7. Olsson M, Thyberg J, Nilsson J. Presence of oxidized low density lipoprotein in nonrheumatic
stenotic aortic valves. Arterioscler Thromb Vasc Biol 1999;19(5):1218–1222.
8. Galante A, Pietroiusti A, Vellini M, et al. C-reactive protein is increased in patients with
degenerative aortic valvular stenosis. J Am Coll Cardiol 2001;38(4):1078–1082.
9. Rajamannan NM, Gersh B, Bonow RO. Calcific aortic stenosis: from bench to the bedside–emerging
clinical and cellular concepts. Heart 2003; 89(7):801–805.
10. Mohler III ER, Gannon F, Reynolds C, et al. Bone formation and inflammation in cardiac valves.
Circulation 2001;103(11):1522–1528.
11. Rajamannan NM, Subramaniam M, Rickard D, et al. Human aortic valve calcification is associated
with an osteoblast phenotype. Circulation 2003;107(17):2181–2184.
12. Alpert JS. Aortic stenosis: A new face for an old disease. Arch Intern Med 2003;163(15):1769–1770.
13. Bache RJ, Vrobel TR, Ring WS. Regional myocardial blood flow during exercise in dogs with
chronic left ventricular hypertrophy. Circ Res 1981; 48(1):76–87.
14. Marcus ML, Doty DB, Hiratzka LF et al. Decreased coronary reserve. A mechanism for angina
pectoris in patients with aortic stenosis and normal coronary arteries. N Engl J Med
1982;307(22):1362–1366.
15. Carabello BA. Evaluation and management of patients with aortic stenosis. Circulation
2002;105(15):1746–1750.
16. Swartz MH. Textbook of Physical Diagnosis: History and Examination. 4th ed. Philadelphia, PA: W.B.
Saunders Company; 2001.
17. Bonow RO, Carabello BA, Chatterjee K, et al. 2008 focused update incorporated into the ACC/AHA
2006 guidelines for the management of patients with valvular heart disease: a report of the
American College of Cardiology/American Heart Association Task Force on Practice Guidelines
(Writing Committee to revise the 1998 guidelines for the management of patients with valvular
heart disease). Endorsed by the Society of Cardiovascular Anesthesiologists, Society for
Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol
2008;52(13):e1–e142.
18. Faggiano P, Aurigemma GP, Rusconi C, et al. Progression of valvular aortic stenosis in adults:
literature review and clinical implications. Am Heart J 1996;132(2 Pt 1):408–417.
19. Wagner S, Selzer A. Patterns of progression of aortic stenosis: a longitudinal hemodynamic study.
Circulation 1982;65(4):709–712.
20. Ross J Jr, Braunwald E. Aortic stenosis. Circulation 1968;38(suppl 1):61–67.
21. Mihaljevic T, Nowicki ER, Rajeswaran J, et al. Survival after valve replacement for aortic stenosis:
implications for decision making. J Thorac Cardiovasc Surg 2008;135(6):1270–1278; discussion
1278–1279.
22. Svensson LG, Tuzcu M, Kapadia S, et al. A comprehensive review of the PARTNER trial. J Thorac
Cardiovasc Surg 2013;145(3 suppl):S11–S16.
23. Kapadia SR, Leon MB, Makkar RR, et al. 5-year outcomes of transcatheter aortic valve replacement
compared with standard treatment for patients with inoperable aortic stenosis (PARTNER 1): a
randomised controlled trial. Lancet 2015;385(9986):2485–2491.
24. Panchal HB, Ladia V, Amin P, et al. A meta-analysis of mortality and major adverse cardiovascular
and cerebrovascular events in patients undergoing transfemoral versus transapical transcatheter
aortic valve implantation using edwards valve for severe aortic stenosis. Am J Cardiol
2014;114(12):1882–1890.
25. Liu Z, He R, Wu C, et al. Transfemoral versus transapical aortic implantation for aortic stenosis
based on no significant difference in logistic EuroSCORE: A meta-analysis. Thorac Cardiovasc Surg
2015.
