Mitral stenosis

Mitral stenosis

1. Pathophysiology of Mitral Valve Diseases Dr. Dharmraj Singh SR, Intensive Care CTVS

2. Mitral Stenosis

3. Outline Anatomy Causes & Pathology Pathophysiology Clinical presentation Diagnosis & Evaluation Disease course Reference- Braunwald Heart Disease, Kaplan Anaesthesia , Sabiston & Spencer Surgery of the Chest, Alpert Valvular heart disease , EAE/ASE Recommendation

4. anatomy The mitral valve apparatus is composed of the mitral annulus, leaflets, chordae tendineae, papillary muscles, and the left ventricular lateral wall. Chordae tendineae and papillary muscles comprise the subvalvular apparatus . Sabiston & Spencer Surgery of the Chest 9 th Edition, page no. 1385

5. Causes & Pathology Rheumatic Fever (RHD) Systemic lupus erythematosus Rheumatoid arthritis ASD with rheumatic MS ( Lutembacher syndrome) LA tumor (LA myxoma) Congenital Mitral Stenosis (rare) Malignant carcinoid disease (pulmonary metastasis or L-R shunting) Braunwald Heart Disease 11 th Edition

6. Causes & Pathology Ball valve thrombosis in the LA Infective endocarditis with large vegetation Congenital membrane in LA ( cor-triatrium ) Extensive mitral annular calcification Methylsergide therapy & Fenfluramine Braunwald Heart Disease 11 th Edition

7. Causes & Pathology Predominant cause of MS – Rheumatic fever Rheumatic changes – 99% of MV excised at the time of MVR Isolated MS - 25% (RHD) Mixed MS and MR – 40% Multivalve – 38% AV- 35% TV- 6% PV- rare Female- 2/3 rd of all rheumatic MS patients Braunwald Heart Disease 11 th Edition

8. Causes & Pathology Initial episode of RF & clinical evidence of MV obstruction is few years to > 20 years. Rheumatic fever results in characteristic changes ( Diagnostic features ) in mitral valve- Thickening at leaflet edges Fusion of the commissures Chordal shortening & fusion Sabiston & Spencer Surgery of the Chest 9 th Edition

9. Pathologic changes of the mitral valve in MS Thickened, rigid, nodular appearance of the mitral valve leaflets as viewed from the atria (A) and ventricle (B). The commissures are calcified and fused, thereby creating the characteristic “ fish mouth ”–shaped valve. B and C, The subvalvular apparatus is thickened, fused, and shortened. D, Healthy mitral valve leaflets. A B C D From Chandrashekar Y, Westaby S, Narula J: Mitral stenosis. Lancet 374:1273, 2009.)

10. Causes & Pathology Earlier stage- relatively flexible leaflets snap open in diastole in to curved shape - restriction of motion at the leaflet tip . Sudden restriction of leaflet opening in diastole – opening snap (OS) on auscultation Interval between S 2 & OS - inverse relationship with LA pressure “ Diastolic doming ” – most evident in motion of anterior leaflet & become less prominent as the leaflets become more fibrotic and calcified, which also muffles the OS. (Anterior leaflet like Hockey stick ) Symmetric fusion of commissures – small , central oval orifice in diastole – fish mouth or buttonhole.

11. Pathologic changes of the mitral valve in MS Parasternal long-axis (left) and short-axis (right) two-dimensional echocardiographic views showing the characteristic findings in rheumatic mitral stenosis. Commissural fusion that results in doming of the leaflets in the long-axis view and in a decrease in the width of the mitral orifice in the short-axis view. Three-dimensional imaging of rheumatic mitral stenosis, obtained by intraoperative epicardial echocardiography. Commissural fusion leaves the mitral valve with a small, circular orifice that has been likened to a fish mouth. Braunwald Heart Disease 11 th Edition

12. Pathologic changes of the mitral valve in MS End- stage disease – thickened leaflet may be so adherent & rigid that they cannot open or shut, with consequent reduction in or, rarely even abolition of S 1 leading to MS+MR RF results exclusively or predominantly in contraction & fusion of the chordae tendineae, with little fusion of valvular commissures – dominant MR Severity of MS- degree of valve opening in diastole, or MVOA Normal adults (MVA)- 4 to 6 cm 2 Orifice is reduced to approximately 2 cm 2 – mild MS, blood can flow from LA to LV only if propelled by a small , although abnormal gradient. MV opening is reduced to 1 cm 2 - severe MS, a left AV pressure gradient of approximately 20 mmHg ( normal LVDP, a mean LAP > 25mmHg) is required to maintain normal CO at rest.

