1. Valvular Heart Disease
Eric D. Grassman, M.D.
Thomas McKiernan M.D

2. Mitral Stenosis

3. ETIOLOGY AND PATHOLOGY
The predominant cause of mitral stenosis (MS) is rheumatic fever
Approximately 25 per cent of all patients with rheumatic heart disease have pure MS, and an additional 40 per cent have combined MS and MR.
Two-thirds of all patients with rheumatic MS are female.
Rheumatic fever results in four forms of fusion of the mitral valve apparatus leading to stenosis: (1) commissural, (2) cuspal, (3) chordal, and (4) combined.

4. ETIOLOGY AND PATHOLOGY
The thickened leaflets may be so adherent and rigid that they cannot open or shut, reducing or rarely even abolishing the first heart sound (S1) and leading to combined MS and MR.
When rheumatic fever results exclusively or predominantly in contraction and fusion of the chordae tendineae, with little fusion of the valvular commissures, dominant MR results.

5. ETIOLOGY AND PATHOLOGY
It probably takes a minimum of 2 years after the onset of acute rheumatic fever for severe MS to develop, and most patients in temperate climates remain asymptomatic for at least a decade more. Symptoms commence most commonly in the third or fourth decade, although mild MS in the aged is becoming a more frequent finding.
Enlargement of the left atrium and resultant elevation of the left main stem bronchus, calcification of the left atrial wall, the development of mural thrombi, and obliterative changes in the pulmonary vascular bed (see [For More Information] ) may all result from chronic MS.

6. Rheumatic mitral stenosis
Rheumatic mitral stenosis. A, Moderate valvular changes including diffuse leaflet fibrosis, commissural fusion, and chordal thickening and fusion. In another case, atrial view (B) and subvalvular and aortic aspects (C) show prominent subvalvular involvement; severe subvalvular distortion is evident (arrow). D, Severe rheumatic mitral stenosis with specimen shown in apical four-chamber echocardiographic view, demonstrating small left ventricle (lv) and enlarged left atrium (la), right ventricle (rv), and right atrium (ra). Note the calcified stenotic valve (arrow) and prominent subvalvular changes (double arrows).

7. Clinical Manifestations
The principal symptom of MS is dyspnea, largely the result of reduced compliance of the lungs. Cough and wheezing may be accompanying symptoms.
Pulmonary edema may be precipitated by effort, emotional stress, respiratory infection, fever, sexual intercourse, pregnancy, atrial fibrillation with a rapid ventricular rate or other tachyarrhythmia, or, indeed, by any condition that increases blood flow across the stenotic mitral valve, either by increasing total cardiac output or by reducing the time available for this flow of blood to occur.

8. Clinical Manifestations
Thromboembolism. Patients older than 35 with atrial fibrillation, especially with a low cardiac output and dilation of the left atrial appendage, are at the highest risk for emboli and therefore should receive prophylactic anticoagulant treatment.
Infective endocarditis
Compression of the left recurrent laryngeal nerve by a greatly dilated left atrium, enlarged tracheobronchial lymph nodes, and dilated pulmonary artery may cause hoarseness

9. Pressure gradient in a patient with mitral stenosis
Pressure gradient in a patient with mitral stenosis. The pressure in the left atrium (LA) exceeds the pressure in the left ventricle (LV) during diastole, producing a diastolic pressure gradient (shaded area).

10. Prominent left atrial (LA) contour
Prominent left atrial (LA) contour. A, The left atrial appendage bulges laterally to the left in this patient with multivalvular rheumatic heart disease (arrow). The double convex contour of enlarged right (curved arrow) and left (arrow) atria is present along the right atrial border (arrow). B, A 40-year-old woman with mitral stenosis. There is left atrial enlargement with a double right-sided heart border (white arrow = right atrium; black arrow = left atrial border). The left main stem bronchus is elevated (black arrow). C, Left atrial (LA) enlargement. A large convex bulge is seen in the area of the LA appendage (white arrow). The LA is grossly enlarged and is border-forming on the right side after traversing the smaller right atrium. The inferior border of the left atrium is visualized (black arrows) as it extends back toward the midline. If this were the right atrial border instead, it would have blended imperceptibly with the right hemidiaphragm and inferior vena cava. D, Enhanced CT demonstrates the anatomical relationship between the anterior RA and the posterior LA. The indentation of lung and fat between the atria (arrow) permits separation of the right-sided borders of both atria as seen in the PA chest radiograph.

