Cardiac catheterization in Aortic stenosis

Describes cardiac catheterization in aortic stenosis

1. Cardiac Catheterization in Aortic Stenosis Dr Anish P G

2. Aortic Stenosis Etiology based on location Supravalvular Subvalvular Valvular Congenital Bicuspid Rheumatic Senile degenerative

3. In subaortic stenosis Gradient is between the main portion of the left ventricle and its outflow tract, although in tunnel subaortic stenosis there may be no discrete subvalvular chamber. In supravalvular stenosis G radient is just beyond the aortic valve, between the initial segment of the proximal aorta (just beyond the aortic valve) and the main segment of the ascending aorta. To facilitate surgical intervention, it is important to identify the site and nature of the obstruction in each instance. This is determined by both hemodynamics and angiography The left ventricle becomes progressively hypertrophied in aortic stenosis. The cardiac output is well maintained until the left ventricle dilates and fails; it then becomes progressively reduced .

4. Pathophysiology LV outflow obstruction i ncreased LV systolic pressure increased LV ejection time ( LVET) increased LV diastolic pressure decreased aortic ( Ao ) pressure. Increased LV systolic pressure with LV volume overload increases LV mass  LV dysfunction and failure. Increased LV systolic pressure, LV mass, and LVET increase myocardial oxygen (O 2 ) consumption. Increased LVET 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 O 2 supply. Increased myocardial O 2 consumption and decreased myocardial O 2 supply myocardial ischemia, which further deteriorates LV function

5. The normal adult aortic valve area – between 3.0 and 4.0 cm 2 . When aortic valve disease is present, the aortic velocity depends on the size of the valve orifice and transaortic volume flow. A normal cardiac output can be maintained without a significant increase in aortic velocity until valve area is reduced to approximately 25% to 30% of normal .

6. In adults outflow obstruction usually develops and increases gradually over a prolonged period In infants and children with congenital AS the valve orifice shows little change as the child grows, thereby intensifying the relative obstruction gradually

7. With decreases in valve area below 1 cm 2 , very small changes in orifice area lead to marked changes in transvalvular pressure gradient and hemodynamic load. LV systolic pressure increases in proportion to the severity of valve obstruction, with the potential energy in the difference between LV and aortic pressure converted into kinetic energy as blood is ejected at high velocity across the valve

8. Bernoulli equation The velocity (V) in the stenotic orifice correlates with the drop in pressure (P) from the LV to the aorta P = 4V 2 Relationship between instantaneous velocity and pressure measurements at any point in systole . The mean systolic pressure gradient by averaging pressure gradients over the systolic ejection period

9. The cross-sectional area of the open aortic valve in systole is a robust measure of stenosis severity. For a given aortic valve area, the aortic velocity and pressure gradient will vary with transaortic volume flow. To account for transaortic volume flow rate, aortic valve area (AVA) can be calculated based on the continuity principle

10. Continuity principle T he stroke volume (SV) in the aortic valve (AV) orifice and the stroke volume just proximal to the valve in the LV outflow tract (LVOT) are equal: SV AV = SV LVOT Stroke volume SV = CSA x VTI Thus the Continuity equation can be solved for aortic valve area: AVA x VTI AV = CSA LVOT x VTI LVOT AVA = (CSA LVOT x VTI LVOT )/VTI AV

11. The standard clinical hemodynamic parameters of aortic stenosis Transaortic velocity Mean transaortic pressure gradient Aortic valve area Others LV stroke work loss R ecovered pressure gradient E nergy loss index V alvuloarterial impedance

12. Aortic stenosis  increased pressure load on the LV  compensatory LV hypertrophy  maintains normal wall stress Wall stress is proportional to LV pressure (P) and radius (r) and inversely related to wall thickness ( Th ): σ = ( P x r )/2 Th Concentric hypertrophy additional sarcomeres aligned in parallel with a corresponding increase in cardiac myocyte size. increase in interstitial tissue with fibrosis, which contributes to the long-term diastolic dysfunction

