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Vascular SurgeryBasic Science and Clinical CorrelationsSecond Edition

Edited by

Rodney A. White, MDProfessor of SurgeryUCLASchool of MedicineChief, Division of Vascular SurgeryHarbor-UCLAMedical CenterTorrance, California

Larry H. Hollier, MDDeanLouisiana State University School of Medicinein New OrleansNew Orleans, Louisiana

Vascular Surgery

Dedication

To our families

Vascular SurgeryBasic Science and Clinical CorrelationsSecond Edition

Edited by

Rodney A. White, MDProfessor of SurgeryUCLASchool of MedicineChief, Division of Vascular SurgeryHarbor-UCLAMedical CenterTorrance, California

Larry H. Hollier, MDDeanLouisiana State University School of Medicinein New OrleansNew Orleans, Louisiana

© 2005 by Blackwell PublishingBlackwell Futura is an imprint of Blackwell Publishing

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First edition 1994 by J.B. Lippincott CompanySecond edition 2005

ISBN: 1-4051-2202-1

Library of Congress Cataloging-in-Publication Data

Vascular surgery : basic science and clinical correlations/edited by Rodney A. White and LarryH. Hollier.–2nd ed.

p. ; cm.Includes bibliographical references and index.ISBN 1-4051-2202-1 (hardback : alk. paper)1. Blood-vessels–Surgery. 2. Blood-vessels–Pathophysiology. 3. Blood-vessels–Physiology.[DNLM: 1. Vascular Surgical Procedures. WG 170 V33132 2004] I. White, Rodney A.II. Hollier, Larry H.

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Contributors, viiPreface, xiiiAcknowledgments, xiv

I Vascular pathology and physiology

1 Embryology and development of the vascular system, 3C. Phifer Nicholson and Peter Gloviczki

2 Vascular wall physiology, 19Christian C. Haudenschild

3 Hemostasis and coagulation, 27Donald L. Jacobs and Jonathan B. Towne

4 Molecular aspects of atherosclerosis, 43J. Jeffrey Alexander and John A. Moawad

5 Localization of atherosclerotic lesions, 55Christopher K. Zarins, Chengpei Xu, Charles A. Taylor, and Seymour Glagov

6 Pathogenesis of arterial fibrodysplasia, 66James C. Stanley

7 Physiology of vasospastic disorders, 80Scott E. Musicant, Jean-Baptiste Roullet, James M. Edwards,and Gregory L. Moneta

8 Buerger’s disease, 92John Blebea and Richard F. Kempczinski

9 Ergotism, 101Roger F.J. Shepherd

10 Arteritis, 114Francis J. Kazmier

11 Adventitial cystic disease, 119Carlos E. Donayre

12 Entrapment syndromes, 126Carlos E. Donayre

13 Intimal hyperplasia, 135Ted R. Kohler

14 Thoracic outlet syndrome, 146Herbert I. Machleder

15 Aneurysmal disease, 162Juan Carlos Jimenez and Samuel Eric Wilson

16 Pathophysiology of renovascular hypertension, 180David L. Robaczewski, Richard H. Dean, and Kimberley J. Hansen

17 Pathophysiology, hemodynamics, and complications ofvenous disease, 192Harold J. Welch, Kevin B. Raftery, and Thomas F. O’Donnell, Jr.

18 Physiologic changes in lymphatic dysfunction, 207Peter Gloviczki

19 Physiologic changes in visceral ischemia, 215Tina R. Desai, Joshua A. Tepper, and Bruce L. Gewertz

20 Natural history of atherosclerosis in the lower extremity,carotid, and coronary circulations, 225Daniel B. Walsh

21 Neurologic basis for sympathetically maintained pain:causalgia and reflex sympathetic dystrophy, 233Marco Scoccianti and Rodney A. White

22 Compartment syndromes physiology, 241Malcolm O. Perry

23 Physiology of reperfusion injury, 245Shervanthi Homer-Vanniasinkam and D. Neil Granger

24 Cerebral ischemia, 251Hao Bui and Christian deVirgilio

25 Pathophysiology of spinal cord ischemia, 257Larry H. Hollier

26 Vascular erectile dysfunction: mechanisms and currentapproaches, 228Ralph G. DePalma

v

Contents

27 Portal hypertension: pathophysiology and clinicalcorrelates, 275David Rigberg and Hugh A. Gelabert

II Noninvasive vascular diagnostics

28 Physiologic basis of hemodynamic measurement, 295R. Eugene Zierler

29 Spectral analysis, 306Christopher R.B. Merritt

30 Ultrasound imaging, 315Christopher R.B. Merritt

31 Radionuclide scanning, 325Robert E. Sonnemaker

32 Computed tomography, 348Anton Mlikotic and Irwin Walot

33 Magnetic resonance imaging, 371David Saloner, Rem van Tyen, Charles M. Anderson, and Gary R. Caputo

III Invasive vascular diagnostics

34 Angiography, 385Anton Mlikotic and C. Mark Mehringer

35 Intravascular ultrasound, 401James T. Lee, George Kopchok, and Rodney A. White

36 Angioscopy in peripheral vascular surgery, 423Arnold Miller and Thomas J. Hölzenbein

IV Medical management

37 Atherosclerosis: risk factors and medical management, 441Ralph G. DePalma and Virginia W. Hayes

38 Pharmacologic intervention: thrombolytic therapy, 454Anthony J. Comerota, A. Koneti Rao, and Mohammad H. Eslami

39 Pharmacologic intervention: vasodilation therapy andrheologic agents, 468George Johnson, Jr.

40 Pharmacologic intervention: lipid-lowering agents, 473Ralph G. DePalma

41 Infections and antibiotics in vascular surgery, 477Martin R. Back

V Endovascular interventions for vasculardisease

42 Catheter-based approaches to the treatment ofatheroembolic disease, 495Frank R. Arko, Christine Newman, and Thomas J. Fogarty

43 Balloon angioplasty and transluminal recanalizationdevices, 503Rajesh Subramanian and Stephen R. Ramee

44 Endovascular stents, 516Frank J. Criado, Youssef Rizk, Gregory S. Domer, and Hilde Jerius

45 Endovascular prostheses for repair of abdominal aorticaneurysms, 520Carlos E. Donayre

VI Comparison of conventional vascularreconstruction and endovascular techniques

46 Surgical and endovascular treatment of chronic ischemiaof the lower limbs, 533Jean-Paul P.M. de Vries, Frans L. Moll, and Jos C. van den Berg

