Cardiac Risk Factors

Functional Status










Heart Failure
NEJM 2007 (update from 2003)


Nearly 5 million Americans have heart failure

Incidence approaching 10 per 1000 population among persons older than 65 years old

Accounts for at least 20% of all hospital admissions among persons older than 65 years

Large randomized trials now include the effect of the stuided intervention on the rate of hospital admissions

ACEi, ARB, BB, Spironolactone, BiV pacing, CABG, and the use of multidisciplinary teams to treat heart failure have all been shown to reduce the rate of hospitalizations substantially, as well as to reduce mortality or improve functional status

There has been an unequivocal reduction in mortality for patients with systolic heart failure; but large epidemiologic surveys (such as Framingham) have not documented meaningful changes in death rates (death is delayed, and occurs a longer time after major cardiac events such as MI)

Symptomatic heart failure confers a worse prognosis than the majority of cancers, with one-year mortality of approximately 45%.


What are the causes of heart failure?

Heart failure is a clinical syndrome arising from diverse causes

Not all patients with HF have poorly contracting ventricles and a low ejection fraction

Many have uncorrected vavular disease, such as AS, or MR, or abnormal filling, resulting in diastolic dysfunction

A large majority of patients are elderly

75% have a history of HTN

Many patients have at least one serious coexisting condition

There are large subgroups of patients who are not well represented in clinical trials 

Heart failure is largely preventable, primarily through the control of blood pressure and other vascular risk factors

What is heart failure?

The syndrome of heart failure

The traditional view that heart failure is a constellation of signs and symptoms caused by inadequate performance of the heart focuses on only one aspect of the pathophysiology involved in the syndrome

A complex blend of structural, functional, and biologic alterations account for the progressive nature of HF and explains the efficacy or failure of therapies

To Beta or not to Beta?


The rationale for beta-blockers in a patient with a poorly contracting heart is based on a conceptual framework broader than that which suggests the treatment of congestion with diuretics and digoxin

The rationale for BB is predicated on an understanding of the role of the sympathetic nervous system in promoting the release of renin and other vasoactive substances that trigger vasoconstriction, tachycardia, and changes in myocytes that lead to disadvantageous ventricular dilatation


 How do you think of heart failure and its therapy?

The hemodynamic model of heart failure

·      Emphasized the effect of an altered load on the failing ventricle

·      And ushered in the era of vasodilators and inotropic agents

The neurohumoral model

·      Recognized the importance of activation of the renin-angiotensin-aldosterone axis and the sympathetic nervous system in the progression of cardiac dysfunction

Most recently

·      Efforts to antagonize the effects of circulating norepinephrine and angiotensin II have shifted with the recognition that these and other vasoactive substances are also synthesized within the myocardium and therefore act in an autocrine and paracrine manner

o   Example:

§  BNP is produced by ventricular myocardium in response to stretch

§  Its vasodilatory and natriuretic effects counteract the opposing actions of angiotensin II and aldosterone

No single model can account for the host of clinical expressions of heart failure, current therapy often targets more than one organ system

Table 1

Figure 1

What then are our treatment options?

1.       ACEi and ARB (Captopril, Lisinopril)

a.       Decrease afterload by interfering with the RAA system, resulting in peripheral vasodilatation

b.      Decreases the degradation of bradykinin (which promotes vasodilatation in the vascular endothelium, and causes natriuresis in the kidney)

c.       Affects LVH, remodeling, and renal blood flow

2.       Aldosterone antagonists (spironolactone, eplerenone)

a.       Aldosterone production by the adrenal glands is increased in heart failure

b.      It stimulates renal sodium retention and potassium excretion and promotes ventricular and vascular hypertrophy

3.       Digoxin

a.       Affects the Na/K-ATPase pump in the myocardial cell, increasing contractility.

4.       Inotropes (dobutatmine, milrinone)

a.       Increase myocardial contractility

5.       Beta-blockers (Carvedilol, metoprolol)

a.       Inhibit the sympathetic nervous system and adrenergic receptors

b.      They slow the heart rate, decrease blood pressure

c.       They have a beneficial effect on the myocardium, enhancing reverse remodeling

d.      Selected agents that also block alpha-adrenergic receptors can cause vasodilation (carvedilol)

e.      Short term effects may result in temporary exacerabation of symptoms

f.        Long term effects are uniformly beneficial - including improved systolic function, reverse remodeling; improvements in survival, morbidity, EF, quality of life, rate of hospitalization, incidence of sudden death

g.       Should be used in all patients in stable condition without substantial fluid retention and without recent exacerbations of heart failure requiring inotropic therapy

h.      Contraindications include RAD, DM with frequent hypoglycemia, bradyarrhythmias or heart block who do not have a pacemaker

