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The subendocardial lymphatics of the canine heart
Exoerimental
Studies
The Subendocardial
Lymphatics of the Canine Heart
A Possible Role of the Lymphatics in the Genesis Conduction Disturbances and Arrhythmias.
HERMAN N. UHLEY, MD, FACC SANFORD E. LEEDS, MD MARY ANNA SUNG, MD with
the technical
SHANTILAL ENRIQUE
assistance
PATEL,
of
ES and
LOBOS
San Francisco,
California
From the Departments of Medicine, Experimental Surgery, and Pathology, Mount Zion Hospital and Medical Center, San Manuscript received Francisco, Calif. March 9, 1971, accepted May 17, 1971. Address for reprints: Herman N.. Uhley, MD, Mount Zion Hospital and Medical Center, 1600 Divisadero St., San Francisco, Calif. 94115.
VOLUME 29, MARCH 1972
of
The subendocardial lymphatics of the canine right ventricle were visualized, and their anatomic relation to the right ventricular conduction system was observed. The lymphatics traversed the main right bundle at many levels and intersected with longitudinal lymphatics following the course of the bundle. In addition, lymphatica crossed the various peripheral branches of the right bundle. The lymphatics anterior to the right bundle tended to be more transversely oriented, whereas those posterior to the bundle were longitudinal, extending from the inferior region to the superior portion of the septum. It is suggested that the lymphatics may play a role in pathologic lesions involving the conduction system, either by direct involvement, or indirectly, by carrying large concentration of potassium from remote damaged areas. The effect of the potassium could be manifested as a conduction defect due to decreased conduction velocity (for example, A-V conduction defects with inferior infarction or right bundle branch block with anteroseptal infarction) or the development of arrhythmias.
Within recent years there has been increased interest in the numerous conduction defects observed in clinical electrocardiography.l Experimental studies have demonstrated the location of the peripheral conduction system by gross staining in man and in the dog,2-4 and the effect of interruption of its various components on the electrocardiogram.5-7 The electrocardiogram that demonstrates a conduction defect may give some insight into localization of disease ; however, the appearance of a conduction defect on the electrocardiogram does not reveal the nature of the underlying pathologic process. Indeed, there is a controversy as to whether certain conduction defects may be due directly to arteriosclerosis or to other pathologic causes.8-11With this in mind, and an awareness of the possible role of the cardiac lymphatics in and experimental conditions,15J6 an other pathologic states12m14 investigation was conducted on the relation of the subendocardial lymphatics to the conduction system of the canine heart.
Methods Twelve dogs were used in this study which was confined to the right ventricle. Evans blue dye was injected into the subendocardial tissue with a no. 30 needle. In 2 dogs, the right ventricIe was opened under
367
UHEY
ET AL
Figure 1.
The large unstained, transversely oriented lymphatic (L) is located in the mid right ventricle anterior to the main right bundle (RB) (white band), and inferior to the small papillary muscle of the septal leaflets of the tricuspid valve.
Figure 4. Extrinsic network of lymphabics (L) transversing and extending along the main right bundle (RB).
cardiopulmonary bypass, and several sites around the right bundle were injected. One heart was injected during inflow occlusion. In the remaining animals the heart was removed and washed free of blood, and injected and studied with use of a Zeiss operating microscope and camera. At times it was possible to see a lymphatic channel which could be cannulated directly and injected (Fig. 1). However, in most instances the dye had to be injected into the subendocardial tissue and, when the lymphatics were entered, blue streaks would project out of the mass of injected dye (Fig. 2). The conduction system was identified by gross staining with Lugol’s solution, and the relation of the lymphatics to the conduction system was observed.
Results
Figure 2. Needle injecting dye in the region of the small . .. papillary muscle of the septal leaflet of the tricuspid valve. Note streaks of lymphatics (L) projecting out of the mass of dye.
Figure 3.
Longitudinal lymphatic (L) of the main right bundle (RB) is filled by way of small transverse lymphatics after injection in the superior portion of the anterior septum.
