Adv. Cardiol., vol. 18, pp. 104-112 (Karger, Basel 1976)

Physical Activity and Coronary Collateral Development 1 J. BARMEYER Department of Clinical Cardiology, University of Freiburg, Freiburg

Supported by a grant from the Stiftung Volkswagenwerk.

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Collaterals can only develop in organs like skeletal muscles, skin, brain and heart which are supplied by so-called net arteries. Collaterals are vessels which are essential for compensating high grade stenoses or complete occlusions and to prevent further ischemia. It has become useful to differentiate between primary and secondary collaterals. Primary collaterals are available immediately in case of an acute arterial occlusion. The acute fate of the affected area depends almost completely on the extent of these interarterial connections. Secondary collaterals, however, develop slowly during weeks or months from capillaries or arterioles and are induced by gradual arterial narrowing. The purpose of this presentation is to investigate the possibility that physical training may promote the growth of collaterals in the coronary patient. The human coronary collaterals form a very complex system of arterioarterial connections with a diameter ranging from 50 to 500 fl, arteriosinusoid vessels and arterioluminal vessels both located in the inner layers of the myocardium, and finally arterio-venous and veno-venous collaterals. The existence of primary collaterals in the human heart has been confirmed by many precise investigations. Anatomical studies have demonstrated predilective sites for these vessels. Primary collaterals can be demonstrated in the interventricular septum and at the apex of the heart connecting the left anterior descending and the right posterior descending artery. Another important primary collateral between left and right coronary artery is the ring of Vieussens connecting the

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conus artery and the proximal left anterior descending artery. A connection between the proximal left circumflex artery and the sinus node artery is called Kugel's artery. Finally, there may be primary connections between the distal left circumflex artery and the posterior branches of the right coronary artery. Primary collaterals in the human heart do not usually prevent myocardial infarction when acute occlusion of a major coronary artery ensues. A typical example demonstrating the incomplete efficacy of primary collaterals is the acute proximal occlusion of the left anterior descending artery in young patients with one vessel disease who without exception, suffer a large anterior wall infarction. Secondary collaterals, however, are much more effective in protecting the myocardium against necrosis. They mostly develop in the interventricular septum, at the apex of the heart and between the right marginal branch and the left anterior descending artery. Figure 1 demonstrates the angiogram of a patient with a so-called infarct at a distance. The extraordinarily well-developed intercoronary connections between right and left coronary artery had fully compensated for the old right coronary artery occlusion. Then, an acute occlusion of the left

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Fig. 1. Postmortem angiogram of a 62-year-old man with acute anterior wall infarction. Old occlusion of the right coronary artery (left arrow) and fresh occlusion of the left anterior descending artery (right arrow).

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anterior descending artery induced a posterior wall infarction by interrupting blood flow in the septal anastomoses. Occasionally, connections between the right marginal branch and the left anterior descending artery can be visualized as demonstrated in figure 2. Collaterals between the conus artery (arrow) and the posterior descending artery are an infrequent finding however (fig. 3). Conditions usually supposed to promote the growth of collaterals are: (1) hypoxia; (2) pressure gradients; (3) increased flow volume, and (4) increased flow velocity. Further analysis of these conditions reveals that the connecting factor (fig. 4) is increased flow velocity and may thus be the causative mechanism triggering the growth of collateral vessels. In which way, however, is still a matter of doubt. Some theoretical reflections may be justified as to how physical training could stimulate collateral development in a patient with coronary artery disease. Many investigations have clarified that pathologic conditions like severe chronic anemia, hypoxemia in pulmonary disease, diseases of the heart valves with hypertrophy and, particularly, occlusive coronary disease, can promote coronary collateral development. It is still a matter of debate as to whether vigorous physical exercise may induce additional collateral growth.

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Fig. 2. Postmortem angiogram of a 59-year-old man who died of acute coronary insufficiency. Dominant right coronary artery with connection between right marginal branch and left anterior descending artery (arrow).

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Fig. 3. Postmortem angiogram of a 56-year-old man without clinical evidence of heart disease. Collateral between conus artery and posterior descending artery compensating a complete occlusion of the right coronary artery (arrow).

artery (arrow).

artery artery (arrow). (arrow).

artery (arrow).

artery artery (arrow). (arrow).