11. Hockey stick deformity
. Long-axis (LX) and short-axis (SX) 2-D echocardiograms of a patient with mitral stenosis. The long-axis view shows typical doming of both leaflets with diminished separation (MS) between the anterior and posterior edges. The short-axis view shows the echo-free orifice in the center of the stenotic valve (MS).

13. Pressure Half Time MVA=220/280 = .78
Mitral Valve Area(cm2) = ______________220___________
Pressure Half Time(ms)

14. Medical Treatment
Patients with rheumatic heart disease should receive penicillin prophylaxis for beta-hemolytic streptococcal infections and prophylaxis for infective endocarditis
Digitalis glycosides do not alter the hemodynamics and usually do not benefit patients with MS and sinus rhythm, but are of great value in slowing the ventricular rate in patients with atrial fibrillation and in the treatment of right-sided heart failure.
Beta blockers may increase exercise capacity by reducing heart rate in patients with sinus rhythm, but especially in patients with atrial fibrillation.

16. Definitive Treatment
Operation (mitral valve replacement or balloon valvuloplasty) should therefore be carried out in symptomatic patients with moderate to severe MS (i.e., a mitral valve orifice size less than approximately 1.0 cm2/m2 body surface area [BSA]—less than 1.5 to 1.7 cm2 in normal-sized adults).
There are further specific guidelines for valvuloplasty

17. Mitral Valvuloplasty
Cineangiogram frame during mitral valvuloplasty using Inoue balloon. The "waist" of the inflating balloon is within the stenotic mitral valve. A pigtail catheter within the left ventricle and a pulmonary artery catheter are also visible.

18. Simultaneous left atrial (LA) and left ventricular (LV) pressure before and after balloon valvuloplasty of the mitral valve in a patient with severe mitral stenosis.

19. Mitral Regurgitation

20. Etiology, Acute MR Infectious endocarditis Trauma
Myxomatous Degeneration
Libman –Sacks lesions (SLE)
CAD ,mi and ischemia
LV dysfunction ,mi,myocarditis
Prosthetic valve dysfunction

21. Etiology,Chronic MR Inflammatory –Rheumatic,SLE
Degenerative - MVP,Marfans ,MAC
Infective Subacute Endocarditis
Structural-Ruptured chordae ,CAD , LV dilatation,Hypertrophic CM ,Prosthetic valve dysfunction
Congenital

22. Top, Mitral regurgitation due to papillary muscle dysfunction
Top, Mitral regurgitation due to papillary muscle dysfunction. At the onset of systole (left), the anterior and posterior mitral valve leaflets (AML and PML) approximate. Later in systole (right), the anterior papillary muscle (P, nonhatched) contracts while the posterior papillary muscle (P, hatched) fails to contract because of ischemia or infarction. Part of the posterior leaflet is allowed to prolapse into the left atrium (LA) during systole, producing regurgitation. This process may involve either papillary muscle. C = chordae tendineae, LV = left ventricle, A = aorta. Bottom, Late systolic murmur (SM) that developed in a patient following an inferior myocardial infarction and is probably due to weakening of the posterior papillary muscle with prolapse of the mitral leaflet into the atrium during late systole.

23. Pressure vs Volume Overload

24. Diagrammatic representation of the changes in the diastolic pressure-volume relationship that occur in valve disease. Hypertrophy without significant ventricular dilatation (e.g., in aortic stenosis) produces a somewhat steeper curve than normal. Acute regurgitation produces a sudden volume load on the ventricle without time for other changes to occur and the ventricle operates at the upper (steep) end of the normal curve (broken line). Chronic aortic and mitral regurgitation with volume overload produces a flattened curve so that large volumes are accommodated without the large rise in end-diastolic pressure which occurs in acute regurgitation.

25. Post-op Death
The probability of postoperative death or persistence of severe heart failure in patients with mitral regurgitation plotted against preoperative echocardiographic end-systolic diameter. As end-systolic diameter exceeded 45 mm, the incidence of a poor postoperative outcome increased abruptly. (Reproduced with permission from Wisenbaugh, T., et al.: Prediction of outcome after valve replacement for rheumatic mitral regurgitation in the era of chordal preservation.

26. Giant V wave
Post Valuloplasty
Intraoperative simultaneous left ventricular (LV) and left atrial (LA) pressures (mm Hg) before (A) and after (B) mitral valvuloplasty for correction of severe acute mitral regurgitation. Note the height of the v wave in the preoperative tracing.