368
The subendocardial lymphatics of the canine heart form a vast network of various shapes and formations which may change at different sites. At times they appear more or less singly in a linear fashion ; at other times the course is tortuous. The lymphatics may have numerous branches intersecting at nearly right angles, or frequently they may form a loose reticular fishnet-like arrangement intersecting at various angles. A given area may be dense with closely interlacing lymphatics, whereas in other areas lymphatics may be less obvious. The vessels vary in size, with some of the larger trunks actually being visible without stain if one looks closely with the light reflecting at a proper angle. A large prominent lymphatic vessel (approximately 1 mm in diameter) can occasionally be seen under the endocardium in the region between the pulmonary outflow tract and the middle course of the right bundle. This vessel generally traverses several millimeters of the anterior septal region of the right heart chambers somewhat perpendicular to the right bundle (Fig. 1). There is an anatomic relation between the subendocardial lymphatics and the main right bundlej (Fig. 3 to 5). Numerous lymphatics traverse the anterior surface of the right septum and cross the The American Journal of CARDIOLOGY
SUBENDOCARDIAL LV~~PHATI~S AND c0N~UcTldN
Figure
5. Transverse lymphatic (L) cmsses ! (RB) and becomes superiorly oriented.
the
right bundle at approximately right angles. They are seen in the middle portion of the right bundle as well as the superior portion near the tricuspid valve and the inferior portion near the base of the anterior papillary muscle. The most striking feature of the relation between the lymphatics and the right bundle is the presence of a generally single longitudinal lymphatic pathway running parallel to the right bundle (Fig. 3 to 5). This channel hugs the right bundle and communicates with the numerous lymphatics that cross the bundle. Other, generally smaller lymphatic vessels cross the anterior (Fig. 6) and posterior branches (Fig. 7) of the right ventricular conduction system. There are also lymphatics crossing the lateral conduction network covering the right mural wall. The lymphatics that come in contact with the various branches of the conduction system beyond the main right bundle tend to be more sparse and have no specific angular relation to the conduction fibers. The lymphatics posterior to the right bundle are longitudinally oriented and may extend from the inferior regions of the heart all the way up to the tricuspid valve (Fig. 8 and 9). On the other hand, lymphatics anterior to the right bundle are more transversely oriented, although shorter more or less longitudinal vessels may be seen. The lymphatics on the papillary muscles were apparent as fine channels near the insertions of the chordae tendineae or on the muscle surface (Fig. 10). Lymphatics could be seen near the base of the small papillary muscle arising from the region near the pulmonary conus as well.
Figure amidst tricular
DEFECTS
6. Lymphatic (L) oriented in a semicircular s#hape the anterior branches of the peripheral right venconduction system.
Lymphatics (L) crossing some of the peripheral Figure 7. conduction fibers (PCF) of the posterior branches of the right ventricular conduction system. Because of the anatomic relationship to some of the posterior branches, it is possible that high potassium concentration from remote tissue damage might cause slower conduction velocities in these fibers thereby enhancing the development of reentry.
Discussion The lymphatics are fine thin-walled delicate structures which are frequently obscured in the postmortem state and are generally very difficult to observe.17 However, informative studies can b& VOLUME 29. MARCH 1972
Lymphatic channel (L) extending from the inFigure 8. ferior regions of the septum to the septal leaflet of the tricuspid valve. 369
UHLEY
ET AL.
Figure 9. Close-up of the lymphatics (L) extending superiorly from the inferior septal region. It is theorized that such lymphatics could ‘carry high concentrations of substances (for example, potassium) from the site of an inferior infarction superiorly to the regions of the A-V conduction system and cause various A-V conduction defects.
made with the use of special dyes or techniques.lQ PateklQ described the anatomy of the cardiac lymphatics and demonstrated that the subendocardial lymphatics connect to a myocardial and subsequently to an epicardial plexus leaving the heart by several main drainage trunks. He noted that valves were uncommon in subendocardial plexus. These studies demonstrate a well defined system of lymphatic vessels beneath the endocardial surface of the right ventricle brought forth by injection of Evans blue dye. The lymphatic vessels exist in various anatomic arrangements (Fig. 11). In general, the lymphatics in the anterior septal
Figure 11. Composite diagram ihustrating the relationship of the canine endocardial lymphatics to the right ventricular conduction system. Note the transverse and longitudinal lymphatics of the right bundle (RB) and the lymphatics crossing some of the peripheral conduction fibers. Lymphatics anterior to the bundle appear somewhat more transversely oriented than the longer longitudinal branches posterior to the bundle.
