Vascular function of the peripheral and coronary circulation: Worthwhile to assess their relation?

Abstract

In this issue of the journal, Scholtens et al report of an absence of any correlation (r = 0.13, SEE = 54; P = .36) between hyperemic myocardial and peripheral blood flows during pharmacological vasodilation with adenosine in a heterogenous group of patients and healthy volunteers as determined with N-ammonia PET. The study is unique in that it concurrently measured the blood flow increase or vasomotor response during pharmacologically induced vasodilation of the arteriolar resistance vessels in the myocardium and upper limb muscle. The current investigation agrees with earlier observations from Bottcher et al but extends them now also to the same stimulus to induce flow increases in the coronary and peripheral circulation. Bottcher et al were first to describe that the peripheral arterial flow responses to transient forearm ischemia did not correlate with dipyridamole-induced hyperemic myocardial blood flow increases. Thus, the current and previous investigations strongly suggest different regulatory mechanisms of the coronary and peripheral microcirculations in the diseased and normal vascular states. Extrapolations between findings in the two vascular beds therefore may not necessarily apply. At the first sight, the results from Scholtens and those from Bottcher et al may indeed contrast the reported association between vascular function of the brachial and epicardial artery from a previous investigation conducted by Anderson et al. In the latter study, the stimuli to provoke the vasomotor response in the peripheral and coronary circulation were different and a different vascular bed was examined, i.e. conductance arteries. Alterations of epicardial artery diameter in response to intracoronary acetylcholine infusion were determined with quantitative coronary angiography (QCA), while the change in brachial artery diameter in response to reactive hyperemia in the peripheral circulation was determined with vascular ultrasound. Thus, endothelial function of the epicardial artery was specifically tested with acetylcholine stimulation of the muscarinergic receptor, whereas flow-mediated brachial artery response was determined in response to hyperemic flow increases. In both the instances, the endothelial vasoreactivity of the conduit vessels of the periphery and coronary circulation was tested. This may explain the observed statistically significant but rather weak correlation between endothelium-dependent vasomotor responses at the site of conduit vessel of the peripheral and coronary circulation in patients with and without angiographically determined CAD (P = .36, P .01) (Figure 1). Interestingly, this weak correlation appeared to be driven by patients without evidence of structural CAD. Conceptually, if these patients without evidence of structural CAD were taken out of the analysis, no association between peripheral and coronary endothelial function would probably exist. Thus, the results from Anderson et al suggest that CADrelated advanced structural alterations may actually dissolve the described association of endothelial function between the peripheral and coronary circulation. The prognostic value of the assessment of endothelial or vascular dysfunction of the peripheral and coronary circulation is well established. In particular, the power of peripheral and coronary endothelial dysfunction in response to various stimuli in the prediction of cardiovascular events appears to be comparable. Cardiovascular events therefore may occur remotely from the site of endothelial dysfunction identified. These observations strongly suggest a systemic nature of vascular dysfunction and its central role in predicting future cardiovascular events. Vascular dysfunction has been appreciated as a useful integrating index of the overall stress burden by various cardiovascular risk factors on the arterial wall, taking into account the cumulative risk of cardiovascular risk factors and as yet unknown variables and genetic predispositions. Despite this, it is From the Department of Internal Medicine, Division of Cardiology, Nuclear Cardiology, University Hospitals of Geneva, Geneva, Switzerland; and Department of Cardiology, Cardiovascular Center, University Hospital Zurich, Zurich, Switzerland. Reprint requests: Thomas H. Schindler, MD, PhD, Department of Internal Medicine, Division of Cardiology, Nuclear Cardiology, University Hospitals of Geneva, 6th Floor, Rue Gabrielle-PerretGentil 4, 1211 Geneva, Switzerland; thomas.schindler@hcuge.ch. J Nucl Cardiol 2011;18:201–3. 1071-3581/$34.00 Copyright 2011 American Society of Nuclear Cardiology. doi:10.1007/s12350-011-9357-0