Current Approaches to the Diagnosis & Management of Heart ...€¦ · Diagnosis of Heart Failure...

transcript

Current Approaches to the

Diagnosis & Management of

Heart Failure

J. Bradley Gibson, D.O.

Cardiology Specialists of Dayton

Which of the Following have been considered

therapies for advanced heart failure refractory to

medical therapy?

A. B. C. D. E.

20% 20% 20%20%20%

A. Heart Transplantaion

B. Ventricular Assist Device Placement

C. Biventricular Pacing

D. Ventricular Reduction Surgery

E. All of the Above

Countdown

Introduction

• The rapidly increasing prevalence and

economic burden of HF represents a

worldwide epidemic and one of the most

important current public health concerns in

cardiovascular medicine today.

Introduction

• The mainstay of HF therapy today remains

reactive treatment for established and

symptomatic disease.

• However, the burden of HF on our society

will continue to grow until effective primary

and secondary prevention strategies are

adopted and employed, as well as

increased awareness of lifestyle choices

that can modify risk factors for developing

Epidemiology

• According to the AHA Heart Disease and

Stroke Statistics-2011 Update, HF affects

approximately 5.7 million Americans, with

the incidence of 670,000 new HF cases in

those ≥45 years of age.

• The prevalence of HF increases by age,

and is more common in men than in

women in those > 40 and <80 years of

Women vs. Men

• Although the incidence of HF is lower, in

general, for women than men, women

comprise about half of the HF burden due

to their longer life expectancy.

• Based on the increasing age of the United

States population and improved survival,

it is projected that an estimated 772,000

new HF cases will be observed in the

year 2040.

Distribution of Types of Heart

Failure

• It is important to recognize that the syndrome of HF includes not only HF with systolic dysfunction, but the increasingly recognized entity of HF with preserved ejection fraction (HFpEF).

• Multiple epidemiological studies have demonstrated that the prevalence of HFpEF is in the range of 50-55%, and is largely predominate in the elderly population.

• Furthermore, HFpEF is more common in women than men in all age groups.

Mortality

• From 1968 to the early 1990s, HF has

increased at least fourfold as the primary

cause of death.

• The degree of HF signs and symptoms

remains the most dismal prognosis for

patients with HF.

• The 10-year survival for patients with

symptomatic HF remains only 20%, with a

median survival of 1.7 years for men and

3.2 years for women.

Hospitalization and Readmission Rates

• HF is the primary reason for 12-15 million

office visits and 6.5 million hospital days

annually.

• According to the Centers for Medicare and

Medicaid Services 2008 statistical report,

HF represents America's largest

diagnosis-related group (DRG) coding

• Readmissions for HF remain disturbingly

common, with significant quality of life and

economic repercussions.

Economic Impact

• More Medicare dollars are spent on HF than on any

other diagnosis.

• An analysis of six countries revealed that 1-2% of

total health care expenditures was for HF, and

approximately 70% was consumed for hospital

costs.

Risk Factors for HF

• The many risk factors for HF may best be

represented by the population attributable

risk (PAR), which may be derived from

large population-based studies, such as

the Framingham and Olmsted County

cohorts.

• PAR takes into account both the hazard

ratio (HR) and the prevalence of the

predisposing condition in a given

population.

•Among the numerous risk factors for HF, the common ones include CAD, hypertension, renal dysfunction,

older age, diabetes mellitus, and obesity, which represent important targets for HF prevention initiatives.

Age and HF

• Increasing age has been consistently shown to be a risk factor for the development of HF and correlates strongly with increasing HF incidence and prevalence.

• The most precipitous rise in HF incidence in recent years has been in individuals >75 years of age.

• Furthermore, these elderly patients generally have three or more comorbid conditions that increase their morbidity and mortality substantially.

CAD and HF • In developed countries today, CAD accounts for

60-75% of all symptomatic HF cases, with a history

of prior MI associated with a fivefold increased

incidence of HF over a 5-year period.

Hypertension and HF

• The incidence of HF can be stratified based on

severity of hypertension.