370
Figure 10. Fine lymphatic on the posterior septum.
channels
longitudinally
oriented
area seem to appear more transversely oriented, whereas lymphatics in the posterior septum appear longitudinal. In regard to the conduction system per se, lymphatics not only traverse the main bundle, but form a longitudinal pathway along the course of the right bundle. The anterior, lateral and posterior branches of the right bundle are also traversed by lymphatics; however, the density of lymphatics seems to be greater in the region of the main right bundle than in the region of the peripheral conduction tissue. Certain lymphatic vessels may at times appear relatively large, in particular, the centrally located lymphatic just anterior to the mid-portion of the main right bundle. The subendocardial lymphatics are part of an extensive transport system capable of returning interstitial materials to the vascular system. Accordingly, if these fine thin-walled transport vessels could become involved with the pathologic process, it is conceivable that adjacent structures might also be affected. For example, inflammation of the perilymphatic structures might lead to subsequent fibrosis and interruption of normal function (delayed or decremental conduction and block). There are specific pathologic entities relating to the conduction system such as sclerosis of the cardiac skeleton described by LevlO and degenerative changes of the conduction system per se described by Yater et a1.8 and Lenegre.9 The question is raised whether these entities as well as myopathies, in part, have their effects on the conduction system mediated by the lymphatics of the heart. Possible role of lymphatics in conduction disCardiac lymph reflects myocardial poturbances: tassium changes.20 Accordingly, one might anticipate that lymphatics draining areas of tissue damage might carry away waste products such as large concentrations of potassium from injured cells. Such relatively high levels of potassium might in turn equilibrate across the lymphatic wall to the immediate environment of the conducThe American
Journal
of CARDIOLOGY
SURENDOCAQDIAL
tion tissue; possibly they would alter conduction velocity, producing transient slowing or block such as is frequently observed in certain myocardial infarctions. Hence, the appearance of intermittent conduction defects might be due to tissue damage in a remote area linked to the conduction system by the lymphatic system as well as to direct damage by the pathologic process to the conduction tissue. The appearance of various degrees of atrioventricular (A-V) block is a frequent transient phenomenon associated with inferior myocardial infarctions. The block is generally thought to be due to occlusive disease in the right coronary artery. However, the block frequently occurs several days after the onset of the inferior infarction, and the terminal branches of the right coronary artery supplying the inferior myocardium are remote from the branches supplying the A-V node. The anatomic study in this paper demonstrates a lymphatic network in the inferior portion of the right heart chambers which drains superiorly to the region of the A-V node (Fig. 8 and 9). Accordingly, it is conceivable that inferior tissue damage would liberate, over a period of time, vast stores of intracellular potassium which would be transported by way of these lymphatics to the region of the A-V node. In so doing, the equilibration of potassium through the lymphatics could alter the extracellular environment of the A-V junction and slow conduction velocity, resulting in a gradual rather than immediate appearance and disappearance of A-V conduction delay after an inferior infarction.
