Download Document

Comprehensive Evaluation
of the Heart Failure Patient
Stephen G. Phillips, M.D.
Assistant Professor of Medicine
Virginia Tech Carilion School of Medicine
September 25, 2015
Outline
•
•
•
•
•
•
Causes of Heart Failure
Inpatient Evaluation at Initial Diagnosis
Medical therapy
Device therapy
Outpatient management
When to refer for advanced therapies
Definition
• Heart Failure is a complex clinical
syndrome that can result from any
structural or functional cardiac disorder
that impairs the ability of the ventricles
to fill with or eject blood
Background
• Heart Failure affects approximately 6
million Americans
• Heart Failure is the most common
Medicare discharge diagnosis
• Admissions rates have increased
approximately 150% over the past 2
decades
• Half of the hospital admissions are
patients with HFpEF
Definition of Heart Failure
Classification
I. Heart Failure with
Reduced Ejection
Fraction (HFrEF)
II. Heart Failure with
Preserved Ejection
Fraction (HFpEF)
Ejection
Fraction
≤40%
≥50%
a. HFpEF, Borderline 41% to 49%
b. HFpEF, Improved
>40%
Description
Also referred to as systolic HF. Randomized clinical trials have
mainly enrolled patients with HFrEF and it is only in these
patients that efficacious therapies have been demonstrated to date.
Also referred to as diastolic HF. Several different criteria have
been used to further define HFpEF. The diagnosis of HFpEF is
challenging because it is largely one of excluding other potential
noncardiac causes of symptoms suggestive of HF. To date,
efficacious therapies have not been identified.
These patients fall into a borderline or intermediate group. Their
characteristics, treatment patterns, and outcomes appear similar to
those of patient with HFpEF.
It has been recognized that a subset of patients with HFpEF
previously had HFrEF. These patients with improvement or
recovery in EF may be clinically distinct from those with
persistently preserved or reduced EF. Further research is needed
to better characterize these patients.
www.cardiosource.com
Classification of Heart Failure
A
B
C
ACCF/AHA Stages of HF
At high risk for HF but without
structural heart disease or symptoms of
HF.
Structural heart disease but without
signs or symptoms of HF.
Structural heart disease with prior or
current symptoms of HF.
NYHA Functional Classification
None
I
I
II
III
IV
D
Refractory HF requiring specialized
interventions.
No limitation of physical activity.
Ordinary physical activity does not
cause symptoms of HF.
No limitation of physical activity.
Ordinary physical activity does not
cause symptoms of HF.
Slight limitation of physical activity.
Comfortable at rest, but ordinary
physical activity results in symptoms of
HF.
Marked limitation of physical activity.
Comfortable at rest, but less than
ordinary activity causes symptoms of
HF.
Unable to carry on any physical activity
without symptoms of HF, or symptoms
of HF at rest.
Case Presentation
• Mr. S is a 51 male with PMH significant for HTN (
on HCTZ 25mg daily) who presents to ED with 1
week h/o fatigue, SOB, and LE edema
• Physical Exam
• Gen: NAD
Vitals: BP =110/70 P=90, afebrile,weight=185lbs
pulse ox 88% RA, 92% on 2LNC
HEENT: JVP, no carotid bruits
Resp: crackles 1/3 way up both lung fields
CV: RRR, normal S1S2, S3 gallop is present
ABD: soft NT/ND
Skin: 2 plus pitting edema to knees bilaterally
Case Presentation-cont
• EKG: NSR, rate=90 bpm, LBBB
QRS=160ms
CXR: cardiomegaly, mild interstitial
edema
• Labs: na=135, K=4.1, CL=100, CO2=
21, Bun=30, crt=1,2
Wbc=7000, Hgb=13.1, plt=250,000,
TSH=3.5 ,NT-proBNP= 1100pg/ml
The Hospitalized Patient
Diagnosis of HF
I IIa IIb III
The diagnosis of heart failure is primarily based on signs and
symptoms derived from a thorough history and physical exam.