13. LV hypertrophy diastolic dysfunction and increased dependence on the atrial contribution to LV filling atrial fibrillation may precipitate symptoms of heart failure due to a combination of increased LV filling pressures and decreased forward cardiac output. L V ejection fraction and wall stress remain normal due to LV compensatory mechanisms to increase wall thickness

14. T he increase in afterload may eventually exceed the compensatory LV response afterload mismatch I mpaired LV systolic function

15. Afterload mismatch P reservation of myocardial contractile function, but impaired systolic function due to high afterload LV systolic function should improve if afterload is relieved with replacement of the stenotic valve average improvement 10 ejection fraction units

16. Decreased contractility ↓ supply to endocardium ↓ coronary flow reserve cytoskeletal abnormalities diastolic dysfunction pathological LVH

17. Subendocardial ischemia Decreased capillary density Impaired coronary flow reserve Perivascular fibrosis- ECM elaboration Large diameter myocytes impairing O2 diffusion High LVEDP Supply demand mismatch Epicardial CAD

18. Cardiac catheterization When noninvasive data are nondiagnostic If there is a discrepancy between clinical and echocardiographic evaluation

19. Correlation between clinical severity of AS and aortic valve area AVA Clinical severity >1 Mild (Symptoms rare in the absence of other heart disease ) 0.7-1 Moderate (Symptoms with unusual stress, AF,Exercise etc ) 0.5-0.7 Moderately severe(Symptoms with activities of daily living ) <0.5 Severe(Symptoms at rest or minimal exertion, biventricular failure)

20. In the hemodynamic assessment of valvular aortic stenosis, primary importance should be placed on obtaining simultaneous measurement of pressure and flow across the aortic valve, whichpermits calculation of the aortic orifice or valve area (AVA). In the typical adult with symptomatic aortic stenosis, AVA is reduced to < / = 0.7 cm 2 . Occasionally , a valve of 0.8 to 0.9 cm 2 results in a symptomatic presentation, especially when there is concomitant coronary artery disease or hypertension or when the absolute value of cardiac output is high (e.g., a large patient, anemia , fever, or thyrotoxicosis). When AVA is </=0.5 cm 2 , severe aortic stenosis is present and cardiac reserve is minimal or absent

21. Catheterization Protocol Right heart catheterization for measurement of right heart pressures and cardiac output. Left heart catheterization for measurement of pressure gradient across aortic valve and LVEDP and assessment of the presence or absence of a transmitral gradient (concomitant mitral stenosis ) Approach Brachial – Sones catheter Brachial /Radial – MP catheter Femoral – Pigtail Left ventriculography the stenotic orifice of the valve during systole as outlined by a jet of contrast material ejected into the aorta. The valve cusps may appear irregular, their mobility may be reduced, and often the number of cusps can be identified In congenital aortic stenosis, the valve may form a funnel during systole. The ascending aorta is dilated ( poststenotic dilatation), but the subvalvular area is widely patent. A subaortic membrane, with a small central orifice, or a subvalvular muscular ring may be seen. The characteristic changes of idiopathic hypertrophic subaortic stenosis may be observed. In supravalvular stenosis, the narrowing of the proximal aorta can be seen

22. Aortography In pure aortic stenosis, aortography often demonstrates a negative jet of radiolucent blood exiting focally from the left ventricle. In the patient with aortic stenosis who also has some aortic regurgitation, aortography permits a rough quantitation of the severity of the regurgitation. If interventional catheter techniques (e.g., balloon aortic valvuloplasty ) are under consideration, determination of the extent of associated aortic regurgitation may become important in clinical decision making .

23. Prussian Helmet sign In congenital aortic stenosis, there may be upward doming of the aortic valve leaflets, which together with the central negative jet gives the so-called Prussian helmet sign.