Figure 5 demonstrates a theoretical model of the possible mechanism for the development of collateral flow around an arterial stenosis that is hemodynamically insignificant under resting conditions. In this model, we have an artery with a 60% reduction of its cross-sectional area. This artery is not critically stenosed under resting conditions. The blood moves in a laminar flow. No pressure gradient is apparent between the pre- and poststenotic arterial segment PI and P2. The result is no flow or very little flow in the preformed collateral pathway. Now physical activity begins and considerably increases flow and flow velocity in the prestenotic segment. As a result, blood pressure rises and the stenosis becomes critical since laminar

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Fig. 4. Collateral development by increased flow velocity.

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Rest

Physical activity

Laminar flow

Turbulent flow LlP:PI -P2 Ipressure gradient) L : Length F :Flow v

:VISCOSlty

R : Radius

Fig. 5. Theoretical model for the development of collateral flow around an arterial

flow may be transformed into turbulent flow. A pressure gradient develops between the pre- and posts ten otic segment of the artery and perfusion of the preformed collateral vessel may ensue which additionally may be encouraged by a so-called Venturi effect in the poststenotic area. So, theoretically, repeated physical activity and other conditions which produce a sufficient increase of flow and flow velocity may induce perfusion of this collateral vessel and encourage gradual enlargement of this pathway. These theoretical considerations make it clear that efficient collateral development may only be encouraged by repeated physical training in cases where there are no significant pressure gradients under resting conditions. Collateral cilculation in myocardial areas which are hypoxic during resting conditions has probably reached its maximum and may not be increased further by physical training. We investigated 70 hearts postmortem in order to determine quantitatively the coronary collateral flow in hearts with different pathological conditions (normal hearts, hearts with all degrees of coronary sclerosis, hypertrophy and valvular disease). Figure 6 demonstrates the principle of measurement of anastomotic flow. At first, both coronary arteries were perfused simultaneously, yielding the flow volume A. Perfusion of intercoronary communications did not occur to any significant extent since pressure gradients were not present, or were so only to a small degree, between the coronary arteries. Then both coronary arteries were perfused separately yielding the flow volume Band

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stenosis.

Physical Activity and Coronary Collateral Development

A

B

109

C

(B+C)-A=anastomoilc flow

Fig. 6. Principle of measurement of intercoronary anastomoses. RAF 11 0 100

..

90 80 70 60 50 40 30 20 10

....

. .... :

.' . . .

'.

'

10 20 30 40 50 60 70 80 90 100

120

140

160 ReF

C. In both cases, pressure gradients developed between the arteries so that fluid could pass through intercoronary channels to the non-perfused artery. The different flow volumes were sampled per minute. Since the sum of the flow volumes Band C always exceeded the flow volume A, the difference between B plus C and A must necessarily give some hints about the extent of intercoronary flow between the two arteries under these experimental conditions. Of course, this relatively coarse method has a lot of shortcomings and can give only hints, but other postmortem methods for providing quantitative information about collateral flow do not as yet exist. The results are presented in figure 7.

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Fig. 7. Relation between relative coronary flow (RCF in mi/IOO g myocardium) and relative anastomotic flow (RAF in %). Correlation coefficient, -0.64, p < 0.001.

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Training

Increase

Decrease

No change

Vigorous (I 1) Slight (12) None (6)

7

6 4

3 3

3

The measurements revealed a strong negative correlation between the decrease of the coronary flow and the increase of the collateral flow. It is evident that below a coronary flow of about 50 ml/lOO g myocardium, being about half the normal flow in these experiments, anastomotic flow rose steeply, indicating that a level had been reached where anastomotic development ensued. According to these results, a patient with moderate coronary sclerosis with a fictive flow of about 60-70 ml/lOO g myocardium would normally not react with coronary collateral development. But one can imagine this patient developing coronary collaterals after taking exercise repeatedly for a sufficient time, since hypoxia and pressure gradients as very strong stimuli may develop according to the theoretical model. There are two possible ways of investigating collateral development by physical training: (1) coronary angiography, and (2) the experimental animal. Selective coronary angiography is a very coarse method. Only extramural collaterals can be visualized. Since no well-documented controlled angiographic studies are available we must still depend on general impressions. HELFANT et al. [4] did not find better coronary collateralization in physically active patients with coronary insufficiency than in sedentary persons. KATTVS and MAC ALPIN [6], however, saw improved collateralization in several patients who had great improvement on exercise therapy in the post-training angiograms. In our clinic, a group of 50 coronary patients have been in physical training for 3 years. Post-exercise coronary angiography in 7 patients did not reveal more or wider collaterals than in non-training patients. In addition to the coronary patients, 60 patients with peripheral arteriosclerotic diesase have been training for 3 years. Pre- and post-training angiograms which were performed in 23 patients were compared with angiograms of an untrained control group of 6 patients.

