Dignan I am glad you posted that, I was reading a related paper yesterday that I was debating making a post on, I'll go ahead and add it here..
FULL TEXT HERE
Quote:
New MRI techniques such as the analysis of magnetization transfer or diffusion have provided evidence for subtle progressive alterations in tissue integrity prior to focal leakage of the blood–brain barrier (BBB) as part of plaque formation in multiple sclerosis. Since inflammation is capable of modulating the microcirculation, we investigated the hypothesis that changes in the local perfusion might be one of the earliest signs of lesion development. 20 patients with definite relapsing–remitting multiple sclerosis were analysed with regard to cerebral blood volume, cerebral blood flow, mean transit time and apparent diffusion coefficient (ADC), as well as conventional MRI parameters, on monthly follow-up scans. Among 89 gadolinium-enhancing lesions, we selected 18 that developed during the study and met strict inclusion criteria. In these, changes of perfusion parameters were detectable not only prior to the BBB breakdown, but also prior to increases in the ADC. Our data indicate that inflammation is accompanied by altered local perfusion, which can be detected prior to permeability of the BBB.
It is interesting how much of this study had to do with blood flow, yet they were primarily interested in inflammation and how that changed microcirculation.
Microcirculation is also changed by increased pressure from venous reflux.
CLICK HERE TO SEE SOURCEQuote:
Local Microcirculation in Chronic Venous Incompetence and Leg Ulcers
Bengt Fagrell
Department of Medicine , Karolinska Institute at St. Erik's Hospital, Stockholm, Sweden
Most chronic leg ulcers (90 to 95%) are caused by incompetence of the deep venous system and/or the perforators of the lower leg. Superficial venous incompetence does not give rise to necrotic skin ulcers. The primary cause of venous leg ulcers is the marked increase in pressure that builds up in the deep veins of the lower leg during walking. This pressure is transformed to the skin vessels through the ankle perforators, out to the nutritional vascular bed of the skin. The intracapillary pressure increases tremendously and this causes the capillaries to dilate and become tortuous. The blood elements leak out through the capillary wall into the surrounding tissue and form a specific microedema, which gives rise to an effective nutritional block between the capillaries and the skin cells. This microedema is most probably the main cause of the development of venous leg ulcers.
Vascular and Endovascular Surgery, Vol. 13, No. 4, 217-225 (1979)
They know that in the case of venous reflux restoring normal circulation usually allows healing of the venous lesions, which in the case of the leg, are skin ulcers.
SOURCE HEREQuote:
Monitoring for 94% of patients lasted a mean 22 months (range, 1 to 107 months). Stenting was performed with no mortality (<30 days) and low morbidity. Thrombotic events were rare (1.5%) during the postoperative period (<30 days) and during later follow-up (3%). At 72 months, primary, assisted-primary, and secondary cumulative patency rates were 79%, 100%, and 100% in nonthrombotic disease and 57%, 80%, and 86% in thrombotic disease, respectively. Cumulative rate of severe in-stent restenosis (>50%) occurred in 5% of limbs at 72 months (10% in thrombotic limbs, 1% in nonthrombotic limbs). The main risk factors associated with stent occlusion were the presence and severity of thrombotic disease; thrombophilia by itself was not a risk factor. The median pain score and degree of swelling decreased significantly poststent. Severe leg pain (visual analogue scale >5) and leg swelling (grade 3) decreased from 54% and 44% prestent to 11% and 18% poststent, respectively. At 5 years, cumulative rates of complete relief of pain and swelling were 62% and 32%, respectively, and ulcer healing was 58%. The mean CIVIQ scores of QOL improved significantly in all categories. Mean hand-foot pressure differential decreased and mean ambulatory venous pressure improved in stented limbs with no concomitant reflux. The hemodynamic response was modified, depending on the presence of deep and superficial reflux in subsets of patients with adjunct saphenous procedures. No increase in venous reflux was observed.
Conclusions
Venous stenting can be performed with low morbidity and mortality, long-term high patency rate, and a low rate of in-stent restenosis. It resulted in major symptom relief in patients with chronic venous disease, which was not consistently reflected in any substantial hemodynamic improvement by conventional measurements. The beneficial clinical outcome occurred regardless of presence of remaining reflux, adjunct saphenous procedures, or etiology of obstruction.
Basically if they opened up the veins people did very well...