27. Diagram depicting the two extremes of the spectrum in pure mitral regurgitation. When severe mitral regurgitation appears suddenly in individuals with previously normal or near-normal hearts (top), the left atrium (LA) is relatively small and the high pressure within it is reflected back into the pulmonary vessels and right ventricle (RV). The anatomical indicator of this latter physiological event is severe hypertrophy of the left atrial and right ventricular walls and marked intimal proliferation and medial hypertrophy of the pulmonary arteries (PA), arterioles, and veins (PV). At the other extreme with severe chronic mitral regurgitation (bottom), the left atrial cavity is of giant size and its wall is thin. It is thus able to "absorb" the left ventricular (LV) pressure without reflecting it back into the pulmonary vessels or right ventricle. As a consequence, pulmonary vessels remain normal, and the right ventricular wall does not thicken. PT = pulmonary trunk; RA = right atrium.

28. Physical Examination

29. . Illustration of great arterial (GA), ventricular (VENT), and atrial pressure pulses with phonocardiogram showing the physiological mechanism of a holosystolic murmur in some forms of mitral regurgitation and in high-pressure tricuspid regurgitation. Ventricular pressure exceeds atrial pressure at the very onset of systole, so regurgitant flow and murmur commence with the first heart sound (S1 ). The murmur persists up to or slightly beyond the second heart sound (S2 ) because regurgitation persists to the end of systole (ventricular pressure still exceeds atrial pressure). V = Atrial v wave.

30. A, Acute post–myocardial infarction papillary muscle dysfunction
A, Acute post–myocardial infarction papillary muscle dysfunction. Acute pulmonary interstitial edema is present but there is no cardiac enlargement. B, Dilated cardiomyopathy. There is diffuse dilatation of the heart in this woman with systemic lupus erythematosus.

31. Clinical Course
Symptoms usually do not develop in patients with chronic MR until the left ventricle fails
The development of symptoms tends to be longer in MR than in MS and often exceeds two decades
Acute pulmonary edema occurs less frequently in chronic MR than in MS, presumably because sudden surges in left atrial pressure are less common.

32. Clinical Course
By the time that symptoms secondary to a reduced cardiac output and/or pulmonary congestion become apparent, serious and sometimes even irreversible left ventricular dysfunction may have developed
In contrast, patients with MS have the benefit of an “early warning system,” i.e., symptoms of pulmonary congestion with frequent, sudden elevations of left atrial pressure.

33. Systole
Diastole
. Diastolic (left) and systolic (right) frames of a left ventricular cineangiogram from a patient with severe mitral regurgitation. Dense opacification of the left atrium was seen in the first systolic frame. Left ventricular contraction is excellent.

34. Mitral Valve Prolapse
Two-dimensional echocardiogram in the parasternal long-axis (A) and apical four-chamber (B) views of a patient with mitral valve prolapse (arrows). LV = left ventricle; AO = aorta; LA = left atrium; RV = right ventricle; RA = right atrium.

35. A large vegetation deforming and perforating the mitral valve
A large vegetation deforming and perforating the mitral valve. The nail probes an abscess that burrowed into the mitral valve annulus.

36. Color flow Doppler study of a patient with mitral regurgitation (MR) as viewed from the four-chamber (A) and two-chamber (B) views. There is acceleration of flow on the left ventricular side of the regurgitant mitral orifice (AC). LV = left ventricle; LA = left atrium; RV = right ventricle; RA = right atrium.

37. Medical Treatment
This includes all the measures used in the treatment of heart failure. Afterload reduction is of particular benefit in the management of MR—both the acute and the chronic forms. By reducing the impedance to ejection into the aorta, the volume of blood regurgitating into the left atrium is reduced
When surgical treatment is contraindicated, chronic afterload reduction with an angiotensin inhibitor or oral hydralazine may improve the clinical state for months or even years in patients with severe, chronic MR

38. Schematic representation of the concept of optimal timing of valve replacement surgery. Early surgery yields low operative mortality and preservation of ventricular function. However, because of a finite postoperative risk of prosthesis-associated complications (the major determinant of the slope of the postoperative survival curve in either early or optimally timed surgery), postoperative risk exceeds that of pure medical treatment at this early phase of the disease. In contrast, if surgery is done too late, operative mortality is increased and ventricular function may progressively deteriorate after surgery. Thus, following late surgery, postoperative survival is primarily determined by both prosthesis-associated complications and congestive heart failure. Optimal timing of surgery balances the risks of maintained medical management with the new risks associated with postoperative complications. With optimally timed surgical intervention, operative mortality is relatively low, ventricular function is almost completely preserved, and postoperative risk is determined, as in early surgery, predominantly in the risk of prosthesis-associated complications. (From Schoen, F. J., and St. John Sutton, M.: Contemporary issues in the pathology of valvular disease.