24. Assessment of stenosis severity Measurement of the pressure gradient Analysis of the pressure waveforms Measurement of cardiac output Calculation of the valve area A ngiocardiography of the chamber upstream to the site of stenosis

25. Pressure gradient D escribed by three invasive measurements: The mean gradient The peak-to-peak gradient T he maximum gradient. The mean and maximum gradients are used to evaluate stenosis severity The rate of rise of LV pressure ( dP / dt ) during isovolumic contraction provides a relatively loadindependent measure of LV systolic function

26. Pressure-Volume Loops by graphing instantaneous pressure (on the vertical axis) against volume (on the horizontal axis). LV stroke volume the distance on the horizontal axis between end-diastole and end-systole LV stroke work (the integral of pressure times volume over the cardiac cycle ) the area enclosed by the pressure-volume loop . Elastance or Emax the slope of the end-systolic pressure-volume relationship under different loading conditions provides a load-independent measure of LV systolic function

27. Central aortic and femoral waveforms

28. Normal Values at Cardiac Catheterization (Supine, Resting Adults)

29. Catheters & Techniques Wires and catheters 0.038-inch standard straight wire pigtail catheter, Judkins right, or Amplatz left Feldman catheter & Rosen wire – specifically designed to cross aortic valve Double lumen pigtail S upravalvular angiography When staright wire does not cross useful to localize the position and orientation of the valve orifice The position and movement of calcium within the valve leaflets may also suggest the location of the valve orifice. H ydrophilic straight wires wire coating may increase the risk for valve leaflet perforation.

30. Probing the aortic valve orifice with the wire should be done in less than 2-minute increments, with the wire removed and the catheter carefully flushed prior to reinsertion and another attempt to cross the valve Risk of Neurologic insult 3 % - clinically significant neurologic event 22% - magnetic resonance imaging evidence of an acute cerebral embolic event. Transseptal puncture S evere aortic valve calcification Critical AS C oexisting mitral stenosis

31. P ressure gradient ( 1) T he mean gradient (2 ) The peak-to-peak gradient (3 ) T he maximum gradient

32. Five invasive methods can be used to measure pressure gradients between the left ventricle and the aorta The single-catheter “pullback technique ” Simultaneous measurement of the proximal aortic and the LV pressures using two transducers yields the most accurate data .

33. 1 st method S ingle arterial puncture 6 French sheath within the femoral artery Advancement of a 6 French double-lumen catheter (Langston dual-lumen catheter, Vascular Solutions, Minneapolis, MN) into the left ventricle S imultaneous measurement of the aortic and LV pressures Following measurement of the gradient, a left ventriculogram is done

34. 2 nd method Two arterial punctures O ne catheter positioned within the left ventricle S econd catheter located within the ascending aorta

35. 3 rd method V enous puncture – Femoral vein T o allow transseptal puncture Catheter is advanced from the left atrium into the left ventricle Arterial puncture Second catheter positioned into the ascending aorta

36. 4 th method S ingle arterial puncture Standard , short 6 French sheath within the femoral artery 4 or 5 French pigtail catheter (through the 6 French sheath) into the left ventricle The femoral artery pressure measured via the side-arm of the sheath used as a surrogate to the central aortic pressure With realignment – G radient is underestimated by approximately 10 mm Hg Without realignment – Gradient is overestimated by approximately 9 mm Hg Therefore, the central aortic pressure should be measured for accuracy

37. LV & Right Femoral artery pressure tracings in AS

38. 5 th method S ingle arterial puncture L ong (55 or 90 cm) 6 French sheath into the ascending aorta with a smaller 4 or 5 French sheath advanced through the long sheath into the left ventricle The side-arm of the long sheath is used to measure the central aortic pressure

39. Newer method Bertog et al Single arterial puncture 4 French catheter into the ascending aorta LV pressure is measured using a 0.014-inch pressure wire (placed through the 4 French catheter ) Correlation with traditional methods was excellent

40. Analysis of pressure waveform Without AS the slope and magnitude of the aortic and LV systolic pressures are similar rise together to a midsystolic peak . With AS the pressure in the aorta rises slowly and achieves a late systolic peak LV hypertrophy limits the ability of the left ventricle to fill at a normal pressure, resulting in a higher end-diastolic pressure.