LYMPHATICS
AND CONDUCTION
DEFECTS
In a similar manner, damage to the tissue of the anterior septum would result in lymph flows toward the right bundle, possibly causing transient complete right bundle branch block. Various peripheral branches of the right ventricular conduction system might also become involved depending on the location of the myocardial damage. Possible role of lymphatics in arrhythmias: The same conditions might be applicable to the development of reentry wherein lymphatics carrying high potassium concentrations from remote damaged areas bring normal myocardium or some strands of Purkinje fibers in contact with a high potassium environment21 thereby delaying the passage of the wave front at a given area. If the involved area has unidirectional block characteristics, and the delayed wave front finds it possible to emerge and activate adjacent myocardium which is no longer refractory, ectopic beats will be set up by means of a reentry mechanism. The effect of local increases in potassium, as determined by the lymphatic pathways, could also bring the resting membrane potential of a given area closer to the threshold of excitability, thereby setting up ectopic foci. On the other hand, delays’ ip conduction velocity of tissue may play a role in the development of exit and protection blocks. Thus, the recognition of an anatomic relation of the lymph system to the conduction fibers might provide some insight into both permanent and transient block patterns and possibly the induction of some arrhythmias seen in clinical electrocardiography.
References 1. Rosenbaum
MB, Elizari MV, Lazzari JO: Los Hemibloqueos. Buenos Aires, Ed. Paidos, 1968 2. Uhlev HN. Rivkin LM: Visualization of the left branch of the human atrioventricular bundle. Circulation 20:
419-421,1958 3. Uhley HN, Rivkin
12.
LM: Peripheral distribution of the conduction system. Amer J Card,iol 5:688-
canine A-V 691,196O 4. Spach SM, Huang S-N, Armstrong SI, et al: Demo,nstration of peripheral conduction system in human hearts. Circulation 28:333-338, 1963 patterns 5. Uhley HN, Rivkin LM: Electrocardiographic following interruption of main and peripheral branches of the canine right bundle of His. Amer J Cardiol 7:810816, 1961 patterns fol6. Uhley HN, Rivkin LM: Electrocardiographic lowing interruption of the main and peripheral branches of the canine left bundle of His. Amer J Cardiol 13:4147, 1964 findings as7. Watt TB Jr, Pruitt RD: Electrocardiographic societed with experimental arborization block in dogs. Amer Heart J 69:642-654,1965 8. Yater WM, Cornell VH, Claytor T: Auriculoventricular heart block due to bilateral bundle-branch lesions. Arch Intern Med (Chicago) ,57:132-173, 1936 9. Lenegre J: Etiology and pathology of bilateral bundle branch block in relation to complete heart block. Progr Cardiovasc Dis 6:409-444, 1964 block. Amer 10. Lev M: Anatomic basis for atrioventricular
VOLUME
29. MARCH 1972
J Med 37:742-748,1964 The coronary circulation and conduction system in acute myocardial infarction. Progr Cardiovasc Dis lQ:410449, 1968 Miller AJ, Pick R, Katz LN: Ventricular endomyocardial pathology produced by chronic cardiac lymphatic obstruction in the dog. Circ Res 8:941-947, 1960 Uhley HN, Leeds SE, Sampson JJ, et al: The cardiac lymphatics in experimental chronic congestive failure. Proc Sot Exp Biol Med 131:379-381, 1969 Foldi M: Diseases of- Lymphatics and Lymph Circulation. Springfield, Ill, Charles C Thomas, 1969, p 313 Leeds SE, Uhley HN, Sampson JJ, et al: The cardiac lymphatics after ligation of the coronary sinus. Proc Sot Exp Biol Med 13559-62, 1970 Symbas PN, Cooper T, Gantner GE Jr, et al: Lymphatics of the heart. Arch Path 81:573-575, 1966 Kline I: Lymphatic pathways in the heart. Arch Path (Chicago) 88:638-644, 1969 Johnson RA, Blake MM: Lymphatics of the heart. Circulation 33:137-142, 1966 Patek PR: The morphology of the lymphatics of the mammalian heart. Amer J Anat 64:203-249, 1939 Areskog NH, Arturson G, Grotte G: Heart lymph: electrolyte composition and changes induced by cardiac glycosides. Biochem Pharmacol 14:783-787, 1965 Sasyniuk B!, Mendez C: A (mechanism for re-entry in canine ventricular tissue. Circ Res 28:3-15, 1971
11. James TN:
13.
14. 15.
