AORTIC STENOSIS + AORTIC REGURGITATION - PowerPoint Presentation

1. AORTIC STENOSIS + AORTIC REGURGITATION Dr Monet Philipose Jr3 Medicine

2. Mixed aortic valve disease (MAVD) was defined as combined moderate regurgitation and moderate stenosis, or a combination of severe aortic stenosis or severe aortic regurgitation, with the second lesion being moderate.

3. EPIDEMIOLOGYMixed aortic stenosis (AS) and aortic regurgitation (AR) is the most frequent concomitant valve disease worldwide and represents a heterogeneous population ranging from mild AS with severe AR to mild AR with severe AS. About 6.8% of patients with at least moderate AS will also have moderate or greater AR, and 17.9% of patients with at least moderate AR will suffer from moderate or greater AS.

4. ETIOLOGYCongenital (Most Commonly A Bicuspid Aortic Valve)Degenerative Rheumatic Disease Prior Balloon Valvuloplasty For AS Prior Mediastinal Irradiation.CardiomyopathyAS complicated by IEParavalvular leakage in post TAVR

5. PATHOPHYSIOLOGY

6. AORTIC STENOSISAORTIC REGURGITATIONIncreased Aortic outflow velocityIncreased Aortic pressure gradientIncreased afterloadLVHDecreased LV ComplianceLVEDP Rises,wall Stress IncreasesClinical Tolerance DecreasesIncreased Aortic Stroke VolumeLV Volume Overload

7. Mixed aortic VHD is characterized by a combination of pressure and volume load that imposes a greater stress on the LV than that induced by isolated AS or ARPure AR is characterized by LV enlargement with increased compliance, enabling a large volume overload to be accommodated with no significant increase in LV end-diastolic pressure. In the presence of AR, stroke volume needs to be increased in order to maintain forward cardiac output.

8. In the presence of concomitant AS with consequent pressure overload, LV hypertrophy, and reduced LV compliance, the AR-induced volume overload leads to LV filling over a steeper portion of the pressure-volume curve, and thereby increases LV diastolic pressure and wall stress . However, the increase in stroke volume resulting from the aortic regurgitant volume may further contribute to increase the transvalvular pressure gradient and thus the severity of LV pressure overload associated with AS LV concentric hypertrophy secondary to AS may prevent the development of LV dilatation in AR.

9. Patients with MAVD may therefore be at higher risk to develop myocardial fibrosis and dysfunction compared with patients with isolated AR, and these patients may progress to heart failure even though neither the AS nor the AR was severe. Reduced coronary flow and increased LV filling pressure also contribute to the development of exercise intolerance. Furthermore, the chronically elevated LV filling pressures may induce secondary pulmonary hypertension and left atrial dilatation, resulting in right ventricular dysfunction and atrial fibrillation.

10. Patients with MAVD should be monitored at the same frequency as asymptomatic patients with severe AS. In patients with MAVD, progression mainly results from the progression of AS.AR severity does not seem to progress markedly over time and may even, albeit infrequently, regress and evolve into predominant AS.

11. CLINICAL DETERMINATION OF THE DOMINANT LESION SYMPTOMSExertional Dyspnea,Angina and Syncope are more in favour of AS.Palpitations in AR>AS

12. SIGNSAS > ARAR > ASPULSELow volume ; Pulsus bisferiensHigh volume collapsing pulseBPLow systolic BP,low pulse pressureHigh systolic BP and low diastolic BP,wide pulse pressurePeripheral signs of AR+_+++ApexHeaving,may be in normal positionHyperdynamic,downwards and outwardsThrillAlways systolic,palpated on aortic area and carotids systolic thrill rarely present, due to functional AS and very rarely diastolic thrill along lsb.S3absentMay be presentS4May be presentabsentEjection clickPresent in mild to moderate ASRare.sometimes present in severe ARDiastolic murmurVery short duration of AR murmurClassical AR murmurSystolic murmurClassical AS murmurFunctional midsystolic ejection murmur may present

13. ASARECGLVHLAHHeart blocksLVHConduction defects

14. ASAR XRAY CHESTMay be normal sized due to concentric LVHPost stenotic dilatation of ascending aortaCalcification of aortic valveCardiomegaly(cor bovinum)Aortic root dilatation and prominent aortic knuckle

15. DOPPLER ECHOCARDIOGRAPHYThe aortic valve area reflects the severity of AS, whereas the effective regurgitant orifice area or regurgitant volume reflects the severity of AR .However, the peak aortic jet velocity and mean gradient increase with AS but also with AR because of increase in transvalvular flow. Peak aortic jet velocity and Doppler mean gradient reflect severity of both AS and AR. Hence, a symptomatic patient with moderate AS and moderate AR having a peak jet velocity ≥4 m/s and a mean gradient ≥40 mm Hg should be considered severe.

