Answer please. Femoral head and acetabulum fractures associated with a posterior hip dislocation--Pipken 4.
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Biomedical subjects
Publications and source records attributed to A Avolio.
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AIM: To determine the effects of wave reflection on the increase in arterial pressure that occurs with age and its association with concomitant changes in both the magnitude and contour of the arterial pressure pulse. RESULTS OF DATA SURVEY: While age-related changes in mean pressure are similar in central and peripheral arteries, changes in pulse pressure and pulse waveform features are different. Because of the specific architectural, geometrical and elastic properties of the arterial vasculature, wave reflection plays an important role in determining peak pressure, the value usually specified as systolic pressure. While the late systolic increase usually determines peak systolic pressure in the central aorta, it is not necessarily related to the peak pressure in the periphery. Peak pressure depends on the timing and intensity of wave reflection, which is a function of the state of the peripheral microvasculature and the elastic properties of the large conduit arteries. Ageing causes changes in both the terminal and central vasculature, so that the intensity of the wave reflection and the transmission properties of arteries affect the arterial pulse to different degrees. Therefore, age-related changes that are observed in the central pressure pulse are different from those observed in the pulse when measured in a limb. Thus the contribution of wave reflection to the determination of peak arterial pressure is not the same at all locations. CONCLUSIONS: These findings have profound implications for therapeutic strategies aimed at altering systolic pressure and for a proper assessment of the alteration in cardiac load that occurs with age or with antihypertensive therapy, when measurements are taken in a limb.
Recorded here is a comprehensive review of the current literature on high tibial osteotomy with emphasis on postponing an inevitable total knee arthroplasty (TKA). Accompanying this review is a confirmatory, retrospective study of 35 patients with 39 high tibial osteotomies with an average follow-up study of 8.5 years (range, 3.8-15.1 years). Twenty-two of the patients (57%) had good results, seven (18%) fair, and ten (25%) poor at final follow-up examination. Nine of the 35 patients required TKA at an average of 4.7 years post-osteotomy. The percentage of good results diminished with time of follow-up study, starting at two years with 87% good results and ending at 15 years with only 57% of the patients remaining in that category. Patients lost an average of 8 degrees of flexion post-osteotomy, regardless of good, fair, or poor result. Patients with favorable results were usually younger than 60 years of age, and had less than 12 degrees of angular deformity, pure unicompartmental disease, ligamentous stability, and a preoperative range of motion are of at least 90 degrees.
Healthy kangaroos are prone to sudden death. To investigate possible causes of this phenomenon, echocardiographic and electrocardiographic studies were conducted in seven healthy sedated (intramuscular ketamine 20 mg/kg, xylazine 2 mg/kg) kangaroos aged 1.5-5 years weighing 5.5-48 kg. As in human hypertrophic cardiomyopathy, kangaroos showed relative left ventricular hypertrophy measured as a ratio of (internal left ventricular end-diastolic diameter)/(septal + posterior wall thickness): 1.7 (SD 0.2) in kangaroos and 1.3 (SD 0.4) in hypertrophic cardiomyopathy cf 2.6 (SD 0.6) in normal man (p less than 0.001 respectively). Peak left ventricular diastolic filling velocity was smaller in kangaroos (2.6 (SD 0.3)/sec) and hypertrophic cardiomyopathy (3.3 (SD 0.7)/sec) than in normal man (4.1 (SD 1.0)/sec) (p less than 0.01, p less than 0.05). The end of T wave occurred earlier than the closing of aortic valve. Corrected QT interval (0.20 (SD 0.02) sec) was shorter than the normal value for man (0.34-0.40 sec). In conclusion, kangaroos have cardiac hypertrophy of unknown aetiology, with impaired diastolic function, as in non-obstructive hypertrophic cardiomyopathy patients. Corrected QT interval was short. These echocardiographic and electrocardiographic findings may explain the mechanism of sudden death in kangaroos, a species which may be used as an experimental model of non-obstructive hypertrophic cardiomyopathy in man.