16. 17. 18. 19. 20.
21.
371
Studies
The Subendocardial
Lymphatics of the Canine Heart
A Possible Role of the Lymphatics in the Genesis Conduction Disturbances and Arrhythmias.
HERMAN N. UHLEY, MD, FACC SANFORD E. LEEDS, MD MARY ANNA SUNG, MD with
the technical
SHANTILAL ENRIQUE
assistance
PATEL,
of
ES and
LOBOS
San Francisco,
California
From the Departments of Medicine, Experimental Surgery, and Pathology, Mount Zion Hospital and Medical Center, San Manuscript received Francisco, Calif. March 9, 1971, accepted May 17, 1971. Address for reprints: Herman N.. Uhley, MD, Mount Zion Hospital and Medical Center, 1600 Divisadero St., San Francisco, Calif. 94115.
VOLUME 29, MARCH 1972
of
The subendocardial lymphatics of the canine right ventricle were visualized, and their anatomic relation to the right ventricular conduction system was observed. The lymphatics traversed the main right bundle at many levels and intersected with longitudinal lymphatics following the course of the bundle. In addition, lymphatica crossed the various peripheral branches of the right bundle. The lymphatics anterior to the right bundle tended to be more transversely oriented, whereas those posterior to the bundle were longitudinal, extending from the inferior region to the superior portion of the septum. It is suggested that the lymphatics may play a role in pathologic lesions involving the conduction system, either by direct involvement, or indirectly, by carrying large concentration of potassium from remote damaged areas. The effect of the potassium could be manifested as a conduction defect due to decreased conduction velocity (for example, A-V conduction defects with inferior infarction or right bundle branch block with anteroseptal infarction) or the development of arrhythmias.
Within recent years there has been increased interest in the numerous conduction defects observed in clinical electrocardiography.l Experimental studies have demonstrated the location of the peripheral conduction system by gross staining in man and in the dog,2-4 and the effect of interruption of its various components on the electrocardiogram.5-7 The electrocardiogram that demonstrates a conduction defect may give some insight into localization of disease ; however, the appearance of a conduction defect on the electrocardiogram does not reveal the nature of the underlying pathologic process. Indeed, there is a controversy as to whether certain conduction defects may be due directly to arteriosclerosis or to other pathologic causes.8-11With this in mind, and an awareness of the possible role of the cardiac lymphatics in and experimental conditions,15J6 an other pathologic states12m14 investigation was conducted on the relation of the subendocardial lymphatics to the conduction system of the canine heart.
Methods Twelve dogs were used in this study which was confined to the right ventricle. Evans blue dye was injected into the subendocardial tissue with a no. 30 needle. In 2 dogs, the right ventricIe was opened under
367
UHEY
ET AL
Figure 1.
The large unstained, transversely oriented lymphatic (L) is located in the mid right ventricle anterior to the main right bundle (RB) (white band), and inferior to the small papillary muscle of the septal leaflets of the tricuspid valve.
Figure 4. Extrinsic network of lymphabics (L) transversing and extending along the main right bundle (RB).
cardiopulmonary bypass, and several sites around the right bundle were injected. One heart was injected during inflow occlusion. In the remaining animals the heart was removed and washed free of blood, and injected and studied with use of a Zeiss operating microscope and camera. At times it was possible to see a lymphatic channel which could be cannulated directly and injected (Fig. 1). However, in most instances the dye had to be injected into the subendocardial tissue and, when the lymphatics were entered, blue streaks would project out of the mass of injected dye (Fig. 2). The conduction system was identified by gross staining with Lugol’s solution, and the relation of the lymphatics to the conduction system was observed.
Results
Figure 2. Needle injecting dye in the region of the small . .. papillary muscle of the septal leaflet of the tricuspid valve. Note streaks of lymphatics (L) projecting out of the mass of dye.
Figure 3.
Longitudinal lymphatic (L) of the main right bundle (RB) is filled by way of small transverse lymphatics after injection in the superior portion of the anterior septum.
