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Regarding “Endothelium-dependent vasodilation is impaired in both microcirculation and macrocirculation during acute hyperglycemia”
JOURNAL OF VASCULAR SURGERY May 1999
942 Letters to the Editors
Reply We thank Lucertini and colleagues for their kind comments concerning our article'! They make two main points. First, they confirm our findings that subfascial endoscopic perforator surgery is not required to correct thc greater proportion of incompetent perforating veins (IPVs) in limbs affected by superficial venous insufficiency alone. Second, they offer three possible explanations for the apparent failure of superficial surgery alone. We would like to make clear, however, that in our study the surgery performed did not involve specific attempts to avulse the IPVs. The perforators were not marked before surgery for the surgeon. We believe that some of the IPVs may have been partially or completely avulsed during phlebectomy. However, the greater proportion of the changes noted in IPV physiology were, we believe, caused by the abolition of main stem reflux in the superficial system that allowed the IPV blood flow to return to normal. We therefore would argue that perforator physiology is to a large part dependent on the main stem venous hemodyamics. We would certainly agree with the final assertion that IPVs in the presence of deep disease require direct surgical correction with the subfascial endoscopic perforator technique. Wesley P. Stuart, MB, ehB, FReSE Andrew W. Bradbury, MD, FReSE
Vascular Surgery Office University Department of Surgery Royal Infirmary Edinburgh, United Kingdom REFERENCES 1. Stuart WP, Adam DJ, Allan PL, Ruddey CV, Bradbury AW.
Saphenous surgery does not correct perforator incompetence in the presence of deep venous reflux. J Vasc Surg 1998;28:834-8.
in the brachial artery diameter after reactive hyperemia is less after glucose ingestion, this is a result of the increased resting diameter. Thus, the decline in flow-mediated dilatation when expressed as a percentage of the resting diameter is likely explained by the increase in the resting diameter rather than by acute impairment of the nitric oxide pathway. Although the authors repeatedly discuss this increase in resting vessel diameter with hyperglycemia, they discount its significance. It has been shown repeatedly that flow-mediated vasodilatation is inversely related to the baseline brachial artery diameter.1· 3 I suspect this is the explanation for their findings in the macrocirculation. The authors are correct in stating that there are difficulties in assessing the microcirculation. Yet, they are confident that the iontophoresis of acetylcholine is likely the "most effective and reliable noninvasive method available" to assess this vascular bed. As previously stated, I am concerned that the apparent difference noted in skin blood flow with hyperglycemia (when expressed as a percent change from baseline) is largely reflective of the significant increase in basal flux after glucose loading. In fact, the absolute change from baseline does not appear to be significantly different between fasting and hyperglycemia. Moreover, recent reports4 ,5 suggest that changes in skin blood flow in response to iontophoresis of acetylcholine are more likely mediated by prostanoids rather than by nitric oxide because NG-monomethyl-L-arginine (L-NMMA; an inhibitor of nitric oxide synthesis) infusion had no effect on the acetylcholine response. Because L-NMMA will most often attenuate the flow-mediated dilatation of the brachial artery, these two noninvasive assays may be examining different effects in the microcirculation versus the macrocirculation. Lawrence Title, MD
Division of Cardiology New Halifax Infirmary Halifax, Nova Scotia, Canada
24/41/97869 REFERENCES 1. Celermajer DS, Sorensen KE, Bull C, Robinson J, Deanfield
Regarding "Endothelium-dependent vasodilatation is impaired in both microcirculation and macrocirculation during acute hyperglycemia"
To the Editors: It was with great interest that I read the article by Akbari et al (J Vasc Surg 1998;28:687-94). However, I do not ibelieve that the results fully support the authors' conclusion that endothelial function is impaired after acute oral glucose loading in healthy subjects. Although there was an apparent decline in flow-mediated dilatation of the brachial artery after glucose ingestion (4.2% vs 11.7%; P < .001), this decline appears to be largely related to the significant increase in the resting brachial artery diameter 60 minutes after the ingestion of the glucose (3.92 mm vs 3.73 mm; P< .02). In contrast, the brachial artery diameter after reactive hyperemia was not significantly different during fasting or hyperglycemia (4.22 vs 4.17 mm; P = .28). Although the absolute change
2.
3.
4.
5.
JE. Endothelium·dependent dilation in the systemic arteries of asymptomatic subjects relates to coronary risk factors and their interaction. J Am Coli CardioI1994;24:1468-74. Jensen· Urstad K, Rosfors S. A methodological study of arterial wall function using ultrasound technique. Clin Physiol 1997;17:557-67. Uehata A, Lieberman EH, Gerhard MD, et al. Noninvasive assessment of endothelium-dependent flow-mediated dilation of the brachial artery. Vasc Med 1997;2:87-92. Noon JP, Walker BR, Hand MF, Webb DJ. Studies with iontophoretic administration of drugs to human dermal vessels in vivo: cholinergic vasodilatation is mediated by dilator prostanoids rather than nitric oxide. Br J Clin Pharmacal 1998;45:545-50. Khan F, Davidson NC, Littleford RC, Litchfield SJ, Struthers AD, Belch JJ. Cutaneous vascular responses to acetylcholine are mediated by a prostanoid-dependent mechanism in man. Vasc Med 1997;2:82-6.