13. Classification of ms severity Mild Moderate Severe Specific findings Valve area (cm) 2 >1.5 1.0-1.5 <1.0 Supportive findings Mean gradient (mmHg)* <5 5-10 >10 Pulmonary artery pressure(mmHg) <30 30-50 >50 * At heart rate between 60 and 80 bpm and in sinus rhythm

14. Stages of Mitral Stenosis STAGE DEFINITION VALVE ANATOMY VALVE HEMODYNAMICS HEMODYNAMICS CONSIQUENCES SYMPTOMS A At risk for MS Mild valve doming during diastole Normal transmitral flow velocity None None B Progressive MS Rheumatic valve changes with commissural fusion and diastolic doming of mitral valve leaflets Planimetered MVA >1.5 cm 2 Increased transmitral flow velocities M VA > 1.5 c m 2 Diastolic pressure half-time <150 msec Mild to moderate LA enlargement Normal pulmonary pressure at rest None C Asymptomatic severe MS Rheumatic valve changes with commissural fusion and diastolic doming of mitral valve leaflets Planimetered MVA ≤1.5 cm 2 (MVA ≤1 cm 2 with very severe MS) M VA ≤ 1.5 c m 2 (MVA ≤1 cm 2 with very severe MS) Diastolic pressure half-time ≥150 msec (Diastolic pressure half-time ≥220 msec with very severe MS) Severe LA enlargement Elevated PASP >30 mm Hg None D Symptomatic severe MS Rheumatic valve changes with commissural fusion and diastolic doming of mitral valve leaflets Planimetered MVA ≤1.5 cm 2 M VA ≤ 1.5 c m 2 (MVA ≤1 cm 2 with very severe MS) Diastolic pressure half-time ≥150 msec (Diastolic pressure half-time ≥220 msec with very severe MS) Severe LA enlargement Elevated PASP >30 mm Hg Decreased exercise tolerance Exertional dyspnea

15. Pathophysiology Transvalvular pressure gradient - square of the transvalvular blood velocity (Bernoulli equation) Doubling of flow rate quadruples the pressure gradient. ↑ LA Pressure - ↑ pulmonary venous and capillary pressures, resulting in exertional dyspnea. First bouts of dyspnea in patients with MS usually are precipitated by tachycardia (exercise, pregnancy, hyperthyroidism, anemia, infection, or AF).

16. Pathophysiology All these leads to- Increase the rate of blood flow across the mitral orifice, resulting in further ↑ LAP & ↓diastolic filling time, resulting in a reduction in forward CO. Because diastole shortens proportionately more than systole as HR ↑, the time available for flow across the mitral valve is reduced at higher HR. At any given SV, therefore tachycardia results in a higher instantaneous volume flow rate and higher transmitral pressure gradient, which further ↑ LAP

17. Pathophysiology This higher transmitral gradient, often in combination with inadequate LV filling explains the sudden occurrence of dyspnea and pulmonary edema in previously asymptomatic patients with MS who develop AF with a rapid ventricular rate. It also accounts for the equally rapid clinical improvement in these patients when the ventricular rate is slowed. Compounding the direct impact of LA pressure on PCWP is the development of reflex pulmonary arterial vasospasm, which may further elevate PAP, leading to right-sided heart failure.

18. Pathophysiology Atrial contraction augments the presystolic transmitral valvular gradient by approximately 30% in patients with MS. AF is common in patients with MS, with an increasing prevalence with age. Severe MS with patients age < 30 years – AF in 10% severe MS with patients age > 50 years – AF in 50 % Withdrawal of atrial transport when AF develops reduces CO by approximately 20% , often resulting in symptom onset.

19. Pathophysiology Elevated LA pressure results in PAH , with secondary effects on the pulmonary vasculature and right-sided cardiac chambers. LA enlargement and stasis of blood flow are associated with an increased risk of thrombus formation and systemic embolism. LV is relatively normal or even small, unless there is coexisting MR Primary LV abnormalities being a small, underfilled chamber and paradoxical septal motion caused by RV enlargement and dysfunction.

20. Hemodynamic consequences of Mitral Stenosis

21. Hemodynamic consequences of MS Schematic representation of left ventricular (LV), aortic, and left atrial (LA) pressures, showing normal (NL) relationships and alterations with mild and severe mitral stenosis (MS).