41. Carabello sign (1987) A rise in arterial blood pressure during left heart catheter pullback in patients with severe aortic stenosis Catheter pullback showed increases in peripheral arterial pressure of 5 mm Hg in 15 of 42 patients . Fifteen of 20 patients (75%) with AVA of 0.6 cm 2 demonstrated this phenomenon N one of 22 patients with AVA of 0.7 cm 2 showed such an increase.

42. Cardiac output FICK TECHNIQUE Oxygen serves as the “indicator ” T he uptake or release of oxygen by a tissue is the product of the amount of oxygen delivered to the tissue times the difference in oxygen content between the blood entering and the blood leaving thetissue THERMODILUTION METHOD A known volume of cold saline is injected into the right atrium while a thermistor in the pulmonary artery continuously records temperature . Cardiac output is then calculated from the known temperature ( T ) and volume ( V ) of the injectate , and the integral of temperature over time (ΔT/ dt ) in the pulmonary artery

43. Assessment of Valve Area

44. Dr. Richard Gorlin , MD 1926–1997 Hibernating myocardium Microvascular angina DIG study

45. Gorlin’s formula (1951) T wo fundamental hydraulic formulas

46. Torricelli's law First formula flow across a round orifice F = flow rate A = orifice area V = velocity of flow C c = coefficient of orifice contraction. The constant C c compensates for the physical phenomenon that, except for a perfect orifice, the area of a stream flowing through an orifice will be less than the true area of the orifice .

47. Second principle relates pressure gradient and velocity of flow according to Torricelli's law V = velocity of flow C v = coefficient of velocity correcting for energy loss as pressure energy is converted to kinetic or velocity energy H=pressure gradient in cm H 2 O g = gravitational constant (980 cm/sec 2 ) for converting cm H 2 O to units of pressure

48. Combining the 2 eqns C =an empirical constant accounting for C V and C C h =in mm Hg

49. The diastolic filling period begins at mitral valve opening and continues until end-diastole. The systolic ejection period begins with aortic valve opening and proceeds to the dicrotic notch or other evidence of aortic valve closure

50. Final equation CO = cardiac output ( cm 3 /minute) SEP = systolic ejection period ( seconds/beat) HR = heart rate ( beats/minute) C = an empirical constant Mitral Valve = constant 0.7 (later changed 0.85) Aortic Valve = 1 P = pressure gradient

51. Example CO = 4000 mL/min HR = 60 beats/min.

52. Planimeter aortic-LV pressure gradients (area = 12.2 cm 2 ) and measure systolic ejection periods (SEPs = 4.1 cm). Next convert cm to time and convert planimetered area to mean systolic pressure gradient. Systolic ejection period of 4.1 cm/beat at paper speed of 100 mm/s = 0.41 s/beat.

53. Mean valve gradient (MVG) = (area x scale factor)/SEP (Scale Factor: 1 cm = 19.6 mm Hg) Aortic valve flow

54. Aortic valve area.

55. As heart rate increases during exercise, the systolic ejection period tends to become shorter, but the tendency is counteracted by both increased venous return and systemic arteriolar vasodilation, factors that normally help to maintain LV stroke volume constant during exercise. The heart rate is increasing but the systolic ejection period is diminishing only slightly so that their product (systolic ejection time per minute) increases. This is the counterpart of the decreased diastolic filling time per minute during exercise

56. With decreasing heart rate, the gradient increases in aortic stenosis for any value of cardiac output. This is opposite to the effect of heart rate in mitral stenosis and reflects the opposite effects of heart rate on systolic and diastolic time per minute. A s the heart rate slows in aortic stenosis, the stroke volume increases if cardiac output remains constant. Thus the flow per beat across the aortic valve increases and so does the pressure gradient

57. Pressures in LV , LVOT & Aorta

58. Pressure recovery Downstream from the orifice, the flow stream expands and decelerates with a corresponding decrease in kinetic and increase in potential energy, a phenomenon called “pressure recovery” The net P between the LV and the mid-ascending aorta is lower than the pressure drop immediately adjacent to the valve Doppler measures velocity at the narrowest orifice, thus Doppler Ps are higher than the net P . The clinical impact of pressure recovery usually is small but can be significant with mild stenosis and a small aortic root or with a doming congenitally stenotic valve