47 Aortoiliac endovascular recanalization compared withsurgical reconstruction, 543Peter L. Faries and Michael L. Marin

48 Endovascular stent–graft repair of thoracic aorticaneurysms and dissections, 554Jason T. Lee and Rodney A. White

49 Brachiocephalic vascular reconstructions compared withendovascular repair, 567Edward B. Diethrich

50 Carotid endarterectomy compared with carotidangioplasty and stenting, 575Mark R. Harrigan, Ricardo A. Hanel, Elad I. Levy, Lee R. Guterman, and L. Nelson Hopkins

51 Endovascular intervention for venous occlusioncompared with surgical reconstruction, 587Patricia E. Thorpe and Francisco J. Osse

Index, 609

Colour plate section follows p.370

Contents

vi

J. Jeffrey Alexander, MDAssociate Professor of SurgeryCase Western Reserve UniversityMetroHealth Medical CenterCleveland, Ohio

Charles M. Anderson, MD, PhDClinical Professor of RadiologyVAMedical CenterUniversity of California, San FranciscoSan Francisco, California

Frank R. Arko, MDDirector, Endovascular SurgeryAssistant Professor of SurgeryStanford University Medical CenterStanford, California

Martin R. Back, MDAssistant Professor of SurgeryUniversity of South Florida;Chief, Vascular SurgeryJames A. Haley Veterans HospitalTampa, Florida

John Blebea, MDProfessor of SurgeryDepartment of SurgeryTemple University School of MedicinePhiladelphia, Pennsylvania

Hao Bui, MDSenior ResidentDepartment of SurgeryHarbor-UCLAMedical CenterTorrance, California

Gary R. Caputo, MDAssociate Professor of RadiologyUniversity of California, San FranciscoSan Francisco, California

Anthony J. Comerota, MD, FACSDirector, Jobst Vascular CenterToledo, Ohio

Frank J. Criado, MDDirector, Center for Vascular InterventionChief, Division of Vascular SurgeryUnion Memorial Hospital/MedStar HealthBaltimore, Maryland

Richard H. Dean, MDPresident and CEOWake Forest University Health SciencesWinston-Salem, North Carolina

Ralph G. DePalma, MD, FACSNational Director of SurgeryProfessor of SurgeryUniformed Services of the Armed Forces;National Director of SurgeryDepartment of Veterans AffairsWashington, District of Columbia

Tina R. Desai, MD, FACSAssistant Professor of SurgeryDepartment of SurgeryThe University of ChicagoChicago, Illinois

Christian deVirgilio, MDVice Chair, EducationDirector, General Surgery ResidencyHarbor-UCLAMedical Center;Associate Professor of SurgeryUCLASchool of MedicineTorrance, California

Jean-Paul P.M. de Vries, MD, PhDVascular SurgeonSt. Antonius HospitalNieuwegeinThe Netherlands

vii

Contributors

Edward B. Diethrich, MDMedical DirectorArizona Heart Institute and Arizona Heart HospitalPhoenix, Arizona

Gregory S. Domer, MDCenter for Vascular Intervention and Division of Vascular SurgeryUnion Memorial Hospital-MedStar HealthBaltimore, Maryland

Carlos E. Donayre, MDAssociate Professor of SurgeryHarbor-UCLAMedical CenterTorrance, California

James M. Edwards, MDChief of SurgeryPortland VAMC;Associate Professor of SurgeryDivision of Vascular SurgeryOregon Health and Science UniversityPortland, Oregon

Mohammad H. Eslami, MDAssistant Professor of SurgeryTemple University School of MedicinePhiladelphia, Pennsylvania

Peter L. Faries, MD, FACSChief of Endovascular SurgeryNew York Presbyterian HospitalWeill Cornell Medical SchoolNew York, New York

Thomas J. Fogarty, MDClinical Professor of SurgeryStanford University Medical CenterStanford, California

Hugh A. Gelabert, MDAssistant Professor of SurgerySection of Vascular SurgeryUCLASchool of MedicineLos Angeles, California

Bruce L. Gewertz, MD, FACSThe Dallas B. Phemister ProfessorChairman, Department of SurgeryThe University of ChicagoChicago, Illinois

Seymour Glagov, MDProfessor Emeritus of Pathology and SurgeryDepartment of SurgerySection of Vascular SurgeryThe University of ChicagoChicago, Illinois

Peter Gloviczki, MDAssociate Professor of SurgeryMayo ClinicRochester, Minnesota

D. Neil Granger, PhDBoyd ProfessorHead, Department of Molecular and Cellular PhysiologyLSU Health Sciences CenterShrieveport, Louisiana

Lee R. Guterman, MD, PhDAssistant Professor, Department of NeurosurgeryCo-Director, Toshiba Stroke Research CenterSchool of Medicine and Biomedical SciencesUniversity at BuffaloState University of New YorkBuffalo, New York

Ricardo A. Hanel, MDAssistant Clinical Instructor of NeurosurgeryNeuroendovascular FellowDepartment of Neurosurgery and Toshiba Stroke Research CenterSchool of Medicine and Biomedical SciencesUniversity at BuffaloState University of New YorkBuffalo, New York

Kimberley J. Hansen, MDProfessor of SurgeryDepartment of General Surgery;Head, Section of Vascular SurgeryDivision of Surgical SciencesWake Forest University School of MedicineWinston-Salem, North Carolina

Mark R. Harrigan, MDAssistant Clinical Instructor of Neurosurgery andNeuroendovascular FellowDepartment of Neurosurgery and Toshiba Stroke Research CenterSchool of Medicine and Biomedical SciencesUniversity at BuffaloState University of New YorkBuffalo, New York

Christian C. Haudenschild, MDProfessor of Pathology and MedicineGeorge Washington University Medical CenterWashington, District of Columbia

Virginia W. Hayes, RN, MS, CFNP, CVNNurse Practitioner for Primary Care and Surgical ResearchVASierra Nevada Health Care SystemReno, Nevada

