Transcript Module 3 chapter 1c - The Association of Physicians of India

MODULE 3 CHAPTER 1C
HYPERTENSION AND HEART
FAILURE
Introduction- Good and Bad news
Good news : Decrease in mortality
Advances in therapy
Evidence based practice
Bad news : Increase in incidence
Advances in therapy
Increase in elderly population
Hypertension and Heart Failure
• Hypertension is the commonest cause of heart
failure (HF)
• Hypertension predisposes to asymptomatic LV
dysfunction,HF with preserved ejection fraction
(HFPEF) as well as HF with reduced ejection
fraction (HFREF)
• One of the most preventable complications from
hypertension management is Heart Failure (HF)
CV Complications of Untreated
Hypertension (N=500)
50
50
45
40
35
Event 30
rate 25
(%) 20
18
15
16
12
8
10
5
2
0
Renal
Failure
Stroke
MI, myocardial infarction; CHF, chronic heart failure.
Perera GA J. Chron Dis. 1955;1:33-42.
Enceph
MI
Angina
CHF
Cumulative Incidence of Heart Failure
by Baseline Hypertension Status
25
Stage 2+
Men aged 60-69 y
Stage 1
20
Normotensive
15
20
Cumulative
15
Incidence
(%)
10
Women aged 60-69 y
Stage 2+
Stage 1
10
5
Normotensive
5
0
2
40
25
4
6
8
0
10 12 14 16
2
40
Men aged 70-79 y
Stage 2+
30
Cumulative
Incidence 20
(%)
Stage 1
Normotensive
10
12
14
Normotensive
2
Time (y)
Levy D et al. JAMA. 1996;275:1557-1562.
Women aged 70-79 y
Stage 1
0
8
10 12 14 16
20
0
6
8
Stage 2+
10
4
6
30
10
2
4
4
6
8
10
12
14
Population-Attributable Risks
for Development of CHF
Women
Men
AP
DM 5%
6%
LVH
4%
VHD
7%
AP
5%
HTN
39%
DM
12%
LVH
5%
VH
D
8%
MI
34%
MI
12%
Population-attributable risk defined as:
(100 x prevalence x [hazard ratio – 1])/(prevalence x [hazard ratio – 1] + 1)
CHF, chronic heart failure; AP, angina pectoris; DM, diabetes mellitus; LVH, left ventricular hypertrophy;
VHD, valvular heart disease; HTN, hypertension; MI, myocardial infarction.
Levy D et al. JAMA. 1996;275:1557-1562.
HTN
59%
Left Ventricular Hypertrophy
Independent Predictor of:
– Myocardial infarction
– Stroke
– Heart Failure
– Total Mortality
– Sudden Death
CV Death Stratified by Time-Varying Presence of Echo-LVH
7
LVH Absent
LVH Present
6
Endpoint Rate (%)
5
HR=0.34, 95% CI 0.17-0.71
P-0.004
4
3
2
1
0
0
6
12
18
24
30
Month
Hazard ratios represent risk reduction associated with absence versus presence of LVH
36
42
48
54
60
Hypertension: A Major Risk Factor for CHF
Obesity
Diabetes
LVH
Diastolic
Dysfunction
Hypertension
CHF
Smoking
Dyslipidemia
MI
Left Ventricular
Remodeling
Systolic
Dysfunction
Subclinical
Left Ventricular
Dysfunction
Time, decades
Vasan RS, Levy D. Arch Intern Med. 1996;156:1789-1796.
Death
Overt Heart
Failure
Time, months
Prevalence of Systolic and Diastolic
Dysfunction by Age
60
45-54
50
55-64
65-74
% of
Population
40
>75
ALL
30
20
10
0
Mild
Moderate
Diastolic Dysfunction
Redfield MM et al. JAMA. 2003;289:194-202.
Severe
EF<50%
EF<40%
Systolic Dysfunction
Heart Failure with Preserved
Ejection Fraction (HF-PEF)
Current Concerts and Treatment
Introduction
• Traditionally HF was thought to be due to systolic function
abnormality shown by EF
• It is now known that about half of cases of HF have
preserved ejection fraction
• Heart failure with a preserved ejection fraction (HFPEF) is
proving to be intriguing with only a few established facts but
many myths.
• Over the past 20 years, significant advances in drug and
device therapy have improved survival in patients with
HFREF, yet evidence-based treatment for reducing
cardiovascular mortality an morbidity in HFPEF is lacking.
Heart Failure with Preserved Ejection
Fraction (HF-PEF)
• HFPEF is defined by heart failure symptoms with a
normal or near-normal EF (>0.50 or 0.45).
• This cut of point does not exclude occult mild systolic
dysfunction. (not normal ejection fraction)
• The term “preserved ejection fraction” is preferred
because ejection fraction is what is commonly
measured for systolic function.
