Download Diastolic congestive heart failure: Treatment is moving to the `burbs

Diastolic congestive heart
failure:
Treatment is moving to the
‘burbs
Asif Serajian, DO FACC
What is HFpEf* and why did we
change the name?
Complex clinical condition initially called diastolic CHF
(congestive heart failure) thought only to be due the
relaxation abnormality of the heart
Soon became clear that it is not simply the opposite
end of the spectrum in comparison to systolic CHF
It is not simply a stiff left ventricle but a stiff ventricle
along with a stiff arterial and venous system
(ventriculo-arterial coupling)
Better termed as Heart Failure with Preserved Ejection Fraction
No effective pharmacological treatment is available
besides symptomatic relief and treatment of risk
factors
Represents over 50% of heart failure in 2015
Exercise has shown to improve functional capacity
and quality of life
Presbycardia
In the 1960’s a certain heart condition in elderly
individuals was described where the left ventricle was
stiff
It was a rare cause of congestive heart failure
It was a poorly understood disease state
Epidemiology
Considered a systemic disease, 30% of patients die
from non cardiac factors vs 17% for heart failure with
reduced ejection fraction (HFrEF)
Accounts for 54% of heart failure diagnosis
Reduced rate of 30 day hospital re-admission in
comparison to HFrEF
Mortality rate
1 year mortality rate is 8%
5 year mortality rate is close to 50% in patients above
age 70
Pulmonary hypertension is a marker of increased
mortality in HFpEF
Even pre-clinical diastolic dysfunction is associated
with increased mortality and with the diagnosis of
diabetes, it many times progresses to overt
congestive heart failure
Men have a higher mortality rate even though more
Mortality
30% of patients die of non-cardiac disorder
emphasizing the systemic nature of disease (17% for
systolic CHF)
Do not ignore pre-clinical
diastolic
dysfunction
You may have seen “stage 1 diastolic dysfunction” on
echocardiograms whereas the patient may not have
signs/symptoms of CHF and ignored this finding as
“pre-clinical”
Seen in 30% of elderly patients
Sometimes referred to as findings of “aging heart”
Combined with diabetes these patients have a rate of
37% of conversion to HFpEF at 5 years!
In elderly patients this finding profoundly increases
mortality
Typical patient with HFpEF
Women: Are especially prone to increased myocardial
and arterial stiffness with aging and these effects are
most prominent with exercise
Diabetes: linked with myocardial steatosis
Hypertension: linked with inflammation in the
myocardial interstitium
Obesity: linked with interstitial fibrosis of the
myocardium
Pathophysiology
It is many times thought of as a stiff ventricle but the
pathophysiology is more complex than that
Studies on myocardial tissue show cardiomyocyte
hypertrophy and interstitial fibrosis, incomplete
relaxation of myocardial tissue with increased
stiffness
The left ventricle goes through a twisting motion much
like wringing a towel
Newer imaging modalities demonstrated
abnormalities of the torsion, untwisting and reduced
longitudinal motion in patients with HFpEF in both
systole and diastole
Basic left ventricular (LV) mechanics and architecture
are affected in HFpEF
In essence the EF is preserved but some of the other
New paradigm
Obesity, COPD and diabetes lead to a
proinflammatory state that induces coronary
microvasculature endothelial inflammation
Inflammation and resultant oxidative stress cause stiff
cardiomyocyte and interstitial fibrosis which
characterize the diastolic abnormalities seen on
echocardiography
Although hypertension is thought to cause HFpEF this
model changes the emphasis to inflammation
However, arterial stiffness in a traditional sense does
affect the diastolic dynamics of the heart
Increased arterial stiffness --> increased reflected
arterial wave --> increased afterload --> decreased
cardiac ouput --> increased diastolic filling pressure
(traditional model)
Breathless, the most common symptom of HFpEF:
causes are pulmonary congestion and subendocardial
ischemia (borderline troponin elevation in these
patients?)
