MULTIVALVULAR HEART DISEASE RNTagore.pptx

multivalvular heart disease in india and clinical evaluation - Mitral stenosis, mitral regurgitation, aortic stenosis , aortic regurgitation

1. Multivalvular heart disease-clinical evaluation Dr. saurabh dhumale Dnb Fellow

2. DEFINITIONS MULTIVALVULAR Heart Disease: the combination of stenotic or regurgitant lesions occurring on ≥2 cardiac valves. MIXED VHD: the combination of stenotic and regurgitant lesions on the same valve.

3. Introduction & epidemiology

4. Multivalvular disease: Multiple valves involved in more than a third of all cases ( 36.8% ) Overall the combination of MS and MR-the commonest followed by the combination of MS and AR. The least common lesion combination was that of MS and AS. Multivalvular disease was seen more often in females in a ratio of 1.2:1. 

5. INCIDENCE PATTERN OF MULTIVALVULAR LESIONS

6. INCIDENCE PATTERN IN RHD: Lesion combination Incidence MS+ MR 46.6% MS+AR 26.5% MR+AR 23.3% MS+AS 2.4% MR+AS 0.9% AS+AR 0.3%

7. ETIOLOGY

8. KEY PRINCIPLES

9. MITRAL STENOSIS + MITRAL REGURGITATION

10. MITRAL STENOSIS + MITRAL REGURGITATION: Etiology is mostly rheumatic.[commissural fusion] Mitral annular calcification leads to predominantly MR but can also produce some degree of stenosis. Congenital lesions , left atrial tumours and infective endocarditis must be considered in differential diagnosis. MR increases the flow rate across the mitral valve. Which frequently results in overestimation of severity of stenosis. left atrial pressure may be markedly increased in patients with mixed mitral VHD, resulting in severe exercise intolerance through an increase in pulmonary venous pressure

11. MS doesn’t significantly effect the hemodynamics and clinical findings of MR however MR can enhance the findings of the MS. When the MVO is smaller than 1.5sq cm stenosis is predominant , when MVO is greater than 2.0sq cm MR is dominant{ref: alperts textbook} ITS VITAL TO DIFFERENTIATE if the early diastolic sound is an opening snap or an LVS3. Presence of a third heart sound practically rules out any significant MS. Usually one lesion dominates severe MS and severe MR can’t coexist.

12. SEVERE MR- Is there ms?

13. Ms or mr, which is severe?

14. OS OR S3?

15. MITRAL STENOSIS + AORTIC REGURGITATION

16. MITRAL STENOSIS + AORTIC REGURGITATION: In Indian study incidence of MS+AR was relatively common compared to western scenario. 10% od MS pts had significant AR. In presence of severe MS the widened pulse pressure and peripheral signs of AR may be absent. Because the CO falls with progressive degrees of MS, transaortic valve flows will decline, masking the potential severity o the aortic valve lesion In isolated MS, le ventricular (LV) preload and diastolic pressure are reduced as a function of the severity of inflow obstruction. With concomitant AR , however, LV filling is enhanced and diastolic pressure may rise depending on the compliance characteristics o the chamber.

17. In a patient with AR , associated MS is suggested by presence of AF, loud S1, presence of opening snap, diastolic thrill over the apex, presence of pre-systolic accentuation for the mid diastolic murmur and evidence of pulmonary arterial hypertension Opening snap may be soft or even inaudible in MS patients who have associated significant AR. This is because of the AR jet impinging on the ventricular side of anterior mitral leaflet restricting the excursion and opening. In the presence of MS, the typical signs of AR , including increased pulse pressure, may be absent.

18. Mdm vs austin flint murmur

19. MITRAL REGURGITATION + AORTIC REGURGITATION

20. MR+ AR MR associated with AR may be primary or secondary to LV remodeling as a consequence of AR. Both AR and MR increase left ventricular (LV) preload, whereas only AR has a significant effect on afterload , as a result of the impact of the increased total stroke volume ejected on systemic vascular resistance, and of the resulting systolic hypertension . Therefore, severe LV dilatation may occur when AR and MR are present together . combination of volume and pressure load further increases wall thickness . Thus, the resulting LV hypertrophy will usually be eccentric, with a wall thickness-to-cavity ratio typically < 0.45, and increased sphericity .