24/41/97877
942 Letters to the Editors
Reply We thank Lucertini and colleagues for their kind comments concerning our article'! They make two main points. First, they confirm our findings that subfascial endoscopic perforator surgery is not required to correct thc greater proportion of incompetent perforating veins (IPVs) in limbs affected by superficial venous insufficiency alone. Second, they offer three possible explanations for the apparent failure of superficial surgery alone. We would like to make clear, however, that in our study the surgery performed did not involve specific attempts to avulse the IPVs. The perforators were not marked before surgery for the surgeon. We believe that some of the IPVs may have been partially or completely avulsed during phlebectomy. However, the greater proportion of the changes noted in IPV physiology were, we believe, caused by the abolition of main stem reflux in the superficial system that allowed the IPV blood flow to return to normal. We therefore would argue that perforator physiology is to a large part dependent on the main stem venous hemodyamics. We would certainly agree with the final assertion that IPVs in the presence of deep disease require direct surgical correction with the subfascial endoscopic perforator technique. Wesley P. Stuart, MB, ehB, FReSE Andrew W. Bradbury, MD, FReSE
Vascular Surgery Office University Department of Surgery Royal Infirmary Edinburgh, United Kingdom REFERENCES 1. Stuart WP, Adam DJ, Allan PL, Ruddey CV, Bradbury AW.
Saphenous surgery does not correct perforator incompetence in the presence of deep venous reflux. J Vasc Surg 1998;28:834-8.
in the brachial artery diameter after reactive hyperemia is less after glucose ingestion, this is a result of the increased resting diameter. Thus, the decline in flow-mediated dilatation when expressed as a percentage of the resting diameter is likely explained by the increase in the resting diameter rather than by acute impairment of the nitric oxide pathway. Although the authors repeatedly discuss this increase in resting vessel diameter with hyperglycemia, they discount its significance. It has been shown repeatedly that flow-mediated vasodilatation is inversely related to the baseline brachial artery diameter.1· 3 I suspect this is the explanation for their findings in the macrocirculation. The authors are correct in stating that there are difficulties in assessing the microcirculation. Yet, they are confident that the iontophoresis of acetylcholine is likely the "most effective and reliable noninvasive method available" to assess this vascular bed. As previously stated, I am concerned that the apparent difference noted in skin blood flow with hyperglycemia (when expressed as a percent change from baseline) is largely reflective of the significant increase in basal flux after glucose loading. In fact, the absolute change from baseline does not appear to be significantly different between fasting and hyperglycemia. Moreover, recent reports4 ,5 suggest that changes in skin blood flow in response to iontophoresis of acetylcholine are more likely mediated by prostanoids rather than by nitric oxide because NG-monomethyl-L-arginine (L-NMMA; an inhibitor of nitric oxide synthesis) infusion had no effect on the acetylcholine response. Because L-NMMA will most often attenuate the flow-mediated dilatation of the brachial artery, these two noninvasive assays may be examining different effects in the microcirculation versus the macrocirculation. Lawrence Title, MD
Division of Cardiology New Halifax Infirmary Halifax, Nova Scotia, Canada
24/41/97869 REFERENCES 1. Celermajer DS, Sorensen KE, Bull C, Robinson J, Deanfield
Regarding "Endothelium-dependent vasodilatation is impaired in both microcirculation and macrocirculation during acute hyperglycemia"
To the Editors: It was with great interest that I read the article by Akbari et al (J Vasc Surg 1998;28:687-94). However, I do not ibelieve that the results fully support the authors' conclusion that endothelial function is impaired after acute oral glucose loading in healthy subjects. Although there was an apparent decline in flow-mediated dilatation of the brachial artery after glucose ingestion (4.2% vs 11.7%; P < .001), this decline appears to be largely related to the significant increase in the resting brachial artery diameter 60 minutes after the ingestion of the glucose (3.92 mm vs 3.73 mm; P< .02). In contrast, the brachial artery diameter after reactive hyperemia was not significantly different during fasting or hyperglycemia (4.22 vs 4.17 mm; P = .28). Although the absolute change
2.
3.
4.
5.
JE. Endothelium·dependent dilation in the systemic arteries of asymptomatic subjects relates to coronary risk factors and their interaction. J Am Coli CardioI1994;24:1468-74. Jensen· Urstad K, Rosfors S. A methodological study of arterial wall function using ultrasound technique. Clin Physiol 1997;17:557-67. Uehata A, Lieberman EH, Gerhard MD, et al. Noninvasive assessment of endothelium-dependent flow-mediated dilation of the brachial artery. Vasc Med 1997;2:87-92. Noon JP, Walker BR, Hand MF, Webb DJ. Studies with iontophoretic administration of drugs to human dermal vessels in vivo: cholinergic vasodilatation is mediated by dilator prostanoids rather than nitric oxide. Br J Clin Pharmacal 1998;45:545-50. Khan F, Davidson NC, Littleford RC, Litchfield SJ, Struthers AD, Belch JJ. Cutaneous vascular responses to acetylcholine are mediated by a prostanoid-dependent mechanism in man. Vasc Med 1997;2:82-6.
24/41/97877