22. Pulmonary Hypertension MS and sinus rhythm- mean LAP elevate, and the LAP curve shows a prominent atrial contraction (a wave), with a gradual pressure decline after mitral valve opening (y descent). In patients with mild to moderate MS without elevated PVR, PAP may be normal or only minimally elevated at rest but rises during exercise. However, in patients with severe MS and those with significantly increased PVR, PAP is elevated when the patient is at rest. Rarely, in patients with extremely elevated PVR, PAP may exceed systemic arterial pressure. Further elevations of LA and pulmonary vascular pressures occur during exercise and tachycardia, particularly with the onset of AF.

23. Pulmonary Hypertension Pulmonary hypertension in patients with MS results from- Passive backward transmission of the elevated LA pressure Pulmonary arteriolar constriction , which presumably is triggered by LA and pulmonary venous hypertension (reactive pulmonary hypertension) Organic obliterative changes in the pulmonary vascular bed , which may be considered a complication of longstanding and severe MS. With moderately elevated PAP (systolic pressure 30 to 60 mm Hg), RV performance is usually maintained Severe PHT results in right-sided HF, with dilation of the RV and its annulus, secondary TR, and sometimes PR.

24. Pulmonary Hypertension Changes in the pulmonary vascular bed may also exert a protective effect ; the ↑precapillary resistance makes the development of symptoms of pulmonary congestion less likely by tending to prevent blood from surging into the pulmonary capillary bed and damming up behind the stenotic mitral valve. This protection, however, occurs at the expense of a reduced cardiac output. In patients with severe MS, pulmonary vein–bronchial vein shunts occur. Their rupture may cause hemoptysis . Patients with severe MS exhibit a reduction in pulmonary compliance, increase in the work of breathing , and redistribution of pulmonary blood flow from base to apex.

25. Left Ventricular Function LV - normal or small, with normal systolic function and normal LVEDP. However, coexisting MR, AoV lesions, systemic hypertension, IHD, and cardiomyopathy all may be responsible for ↑ LVDP.

26. Exercise hemodynamics At any given severity of stenosis, the clinical picture is dictated largely by the levels of cardiac output and PVR with exertion. High transvalvular pressure gradient with exertion ↑ LA and pulmonary capillary pressures, leading to pulmonary congestion during exertion. inadequate rise in CO during exertion, resulting in a smaller rise in pulmonary venous pressure. In these patients, symptoms are caused by a low cardiac output rather than by pulmonary congestion. Critical MS (MVA <1 cm 2 ) , particularly when PVR is elevated, CO usually is depressed at rest and may fail to rise at all during exertion. resting weakness and fatigue secondary to a low CO, with low-output and pulmonary congestion symptoms with exercise.

27. Left Atrial changes Combination of mitral valve disease and atrial inflammation secondary to rheumatic carditis causes- (1) LA dilation , (2 ) fibrosis of the atrial wall, and (3) disorganization of the atrial muscle bundles . These changes lead to disparate conduction velocities and inhomogeneous refractory periods. Premature atrial activation, caused by an automatic focus or reentry , may stimulate the left atrium during the vulnerable period, thereby precipitating AF. AF often is episodic at first but then becomes more persistent. AF causes diffuse atrophy of atrial muscle, further atrial enlargement, and further inhomogeneity of refractoriness and conduction. These changes lead in turn to irreversible AF.

28. Clinical presentation

29. Symptoms & complications Pulmonary Venous Hypertension: Dyspnea, Orthopnea, Paroxysmal Nocturnal Dyspnea Acute Pulmonary Edema Hemoptysis Winter bronchitis

30. Other complications Atrial Fibrilation Systemic Embolism Infective Endocarditis

31. Dyspnea The most common presenting symptoms of MS are dyspnea, fatigue, and decreased exercise tolerance. Caused by a reduced ability to increase CO normally with exercise or elevated pulmonary venous pressures and reduced pulmonary compliance. Dyspnea may be accompanied by cough and wheezing. Vital capacity is reduced, presumably because of the presence of engorged pulmonary vessels and interstitial edema . Patients who have critical obstruction to LA emptying and dyspnea with ordinary activity (NYHA III) generally have orthopnea as well and are at risk for attacks of frank pulmonary edema .