Larry H. Hollier, MDDean, Louisiana State University School of Medicine in New OrleansNew Orleans, Louisiana

Contributors

viii

Thomas J. Hölzenbein, MDFellow in Vascular ResearchHarvard Medical SchoolDivision of Vascular SurgeryHarvard-Deaconess Surgical ServiceNew England Deaconess HospitalBoston, Massachusetts

Shervanthi Homer-Vanniasinkam, IBSc, MD, FRCSEd, FRCSProfessor, Consultant Vascular SurgeonVascular Surgery UnitLeeds General InfirmaryLeedsUnited Kingdom

L. Nelson Hopkins, MDProfessor and Chairman, Department of Neurosurgery;Professor, Department of Radiology; and DirectorToshiba Stroke Research Center;School of Medicine and Biomedical SciencesUniversity at BuffaloState University of New YorkBuffalo, New York

Donald L. Jacobs, MD, MSAssociate Professor of SurgerySt. Louis UniversitySt. Louis, Missouri

Hilde Jerius, MDCenter for Vascular Intervention and Division of Vascular SurgeryUnion Memorial Hospital-MedStar HealthBaltimore, Maryland

Juan Carlos Jimenez, MDDepartment of SurgeryUniversity of California, IrvineIrvine, California

George Johnson, Jr., MDRoscoe B.G. Cowper Distinguished Professor of SurgeryVice Chairman, Department of SurgeryUniversity of North Carolina at Chapel Hill School of MedicineChapel Hill, North Carolina

Francis J. Kazmier, MD, FACCOchsner Clinic FoundationNew Orleans, Louisiana

Richard F. Kempczinski, MDProfessor of Surgery EmeritusUniversity of Cincinnati School of MedicineCincinnati, Ohio

Ted R. Kohler, MDChief of Vascular SurgerySurgical Service of the Veterans Affairs Puget Sound Health CareSystem;

Professor of SurgeryDepartment of SurgeryUniversity of WashingtonSeattle, Washington

George Kopchok, BSBiomedical EngineeringResearch and Education InstituteDivision of Vascular SurgeryHarbor-UCLAMedical CenterTorrance, California

James T. Lee, MDClinical Faculty, Surgical ServicesUCLASchool of MedicineHarbor-UCLAMedical Center Campus;Peripheral Vascular and Endovascular SurgerySouthern California Permanente Medical GroupBellflower Medical CenterBellflower, California

Jason T. Lee, MDVascular Surgery FellowDivision of Vascular SurgeryStanford University Medical CenterStanford, California

Elad I. Levy, MDAssistant Clinical Instructor of Neurosurgery andNeuroendovascular FellowDepartment of Neurosurgery and Toshiba Stroke Research CenterSchool of Medicine and Biomedical SciencesUniversity at BuffaloState University of New YorkBuffalo, New York

Herbert I. Machleder, MDDepartment of SurgeryUCLAMedical CenterLos Angeles, California

Michael L. Marin, MD, FACSChief, Division of Vascular SurgeryMount Sinai School of MedicineNew York, New York

C. Mark Mehringer, MDProfessor of Radiological SciencesDavid Geffen School of Medicine at UCLAHarbor-UCLAMedical CenterTorrance, California

Christopher R.B. Merritt, MD, FACRProfessor of RadiologyDepartment of RadiologyThomas Jefferson University HospitalPhiladelphia, Pennsylvania

Contributors

ix

Arnold Miller, MDAttending Vascular SurgeonDepartment of SurgeryMetroWest Medical CenterFramingham-Natick, Massachusetts;Assistant Clinical Professor of Surgery, Harvard Medical School,Boston, Massachusetts

Anton Mlikotic, MDAssistant Professor of Radiological SciencesDavid Geffen School of Medicine at UCLAHarbor-UCLAMedical CenterTorrance, California

John A. Moawad, MDAssistant Professor of SurgeryCase Western Reserve UniversityMetroHealth Medical CenterCleveland, Ohio

Frans L. Moll, MD, PhDProfessor of Vascular SurgeryHead of the Department of Vascular SurgeryUniversity Medical Center UtrechtUtrechtThe Netherlands

Gregory L. Moneta, MDProfessor of SurgeryChief, Division of Vascular SurgeryOregon Health and Science UniversityPortland, Oregon

Scott E. Musicant, MDResearch Fellow in Vascular SurgeryDivision of Vascular SurgeryOregon Health and Science UniversityPortland, Oregon

Christine Newman, RNFogarty ResearchPortola Valley, California

C. Phifer Nicholson, MDSurgical Consultants, P.A.Edina, Minnesota

Thomas F. O’Donnell, Jr., MDProfessor of SurgeryPresident and CEONew England Medical CenterTufts University School of MedicineBoston, Massachusetts

Francisco J. Osse, MDAssociate Professor of RadiologyDivision of Vascular and Interventional Radiology

University of IowaIowa City, Iowa

Malcolm O. Perry, MDProfessor EmeritusThe University of Texas Southwestern Medical SchoolDallas, Texas

Kevin B. Raftery, MDLahey Clinic Medical CenterBurlington, Massachusetts

Stephen R. Ramee, MD, FACCSection Head, Interventional CardiologyOchsner Clinic FoundationNew Orleans, Louisiana

A. Koneti Rao, MDProfessor of MedicineTemple University School of MedicinePhiladelphia, Pennsylvania

David Rigberg, MDClinical FellowSection of Vascular SurgeryUCLASchool of MedicineLos Angeles, California

Youssef Rizk, DOCenter for Vascular Intervention and Division of Vascular SurgeryUnion Memorial Hospital-MedStar HealthBaltimore, Maryland

David L. Robaczewski, MDBradshaw Fellow of Surgical ResearchDepartment of General SurgeryDivision of Surgical SciencesWake Forest University School of MedicineWinston-Salem, North Carolina

Jean-Baptiste Roullet, PhDDirector, Basic Science ResearchDivision of Vascular SurgeryOregon Health and Science UniversityPortland, Oregon

David Saloner, PhDProfessor of RadiologyVAMedical CenterUniversity of California, San FranciscoSan Francisco, California