Clinicians should determine the following:
New
a. adequacy of systemic perfusion;
b. volume status;
c. the contribution of precipitating factors and/or comorbidities
d. if the heart failure is new onset or an exacerbation
of chronic disease; and
e. whether it is associated with preserved normal or reduced
I IIa IIb III
ejection fraction.
Chest radiographs, echocardiogram, and echocardiography are key
tests in this assessment.
New
High Risk Features






Elevated BUN(>43mg/dl) or creatinine >2.75
Low SBP(<115mmhg)
Hyponatremia
Elevated BNP
Elevated troponin
Ischemic EKG changes
The Hospitalized Patient
I IIa IIb III
Precipitating Factors for Acute HF
It is recommended that the following common
potential precipitating factors for acute HF be
identified as recognition of these comorbidities,
New
is critical to guide therapy:
• acute coronary syndromes/coronary
ischemia
• severe hypertension
• atrial and ventricular arrhythmias
• infections
• pulmonary emboli
• renal failure
• medical or dietary noncompliance
Cardiosource, 2011
BNP
Cardiosource, 2011
Hospitalized/Acute
I IIa IIb III
Measurement of BNP or NT-proBNP is useful to support
clinical judgment for the diagnosis of acutely
decompensated HF, especially in the setting of
uncertainty for the diagnosis.
I IIa IIb III
Measurement of BNP or NT-proBNP and/or cardiac
troponin is useful for establishing prognosis or disease
severity in acutely decompensated HF.
Ambulatory/Outpatient
I IIa IIb III
In ambulatory patients with dyspnea, measurement of
BNP or N-terminal pro-B-type natriuretic peptide (NTproBNP) is useful to support clinical decision making
regarding the diagnosis of HF, especially in the setting of
clinical uncertainty.
I IIa IIb III
Measurement of BNP or NT-proBNP is useful for
establishing prognosis or disease severity in chronic HF.
Ambulatory/Outpatient (cont.)
I IIa IIb III
BNP- or NT-proBNP guided HF therapy can be useful to
achieve optimal dosing of GDMT in select clinically
euvolemic patients followed in a well-structured HF
disease management program.
I IIa IIb III
I IIa IIb III
The usefulness of serial measurement of BNP or NTproBNP to reduce hospitalization or mortality in patients
with HF is not well established.
Measurement of other clinically available tests such as
biomarkers of myocardial injury or fibrosis may be
considered for additive risk stratification in patients with
chronic HF.
Case Presentation-cont
• Pt received 40mg IV Lasix in the ED and
transferred to telemetry unit
• UOP 1.5 L after 2 hours
• BMP in AM essentially unchanged; Pt started on
40mg Lasix IV bid w/ KCL supplements
• TTE performed
mildly dilated LV ( 5.3cm)
Severe global hypokinesis, EF=25%
- mildly dilated LA
- mild mitral regurgitation
Diuretics in Hospitalized Patients
I IIa IIb III
I IIa IIb III
Patients with HF admitted with evidence of significant fluid
overload should be promptly treated with intravenous loop
diuretics to reduce morbidity.
If patients are already receiving loop diuretic therapy, the
initial intravenous dose should equal or exceed their
chronic oral daily dose and should be given as either
intermittent boluses or continuous infusion. Urine output
and signs and symptoms of congestion should be serially
assessed, and the diuretic dose should be adjusted
accordingly to relieve symptoms, reduce volume excess,
and avoid hypotension.
More than 50% of Patients Have Little or
No Weight Loss During Hospitalization
35
30
24%
Patients (%)
25
Current treatment options
33% • Loop diuretics
• IV inotropes
• Nitrates
• Nesiritide
20
15
10
13%
7%
15%
6%
5
3%
2%
0
(<-20)
(-20 to -15)
(-15 to -10)
(-10 to -5)
(-5 to 0)
Change in Weight (lbs)
Fonarow GC. Rev Cardiovasc Med. 2003;4(suppl 7): 21.
