Vascular Medicine

Measurement of the ankle—brachial index (ABI) can provide important information about the presence of subclinical atherosclerosis. Performing the ABI in the overall population is not feasible, but it can be used in a selected population. A simple prediction rule could be of much use to estimate the risk of an abnormal ABI. This was designed as an observational study in the setting of 955 general practices in The Netherlands. A total of 7454 patients aged ≥ 55 years presenting with at least one vascular risk factor (smoking, hypertension, diabetes, and hypercholesterolemia) and no complaints of intermittent claudication were included. Patients were selected by the general practitioner during visiting hours and from medical records. Main outcome measures included the prevalence of PAD, defined as an ABI below 0.9, which was related to vascular risk factors using regression analyses on which the PREVALENT clinical prediction model was developed. The overall prevalence of PAD was 18.4%. Since the treatment of individuals with a history of coronary heart disease and cerebrovascular disease will not be influenced by the finding of asymptomatic PAD, these individuals were not taken into account for the development of the clinical prediction model. Analyses showed a significantly increased risk for PAD with increasing age, smoking, and hypertension. The clinical prediction model giving risk factor points per factor (age: 1 point per 5 years starting at 55 years; ever smoked: 2 points; currently smoking: 7 points; and hypertension: 3 points), showed a proportional increase of the PAD prevalence with each increasing risk profile (range: 7.0—40.6%). In conclusion, based on the PREVALENT clinical prediction model, the general practitioner is able to identify a high-risk population in which measurement of ABI is useful.

Until now, peripheral vascular endothelial function testing has been performed in research laboratories under highly controlled conditions, thus limiting its clinical applicability. In this study, we evaluated endothelial function in two peripheral vascular beds before and during reactive hyperemia in an outpatient clinic setting. The brachial artery was imaged with a portable ultrasound device and changes in vessel diameter were expressed as percent flow-mediated dilation (%FMD). Pulse wave amplitude of the finger was detected by peripheral arterial tonometry (PAT) and PAT hyperemia was defined as the maximal plethysmographic recording compared to baseline. Sixty individuals (43 men) were enrolled with an average age 53 ± 2 years (mean ± SE). The 31 individuals with more than two cardiac risk factors (CRF) had lower FMD (7.0 ± 1.1%) and PAT hyperemia (2.1 ± 0.9) compared to the 29 individuals with 0—2 CRF (FMD 11.3 ± 0.8%, PAT hyperemia 2.4 ± 0.1; p < 0.05 for both). The 32 individuals with coronary artery disease (CAD) had lower FMD (6.8 ± 1.1%) and PAT hyperemia (2.0 ± 0.1) compared to the 28 individuals without CAD (FMD 11.5 ± 0.8%, PAT hyperemia 2.4 ± 0.1; p < 0.05 for both). Thus, peripheral vascular endothelial function testing in the ambulatory setting correlates with the extent of CAD risk and the presence or absence of CAD. In conclusion, these data suggest that peripheral vascular endothelial function testing is feasible in ambulatory patients, and this is an important next step in bringing this technology to clinical applicability.

Erectile dysfunction (ED) is frequently associated with cardiovascular disease. Epidemiological data on the frequency of ED in vascular surgery patients is rarely reported. We evaluated the prevalence of this comorbidity in patients consulting the vascular surgery outpatient clinic. Over a 6-month period, a short version of the International Index of Erectile Function (IIEF) questionnaire consisting of six EDrelevant questions was handed out to 440 vascular surgery outpatients. Clinical data were collected from patients' records. Linear regression models with forward selection were used to investigate associations between erectile function score and possible risk factors. The return rate was 31% (137 patients). Eight patients (6%) were taking phosphodiesterase inhibitors. ED, as defined by an erectile function score of 25 or less and/or use of phosphodiesterase inhibitors, was found in 90% (95% CI: 84% to 95%) of cases. Moderate or severe ED, as defined by an erectile function score of 16 or less and/or use of phosphodiesterase inhibitors, was found in 70% (95% CI: 62% to 78%) of cases. Increased age, abdominal aortic aneurysm, peripheral arterial disease, urologic disease, insulin-dependent diabetes mellitus, and use of beta-blockers were significantly associated with a lower erectile function score. In conclusion, erectile dysfunction is a frequent and often missed comorbidity in vascular surgery patients. While ED may have a profound impact on the patient's quality of life, attention should also be paid to the patient's preoperative sexual function, considering the availability of oral pharmacotherapies and possible consequences concerning liability in postoperative patients in whom pre-existing ED was not identified properly.

A plethora of evidence supports a link between inflammation and atherogenesis. Both the vasoactive peptide angiotensin II (ANG II) as well as the CD40/CD154 signaling pathway exhibit proinflammatory properties with a direct influence on atherogenesis. We therefore tested the hypothesis that ANG II interacts with CD40/CD154 in human vascular smooth muscle cells (SMC). ANG II did not increase expression of CD40 in human SMC. However, when SMC were prestimulated with ANG II and thereafter stimulated with CD154, the ligand for CD40, the release of IL-6 as a marker of inflammatory activation was augmented compared to cells not primed with ANG II. TNF receptor-associated factor 2 (TRAF-2), an important adaptor protein involved in CD40 signaling, but not TRAF-5 or -6, was increased by ANG II via activation of the angiotensin II type 1 (AT1) receptor subtype. These results suggest that a signaling pathway downstream of CD40 may be altered by ANG II prestimulation. Thus, ANG II can also indirectly cause inflammatory activation of vascular SMC. The data show a novel link between the proatherogenic vasoactive peptide ANG II and cell—cell contact-mediated inflammatory pathways and implicate options for the prevention and therapy of atherosclerotic disease.

Purple glove syndrome (PGS) is a rare complication of intravenous phenytoin use that typically presents with pain, edema, and discoloration at the injection site that spreads to the distal limb. Several risk factors have been associated with the development of PGS; however, the etiology remains unknown. We present a case of PGS and briefly review the current understanding of this syndrome.