• The lifetime risk of developing HF doubles if blood

pressure is >160/90 mm Hg compared with those

with a blood pressure of <140/90 mm Hg.

Staging of Heart Failure

• This is the basis of the staging concept of

HF, as outlined in the American College of

Cardiology Foundation/American Heart

Association (ACCF/AHA) 2009 Focused

Update of the 2005 Guidelines for the

Diagnosis and Management of Heart

Failure in Adults.

Mechanisms of Heart Failure

• Myocardial contraction and relaxation are mediated by

interaction of the proteins that compose the thick and thin

filaments of the sarcomere.

• The troponins are also found in the thin filament. They serve

both structural and regulatory functions that facilitate actin and

myosin interaction.

The Length-Tension Relationship (Frank-

Starling Mechanism)

• Increases in end-diastolic volume lead to stretch of ventricular

myocytes and increased tension generation leading to stronger

contraction. This allows the heart to increase stroke volume

when there is increased venous return.

• However, increasing chamber volume beyond a certain point

does not result in further increases, but rather in decreases in

tension generation.

Heart Failure With Reduced Ejection Fraction

• HF is the clinical syndrome that results

from structural or functional abnormalities

that impair the ability of the heart to fill with

or eject blood.

• All forms of cardiac disease can lead to

heart failure with reduced ejection fraction

(HFREF).

• HFREF typically progresses gradually from

asymptomatic LV systolic dysfunction to a

symptomatic state characterized by

dyspnea, fatigue, and volume overload.

The Role of Neurohormones in Heart Failure

• The earliest response to decreased

cardiac output is activation of the

sympathetic nervous system (SNS).

The Role of Neurohormones in Heart Failure

• While initial effects of SNS activation may be

beneficial by augmenting cardiac output,

unopposed sustained SNS activity has deleterious

effects on the myocardium.

– SNS activity increases MVO2 in circumstances in

which there is negative oxygen balance (greater

demand than supply) such as ischemia and pressure

or volume overload with increased wall stress.

– Sustained SNS activation causes downregulation

and uncoupling of beta-1 adrenergic receptors, which

desensitizes the myocardium to the effects of

norepinephrine.

– Persistent activation of the sympathetic nervous and

RAAS after myocardial injury promotes ventricular

remodeling.

Heart Failure With Preserved Ejection Fraction

• Heart failure with preserved ejection

fraction (HFPEF) is a complex and

multifactorial disorder characterized by

exercise intolerance, resulting from

elevated cardiac filling pressures due to

slow and incomplete ventricular relaxation

and increased chamber and arterial

stiffness.

– It affects primarily elderly patients, and is

particularly prevalent in women, and people

with hypertension, diabetes, and obesity.

Heart Failure With Preserved Ejection Fraction

• In addition to diastolic abnormalities, individuals

with HFPEF have increased myocardial systolic

stiffness, reduced contractile reserve, and show

dramatic blood pressure changes in response to

relatively small changes in afterload.

• These changes result in objectively impaired

cardiopulmonary performance.

• The principal pathologic mechanism considered to

produce symptoms in HFpEF is diastolic

dysfunction, characterized by elevated “passive”

chamber stiffness and/or delayed myocardial

relaxation during early diastole

Prognosis

• Despite advances in pharmacological and device therapies,

heart failure is still associated with a particularly poor prognosis.

• A number of individual risk factors are associated with worse

prognosis

Prognosis

• A number of studies have been performed to help develop predictive models of prognosis in heart failure.

• The two most commonly utilized models are the Heart Failure Survival Score (HFSS) and the Seattle Heart Failure Model (SHFM).

• They allow physicians to discuss prognostic information with individual patients and aid in decision-making with regard to the need for transplant or mechanical circulatory support in heart failure patients.

Heart Failure Survival Score (HFSS)

• Patients are subsequently stratified into low, medium, and high risk.

• These strata correlate to 1-year survival rates of 88%, 60%, and 35%, respectively.

• Thus, those considered medium and high risk might be considered for advanced therapeutic interventions (e.g., heart transplantation).