(0 to 5)
(5 to 10)
(>10)
Dosing of diuretics in renal
disease
Cardiosource,2011
Diuretics in Heart Failure
Study Design of DOSE Trial
Acute Heart Failure (1 symptom AND 1 sign)
Home diuretics dose ≥ 80 mg and ≤240 mg furosemide
<24 hours after admission
2x2 factorial randomization
High Dose (2.5x oral)
Continuous infusion
High Dose (2.5x oral)
Q12 IV bolus
Low Dose (1x oral)
Continuous infusion
48 hours
1) Change to oral
2) continue current dose
3) 50% increase in dose
72 hours
Co-Primary endpoints:
Change in creatinine from baseline to 72 hours
PGA VAS area under curve over 72 hours
Low Dose (1 x
oral)
Q12 IV bolus
DOSE Trial
Cardiosource, 2014
Diuretics in Hospitalized Patients (cont.)
I IIa IIb III
I IIa IIb III
The effect of HF treatment should be monitored with
careful measurement of fluid intake and output, vital signs,
body weight that is determined at the same time each day,
and clinical signs and symptoms of systemic perfusion and
congestion. Daily serum electrolytes, urea nitrogen, and
creatinine concentrations should be measured during the
use of intravenous diuretics or active titration of HF
medications.
When diuresis is inadequate to relieve symptoms, it is
reasonable to intensify the diuretic regimen using either:
a. higher doses of intravenous loop diuretics.
b. addition of a second (e.g., thiazide) diuretic.
Noninvasive Cardiac Imaging
I IIa IIb III
Patients with suspected or new-onset HF, or those presenting with acute
decompensated HF, should undergo a chest x-ray to assess heart size and
pulmonary congestion, and to detect alternative cardiac, pulmonary, and
other diseases that may cause or contribute to the patients’ symptoms.
I IIa IIb III
A 2-dimensional echocardiogram with Doppler should be performed during
initial evaluation of patients presenting with HF to assess ventricular
function, size, wall thickness, wall motion, and valve function.
I IIa IIb III
Repeat measurement of EF and measurement of the severity of structural
remodeling are useful to provide information in patients with HF who have
had a significant change in clinical status; who have experienced or
recovered from a clinical event; or who have received treatment, including
GDMT, that might have had a significant effect on cardiac function; or who
may be candidates for device therapy.
Noninvasive Cardiac Imaging (cont.)
I IIa IIb III
Noninvasive imaging to detect myocardial ischemia and
viability is reasonable in patients presenting with de novo
HF who have known CAD and no angina unless the
patient is not eligible for revascularization of any kind.
I IIa IIb III
Viability assessment is reasonable in select situations
when planning revascularization in HF patients with
CAD.
I IIa IIb III
Radionuclide ventriculography or magnetic resonance
imaging can be useful to assess LVEF and volume when
echocardiography is inadequate.
Noninvasive Cardiac Imaging (cont.)
I IIa IIb III
Magnetic resonance imaging is reasonable when
assessing myocardial infiltrative processes or
scar burden.
I IIa IIb III
No Benefit
Routine repeat measurement of LV function
assessment in the absence of clinical status
change or treatment interventions should not be
performed.
Case Presentation
• Mr. S went for LHC on HD #2 which
demonstrated mild non-obstructive CAD;
LVEDP= 20.
• Pt started on carvedilol 3.125mg po bid
and Lisinopril 5mg po daily
• By HD #3, IV Lasix converted to PO
Lasix 40mg daily
• Pt discharged home on HD#4
Causes of Heart Failure in Western World
Most Common Causes of Heart Failure
1. Coronary Artery Disease
2. Hypertension
3. Valvular Heart Disease
4. Cardiomyopathy
Pharmacologic Treatment for Stage C HFrEF
HFrEF Stage C
NYHA Class I – IV
Treatment:
Class I, LOE A
ACEI or ARB AND
Beta Blocker
For all volume overload,
NYHA class II-IV patients
For persistently symptomatic
African Americans,
NYHA class III-IV
For NYHA class II-IV patients.
