Diastolic Dysfunction: Nuts, bolts & who cares ? Kunjan Bhatt MD Austin Heart
Background • For patients > 65 years old, CHF is the most common diagnosis at discharge. • The population is aging • In the early 1900s, ~ 4% population was > 65. • By 2010, 1/3 population will be > 65.
Background • Among the elderly, cardiovascular disease is the MOST common cause of mortality and morbidity. • In the US, 5 million people have CHF. ½ these cases are from CHF with preserved LV function.
Background • Classically, we’ve sought out causes of CHF as a result of systolic dysfunction. • Now we are discovering that ½ cases of CHF is being caused by diastolic dysfunction, where LV systolic function is preserved.
Misconception #1 Diastolic dysfunction is uncommon as is Diastolic congestive heart failure. • Fact #1 • Everyone and their mother over the age of 40-50 has E/A reversal, during resting 2D echo. The actual incidence is ~25-30% in individuals > 45 years. • Over the past 10 years, incidence of Diastolic CHF has increased. • 70 y.o pts’ incidence of CHF: SHF = DHF • 80 y.o pts’ incidence of CHF: DHF > SHF
Misconception #2 • Discussions of Diastolic dysfunction cause people to vasovagal, fall asleep, and bore them ½ to death. Diastolic dysfunction is simple, SEE? • E/A normal great! Normal Diastolic function! Stop pestering me! • E/A reversed whoop-dee-do. Abnormal diastolic dysfunction. Can we stop talking about this now?
FACT #2 • This is actually ½ true – this subject is great to put most people to sleep. • HOWEVER, Diastolic dysfunction classification should not be normal or abnormal. It’s patronizing to patient’s who have rip-roaring CHF with preserved LV function. • Spectrum of disease. LOAD DEPENDENT!! • This is why I’m giving the talk!
Misconception #3 • Diastolic dysfunction = Diastolic CHF • Not quite! • Fact #3 • Diastolic dysfunction characterizes abnormal relaxation of the LV, and for the purposes of this talk, an echo finding. • Diastolic CHF describes a clinical syndrome of CHF in patient with preserved LV function.
Causes of Diastolic dysfunction Heart Failure • Hypertension • Hypertension • Hypertension • Hypertension • Hypertension • Hypertension • Hypertension
Other Causes of abnormal Diastolic filling • Cardiomyopathy • Hypertrophic • Restrictive • Infiltrative • CAD • Valvular heart disease • Diabetes • Obesity • Sleep Apnea • *** Constrictive Pericarditis
Determinants of Diastolic filling Quinones ASE Review 2007
Topics for Discussion • Brief Review of Diastolic physiology • MV inflow patterns • IVRT – Isovolumic Relaxation time • DT – Deceleration time • Velocity of propagation • Tissue Doppler of the MV annulus • E/E’ • Atrial Fib and Sinus Tachycardia • Diseases of the Pericardium • The “who cares factor”
Normal Diastolic function • Occupies about 2/3 of the cardiac cycle. Takes longer than systole • Active process, requires energy • Abnormalities of diastolic function ALWAYS precede those of systolic function. • Ex: Acute MI
Normal Diastolic filling 1. Isovolumic Relaxation 2. Early rapid diastolic filling phase 3. Diastasis 4. Late diastolic filling due to atrial contraction Quinones, ASE Review 2007
Normal Diastolic function • When LV pressure becomes less than LA pressure, MV opens • Rapid early diastolic filling begins. • Driving force is predominantly elastic recoil and normal relaxation. • ~80% LV filling during this phase
Normal Diastolic function • As a result of rapid filling, LV pressure rapidly equilibrates with and may exceed LA pressure. • Results in deceleration of MV inflow. • Late diastolic filling is from atrial contraction. It’s ~ 20% LV filling.
MV inflow Patterns • 5 stages – Normal and Stages I – IV diastolic dysfunction • Stage I – Impaired relaxation • Stage II – Pseudo-normal • Stage III – Restrictive Filling, reversible • Stage IV – Restrictive Filling, irreversible
MV inflow pattern limitations Advantages Disadvantages
IVRT – Isovolumic relaxation time • Time interval between aortic valve closure and mitral valve opening. Usually obtained from Apical view with Doppler sample between AV and MV • It will lengthen with impaired LV relaxation and decrease with with increase in LV filling pressures. • Normal = 70 – 90 ms.
DT and IVRT • DT - Peak of the E wave – time interval for the E wave velocity to reach 0. • PHT = 0.29 * DT • IVRT – time interval of AV closure to MV opening.
Deceleration time • Nl = 160 – 220 ms • Deceleration time increases, if there is abnormal relaxation. It decreases in elevated LV filling pressures • The LV can also relax vigorously from tremendous elastic recoil such as young healthy people (short DT but normal) • Conversely, if there is a decrease in LV compliance or a significant increase in LA pressure DT decreases (pathologic – suggests elevated filling pressures)
IVRT + DT: Strengths and Weaknesses StrengthsWeaknesses Lester et al, JACC 2008; 51; 679 - 689
Velocity of Propogation (color M-mode of MV inflow)
Velocity of propagation of mitral inflow • Normally, there is a intraventricular pressure gradient. • Apical < Base • This gradient decreases with a decrease in myocardial relaxation • Color M mode displays color coded mean velocities from the annulus to the apex over time.
