. Finally, measurements are somewhat operatordependent, and influenced by physiological variables such as heart rate, hydration status and posture, limitations that also affect the accepted gold standard method of RHC [4].Magnetic resonance imaging (MRI) is an attractive modality for studying the complex geometry of the right ventricle and pulmonary vasculature since no assumptions need to be made about the shape or location of the structure being studied. It provides three-dimensional anatomical measurements of right ventricular morphology that are unaffected by physiological variables and more likely to be reproducible than dynamic, planar measurements made at ECHO. Furthermore, these anatomical variables assess the right ventricular response to chronic pulmonary vascular disease and may provide a more clinically relevant assessment of disease severity.MRI has been extensi...
Blood flow velocity was recorded from the middle or anterior cerebral and extracranial internal carotid arteries using transcranial Doppler sonography (TCD) in 121 unselected consecutive patients with acute aneurysmal subarachnoid hemorrhage (SAH). Recordings were made daily or every 2nd day after SAH for a 14-day period. The highest recorded velocity was greater in the 47 patients who developed a delayed ischemic neurological deficit (186 +/- 6 cm sec-1; mean +/- standard error of the mean) than in the 74 patients who did not develop a neurological deficit (149 +/- 5 cm sec-1) (p < 0.001, Mann-Whitney test). Peak velocity recordings can thus assist in the diagnosis of delayed ischemic neurological deficit; however, peak velocity was often recorded only after the onset of neurological deficit. When only those readings made before the onset of neurological deficit were considered, there was no significant difference in peak velocity between the groups (157 +/- 8 cm sec-1 vs. 149 +/- 5 cm sec-1, respectively). Alternative TCD parameters for predicting delayed neurological deficit were therefore sought. The rate of increase in TCD velocity, recorded during the first few days after SAH, was significantly higher in the patients who later developed a neurological deficit. A maximum velocity increase of 65 +/- 5 cm sec-1 per 24-hour period was recorded in patients who later developed a neurological deficit, compared to 47 +/- 3 cm sec-1 24 hrs-1 in patients who did not develop a delayed neurological deficit (p = 0.003). A rise of more than 50 cm sec-1 24 hrs-1 identifies those patients who are most likely to develop a delayed ischemic neurological deficit after SAH. This can be applied prospectively to individual cases. Serial TCD studies in the early period after SAH are thus of value to identify patients who can be selected for prophylactic therapy, which may prevent or ameliorate development of delayed ischemic neurological deficits.
The predictive value of cranial computed tomography (CT) blood load and serial transcranial Doppler sonography for the development of delayed ischaemic neurological deficit was assessed in 121 patients following subarachnoid haemorrhage. Of the 121 patients, 81 (67%) had thick layers of blood or haematoma, including intraventricular bleeding. The proportion of patients who developed delayed deficit was higher with increasing amounts of subarachnoid blood on the admission CT (51% of 53 cases in Fisher grade 3; 35% of 33 cases in grade 2; 28% of 7 cases in grade 1, P < 0.01). Doppler velocities obtained from readings at least every 2 days following admission were higher in patients with delayed neurological deficit (peak velocity for grade 3 patients 176 +/- 6 cm/s (mean +/- SE), versus grade 2: 164 +/- 7 cm/s; grade 4 149 +/- 9, both P = 0.04, Mann-Whitney). Peak velocity and maximal 24-h rise tended to be higher within different CT grades in patients with a deficit than in those without; this difference was significant for grade 3 patients (P < 0.01). We conclude that a combined approach with CT and Doppler sonography provides greater predictive value for the development of delayed ischaemic neurological deficit than either test considered independently. The value of Doppler sonography may be greatest for patients with Fisher grade 3 blood, in whom the risk of delayed ischaemia is greatest.
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