Cardiology Review:Heart Failure and Valve Disease

March 30, 2009

Dr. Lisa Mielniczuk

Assistant Professor Medicine

University of Ottawa Heart Institute

Outline

• Heart Failure– Causes– Symptoms– Treatments

• Approach to valve disease– Aortic stenosis and regurgitation– Mitral stenosis and regurgitation

Leadership. Knowledge. Community.4

HF Prevalence in Canada

Chow C-M et al. Can J Cardiol 2005;21(14):1265-71.

Leadership. Knowledge. Community.5

Majority of HF Patients Treated by GPs/FPs

Tu K et al. Can J Cardiol 2004;20:282-91.

Why Heart Failure?

Projected number of incident hospitalizations for CHF patients, using high, medium and low population growth projections in Canada 1996-2050

HF Cases are on the rise!

Definition

• Condition where the heart cannot pump an adequate supply of blood at normal filling pressures to meet the metabolic needs of the body

• Clinically– Ventricular dysfunction– Reduced exercise capacity– Impaired quality of life– Shortened life expectancy

Cardiomyopathy

• Characterized by ventricular – Dilatation– Hypertrophy

• Frank Starling: CO = SV x HR

• Laplace: Tension = Press x rad/ 2 x thick

Gross Pathologic Findings

• Enlargement of all 4 chambers

• Normal valves with regurgitation– Enlargement and distortion of the subvalvular

apparatus

• Intracavitary thrombi

Heart Failure

Increased contractility

Normal

Heart Failure

Left ventricular end diastolic pressure (volume)

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Pulmonary congestion

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Classification of Cardiomyopathy

• Multiple ways to consider classification:– Etiologic– Systolic vs. Diastolic– Right vs. Left – Pathologic

General Causes of HF

• Coronary artery disease

• Myocardial infarction

• Valve disease

• Idiopathic cardiomyopathy

• Hypertension

• Myocarditis / pericarditis

• Arrhythmias

• Thyroid disease

• Pregnancy

• Toxins (alchohol, chemotherapy)

Dilated Cardiomyopathy

• CAD is the most common cause of systolic dysfunction

• What are the other non-ischemic causes of a dilated cardiomyopathy?

• Idiopathic (50%)• Familial• Substance abuse

• Myocarditis• Infiltrative disease• Peripartum• HIV• Chemotherapy• Electrolyte imbalance• Nutritional: thiamine,scurvy

Mechanisms and Causes of HF

Left Sided HF

Impaired ContractilityMyocardial infarctionTransient ischemiaChronic volume overload

MR/ARDilated cardiomyopathy

Increased AfterloadASUncontrolled HTN

Systolic Dysfunction

Diastolic Dysfunction

Impaired ventricular relaxationLVHHypertrophic cardiomyopathyRestrictive cardiomyopathyTransient ischemia

Obstruction of LV fillingMSPericardial constriction or tamponade

Mechanisms and Causes of HF

Right Sided HF

Cardiac CausesLeft sided HFPulmonary stenosisRight ventricular infarction

Parenchymal pulmonary diseaseCOPDInterstitial lung diseaseChronic infections Adult respiratory distress syndrome

Pulmonary Vascular DiseasePulmonary emobolismPulmonary HTNRight ventricular infarction

The Heart Failure Continuum

STAGE A•High risk for developing HF (diabetes, CKD, HTN)•No structural disorder of the heart

STAGE B•Structural disorder of the heart (e.g.. Previous MI)•Not yet developed symptoms of HF

STAGE C•Past or current symptoms of HF•Symptoms associated with underlying structural heart disease

STAGE D•End stage disease•Requires specialized treatment strategies

CLASS I•No symptoms and no limitations in physical activity•No shortness of breath when walking, climbing stairs etc.