Marco Scoccianti, MD, EBSQ (vasc)Head, Endovascular Surgery UnitDivision of Vascular SurgeryS. Giovanni-Addolorata Hospital ComplexRomeItaly

Contributors

x

Roger F.J. Shepherd, MB, BChAssistant Professor of MedicineMayo Clinic College of MedicineMayo ClinicRochester, Minnesota

Robert E. Sonnemaker, MDMedical DirectorPET ImagingDepartment of Nuclear MedicineSt. John’s Health SystemSpringfield, Missouri

James C. Stanley, MDProfessor of SurgeryHead, Section of Vascular SurgeryUniversity of Michigan Medical CenterAnn Arbor, Michigan

Rajesh Subramanian, MD, FACCOchsner Clinic FoundationNew Orleans, Louisiana

Charles A. Taylor, PhDAssistant Professor of Mechanical Engineering, Surgery and Pediatrics (by courtesy)Stanford UniversityStanford, California

Joshua A. Tepper, MDResident in General SurgeryDepartment of SurgeryThe University of ChicagoChicago, Illinois

Patricia E. Thorpe, MDProfessor of RadiologyUniversity of IowaIowa City, Iowa

Jonathan B. Towne, MDProfessor of SurgeryChairman, Division of Vascular SurgeryMedical College of WisconsinMilwaukee, Wisconsin

Jos C. van den Berg, MD, PhDInterventional RadiologySan Antonio HospitalNieuwegeinThe Netherlands

Rem van Tyen, PhDAssistant Research PhysicistVAMedical CenterUniversity of California, San FranciscoSan Francisco, California

Irwin Walot, MDAssociate Professor of Radiological SciencesChief, Cardiovascular/Interventional RadiologyHarbor-UCLAMedical CenterTorrance, California

Daniel B. Walsh, MDSection of Vascular SurgeryDartmouth-Hitchcock Medical CenterDartmouth Medical SchoolLebanon, New Hampshire

Harold J. Welch, MDLahey Clinic Medical CenterBurlington, Massachusetts

Rodney A. White, MDProfessor of SurgeryUCLASchool of Medicine;Chief, Division of Vascular SurgeryHarbor-UCLAMedical CenterTorrance, California

Samuel Eric Wilson, MD, FACSProfessor and ChairDepartment of Surgery;Associate DeanUniversity of California, IrvineIrvine, California

Chengpei Xu, MD, PhDSenior Research ScientistDivision of Vascular SurgeryStanford University School of MedicineStanford, California

Christopher K. Zarins, MDProfessor of SurgeryDivision of Vascular SurgeryStanford University School of MedicineStanford, California

R. Eugene Zierler, MDProfessor of SurgeryMedical DirectorVascular Diagnostic ServicesUniversity of Washington Medical CenterSeattle, Washington

Contributors

xi

xiii

This revised edition of Vascular Surgery: Basic Science and Clini-cal Correlations was developed in order to address significantchanges that have occurred in contemporary vascular surgeryand to highlight new information that has developed regard-ing vascular imaging and interventional and endovascularprocedures. The overall length of the text is slightly shorterthan the first edition with relevant core chapters being retained to emphasize the basic science nature of the text, with approximately 60 percent of the material undergoingmajor revisions or being new chapters.

The significant change from the first text is an emphasis onvascular pathology and physiology that is relevant to currentpractice, including information that is currently included on the vascular board examinations. A new emphasis on endovascular therapies has been added by including fivechapters on endovascular techniques and an additional section with six chapters comparing conventional vascular

xiii

Preface

reconstruction with endovascular methods. These new chapters address the most important issue in contemporaryvascular surgery, i.e. the role of endovascular methods in treating vascular lesions and the impact that this has on training and credentialing. A unique aspect of this book differentiating it from other texts is a comparison of conven-tional methods with the endovascular techniques.

Overall, the text provides a comprehensive approach to contemporary vascular surgery and future perspectives. Theauthors are preeminent in the field and are most capable foraddressing the assigned topics, with the goals being to providean updated and forward-looking text that accommodates theneeds of practicing and training vascular surgeons.

Rodney A. WhiteLarry H. Hollier

xiv

We would like to acknowledge the efforts of Blackwell Pub-lishing, Futura Division, for the timely preparation of this text.In particular, we appreciate the efforts of Steve Korn, Jacques

xiv

Acknowledgments

Strauss, and the invaluable expertise of Joanna Bellhouse, Development Editor, who has meticulously and efficiently organized materials and prepared the text for publication.

Vascular pathology and physiology

I

3

The vascular system develops between the third and eighthweeks of gestation. In the middle of the third week, the embryois no longer able to meet its nutritional requirements by diffu-sion alone, thus prompting differentiation of extraembryonicmesodermal cells (angioblasts) located in the wall of the yolksac. These angioblasts form angiogenic cell clusters, whichcanalize to form early blood vessels. Cells that are centrally lo-cated in these clusters differentiate into blood cells, whilethose at the periphery flatten and form endothelial cells.1

Similarly, during this same period, intraembryonic mesoder-mal cells differentiate to form the heart tube, paired dorsal aor-tae, visceral arteries, and axial arteries of the developing limbbuds. Woollard2 described the above events in the develop-ment of the vascular system in three stages: (1) the capillarynetwork stage, an undifferentiated network of primitive bloodlakes; (2) the retiform stage, when separation of the primitivearterial and venous channels occurs; and (3) the gross differen-tiation phase with the appearance of mature vascular chan-nels. By the end of the eighth week of gestation, developmentof the vascular system is virtually complete with only minorchanges occurring after this time.

Arterial system

Aortic arch and great vessels

The aortic arch and its major branches develop from the sixembryologic aortic arches, which, in turn, originate from theaortic sac. Each branchial arch is supplied by one of the aorticarches. The fifth aortic arch is often not formed at all (Fig. 1.1).In the 4-mm embryo (end of fourth week), the first aortic archhas nearly disappeared with only a small portion persisting onthe maxillary artery (Fig. 1.2). The second aortic arch also regresses with portions persisting as the hyoid and stapedialarteries.1

In the 10-mm embryo (beginning of sixth week), the first andsecond aortic arches have disappeared and the third, fourth,and sixth aortic arches enlarge (Fig. 1.3). The third aortic arch is

the anlage of the common carotid artery and the first portion ofthe internal carotid artery with the remainder of the internalcarotid artery formed by the dorsal aorta (Fig. 1.4).1 The proxi-mal right subclavian artery develops from the right fourth aor-tic arch. Its distal portion is formed by a portion of the rightdorsal aorta and the seventh intersegmental artery (see Fig.1.4). The embryologic left fourth aortic arch forms the arch ofthe aorta between the left common carotid and left subclavianarteries.

