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Recall: The underlying disorder is one of severely impaired left ventricular filling (diastolic dysfunction) due to increased wall thickness, impaired ventricular relaxation, and the development of ischemic induced myocardial fibrosis (increased ventricular stiffness). Systolic function is relatively preserved (at least until late in the disease process).

Principles of therapy:

  1. With respect to the obstructive form of HCM we traditionally expect the following hemodynamic changes to reduce the degree of obstruction
  • A decrease in contractility
  • A decrease in heart rate
  • An increase in preload
  • An increase in afterload
  1. Attempt to improve left ventricular diastolic function (as ventricular filling is improved, stroke volume will increase and therefore pulmonary edema will decrease)

Beta-blockers improve diastolic function indirectly by reducing heart rate and improving myocardial perfusion, thereby enhancing ventricular filling. Their negative inotropic properties reduce myocardial oxygen demand/consumption and thus may reduce ischemia. Beta-blockers also have antiarrhythmic properties that may be of benefit in this disorder. Beta-blockers reduce or abolish dynamic LVOT obstruction, and are therefore often used in the obstructive form of HCM. And finally, blockade of the deleterious effects of chronic sympathetic nervous system activation (vasoconstriction increasing afterload, myocardial necrosis, coronary vasospasm, arrythmogenesis) may be of benefit. Beta-blockers are the therapy of choice in humans with obstructive HCM or with exertional dyspnea and exercise intolerance.

  • Atenolol: 6.25-12.5 mg/cat SID-BID (PO)
  • Metoprolol: 0.5-1 mg/kg TID (PO)

Calcium channel blockers, like beta blockers, reduce heart rate and myocardial oxygen consumption. They also may improve the active process of myocardial relaxation directly. In humans and in cats, the tendency in the past was to treat non-obstructive HCM with calcium channel blockers (diltiazem). However the most recent therapeutic consensus guidelines for human HCM do not include the use of calcium channel blockers as there is no conclusive evidence that calcium channel blocker improve symptoms, hemodynamics, or survival.

  • Diltiazem: 1-2 mg/kg TID (PO) or 7.5 mg per cat TID

Angiotensin converting enzyme (ACE) inhibitors – Traditionally, treatment of HCM has focused on negative inotropic/chronotropic therapy (beta blockers, calcium channel blockers), and ACE inhibitors have been avoided (particularly in obstructive HCM) due to the impression that any arterial vasodilation may promote hypotension. However, the renin-angiotensin-aldosterone system (RAAS) plays an important role in stimulation of myocardial hypertrophy and fibrosis (which adversely affects diastolic function) and progression of heart failure. Therefore ACE-inhibitors may theoretically have some benefit in the setting of HCM. Recent work in veterinary medicine suggests that ACE-inhibition does not worsen dynamic LVOT obstruction or promote hypotension in HCM cats and that ACE-inhibitors are tolerated well in this population. Interim analysis of an ongoing prospective randomized clinical trial of therapy in feline CHF due to HCM suggests that cats treated with ACE-inhibitors tend to have a better outcome (not statistically significant) than those treated with either beta-blockers or calcium channel blockers. As the final results of this trial have yet to be published, any conclusions at this point are premature. However in the asymptomatic (pre-CHF) stage of HCM, two recent placebo-controlled feline studies showed no improvement in LV wall thickness, mass, or diastolic function with ACE-inhibitor therapy for 6-12 months (MacDonald et al JVIM 2006, Taillefer et al CVJ 2006). Note also that ACE-inhibitors are not featured in the most recent therapeutic consensus guidelines for human HCM.

  1. Reduce pulmonary edema and pleural effusion for cats in CHF:
  • Diuretics – furosemide (Lasix): 1-2 mg/kg BID-TID (PO, IM, IV); do not exceed 2 mg/kg (IV)
  • Although diuretics are very useful initially when pulmonary edema is present, as pulmonary edema resolves and additional therapy is in progress, one should attempt to use the least diuretic dose/reduce the dose (these individuals require as much preload as possible to prime their stiff left ventricle). Dramatic improvement may be noted with conservative doses.
  • ACE-inhibitors likely have a role to play in the management of CHF by blocking the RAAS when furosemide therapy is used
    • enalapril or benazepril: 0.25-0.5 mg/kg Q 24 hrs PO
  • Renal parameters and electrolytes must be monitored
  • Periodic thoracocentesis for pleural effusion may be necessary
  1. Direct arteriolar dilators will potentially exacerbate the situation; they reduce afterload and can promote hypotension as the left ventricle (already contracting maximally) cannot substantially augment stroke volume to raise blood pressure. Don’t use them.
  2. Prevent thromboembolic disease. See Question 19 above.
  3. Treat underlying disorders if present.
  • Hyperthyroidism for management.
  • Systemic hypertension – it is important to rule out hypertension as etiologic.