39. Mitral Valve Replacement vs Repair

40. Graph of the late survival of operative survivors of surgical correction of MR according to preoperative echocardiographic ejection fraction (EF). Number at risk for each interval is indicated at bottom. (Reproduced with permission from Enriquez-Sarano, M., et al.: Echocardiographic prediction of survival after surgical correction of organic mitral regurgitation.

41. Mitral Valve Prolapse
PE: mid systolic click

43. . Left panel, The dynamic spectrum, time in years, and the progression of mitral valve prolapse (MVP) are shown. A subtle gradation (cross-hatched area) exists between the normal mitral valve and valves that produce mild MVP without mitral regurgitation (no MR). Progression from the level MVP–no MR to another level may or may not occur. Most of the MVP syndrome cases occupy the area above the dotted line, while progressive mitral valve dysfunction cases occupy the area below the dotted line. Right panel, The large circle represents the total number of patients with MVP. Patients with MVP may be symptomatic or asymptomatic. Symptoms may be directly related to mitral valve dysfunction (black circle), or to autonomic dysfunction (cross-hatched circle). Certain patients with symptoms directly related to mitral valve dysfunction may present with and continue to have symptoms secondary to autonomic dysfunction.

44. Aortic Stenosis

45. ETIOLOGY AND PATHOLOGY
Congenitally bicuspid valves may be stenotic with commissural fusion at birth, but more commonly they are not responsible for serious narrowing of the aortic orifice during childhood
In a majority of cases, a bicuspid valve is not stenotic at birth and the changes causing stenosis resemble those occurring in senile, degenerative calcific stenosis of a tricuspid aortic valve except that in the congenitally bicuspid valve these changes occur several decades earlier

46. ETIOLOGY AND PATHOLOGY
Rheumatic AS results from adhesions and fusions of the commissures and cusps and vascularization of the leaflets of the valve ring, leading to retraction and stiffening of the free borders of the cusps, with calcific nodules present on both surfaces and an orifice that is reduced to a small round or triangular opening. As a consequence, the rheumatic valve is often regurgitant as well as stenotic
In degenerative (senile) calcific AS, the cusps are immobilized by a deposit of calcium along their flexion lines at their bases. This most common cause of AS in adults. Both diabetes mellitus and hypercholesterolemia are risk factors for the development of this lesion
In atherosclerotic aortic valvular stenosis, severe atherosclerosis involves the aorta and other major arteries; this form of AS occurs most frequently in patients with severe hypercholesterolemia

47. Types of aortic valve stenosis. A, Normal aortic valve
Types of aortic valve stenosis. A, Normal aortic valve. B, Congenital aortic stenosis. C, Rheumatic aortic stenosis. D, Calcific aortic stenosis. E, Calcific senile aortic stenosis.

48. RHEUMATIC
Aortic stenosis

49. Bicuspid Calcium Tricuspid
Calcific aortic stenosis. A, Congenitally bicuspid aortic valve, characterized by two equal cusps with basal mineralization. B, Congenitally bicuspid aortic valve having two unequal cusps, the larger with a central raphe (arrow). C, Otherwise anatomically normal tricuspid aortic valve in an elderly patient, characterized by isolated cusps with calcification localized to basilar aspect; cuspal free edges are not involved. D and E, Photomicrographs of calcific deposits in calcific aortic stenosis; deposits are rimmed by arrows (hematoxylin and eosin, ×15). D, Deposits with underlying cusp largely intact; transmural calcific deposits are shown in E

50. Pathophysiology of aortic stenosis
Pathophysiology of aortic stenosis. Left ventricular (LV) outflow obstruction results in an increased LV systolic pressure, increased left ventricular ejection time (LVET), increased left ventricular diastolic pressure, and decreased aortic (Ao) pressure. Increased LV systolic pressure with LV volume overload increases LV mass, which may lead to LV dysfunction and failure. Increased LV systolic pressure, LV mass, and LVET increase myocardial oxygen (O2 ) consumption. Increased LVET results in a decrease of diastolic time (myocardial perfusion time). Increased LV diastolic pressure and decreased Ao diastolic pressure decrease coronary perfusion pressure. Decreased diastolic time and coronary perfusion pressure decrease myocardial O2 supply. Increased myocardial O2 consumption and decreased myocardial O2 supply produce myocardial ischemia, which further deteriorates LV function (­ = increased, ¯ = decreased).