Seattle Heart Failure Model

• The SHFM is another prospectively validated scoring system that was studied in a much broader patient population than the HFSS.

• The model was validated in multiple studies (totaling nearly 10,000 patients), and it estimates 1-, 2-, and 5-year survival across many diverse populations.

• The model also allows the clinician to add or subtract an assortment of treatment regimens, including medical therapies and devices, to assess how these changes affect mortality.

Seattle Heart Failure Model

• There is a simple, free, online score

calculator that is readily accessible to most

clinicians

• http://depts.washington.edu/shfm/

Prognosis

• The early recognition of subclinical heart failure (Stage B) and at-risk populations (Stage A) represents an opportunity for clinicians to intervene before the development of significant heart failure morbidity and mortality.

• Improved understanding of the prognostic implications of a wide range of variables will assist clinicians in determining which patients truly warrant advanced therapeutics (e.g., transplantation, ventricular assist device).

Establishing the Diagnosis

• The clinical diagnosis of heart failure is often challenging because of the nonspecific nature of the presenting symptoms.

• It is common for patients to receive multiple courses of antibiotics for suspected pneumonia, or to receive bronchodilators for suspected asthma or chronic obstructive pulmonary disease (COPD) before the accurate diagnosis of heart failure is established.

• In other cases, many patients with lower extremity edema are falsely assumed to have heart failure, when in fact there may be an underlying nephrotic syndrome, cirrhosis, chronic venous stasis, or an adverse medication effect (e.g., with calcium channel blockers).

History

• Most symptoms in patients presenting with

heart failure are related to elevated filling

pressures.

• Dyspnea is the most common symptom

and can be abrupt in onset (e.g., acute

pulmonary edema) or may present with

subtle progression with lessening activity.

• It may occur with exertion, at rest, or in the

recumbent position (orthopnea and

paroxysmal nocturnal dyspnea).

History

• Other common symptoms of congestion

relate to the manifestations of tissue

edema.

• Swelling in the lower extremities, abdomen

(ascites), and scrotum are common.

• The presence of nausea/vomiting, early

satiety, or right upper quadrant discomfort

suggests hepatic congestion and can

mimic a variety of other clinical

presentations (e.g., gastritis, hepatitis,

biliary disease).

Echocardiography

• Echocardiography provides extensive

information about the etiology and severity

of heart failure and enables an accurate

assessment of chamber dimensions,

biventricular function, valvular

stenosis/regurgitation, and filling

pressures/patterns (diastolic function).

Cardiac Magnetic Resonance Imaging

• The clinical utility of cardiac magnetic

resonance imaging (cMRI) continues to

expand. In addition to providing

remarkable anatomic detail, cMRI allows

accurate assessment of biventricular

function, quantitation of valvular

regurgitation and/or stenosis, tissue

characterization, and assessment of both

microvascular and epicardial perfusion.

Diagnosis of Heart Failure With Preserved

Ejection Fraction

• Whereas the diagnosis of heart failure with

reduced EF can be made readily through

echocardiography in symptomatic patients,

the diagnosis of heart failure with

preserved EF is more difficult.

• Current data suggest that nearly 50% of

patients with heart failure have preserved

EF. Despite having preserved systolic

function, the prognosis of patients with

HFpEF mirrors that of HFrEF, with similar

mortality rates.

Diagnosis of Heart Failure With Preserved

Ejection Fraction

• Multiple diagnostic criteria have been proposed to define HFpEF; they all generally include the presence of signs and symptoms of heart failure in the setting of preserved EF, when other etiologies have been ruled out (e.g., valvular heart disease, infiltrative diseases).

• A sample algorithm developed by the Heart Failure and Echocardiography Societies of the European Society of Cardiology is available.

Staging of Heart Failure

• In 2005, the American College of Cardiology/American Heart Association (ACC/AHA) heart failure guideline writing committee developed a new staging system for heart failure with the purpose of highlighting that heart failure is a spectrum ranging from asymptomatic patients with risk factors to end-stage disease requiring advanced therapeutics.

• By categorizing patients into one of four categories, the clinician can appropriately tailor recommended therapies.

