Vascular protection in peripheral artery disease: systematic review and modelling study.

AIMS: To ascertain the effectiveness of medical therapy for reducing risk in peripheral artery disease (PAD) and to model the potential impact of combining multiple efficacious approaches. METHODS AND RESULTS: 17 electronic databases, reference lists of primary studies, clinical practice guidelines, review articles, trial registries and conference proceedings from cardiology, vascular surgery and atherosclerosis meetings were screened. Eligible studies were randomized trials or meta-analyses of randomized trials of medical therapy for PAD which reported major cardiovascular events (myocardial infarction, stroke and cardiovascular death). Baseline event rates for modelling analyses were derived from published natural history cohorts. Overall, three strategies had persuasive evidence for reducing risk in PAD: antiplatelet agents (pooled RRR 26%, 95% CI 10 to 42), statins (pooled RRR 26%, 95% CI 18 to 33) and angiotensin-converting enzyme inhibitors (individual trial RRR 25%, 95% CI 8 to 39). The estimated cumulative relative risk reduction for all three strategies was 59% (CI 32 to 76). Given a 5-year major cardiovascular event rate of 25%, the corresponding absolute risk reduction and number needed to treat to prevent one event were 15% (CI 8 to 19) and 7 (CI 5 to 12), respectively. Population level analyses suggest that increased uptake of these modalities could prevent more than 200 000 events in patients with PAD each year. CONCLUSION: The use of multiple efficacious strategies has the potential to substantially reduce the cardiovascular burden of PAD. However, these data should be regarded as hypothetical, since they are based on mathematical modelling rather than factorial randomized trials.

Trapped renal arteries: functional renal artery stenosis due to occlusion of the aorta in the arch and below the kidneys.

Acute renal failure is a well recognized complication from the use of angiotensin-converting enzyme inhibitors in patients with severe bilateral renovascular disease. A 54-year-old woman presented with acute pulmonary edema with intractable hypertension and a history of lower limb claudication. The addition of lisinopril to her antihypertensive regimen resulted, within 48 h, in the development of acute renal failure that remitted with cessation of the drug. She was found to have a heavily calcified occlusion of her aortic arch and another occlusion of the aorta below the renal arteries. Angiography and Doppler ultrasonography showed normal renal arteries. This is the first reported case of angiotensin-converting enzyme inhibitor-induced renal failure occurring in a patient with atherosclerotic occlusion of the aorta. The literature on suprarenal aortic occlusion is reviewed to determine the manner of presentation, prevalent risk factors and physical findings that typify this unique clinical entity.

What level of plasma homocyst(e)ine should be treated? Effects of vitamin therapy on progression of carotid atherosclerosis in patients with homocyst(e)ine levels above and below 14 micromol/L.

High levels of plasma homocyst(e)ine (H[e]) are associated with increased vascular risk. Treatment is being contemplated, but the level at which patients should be treated is not known. We compared the response of carotid plaque to vitamin therapy in patients with H(e) above and below 14 micromol/L, a level commonly regarded as high enough to warrant treatment. Two-dimensional B-mode ultrasound measurement of carotid plaque was used to assess the response to vitamin therapy with folic acid 2.5 mg, pyridoxine 25 mg, and cyanocobalamin 250 microg daily, in 101 patients with vascular disease (51 with initial plasma levels above, and 50 below 14 micromol/L). Among patients with plasma H(e) >14 micromol/L, the rate of progression of plaque area was 0.21 +/- 0.41 cm2/year before vitamin therapy, and -0.049 +/- 0.24 cm2/year after vitamin therapy (P2 = .0001; paired t test). Among patients with levels <14 micromol/L, the rate of progression of plaque was 0.13 +/- 0.24 cm2/year before vitamin therapy and -0.024 +/- 0.29 cm2/year after vitamin therapy (P2 = .022, paired t test). The change in rate of progression was -0.15 +/- .44 cm2/year below 14 micromol/L, and -0.265 +/- 0.46 cm2/year above 14 micromol/L (P = 0.20). Vitamin therapy regresses carotid plaque in patients with H(e) levels both above and below 14 micromol/L. These observations support a causal relationship between homocyst(e)ine and atherosclerosis and, taken with epidemiologic evidence, suggest that in patients with vascular disease, the level to treat may be <9 micromol/L.

Congenital entrapment of the lateral cutaneous nerve of the calf presenting as a personal sensory neuropathy.

OBJECTIVE: Presentation of an unusual case of congenital entrapment of the lateral cutaneous nerve of the calf (LCNC) mimicking a peroneal sensory neuropathy. METHODS: We report the case of as 16-year-old girl with a 3 year history of progressive tingling, numbness and pain in her right calf precipitated by athletic activities involving repeated flexion and extension of the knee. A Tinel's sign was present over the common peroneal nerve in the distal popliteal fossa but absent at the fibular neck. Motor and sensory examination of the common peroneal nerve was normal as were electrophysiological studies and MRI. RESULTS: At surgery, the LCNC, a sensory branch of the common peroneal nerve, was entrapped at a point where it pierced the tendon of the biceps femoris muscle. Transection of the part of the tendon overlying the LCNC resulted in complete and permanent relief of symptoms. SIGNIFICANCE AND CONCLUSION: The proximal location of the Tinel's sign, absence of motor or sensory deficits and normal electrophysiology suggested, preoperatively, that this was not an entrapment of the common peroneal nerve at the fibular neck but rather a more proximal abnormality likely involving only a part of the peroneal nerve or one of its sensory branches. As a result, the more proximal exposure of the peroneal nerve within the popliteal fossa revealed entrapment of the neuropathy of the common peroneal nerve or one of its branches, due to a normal nerve piercing an otherwise normal tendon. Secondly, there are no previously reported cases of surgically documented compression of the LCNC in an otherwise normal patient (i.e. non-diabetic).