59. In calculating aortic valve area, the gradient between sites 1 and 3, which records gradient before pressure recovery, is probably the most accurate reflection of the pressure drop across the valve. When the aortic catheter is placed at a more distal site, it records the effect of pressure recovery, which reduces gradient as blood flow again becomes laminar. The more proximal aortic position is probably the ideal location for measuring the gradient for the valve area calculation

60. limitations of the Gorlin -derived orifice area As the square root of the mean gradient is used in the Gorlin formula, the valve area calculation is more strongly influenced by the cardiac output than the pressure gradient

61. Transducer Calibration Pullback Hemodynamics An augmentation in peripheral systolic pressure of more than 5 mm Hg at the time of LV catheter pullback indicates that significant aortic stenosis is present. This sign is present in >80% of patients with an aortic valve area of 0.5 cm 2 or less

62. Hakki’s formula The product of heart rate, SEP or DFP, and the Gorlin formula constant was nearly the same for all patients whose hemodynamics were measured in the resting state, and the value of this product was close to 1.0

63. Valve resistance Helps to separate patients with severe aortic stenosis from those patients who had similarly small calculated aortic valve areas, but who were subsequently demonstrated to have mild disease. Resistance appears less flow dependent than valve area Resistance is unlikely to supplant the Gorlin formula in assessing stenosis severity, but may be an important adjunct to it in patients with low cardiac output.

64. Resistance also has been shown to be more constant under conditions of changing cardiac output than valve area. Resistance thus necessarily has a close relationship to valve area. Resistance rises sharply below a valve area of 0.7 cm 2 . The shoulder of this curve is between 0.7 and 1.1 cm 2 , which is the common area of indeterminate significance of Gorlin aortic valve area. Some patients in this gray zone tend to have higher valve resistance than others. T he patients with resistance >250 dynes x s x cm –5 are more likely to have significant obstruction, whereas those with resistance below 200 dynes x s x cm –5 are less likely. Valve resistance is not expected to remain consistent.

65. Valve resistance before and after valvuloplasty

66. Low Gradient AS

67. D obutamine or nitroprusside for patients with a cardiac output of <4.5 L/minute who have a transvalvular gradient of <40 mm Hg and a valve resistance of <275 dyn sec/cm -5 . If patients respond by substantially increasing the measured gradient, they probably have truly severe aortic stenosis and may benefit from aortic valve replacement. If cardiac output increases substantially but gradient increases only slightly or actually declines, the aortic stenosis is mild and the patient is unlikely to benefit from aortic valve replacement

68. True Vs. Pseudo AS O btain baseline measurements of cardiac output, heart rate, and simultaneous LV and aortic pressures Initiate dobutamine by continuous infusion at 5 μg / kg/min The dose is increased by 3 to 10 μg /kg/min every 5 minutes until a maximum dose of 40 μg /kg/min is achieved The mean gradient increases to more than 40 mm Hg, cardiac output increases by 50%, heart rate increases to more than 140 beats per minute ( bpm ), or intolerable symptoms or side effects ( arrhythmias) occur .

69. Low flow low gradient AS

70. Patients with true, severe AS (1) mean aortic valve gradient greater than 30 mm Hg (2) an aortic valve area remains 1.0 cm2 or less Patients with pseudo–aortic stenosis (1) cardiac output increases (2) mean aortic valve gradient remains less than 30 mm Hg these findings indicate a component of a primary cardiomyopathy and mild to moderate AS.

71. Angiocardiography Left ventriculography should be routinely performed provides assessment of LV systolic function the anatomy of the aortic valve coexisting mitral regurgitation The aortic valve should be assessed for Calcification Leaflet morphology ( bicuspid) leaflet mobility. A bicuspid aortic valve may show systolic doming of the leaflets.

72. Thank you