26. Greason KL, Suri RM, Nkomo VT, et al. Beyond the learning curve: transapical versus transfemoral
transcatheter aortic valve replacement in the treatment of severe aortic valve stenosis. J Card Surg
2014;29(3):303–307.
27. Leshnower BG, Myung RJ, McPherson L, et al. Midterm results of DavidV valve-sparing aortic root
replacement in acute type A aortic dissection. Ann Thorac Surg 2015;99(3):795–800.
28. Leontyev S, Trommer C, Subramanian S, et al. The outcome after aortic valve-sparing(David)
operation in 179 patients: a single-centre experience. Eur J Cardiothorac Surg 2012;42(2):261–266.
2382
29. Patel ND, Weiss ES, Alejo DE, et al. Aortic root operations for Marfan syndrome: a comparison of
the Bentall and valve-sparing procedures. Ann Thorac Surg 2008;85(6):2003–2010.
30. Schoenhoff FS, Langhammer B, Wustmann K, et al. Decision-making in aortic root surgery in
Marfan syndrome: bleeding, thromboembolism and risk of reintervention after valve-sparing or
mechanical aortic root replacement. Eur J Cardiothorac Surg 2015;48(6):931–935; discussion 935–
936.
31. Rowe JC, Bland EF, Sprague HB, et al. The course of mitral stenosis without surgery: ten and
twenty year perspectives. Ann Intern Med 1960;52:741–749.
32. Wood P. An appreciation of mitral stenosis. I. Clinical features. Br Med J 1954;1:1051–1063.
33. Olesen KH. The natural history of 271 patients with mitral stenosis under medical treatment. Br
Heart J 1962;24:349–357.
34. Selzer A, Cohn KE. Natural history of mitral stenosis: a review. Circulation 1972;45(4):878–890.
35. Roberts WC, Perloff JK. Mitral valvular disease. A clinicopathologic survey of the conditions
causing the mitral valve to function abnormally. Ann Intern Med 1972;77(6):939–975.
36. Inoue K, Owaki T, Nakamura T, et al. Clinical application of transvenous mitral commissurotomy
by a new balloon catheter. J Thorac Cardiovasc Surg 1984;87(3):394–402.
37. Wilkins GT, Weyman AE, Abascal VM, et al. Percutaneous balloon dilatation of the mitral valve: an
analysis of echocardiographic variables related to outcome and the mechanism of dilatation. Br
Heart J 1988;60(4):299–308.
38. Cohen DJ, Kuntz RE, Gordon SP, et al. Predictors of long-term outcome after percutaneous balloon
mitral valvuloplasty. N Engl J Med 1992; 327(19):1329–1335.
39. Feldman T. Hemodynamic results, clinical outcome, and complications of Inoue balloon mitral
valvotomy. Cathet Cardiovasc Diagn 1994;(suppl 2):2–7.
40. Davis K. Multicenter experience with balloon mitral commissurotomy: NHLBI balloon valvuloplasty
registry report on immediate and 30-day follow-up results. Circulation 1992;85(2):448–461.
41. Dean LS. Complications and mortality of percutaneous balloon mitral commissurotomy: a report
from the National Heart, Lung, and Blood Institute Balloon Valvuloplasty Registry. Circulation
1992;85(6):2014–2024.
42. Palacios IF, Sanchez PL, Harrell LC, et al. Which patients benefit from percutaneous mitral balloon
valvuloplasty? Prevalvuloplasty and postvalvuloplasty variables that predict long-term outcome.
Circulation 2002;105(12):1465–1471.
43. Kang DH, Park SW, Song JK, et al. Long-term clinical and echocardiographic outcome of
percutaneous mitral valvuloplasty: randomized comparison of Inoue and double balloon techniques.
J Am Coll Cardiol 2000;35:169–175.
44. Fawzy ME, Hegazy H, Shoukri M, et al. Long-term clinical and echocardiographic results after
successful mitral balloon valvotomy and predictors of long-term outcome. Eur Heart J
2005;26(16):1647–1652.
