Real world data from a multi-centre study on the effects of cilostazol on pain symptoms and walking distance in patients with peripheral arterial disease.

OBJECTIVE: to assess the effects of cilostazol on pain-free walking distance in PAD patients with IC at 3 and 6 months in a real world, prospective, observational study. We included 1015 PAD patients presenting with IC (71.3% men, 93.5% white, mean age 69.2 ± 8.7 years). Patients were followed up for 6 months by their physicians. RESULTS: Cilostazol significantly increased pain-free walking distance by a median of 285 and 387 m at 3 and 6 months, respectively (p < 0.01 for all comparisons). This effect was significant for patients 50-74 years (but not for those aged ≥ 75 years) and independent of smoking status, changes in physical activity, comorbidities and concomitant medication for PAD (i.e., acetylsalicylic acid and clopidogrel). Furthermore, significant reductions were observed in systolic (from 139 ± 16 to 133 ± 14 mmHg; p < 0.001) and diastolic blood pressure (from 84 ± 9 mmHg to 80 ± 10 mmHg; p < 0.001). Smoking cessation and increased physical activity were reported by the majority of participants. In conclusion, cilostazol was shown to safely decrease pain symptoms and improve pain-free walking in PAD patients with IC in a real world setting. Benefits also occurred in terms of BP and lifestyle changes.

Chronic ergot toxicity presenting with bilateral external iliac artery dissection and lower extremity rest pain.

Chronic use of ergot alkaloids has been recognized as a rare cause of lower extremity ischemia. Most patients with ergot toxicity present with symptoms of lower extremity claudication. Herein we present a woman with bilateral lower extremity rest pain and a history of chronic ergot use for migraine headaches. Arteriography demonstrated extensive pruning of the distal arterial tree along with bilateral external iliac artery dissections - a finding that is not often associated with young, normotensive patients with chronic ergot toxicity. This patient was treated with endovascular stenting of the dissections along with cessation of ergot. Her symptoms improved markedly, and follow-up arteriography 6 weeks later demonstrated resolution of the iliac dissections along with restoration of nearly normal lower extremity runoff vessels. Discontinuation of ergot-containing products and cessation of tobacco and caffeine use is the cornerstone of therapy in chronic ergot toxicity. The association of ergot toxicity and iliac dissection has not been previously described. Endovascular or surgical interventions may be considered in patients with ergot toxicity for specific indications or those whose symptoms progress despite conservative management.

Chronic ergot toxicity: A rare cause of lower extremity ischemia.

Chronic ergot toxicity is a rare cause of lower extremity ischemia. The cornerstone of therapy in ergot toxicity is to discontinue the use of caffeine, cigarettes, and all ergot-containing medications. Although multiple different therapies have been recommended for acute toxicity, no specific treatment is uniformly recommended in chronic toxicity. We present a case of long-term ergot use for migraine headaches in a woman who had severe chronic lower extremity claudication. This case demonstrates the unique features associated with the diagnosis and management of chronic ergot toxicity. We recommend a conservative approach consisting of observation, antiplatelet agents, and the discontinuance of ergots. If symptoms progress to rest pain or gangrene, surgical treatment should be considered.

Ergotamine-induced intermittent claudication.

We report about a female patient with intermittent claudication caused by ergotamine. She used ergotamine as a treatment for migraine headaches for more than 4 years. The claudication began 7 month before admission. Colour Doppler sonography and angiography showed severe stenosis of the left external iliac and superficial femoral artery. The patient was treated with phenprocoumon for one year after withdrawal of ergotamine. After that the superficial femoral stenosis disappeared completely, but the external iliac stenosis was still present and was consequently successfully treated by atherectomy. The histology showed a fibrosis of the intima and a hypertrophy of the media.

The influence of chronic treatment with betablockade and angiotensin converting enzyme inhibition on the peripheral blood flow in hypertensive patients with and without concomitant intermittent claudication. A comparative cross-over trial.

In a comparative cross-over trial we examined the influence of the betablocker bisoprolol and the ACE-inhibitor lisinopril on the peripheral blood flow of 2 groups of hypertensive patients with and without concomitant intermittent claudication. In 11 patients with hypertension without peripheral arterial obstructive disease and 11 patients with hypertension and claudication we assessed the blood pressure, leg blood flow, vascular resistance, walking distance, transcutaneous oxygen consumption and Laser-Doppler flow after treatment of one month with 10 mg bisoprolol once daily or 20 mg lisinopril once daily. The walking distance of patients with claudication improved in all patients while participating in an exercise program. For both treatment groups this improvement was significant (p < 0.05) compared to baseline, from 264 m at baseline to 313 m with bisoprolol and to 400 m with lisinopril. The difference was not significant between the both drugs. In patients without peripheral vascular obstructive disease we found a significant (p < 0.05) reduction in blood flow for both drugs. The peripheral blood flow parameters of 38 legs showed no statistical significant effect of bisoprolol nor lisinopril on the local vascular resistance at rest, after occlusion or after exercise.

Misleading cause of acute arterial insufficiency: ergotamine intoxication. Case report.

In a woman arteriographically indicated spasm of the iliac, femoral and popliteal arteries did not respond to intra-arterial tolazoline. At operation groin pulsations were normal. Bilateral lumbar sympathectomy was performed. Subsequently it emerged that she had been using ergotamine. Surgery could have been avoided if nitroprusside had been given.

Beta-adrenergic blocker therapy does not worsen intermittent claudication in subjects with peripheral arterial disease. A meta-analysis of randomized controlled trials.

Beta-Adrenergic blockers have been considered relatively contraindicated in peripheral arterial disease because of the perceived risk that these drugs could worsen intermittent claudication. Therefore, we conducted a meta-analysis of available randomized controlled trials from the English-language literature to determine whether or not beta-blockers exacerbate intermittent claudication. The primary focus of this analysis was the effect of beta-blockers on exercise duration, measured as walking capacity or endurance time. Outcomes were pooled where appropriate. Of 11 eligible reports, six included 11 individual controlled treatment comparisons that provided data for an analysis of pain-free exercise capacity; no effect size was statistically significant. The pooled effect size for pain-free walking distance was -0.24 (95% confidence interval, -0.62 to 0.14), indicating no significant impairment of walking capacity compared with placebo. Only one study reported that certain beta-blockers were associated with worsening of intermittent claudication. These results strongly suggest that beta-blockers do not adversely affect walking capacity or symptoms of intermittent claudication in patients with mild to moderate peripheral arterial disease. In the absence of other contraindications, beta-blockers can probably be used safely in such patients.

Claudication: an unusual side effect of DHE administration.

DHE is effective in the treatment of acute and chronic migraine. The side effects most commonly observed are abdominal discomfort, muscle pain, diarrhea and anxiety. DHE is a dehydrogenated amino acid ergot alkaloid and, as such, causes only limited vasoconstriction; indeed, its overall effects include peripheral vasodilation. The literature is replete with reports of clinical vasospasm and claudication occurring with therapeutic doses of ergotamine. There has not been any previous description of claudication caused by DHE. This paper describes pulselessness in two patients during relatively short courses of DHE. Treatment consisted of calcium channel blockers and discontinuation of DHE. Recovery was complete.