• The first two stages (A and B) comprise asymptomatic patients.

Stage A is the new target

• Stage A includes only patients with risk

factors for the development of heart failure

• Current estimates suggest that this group

represents as much as 22% of the general

population older than 45 years

• Early preventive strategies targeting this

population could have a significant global

impact.

Stage B

• Stage B includes patients with evidence of

structural heart disease in the absence of

symptoms.

• Early appropriate therapies such as the

use of beta-blockers and ACE inhibitors in

patients with asymptomatic low EF

reduces mortality and delays the

development of symptomatic disease.

Medical Therapy for HF

• Over the past two decades, medical therapy for HF has transformed from focusing on symptom management and palliation to improving natural history, reducing adverse outcomes, and improving survival.

• Much of this advance has centered on approaches that inhibit neurohormonal activation, particularly the adrenergic nervous system and renin-angiotensin-aldosterone axis, in patients with HF and reduced left ventricular ejection fraction.

ACE Inhibitors

• Multiple clinical trials have demonstrated the ability

of ACE inhibitors to reduce mortality and HF

hospitalizations in patients with reduced LVEF.

ACE Inhibitors

• ACE inhibitors were the first agents shown

to reduce the rate of progression of LV

remodeling, as evidenced by diminishing

or preventing the progressive LV dilation

observed in patients following large MIs,

and in those with reduced LVEF and LV

dilation treated with placebo.

• ACE inhibitors also been demonstrated to

prevent recurrent MIs.

ACE Inhibitors

• The American College of Cardiology

Foundation/American Heart Association

(ACCF/AHA) 2009 Focused Update of the

2005 Guidelines for the Diagnosis and

Management of Heart Failure in Adults, as

well as the Heart Failure Society of

America (HFSA) 2010 comprehensive

heart failure practice guideline both

recommend the routine use of ACE

inhibitors in symptomatic and

asymptomatic patients with HF and LVEF

≤40%.

ACE Inhibitors

• Intolerance due to cough represents an indication to switch to an angiotensin-receptor blocker (ARB).

• Intolerance due to hyperkalemia, hypotension, or renal insufficiency, which does not respond adequately to dose reduction, is likely to be replicated by an ARB, and warrants consideration of switching to the combination of hydralazine and isosorbide dinitrate (ISDN).

• Development of angioedema warrants immediate discontinuation of the ACE inhibitor.

Beta Blockers

• Beta-adrenergic blocking agents, long

considered contraindicated in patients with

HF on the grounds that increased

adrenergic tone represented an

appropriate compensatory mechanism in

this condition, were originally purported to

have salutary effects based on

observational studies in patients with

dilated cardiomyopathy in the 1970s.

Beta Blockers

• The mechanistic basis for those

investigations lay in the assumption that,

despite supporting blood pressure and

cardiac output in patients with HF, chronic,

sustained cardiac adrenergic stimulation

accelerated the progression of myocardial

pathology, as well as being proischemic

and proarrhythmic.

Beta Blockers

• More than any other class of agents, beta-

blockers reduce and even reverse the

progression of LV remodeling, as gauged

by the longitudinal assessment of LV

volumes.

• Based on the COMET and MERTIT-HF

studies, the 2 most appropriate beta

blockers for heart failure are Coreg

(Carvedilol) and Toprol XL (Metoprolol

Succinate).

Angiotensin-Receptor Blockers

• Comprehensive heart failure practice guidelines recommend ARBs as first-line therapy for symptomatic and asymptomatic patients with HF and LVEF ≤40% who are intolerant for reasons other than hyperkalemia or renal insufficiency.

• ARBs are also considered reasonable alternatives to ACE inhibitors as first-line therapy for patients with mild to moderate HF and reduced LVEF, especially in those patients already receiving ARBs for other indications.

Hydralazine-Isosorbide Dinitrate

• The combination of hydralazine and ISDN was first investigated in the V-HeFT trial, comparing this regimen with prazosin and with placebo.