CLASS II•Mild symptoms and slight limitation during ordinary physical activity

CLASS III•Marked limitation in activity due to symptoms (fatigue, shortness of breath) with less than ordinary activity (e.g.. Short distances or ADL’s)

CLASS IV•Severe limitation, may experience symptoms at rest

NYHA FUNCTIONAL CLASS

ACC/AHA STAGES OF HEART FAILURE

INCREASING SEVERITY OF HEART FAILURE

Functional Classification

Stages of Heart Failure

STAGE A

High risk but no structural heart disease

STAGE B

Structural heart disease but no symptoms

STAGE C

Current or prior symptoms HF

STAGE D

Refractory HF

•HTN, ASCD•DM, obesity•FH•cardiotoxins

•Structural disease plus symptoms

•Previous MI•LVH, low EF•Valvular disease

•Marked symptoms despite maximal meds•hospitalized

Treat HTN, lipidsSmoking cessationACE or ARB if appropriate

Routine: ACE, BB and diureticsSelected: aldo agents, ARBs, dig, nitratesDevices:CRT/ICD

ACE or ARBBB

End of lifeMCStransplant

Diagnosis of HF

• Constellation of symptoms and signs• CXR

• Alternative Methods– Invasive hemodynamic studies– Echocardiogram– Serum BNP testing

Symptoms and Signs of HF

Increased filling pressures

Congestion Poor Perfusion

Poor Cardiac Output

Evaluating the JVP

• Consensus: <2 cm above the sternal angle considred normal and >4cm ASA is abnormal

• http://cal.fmc.flinders.edu.au/gemp/ClinicalSkills/clinskil/year1/cardio/cardio04.htm

Congestion

• Left-Sided– Symptoms

• Dyspnea• Orthopnea• Paroxysmal

nocturnal dyspnea

• Fatigue– Signs

• S3 gallop• Displaced apex• MR• Pulmonary rales• Loud P2

• Right-Sided– Symptoms

• Peripheral edema• Abdominal bloating• Nausea• Anorexia

– Signs• Elevated JVP• Hepatomegaly• Ascites• Edema

Assessing Perfusion

• Symptoms– Fatigue– Confusion– Dyspnea– sweating

• Signs– Hypotension– Tachycardia– Cool extremities– Altered mental status– Rising creatinine– Liver enzyme

abnormalities

Pulmonary Edema

• General Considerations

– Increase in the fluid in the lung – Generally, divided into cardiogenic and non-cardiogenic categories.

• Pathophysiology

– Fluid first accumulates in and around the capillaries in the interlobular septa (typically at a wedge pressure of about 15 mm Hg)

– Further accumulation occurs in the interstitial tissues of the lungs – Finally, with increasing fluid, the alveoli fill with edema fluid (typically

wedge pressure is 25 mm Hg or more)

Cardiogenic vs. Noncardiogenic pulmonary edema

• Cardiogenic pulmonary edema – Heart failure – Coronary artery disease with

left ventricular failure. – Cardiac arrhythmias – Fluid overload -- for example,

kidney failure. – Cardiomyopathy – Obstructing valvular lesions --

for example– Myocarditis and infectious

endocarditis

• Non-cardiogenic pulmonary edema -- due to changes in capillary permeability – Smoke inhalation. – Head trauma – Overwhelming sepsis. – Hypovolemia shock – Acute lung re-expansion– High altitude pulmonary edema – Disseminated intravascular

coagulopathy (DIC) – Near-drowning – Overwhelming aspiration– Acute Respiratory Distress

Syndrome (ARDS)

CXR Findings of Pulmonary Edema

• cardiogenic pulmonary edema • Kerley B lines (septal lines)

– Seen at the lung bases, usually no more than 1 mm thick and 1 cm long, perpendicular to the pleural surface

• Pleural effusions – Usually bilateral, frequently the

right side being larger than the left

– If unilateral, more often on the right

• Fluid in the fissures – Thickening of the major or minor

fissure • Peribronchial cuffing

– Visualization of small doughnut-shaped rings representing fluid in thickened bronchial walls