16. CARDIAC CATHETERIZATIONCardiac catheterization is currently recommended in situations where noninvasive evaluation is inconclusive or discordant with clinical findings and remains commonly performed in patients with multiple VHDSTRESS ECHOCARDIOGRAPHYLow-dose dobutamine stress echocardiography may be helpful to distinguish true severe AS from pseudosevere AS and to assess LV flow reserve, when the pressure gradient is low and LV ejection fraction is reducedMULTIDETECTOR COMPUTED TOMOGRAPHYMultidetector computed tomography is used when there is evidence of low-flow, low-gradient AS and preserved LV ejection fraction. High calcium scores are consistent with increased severe AS.

17. poorer prognosis IN mixed aortic valve disease (MAVD).Increased aortic flow rate Peak aortic velocity ≥4 m/s Peak aortic valve pressure gradient >45 mm Hg LV remodeling Relative wall thickness LV longitudinal dysfunction

18. DIFFERENTIAL DIAGNOSISPDA- Water hammer pulse, best audible in left infraclavicular area and left 2nd ICS .Systolo- diastolic thrill present.Rupture of sinus of Valsalva- chest pain with continuous murmur along left sternal border.Coronary AV fistula- Along left sternal edge,superficial ,harshPulmonary AV fistula- Along left 2nd ICS.Aortopulmonary window- Along left 3rd ICS.VSD with AR , MS with MR.

19. MANAGEMENT OF MAVD MAVD may present asThe combination of severe stenosis and regurgitationThe combination of severe stenosis and non severe regurgitation The combination of severe regurgitation and non severe stenosisThe combination of moderate stenosis and moderate regurgitation If one severe lesion is associated with ≥1 non severe lesions , the management of the most severely diseased valve is defined by current guidelines.

20. Mild AR Moderate AR Severe ARMild ASMild/moderate MAVD No indication for AV InterventionModerate MAVD No indication for AV InterventionSevere MAVD (class I) if: Symptoms, LVEF ≤50%, and/or undergoing other cardiac surgery. (Class IIa) if: Asymptomatic, LVEF >50% and LVESD ≥50mm.Moderate ASModerate MAVD No indication for AV Intervention Likely severe MAVD(Class I) if High gradient,Symptoms, LVEF ≤50%, and/or undergoing other cardiac surgery.(class IIa) if: Low gradient, Symptoms, LVEF ≤50%, and/or LVESD ≥50mm.Severe MAVD (class I) if: Symptoms, LVEF ≤50%, and/or undergoing other cardiac surgery. (class IIa) if: Asymptomatic, LVEF >50%and LVESD ≥50mm.

21. Mild ARModerate ARSevere ARSevere ASSevere MAVDAV intervention (class I) if:► High gradient.► Symptoms, LVEF <50%and/or undergoing othercardiac surgery. (class IIa) if:► Low flow, low gradient.► Symptoms and/or LVEF <50%.► Confirmation of severe AS by MDCT.AV intervention (class IIa) if:► High gradient.► Asymptomatic and LVEF ≥50%.► Low surgical risk.Severe MAVDAV intervention (class I) if:► High gradient.► Symptoms, LVEF <50%and/or undergoing othercardiac surgery.(class IIa) if:► Low flow, low gradient.► Symptoms and/or LVEF <50%.► High gradient.► Asymptomatic and LVEF ≥50%.► Low surgical risk.Severe MAVDAV intervention (class I) if:► Symptoms, LVEF ≤50%and/or undergoing othercardiac surgery.(class IIa) if:► Asymptomatic, LVEF >50% and LVESD ≥50mm.► Low surgical risk.

22. Surgery: The decision is made on an individual basis, taking into consideration the symptoms, transvalvular gradient, aortic valve area, and left ventricular size and function.TAVR and SAVRPharmacotherapy: Depends on the dominant lesion. vasodilators used for AR may increase the transvalvular gradient of AS; agents that slow the heart rate (beta-blockers) may increase regurgitant volumes in AR.Treatment for complications like CCF and Prevention of Infective endocarditis