• With the subsequent V-HeFT-2 (Valsartan Heart Failure Trial-2) study, which demonstrated superiority of enalapril over hydralazine/ISDN, the latter combination became incorporated into clinical recommendations as an alternative to ACE inhibitors when ACE inhibitors were considered contraindicated or were not tolerated.

• Post-hoc subset analyses of V-HeFT data

suggested preferential benefit for

hydralazine/ISDN among African-

American patients.

• Clinical adoption of the hydralazine/ISDN

combination has been much lower than

that of other HF treatments, perhaps in

part by the requirement for three times

daily dosing and, in part, by the adverse

effects.

• Comprehensive heart failure practice guidelines recommend hydralazine/ISDN to improve outcomes in African Americans with moderate to severe HF symptoms and reduced LVEF or LV dilation, on top of optimal ACE inhibitor/ARB, beta-blocker, and diuretic treatment.

• This combination is considered "reasonable" (though not firmly evidence-based) for non-African Americans with persistent symptoms despite standard treatment and for those intolerant of ACE inhibitors or ARBs.

Aldosterone-Receptor Blockers

• Circulating levels of aldosterone are

markedly increased in patients with HF.

• ACE inhibition and angiotensin-receptor

blockade diminish, but do not abolish,

aldosterone secretion, which tends to

"escape" over time following institution of

renin-angiotensin system inhibition.

• Comprehensive heart failure practice guidelines recommend aldosterone-receptor blockers for patients with HF (NYHA class IV or class III with prior class IV symptoms) and LVEF ≤35% and consideration of this therapy in patients post-MI with clinical HF and LVEF <40%.

• This therapy is not recommended for patients with serum creatinine >2.5 mg/dl (or estimated glomerular filtration rate of <30 ml/min) or serum potassium >5.0 mmol/L, or in those receiving other potassium-sparing diuretics.

• The principal side effect of aldosterone-

receptor blockers is hyperkalemia.

Gynecomastia is an additional side effect

with spironolactone, reported in

approximately 9% of men.

Digoxin

• Digoxin, an age-old remedy for HF, and a

long-time mainstay of its treatment

regimen, is now far from universally-

prescribed, yet remains an effective form

of therapy.

• Clinical trial evidence supports the efficacy

of digoxin, although this evidence falls

short of that available for ACE inhibitors,

ARBs, beta-blockers, and aldosterone-

receptor blockers.

Digoxin

• Comprehensive heart failure practice guidelines recommend consideration of the addition of digoxin to standard therapy for patients with LVEF ≤40% who have current or prior HF symptoms and who are receiving standard therapy, to improve symptoms and reduce HF hospitalizations.

• Dosing should be based on lean body mass, renal function, and concomitant medications. The majority of patients should be treated with 0.125 mg daily, targeting a level <1.0 ng/ml.

Digoxin

Diuretics

• Diuretics are a mainstay of treatment for

patients with HF and evidence of volume

overload.

• Although thiazide diuretics alone may be

considered in patients with minimal fluid

excess, the vast majority of patients are

better-treated with loop diuretics, such as

furosemide, bumetanide, or torsemide.

Diuretics

• Treatment approaches to refractoriness to

loop diuretics include increased dose,

dividing into multiple daily doses, switching

from furosemide to torsemide, and adding

a thiazide diuretic, such as chorthiazides

or metolazone (recognizing the greater

potential for electrolyte perturbation with

daily metolazone use).

Key Points

• In general, all patients with HF and

reduced LVEF should have ACE inhibitors

and beta-blockers instituted and titrated to

the target doses used in clinical trials.

• ARBs should be prescribed in the event of

ACE inhibitor intolerance due to cough or

angioedema. ARBs do not provide any

particular benefit over ACE inhibitors if

cardiorenal limitations (e.g., hypotension,

renal insufficiency, hyperkalemia) are the

reason for ACE inhibitor intolerance.

Key Points

• Digoxin may have symptomatic benefits in

patients with HF, but effective serum levels

rarely require doses >0.125 mg daily.

• Diuretics should be used in the lowest

doses tolerated to maintain a stable

compensated volume status.

