Biomedical subjects

Einar Stranden

Publications and source records attributed to Einar Stranden.

4 recordsLinked to original sources

PubMed2006

Prothrombotic activity is associated with the anatomical as well as the functional severity of peripheral arterial occlusive disease.

The importance of prothrombotic activity in cardiovascular disease has been well established. However, limited data exist on the relationship between prothrombotic activity and the severity of peripheral arterial occlusive disease (PAD). The objective of the present study was to investigate the relationship between markers of haemostasis and the diagnostic measures of PAD: ankle-brachial-index (ABI), maximum treadmill walking distance and angiographic score. In a cross-sectional study of 127 patients (mean age 66 years; 64% males) with angiographically verified PAD, fasting blood samples were drawn, and citrated plasma was obtained for determination of selected haemostatic variables: von Willebrand factor (vWF), thrombomodulin (sTM), thrombin-antithrombin complex (TAT), soluble tissue factor (sTF), tPA antigen (tPAag) and D-dimer were all significantly correlated with the angiographic score (p < 0.05 for all). D-dimer, tPAag and fibrinogen were inversely correlated with the maximum treadmill walking distance, (p < 0.0001, p < 0.04 and p < 0.05, respectively), whereas fibrinogen was the only variable correlating to ABI (r = -0.223, p < 0.05). After adjustment for relevant covariates, D-dimer and TAT remained statistically significantly associated with the angiographic score (p < 0.001), and fibrinogen was, independent of other risk factors, inversely related with both the maximum treadmill walking distance and the ABI (p < 0.01 for both). This rather large study in patients with PAD showed that plasma levels of D-dimer, TAT and fibrinogen significantly predicted the extent of atherosclerosis, evaluated by angiographic score, maximum treadmill walking distance and ABI, respectively. These findings demonstrate a prothrombotic state in PAD patients, which might be of importance in future diagnosis and treatment of the disease.

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PubMed2005

[Venous leg ulcers].

Patients with venous leg ulcers usually have extensive symptoms both related to their venous insufficiency and to the wound itself, often combined with a reduced quality of life. Prevalence of venous leg ulcers varies from 0.1 to 1.0%. Treatment costs are high and may amount to 1.5% of a nation's total spending on health care. Venous hypertension is the common denominator for all patients with venous leg ulcers. Isolated superficial as well as deep or combined venous insufficiency with or without insufficient perforators may cause ulceration. In the microcirculation, inflammation is involved, but the exact mechanisms behind the ulcer formation remain unresolved. During the examination, a presence of superficial venous insufficiency accessible for superficial resection must be established. In addition to a clinical examination, venous pressure measurements/plethysmography and colour duplex scanning is recommended in order to locate and evaluate the significance of the venous insufficiency. The key element in the treatment of venous ulcers is to reduce oedema and venous hypertension by adequate compression and elevation. If primary superficial venous insufficiency is established, venous resection is recommended. This may improve healing and reduce recurrences. In selected patients, deep venous reconstruction is an alternative approach.

Bandages↗

PubMed2005

[Arterial ischemic ulcers].

Arterial ischaemic ulcers develop because of inadequate perfusion leading to local ischaemia in the skin and underlying tissue. The most common cause is peripheral arterial disease, giving rise to symptoms like intermittent claudication, rest pain and gangrene, in addition to local ulceration. Diabetes mellitus increases the risk of ulcer formation; admittedly mainly neuropathic ulcers with a low component of peripheral arterial disease. Yet a combination of neuropathy and ischaemia is common ("neuro-ischaemic ulcer"). A thorough patient history and clinical examination can help discriminate arterial ulcers from venous, pressure, traumatic and vasculitis ulcers. Reduction of ankle systolic pressure and calculated ankle/brachial index, sometimes additional other non-invasive laboratory tests, confirm peripheral arterial disease. The primary treatment of arterial ischaemic ulcer is to increase blood supply to the affected area, primarily by endovascular treatment or open arterial reconstruction. Endovascular treatment (balloon angioplasty) is the method of choice because of graft infection risk in patients with open ulcers. Most arterial ischaemic ulcers will progress to healing if the blood supply is reestablished.

Angioplasty, Balloon↗

PubMed2003

Quantification of leg oedema in postmenopausal hypertensive patients treated with lercanidipine or amlodipine.

OBJECTIVE: Of the study was to compare the leg oedema-forming potential of two different dihydropyridine calcium channel blockers in postmenopausal women. DESIGN: A total of 92 postmenopausal hypertensive patients [systolic blood pressure (SBP) 150-179 mmHg or diastolic blood pressure (DBP) 95-109 mmHg were randomized to receive a 4-week treatment with either 10 mg/day lercanidipine (n = 48) or 5 mg/day amlodipine (n = 44), with force-titration to 20 and 10 mg/day, respectively for an additional 4 weeks. METHODS: Leg volume was measured by water displacement volumetry, patients were questioned for symptoms and a physical examination was performed to detect the presence of oedema. RESULTS: A total of 77 patients completed the study, without a major protocol violation and were included in the primary analysis. Leg volume increase from baseline was significantly higher in the amlodipine than in the lercanidipine group (60.4 +/- 8.6 versus 5.3 +/- 8.1 ml; P < 0.001). The percentage of patients with evidence of oedema on physical examination (33.3 versus 9.8%, P = 0.011) and with symptoms of leg swelling (63.9 versus 22%, P < 0.001) and leg heaviness (47.2 versus 12.2%, P < 0.001) was also greater with amlodipine compared with lercanidipine. A positive correlation was found between leg volume and sign or symptoms of oedema (P < 0.001). Both drugs reduced SBP and DBP, with no significant differences between treatments. No correlation was found between leg volume changes from baseline and the antihypertensive effect of either drug. CONCLUSIONS: In postmenopausal females with mild to moderate hypertension the oedema formation of Lercanidipine was significantly less than that of Amlodipine, despite no significant differences in the antihypertensive effect.

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