Significant lower limb arterial obstruction is usually detected by Doppler ankle-brachial pressure index (ABPI) measurement. However, ABPI is non-contributory in cases of diabetic medial sclerosis or calcifications and is unsuitable for the detection of small vessel involvement. Thallium-201, a perfusion agent, is frequently used for the investigation of coronary artery disease, and whole-body (201)Tl scintigraphy (WBS) has also been reported to be useful in the assessment of peripheral artery disease (PAD). Thus, we evaluated the clinical feasibility of simultaneous myocardial and lower limb perfusion assessment. WBS was performed after treadmill exercise and myocardial scintigraphy, and again 4 h later. Calf (201)Tl fractional activities (percentage of whole-body (201)Tl uptake) were calculated. We determined a threshold value of normal post-exercise calf (201)Tl uptake (mean of the (201)Tl fractional uptakes minus 2 SD) in a control group of nine healthy volunteers. We checked its accuracy in a pilot group of 25 diabetic patients with proven PAD. This method permitted the detection of lower limb perfusion abnormalities in 38% of 47 asymptomatic diabetic patients with no evidence of PAD. In conclusion, for asymptomatic diabetic patients, whole-body (201)Tl scintigraphy after a treadmill test seems an efficient method of showing lower limb perfusion abnormalities not detected by ABPI measurement. It allows the evaluation of vascular status with no additional inconvenience for patients when performed after myocardial scintigraphy.
We infused prostacyclin (PGI2) (7.5 ng/kg/min) during 5 h, three times at weekly intervals in 8 patients with Raynaud's phenomenon (RP). In 4 patients, improvement was long-term, more than 90 days after the last infusion (good responders); in 3 patients, improvement was mild, less than 15 days, and in one patient no improvement was observed (poor responders). Clinical response was always accompanied by improvement, although less prolonged, of capillary appearance and/or function, as judged by microscopy and/or hemodynamic tests (pulse volume index; radial artery blood flow). Lastly, increased catabolism of PGI2 seemed to be excluded in poor responders, since no statistical difference in PGI2 metabolism could be observed between the two groups.
Changes in systolic and diastolic blood pressure, heart rate, arterial blood flow and vascular resistance in the arm and in the leg were investigated in 9 healthy volunteers (22-40 years) after oral dosing with bisoprolol 10 mg, propranolol 40 mg, and placebo in a randomized double-blind cross-over study. Arterial blood flow and vascular resistance were determined in brachial and femoral arteries with unimpeded circulation, after exclusion of the hand or foot by placing a tourniquet on the wrist or ankle, and during post-ischaemic hyperaemia. Distal arterial occlusion allows one to isolate a predominantly muscular circulation in the forearm or, to a lesser extent, in the leg. Both active drugs induced a significant fall in heart rate and systolic blood pressure versus placebo with no significant difference between the drugs. Brachial and femoral flow rates were reduced by both drugs probably due to a fall in cardiac output, but the two beta blockers produced different effects on vascular resistance: propranolol significantly increased brachial vascular resistance compared with placebo and bisoprolol, both during unimpeded circulation and during occlusion of the hand by a wrist tourniquet. Bisoprolol had no influence on brachial vascular resistance. Both drugs induced small increases in femoral vascular resistance. The different action on local vascular resistance in the brachial artery territory could be interpreted as the expression of the high beta 1 selectivity of bisoprolol leaving the vascular beta 2 receptors unopposed, whereas non-selective propranolol acts on both beta-adrenoceptor subtypes.
"Raynaud's phenomenon (R.P.) is characterized by a spastic vasoconstriction of hand and/or feet extremities leading to painful ischemic attacks. In the pathogeny of this syndrome the role of a platelet hyperactivation was evidenced. Nevertheless, the responsibility of platelet aggregation remains controversial. We report here the case of a patient presenting with a Glanzmann thrombasthenia defined by the complete lack of platelet aggregation, and showing a typical RP which was confirmed by the measurement of hand temperature and the decrease of digital and hand blood flow. Thus, the description of this case shows that platelet aggregation by itself is not necessary for the occurrence of RP, and encourages for therapeutic purposes the development of vasodilatators rather than platelet antiaggregants agents."
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