Cutaneous Blood Flow Abnormalities in Hypertriglyceridemia

The microcirculation in atherogenesis

“…Using single photon emission computed topographic imaging studies on patients without hemodynamically significant epicardial coronary artery lesions (not associated with angina pectoris), these authors could demonstrate that exercise-induced myocardial ischemia was associated with impaired endotheliumdependent vasodilation of the coronary microcirculation [ 111. In agreement with the previously mentioned improvement of the postischemic hyperemic response by lipidlowering agents [5], the reduced vasodilator response in the myocardial microcirculation of hypercholesterolemic patients could be restored by lipid-lowering therapy [ 121. These and earlier studies [13,14] have attributed the impaired vasodilator response of microvessels in atherosclerotic subjects to the prevailing high levels of circulating lipid and cholesterol.…”

“…Similar observations have been made in hypertriglyceridemic patients, in which postischemic reactive hyperemia is significantly impaired [5]. Of particular interest is the fact that these changes are entirely reversible by dietary or pharmacological correction of the hypertriglyceridemic state [5]. Others have performed experiments with various endothelium-dependent and endothelium-independent vasodilators and have suggested that endothelium-dependent vascular relaxation is abnormal in the coronary microcirculation of atherosclerotic animals [6,7].…”

“…For instance, laser Doppler fluxmetry on toe pulp and leg skin has revealed marked retardation and complete loss of vasodilator response during postischemic reactive hyperemia in patients with lower limb atherosclerosis, contributing to intermittent claudication or critical ischemia [4]. Similar observations have been made in hypertriglyceridemic patients, in which postischemic reactive hyperemia is significantly impaired [5]. Of particular interest is the fact that these changes are entirely reversible by dietary or pharmacological correction of the hypertriglyceridemic state [5].…”

Evidence of microvascular dysfunction in patients with cystic fibrosis

“…Bearing in mind the same considerations of elevated prostanoids in patients with CF previously described (10) and the contribution of these mediators in an impaired vascular response (21), it is not surprising that patients with CF also exhibit a lower microvascular response to the ACh iontophoresis. However, TTP values were similar between both groups, confirming that the microvascular integrity and structure are intact and unlikely affecting the ACh response (41,51). In addition, a previously described reliance of the iontophoresis response to ACh on endothelial function was assessed through brachial artery flowmediated dilatation, which is also impaired in CF (11).…”

“…Expression of the values as a relative change, as reported by others (55), eliminates possible spatial variations and allows for a more accurate comparison not only between groups, but also between sites on the same individual. In addition, our results may suggest that the structure of the blood microvessels is preserved (41,51), despite impairment of the mechanisms that contribute to the reactive hyperemia response. The exact mechanism is unknown; however, prostanoids are key players in the PORH response (21), and many factors, including metabolic and endothelial vasodilators, sensory nerves, and NO, have also been shown to be involved (23,50).…”