• Non-cardiogenic pulmonary edema – Bilateral, peripheral air space

disease with air bronchograms or central bat-wing pattern

– Kerley B lines and pleural effusions are uncommon

– Typically occurs 48 hours or more after the initial insult

– Stabilizes at around five days and may take weeks to completely clear

– On CT • Gravity-dependent consolidation

or ground glass opacification • Air bronchograms are common

cuffing

Kerley B

Alveolar edema

Goals of Therapy

• Identify and Treat the Underlying Cause

• Eliminate the acute precipitant

• Manage HF symptoms

• Modulate the neurohormonal response

• Improve long-term survival

Precipitants of HF

• Increased metabolic demands– Fever, anemia, infection, tachycardia, hyperthyroidism, pregnancy

• Increased circulating volume– Excessive salt or fluid in diet– Renal failure

• Increased afterload– Hypertension– PE

• Impaired contractility– Negative inotropes– Ischemia

• Failure to take medications

Progression of Progression of underlying diseaseunderlying disease

Pharmacotherapy

↓cardiac function

vascular resistance

↓renal/tissue perfusion

Neurohormonal changes

Na/fluid accumulation

Peripheral/pulmonary edema

wall stress

norepinephrine

angiotensin II

aldosterone

ANF

+ inotropes

diuretics

vasodilatorsBB

ACE I

sprionolactone

Management Strategy

Severe symptoms: refer to specialist, ER or HF clinic

If EF>40%: treat cause (HTN)

If EF<40%

ACE I +Beta blocker

Titrate to target doses

NYHA III

Prescribe ARB

Clinically stable

Consider nitrates

Continue therapy

•Add ARB

•Digoxin or nitrates

Class IIIb-IV•Combo diuretics

•spironolactone

Education

Risk factor reduction

Fluid/salt regimen

If EF<30% consider ICD

If QRS>120, consider CRT

intolerant

Can J Cardiol 2007; 23

MERIT HF Study

The MERIT-HF Study Group, Lancet 1999; 353:2001

Exner, DV, Dries, DL, Waclawiw, MA, et al. J Am Coll Cardiol 1999; 33:916.

SOLVD-P

US CARVEDILOL TRIAL

CONSENSUS Trial Study Group, N Engl J Med 1987; 316:1429

meta-analysis of five trials involving 12,763 patients

Flather, MD, Yusuf, S, Kober, L, et al. Lancet 2000; 355:1575

Valvular Disease

Mitral Stenosis

• Restriction and narrowing of mitral valve

• Impairment of left ventricular filling

Mitral Stenosis - Causes

• Rheumatic Fever (>90% cases)– 50% patients will have known history– Average 20 years prior to clinical symptoms

• Congenital stenosis of MV

• Extensive calcification

• endocarditis

MS - Pathophysiology

• LA pressure increases – Increased pulmonary

pressures

• LA dilatation– Atrial fibrillation

• Stagnation of blood in LA– thromboembolism

MS - Clinical Presentation

• Natural history variable• 10 year survival (symptoms)

– 50-60%

• Early onset– Dyspnea and reduced exercise capacity

• Advanced– SOB at rest– Pulmonary congestion (orthopnea, PND etc)– Pulmonary HTN (RHF)– Hoarseness from laryngeal nerve compression

MS - Examination

• Loud S1– From high pressure gradient from LA and LV

• Opening snap– Sudden tensing of chordae and stenotic leaflets on

valve opening

• Diastolic murmur– Low frequency– Severity relates to duration

MS - Diagnosis

• ECG– LAE, RVH– Atrial fibrillation

• CXR– LAE, pulmonary vascular

redistribution– Prominent pulmonary

arteries

• Echo– Thickened MV– LAE

MS - Treatment

• Percutaneous balloon valvuloplasty

• Surgical repair

• Antibiotics at time of risk

• Diuretics for vascular congestion

• Decrease HR if AF• anticoagulation

Mitral Regurgitation

• Structural abnormality of mitral valve apparatus resulting in leaking of blood back to LA during systole

MR - Causes

Mitral Annulus•Annular calcification

Leaflets•Rheumatic disease•Endocarditis•Myxomatous disease•prolapse

Chordae Tendinae•Rupture•endocarditis

Papillary muscle•Dysfunction (MI or ischemia)