368
The subendocardial lymphatics of the canine heart form a vast network of various shapes and formations which may change at different sites. At times they appear more or less singly in a linear fashion ; at other times the course is tortuous. The lymphatics may have numerous branches intersecting at nearly right angles, or frequently they may form a loose reticular fishnet-like arrangement intersecting at various angles. A given area may be dense with closely interlacing lymphatics, whereas in other areas lymphatics may be less obvious. The vessels vary in size, with some of the larger trunks actually being visible without stain if one looks closely with the light reflecting at a proper angle. A large prominent lymphatic vessel (approximately 1 mm in diameter) can occasionally be seen under the endocardium in the region between the pulmonary outflow tract and the middle course of the right bundle. This vessel generally traverses several millimeters of the anterior septal region of the right heart chambers somewhat perpendicular to the right bundle (Fig. 1). There is an anatomic relation between the subendocardial lymphatics and the main right bundlej (Fig. 3 to 5). Numerous lymphatics traverse the anterior surface of the right septum and cross the The American Journal of CARDIOLOGY
SUBENDOCARDIAL LV~~PHATI~S AND c0N~UcTldN
Figure
5. Transverse lymphatic (L) cmsses ! (RB) and becomes superiorly oriented.
the
right bundle at approximately right angles. They are seen in the middle portion of the right bundle as well as the superior portion near the tricuspid valve and the inferior portion near the base of the anterior papillary muscle. The most striking feature of the relation between the lymphatics and the right bundle is the presence of a generally single longitudinal lymphatic pathway running parallel to the right bundle (Fig. 3 to 5). This channel hugs the right bundle and communicates with the numerous lymphatics that cross the bundle. Other, generally smaller lymphatic vessels cross the anterior (Fig. 6) and posterior branches (Fig. 7) of the right ventricular conduction system. There are also lymphatics crossing the lateral conduction network covering the right mural wall. The lymphatics that come in contact with the various branches of the conduction system beyond the main right bundle tend to be more sparse and have no specific angular relation to the conduction fibers. The lymphatics posterior to the right bundle are longitudinally oriented and may extend from the inferior regions of the heart all the way up to the tricuspid valve (Fig. 8 and 9). On the other hand, lymphatics anterior to the right bundle are more transversely oriented, although shorter more or less longitudinal vessels may be seen. The lymphatics on the papillary muscles were apparent as fine channels near the insertions of the chordae tendineae or on the muscle surface (Fig. 10). Lymphatics could be seen near the base of the small papillary muscle arising from the region near the pulmonary conus as well.
Figure amidst tricular
DEFECTS
6. Lymphatic (L) oriented in a semicircular s#hape the anterior branches of the peripheral right venconduction system.
Lymphatics (L) crossing some of the peripheral Figure 7. conduction fibers (PCF) of the posterior branches of the right ventricular conduction system. Because of the anatomic relationship to some of the posterior branches, it is possible that high potassium concentration from remote tissue damage might cause slower conduction velocities in these fibers thereby enhancing the development of reentry.
Discussion The lymphatics are fine thin-walled delicate structures which are frequently obscured in the postmortem state and are generally very difficult to observe.17 However, informative studies can b& VOLUME 29. MARCH 1972
Lymphatic channel (L) extending from the inFigure 8. ferior regions of the septum to the septal leaflet of the tricuspid valve. 369
UHLEY
ET AL.
Figure 9. Close-up of the lymphatics (L) extending superiorly from the inferior septal region. It is theorized that such lymphatics could ‘carry high concentrations of substances (for example, potassium) from the site of an inferior infarction superiorly to the regions of the A-V conduction system and cause various A-V conduction defects.
made with the use of special dyes or techniques.lQ PateklQ described the anatomy of the cardiac lymphatics and demonstrated that the subendocardial lymphatics connect to a myocardial and subsequently to an epicardial plexus leaving the heart by several main drainage trunks. He noted that valves were uncommon in subendocardial plexus. These studies demonstrate a well defined system of lymphatic vessels beneath the endocardial surface of the right ventricle brought forth by injection of Evans blue dye. The lymphatic vessels exist in various anatomic arrangements (Fig. 11). In general, the lymphatics in the anterior septal
Figure 11. Composite diagram ihustrating the relationship of the canine endocardial lymphatics to the right ventricular conduction system. Note the transverse and longitudinal lymphatics of the right bundle (RB) and the lymphatics crossing some of the peripheral conduction fibers. Lymphatics anterior to the bundle appear somewhat more transversely oriented than the longer longitudinal branches posterior to the bundle.