• Aldosterone antagonists should be

considered in patients with symptomatic

HF, as long as serum creatinine is <2.5

mg/dl and potassium levels are <5.0

mEq/dl.

Key Points

• Hydralazine and ISDN in combination

should be considered, particularly in

African-American populations, if advanced

symptoms (e.g., HF of NYHA class III-IV)

persist.

• To avoid complications of polypharmacy,

close, frequent surveillance of symptoms,

clinical status, and laboratories is required.

LV RemodelingLV Remodeling

•• ACE InhibitorsACE Inhibitors

•• ARBsARBs

•• Beta BlockersBeta Blockers

SurvivalSurvival

•• HydralazineHydralazine//IsordilIsordil

•• AldactoneAldactone (Class II(Class II--IV)IV)

SymptomsSymptoms

•• DiureticsDiuretics

•• DigoxinDigoxin

•• ARBsARBs

Advanced Therapies

• Recent studies have demonstrated that more than 6 million people are living with HF and that >1 million hospitalizations occur for a primary diagnosis of HF each year in the United States.

• Most HF-related hospitalizations and deaths occur in a subgroup of patients who are refractory to guideline-based medical management, a group commonly categorized as having advanced HF.

• Studies have estimated that >200,000 Americans are living with end-stage HF, with a 1-year mortality rate of 70-90%.

Advanced Therapies

• Beyond evidence-based medications,

device therapy in the form of defibrillators

(e.g., implantable cardioverter-defibrillators

[ICDs]) and cardiac resynchronization

therapy have demonstrated clear mortality

benefits in patients with advanced HF.

• Referral of patients with refractory HF to a

HF program with the expertise in the

management of end-stage HF may also be

useful.

Heart Transplantation

• Within years of the first human heart

transplantation performed in South Africa

by Christiaan Barnard in 1967, enthusiasm

for the procedure waned, as few patients

survived even 1 year after surgery.

• Currently, with the 1-year survival rate

approaching 90%, the 5-year survival rate

of 70%, and the 10-year survival rate of

50%, heart transplantation is established

as a valuable option for acceptable

patients with advanced HF.

• Determination of transplantation candidacy

requires that two basic questions be

answered: 1) Is the patient sick enough

that the prognosis would benefit

significantly from heart transplantation?

and 2) Is there some characteristic of this

particular patient that would make a poor

transplant outcome?

Causes of Death in Heart Transplantation

• The causes of death are dependent on the time

period after transplantation.

CAV=Cardiac Allograft Vasculopathy

Transplant Centers in Ohio

• Childrens Hospital Medical Center

Cincinnati – Transplant

• The Cleveland Clinic Foundation

• Nationwide Children’s Hospital

• The Ohio State University Medical Center

Mechanical Circulatory Support

• While heart transplantation has become

the accepted form of treatment for

selected patients with end-stage HF,

limited donor hearts dictate that

transplantation is a treatment for a minority

of these patients.

• MCS has attracted increased interest as

an option for patients waiting for transplant

(bridge to transplant [BTT]) and for

patients who are not transplant candidates

(destination therapy [DT]).

Mechanical Circulatory Support

• Incremental improvements in the design of

LVADs and management of patients with

MCS have made its wider use a reality.

• VADs can be divided into two main

categories: 1) pulsatile-flow pumps, and 2)

continuous-flow pumps.

• Currently used pulsatile-flow LVADs

include the Thoratec HeartMate XVE and

Thoratec IVAD.

• Currently, the FDA has approved the use

of the Thoratec HeartMate II (axial-flow

pump) and the MicroMedDeBakey VAD

(axial-flow pump, approved by the FDA for

use in children).

Bridge to Transplantation

• Both of the following criteria must be fulfilled in order for Medicare coverage to be provided for a VAD used as a BTT: 1) The patient is approved and listed as a candidate for heart transplantation by a Medicare-approved heart transplant center, and 2) the implanting site, if different than the Medicare-approved transplant center, must receive written permission from the Medicare-approved heart transplant center under which the patient is listed prior to implantation of the VAD.

