Case 1 Clinical History (73,M) Cardiovascular Surgical Pathology Case 1. Case 1 Clinical History (73,M) Case 1 Clinical History (73,M)
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1 Cardiovascular Pathology Specialty Conference USCAP, Boston, MA March 11, 2009 Cardiovascular Surgical Pathology (No Disclosures; No Conflicts of Interest) William D. Edwards, M.D. Dept of Lab Medicine & Pathology Mayo Clinic, ochester, MN Clinical History (73,M) eferral to Mayo Clinic Worsening chest pain and SOB Past medical history Exertional chest discomfort (2 yr) History of present illness Exertional chest pain (2 wk) More frequent than previously More intense than previously Now radiates to left shoulder Nocturnal chest pain (2 wk) Clinical History (73,M) Coronary angiography 100% occlusion of prox CA 99% stenosis of prox LAD 80% stenosis of LAD-D1 80% stenosis of LCX-OM1 Echocardiography Severe aortic stenosis (0.6 cm 2 ) Moderate mitral regurgitation LV EF 34% (normal, 50-70%) Moderate LV and LA dilatation Clinical History (73,M) Clinical diagnoses Severe coronary artery disease Unstable angina pectoris Severe aortic stenosis Moderate systolic dysfunction Surgical procedures Coronary artery bypass surgery Aortic valve replacement, with 23-mm Carpentier-Edwards bovine pericardial bioprosthesis Aortic Valve Aortic Valve Ao Aspect LV Aspect Fibrocalcific Cusps (Gross & Micro) 1
2 Aortic Valve Diagnosis Aortic Valve Heart, aortic valve, excision: fibrocalcific aortic valve disease, associated with clinically severe aortic stenosis and no aortic regurgitation Microscopy None! Normal AV Mechanisms What processes interfere with valve opening? Calcification Any region Fibrosis Cusps Fusion Commissures Causes and Demographics Causes % Age* M:F : : :1 Other 5 <70 1:1 * Age at time of surgery (in years) 2
3 Type Calcium in Valve Pockets (Autopsy) Type Type 3 Cusps (Surgical) Calcium (X-ay) Mild Commissural Fusion (Surgical) Type Type Unequal Sized Cusps (Surgical) Fenestrations and Strands (Surgical) 3
4 Type Type Age-related abnormalities In U.S. population >65 yr old * Aortic valve sclerosis: 25% Aortic valve stenosis: 5% Pathogenesis of aortic stenosis Not by random wear-and-tear Interplay of numerous factors * Assessed by echocardiography Atherosclerotic risk factors Hyperlipidemia (esp apolipoprotein B, 2, & E), with Ox-LDL in valve; hypertension, age, & diabetes Inflammation and proliferation T cells, macrophages, monocytes, plasma cells, B cells, mast cells CAM s, TGF-β, TNF-α, MMP, BMP Myofibroblasts (GF, angio II, NO) Neoangiogenesis (VEG-F, PDGF) Type Type Calcification and ossification Cellular osteoblast-like phenotype Alkaline phosphatase, osteopontin, osteocalcin, osteonectin, bone sialoprotein, & tenascin-c Microfocal gross mass (CaPO4) Genetic and metabolic factors Osteoporosis and aortic stenosis Vitamin D receptor polymorphism Apolipoprotein E4 allele Diagram (Circulation 2005;111:3316) Type Type Inflammation Calcium Calcium and Inflammation (H&E) Chronic Inflammation (H&E, High Power) 4
5 Type T Cells (CD3) B Cells (CD20) Mac s (CD68) Mast Cells (SAB) Inflammation (Special Stains) Congenitally Valve Congenitally Valve (AY-fee) Two Cusps (Autopsy) 2 Cusps (Surgical) Calcium (X-ay) Congenitally Valve Congenitally Valve Location of (n = 567; 7 Studies) elative Size of Cusps (n = 524) P P L ight-left 460 (81%) 150º P L ight-post 90 (16%) L Left-Post 17 (3%) Diagram (Mayo Clin Proc 1999;74:14-26) 180º 30º 0º Equal 27 (5%) Unequal 484 (92%) Thirds 13 (2%) Diagram (Mayo Clin Proc 1999;74:14-26) 5
6 Congenitally Valve Congenitally Valve Equal (5%) Unequal (90%) elative Cusp Size (Surgicals) Thirds (5%) Commissural Fusion (Surgical) Congenitally Valve Congenitally Valve Seen With egurgitation > Stenosis Atypical BAV Commissural Fusion (Surgical) Fenestrated (Surgical) Congenitally Valve Occurrence Incidence (%): 1-2 Sex (M:F ratio): 2-3:1 Fate (by age 75) % Stenosis 85 egurgitation 10 Infection 3 Dissection 2 Normal 0 Congenitally Valve Etiology Inheritance: autosomal dominant trait, with incomplete penetrance Mutation: Notch-1 gene encoding for membrane receptor important for normal cardiac development Association: defective microfibrils in aortic valve & ascending aorta esult: weak mechanical support (fibrocalcific valve, dilated aorta) 6