Arterial pressure waves were recorded noninvasively from the carotid, radial, femoral, or all three of these arteries of 1,005 normal subjects, aged 2-91 years, using a new transcutaneous tonometer containing a high fidelity Millar micromanometer. Waves were ensemble-averaged into age-decade groups. Characteristic changes were noted with increasing age. In all sites, pulse amplitude increased with advancing age (carotid, 91.3%; radial 67.5%; femoral, 50.1% from first to eighth decade), diastolic decay steepened, and diastolic waves became less prominent. In the carotid pulse, there was, in youth, a second peak on the downstroke of the waves in late systole. After the third decade, this second peak rose with age to merge with and dominate the initial rise. In the radial pulse, a late systolic wave was also apparent, but this occurred later; with age, this second peak rose but not above the initial rise in early systole, even at the eighth decade. In the femoral artery, there was a single systolic wave at all ages. Aging changes in the arterial pulse are explicable on the basis of both an increase in arterial stiffness with increased pulse-wave velocity and progressively earlier wave reflection. These two factors may be separated and effects of the latter measured from pressure wave-contour analysis using an "augmentation index," determined by a computer algorithm developed from invasive pressure and flow data. Changes in peak pressure in the central (carotid) artery show increasing cardiac afterload with increasing age in a normal population; this can account for the cardiac hypertrophy that occurs with advancing age (even as other organs atrophy) and the predisposition to cardiac failure in the elderly. Identification of mechanisms responsible offers a new approach to reduction of left ventricular afterload.
We compared dilevalol (an isomer of labetalol), 200-400 mg daily, against atenolol, 50-100 mg daily, in a double-blind, crossover, placebo-controlled trial with respect to effects on arterial distensibility (measured as pulse wave velocity [PWV]) and wave reflection (assessed from carotid pressure wave contour). Twelve patients of mean age 58 years (range 44-73 years) with essential hypertension (supine diastolic blood pressure 95-114 mm Hg) took active therapy for 12 weeks, separated by a 2-4 week placebo period. Carotid pressure waveforms were recorded noninvasively by applanation tonometry with a Millar micromanometer-tipped probe. PWV was measured between carotid and femoral arteries (aortic PWV), carotid and radial arteries (arm PWV), and femoral and pedal arteries (leg PWV). Early wave reflection was calculated from the ratio of the height of the peak of the carotid wave above its shoulder to the pulse pressure and was expressed as an augmentation index. Both drugs were equally effective in reducing brachial sphygmomanometric pressure and PWV in all three regions (active vs. placebo, p less than 0.001), but there was no significant difference between the two active therapies. However, the augmentation index (averaged during the treatment period) was significantly lower with dilevalol (19%) than with atenolol (28%, p less than 0.01), corresponding to a greater decrease of 5-8 mm Hg in carotid systolic pressure compared with the brachial artery. Although both drugs were equally effective in reducing arterial distensibility, the vasodilating action of dilevalol gave added benefit in reducing wave reflection, presumably through its vasodilatory effect on peripheral conduit arteries.
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Effects of sublingual glyceryl trinitrate (GTN) were studied in ten patients without heart failure during diagnostic cardiac catheterisation following angiography. GTN caused substantial reduction in peak left ventricular and aortic pressure (19 mmHg) with lesser reduction in mean aortic pressure (9 mmHg) and no change in diastolic aortic pressure. Reduction in stroke volume (by 15%), associated with fall in left ventricular end diastolic pressure (by 4 mmHg) was insufficient to explain the marked (17 mmHg - 34%) reduction in pulse pressure. Decrease in pulse pressure was associated with loss of the late systolic peak on both the aortic and left ventricular pressure wave. This peak is caused by pulse wave reflection. GTN caused no change in peripheral resistance or in indices of aortic compliance (characteristic impedance, total arterial compliance) but was associated with reduction in fluctuations of both modulus and phase of aortic impedance. All these changes in pressure waves and in impedance spectra are explicable on the basis of decreased peripheral wave reflection. This can be attributed to the known vasodilatory effect of GTN on the peripheral arteries. Simulation of arterial vasodilatation in a multi-branched model of the systemic arterial system confirmed this interpretation. Dilatation of peripheral arteries explains in part the beneficial effects of GTN in adult man.
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