32. Dyspnea The latter may be precipitated by effort, emotional stress, respiratory infection, fever pregnancy, or AF with a rapid ventricular rate or other tachyarrhythmia. Pulmonary edema may be caused by any condition that increases the flow rate across the stenotic mitral valve, either because of an increase in total cardiac output or a reduction in the time available for blood flow across the mitral orifice to occur. In patients with a markedly elevated PVR, RV function often is impaired, and the presentation also may include symptoms and signs of right-sided HF. MS is a slowly progressive disease, and many patients remain seemingly asymptomatic merely by readjusting their lifestyles to a more sedentary level.

33. Hemoptysis Rupture of thin-walled, dilated bronchial veins Sudden rise in LA pressure, or it may be milder, with only blood-stained sputum associated with attacks of paroxysmal nocturnal dyspnea. Pink, frothy sputum characteristic of acute pulmonary edema with rupture of alveolar capillaries Also may be caused by pulmonary infarction, a late complication of MS associated with HF.

34. Chest pain Not a typical symptom of MS, Indistinguishable from that of angina pectoris Severe RV hypertension secondary to the pulmonary vascular disease or by concomitant coronary atherosclerosis. Secondary to coronary obstruction caused by coronary embolization.

35. Palpitations and Embolic Events Often are initially diagnosed when they present with AF or an embolic event.

36. Other Symptoms Compression of Lt RLN by a greatly dilated LA, enlarged tracheobronchial lymph nodes, and dilated pulmonary artery may cause hoarseness ( Ortner syndrome ). Repeated hemoptysis is common in patients with pulmonary hemosiderosis Systemic venous hypertension, hepatomegaly, edema , ascites, and hydrothorax are all signs of severe MS with elevated PVR and right-sided HF.

37. Physical examination Irregular puls e caused by AF and signs of left- and right-sided HF Classic diastolic murmur & loud S 1 often are difficult to appreciate Severe chronic MS, a low CO, and systemic vasoconstriction may exhibit the so-called mitral facies , characterized by pinkish purple patches on the cheeks. Arterial pulse is usually normal, but in patients with a reduced stroke volume, the pulse may be low in volume JVP usually exhibits a prominent a wave in patients with sinus rhythm and elevated PVR. With AF, the x descent of the JVP disappears, and there is only one crest, a prominent v or c-v wave, per cardiac cycle.

38. Physical examination Palpation of the cardiac apex usually reveals an inconspicuous left ventricle; the presence of a palpable presystolic expansion wave or an early diastolic rapid filling wave speaks strongly against serious MS. Readily palpable, tapping S 1 suggests that the anterior mitral valve leaflet is pliable. RV lift is felt in the left parasternal region in patients with pulmonary hypertension. A loud P 2 may be palpable in the second left intercostal space in patients with MS and pulmonary hypertens ion.

39. Auscultation Opening snap : sudden tensing of the valve leaflets after the valve cusps have completed their opening excursion. movement of the mitral dome into the left ventricle suddenly stops most readily audible at the apex The mitral OS follows A2 by 0.04 to 0.12 second; this interval varies inversely with the LA pressure A short A2 -OS interval is a reliable indicator of severe MS

40. Auscultation Diastolic Murmur : low-pitched, rumbling murmur of MS is best heard at the ape pitch and duration of the murmur are a guide to the severity of mitral valve narrowing intensity of the diastolic murmur is not closely related to the severity of stenosis murmur usually commences immediately after the OS. severe MS the murmur persists until end-diastole, with presystolic accentuation while sinus rhythm is maintained

41. Auscultation Other Auscultatory findings : pansystolic murmur of TR and a S3 originating from the RV may be audible in the 4 th ICS in the left parasternal region in patients with severe MS. These signs, which are secondary to pulmonary hypertension, may be confused with the findings of MR. inspiratory augmentation of the murmur and of the S3 and the prominent v wave in the jugular venous pulse aid in establishing that the murmur originates from the tricuspid valve. A high- pitched decrescendo diastolic murmur along the left sternal border in patients with MS and pulmonary hypertension may be audible pulmonic regurgitation ( Graham Steell murmur ) but more often is caused by concominant AR

42. Diagnosis & Evaluation Differential Diagnosis: MS is rare dx in developed countries & most apical diastolic murmur have other causes. Older patients- mitral annular calcification VSD LA myxoma HCM

