(Circulation. 2004;109:452-456.)
© 2004 American Heart Association, Inc.
Clinician Update |
From the Hypertrophic Cardiomyopathy Center and Cardiac Catheterization Laboratory, Division of Cardiology, Tufts-New England Medical Center, Boston, Mass (C.D.K.), and The Hypertrophic Cardiomyopathy Center, Minneapolis Heart Institute Foundation, Minneapolis, Minn (B.J.M.).
Correspondence to Carey D. Kimmelstiel, MD, Tufts-New England Medical Center, 750 Washington St, Boston, MA 02111-5913. E-mail ckimmelstiel@tufts-nemc.org
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
| Introduction |
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Physical examination was notable for a bifid carotid pulse and loud apical systolic ejection murmur. Echocardiography documented hyperdynamic left ventricular (LV) systolic function and asymmetric hypertrophy confined to the basal ventricular septum (measuring 20 mm in thickness) consistent with hypertrophic cardiomyopathy (HCM). Continuous wave Doppler estimated a 65 mm Hg subaortic gradient due to dynamic systolic anterior motion of the mitral valve with septal contact. Coronary angiography showed patent bypass grafts.
Medical management with ß-blockers and verapamil was ineffective in controlling symptoms. Catheter-based intervention was considered for this patient to reduce outflow obstruction and symptoms.
HCM is a relatively common genetic disease with important clinical consequences, including sudden death in the young and disability due to heart failure at any age.1,2 It is estimated that progression to NYHA functional classes III/IV associated with obstruction to LV outflow occurs in about 10% of HCM patients who are limited largely by exertional dyspnea, chest pain, fatigue, and occasionally orthopnea or nocturnal dyspnea.1,2 Long-term consequences of HCM attributable to outflow obstruction have been emphasized, particularly progression of disabling symptoms and death related to heart failure.2
| Therapeutic Options in Obstructive HCM |
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