Provided estimated creatinine
>30 mL/min and K+ <5.0 mEq/dL
Add
Add
Add
Class I, LOE C
Loop Diuretics
Class I, LOE A
Hydral-Nitrates
Class I, LOE A
Aldosterone
Antagonist
Neprilysin Inhibition Potentiates Actions of
Endogenous Vasoactive Peptides That Counter
Maladaptive Mechanisms in Heart Failure
Endogenous
vasoactive peptides
(natriuretic peptides,
adrenomedullin,
bradykinin, substance P,
calcitonin gene-related peptide)
Neprilysin
Inactive metabolites
Neurohormonal
activation
Vascular tone
Cardiac fibrosis,
hypertrophy
Sodium retention
Neprilysin
inhibition
LCZ696: Angiotensin Receptor Neprilysin
Inhibition
LCZ696
Angiotensin
receptor blocker
Inhibition of
neprilysin
PARADIGM-HF: Study Design
Randomization
Single-blind run-in period
Double-blind period
LCZ696 200 mg BID
Enalapril
LCZ696
(1:1 randomization)
10 mg
BID
100 mg
BID
200 mg
BID
Enalapril 10 mg BID
2 weeks
1-2 weeks
2-4 weeks
PARADIGM-HF: Cardiovascular Death or Heart
Failure Hospitalization (Primary Endpoint)
Kaplan-Meier
Estimate of
Cumulative Rates
(%)
4
0
Enalapril
3
2
(n=4212)
914
2
4
LCZ696
(n=4187)
1
6
8
0
0
180
360
540
720
900
1080
1260
896
853
249
236
Days After Randomization
Patients at Risk
LCZ696
Enalapril
1117
4187
4212
3922
3883
3663
3579
3018
2922
2257
2123
1544
1488
Ivabradine
• Specifically binds the Funny
channel
– Reduces the slope for diastolic
depolarization
• Prolongs diastolic duration
• Does not alter…
• Ventricular repolarization
• Myocardial contractility
• Blood pressure
44
Systolic Heart failure treatment with
the If inhibitor ivabradine Trial
Heart rate at baseline influences the effect of
ivabradine on cardiovascular outcomes in chronic
heart failure:
analysis from the SHIFT study
Effect of ivabradine on outcomes in patients with chronic heart failure and HR 75 bpm
Böhm M, Borer J, Ford I, et al. Clin Res Cardiol. 2013;102(1):11-22
www.shift-study.com
Effect of ivabradine on primary outcome
CV death or hospitalization for HF
Patients with primary composite end point (%)
Hazard ratio=0.76
P<0.0001
40
Placebo
30
Ivabradine
20
10
0
0
6
12
18
24
30
Time (months)
Böhm M, Borer J, Ford I, et al. Clin Res Cardiol. 2013;102(1):11-22
www.shift-study.com
Inpatient and Transitions of Care
I IIa IIb III
The use of performance improvement systems
and/or evidence-based systems of care is
recommended in the hospital and early
postdischarge outpatient setting to identify
appropriate HF patients for GDMT, provide
clinicians with useful reminders to advance
GDMT, and to assess the clinical response.
Inpatient and Transitions of Care
I IIa IIb III
Throughout the hospitalization as appropriate, before hospital
discharge, at the first postdischarge visit, and in subsequent
follow-up visits, the following should be addressed:
a. initiation of GDMT if not previously established and not contraindicated;
b. precipitant causes of HF, barriers to optimal care transitions, and
limitations in postdischarge support;
c. assessment of volume status and supine/upright hypotension with
adjustment of HF therapy, as appropriate;
d. titration and optimization of chronic oral HF therapy;
e. assessment of renal function and electrolytes, where appropriate;
f. assessment and management of comorbid conditions;
g. reinforcement of HF education, self-care, emergency plans, and need for
adherence; and
h. consideration for palliative care or hospice care in selected patients.
Inpatient and Transitions of Care
I IIa IIb III
I IIa IIb III
I IIa IIb III
Multidisciplinary HF disease-management programs are
recommended for patients at high risk for hospital readmission,
to facilitate the implementation of GDMT, to address different
barriers to behavioral change, and to reduce the risk of
subsequent rehospitalization for HF.