43. Echocardiography Rheumatic mitral stenosis. Parasternal long-axis view (diastolic frame) of a rheumatic mitral valve. Diastolic doming of the anterior mitral leaflet ( arrow ) is present, as well as a fixed posterior leaflet. Inset, Doming and fish-mouth appearance of the valve, as seen by 3D TTE from the LV aspect. LA, Left atrium. Most accurate approach for Diagnosis & evaluation of Mitral Stenosis. Recommended for all patients with MS at initial presentation, for reevaluation of changing symptoms or signs. EAE/ASE Recommendation. (European Association of Echocardiography/American Society of Echocardiography)

44. ECHO EVALUATION OF Mitral Stenosis A. Appearance of the MV & the mobility of its leaflets

45. ECHO EVALUATION OF Mitral Stenosis B. Determine the valve area 1. Planimetry 2. Pressure Half Time MVA = 220/PHT 3. Continuity Equation 4. PISA EAE/ASE Recommendation. (European Association of Echocardiography/American Society of Echocardiography)

46. ECHO EVALUATION OF Mitral Stenosis B. Determine the valve area 1. Planimetry 2. Pressure Half Time MVA = 220/PHT 3. Continuity Equation 4. PISA

47. ECHO EVALUATION OF Mitral Stenosis PHT= 211 MVA= 1.04 cm 2 PHT= 159 MVA= 1.38 cm 2

48. ECHO EVALUATION OF MS C. Determine the Mean valve gradient

49. Recommendation for Classification of MS severity Mild Moderate Severe Specific findings Valve area (cm) 2 >1.5 1.0-1.5 <1.0 Supportive findings Mean gradient (mmHg)* <5 5-10 >10 Pulmonary artery pressure(mmHg) <30 30-50 >50 * At heart rate between 60 and 80 bpm and in sinus rhythm European Association of Echocardiography/American Society of Echocardiography

50. Assessment of MV according to the Wilkins Score GRADE LEAFLET MOBILITY VALVE THICKENING CALCIFICATION SUBVALVULAR THICKENING 1 Highly mobile valve with only leaflet tips restricted Leaflets near normal in thickness (4-5 mm) Single area of increased echo brightness Minimal thickening just below the mitral leaflets 2 Leaflet mid and base portions have normal mobility Mid leaflets normal, considerable thickening of margins (5-8 mm) Scattered area of brightness confined to leaflet margins Thickening of chordal structures extending to one-third of the chordal length 3 Valve continues to move forward in diastole, mainly from base Thickening extending through the entire leaflet (5-8 mm) Brightness extending into mid-portions of the leaflets Thickening of chordal structures extending to one-third of the chordal length 4 No or minimal forward movement of the leaflet in diastole Considerable thickening of all leaflet tissue (> 8-10 mm) Extensive brightness throughout much of the leaflet tissue Extensive thickening and shortening of all chordal structures extending down to the papillary muscles Total score is the sum of the four items & ranges between 4 and 16

51. Recommendations for data recording and measurement in routine use for MS quantitation

52. Measures of MS severity obtained by Doppler-echocardiography Level of recommendations: (1) appropriate in all patients (yellow); (2) reasonable when additional information is needed in selected patients (green); and (3) not recommended (blue).

53. Exercise Testing with Doppler Echo Useful for many patients with MS to ascertain the level of physical conditioning and elicit covert cardiac symptoms. Recommended when a discrepancy exists between resting echocardiographic findings and severity of clinical symptoms Useful parameter on exercise testing includes- Exercise duration, BP & HR response, change in mitral peak and (especially) mean gradient, and increase in pulmonary pressures with exercise, compared with the expected normal changes. An exercise pulmonary systolic pressure greater than 60 mm Hg can be a key data point in the management of these patients.

54. Electrocardiography LA enlargement- broad, bifid P wave in lead II (P mitrale ) and enlarges the terminal negative portion of the P wave in V1. Lead II: Bifid P wave with > 40 ms between the two peaks, Total P wave duration > 110 ms  Lead V1: Biphasic P wave with terminal negative portion > 40 ms duration, Biphasic P wave with terminal negative portion > 1mm deep Right Ventricular Hypertrophy: Right axis deviation of +90 degrees or more, RV1 = 7 mm or more, RV1 + SV5 or SV6 = 10 mm or more, Right Axis Deviation: Pulmonary hypertension Atrial Fibrillation:  irregularly irregular rhythm with absent P waves

55. Electrocardiography

56. Roentgenographic Finding Left atrial enlargement (straightening of Lt heart border, double density sign) Redistribution of venous and arterial flow to upper lobes (correlate with degree of MS) Calcification of mitral valve Kerley B lines Enlarged pulmonary artery Enlarged right ventricle

57. Roentgenographic Finding

58. Cardiac CT & MRI Cardiac CT - MVA estimates in MS by planimetry after multiplanar reconstruction- larger than those obtained by echocardiography or catheterization CMR estimate the stenotic valve area either by planimetry or continuity close to ECHO value than CT These techniques can also provide information on LA cavity and appendage thrombi.