45. Tomai F, Gaspardone A, Versaci F, et al. Twenty year follow-up after successful percutaneous
balloon mitral valvuloplasty in a large contemporary series of patients with mitral stenosis. Int J
Cardiol 2014;177(3):881–885.
46. Gross RI, Cunningham JN Jr, Snively SL. Long-term results of open radical mitral commissurotomy:
ten year follow-up study of 202 patients. Am J Cardiol 1981;47(4):821–825.
47. Halseth WL, Elliott DP, Walker EL, et al. Open mitral commissurotomy. A modern re-evaluation. J
Thorac Cardiovasc Surg 1980;80(6):842–848.
48. Farhat MB, Ayari M, Maatouk F, et al. Percutaneous balloon versus surgical closed and open mitral
commissurotomy: seven-year follow-up results of a randomized trial. Circulation 1998;97(3):245–
250.
49. Cotrufo M, Renzulli A, Ismeno G, et al. Percutaneous mitral commissurotomy versus open mitral
commissurotomy: a comparative study. Eur J Cardiothorac Surg 1999;15(5):646–651.
50. David TE, Uden DE, Strauss HD. The importance of the mitral apparatus in left ventricular function
after correction of mitral regurgitation. Circulation 1983;68(3 Pt 2):II76–II82.
51. David TE, Burns RJ, Bacchus CM. Mitral valve replacement for mitral regurgitation with and
without preservation of chordae tendineae. J Thorac Cardiovasc Surg 1984;88(5 Pt 1):718–725.
52. Hennein HA, Swain J, McIntosh CL, et al. Comparative assessment of chordal preservation versus
2383
chordal resection during mitral valve replacement. J Thorac Cardiovasc Surg 1990;99(5):828–836.
53. Rozich JD, Carabello BA, Usher BW, et al. Mitral valve replacement with and without chordal
preservation in patients with chronic mitral regurgitation: mechanisms for differences in
postoperative ejection performance. Circulation 1992;86(6):1718–1726.
54. Horskotte D, Schulte HD, Bircks W, et al. The effect of chordal preservation on late outcome after
mitral valve replacement: a randomized study. J Heart Valve Dis 1993;2(2):150–158.
55. Hammermeister K, Sethi GK, Henderson WG, et al. Outcomes 15 years after valve replacement
with a mechanical versus a bioprosthetic valve: final report of the Veterans Affairs randomized
trial. J Am Coll Cardiol 2000;36(4):1152–1158.
56. Ling LH, Enriquez-Sarano M, Seward JB, et al. Clinical outcome of mitral regurgitation due to flail
leaflet. N Engl J Med 1996;335(19):1417–1423.
57. Gillinov AM, Mihaljevic T, Blackstone EH, et al. Should patients with severe degenerative mitral
regurgitation delay surgery until symptoms develop? Ann Thorac Surg 2010;90:481–488.
58. Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC Guideline for the management of
patients with valvular heart disease: executive summary a report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation
2014;129(23):2440–2492.
59. Enriquez-Sarano M, Schaff HV, Orszulak TA, et al. Valve repair improves the outcome of surgery
for mitral regurgitation: a multivariate analysis. Circulation 1995;91(4):1022–1028.
60. Algarni KD, Suri RM, Schaff H. Minimally invasive mitral valve surgery: does it make a difference?
Trends Cardiovasc Med 2015;25(5):456–465.
61. McClure RS, Athanasopoulos LV, McGurk S, et al. One thousand minimally invasive mitral valve
operations: early outcomes, late outcomes, and echocardiographic follow-up. J Thorac Cardiovasc
Surg 2013;145:1199–1206.
62. Svensson LG, Atik FA, Cosgrove DM, et al. Minimally invasive versus conventional mitral valve
surgery: a propensity-matched comparison. J Thorac Cardiovasc Surg 2010;139:926–932.