Scheduling an early follow-up visit (within 7 to 14 days) and
early telephone follow-up (within 3 days) of hospital discharge
is reasonable.
Use of clinical risk prediction tools and/or biomarkers to identify
patients at higher risk for postdischarge clinical events is
reasonable.
Stage C: Nonpharmacological Interventions
I IIa IIb III
Patients with HF should receive specific education to
facilitate HF self-care.
I IIa IIb III
Exercise training (or regular physical activity) is
recommended as safe and effective for patients with HF
who are able to participate to improve functional status.
I IIa IIb III
Sodium restriction is reasonable for patients with
symptomatic HF to reduce congestive symptoms.
Stage C: Nonpharmacological Interventions
(cont.)
I IIa IIb III
I IIa IIb III
Continuous positive airway pressure (CPAP) can be
beneficial to increase LVEF and improve functional
status in patients with HF and sleep apnea.
Cardiac rehabilitation can be useful in clinically stable
patients with HF to improve functional capacity,
exercise duration, HRQOL, and mortality.
Case Presentation-cont
• Patient seen every 2 weeks for 6 weeks in
HF clinic for uptitration of carvedilol and
Lisinopril.
• At week 6 post-discharge, spironolactone
25mg po daily added. BMP check at 5 days
and at 30 days.
• At week 16 post-discharge, patient still with
NYHA class II symptoms. Repeat echo
essentially unchanged with Ef=25-30%.
Device Therapy for Stage C HFrEF
I IIa IIb III
I IIa IIb III
NYHA Class III/IV
I IIa IIb III
NYHA Class II
ICD therapy is recommended for primary prevention of SCD to
reduce total mortality in selected patients with nonischemic DCM
or ischemic heart disease at least 40 days post-MI with LVEF of
35% or less, and NYHA class II or III symptoms on chronic
GDMT, who have reasonable expectation of meaningful survival
for more than 1 year.
CRT is indicated for patients who have LVEF of 35% or less,
sinus rhythm, left bundle-branch block (LBBB) with a QRS
duration of 150 ms or greater, and NYHA class II, III, or
ambulatory IV symptoms on GDMT.
Device Therapy for Stage C HFrEF
(cont.)
I IIa IIb III
CRT is not recommended for patients with NYHA class I or
II symptoms and non-LBBB pattern with a QRS duration of
less than 150 ms.
No Benefit
I IIa IIb III
No Benefit
CRT is not indicated for patients whose comorbidities
and/or frailty limit survival with good functional capacity to
less than 1 year.
Indications for CRT Therapy
Patient with cardiomyopathy on GDMT for >3 mo or on GDMT and >40 d after MI, or
with implantation of pacing or defibrillation device for special indications
LVEF <35%
Evaluate general health status
Comorbidities and/or frailty
limit survival with good
functional capacity to <1 y
Continue GDMT without
implanted device
Acceptable noncardiac health
Evaluate NYHA clinical status
NYHA class I
·
·
·
·
·
·
LVEF ≤30%
QRS ≥150 ms
LBBB pattern
Ischemic
cardiomyopathy
QRS ≤150 ms
Non-LBBB pattern
NYHA class III &
Ambulatory class IV
NYHA class II
·
·
·
·
·
·
·
·
·
·
·
·
·
·
LVEF ≤35%
QRS ≥150 ms
LBBB pattern
Sinus rhythm
LVEF ≤35%
QRS 120-149 ms
LBBB pattern
Sinus rhythm
LVEF ≤35%
QRS ≥150 ms
Non-LBBB pattern
Sinus rhythm
QRS ≤150 ms
Non-LBBB pattern
·
·
·
·
·
·
·
·
·
·
·
·
·
·
·
·
LVEF ≤35%
QRS ≥150 ms
LBBB pattern
Sinus rhythm
LVEF ≤35%
QRS 120-149 ms
LBBB pattern
Sinus rhythm
LVEF≤35%
QRS ≥150 ms
Non-LBBB pattern
Sinus rhythm
LVEF ≤35%
QRS 120-149 ms
Non-LBBB pattern
Sinus rhythm
·
·
Special CRT
Indications
Anticipated to require
frequent ventricular
pacing (>40%)
Atrial fibrillation, if
ventricular pacing is
required and rate
control will result in
near 100%
ventricular pacing
with CRT
Colors correspond to the class of recommendations in the ACCF/AHA Table 1.