Destination Therapy

• The current criteria established by the

CMS for DT include: 1) NYHA functional

class IV symptoms in patients ineligible for

heart transplantation; 2) failure to respond

to optimal medical therapy for at least 45

of the last 60 days, or being balloon pump

dependent for 7 days, or intravenous-

inotrope dependent for 14 days; 3) LVEF

<25%; and 4) demonstrated function

limitation with a peak oxygen consumption

of 14 ml/kg/min.

• Patients are at risk for development of von

Willebrand syndrome type 2, so assessment for

bleeding risk and bleeding history prior to surgery is

mandatory.

• Oral anticoagulation and antiplatelet therapy are

necessary for patients undergoing LVAD

placement, due to the potential for thrombus

formation in the device and subsequent risk for

thromboembolic complications. Data from the

second INTERMACS annual report demonstrate

that stroke (14.1%) and bleeding (6.7%) are

accountable for more than one-fifth of the deaths

that occur after MCS surgery.

Infection

• Infection accounts for 15% of the deaths in

patients on LVAD therapy, the

transcutaneous drive line increases the

likelihood that bacteria will enter the body,

and the position of the mechanical pump

hardware makes it difficult to successfully

treat a device infection. Patients with an

infection on LVAD support have

significantly prolonged hospital stays and

tend to have a higher risk of mortality.

Ventricular Reduction Surgery

• In the setting of ischemic heart disease, ventricular reconstruction in the form of endoventricular patch plasty repair, as described by Dor, has generated a great deal of recent interest.

• Initial series demonstrated that surgical ventricular reconstruction was associated with reduced ventricular volumes, increased EF, and improved ventricular function.

• A substudy of the STICH (Surgical Treatment for Ischemic Heart Failure) trial showed no benefits demonstrated with respect to symptoms, exercise tolerance, hospitalizations, or deaths.

Biventricular Pacing (Cardiac

Resynchronization Therapy)

• As Ventricular dilation and LV function worsens, conduction often worsens.

• Many patient develop conduction delay and Bundle Branch Blocks.

• Biventricular pacing improves LV contraction by ensuring a delayed yet synchronous contraction and thereby improving intraventricular synchrony.

• Improved synchrony results in more effective systolic function, and therefore, improvement in EF, stroke volume, and cardiac output.

The LV lead

• The implantation of an LV lead is most often performed transvenously into a branch vessel of the coronary sinus.

• In approximately 7% of cases, transvenous LV lead implantation is unsuccessful. This may be due to patient anatomy, inability to access the coronary sinus, inadequate target vessels, high capture threshold, or phrenic nerve stimulation. In these cases, the patient can consider epicardial lead placement via surgical approach.

• CRT improves mortality, hospitalizations,

and reverse remodeling in HF with systolic

dysfunction and wide QRS.

• Two thirds of appropriately selected

patients respond to CRT.

• Recently, evidence has supported the use

of CRT in mild HF as well as moderate to

severe HF.

Key points on Advanced Therapies

• Consideration of advanced HF therapies

should be entertained when either HF

symptoms become refractory to

conventional medical, surgical, and device

interventions or when end-organ

dysfunction becomes apparent.

• Heart transplantation is the treatment of

choice for end-stage HF, but remains

limited by donor organs and comorbidities

in potential candidates.

• Survival following heart transplantation is >85% at 1 year, 70% at 5 years, and 50% at 10 years.

• Complications following transplantation include rejection, infection, renal insufficiency, malignancy, and cardiac allograft vasculopathy.

• The continuous flow LVAD is now an established therapeutic option as a permanent solution for advanced HF, as well as a "bridge" to transplantation, myocardial recovery, and/or further consideration of long-term options (e.g., "bridge to decision").

• Myocardial recovery after VAD support

remains uncommon, but will likely evolve

over time as VAD support will be used as

a platform for direct myocardial therapies.

• Current evidence does not support

surgical ventricular remodeling or mitral

valve repair for most patients with severe

systolic HF.

Which of the Following have been considered

therapies for advanced heart failure refractory

to medical therapy?

