Number 24, 2004
Angina Pectoris

Assessment of collateral circulation

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Gerald S. Werner
Clinic for Internal Medicine I, Friedrich-Schiller-University Jena, Jena, Germany
Correspondence: Gerald S. Werner, Klinik für Innere Medizin I, Friedrich-Schiller-Universität, Erlanger Allee 101, D-07740 Jena, Germany.
Tel: +493641939538, fax: +493641939363, e-mail: gerald.werner@med.uni-jena.de

Historical background
Among the first to describe connections between the major coronary arteries was the Dutch anatomist Richard Lower, in the 17th century. Ever since, there has been continuing dispute over whether these connections exist as preformed interarterial connections or develop only as the consequence of an occluded coronary artery. These so-called collaterals are often capable of fully supplementing blood flow to the myocardium distal to a coronary occlusion, preserving myocardial function (Figure 1), but collaterals are also observed in patients after myocardial infarction, and the question arises whether these collaterals had been insufficient to prevent the myocardial infarction or started to develop only after the acute coronary occlusion.

Angiographic assessment of collaterals
Assessment of collaterals in man became possible with the development of coronary angiography [1,2]. This is the most widely used method, being available during routine diagnostic angiography, but it is only semiquantitative, based on the description of collateral filling by Rentrop and Cohen [3] (Table I). Even in early angiographic studies, detailed analysis was made of the collateral anatomy, but no relationship was found between specific patterns of collaterals and well preserved or impaired myocardial function [1]. This limitation is probably technique related, and semiquantitative assessment of the collateral diameters may help to refine the classic Rentrop grading [4] (Table I). This approach is also of potential value to assess collateral development over the course of time [5].

Table I. Semiquantitative angiographic assessment of the collateral circulation. ^aAccording to Rentrop and Cohen [3]; ^bModified from [2,4], with permission.

Experimental assessment of collaterals
The collateral circulation has been extensively studied in experimental animal models, but species differences in the coronary anatomy limit extrapolation of these findings to man [6,7]. Better understanding of collateral circulation in man would provide insight to specific features of human coronary pathophysiology; however, recent therapeutic attempts to induce collateral development in man now also make more refined methods a necessity, to enable assessment of this angiogenesis [8]. A quantitative assessment of new therapeutic strategies would be superior to angiographic methods [9].
One important finding from animal experiments is that collateral perfusion is best achieved through large epicardial channels, developed in a process called arteriogenesis that is triggered by pressure gradients along arterioles and resulting shear stress, and not through capillary structures developed in response to ischemia in a process called angiogenesis [10].

Invasive assessment of collaterals in man
Noninvasive methods allow accurate assessment of coronary perfusion if the coronary anatomy is known [11], but their interpretation is impaired in multivessel disease [12,13].
Physiologically viewed, collateral function is characterized by the ability of the collaterals to maintain adequate perfusion pressure and perfusion volume to the myocardium distal to an occluded or severely obstructed artery. Assessment of pressure and flow in the collateralized vascular region would provide the best physiologic measure of collateral function; they are the basic parameters describing the fluid dynamics of blood flow from which the properties (vascular resistances) can be derived.
Direct assessment of collaterals became available with the development of percutaneous transluminal coronary angioplasty (PTCA). The pressure measured through balloon catheters during a balloon occlusion is a measure of collateral supply, and patients with greater distal occlusion pressures less often had angina during balloon occlusion [14]. The small fluid-filled central lumen of these catheters provided only damped pressure recordings, but the approach was similar to that used when microsensors became available to record pressure at the tip of 0.36mm (0.014 inch) wires and to record coronary flow velocity [15]. The first studies of collateral circulation with these new tools were carried out during PTCA of high-grade coronary lesions, and quantitative indices of collateral function were introduced [16–19] (Table II). The collaterals in these patients either were already visible during diagnostic angiography or become visible during balloon occlusion, as recruitable collaterals.

Table II. Calculation of physiologic components of collateral circulation.

Determinants of collateral function
About every fifth person appears to have some well-developed, preformed interarterial connections that can serve immediately as collaterals during a coronary occlusion [25] and which remain as a functional reserve if a coronary lesion is treated successfully [26]. In contrast, the majority of collaterals disappear immediately after angioplasty and may not be able to prevent an acute myocardial infarction [20].
Collateral development is determined by the severity of stenosis of the artery to which they connect, and they are best developed in totally occluded arteries [27]. If a stenosis deteriorates gradually, collaterals have time to develop, but in cases of acute myocardial infarction without prior collateral formation, they start to appear within a few days [28], and reach full functional competence within 3 months [21].
Differences in the angiographic grading of collaterals between diabetic and nondiabetic patients have led to continuing debate as to whether diabetes would affect collateral development [29]. However, a number of studies contradict this observation [30,31]. When invasive methods were applied, no adverse influence of diabetes on collateral development was observed [32,33]; however, the development of collaterals may be delayed compared with that in nondiabetic patients [33].

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REFERENCES

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