Long mitral valve leaflets determine left ventricular outflow tract obstruction during exercise in hypertrophic cardiomyopathy
2016 (English)In: International Journal of Cardiology, ISSN 0167-5273, E-ISSN 1874-1754, Vol. 212, 47-53 p.Article in journal (Refereed) Published
BACKGROUND: Development of left ventricular outflow tract obstruction (LVOTO) in patients with hypertrophic cardiomyopathy (HCM) is important for explaining symptoms and designing management. LVOTO is mostly caused by a combination of septal hypertrophy and systolic anterior movement of the mitral valve (SAM). The aim of the present study was to determine predictors of exercise induced LVOTO in a group of HCM patients.
METHODS: We performed supine exercise Doppler echocardiography, including measurements of LV morphology and function and anterior mitral leaflet length, in 51 mildly symptomatic HCM (septal thickness≥15mm) and compared them with 50 healthy controls. Measurements were made at 1) rest, 2) Valsalva maneuver, 3) peak exercise and 4) post exercise. LVOTO was diagnosed as a LVOT gradient of >30mmHg at rest, after Valsalva and after exercise or ≥50mmHg at peak exercise.
RESULTS: All patients stopped exercise because of exhaustion. 35% of the patients had resting LVOTO and 48% during Valsalva. At peak exercise, only 37% had LVOTO, who increased to 64% post exercise. Patients who developed LVOTO at peak exercise were more prone to continue having it post exercise (p<0.001), to have attenuated systolic blood pressure rise (p=0.011) and to have long anterior mitral valve leaflets (p<0.001). Backward multiple regression analysis showed the anterior mitral leaflet length as the strongest single independent predictor (β=0.36, p=0.010) for increased LVOT velocities, followed by basal septal thickness.
CONCLUSION: In patients with HCM, LV outflow tract obstruction seems to be relatively uncommon during exercise but rather occurring minutes after stopping exercise. Exercise LVOTO seems to be determined by long anterior mitral leaflets in addition to the well established septal hypertrophy.
Place, publisher, year, edition, pages
Elsevier, 2016. Vol. 212, 47-53 p.
transthyretin, Amyloidosis hereditary, echocardiography, scintigraphy, amyloid cardiomyopathy, VEREUX RB, 1986, AMERICAN JOURNAL OF CARDIOLOGY, V57, P450 bue G, 2003, AMYLOID-JOURNAL OF PROTEIN FOLDING DISORDERS5th Int Symp on Familial yloidotic Polyneuropathy and Other Transthyretin Related Disorders/4th Int Workshop on Liver ansplantation in Familial Amyloid Polyneuropathy, SEP 24-27, 2002, MATSUMOTO, JAPAN, V10, P32 gueh Sherif F., 2009, EUROPEAN JOURNAL OF ECHOCARDIOGRAPHY, V10, P165 ille M, 2002, EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING, V29, P376
Cardiac and Cardiovascular Systems
IdentifiersURN: urn:nbn:se:umu:diva-119478DOI: 10.1016/j.ijcard.2016.03.041ISI: 000374474600012PubMedID: 27031819OAI: oai:DiVA.org:umu-119478DiVA: diva2:921435