module 3 chapter 1c hypertension and heart failure

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)

20

5

10

15

20

25

30

35

40

45

50

18

128

16

50

RenalFailure

Stroke Enceph MI Angina CHF

MI, myocardial infarction; CHF, chronic heart failure.Perera GA J. Chron Dis. 1955;1:33-42.

Eventrate(%)

CumulativeIncidence

(%)

Cumulative Incidence of Heart Failure by Baseline Hypertension Status

Stage 1

25

20

15

10

5

02 4 6 8 10 12 14 16

Stage 2+Men aged 60-69 y

Normotensive

25

20

15

10

5

02 4 6 8 10 12 14 16

Stage 2+

Stage 1

Women aged 60-69 y

Normotensive

40

CumulativeIncidence

(%)

Time (y)

Levy D et al. JAMA. 1996;275:1557-1562.

Stage 1

Normotensive

Stage 2+30

20

10

02 4 6 8 10 12 14

Women aged 70-79 y

2 4 6 8 10 12 14

Men aged 70-79 yStage 2+

Stage 1

Normotensive

40

30

20

10

0

Population-Attributable Risks for Development of CHF

AP5%DM

6%LVH4%

VHD7%

MI34%

HTN 39%

Men Women

HTN 59%

DM12%

LVH5%

VHD

8%

AP5%

MI12%

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.

Left Ventricular HypertrophyIndependent Predictor of:

– Myocardial infarction– Stroke– Heart Failure– Total Mortality– Sudden Death

0 6 12 18 24 30 36 42 48 54 60

Month

0

1

2

3

4

5

6

7

End

poin

t Rat

e (%

)

CV Death Stratified by Time-Varying Presence of Echo-LVH

LVH AbsentLVH Present

HR=0.34, 95% CI 0.17-0.71P-0.004

Hazard ratios represent risk reduction associated with absence versus presence of LVH

Hypertension: A Major Risk Factor for CHF

Time, decades

Vasan RS, Levy D. Arch Intern Med. 1996;156:1789-1796.

Death

ObesityDiabetes

SmokingDyslipidemia

Systolic Dysfunction

Diastolic Dysfunction

SubclinicalLeft Ventricular

Dysfunction

CHF

Overt HeartFailure

Time, months

Hypertension

LVH

MI

Left VentricularRemodeling

Prevalence of Systolic and Diastolic Dysfunction by Age

Redfield MM et al. JAMA. 2003;289:194-202.

% of Population

0

10

20

30

40

50

EF<50% EF<40%

Diastolic Dysfunction Systolic DysfunctionMild Moderate Severe

45-54

55-64

65-74

>75

ALL

60

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

67%

10%

23%

Women

Normal (55%)

Mildly Reduced(45% - 54%)

Moderately (30-44%) or severely reduced (< 30%)

Kitzman, et. al.Am. J. Cardiol. 87:413-419 (2001)

27%

31%42%

Men

4,842 community-dwelling elderly (>66 yr.) subjects; CHF prevalence 8.8%

80% had normal EF(>45%)

3 Mechanisms1.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 volume-dependent elevation of filling pressures

↑ Vascular Stiffness ↓Vasodilitation Systemic Pulmonary

↑ LV Stiffness ↓Relaxation

LVH, Fibrosis, AGE, Titin, Myocyte Δs

↑ RV Load Rest Exercise

↑ Exertional BP Load → Diastolic Dysf

↓ Systolic Reserve

Atrial Dysfunction Atrial Failure (AF)

Renal Dysfunction Anemia Infection

Obesity

HFPEF

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 HypertensionRegression 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

• P.N.D. OR ORTHOPNOEA

• NECK VEIN DISTENTION

• RALES

• CARDIOMEGALY

• ACUTE PULMONARY EDEMA

• S3 GALLOP

• VENOUS PRESSURE > 16 Cm H2O

• HEPATO JUGULAR REFLEX

MINOR CRITERIA

• ANKLE EDEMA

• NIGHT COUGH

• EXERTIONAL DYSPNOEA

• HEPATOMEGALY

• PLEURAL EFFUSION

• TACHYCARDIA ( > 120 / Min )

SIMULTANEOUS PRESENCE OF2 MAJORS OR I MAJOR AND3 MINORS

(Porth, 2009). Picture retrieved from http://www.starsandseas.com/SAS

%20Physiology/Cardiovascular/Cardiovascular.htm

Goals of therapy

To relieve symptomsTo give good quality of life

To halt the progress of diseaseTo reduce mortality

Patient is happy

Doctor is happy

The ultimate goal is to make both doctor and patient happy

Types of therapy 1I – Mortality reducing drugs

Angiotensin converting enzyme inhibitorBeta blockersAldosterone antagonistsAngiotensin receptor blockersNitrates + Hydralazine

II - Morbidity reducing drugs Diuretics (Loop and Thiazide) Digoxin

III - Metabolically Active Drugs Trimetazidine L-Carnitine Co enzyme Q

IV – Newer, emerging drugsIvabradineOmega 3 fatty acids

Types of therapy 2- Supportive Drugs• Anemia – Iron,Erhythropoitin• Oral anticoagulants• Electrolytes- Na, K correcting drugs• Drugs for Co-MorbidsTypes 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 increase survival

+_ symptomsACEIB.Blockers

Aldosterone antagonists

ARBNitrates +

Hydralazine

MUSTIn all

patients

Doctor feels good

Symptom relieving quality of life providing

drugsDecrease

symptoms- survival

DiureticsDigoxin

More often

symptomatic

patients

Patient

feels good

Metabolically acting drugs? Symptoms

? survival

Trimetazidine

L-CarnitineCo enzyme

Q

Sometimes in

selected patients

Industry

feels good

Newer drugsYet to be proven

IvabradineOmega 3

fatty acids

Individualize

Who will feel

good?

1-4A-D

2-4C,D

Treatment of Hypertension and CVD Outcomes Placebo Controlled Trials

-16-21

-38

-50

-40

-30

-20

-10

0

Heartfailure

Fatal/nonfatalstrokes CVD deaths

Fatal/nonfatalCHD events

Riskreduction

(%)

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.

-52-60

THE VERY ESSENCE OF CARDIOVASCULAR PRACTICE IS THE PREVENTION OF HEART FAILURE

PRACTICE IMPLICATION2013

THE VERY ESSENCE OF CARDIOVASCULAR PRACTICE IS THE EARLY DETECTION OF HEART FAILURE SIR THOMAS LEWIS 1933

CONCLUSION

• THE GREATEST BENEFIT OF TREATING HYPERTENSION IS THE PREVENTION OF HEART FAILURE AND STROKE

END OF MODULE 3 CHAPTER 1C