• HF-PEF is often equated with diastolic heart failure but
it is not so simple
Diagnostic Criteria
• Symptoms and signs compatible with heart
failure
• Left ventricular ejection fraction >50%
• LV EDV < 97ml/m2
• Exclusion of severe valvular disease and
pericardial disease
Hunt SA et al. ACC/AHA 2005 Guideline Update for the Diagnosis and Management
of Chronic Heart Failure in the Adult. Circulation 112: e154–e235
Ejection Fraction in Subjects with CHF
in the Cardiovascular Health Study
4,842 community-dwelling elderly (>66 yr.) subjects; CHF prevalence 8.8%
80% had normal EF(>45%)
Men
Women
10%
Normal (55%)
31%
42%
27%
Kitzman, et. al.Am. J. Cardiol. 87:413-419 (2001)
Mildly Reduced
(45% - 54%)
Moderately (30-44%) or
severely reduced (< 30%)
23%
67%
3 Mechanisms
1.An increase in intrinsic myocardial stiffness and
impaired relaxation in diastole result in higher left
atrial pressures to fill adequately
2.Increased systolic ventricular and arterial stiffening—
that is, deranged ventriculoarterial coupling, may
contribute to the pathophysiology of HFPEF
3.Enhanced sensitivity to volume overload from
increased LV remodelling and dilatation with volumedependent elevation of filling pressures
↑ Vascular Stiffness
↓Vasodilitation
Systemic Pulmonary
↑ RV Load
Exercise
Rest
↑ LV Stiffness
↓Relaxation
LVH, Fibrosis, AGE, Titin,
Myocyte Δs
↑ Exertional BP
Load → Diastolic Dysf
↓ Systolic Reserve
Atrial Dysfunction Atrial
Failure (AF)
Renal Dysfunction
Anemia
Infection
Obesity
Ejection fraction
• The misunderstanding of the pathophysiology began
when we defined systolic function solely on the basis of
ejection fraction
• EF DOES NOT REPRESENT WHOLE SYSTOLIC FUNCTION
• Ejection fraction does not take into account systolic
function in the longitudinal axis. A number of studies
have now shown that LV longitudinal function is
reduced not only in diastole but also in systole even
though LV ejection fraction is within normal limits
The exact understanding of mechanisms that
contribute to development of HFPEF is still evolving
• However, the main physiological difference between SHF and HFPEF is the
increase in ventricular volume and change in shape due to ventricular
remodeling.
• Remodeling leads to increased ventricular volumes and reduced ejection
fraction. The rate of occurrence of remodeling is a major differentiating factor.
• For example; A myocardial infarction (or viral myocarditis) appears to be a
potent stimulant for the remodeling process resulting in rapid progression to
SHF compared to Hypertensive heart disease where remodeling is a slower
process. In HHD compensatory increased radial contraction tends to normalize
the ejection fraction however at later stages further remodeling will occur and
the patient will slip from HFPEF to SHF hence DCM in “burnt out”
hypertension.
Echocardiography
Bursi F, et al. JAMA 2006;296:2209-2216.
HF-PEF
Current treatment targets and options
• LV volume & edema:
Diuretics, salt restriction, nitrates
• Rx HTN:
Diuretics, CCB, BB, ACEI, ARB
• Reverse LVH:
ACEI,ARBS
• Prevent ischemia:
BB, CA, nitrates
• Reduce HR, prevent AF:
BB, rate lowering CA, ARB
• Bradycardia:
Atrial Pacing
• Enhance relaxation:
No current treatment
• Prevent vascular events:
ACEI, ARB, BB
ANEMIA,KIDNEY DISEASE,PHT,FLUID OVERLOAD
Control of Hypertension
Regression of LVH is an important therapeutic goal, since it has been
shown to play a significant role in the pathophysiology of HFPEF
Effect of therapy with each of five antihypertensive drug classes on reduction in left ventricular mass in patients
with hypertension. These data represent a meta-analysis of 80 trials of over 4100 patients. The decrease in left
ventricular mass index, adjusted for the duration of therapy and diastolic pressure, was significantly higher with
angiotensin II receptor blockers (13 percent), calcium channel blockers (11 percent), and angiotensin converting
enzyme inhibitors (10 percent) compared to beta blockers (6 percent).
Data from Klingbeil, AU, Schneider, M, Martus, P, et al, Am J Med 2003; 115:41.