51. A, Phonocardiogram over the left ventricular impulse in a patient with mild congenital bicuspid aortic valve stenosis. The aortic ejection sound (E) is louder than the first heart sound (S1 ). A2 = Aortic component of the second heart sound. B, Left ventriculogram (LV) in another patient with congenital aortic valve stenosis. The cephalad systolic doming of the stenotic valve (arrows) produces the ejection sound.

52. . A, Aortic stenosis. The left ventricular border is rounded and prominent due to left ventricular hypertrophy. The proximal ascending aorta is prominent due to poststenotic dilatation (arrow). B, Aortic regurgitation in a patient with Marfan syndrome. Prominent left ventricular border (arrow). The LV chamber is dilated due to aortic regurgitation and the ascending aorta is convex (curved arrows). The descending aorta is dilated. C, The ascending aorta is enlarged, and there is a thin mural calcification within the left ventricle due to a large aneurysm (arrows).

53. Long-axis (LAX) and short-axis (SAX) views from a patient with aortic stenosis (AS). The long-axis examination shows classic doming, restricted motion, and reduced separation of the leaflets. The elliptical orifice occasionally can be identified in the short-axis examination. LV = left ventricle; AO = aorta; LA = left atrium; RVOT = right ventricular outflow tract; RA = right atrium.

54. Principles of using Doppler echocardiography and the continuity equation for calculating the area of a stenotic orifice. A1 = area proximal to the stenosis; A2 = area of the stenosis; V1 = velocity proximal to the stenosis; V2 = velocity through the stenosis.

55. Natural history of aortic stenosis without operative treatment.

57. Physical Examination
S2 may be single because calcification and immobility
of the aortic valve make A2 inaudible
An aortic ejection sound occurs simultaneously with
the halting upward movement of the aortic valve
It is dependent on mobility of the valve cusps and
disappears when they become severely calcified.
The systolic murmur of AS is usually late-peaking
and heard best at the base of the heart but is often
well transmitted along the carotid vessels and to the apex
The systolic murmur may be cooing or musical when AS becomes severe and associated with a precordial thrill

58. Treatment - mechanical
Balloon Aortic Valvuloplasty - The major disadvantage of balloon valvuloplasty in adults with critical, calcified AS is restenosis due to scarring, which occurs in about half of the patients within 6 months. This option is only as a bridge to AVR or in patients with severe CHF and no surgical options.
Otherwise the treatment is AVR

60. Aortic valve Replacement

61. Percutaneous Aortic Valve
Surgery Insight: current advances in percutaneous heart valve replacement and repair
Vasilis Babaliaros, Alain Cribier and Carla Agatiello
Nature Clinical Practice Cardiovascular Medicine (2006) 3,

62. Aortic Regurgitation

63. Etiology
Aortic regurgitation (AR) may be caused by primary disease of either the aortic valve leaflets (rheumatic fever) or the wall of the aortic root or both. Among patients with pure AR coming to valve replacement, the percentage with aortic root disease has been increasing steadily during the past few decades and now accounts for more than one-half of the patients

64. Pathophysiology of aortic regurgitation
Pathophysiology of aortic regurgitation. Aortic regurgitation results in an increased left ventricular (LV) volume, increased stroke volume, increased aortic (Ao) systolic pressure, and decreased effective stroke volume. Increased LV volume results in an increased LV mass, which may lead to LV dysfunction and failure. Increased LV stroke volume increases systolic pressure and prolongation of left ventricular ejection time (LVET). Increased LV systolic pressure results in a decrease in diastolic time. Decreased diastolic time (myocardial perfusion time), diastolic aortic pressure, and effective stroke volume reduce myocardial O2 supply. Increased myocardial O2 consumption and decreased myocardial O2 supply produce myocardial ischemia, which further deteriorates LV function (­ = increased, ¯ = decreased).

65. Hemodynamics of Aortic Regurgitation

66. A, Phonocardiogram recorded from the mid-left sternal edge of a patient with chronic pure severe aortic regurgitation. An early diastolic murmur (EDM) proceeds immediately from the aortic component (A2 ) of the second heart sound. The murmur has an early crescendo followed by a late long decrescendo. There is a prominent midsystolic flow murmur (SM) across an unobstructed aortic valve. S1 = First heart sound. B, Phonocardiogram in the third left intercostal space (3LICS) records a high-frequency, musical, early diastolic decrescendo murmur (EDM) caused by eversion of an aortic cusp. S1 = First heart sound; SM = midsystolic murmur; A2 = aortic component of the second sound.