21. Presenting symptoms are not likely to aid in the recognition of this combination. Because of the regurgitation of the blood in the systole forward stroke volume into the aorta is reduced there by producing the systolic decapitation of the BP. mitral valve competency normally protects the left atrium and the pulmonary veins from the deleterious effects of the increased LV pressure related to AR. However, the coexistence of AR and MR exacerbates the impact of LV volume and pressure overload on the left atrium, pulmonary circulation, and right chambers. Hence, this combination is poorly tolerated, and postoperative LV dysfunction is more likely to occur than in isolated valve regurgitation. MR is an independent risk factor for reduced survival in patients with severe AR , with mortality increasing with each grade of MR severity.

22. Presence of S4 indicates a dominant AR or a relatively recent onset MR. Evidence of A.fib or PH may indicate a significant MR

23. AORTIC STENOSIS + AORTIC REGURGITATION

24. AS+ AR Approximately 2/3 rd of the patients with calcific aortic stenosis will have some degree of aortic regurgitation. Likely causes of predominant aortic regurgitation with minor degrees of stenosis are rheumatic and congenital bicuspid aortic valve. Mixed aortic VHD is characterised by a combination of pressure and volume load that imposes a greater stress on the LV than that induced by isolated AS or AR. The stenotic component imposes a pressure overload that aggravates LV hypertrophy, resulting in decreased LV compliance and thus in a disproportionate increase in LV diastolic pressure per unit of volume increase during diastole.

25. the increase in stroke volume resulting from the regurgitant flow may further contribute to severe pressure overload even when the aortic valve area is >1.0 cm2 The pulse volume will depend on the significance of AS, but generally high volume even with severe AS if AR is atleast moderate or severe. The systolic decapitation effect of AS will make the pulse pressure narrow. Cardiomegaly indicates significant AR.

26. In severe AR- is there as?

27. As or ar , which is severe?

28. MITRAL REGURGITATION + AORTIC STENOSIS: Very undesirable set of hemodynamic consequences. Hemodynamic abnormalities of both the lesions are in systole. secondary MR may develop as a result of leaflet tethering and mitral annular dilatation. Because of the high prevalence of concomitant coronary artery disease, ischemic MR is also not uncommon in the elderly population. Elderly patients may also present primary MR as a result of mitral annular calcifications or pro-lapse

29. As a direct consequence of the increased afterload because of AS, the transmitral systolic pressure gradient increases, therefore, leading, for any given mitral effec t ive regurgitant orifice, to higher regurgitant volume. the presence of significant MR may decrease the forward flow across the aortic valve. This MR-induced low-flow state may reduce the transaortic pressure gradient and yield to an underestimation of AS Low cardiac output combined with increased pulmonary venous pressure.

30. MS+AS This infrequent combination is usually poorly tolerated, and the reduction in cardiac output is usually greater than what is seen in isolated AS or MS. Hence, both aortic and mitral pressure gradients may be lower than expected, which can lead to underestimation of the severity of both AS and MS. Similar to MR, severe MS may lead to low LV outflow and, therefore, result in paradoxical low-flow, low-gradient AS.

31. In presence of significant aortic stenosis the symptoms of MS can get exaggerated with attenuation of the auscultatory findings. The elevated LV end diastolic pressures in aortic stenosis will lessen the LV-LA gradient in late diastole thus shortening the length of mitral diastolic murmur. The diastolic murmur may all together absent making it a silent MS.

32. Patients will have low volume pulse. Sytolic blood pressure will be normal or low. Presence of atrial fibrillation in aortic stenosis will give a clue as to the presence of mitral valve disease. Severe aortic stenosis will soften S1. A2 intensity is also reduced.

33. Ts in combined valvular disease Ts very rarely presents as an isolated lesion. In most cases its secondary to rheumatic valvulitis and coexists with mitral and aortic valve disease. Ts of varying degrees was has been found in 10-23% of autopsies of patients with rhd . Ts is therefore a lesion that commonly escapes detection on clinical examination. Paucity of pulmonary symptoms in he form of PND, pulmonary edema , hemoptysis in a patient of severe rheumatic ms, should prompt a thorough evaluation of ts . Clinically, giant ’A’ waves in jvp , slipt s1 and an absence of signs of rvh are classical features.

34. Thank you