New model
Incorporates:
Arterial/venous stiffness
Ventricular stiffness from stiff myocytes and
interstitial fibrosis
Ventricular torsional abnormalities (not clearly seen
on echocardiography)
Inflammation at level of the muscle altering oxygen
metabolism
Diagnosis of HFpEF
European Society of Cardiology calls
for:
1. signs or symptoms of heart failure
2. normal or mildly abnormal systolic function
3. evidence of LV diastolic dysfunction
Evidence of LV diastolic
dysfunction
Can be tricky as many times the echocardiogram is
performed when volume status has improved
Diastolic parameters at that point in time may be only
mildly abnormal (stage 1)
Tissue doppler index which correlates with diastolic
filling pressures may not be elevated post diuresis or
technical reason in measurement
Must look for clues to fit the clinical diagnosis
Remember it is clinical diagnosis
Diastolic parameters by
echocardiography
Measure the relaxation velocity of the LV in early
diastole (e’ should be < 9)
Measure mitral early diastolic inflow (E) and measure
the ratio E/e’
If E/e’ is above 13 then the diagnosis of significant
diastolic dysfunction is established
If these criteria are not noted then other factors must
be reviewed
Other factors
Echocardiographic: *Left atrial dilation *Pulmonary
vein flow *Pulmonary arterial hypertension *Doppler
parameters with valsalva and exercise
Clinical: *Elevated BNP *Presence of atrial fibrillation
If 2 or more of these are present then the diagnosis is
established
Cardiac catheterization can be used in cases where
the etiology of breathlessness remains elusive
One challenge of the assessment of the
echocardiographic markers is whether the delayed
relaxation noted on echocardiography is pre-clinical
diastolic dysfunction i.e. the aging heart or HFpEF
Increased left atrial (LA) volume and pulmonary
hypertension would indicate that this patient has
HFpEF
Think of LA volume as hemoglobin A1C of diastolic
heart failure, it tells us about the past
Treatment
Unlike systolic heart failure, treatment is disappointing
No agents have been shown to improve survival,
enhance quality of life, exercise tolerance or diastolic
function
Trials have studied spironolactone, sildenafil and
other agents all with disappointing results
Symptomatic relief with diuretics, heart rate and blood
pressure control have been the mainstay of therapy
Dietary salt restriction to 2 grams of sodium is
recommended
Data suggests that dietary sodium restriction
improves LV diastolic function
In diabetic patients with elevated triglycerides,
prolonged caloric restriction reduces myocardial
steatosis and improves diastolic function
Exercise for HFpEF
No effective medication exists for HFpEF but an
approach to the musculoskeletal system has merit
Data suggests that impaired oxidative metabolism in
the skeletal musculature which is caused by greater
intramuscular fat content and decreased supply or
utilization of oxygen is the major contributor to the
decreased functional capacity experienced by
patients with HFpEF
One study demonstrated that after exercise training
16% of improvement in exercise capacity takes place
at the myocardial level and the remaining 84% is
attributed to changes at the skeletal muscle level
Improved functionality can be achieved with exercise
training driven efficiency in perfusion, oxygen transfer
and use of oxygen at the level of the muscle
Trials
6 small randomized controlled trials have assessed
the impact of exercise training on aerobic fitness and
QOL
Overall outcomes showed benefits of exercise training
Exercise programs used low to moderate intensity
walking or cycling and occasionally resistance training
Typical exercise was 30 minutes per day, 3 times a
week at an intensity based on previous exercise
stress test with a duration of 12-24 weeks
Outcomes measured
Fitness outcomes were measured by
6-minute walk distance
peak oxygen consumption (VO2)
Diastolic echocardiographic parameters
Results
Patients with exercise training demonstrated
improved exercise capacity
Peak exercise capacity improved by a threshold of
10%
Exercise training prescription
Candidates should be evaluated for cardiac ischemia
by means of stress testing prior to initiation of
exercise training program
Once stable disease is confirmed, patients with
HFpEF should initiate 3 to 5 weekly sessions of large
muscle group endurance activities such as walking,
cycling, upper and lower extremity ergometry for a
period of 20-60 minutes
Intensity target should be perceived “somewhat hard”
In elderly patients with multiple comorbidities, slow
goal-oriented up-titration of duration must be
undertaken
If there is concern about stability of patient, initial
exercise should be supervised
Prevention
Because there are no pharmacological treatment for
HFpEF prevention represents treatment of risk factors
Stage A heart failure is considered in those with risk
factors of congestive heart failure without known CHF
by the American College of Cardiology classification
Stage B is with structural changes and no symptoms
Exercise for prevention
Patients with higher levels of exercise across their
lifetime have more compliant left ventricles (LV)
The Cooper Center Longitudinal Study look at 1678
men and 1247 women demonstrating:
low fitness was associated with smaller heart size
and diastolic dysfunction with concentric
remodeling
higher fitness was associated with lower
prevalence of diastolic dysfunction and lower LV
filling pressures
Prevention comes back to risk
factors
Fitness, stiffness and age interact to lead to heart
failure
Perhaps exercise training might halt or even reverse
diastolic dysfunction
Summary
HFpEF is the most common form of heart failure
Complex disorder where patients have a stiff LV and
a stiff arterial and venous system
Typical patient has multiple comorbid conditions such
as hypertension, diabetes, renal disease, lung
disease, obesity
Clinical presentation is of dyspnea and fatigue
however signs of heart failure may be less common
and diagnosis can be elusive at times
Management is directed at treatment of comorbid
conditions and diuresis as necessary
Musculoskeletal system plays an important role in the
disorder
There are peripheral vascular function and skeletal
muscle abnormalities in patients with HFpEF and
contribute to patient’s symptoms of fatigue and
exertional intolerance
Short-term, low to moderate intensity aerobic exercise
training increases functional capacity and QOL
scores-improvements attributed to skeletal muscle
function and not the pump itself
Long-term exercise is associated with lower
prevalence of diastolic dysfunction, less adverse LV
remodeling and lower LV filling pressures
Brings us back to what we have been telling our
patients all these years.... diet and exercise
However, now you can make a better case for
exercise in patients with HFpEF with the knowledge
provided here
Thank you.