7 Congenitally Unicommissural Valve Congenitally Unicommissural Valve Opened and Closed (Autopsy) Fibrosis (Surgical) Congenitally Unicommissural Valve Congenitally Unicommissural Valve Calcification (Surgical) 1 Cusp (Surgical) Calcium (X-ay) Type Fibrocalcific (Autopsy) Candlewax 7
8 Type Type C C C Fibrosis (Surgical) Calcium (X-ay) Three Fused Commissures (Surgical) Type What Type Is It?,, or? Two Fused Commissures (Surgical) One Fused Commissure (Surgical) What Type Is It? Type What if no history of rheumatic fever? Postinflammatory (probably rheumatic) One Fused Commissure (Surgical) 8
9 Subaortic Septal Myectomy LV V Angled Septum in Elderly (Autopsy) Ao LA Long-Axis View Subaortic Septal Myectomy Gross Usually <10 g Multiple pieces Microscopy Hypertrophy & focal fibrosis H&E stain only Amyloid stain if >65 years old (C or SAB) Surgical Tissue Past Trends Cases (%) 1159 Surgically Excised Valves Year Past and Future Trends Future Trends Changes ( ) & Projections ( ) 65 and over 85 and over U.S. Census Bureau (1993) Prevalence of various causes : steady increase valve: stable rate (1-2%) : steady decrease Natural history of symptomatic AS High risk for sudden death ( CP) 5-yr survival: 50% (worse than CA) Effective therapy for aortic stenosis Aortic valve replacement (surgery) Major impact on health care costs 9
10 Summary Handling surgical specimens Diagnostic versus research purposes outine diagnostic evaluation Gross examination (no microscopy) vs commissural fusion : shallow, single ridge, obtuse Fusion: high, two cusps, acute angle Calcium: difficult distinction if marked Summary Cardiovascular Pathology Specialty Conference USCAP, Boston, MA March 11, 2009 Surgical Pathology of Aortic Valve Stenosis Comparison of Surgical Specimens William D. Edwards, M.D. Dept of Lab Medicine & Pathology Mayo Clinic, ochester, MN Textbooks eferences Schoen FJ, Edwards WD. Valvular heart disease: general principles and stenosis. In Cardiovascular Pathology, 3/e. MD Silver, AI Gotlieb, FJ Schoen (ed). Churchill Livingstone, New York, 2001: Virmani, A Burke, A Farb, JB Atkinson. Pathology of cardiac valves. In Cardiovascular Pathology, 2/e. WB Saunders Co, Philadelphia, 2001: Surgical Pathology eferences Butany J, Collins MJ, El Demellawy D, et al. Morphological and clinical findings in 247 surgically excised native aortic valves. Can J Cardiol 2005;21: Chuangsuwanich T, Warnnissorn M, Leksrisakul P, et al. Pathology and etiology of 110 consecutively removed aortic valves. J Med Assoc Thai 2004;87:
11 Surgical Pathology eferences Dare AJ, Veinot JP, Edwards WD, Tazelaar HD, Schaff HV. New observations on the etiology of aortic valve disease: a surgical pathologic study of 236 cases from Hum Pathol 1993;24: Turri M, Thiene G, Bortolotti U, et al. Surgical pathology of aortic valve disease: a study based on 602 specimens. Eur J Cardiothorac Surg 1990;4: Surgical Pathology eferences Peterson MD, oach M, Edwards JE. Types of aortic stenosis in surgically removed valves. Arch Pathol Lab Med 1985;109: Subramanian, Olson LJ, Edwards WD. Surgical pathology of pure aortic stenosis: A study of 374 cases. Mayo Clin Proc 1984;59: Aortic Valve eferences Sievers HH, Schmidtke C. A classification system for the bicuspid aortic valve from 304 surgical specimens. J Thorac Cardiovasc Surg 2007;133: Sabet HY, Edwards WD, Tazelaar HD, Daly C. Congenitally bicuspid aortic valves: a surgical pathology study of 542 cases (1991 through 1996) and a literature review of 2,715 additional cases. Mayo Clin Proc 1999;74: eferences Temporal Changes in Etiology Edwards WD. The changing spectrum of valvular heart disease pathology. In: Harrison s Advances in Cardiology. E Braunwald (ed). McGraw-Hill, New York, 2003: Passik CS, Ackermann DM, Pluth J, Edwards WD. Temporal changes in the causes of aortic stenosis: a surgical pathologic study of 646 cases. Mayo Clin Proc 1987;62: Histopathology eferences Somers P, Knaapen M, Mistiaen W. Histopathology of calcific aortic valve stenosis. Acta Cardiol 2006;61: Matthias Bechtel JF, Noack F, Sayk F, et al. Histopathological grading of ascending aortic aneurysm: comparison of patients with bicuspid versus tricuspid aortic valve. J Heart Valve Dis 2003;12: eferences Subaortic Septal Myectomy Allen D, Edwards WD, Tazelaar HD, Danielson GK. Surgical pathology of subaortic septal myectomy not associated with hypertrophic cardiomyopathy: a study of 98 cases ( ). Cardiovasc Pathol 2003;12:
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