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.

Let’s Clarify some misconceptions…

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

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

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 PW inflow patterns

MV inflow pattern limitations Advantages Disadvantages

DT and IVRT

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 Strengths Weaknesses 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

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 Vein Profile

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.

PV profiles in diastolic dysfunction.

Pulmonary Vein flow: Strengths and Weaknesses Strengths Weaknesses Lester et al, JACC 2008; 51; 679 - 689

(here’s where it gets ugly) Tissue Doppler (here’s where it gets ugly)

Tissue doppler Measuring tissue velocity and NOT blood 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

WHAT ARE THE 3 profiles seen on Tissue Doppler? QUESTION WHAT ARE THE 3 profiles seen on Tissue Doppler?

Tissue doppler S’ – systolic velocity of the MV annulus. 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 (akinetic vs 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

Tissue Doppler E’ decreases with aging (precedes even E/A reversal) Load independent! Reproducible One of the earliest markers for diastolic dysfunction Correlates with filling pressures, especially when used as a ratio E/E’

Tissue Doppler STRENGTHS WEAKNESSES 1. Can be obtained in most patients 2. Early marker of diastolic dysfunction 3. Not influenced by changes in heart rate 4. Primarily load independent in disease states WEAKNESSES 1. Influenced by local changes in wall motion (infarction) 2. Not accurate in significant MV disease – - MAC - MVR

Who cares about Tissue Doppler? (beyond the Echo Nerd Herd) E/E’ can guesstimate PCWP >15  wedge > 20 < 8 – normal 8 - 15 ?? E/E’ has been validated in clinical studies as a marker of elevated PCWP (> 15). Elevated E/E’ is predictive of poor outcomes in MI Significantly decreased E’ associated with higher mortality.

E/E’ is a robust clinical marker What the ratio means? > 15  elevated filling pressures < 8  Nl 8 – 15  ??? Nagueh et al, JACC 1997; 30: 1527 - 1533

Assessment of Diastolic filling in A-fib and Sinus Tachycardia No A wave from Mv inflow and blunted PVs wave DT time measurement is tricky, variable Can use E/E’ Can use DT of the PVd wave Sinus Tachycardia E and A waves may fuse. Use E/E’

Let’s Review

Normal MV inflow E/A = 0.9-1.5 DT = 160-240 ms IVRT 70-90 ms Vp > 50 cm/s S – dominant PV pattern

Stage I DT > 240 ms E/A < 0.9 IVRT - > 90 ms LAVI>28 ml/m2 Vp < 50 cm/s S – dominant PV pattern

Stage II Looks the same like normal – hence the name “pseudonormal” Many of the parameters are the same as Normal LV inflow. PV – S blunting or D dominant PV

How do I differentiate between Stage II and normal? Valsalva – shouldn’t change normal but pseudonormal should look like Stage I. Also Stage III should look like stage I E’ (Tissue Doppler) – Normal is normal. Lower velocities with diastolic dysfunction (E’m <10, E’l < 15). Left atrial volume – With elevated filling pressures, the left atrium will remodel and enlarge (LA Volume Index > 28 ml / m2) Velocity of propagation - > 50 cm/s (normal) or < 50 cm/s (abnormal) D – dominant pulmonary veins

Stage II Valsalva 

The 4 Phased Valsalva Maneuver PHASES I - AO pressure increases (increase in IT pres.) II – AO and PP decrease because dec. in preload. Reflex tachycardia. III – AO pressure decreases more in response to release of IT pressure IV – recovery period. Preload, AO, PP + increase. Nishimura et al. Mayo clinic proceedings. 2004;79: 577-578.

Stage III – Restrictive,reversible DT < 160 ms IVRT < 70 ms E/A > 2:1 E’ < 5cm/s Vp < 50 cm/s LAVI > 35 ml / m2 D>>S (PV Pattern)

Stage III – Restrictive, reversible Valsalva 

Stage IV – restrictive irreversible DT < 130ms E/A > 2.5 E’ < 5 cm/s Vp < 50 cm/s IVRT < 70ms LAVI > 40 No valsalva change D>>S (PV pattern)

What about other causes of CHF with preserved LV function TEE 5C view

Causes of pericardial constriction Prior Cardiac surgery Idiopathic Pericarditis Prior Radiation Collagen Vascular Infection (TB)

Constrictive Pericarditis Everything we’ve spoken about for diastolic dysfunction DOES NOT APPLY HERE. Not uncommon Escapes clinical and echo detection Pericardial Thickness may be normal in 1/5th of cases Calcification of the pericardium may only occur in ~ 20% pts on CXR

Constrictive Pericarditis – some Echo findings Thickened pericardium (~ 80%) Abnormal ventricular septal motion Flattening of the posterior wall during diastole Respirophasic variation of Ventricular cavity size Dilated IVC

Echo criteria to diagnose Pericardial Constriction 1)Disassociation between intrathoracic and intra-pericardial pressures. (normally they’re related) 2)Exaggerated ventricular interdependence (i.e. the filling of one, significantly impacts the filling of the other)

Doppler Findings in Constrictive Pericarditis Respiratory variation of >25% in mitral E velocity

Doppler Findings in Constrictive Pericarditis OH Figure 17-29 Increased DFR with expiration in the hepatic vein.

Other features of constriction Tissue doppler that is > 7 cm/s (annulus paradoxus) Unless the myocardium is involved, myocardial relaxation is intact. Septal annular velocities are normal or even increased (not close to the pericardium like the lateral annulus) PW MV inflow that looks like restrictive filling pattern  E/A > 1.5 and DT < 160 ms. E/E’ is inversely proportional to the PCWP (as opposed to myocardial diseases).

WHO CARES?

Who cares about diastolic dysfunction? Steady rise in prevalence of CHF with preserved LV function. By the 7th decade, incidence of diastolic CHF = systolic CHF By the 8th decade, incidence of diastolic CHF > systolic CHF The survival of patients with the clinical syndrome of heart failure is similar in those with persevered versus those with a reduced LV ejection fraction

Summary Diastolic Dysfunction is a real, dynamic process. Much information can be gained on LV filling pressures without a drop of blood (no cath) Prognostic information and therapeutic options stem from the results (myocardial, pericardial). You are in the front line to look for this stuff. Keep a sharp look out, you’ll favorably alter patient care. That’s the bottom line.

(for not falling asleep) Thank you ! (for not falling asleep)