67. Aortic regurgitation. There is massive aortic dilatation in this man with severe aortic regurgitation related to annuloaortic ectasia. A, PA projection. B, Lateral projection.

68. Color flow mapping in a patient with aortic regurgitation
. Color flow mapping in a patient with aortic regurgitation. The brightly colored, high-velocity jet can be seen passing from the aorta (AO) to the left ventricle (LV). The center of the jet is white, and the edges are shades of blue. Even though the velocity is extremely high, most of the jet is blue because the flow is almost perpendicular to the ultrasonic beam, and the velocities are registered as being lower than they actually are.

69. Treatment Symptomatic patients – AVR Asymptomatic patients:
Patients with severe AR and an end-systolic diameter less than 40 mm almost invariably remain stable without cardiac failure or death, whereas those with an end-systolic diameter greater than 55 mm (Fig. 32–42 Fig. 32–42 ), an end-systolic volume greater than 55 ml/m2, an end-diastolic volume greater than 200 ml/m2, or an ejection fraction less than 50 per cent have an increased risk of death secondary to left ventricular dysfunction.
In a comparison of digoxin with nifedipine in asymptomatic patients with severe AR, the latter delayed the need for operation (the development of symptoms or of left ventricular dysfunction)

70. Relation of preoperative ventricular function to postoperative survival. Data of Greves et al. (left) and those of Bonow et al. (right) show remarkable agreement: Both groups incorporated limits clearly in abnormal range. Cunha et al. (center) selected a limit that was well within normal range. These and other published data indicate that preoperative ventricular function is an important determinant of postoperative survival. SEF = systolic ejection fraction; ESD = echocardiographically measured dimension at end-systole; angio = angiography; echo = echocardiography.

71. Designs and flow patterns of major categories of prosthetic heart valves: caged-ball, caged-disc, tilting-disc, bi-leaflet tilting-disc, and bioprosthetic (tissue) valves. Whereas flow in mechanical valves must course along both sides of the occluder, bioprostheses have a central flow pattern.

72. A, The Starr-Edwards ball and cage valve. B, The Omniscience valve
A, The Starr-Edwards ball and cage valve. B, The Omniscience valve. C, The Medtronic-Hall valve. D, The St. Jude valve. E, The Carbomedics bileaflet valve.
Medtronic St Jude Valve the most commonly used

73. A, The Hancock porcine valve. B, The Carpentier-Edwards porcine valve
A, The Hancock porcine valve. B, The Carpentier-Edwards porcine valve. C, Carpentier pericardial valve. D, Cryopreserved homograft valve. E, Incisions for placement of pulmonary autograft valve into the aortic position.
Ross Procedure

74. Unified model for bioprosthetic heart valve failure relating isolated tissue processes of mineralization and collagen degeneration to gross clinical failures. Such failures have calcification with cuspal stiffening (1), cuspal defects without calcific deposits (2), or cuspal tears associated with mineralization (1 and 2). These processes may occur independently or they may be synergistic. Specifically, implant and host factors interact to induce the collagen-oriented and cell-oriented calcific deposits noted ultrastructurally. The deposits predominate in the central portions of valve cusps, particularly at flexion points such as the commissures (Pathway 1). Stress causes shear between and fracture of collagen fibers, which may create gross cuspal defects (Pathway 2). Although dynamic mechanical activity is not a prerequisite for calcification, stress may promote (i.e., accelerate) this process through unknown mechanisms.

75. Aortic valve replacement for aortic insufficiency

76. TRICUSPID REGURGITATION
The most common cause of tricuspid regurgitation (TR) is not intrinsic involvement of the valve itself but dilatation of the right ventricle and of the tricuspid annulus, which may be complications of right ventricular failure of any cause and which cause secondary, functional TR.
The response of the murmur to respiration and other maneuvers is of considerable aid in establishing the diagnosis of tricuspid regurgitation. It is usually augmented during inspiration (Carvallo’s sign).
TR in the absence of pulmonary hypertension usually does not require surgical treatment. Indeed, both patients and experimental animals with normal pulmonary artery pressure may tolerate total excision of the tricuspid valve, as long as right ventricular systolic pressure is normal for a period of time.
Surgical treatment of acquired regurgitation secondary to annular dilatation was greatly improved when Carpentier introduced the concept of suturing the annulus to a right prosthetic ring of appropriate dimensions.

77. The End