Biphasic changes in left ventricular end-diastolic pressure during dynamic exercise in patients with nonobstructive hypertrophic cardiomyopathy

Yasushi Takeichi, Mitsuhiro Yokota, Mitsunori Iwase, Hideo Izawa, Takao Nishizawa, Ryoji Ishiki, Fuji Somura, Kohzo Nagata, Satoshi Isobe, Akiko Noda

Research output: Contribution to journalArticle

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Abstract

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.

Original languageEnglish
Pages (from-to)335-343
Number of pages9
JournalJournal of the American College of Cardiology
Volume38
Issue number2
DOIs
Publication statusPublished - 18-08-2001
Externally publishedYes

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Hypertrophic Cardiomyopathy
Exercise
Blood Pressure
Ventricular Pressure
Thallium
Heart Rate
Left Ventricular Hypertrophy
Microcirculation
Left Ventricular Function
Propranolol
Adrenergic Agents
Perfusion

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

Takeichi, Yasushi ; Yokota, Mitsuhiro ; Iwase, Mitsunori ; Izawa, Hideo ; Nishizawa, Takao ; Ishiki, Ryoji ; Somura, Fuji ; Nagata, Kohzo ; Isobe, Satoshi ; Noda, Akiko. / Biphasic changes in left ventricular end-diastolic pressure during dynamic exercise in patients with nonobstructive hypertrophic cardiomyopathy. In: Journal of the American College of Cardiology. 2001 ; Vol. 38, No. 2. pp. 335-343.
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abstract = "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.",
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Biphasic changes in left ventricular end-diastolic pressure during dynamic exercise in patients with nonobstructive hypertrophic cardiomyopathy. / Takeichi, Yasushi; Yokota, Mitsuhiro; Iwase, Mitsunori; Izawa, Hideo; Nishizawa, Takao; Ishiki, Ryoji; Somura, Fuji; Nagata, Kohzo; Isobe, Satoshi; Noda, Akiko.

In: Journal of the American College of Cardiology, Vol. 38, No. 2, 18.08.2001, p. 335-343.

Research output: Contribution to journalArticle

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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

PY - 2001/8/18

Y1 - 2001/8/18

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.

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