TY - JOUR
T1 - Biphasic changes in left ventricular end-diastolic pressure during dynamic exercise in patients with nonobstructive hypertrophic cardiomyopathy
AU - Takeichi, Yasushi
AU - Yokota, Mitsuhiro
AU - Iwase, Mitsunori
AU - Izawa, Hideo
AU - Nishizawa, Takao
AU - Ishiki, Ryoji
AU - Somura, Fuji
AU - Nagata, Kohzo
AU - Isobe, Satoshi
AU - Noda, Akiko
N1 - Funding Information:
Supported in part by a grant-in-aid for scientific research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan to Dr. Yokota.
PY - 2001
Y1 - 2001
N2 - OBJECTIVES: The aim of this study was to clarify the serial changes in left ventricular (LV) end-diastolic pressure (LVEDP) during dynamic exercise in patients with hypertrophic cardiomyopathy (HCM). BACKGROUND: Although HCM is characterized by impaired resting LV diastolic function, serial changes in LVEDP during exercise have not been characterized. METHODS: We simultaneously measured LV pressure and LV dimensions during symptom-limited supine bicycle exercise in 5 healthy individuals and 20 patients with HCM. Exercise thallium-201 scintigraphic studies were also performed. RESULTS: The LVEDP (baseline: 12 ± 5 mm Hg) progressively increased to a maximum value at peak exercise (28 ± 8 mm Hg) in 11 patients with HCM (group I). In the remaining nine patients with HCM (group II), changes in LVEDP during exercise were biphasic, with an initial progressive increase and a subsequent gradual decline up to peak exercise (14 ± 4 mm Hg at baseline, 27 ± 5 mm Hg at the critical heart rate, 16 ± 3 mm Hg at peak exercise). Exercise-induced changes in LV dimensions and LV peak systolic pressures were similar in both groups. However, the maximum first derivative of LV pressure was greater and the LV pressure half-time was shorter in group II than in group I at a similar peak exercise heart rate. The biphasic changes in LVEDP disappeared by pretreatment with propranolol. The LV hypertrophy scores were higher in group I than in group II. Exercise thallium-201 images showed more severe perfusion defects in group I than in group II patients. CONCLUSIONS: The biphasic changes in LVEDP seen during exercise may be related to improved coronary microcirculation in response to beta-adrenergic stimulation in patients with mild to moderate HCM.
AB - OBJECTIVES: The aim of this study was to clarify the serial changes in left ventricular (LV) end-diastolic pressure (LVEDP) during dynamic exercise in patients with hypertrophic cardiomyopathy (HCM). BACKGROUND: Although HCM is characterized by impaired resting LV diastolic function, serial changes in LVEDP during exercise have not been characterized. METHODS: We simultaneously measured LV pressure and LV dimensions during symptom-limited supine bicycle exercise in 5 healthy individuals and 20 patients with HCM. Exercise thallium-201 scintigraphic studies were also performed. RESULTS: The LVEDP (baseline: 12 ± 5 mm Hg) progressively increased to a maximum value at peak exercise (28 ± 8 mm Hg) in 11 patients with HCM (group I). In the remaining nine patients with HCM (group II), changes in LVEDP during exercise were biphasic, with an initial progressive increase and a subsequent gradual decline up to peak exercise (14 ± 4 mm Hg at baseline, 27 ± 5 mm Hg at the critical heart rate, 16 ± 3 mm Hg at peak exercise). Exercise-induced changes in LV dimensions and LV peak systolic pressures were similar in both groups. However, the maximum first derivative of LV pressure was greater and the LV pressure half-time was shorter in group II than in group I at a similar peak exercise heart rate. The biphasic changes in LVEDP disappeared by pretreatment with propranolol. The LV hypertrophy scores were higher in group I than in group II. Exercise thallium-201 images showed more severe perfusion defects in group I than in group II patients. CONCLUSIONS: The biphasic changes in LVEDP seen during exercise may be related to improved coronary microcirculation in response to beta-adrenergic stimulation in patients with mild to moderate HCM.
UR - http://www.scopus.com/inward/record.url?scp=0034900987&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0034900987&partnerID=8YFLogxK
U2 - 10.1016/S0735-1097(01)01384-5
DO - 10.1016/S0735-1097(01)01384-5
M3 - Article
C2 - 11499721
AN - SCOPUS:0034900987
SN - 0735-1097
VL - 38
SP - 335
EP - 343
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 2
ER -