The fifth aortic arch is transient and never well developed.No portion persists in the extrauterine life.

The sixth aortic arch (pulmonary arch) gives off branchesthat grow toward the developing lung bud. The right sixth aor-tic arch forms the proximal segment of the right pulmonaryartery, while the distal left sixth aortic arch persists as the duc-tus arteriosus; it later becomes the ligamentum anteriosum(see Fig. 1.4).

Formation of the neck causes the heart to descend from itsinitial cervical position into the thoracic cavity. This results inelongation of the innominate and carotid arteries and a shift ofthe origin of the left subclavian artery from the level of the sev-enth intersegmental artery to a point closer to the origin of theleft common carotid artery (Fig. 1.5). In embryologic develop-ment, the recurrent laryngeal nerves supply the sixthbranchial arches. With the caudal shift of the heart and disap-pearance of portions of the right fifth and sixth aortic arches,the right recurrent laryngeal nerve moves up to hook aroundthe fourth aortic arch while the left recurrent laryngeal nervehooks around the ligamentum anteriosum (see Figs. 1.4 and1.5).

Visceral arteries

Most of the differentiation of the arterial supply to the abdomi-nal viscera has occurred by the end of the eighth week. The pri-mordium of the celiac artery is represented by the pairedcephalic roots of the vitelline arteries at the level of the 10th ven-tral segmental artery. The superior mesenteric artery originatesby fusion of the paired vitelline arteries at the level of the 13th

Embryology and development of the vascular system

C. Phifer NicholsonPeter Gloviczki

1

ventral segmental artery. Fusion of the vitelline arteries in amore caudal location forms the inferior mesenteric artery.

Renal arteries

The adult kidney (metanephros) begins to develop in the fifth week of gestation and is initially located in the pelvis. With diminution of the body curvature and growth

of the body in the lumbar and sacral regions, the kidney ascends into the abdomen. The metanephros receives its origi-nal blood supply from a pelvic branch of the aorta but as it ascends, arteries originating from successively higher levels ofthe abdominal aorta supply the kidney while the lower vesselsdegenerate.1

PART I Vascular pathology and physiology

4

Figure 1.1 Aortic arches supplying branchial

clefts and pharyngeal pouches.

Figure 1.2 Aortic arches at the end of fourth week of development.

Figure 1.3 Aortic arches at the beginning of sixth week of development

with early pulmonary arteries.

Arteries to the lower extremity

During the fifth week of development (6-mm embryo), theumbilical artery gives rise to the sciatic artery. The sciaticartery is a continuation of the internal iliac artery, which devel-ops with the lower limb bud as its axial artery. The femoralartery, an extension of the external iliac artery, replaces the sci-atic artery and its branches to the thigh during the eighth weekof development.3 Adult derivatives of the sciatic system include the popliteal, anterior tibial, and peroneal arteries.

Proximal portions of the umbilical arteries persist to form the internal iliac and superior vesical arteries.1

Venous system

During the fifth week of gestation, three major pairs of veinsare present in the embryo: (1) vitelline or omphalomesentericveins between the yolk sac and the sinus venosus; (2) umbilicalveins, which course between the chorionic villi and the embryo; and (3) cardinal veins, which drain the body of theembryo (Fig. 1.6).

Vitelline vein derivatives

The vitelline veins pass from the yolk sac to the venous plexussurrounding the duodenum prior to passing into the septumtransversum (Fig. 1.7). Liver cords budding from the duode-num grow into the septum transversum, interrupting thecourse of the vitelline veins to form the hepatic sinusoids. Theleft and right hepatocardiac channels drain the hepatic sinu-soids into the sinus venosus (Fig. 1.8). With obliteration of theleft hepatocardiac channel, the right hepatocardiac channelbecomes the posthepatic (suprahepatic) inferior vena cava.The portal vein forms as the venous plexus surrounding theduodenum coalesces into a single vein. The superior mesen-teric vein develops from the distal right vitelline vein.

Umbilical vein derivatives

The entire right umbilical vein and the proximal portion of theleft umbilical vein disappear, while the distal left umbilicalvein persists to carry blood to the liver from the placenta. Acommunication, the ductus venosus, later forms between the

CHAPTER 1 Embryology and development of the vascular system

5

Figure 1.4 Transformation of aortic arches

into adult configuration.

Figure 1.5 Adult configuration of great vessels. Note position of recurrent

laryngeal nerves.


6

Figure 1.7 Vitelline veins forming venous plexus around duodenum.

Figure 1.8 Liver cords interrupting course of vitelline veins.

Figure 1.6 Venous system at end of fifth week

of gestation.

left umbilical vein and the right hepatocardiac channel, by-passing the sinusoids of the liver (Fig. 1.9). After birth, the leftumbilical vein and the ductus venosus are obliterated to form the ligamentum teres hepatis and ligamentum venosum,respectively.

Cardinal vein derivatives

In early embryologic development, the cardinal venous sys-tem is composed of three pairs of veins: (1) the anterior cardi-nal veins, which drain the cephalic embryo; (2) the posteriorcardinal veins, which drain the remainder of the embryo; and

(3) the common cardinal veins, which are formed by the junc-tion of the anterior and posterior cardinal veins (see Fig. 1.6).During the fifth to seventh weeks of gestation, the followingveins form: (1) the subcardinal veins, which drain the kidneys;(2) the sacrocardinal veins, which drain the lower extremities;and (3) the supracardinal veins, which drain the body wall viaintercostal veins (Fig. 1.10).

In the formation of the vena cava, anastomoses develop be-tween the left and right sides of the cardinal system, channel-ing blood from left to right. The communication between theanterior cardinal veins develops into the left brachiocephalicvein. The right common cardinal vein and the proximal por-tion of the right anterior cardinal vein form the superior venacava.