370
Figure 10. Fine lymphatic on the posterior septum.
channels
longitudinally
oriented
area seem to appear more transversely oriented, whereas lymphatics in the posterior septum appear longitudinal. In regard to the conduction system per se, lymphatics not only traverse the main bundle, but form a longitudinal pathway along the course of the right bundle. The anterior, lateral and posterior branches of the right bundle are also traversed by lymphatics; however, the density of lymphatics seems to be greater in the region of the main right bundle than in the region of the peripheral conduction tissue. Certain lymphatic vessels may at times appear relatively large, in particular, the centrally located lymphatic just anterior to the mid-portion of the main right bundle. The subendocardial lymphatics are part of an extensive transport system capable of returning interstitial materials to the vascular system. Accordingly, if these fine thin-walled transport vessels could become involved with the pathologic process, it is conceivable that adjacent structures might also be affected. For example, inflammation of the perilymphatic structures might lead to subsequent fibrosis and interruption of normal function (delayed or decremental conduction and block). There are specific pathologic entities relating to the conduction system such as sclerosis of the cardiac skeleton described by LevlO and degenerative changes of the conduction system per se described by Yater et a1.8 and Lenegre.9 The question is raised whether these entities as well as myopathies, in part, have their effects on the conduction system mediated by the lymphatics of the heart. Possible role of lymphatics in conduction disCardiac lymph reflects myocardial poturbances: tassium changes.20 Accordingly, one might anticipate that lymphatics draining areas of tissue damage might carry away waste products such as large concentrations of potassium from injured cells. Such relatively high levels of potassium might in turn equilibrate across the lymphatic wall to the immediate environment of the conducThe American
Journal
of CARDIOLOGY
SURENDOCAQDIAL
tion tissue; possibly they would alter conduction velocity, producing transient slowing or block such as is frequently observed in certain myocardial infarctions. Hence, the appearance of intermittent conduction defects might be due to tissue damage in a remote area linked to the conduction system by the lymphatic system as well as to direct damage by the pathologic process to the conduction tissue. The appearance of various degrees of atrioventricular (A-V) block is a frequent transient phenomenon associated with inferior myocardial infarctions. The block is generally thought to be due to occlusive disease in the right coronary artery. However, the block frequently occurs several days after the onset of the inferior infarction, and the terminal branches of the right coronary artery supplying the inferior myocardium are remote from the branches supplying the A-V node. The anatomic study in this paper demonstrates a lymphatic network in the inferior portion of the right heart chambers which drains superiorly to the region of the A-V node (Fig. 8 and 9). Accordingly, it is conceivable that inferior tissue damage would liberate, over a period of time, vast stores of intracellular potassium which would be transported by way of these lymphatics to the region of the A-V node. In so doing, the equilibration of potassium through the lymphatics could alter the extracellular environment of the A-V junction and slow conduction velocity, resulting in a gradual rather than immediate appearance and disappearance of A-V conduction delay after an inferior infarction.