Velocity of propagation of mitral inflow • Color flow baseline needs to be shifted to lower the nyquist limit. • The central highest velocity jet should be blue. • Trace the slope of the first aliasing line. • > 50 cm/s normal • < 50cm/s abnormal • Load dependent. • Hard to do accurately
Velocity of propagation of mitral inflow • Vp has been used to estimate filling pressures (PCWP) 1. E/Vp > 1.5 PCWP > 15 mmHg 2. PCWP = 4.5 [1000/(2 x IVRT) + Vp] – 9 3. PCWP = (5.27 x E/Vp) + 4.6 • Falsely high in restrictive Cardiomyopathy and HOCM.
MV inflow propagation velocity: Strengths and Weaknesses Strengths Weaknesses Lester et al, JACC 2008; 51; 679 - 689
LA Volume Index • EASY TO DO!! • The new echo GOLD STANDARD for LA size. • LA 2D dimension extrapolates that LA enlarges in an AP diameter. Erroneous assumption. • Correlates much better with the true gold standard which is MRI. • Has been called the HbAIC of cardiac disease. Robust marker of clinical outcomes • WHAT DO YOU NEED: • BSA (remember, it’s an index) • A4C and A2C traced LA’s • Shortest length
LA volume • Divide the LA volume by BSA!! • A-L method is used most commonly (we don’t like calculus) • 22 +/- 6 ml / m2 (normal) • 28-34 - mild • 34-40 - moderate • >40 - severe
LA volume: Strengths and Weaknesses Strengths Weaknesses Lester et al, JACC 2008; 51; 679 - 689
Pulmonary venous flow • Normally 4 different waves seen – S1/S2/D/A • Normal S – dominance. • Young people can have a D dom normally
Pulmonary Vein Profile • PVs1 – early in systole and relates to atrial relaxation. A decrease in LA pressure promotes forward flow. • PVs2 – mid systole. Represents the increase in pulmonary venous pressure. • Normally the S2>S1 • Distinction only identifiable in about 30% people, normally.
Pulmonary Vein Profile • PVd – occurs after opening of the MV and in conjunction with decrease in LA pressure • Pva – increase with atrial contraction. May result in a flow reversal into the PV. Depends upon • LV diastolic pressure • LA compliance • HR
Pulmonary Vein Profile • Think of PVd and Pva as extensions of MV inflow E and A. • The peak velocity and DT correlate well with those of mitral E velocity because the LA acts as a passive conduit for flow during early diastole. • DT becomes shorter as PCWP increases. • Both Pva velocity and duration increase with higher LVEDP.
Pulmonary Vein flow: Strengths and Weaknesses Strengths Weaknesses Lester et al, JACC 2008; 51; 679 - 689
Tissue Doppler (here’s where it gets ugly)
Tissue doppler • Measuring tissue velocity and NOTblood flow • Speed of tissue is ~ 1/10 of arterial blood. • Arterial blood velocity ~ 150 cm/s • Venous Blood velocity ~ 10 cm/s • Myocardial Tissue velocity ~ 1 – 20 cm/s • Speed usually expressed in cm/s
Tissue Doppler – What we change on echo Machines • Doppler instruments are altered to reject the high velocity of blood • Requires a high frame rate • DECREASE GAIN! • Lower aliasing velocities
QUESTION WHAT ARE THE 3 profiles seen on Tissue Doppler?
Tissue doppler • 3 velocity profiles are seen – systolic (S’), Early Diastolic (E’) and late diastolic (A’) • S’ – systolic velocity of the MV annulus. • Normally should be > 6 cm/s • Can perform segmental or regional functional assessment • E’ – Early Diastolic velocity • 2 sites are typically measured – medial and lateral – Normal Range… • E’m – > 10 cm/s • E’l > 15 cm/s • A’ - Late diastolic velocity. • Atrial contraction • Correlates with LA function • Increases in early diastolic dysfunction • decreases with LA dysfunction (later diastolic dysfunction)
TDI - applications • Beyond E’ and E/E’, mostly in research… • Evaluation of Thick Walls • LVH, HCM, Infiltrative CM, Restrictive CM, & Athlete's Heart • Normal TDI and strain vs abnormal TDI and strain • Assessment of viability (akineticvs scar). • Relates to Tissue velocity gradients
Tissue Doppler – Normal Profiles Lateral > 15 cm/s Medial > 10 cm/s
Tissue Doppler • E’ velocity is essential for classifying the diastolic filling pattern and estimating filling pressures. • Helpful to differentiate myocardial disease from pericardial disease • Normally E’ increases with an increase in the transmitral gradient (exertion or increase preload) • In Diastolic Dysfunction – it’s low & doesn’t increase as much with exertion or inc. preload