Systolic Heart Failure

Susan C. Brozena, M.D., F.A.C.C., F.A.H.A
Disclosures		Relationship: Yes Grants/Research Support: Wyeth/Pfizer and Medtronics

Mariell L. Jessup, M.D., F.A.C.C.
Disclosures		Relationship: Yes Honorarium: Advisory Board Member for Medtronics, Acorn, Cardiomems and Ventracor

The Planners of this activity have no relationships to disclose.

This lecture and the post-test is worth 1.5 credit hours.

Two noted medical directors of the University of Pennsylvania's highly regarded Heart Failure/Transplant Program define heart failure and its causes ... and review the current classification system that divides heart failure into four stages – A being high risk; B denoting structural cardiac abnormality but no symptoms; C structural abnormality with symptoms; and D end-stage symptoms that don't respond to treatment.

With illustrations that clarify and expand upon their discussion, the authors explain concentric versus eccentric hypertrophy and how reduced output leads to decreased perfusion and activates the renin-angiotensin-aldosterone system.

They also detail the various compensatory mechanisms that come into play. Describing the importance of the renin- angiotensin- aldosterone system in controlling blood pressure, the authors review its effects which include sodium retention and concomitant loss of potassium and magnesium as well as the consequences of long- term activation.

Atrial- and brain natriuretic peptides (ANP and BNP) levels increase in congestive heart failure (CHF), and the authors define the benefits and pitfalls of using BNP to identify patients with left ventricular dysfunction.

How to evaluate patients with heart failure, including a detailed discussion of history and physical examination, is followed by treatment recommendations for Stage A – principally, controlling such risk factors as hypertension, diabetes, and coronary artery disease (CAD); and Stages B, C, and D – delaying remodeling and employing diuretics.

The rationale for various pharmacologic and non- pharmacologic treatments is detailed. Following infarction and other "insults" to the heart the ventricles remodel themselves for several months with such effects as dilatation, hypertrophy and mitral regurgitation.

Both post-myocardial infarction patients and those with dilated cardiomyopathy benefited from ACE inhibitors, beta-adrenergic antagonists, or cardiac resynchronization. ACE inhibitors, in particular, improve post-myocardial infarction and heart failure survival, reduce symptoms, and improve cardiac performance.

The authors conclude that CHF is a systemic disease that can progress markedly if compensatory mechanisms are left unchecked.