The communication between the subcardinal veins formsthe left renal vein. After development of this communication,the proximal left subcardinal vein disappears with its distalportion persisting as the left gonadal vein.1 Hence, the rightsubcardinal vein becomes the renal segment of the inferiorvena cava (see Fig. 1.10).

The communication between the sacrocardinal veins be-

comes the left common iliac vein. The left sacrocardinal veinthen involutes while the right sacrocardinal vein persists to become the sacrocardinal segment of the inferior vena cava.1

As portions of the posterior cardinal veins disappear, thesupracardinal veins become more important. The azygos vein,into which the 4th through 11th intercostal veins empty, formsfrom the right supracardinal vein and a portion of the right


7

Figure 1.9 Formation of hepatic veins, hepatic

portion of inferior vena cava, and portal vein.

A B

Figure 1.10 Development of the venous system. (A) In seventh week. (B) At birth.

Interrupted aortic arch is also a relatively rare anomaly, resulting from obliteration of the left fourth aortic arch (Fig. 1.13). The ductus arteriosus remains widely patent, supplying blood of low oxygen content to the systemic circula-tion while the aortic trunk supplies the two common carotidarteries.

Anomalies of the aortic arch branches

Common ostial origin of the innominate and left common carotid ar-teries, the most common anomaly of the arch branches, occursin approximately 10% of patients. Origin of the left vertebralartery from the aortic arch proximal to the left subclavian arteryoccurs in 5% of patients.

Aberrant right subclavian artery (arteria lusoria) occurs in ap-proximately 2% of patients, resulting from obliteration of theright fourth aortic arch and proximal right dorsal aorta (Fig.1.14). In this anomaly, the right subclavian artery arises fromthe aortic arch just distal to the left subclavian artery, passingbehind the esophagus to the right arm, frequently compress-ing the esophagus (dysphagia lusoria). Absence of the normalorigin of the right subclavian artery results in a nonrecurrentright recurrent laryngeal nerve.

Coarctation of the aorta

Coarctation of the aorta may be congenital or acquired and


8

Figure 1.11 Adult configuration of major lymphatic channels.

posterior cardinal vein (see Fig. 1.10). The hemiazygous vein,into which the fourth through seventh intercostal veins empty,develops from the left supracardinal vein.1

Lymphatic system

Disagreement remains as to the origin of the lymphatics butthe leading theories are the centrifugal theory proposed byLewis4 and Sabin5 and the centripetal theory proposed byHuntington.6 According to the centrifugal theory, the lym-phatics are believed to arise by proliferation from the venoussystem. The centripetal theory, however, suggests that lym-phatics form from coalescence of mesenchymal spaces into asystem of vessels.

By the sixth week of gestation, paired jugular lymph sacs areidentifiable in the vicinity of the anterior cardinal veins. Thecisterna chyli dorsal to the aorta and retroperitoneal lymphsacs at the root of the mesentery are present by the end of theeighth week of development. Communications between thejugular lymph sacs and the cisterna chyli develop, forming apaired system of lymphatic trunks with numerous anasto-moses across the midline. Portions of the right and left systemswill involute so that in adults the major lymphatic system consists of left and right lumbar lymphatic trunks, whichdrain into the cisterna chyli and then the thoracic duct. The thoracic duct has an inferior right portion, then crosses themidline at the level of the fourth to sixth thoracic vertebrae to eventually empty into the left subclavian vein at its junction with the left internal jugular vein (Fig. 1.11). The thoracic duct, therefore, provides lymph drainage for the left upper extremity, the chest, abdomen, and the lower extremities. Lymph from the head, neck, and right upper extremity drains into the right subclavian vein via the rightcervical lymphatic trunk.

Embryologic derangements in vascular pathology

Arterial anomalies

Anomalies of the aortic arch

True anomalies of aortic arch are rare; they occur in less than2% of adults.

Right aortic arch results from obliteration of the left fourthaortic arch and the left dorsal aorta, which are replaced by cor-responding vessels on the right side.

Double aortic arch or aortic ring results from persistence ofthe right dorsal aorta between the seventh intersegmentalartery and its junction with the left dorsal aorta (Fig. 1.12). Theaortic ring thus formed surrounds the trachea and the esopha-gus, compressing these structures.

may occur in the descending thoracic aorta or the abdominalaorta. Our discussion will focus on congenital coarctation.

Several hypotheses have been proposed as causes of congenital coarctation of the aorta. According to Dean andcoworkers,7 congenital coarctations result from either failureof maturation of the mesenchymal cell component or arresteddevelopment of the artery during the period of gross differen-tiation. If arrest occurs during the mesenchymal cell stage, theartery may appear as a fibrous cord. With developmental arrest during the gross differentiation phase, the aorta may appear normal in early childhood, but later may be recognizedas a nonexpanding portion of aorta adjacent to a normallygrowing segment.

With aortic coarctation from anomalous mesenchymal cellmaturation, luminal fibrous clefts and ridges causing partialobstruction may be noted on arteriography. Microscopically,dysplastic mesenchymal cell layers compose a disorganizedmedia.

Coarctation of the thoracic aorta may be preductal or postduc-tal. In preductal aortic coarctation, the ductus arteriosus per-sists supplying poorly oxygenated blood to the lower body. Inthe postductal type, this channel is obliterated and numerouscollaterals from the subclavian and axillary arteries supply thelower body.

Coarctation of the abdominal aorta is rare, accounting for 0.5%to 2% of clinically recognized coarctations of the thoracic and


9

Figure 1.12 Persistent right dorsal aorta,

which forms double aortic arch (aortic ring)

surrounding trachea and esophagus.

Figure 1.13 (A) Interrupted aortic arch.