63. Chitwood WR Jr, Rodriguez E, Chu MW, et al. Robotic mitral valve repairs in 300 patients: a
single-center experience. J Thorac Cardiovasc Surg 2008;136(2):436–441.
64. Mihaljevic T, Jarrett CM, Gillinov AM, et al. Robotic repair of posterior mitral valve prolapse
versus conventional approaches: potential realized. J Thorac Cardiovasc Surg 2011;141(1):72–80.
65. Mihaljevic T, Koprivanac M, Kelava M, et al. Value of robotically assisted surgery for mitral valve
disease. JAMA Surg 2014;149(7):679–686.
66. Suri RM, Antiel RM, Burkhart HM, et al. Quality of life after early mitral valve repair using
conventional and robotic approaches. Ann Thorac Surg 2012;93:761–769.
67. Mauri L, Foster E, Glower DD, et al. 4-year results of a randomized controlled trial of percutaneous
repair versus surgery for mitral regurgitation. J Am Coll Cardiol 2013;62(4):317–328.
68. Reynen K. Frequency of primary tumors of the heart. Am J Cardiol 1996; 77(1):107.
69. Lam KY, Dickens P, Chan AC. Tumors of the heart. A 20-year experience with a review of 12,485
consecutive autopsies. Arch Pathol Lab Med 1993; 117(10):1027–1031.
70. Shapiro LM. Cardiac tumours: diagnosis and management. Heart 2001; 85(2):218–222.
71. Goodwin JF. Diagnosis of left atrial myxoma. Lancet 1963;1(7279):464–468.
72. Hall RJ, Cooley DA, McAllister HA. Neoplastic heart disease. In: Hurst JW, ed. The Heart, Arteries,
and Veins. 7th ed. New York, NY: McGraw-Hill; 1990:1382–1403.
73. McAllister HA, Fenoglio JJ. Tumors of the cardiovascular system, fascicle 15. In: Hartman WH,
Cowan W, eds. Atlas of Tumor Pathology. 2nd ed. Washington, DC: Armed Forces Institute of
Pathology; 1978:1–20.
74. Prichard RW. Tumors of the heart; review of the subject and report of 150 cases. AMA Arch Pathol
1951;51(1):98–128.
75. Bortolotti U, Maraglino G, Rubino M, et al. Surgical excision of intracardiac myxomas: a 20-year
follow-up. Ann Thorac Surg 1990;49(3):449–453.
76. Fyke FE III, Seqard JB, Edwards WD, et al. Primary cardiac tumors: experience with 30 consecutive
patients since the introduction of two-dimensional echocardiography. J Am Coll Cardiol
1985;5(6):1465–1473.
2384
77. Goodwin JF. The spectrum of cardiac tumors. Am J Cardiol 1968;21(3):307–314.
78. Fang BR, Chiang CW, Hung JS, et al. Cardiac myxoma–clinical experience in 24 patients. Int J
Cardiol 1990;29(3):335–341.
79. Hanson EC, Gill CC, Razavi M, et al. The surgical treatment of atrial myxomas. Clinical experience
and late results in 33 patients. J Thorac Cardiovasc Surg 1985;89(2):298–303.
80. St John Sutton MG, Mercier LA, Giuliani ER, et al. Atrial myxomas: a review of clinical experience
in 40 patients. Mayo Clin Proc 1980;55(6): 371–376.
81. Yang M, Yao M, Wang G, et al. Comparison of postoperative quality of life for patients who
undergo atrial myxoma excision with robotically assisted versus conventional surgery. J Thorac
Cardiovasc Surg 2015;150(1):152–157.
82. Schilling J, Engel AM, Hassan M, et al. Robotic excision of atrial myxoma. J Card Surg
2012;27(4):423–426.
83. Russo MJ, Martens TP, Hong KN, et al. Minimally invasive versus standard approach for excision of
atrial masses. Heart Surg Forum 2007;10(1):E50–E54.
84. Corno A, de Simone G, Catena G, et al. Cardiac rhabdomyoma: surgical treatment in the neonate. J
Thorac Cardiovasc Surg 1984;87(5):725–731.