LYMPHATICS
AND CONDUCTION
DEFECTS
In a similar manner, damage to the tissue of the anterior septum would result in lymph flows toward the right bundle, possibly causing transient complete right bundle branch block. Various peripheral branches of the right ventricular conduction system might also become involved depending on the location of the myocardial damage. Possible role of lymphatics in arrhythmias: The same conditions might be applicable to the development of reentry wherein lymphatics carrying high potassium concentrations from remote damaged areas bring normal myocardium or some strands of Purkinje fibers in contact with a high potassium environment21 thereby delaying the passage of the wave front at a given area. If the involved area has unidirectional block characteristics, and the delayed wave front finds it possible to emerge and activate adjacent myocardium which is no longer refractory, ectopic beats will be set up by means of a reentry mechanism. The effect of local increases in potassium, as determined by the lymphatic pathways, could also bring the resting membrane potential of a given area closer to the threshold of excitability, thereby setting up ectopic foci. On the other hand, delays’ ip conduction velocity of tissue may play a role in the development of exit and protection blocks. Thus, the recognition of an anatomic relation of the lymph system to the conduction fibers might provide some insight into both permanent and transient block patterns and possibly the induction of some arrhythmias seen in clinical electrocardiography.
References 1. Rosenbaum
MB, Elizari MV, Lazzari JO: Los Hemibloqueos. Buenos Aires, Ed. Paidos, 1968 2. Uhlev HN. Rivkin LM: Visualization of the left branch of the human atrioventricular bundle. Circulation 20:
419-421,1958 3. Uhley HN, Rivkin
12.
LM: Peripheral distribution of the conduction system. Amer J Card,iol 5:688-
canine A-V 691,196O 4. Spach SM, Huang S-N, Armstrong SI, et al: Demo,nstration of peripheral conduction system in human hearts. Circulation 28:333-338, 1963 patterns 5. Uhley HN, Rivkin LM: Electrocardiographic following interruption of main and peripheral branches of the canine right bundle of His. Amer J Cardiol 7:810816, 1961 patterns fol6. Uhley HN, Rivkin LM: Electrocardiographic lowing interruption of the main and peripheral branches of the canine left bundle of His. Amer J Cardiol 13:4147, 1964 findings as7. Watt TB Jr, Pruitt RD: Electrocardiographic societed with experimental arborization block in dogs. Amer Heart J 69:642-654,1965 8. Yater WM, Cornell VH, Claytor T: Auriculoventricular heart block due to bilateral bundle-branch lesions. Arch Intern Med (Chicago) ,57:132-173, 1936 9. Lenegre J: Etiology and pathology of bilateral bundle branch block in relation to complete heart block. Progr Cardiovasc Dis 6:409-444, 1964 block. Amer 10. Lev M: Anatomic basis for atrioventricular
VOLUME
29. MARCH 1972
J Med 37:742-748,1964 The coronary circulation and conduction system in acute myocardial infarction. Progr Cardiovasc Dis lQ:410449, 1968 Miller AJ, Pick R, Katz LN: Ventricular endomyocardial pathology produced by chronic cardiac lymphatic obstruction in the dog. Circ Res 8:941-947, 1960 Uhley HN, Leeds SE, Sampson JJ, et al: The cardiac lymphatics in experimental chronic congestive failure. Proc Sot Exp Biol Med 131:379-381, 1969 Foldi M: Diseases of- Lymphatics and Lymph Circulation. Springfield, Ill, Charles C Thomas, 1969, p 313 Leeds SE, Uhley HN, Sampson JJ, et al: The cardiac lymphatics after ligation of the coronary sinus. Proc Sot Exp Biol Med 13559-62, 1970 Symbas PN, Cooper T, Gantner GE Jr, et al: Lymphatics of the heart. Arch Path 81:573-575, 1966 Kline I: Lymphatic pathways in the heart. Arch Path (Chicago) 88:638-644, 1969 Johnson RA, Blake MM: Lymphatics of the heart. Circulation 33:137-142, 1966 Patek PR: The morphology of the lymphatics of the mammalian heart. Amer J Anat 64:203-249, 1939 Areskog NH, Arturson G, Grotte G: Heart lymph: electrolyte composition and changes induced by cardiac glycosides. Biochem Pharmacol 14:783-787, 1965 Sasyniuk B!, Mendez C: A (mechanism for re-entry in canine ventricular tissue. Circ Res 28:3-15, 1971
11. James TN:
13.
14. 15.
16. 17. 18. 19. 20.
21.
371