Abnormal obliteration of right and left fourth

aortic arches with persistence of portion of

right dorsal aorta. (B) Aorta supplies head while

pulmonary artery via patent ductus arteriosus

supplies remainder of body.

abdominal aorta. Reconstruction may be challenging becausethe stenosis may extend from the celiac axis to the infrarenalabdominal aorta. In about 80% of patients, renal artery steno-sis with renovascular hypertension is present. Untreated ab-dominal coarctation may eventually result in cardiac failure orcerebral hemorrhage, the major causes of death from thisanomaly.8 Repair often requires renal revascularization andbypass or replacement of the narrowed aorta in the second orthird decade of life.9

Anomalies of the visceral arteries

Congenital anomalies of the visceral arteries are not uncom-mon; however, visceral arterial anomalies requiring vascularsurgical intervention are rare. We define a visceral artery anom-aly as a difference in number or origin of the arterial supply toan organ from the accepted normal. The normal arterial sup-ply of an organ is that pattern of arteries to a viscus that occursmost commonly. Celiac, hepatic, and renal arterial anomaliesof importance to the vascular surgeon are described.

Celiac artery anomalies are found in 11% to 40% of patients.

The typical celiac axis, which branches into left gastric, splenic,and common hepatic arteries, is found in 60% to 89% of pa-tients. The most common variation is a gastrosplenic trunkwith the common hepatic artery arising from the aorta or thesuperior mesenteric artery occurring in 5% to 8% of patients.10

Hepatosplenic and hepatogastric trunks occur less frequentlyand, rarely, the celiac axis may be combined with the superiormesenteric artery (Fig. 1.15).

Hepatic artery anomalies may be of two types: replaced or ac-cessory. A replaced hepatic substitutes for a normal hepaticartery that is absent, while an accessory hepatic is an additionto the normal one that is present. Michels,11 from 200 anatomicdissections, found one or more hepatic artery anomalies in 83cases (41%). The four most common variations in the arterialsupply to the liver were (1) replaced right hepatic artery, 17%;(2) replaced left hepatic artery, 16%; (3) accessory left hepaticartery, 12%; and (4) accessory right hepatic artery, 8% (Fig.1.16). In 2.5% of his dissections, Michels noted the common he-patic artery originated from the superior mesenteric artery.

As previously described, during embryologic develop-ment, the kidney arterial supply originates from the aorta at


10

Figure 1.15 Celiac artery anomalies.

Figure 1.14 (A) Aberrant right subclavian

artery. Abnormal obliteration of right fourth

aortic arch and proximal right dorsal aorta. (B)

Aberrant right subclavian artery passing

posterior to trachea and esophagus.

successively higher levels as the kidney ascends from thepelvis. Failure of lower vessels to degenerate results in multi-ple renal arteries, present in 25% to 33% of adults. Multiplerenal arteries are slightly more common on the left than theright and may enter the renal hilum or directly into theparenchyma of one of the poles of the kidney. Supernumeraryarteries most commonly enter the upper pole of the kidneyand are more common in ectopic kidneys. Lower pole super-numerary arteries to the right kidney typically cross anteriorto the inferior vena cava.12

As the kidneys ascend from the pelvis, they must pass be-tween the umbilical arteries. The kidneys are closely opposedand may come into contact with each other as they ascend be-tween the umbilical arteries. If they come into contact, theirlower poles may fuse, resulting in a horseshoe kidney, which isfound in 1 in 600 persons. Similarly, one or the other kidneymay fail to ascend, resulting in a pelvic kidney. Usually, theseectopic kidneys are located in the pelvis close to the commoniliac artery.1 Multiple renal arteries often supply horseshoeand pelvic kidneys, commonly arising from the aorta near theaortic bifurcation or from the common iliac arteries.

The Arc of Buhler is represented in intrauterine life as a longi-tudinal anastomosis that connects the 10th through 13th ventral segmental arteries. The 10th ventral segmental arterycontributes to the formation of the celiac artery; the 11th andthe 12th segmental arteries regress; and the 13th ventral seg-mental artery contributes to the development of the superiormesenteric artery. Normally, this longitudinal communicationregresses by the eighth week of embryonic life; however, if itpersists, the Arc of Buhler forms a communication between theceliac and superior mesenteric arteries. Discovered in 2% ofautopsy cases and usually found in the location of the pancre-aticoduodenal arteries, the Arc of Buhler may undergoaneurysmal degeneration and rupture, probably related to in-herent weakness in the persistent embryonic artery13 (Fig.


11

Figure 1.16 Hepatic artery anomalies (C.A.,

celiac axis; L.G., left gastric; H, hepatic; M.H.,

middle hepatic; R.H., right hepatic; L.H., left

hepatic).

Figure 1.17 Persistent arc of Buhler with associated aneurysm.

1.17). If an aneurysm of this artery is identified, recommenda-tions pertinent to other visceral artery aneurysms should befollowed.

Persistent sciatic artery

Persistent sciatic artery is a congenital anomalous continuationof the internal iliac artery, which in 63% of these cases serves asthe major blood supply to the lower extremity.3 If the sciaticartery is the major artery of the lower extremity, the superficialfemoral artery is hypoplastic or absent. Following the courseof the inferior gluteal artery, the sciatic artery passes with thesciatic nerve through the greater sciatic foramen below the pir-iformis muscle and enters the thigh (Fig. 1.18).14 The arterythen courses along the posterior aspect of the adductor

magnus muscle to the popliteal fossa, where it continues as the popliteal artery. Early atheromatous degeneration andaneurysm formation are common. Due to its proximity to thesciatic nerve, a sciatic artery aneurysm may present as apainful buttock mass or with sciatic pain. Sciatic arteryaneurysms are bilateral in 12% of the cases. Palpable poplitealand pedal pulses without palpable femoral pulses are clinicalfindings highly suggestive of persistent sciatic artery. Mag-netic resonance imaging (MRI) and arteriography provide adefinitive diagnosis. Proximal and distal ligation of theaneurysm and femoropopliteal bypass graft3 is the preferredtreatment.

Venous anomalies

Anomalies of the superior vena cava

Anomalies of the superior vena cava of importance to the vas-cular surgeon include left superior vena cava and double superior vena cava.

Persistence of the left anterior cardinal vein and obliterationof the right common cardinal and proximal right anterior car-dinal veins after the eighth week of gestation results in a left-

sided superior vena cava (Fig. 1.19).10 Blood from the right upperextremity and right side of the head drains into the brachio-cephalic vein and then into the left superior vena cava, whichcourses anterolateral to the aortic arch and anterior to thehilum of the left lung.1 The left-sided superior vena cava thendrains into the coronary sinus.