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Table I. Physical training and collateral development in peripheral arteriosclerotic disease

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Physical Activity and Coronary Collateral Development

Table II. Physical activity and collateral development (experimental studies) Authors

Animals Physical training

Technique

Method

Collateral development

TEPPERMAN and PEARLMAN [7]

rat

swimming

corrosion cast

no constriction

ECKSTEIN [3]

dog

running

back flow

constriction

+ +

BURT and JACKSON [2]

dog

running

back flow angiography

no constriction

KAPLINSKI et al. [5]

dog

running

angiography

constriction

AMANN et al. [1]

dog

running

angiography

no constriction

SCHAPER et al. [8]

dog, pig

running

peripheral coronary pressure

constriction

+

One group was training vigorously, another lightly, and a third group served as a control group. Table I reveals that there was no significant difference in collateral development between the exercising and non-exercising patients, a finding which corresponds to our angiographic experience in coronary patients. TEPPERMAN and PEARLMAN [7] found an increase in the cross-sectional area of extramural collaterals in rats after swimming. ECKSTEIN'S [3] studies revealed a significantly better collateralization after coronary arterial narrowing in running dogs than in non-running dogs. On the other hand, BURT and JACKSON [2], KAPLINSKI et al. [5], AMANN et at. [1], and SCHAPER et al. [8] were not able to demonstrate more collaterals in dogs after exercise. Only SCHAPER et al. [8] found some suggestion that physical training may improve collateral development in the pig (table II).

If we summarize the results of experimental and angiographic studies, it must be said that at the present time we are not justified in concluding that physical training promotes the growth of collaterals. On the other hand, we cannot exclude the possibility of their development on exercise either since we have no method yet to determine collateral flow quantitatively in the human being.

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Conclusions

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In my opinion, the chronically hypoxic myocardium has already developed a maximum of collateral circulation which cannot be increased further by physical training. However, in a patient with moderate coronary sclerosis without any ischemic myocardial areas under resting conditions, collateral improvement may well be induced by regular and substantial exercise. This, however, is still only a hypothesis.

References

2 3 4 5

6 7

8

AMANN, L.; MEESMANN, W.; SCHULZ, F. W.; SCHLEY, G.; WILDE, A. und TOTTEMANN, J.: Untersuchungen tiber die Collateralentwicklung am gesunden Herzen nach kiirperlichem Training. Verh. dt. Ges. KreislForsch. 37: 150-154 (1971). BURT, J. J. and JACKSON, R.: Coronary collateral development. J. Sportmed. 5: 203 (1965). ECKSTEIN, R. W. : Effect of exercice and coronary artery narrowing on coronary collateral circulation. Circulation Res. 5: 230-235 (1957). HELFANT, R.; VOKONAS, P., and GORLIN, R.: Functional importance of the human collateral circulation. New Eng!. J. Med. 284: 1277-1281 (1971). KAPLINSKY, E.; HOOD, W. B.; MCCARTHY, B.; MCCOMBS, H. L., and LowN, B. : Effect of physical training in dogs with coronary artery ligation. Circulation 37: 556- 565 (1968). KATTUS, A. A. and McALPIN, R . N.: Role of exercise in discovery, evaluation and management of ischemic heart disease. Cardiovasc. Clin. 1: 355 (1969). TEPPERMAN, J. and PEARLMAN, D . : Effect of exercise and anemia on coronary arteries of small animals as revealed by the corrosion-cast technique. Circulation Res. 9: 576-584 (1961). SCHAPER, W.; FLAMENG, W.; SNOECKX, L. und JAGENEAU, A.: Der Einfluss kiirperlichen Trainings auf den Collateralkreislauf des Herzens. Verh. dt. Ges. KreislForsch. 37: 112-121 (1971).

Dozent Dr. JORGEN BARMEYER, Department of Clinical Cardiology, University of Freiburg, D-7800 Freiburg (FRG)

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Physical activity and coronary collateral development.

Adv. Cardiol., vol. 18, pp. 104-112 (Karger, Basel 1976) Physical Activity and Coronary Collateral Development 1 J. BARMEYER Department of Clinical C...
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