A. B. C. D. E.

20% 20% 20%20%20%A. Heart Transplantation

B. Ventricular Assist

Device Placement

C. Biventricular Pacing

D. Ventricular Reduction

Surgery

E. All of the Above

Countdown

Which of the Following have been considered therapies

for advanced heart failure refractory to me...

Ventricular Assist Device

Placement

Biventricular Pacing

Ventricular Reduction

Surgery

All of the Above

First Slide Second Slide

Questions?

References 1. Hunt SA, Abraham WT, Chin MH, et al. 2009 focused update incorporated into the ACC/AHA 2005 Guidelines for the

Diagnosis and Management of Heart Failure in Adults: a report of the American College of Cardiology Foundation/American

Heart Association Task Force on Practice Guidelines: developed in collaboration with the International Society for Heart and

Lung Transplantation. J Am Coll Cardiol 2009;53:e1-e90.

2. Roger VL, Go AS, Lloyd-Jones DM, et al., on behalf of the American Heart Association Statistics Committee and Stroke

Statistics Subcommittee. Heart disease and stroke statistics--2011 update: a report from the American Heart Association.

Circulation 2011;123:e18-e209.

3. McMurray JJ, Petrie MC, Murdoch DR, Davie AP. Clinical epidemiology of heart failure: public and private health burden. Eur

Heart J 1998;19 Suppl P:P9-16.

4. Swedberg K, Cleland J, Dargie H. Guidelines for the diagnosis and treatment of chronic heart failure: executive summary

(update 2005): The Task Force for the Diagnosis and Treatment of Chronic Heart Failure of the European Society of

Cardiology. Eur Heart J 2005;26:1115-40.

5. Lloyd-Jones DM, Larson MG, Leip EP, et al. Lifetime risk for developing congestive heart failure: the Framingham Heart

Study. Circulation 2002;106:3068-72.

6. Owan TE, Redfield MM. Epidemiology of diastolic heart failure. Prog Cardiovasc Dis 2005;47:320-32.

7. Owan TE, Hodge DO, Herges RM, Jacobsen SJ, Roger VL, Redfield MM. Trends in prevalence and outcome of heart failure

with preserved ejection fraction. N Engl J Med 2006;355:251-9.

8. Ceia F, Fonseca C, Mota T, et al. Prevalence of chronic heart failure in southwestern Europe: the EPICA study. Eur J Heart

Fail 2002;4:531-9.

9. Tobacman LS. Thin filament-mediated regulation of cardiac contraction. Annu Rev Physiol 1996;58:447-81.

10. Aaronson KD, Schwartz JS, Chen TM, Wong KL, Goin JE, Mancini DM. Development and prospective validation of a clinical index to predict

survival in ambulatory patients referred for cardiac transplant evaluation. Circulation 1997;95:2660-7.

11. Levy W C et al. Circulation. 2006;113:1424-1433

12. Ammar KA, Jacobsen SJ, Mahoney DW, et al. Prevalence and prognostic significance of heart failure stages: application of the American

College of Cardiology/American Heart Association heart failure staging criteria in the community. Circulation 2007;115:1563-70.

13. Kramer DG, Trikalinos TA, Kent DM, Antonopoulos GV, Konstam MA, Udelson JE. Quantitative evaluation of drug or device effects on

ventricular remodeling as predictors of therapeutic effects on mortality in patients with heart failure and reduced ejection fraction: a meta-analytic

approach. J Am Coll Cardiol 2010;56:392-406.

14. Poole-Wilson PA, Swedberg K, Cleland JG, et al, and the Carvedilol Or Metoprolol European Trial Investigators. Comparison of carvedilol and

metoprolol on clinical outcomes in patients with chronic heart failure in the Carvedilol Or Metoprolol European Trial (COMET): randomised

controlled trial. Lancet 2003;362:7-13.

15. Menicanti L, Castelvecchio S, Ranucci M, et al. Surgical therapy for ischemic heart failure: single-center experience with surgical anterior

ventricular restoration. J Thorac Cardiovasc Surg 2007;134:433-41.

16. Cardiosource. ACCSAP 8.

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