Persistence of the left anterior cardinal vein and failure ofthe left brachiocephalic vein to form results in double superiorvena cava (Fig. 1.20). The left superior vena cava drains into thecoronary sinus as previously described.


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Figure 1.19 Left superior vena cava draining into coronary sinus.

Figure 1.20 Double superior vena cava.Figure 1.18 Persistent sciatic artery and sciatic artery aneurysm.

Anomalies of the inferior vena cava

Embryologic abnormalities of the inferior vena cava and renalveins pose potentially difficult problems for the vascular sur-geon during abdominal aortic surgery. Important anomaliesof the inferior vena cava include double inferior vena cava andleft inferior vena cava.

Double inferior vena cava results when the left sacrocardinalvein fails to lose its communication with the left subcardinalvein. With this anomaly, the left iliac vein may or may not bepresent but the left gonadal vein is found in its normal loca-tion1 (Fig. 1.21).

Left inferior vena cava results from regression of the rightsacrocardinal vein, the normal precursor of the lower in-frarenal inferior vena cava, and persistence of the left sacrocar-dinal vein, which maintains its communication with the leftsubcardinal vein1 (Fig. 1.22).

If the right subcardinal vein fails to make communicationwith the liver, absence of the suprarenal inferior vena cava results.Blood from the caudal part of the body is shunted directly intothe right supracardinal (azygous) vein (Fig. 1.23). The hepaticveins enter the right atrium at the site normally occupied bythe inferior vena cava.15

Renal vein anomalies

Important renal vein anomalies include a circumaortic renal


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Figure 1.21 Double inferior vena cava.

Figure 1.22 Left inferior vena cava.

collar and a posterior (retroaortic) left renal vein. In utero,communications between the subcardinal and supracardinalveins form a venous ring around the aorta at the level of therenal veins. Failure of the dorsal portion of the ring to regressresults in either a posterior renal vein if the ventral portion of

Figure 1.23 Absent inferior vena cava. Suprarenal inferior vena cava drains

into axygos vein.

had an aneurysm of the retrohepatic vena cava. The patientSweeny et al. reported presented with thrombosis of an in-frarenal vena cava aneurysm following strenuous exercise.

Arteriovenous malformations

Congenital arteriovenous malformations (AVMs) result fromanomalous development of the primitive vascular system.18

AVMs are usually present at birth although signs and symp-toms may not be manifest until later in life.19 Associated withmany different syndromes, AVMs have multiple clinical pre-sentations (Table 1.2). Progression is usually the result of hemodynamic factors because tumor-like behavior with en-dothelial proliferations is not characteristic.20

In AVMs, the pathologic vasculature is mixed arteriove-nous. The amount of blood shunted through the abnormalvessels and the resultant hemodynamic factors determine thesecondary morphologic changes in the feeding arteries anddraining veins.19

Although multiple classifications have been suggested, theaccepted classification by Szilagyi and coworkers18,21 is basedon the developmental stages of the vascular system. As previ-ously noted, the developmental stages of the vascular systemare the capillary network phase, the retiform stage, and thegross differentiation phase. Hemangiomas result from devel-opmental abnormalities in the capillary network stage, whilecongenital arteriovenous fistulas result from arrest in devel-opment in the retiform stage. Arteriovenous fistulas have beenfurther subdivided into microfistulous or macrofistulousAVMs, depending on the size of the abnormal communicatingvessel and whether or not angiography can demonstrate thesite of the arteriovenous connections (Fig. 1.25). According to Mulliken and Glowacki,20 the term hemangioma appliesto those lesions that clinically undergo growth and usually resolution with endothelial hyperplasia present during theproliferative phase. In the proliferative phase, hemangiomasincorporate [3H] thymidine and have an increased mast cellcount.22 The term vascular malformation (such as arteriovenous,venous or lymphatic malformations, and port wine stains) ap-plies to clinically and cellularly adynamic lesions. Seventypercent of congenital AVMs, however, include not only microfistulous or macrofistulous communications but also include hemangiomatous lesions.21

Congenital AVMs may be located anywhere on the body;however, lesions involving the upper extremity are most fre-quent, followed by lesions of the head and neck. AVMs of thehead and neck are classified as intraaxial if arising from arter-ies supplying brain tissue (carotid artery or vertebral arteries)or extraaxial if arising from arteries supplying dura, bone, ormuscle.23 Other locations of AVMs include the lower extrem-ity, the pelvis, and the viscera (lung, gastrointestinal tract, kid-neys, and liver).

Schwartz and colleagues24 reviewed 185 patients at theMayo Clinic with AVMs of the extremities and pelvis. Lesions


14

the ring regresses, or a circumaortic venous collar if the ventralportion persists (Fig. 1.24).

Brener and colleagues16 reviewed venous anomalies foundduring abdominal aortic reconstructions at the MassachusettsGeneral Hospital between 1959 and 1973. During that period,31 anomalies of the inferior vena cava or renal veins werefound and 11 of these resulted in complications. The most com-mon venous anomaly was posterior left renal vein, followedby duplication of the inferior vena cava. In their review of theliterature, the most frequent major venous anomaly was thecircumaortic renal collar (1.5% to 8.7%) (Table 1.1). Of theabove anomalies, the circumaortic renal collar and the posteri-or left renal vein pose the greatest threat since the posteriorveins may be easily injured during dissection prior to placement of an aortic cross clamp. Meticulous attention to de-tail during dissection of the infrarenal aorta and common iliacarteries is essential to avoid potentially disastrous hemor-rhage from anomalous veins.

Arare, congenital venous anomaly is an aneurysm of the in-ferior vena cava. In Sweeny et al.’s review,17 only three caseshad been reported before 1990: two patients had aneurysms ofthe supradiaphragmatic inferior vena cava and one patient

Figure 1.24 Circumaortic renal collar.

Venous anomaly Incidence percentage

Circumaortic renal collar 1.5–8.7

Double inferior vena cava 2.2–3.0

Posterior left renal vein 1.8–2.4

Left inferior vena cava 0.2–0.5

Table 1.1 Incidence of major inferior vena caval and renal vein anomalies

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