85. Brizard C, Latremouille C, Jebara VA, et al. Cardiac hemangiomas. Ann Thorac Surg
1993;56(2):390–394.
86. Choi JY, Bae EJ, Noh CI, et al. Cardiac rhabdomyoma in childhood tuberous sclerosis. Cardiol
Young 1995;5(02):166–171.
87. Alkalay AL, Ferry DA, Lin B, et al. Spontaneous regression of cardiac rhabdomyoma in tuberous
sclerosis. Clin Pediatr (Phila) 1987;26(10):532–535.
88. Beghetti M, Gow RM, Haney I, et al. Pediatric primary benign cardiac tumors: a 15-year review.
Am Heart J 1997;134(6):1107–1114.
89. Gutiérrez de Loma J, Villagrá F, Perez de León J, et al. Rhabdomyoma of the heart: surgical
treatment. J Cardiovasc Surg (Torino) 1982;23(2):149–154.
90. Foster ED, Spooner EW, Farina MA, et al. Cardiac rhabdomyoma in the neonate: surgical
management. Ann Thorac Surg 1984;37(3):249–253.
91. Edwards FH, Hale D, Cohen A, et al. Primary cardiac valve tumors. Ann Thorac Surg
1991;52(5):1127–1131.
92. Ryan PE Jr, Obeid AI, Parker FB Jr. Primary cardiac valve tumors. J Heart Valve Dis 1995;4(3):222–
226.
93. Darvishian F, Farmer P. Papillary fibroelastoma of the heart: report of two cases and review of the
literature. Ann Clin Lab Sci 2001;31(3):291–296.
94. Gallo R, Kumar N, Prabhakar G, et al. Papillary fibroelastoma of mitral valve chorda. Ann Thorac
Surg 1993;55(6):1576–1577.
95. Topol EJ, Biern RO, Reitz BA. Cardiac papillary fibroelastoma and stroke. Echocardiographic
diagnosis and guide to excision. Am J Med 1986; 80(1):129–132.
96. Roberts WC. Primary and secondary neoplasms of the heart. Am J Cardiol 1997;80(5):671–682.
97. Thomas CR Jr, Johnson GW Jr, Stoddard MF, et al. Primary malignant cardiac tumors: update
1992. Med Pediatr Oncol 1992;20(6):519–531.
98. Hajar R, Roberts WC, Folger GM Jr. Embryonal botryoid rhabdomyosarcoma of the mitral valve.
Am J Cardiol 1986;57(4):376.
99. Hui KS, Green LK, Schmidt WA. Primary cardiac rhabdomyosarcoma: definition of a rare entity. Am
J Cardiovasc Pathol 1988;2(1):19–29.
100. Shirani J, Roberts WC. Clinical, electrocardiographic and morphologic features of massive fatty
deposits (“lipomatous hypertrophy”) in the atrial septum. J Am Coll Cardiol 1993;22(1):226–238.
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Chapter 83
Ischemic Heart Disease
Jonathan W. Haft
Key Points
1 Because of its unique physiology, the heart is particularly susceptible to ischemic injury.
2 Atherosclerotic plaques cause ischemia from chronic flow limitations or from unstable plaque
rupture.
3 Patients with coronary artery disease will present with either chronic stable angina or an acute
coronary syndrome (ACS), which consists of unstable angina, a non–ST-segment myocardial
infarction, or an ST-segment myocardial infarction.
4 Several well-described complications from myocardial infarctions must be anticipated and recognized
early.
5 Medical treatment of coronary artery disease includes lifestyle modifications and medications to
slow the progression and stabilize atherosclerotic plaques.
6 Percutaneous intervention (PCI) of coronary lesions has improved dramatically in recent years to
include drug-eluting intracoronary stents.
7 Coronary artery bypass grafting (CABG) involves creation of alternative conduits from the systemic
circulation to the epicardial coronary arteries.