59. Cardiac catheterization Routine diagnostic cardiac catheterization is not recommended for the evaluation of MS. Measurement of LA and LV pressures shows the expected hemodynamics Measurement of the mean transmitral pressure gradient and, in conjunction with measurement of transmitral volume flow rate, calculation of the valve area using the Gorlin formula Occasionally, diagnostic cardiac catheterization is necessary when echocardiography is nondiagnostic or results are discrepant with clinical findings. More often these measurements now are recorded for monitoring before, during, and after percutaneous BMV.

60. Disease course In temperate zones (United States and Western Europe) ARF to MS (15 to 20 years before symptoms of MS develop). 5 to 10 years for most patients to progress from mild disability (i.e., early NYHA Class II) to severe disability (NYHA Class III or IV) The progression is much more rapid in patients in tropical and subtropical areas, in Polynesians, and in Native Alaskans. In India , critical MS may be present in children as young as 6 to 12 years of age. In North America and Western Europe, however, symptoms develop more slowly, with onset usually between ages 45 and 65 years.

61. Disease course Interval between active rheumatic fever and clinical symptoms of valve disease in 177 patients with mitral stenosis ( yellvow bars ) and 121 with aortic stenosis ( blue bars ).

62. Disease course Hemodynamic Progression: The initial MVA was 1.7 ±0.6 cm2, and the overall rate of progression was a decrease in valve area of 0.09 cm2/yr . Approximately one third of patients showed rapid progression, defined as a decrease in MVA of more than 0.1 cm2/yr. Rate of hemodynamic progression of rheumatic MS in underdeveloped countries, where the age at symptom onset is much younger.

63. Disease course Clinical Outcomes: Symptomatic patients with MS have a poor outlook, with 5-year survival rates of 62% for MS patients in NYHA Class III but only 15% in Class IV 5-year survival rate of only 44% in patients with symptomatic MS who refused valvotomy Overall clinical outcomes are greatly improved in patients who undergo surgical or percutaneous relief Complications of the disease process (AF, systemic embolism, pulmonary hypertension) and side effects of therapy (e.g., prosthetic valves, anticoagulation).

64. Disease course Natural history of the respective valvular lesion in 159 patients with isolated mitral stenosis (MS) ( solid blue line ) or mitral regurgitation (MR) ( solid purple line ) who did not have surgery, even though operation was indicated, compared with patients treated with valve replacement for MS ( dashed blue line ) or MR ( dashed purple line ). The expected survival rate in the absence of mitral valve disease is indicated by the upper curve ( dashed black line )

65. Complications AF : most common complication The prevalence of AF in patients with MS is related to the severity of valve obstruction and patient age 17%- age 21-30 years 45%- age 31-40 years 60%- age 41-50 years 80%- older than 51 years AF may precipitate or worsen symptoms. AF predisposes affected patients to LA thrombus formation and systemic embolic events.

66. Complications Systemic Embolism: c aused by LA thrombus formation Most often occurs in patients with AF, 20% of patients with MS and a systemic embolic event are in sinus rhythm When embolization occurs in patients in sinus rhythm, the possibility of transient AF or underlying infective endocarditis should be considered. Loss of atrial appendage contractile function, despite electrical evidence of sinus rhythm, leads to blood flow stasis and thrombus formation Risk of embolism correlates directly with patient age and LA size Inversely with the CO Half of all clinically apparent emboli are found in the cerebral vessels.

67. Complications Coronary embolism may lead to myocardial infarction (MI) and angina pectoris, and renal emboli may be responsible for the development of systemic hypertension. Emboli are recurrent and multiple in approximately 25% of patients who develop this complication.

68. Complications Infective Endocarditis: MS is a predisposing factor for endocarditis in less than 1% of cases in clinical series of bacterial endocarditis The estimated risk of endocarditis in patients with MS is 0.17 per 1000 patient-years, which is much lower than the risk in patients with MR or aortic valve disease.

69. Thank you