Benefit for NYHA class I and II patients has only been shown in CRT-D trials, and while patients may not experience immediate symptomatic benefit, late remodeling may be avoided along
with long-term HF consequences. There are no trials that support CRT-pacing (without ICD) in NYHA class I and II patients. Thus, it is anticipated these patients would receive CRT-D
unless clinical reasons or personal wishes make CRT-pacing more appropriate. In patients who are NYHA class III and ambulatory class IV, CRT-D may be chosen but clinical reasons and
personal wishes may make CRT-pacing appropriate to improve symptoms and quality of life when an ICD is not expected to produce meaningful benefit in survival.
Case Presentation-cont
• Pt receives CRT-D 2 weeks after repeat
echo( which demonstrated EF still 2530% range)
• Pt feels better with more energy for
about 12 months after device implant
• Pt admitted in June 2015 for ADHF
- treated with IV diuretics for 3 days
- Cardiomems implanted HD#4
Cardiosource 2014
TeleHealth in Heart Failure
Why is it Likely to Become Essential?
1. More patients with long-term conditions
–
–
–
More older people
Longer survival with illness
Better primary & secondary prevention
2. More monitoring required
–
–
–
Higher expected standards of care
More things that can be monitored
More treatments that can be monitored
3. Patient preference and convenience
4. Reduced Cost
Telemonitoring
MEMS-based pressure sensor
Device
Implant
Non-Invasive
Home
Monitoring
Structured Telephone Support
Cardiosource, 2014
Clinical Events and Findings Useful for
Identifying Patients With Advanced HF
Repeated (≥2) hospitalizations or ED visits for HF in the past year
Progressive deterioration in renal function (e.g., rise in BUN and creatinine)
Weight loss without other cause (e.g., cardiac cachexia)
Intolerance to ACE inhibitors due to hypotension and/or worsening renal function
Intolerance to beta blockers due to worsening HF or hypotension
Frequent systolic blood pressure <90 mm Hg
Persistent dyspnea with dressing or bathing requiring rest
Inability to walk 1 block on the level ground due to dyspnea or fatigue
Recent need to escalate diuretics to maintain volume status, often reaching daily
furosemide equivalent dose >160 mg/d and/or use of supplemental metolazone therapy
Progressive decline in serum sodium, usually to <133 mEq/L
Frequent ICD shocks
Adapted from Russell et al. Congest Heart Fail. 2008;14:316-21.
Cardiac Transplantation
I IIa IIb III
Evaluation for cardiac transplantation is indicated
for carefully selected patients with stage D HF
despite GDMT, device, and surgical
management.
Mechanical Circulatory Support
I IIa IIb III
MCS use is beneficial in carefully selected* patients with
stage D HFrEF in whom definitive management (e.g.,
cardiac transplantation) or cardiac recovery is anticipated
or planned.
I IIa IIb III
I IIa IIb III
Nondurable MCS, including the use of percutaneous and
extracorporeal ventricular assist devices (VADs), is
reasonable as a “bridge to recovery” or a “bridge to
decision” for carefully selected* patients with HFrEF with
acute, profound hemodynamic compromise.
Durable MCS is reasonable to prolong survival for carefully
selected* patients with stage D HFrEF.
Heart Mate II
 A surgically implanted,
rotary continuous-flow
device in parallel with
the native left ventricle
– Left ventricle to ascending aorta
 Percutaneous driveline
 Electrically powered
– Batteries & line power
 Fixed speed operating
mode
 Home discharge
69
Post-op management
• Aspirin 81mg and coumadin with INR
1.5 to 2.5
• MAP of 70-80mmhg
• Acquired von-Willebrand syndrome- GI
bleeding
• 10% chance of CVA per year