Specialty Spotlight: Beta-blockers in the Management of Hypertrophic Heart Disease

Beta-blockers in the Management of Hypertrophic Heart Disease
Andrew Waxman, DVM, DACVIM (Cardiology)

Why are beta-blockers so commonly used in the management of hypertrophic heart disease?

It is first important to remember the determinants of myocardial oxygen demand.  The amount of oxygen demanded by the myocardium is impacted by afterload (of which a large portion is blood pressure), contractility, and heart rate.  Oxygen starved tissue can promote myocyte necrosis.   It can also serve as a focus for arrhythmias, hence why beta-blockers can also be effective antiarrhythmic medications.  In non-hypertensive patients, lowering of heart rate and contractility are appropriate targets to lower oxygen demand.

So this is when I convince you that beta-blockers are now a good idea.  Remember that beta-stimulation increases contractility and heart rate.  By truncating the beta-stimulatory effects on the heart we target two of the three determinants of myocardial oxygen demand.

Why is concentric hypertrophy bad?

Blood supply to the heart is arranged in a manner that provides the highest oxygen and nutrient load to the epicardium and the least the endocardial surface.  Unfortunately, the tissue demands are arranged in the exact opposite manner as the highest demand is the endocardium with the papillary muscles demanding the most.  The tissue with the highest demand receives the lowest concentration of oxygen and nutrients.

Any myocardial disease process that results in increased wall thickness such as primary hypertrophic cardiomyopathy or obstructive heart disease (valvular stenoses) substantially affects the delivery of oxygen.  The highest demanding tissues are now further from the highest concentrations of oxygen.  This leads to endocardial necrosis, fibrosis, and sometimes mineralization.

Decreased coronary reserve has been documented in several studies in hypertrophic patients.  This means that as the heart rate increases coronary flow cannot increase enough to adequately deliver oxygen.  This is due to coronary narrowing as well as vasomotor and endothelial dysfunction.

Recall those cats that have rate-dependent murmurs?

Many of these are created by systolic anterior motion (SAM) of the mitral valve.  Drag in the left ventricular outflow tract carries the anterior mitral valve leaflet into the path of ejected blood.  This creates obstruction of varying degrees that often worsens with increasing heart rate.  Studies have shown that a decrease in the early systolic acceleration can reduce this drag effect on the leaflet effectively reducing and eliminating SAM in many patients.  Beta-blockers, by reducing heart rate and contractility, can be effective at reducing systolic anterior motion.  In many cats the murmur created by SAM can be reduced and sometimes eliminated.

Should I worry about reducing systolic function with beta-blockers?

Most diseases which promote hypertrophy are not true systolic disorders.  The excessive myocardial muscle mass does not have trouble generating pressure until end stage remodeling occurs.  The real problem is that excessive myocardial mass cannot relax properly leading to diastolic dysfunction.  Progressive increases in filling pressure lead to congestive heart failure.  Beta-blockers, by decreasing heart rate and increasing the diastolic period, allow a longer filling period in the face of diastolic dysfunction.

When should a patient be started on a beta-blocker?

It may be hard to determine if a patient should be started on a beta-blocker based solely on physical examination findings.  An echocardiogram is extremely useful in determining the cause of a murmur and assessing systolic function.  If deemed an appropriate therapy for a patient beta-blockers are introduced slowly with owners instructed to observe for lethargy, weakness, or changes in appetite.  Rarely, patients may wheeze on high doses of beta-blockers.  This is most common in patients with underlying airway disease such as feline asthma.  Increase in dosing can be instructed every 1-2 weeks until the optimal dose is reached or an appropriate reduction in heart rate or obstruction is observed.  If a side effect is noted, the highest tolerated dose should be continued.

While beta-blockade may reduce the risk, it is not recommended to initiate beta-blocker therapy in the setting of congestive heart failure.  Once a patient is stabilized it may be introduced slowly.

-Andrew Waxman, DVM, DACVIM (Cardiology)