Digital blood flow response to body warming, cooling, and rewarming in patients with Raynaud's phenomenon

Abstract

Although the diagnosis of Raynaud's phenomenon (RP) is usually made easily from a careful history, the assessment of RP severity is difficult, for the vasopastic attacks are not easily induced under experimental conditions. In this study, the laser Doppler flowmetry (LDF) technique was used to quantify digital blood flow, which was standardized by body cooling and warming in patients with RP. Twenty-one healthy subjects and 56 RP patients were studied: 7 had primary RP, 22 had suspected secondary Raynaud's syndrome (susp RS), and 27 had systemic sclerosis (SSc)-associated secondary Raynaud's syndrome (SSc RS). The inherent variability in the acral cutaneous circulation was minimized by whole-body warming and cooling. Digital blood flow values at environmental temperatures of 40°C, 12°C, and after rewarming, to 40°C were recorded, as was the time taken for blood flow to reach 25%, 50%, and 75% of the full effects of whole-body cooling and rewarming. Patients with primary RP and susp RS had normal blood flow values at ambient temperatures of 40°C, 12 °C, and after rewarming to 40 °C when compared with controls, but they had significantly faster vasoconstrictor responses to whole-body cooling, suggesting a heightened sympathetic activity. Additionally, they had slower vasodilator responses with longer 25%(max) response time to whole-body rewarming. Patients with SSc RS had significantly lower blood flow values at 40°C after initial warming and following subsequent rewarming, and despite a normal vasoconstrictor response to cooling, it took longer for them to vasodilate during rewarming, suggesting that poor digital blood flow in these patients may be more related to digital vasculature abnormalities and not an increase in sympathetic activity. In conclusion, our assessment technique can be used to quantify digital blood flow in patients with RP and may be potentially useful in the investigation of the etiologic role of the sympathetic nervous system in RP.