SCVS Annual Meeting 2006 Abstracts: Modifiable Vascular Risk Factors in Peripheral Arterial Disease: Can we do Better?
December 23, 2005
Modifiable Vascular Risk Factors in Peripheral Arterial Disease: Can we do Better?
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Stella S. Daskalopoulou, MD, MSc, DIC, PhD, FASA, Mariasoosai Pathmarajah, MD, Stavros K. Kakkos, MD, MSc, DIC, PhD, Marios E. Daskalopoulos, MD, MSc, DIC, PhD, FASA, P AH Holloway, MD, Dimitri P. Mikhailidis, BSc, MSc, MD, FACB, FASA, FFPM, FRCP, FRCPath, George Geroulakos, MD, PhD, FRCS.
Ealing Hospital and Imperial College London, London, United Kingdom. OBJECTIVES: Patients with peripheral arterial disease (PAD) have a markedly increased risk of vascular events. Nevertheless, PAD remains underdiagnosed and not aggressively managed. We evaluated the vascular risk factor status of claudicants attending a Vascular Outpatient Clinic.
METHODS: We assessed 148 claudicants (age 68.9±10.4 years; 111 men) at presentation. A fasting venous blood sample was collected.
RESULTS: The ankle brachial pressure index (ABPI) was 0.64±0.14. The systolic/diastolic blood pressure was 141±19/77±11 mmHg; 71.6% of the patients were on antihypertensive treatment; 58 patients (39.2%) were smokers, 72 (48.6%) ex-smokers; 55 patients (37.2%) had diabetes. Most patients (81.1%) were on antiplatelet drugs. The fasting lipids were (mg/dl): total cholesterol=208±39, HDL-cholesterol=50±12, LDL-cholesterol=127±35, triglycerides=159±80. Of the patients, 80% had LDL-cholesterol>100 (NCEP ATP III target), 20.7% HDL-cholesterol<40 (NCEP ATP III recommended value) and 41.4% triglycerides>150 (borderline raised level). Only 57.9% of the patients were on statins at presentation; 69.4% of these had not reached the LDL-cholesterol goal. In patients not on lipid-lowering drugs, LDL-cholesterol inversely correlated with the ABPI (r=-0.44, p=0.006). The median high-sensitivity CRP (hsCRP) was 5.0 mg/l (interquartile range=3.0-8.0). Fibrinogen was 360±90 mg/dl; 73.6% of the patients had levels associated with a higher risk of vascular events (>300 mg/dl). The ABPI inversely correlated with hsCRP (r=-0.23, p=0.039) and fibrinogen (r=-0.28, p=0.007). Homocysteine was 15.7±6.3 μmol/l; 67.6% had >12 μmol/l (suggested treatment threshold for high-risk patients). Serum creatinine (another emerging predictor) was 1.20±0.38 mg/dl; this may reflect early renal atherosclerosis.
CONCLUSIONS: Despite evidence-based medicine and guidelines, modifiable vascular risk factors in claudicants remain poorly controlled. We showed, for the first time, a significant inverse correlation between ABPI and LDL-cholesterol in patients not on lipid-lowering drugs and also between ABPI and fibrinogen and hsCRP, in all patients, supporting a link between the severity of PAD and atherogenic and inflammatory risk factors. Further studies need to confirm these findings. Furthermore, prospective studies need to establish whether multi-targeted aggressive risk factor modification can decrease PAD progression and the occurrence of vascular events.
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