6.       Vasodilator therapy (eg. Combination hydralazine and isosorbide dinitrate)

a.       Decreased afterload by counteracting peripheral vasoconstriction

7.       Cardiac resynchronization therapy with biventricular pacing

a.       Improves left ventricular function

b.      Favors reverse remodeling

8.       Nesiritide (BNP)

a.       Decreases preload by stimulating dieresis and decreases afterload by vasodilation

9.       Exercise

a.       Improves peripheral blood flow by eventually counteracting peripheral vasoconstriction

b.      Also improves skeletal muscle physiology


A patient with pulmonary congestion, dyspnea, edema but with normal EF… heart failure?
Diastolic Heart failure

·         20-50% of patients with HF have preserved systolic function or a normal LVEF

·         Such hearts contract normally, but relaxation is abnormal

·         Cardiac output is limited

·         Patients are typically elderly, female, obese, with HTN, and DM

·         Few clinical trials, little guidance

What are the stages of Heart failure?
Management of Heart failure

Clinical Assessment:

·         Breathlessness, fatigue, edema

·         Fluid overload, cardiac findings

·         BNP, serial weight measurement

·         Evaluate at 45 degrees

·         JVP, HJR, gallop rhythm, peripheral edema

Treatment of patients with Stage A Heart Failure – High risk with no symptoms
Figure 3

·         Prevent remodeling

·         Control risk factors

·         Effective treatment of HTN decreases the occurrence of LVH and CV mortality, as well as reducing the incidence of heart failure by 30-50%

·         Target diastolic blood pressure in high risk pts < 80

·         ACEi treatment in asymptomatic high-risk patients with diabetes or vascular disease and no history of heart failure significantly reduces rates of death, MI, stroke

·         ARB (losartan) delays first hospitalization for HF in patients with DM and nephropathy

Stage B – Structural heart disease, no symptoms

·         ACEi or ARBs in all patients, BB in selected patients

Stage C – structural disease, previous or current symptoms

·         ACEi and BB in all patients

Stage D – Refractory symptoms requiring special intervention

·         Inotropes, VAD, transplant

Treatment of Stage B, C, D; with or without symptoms

·         HF and low EF

·         Improve survival

·         Slow progression of disease

·         Alleviate symptoms

·         Minimize risk factors

·         Control the sx of HF with basic habits

o   Sodium restriction, weight monitoring, adherence to medication schedules

o   Moderation of EtOH

o   Avoidance of NSAIDs, which are associated with an increase in the incidence of new heart failure, decompensated chronic heart failure, and hospitalizations for heart failure


Common Clinical Problems

The patient has classic symptoms of heart failure with a normal LVEF...




...Consider diastolic heart failure, valvular heart disease, hypertensive heart disease, and ischemia




The patient has hypotension: when is the systolic blood pressure too low?...




... asymptomatic patients with dilated cardiomyopathy often tolerate a sytolic blood pressure of 90mmHg.  If the patient has no lightheadedness or undue fatigue, peripheral perfusion is adequate, and blood urea nitrogen and creatinine are unchanged, continue the same doses of medications.

... in symptomatic patients, decrease the dose of diuretic.  if symptoms persist, adjustment of the timing of concomitant medicaitons may be helpful.  Decreasing the dose of the ACE inhibitor, beta-blocker, ARB, or vasodilator.




The patient has hyperkalemia...




... ensure the patient is not taking exogenous potassium supplementation. 
... Avoid hypovolemia. 
... Consider decreasing the dose of a potassium-sparing diuretic. 
... Concomitant use of an ACE inhibitor or ARB and spironolactone may increase the risk of hyperkalemia. 
... Avoid high doses of ACE inhibitors and ARBS in patients receiving spironolactone. 
... Avoid use of spironoloactone in patients with renal failure, and use lose doses of ACEi and ARB.




The patient has increasing azotemia while taking ACE inhibitors...




... Decrease the dose of diuretic.  Consider renal-artery stenosis.




The patient has a cough while taking ACEi...




... rule out worsening CHF.  Change to ARB.




Should the dose of the ACEi be increased or should beta-blocker be added in a symptomatic patient...




... Start BB therapy if there are no contraindications




The patient has worsening sx of CHF after starting beta-blocker therapy...




... increase the dose of diuretic and slow the titration of beta blocker.




The patient has worsening bronchospasm after starting beta-blocker therapy




... decrease the dose of the beta-blocker.  Consider a beta-selective agent.  Discontinue treatment with the drug if the problem persists.




Persistent paroxysmal nocturnal dyspnea or orthopnea or daytime fatigue despite absence of fluid retention on physical exam...




... consider obstructive sleep apnea




The patient requires repeat hospitalizations...



... multidisciplinary approach, visiting nurse in the home, referral for heart failure