HFREF
NYHA
• Cl. I – 1 year – 5% ; 4 year mortality – 19%
• Cl.II / III - 1 year – 15% ; 4 year mortality – 40%
• CL.IV – 6 months – 44%; 12 months 64%
(without ACEI)
FRAMINGHAM CRITERIA : HEART FAILURE
MAJOR CRITERIA
MINOR CRITERIA
•
P.N.D. OR ORTHOPNOEA
•
ANKLE EDEMA
•
NECK VEIN DISTENTION
•
NIGHT COUGH
•
RALES
•
•
EXERTIONAL DYSPNOEA
CARDIOMEGALY
•
ACUTE PULMONARY EDEMA
•
HEPATOMEGALY
•
S3 GALLOP
•
PLEURAL EFFUSION
•
VENOUS PRESSURE > 16 Cm H2O
•
TACHYCARDIA ( > 120 / Min )
•
HEPATO JUGULAR REFLEX
SIMULTANEOUS PRESENCE OF
2 MAJORS OR I MAJOR AND
3 MINORS
(Porth, 2009). Picture retrieved from
http://www.starsandseas.com/SAS%20Physiolog
y/Cardiovascular/Cardiovascular.htm
Goals of therapy
To relieve symptoms
To give good quality of life
To halt the progress of disease
To reduce mortality
Patient is happy
Doctor is happy
The ultimate goal is to make both doctor and patient happy
Types of therapy 1
I – Mortality reducing drugs
Angiotensin converting enzyme inhibitor
Beta blockers
Aldosterone antagonists
Angiotensin receptor blockers
Nitrates + Hydralazine
II - Morbidity reducing drugs
 Diuretics (Loop and Thiazide)
 Digoxin
III - Metabolically Active Drugs
 Trimetazidine
 L-Carnitine
 Co enzyme Q
IV – Newer, emerging drugs
Ivabradine
Omega 3 fatty acids
Types of therapy 2- Supportive Drugs
• Anemia – Iron,Erhythropoitin
• Oral anticoagulants
• Electrolytes- Na, K correcting drugs
• Drugs for Co-Morbids
Types of therapy 3- harmful drugs
• Routine inotropes
• Anti arrhythmics (except B Blockers and
Amiodarone)
• Calcium blockers ( non DHP)
• High dose Digoxin
MANAGEMENT: GENERAL MEASURES
•
•
•
•
•
•
•
•
•
Correctable causes
Daily weighing – Report if >2kgs in 1-3 days
Self management of diuretics
Compliance with medication
Regular exercise
Stop smoking, Alcohol
Salt , fluid management- careful in summer,powercuts
Vaccination
Warning about other drugs (NSAIDS,VIT E, ALTERNATIVE
MEDICINES)
• Treating precipitating factors of HF
Precipitating causes of Heart Failure
•
•
•
•
•
•
•
•
•
Anemia,arrhythmia, alcohol
Beri beri
Cardiac toxins
Drugs – NSAIDS,Glitazones,Steroids
Exercise – severe, emotion, embolism
Fever
Goitre
Hypertension, hypoxia
Infections , iatrogenic, iv fluids
SUMMARY
Disease Modifying mortality
reducing drugs
Symptom relieving quality of
life providing drugs
Metabolically
acting drugs
Newer drugs
increase survival
Decrease symptoms
? Symptoms
Yet to be proven
+_ symptoms
- survival
? survival
ACEI
B.Blockers
Diuretics
Aldosterone antagonists
Digoxin
Trimetazidine
Ivabradine
L-Carnitine
Omega 3 fatty
acids
Co enzyme Q
ARB
Nitrates + Hydralazine
More often
symptomatic
patients
MUST
In all
patients
Individualize
Industry
feels good
Who will feel
good?
1-4
A-D
Patient feels
good
Doctor feels
good
2-4
C,D
Sometimes in
selected
patients
Treatment of Hypertension and CVD Outcomes
Placebo Controlled Trials
0
Heart
failure
Fatal/nonfatal
Fatal/nonfatal
strokes
CVD deaths CHD events
-10
-20
Risk
reduction
(%)
-16
-21
-30
-40
-38
-50
-60
-52
17 randomized, placebo-controlled trials (48,000 subjects)—14 diuretic and 3 beta blocker based trials.
All differences are statistically significant.
CVD, cardiovascular disease; CHD, coronary heart disease.
Herbert PR et al. Arch Intern Med. 1993;153:578-581.
Moser M, Herbert PR. J Am Coll Cardiol. 1996;27:1214-1218.
THE VERY ESSENCE OF CARDIOVASCULAR
PRACTICE IS THE EARLY DETECTION OF
HEART FAILURE
SIR THOMAS LEWIS 1933
THE VERY ESSENCE OF
CARDIOVASCULAR PRACTICE IS THE
PREVENTION OF HEART FAILURE
PRACTICE IMPLICATION
2013
CONCLUSION
• THE GREATEST BENEFIT OF
TREATING HYPERTENSION IS THE
PREVENTION OF HEART FAILURE
AND STROKE
END OF MODULE 3 CHAPTER 1C