Left ventricle•Cavity dilatation

MOST COMMON:

MOST COMMON:

Myxomatous degeneration

Myxomatous degeneration

Papillary muscle dysfunction or cavity dilatation

Papillary muscle dysfunction or cavity dilatation

MR - Pathophysiology

• Portion of the LV stroke volume ejected into LA– Forward CO is les than total LV CO

• Elevation of LA volume• Reduction of forward CO• Volume related stress on LV• Severity depends on:

– Size of orifice during regurge– SVR opposing LV blood flow– LA compliance– Duration of regurgitation

MR – Clinical Presentation

• Chronic– Fatigue– If LV contractile dysfunction – heart failure

• Acute– Pulmonary edema– hypotension

MR - Examination

• Murmur– Pansystolic murmur heard at apex

• S3– Reflects increased volume returning to LV in

early diastole

• LV displacement– If LV enlargement present

MR - Diagnosis

• CXR– Pulmonary edema if

acute– Left atrial and ventricular

dilatation– Calcification of MV

• Echo– Identifies structural

cause of MR– LV /LA size and function

MR - Treatment

• Acute MR– Vasodilators and

diuretics– Reduce the resistance

to forward flow– Relieve pulmonary

edema

• Chronic– Operative repair once

symptoms develop or LV starts to dilate

Aortic Stenosis

• Thickened and restricted opening of aortic valve

• Obstruction to LV outflow

AS - Causes

• Age related calcification of valve

• Rheumatic heart disease

• Congenital bicuspid AV

AS - Pathophysiology

• Blood flow across the AV is impeded• Once AVA reduced by 50%:

– Significant LV pressure needed to drive blood into aorta

– Results in LV hypertrophy– Reduced LV compliance

• Increased end diastolic pressure

AS – Clinical Presentation

• Angina– Imbalance b/w myocardial

oxygen supply and demand

• Syncope– Peripheral vasodilation with

inability to augment CO with exercise

• HF– Increased LAP from high

LVEDP– Contractile dysfunction if

longstanding pressure overload

Symptom Median survival

Angina 5 yrs

Syncope 3 years

HF 2 years

AF 6 months

AS -Exam

• Murmur– Late peaking systolic ejection murmur

• Carotid pulse– Weakend (parvus) and delayed (tardus) due

to LV obstruction

• S4– Atrial contraction into stiff LV

AS - Treatment

• Only effective treatment for severe symptomatic disease is surgical correction

• What if asymptomatic?– 20% of patients will progress over 20 years if

mild disease only– Endocarditis prophylaxis

Aortic Regurgitation

AR - Causes

• Abnormalities of valve leaflets– Congenital (bicuspid valves)– Endocarditis– Rheumatic

• Dilatation of aortic root– Aortic aneursym – Aortic dissection– syphilis

AR - Pathophysiology

• Severity of AR– Size of regurgitant orifice– Pressure gradient across valve in diastole– Duration of diastole

• Acute– LV noncompliant– LVEDP rises quickly – pulmonary edema

• Chronic– Chronic volume/pressure overload– Dilates – well compensated

AR – Clinical Manifestations

• SOB on exertion

• Fatigue

• Decreased exercise tolerance

AR - Examination

• Murmur– Blowing diastolic along LSB

• Widened pulse pressure

Name Description

Bisferins Double impulse

Corrigans Marked distention and collapse

deMusset Head bobbing

Duroziez To and fro murmur

Hill Greater popliteal SBP

Muller Uvula pulsations

Quincke Nail bed pulsation

Traube Pistol shot femoral art

AR - Treatment

• Asymptomatic disease progresses very slowly

• Surgery if:– Symptoms– Impaired LV function

• Death occurs within 4 years after angina or 2 years after HF

Summary Slide

• Heart Failure– Understand causes of

systolic and diastolic HF

– Awareness of the presentation of left vs. right HF

– Know treatment priniciples

• Valve Disease– Identify the most

common causes of 4 common valve lesions

– Remember clinical presentations

– Surgery treatment of choice any time symptoms present