8 The left internal mammary artery is the superior conduit for CABG.
9 CABG remains superior to both medical treatment and PCI for patients with left main or three-vessel
disease or for patients with two-vessel disease involving the left anterior descending artery
associated with left ventricular dysfunction.
CORONARY ANATOMY AND PHYSIOLOGY
The right and left coronary arteries originate from the aorta just above the aortic valve cusps (Fig. 83-
1). The orifices of the two arteries within the sinuses of Valsalva designate the right and left coronary
cusps. The third aortic valve cusp is referred to as the noncoronary cusp. The coronary circulation is
traditionally divided into three major territories: The left anterior descending (LAD) and the circumflex
territories originate from the left coronary artery, and the right coronary territory usually comes from
the right coronary artery.
The origin of the left coronary artery is referred to as the left main and travels posterolaterally to the
left behind the pulmonary artery, where it divides into two main branches, the LAD and the circumflex
coronary artery. The length of the left main coronary artery is variable, but rarely exceeds 2 cm.
Unusually, the left main is absent, where the circumflex and LAD originate from the aorta via two
separate ostia.
The LAD coronary artery emerges from behind the pulmonary artery and travels inferiorly within the
interventricular groove to the cardiac apex, sometimes wrapping around it onto the posterior
interventricular groove. The LAD gives off two different types of branches: diagonals and septals, both
of which are highly variable in size and number. The diagonals take off at acute angles and perfuse the
anterolateral surface of the left ventricle. Septal branches, the first of which is typically quite
prominent, emerge at a right angle from the LAD and supply the interventricular septum. The LAD is
the most prominent of the three coronary territories described, and carries approximately 50% of left
ventricular myocardial blood flow, supplying the anterior, anterolateral, septal, and apical walls.
The circumflex coronary artery continues from the left main coronary and travels within the posterior
atrioventricular groove. Branches from the circumflex are called obtuse marginal arteries, and also vary
greatly in size and number. In 80% to 90% of people, the terminal branch of the circumflex supplies the
posterolateral wall of the left ventricle. In the remaining 10% to 20%, the circumflex continues to the
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posterior interventricular septum and terminates as the posterior descending artery (PDA). This is
referred to as a left dominant heart, where the left main coronary artery is supplying the posterior
interventricular septum. Some patients will have a third branch of the left main referred to as the ramus
intermedius, or intermediate branch. If present, this vessel is typically large, and supplies much of the
anterolateral wall of the left ventricle.
The right coronary artery originates from the anterior right sinus of Valsalva and descends in the
right atrioventricular groove. One or more acute marginal branches feed the right ventricular free wall.
In 80% to 90% of patients, the right coronary artery continues to the posterior interventricular septum
and supplies the PDA and often a variable-sized right posterolateral artery. This is referred to as a right
dominant heart. Near the origin of the posterior descending branch, a small characteristic vessel can be
seen supplying the atrioventricular node. This branch can become important in acute right coronary
artery occlusions, resulting in life-threatening heart block and bradycardia. A small proximal branch of
the right coronary artery supplies the sinus node on the anterolateral surface of the superior vena cava.
Anomalous origin of the coronary arteries is common, occurring in 0.3% to 1% of the population, and
their anatomy is varied and complex. Rarely, the left coronary arises from the pulmonary artery. This
pathology is diagnosed in infancy, as the myocardium becomes profoundly ischemic when pulmonary
vascular resistance falls and myocardial perfusion decreases. If left uncorrected, it is universally fatal.
The coronaries may also originate from atypical aortic root sinuses, and their trajectory is variable. The
most worrisome problem occurs when the LAD or left main coronary artery originates from the right
sinus of Valsalva. When the LAD travels posteriorly and to the left, it courses between the pulmonary
artery and the aortic root. This trajectory is described as “malignant” because of the potential for
compression between the great vessels, particularly during accentuated wall stress, such as with
exercise. Although there is little evidence, it is generally accepted that a revascularization strategy
should be considered in symptomatic patients with “malignant” coronary anomalies or in asymptomatic
patients with demonstrable ischemia on noninvasive testing.1
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