CLINICAL STUDY
Biphasic changes in left ventricular end-diastolic pressure during dynamic exercise in patients with nonobstructive hypertrophic cardiomyopathy
Yasushi Takeichi, MD ,
Mitsuhiro Yokota, MD, PhD, FACC*,1,
Mitsunori Iwase, MD, PhD ,
Hideo Izawa, MD, PhD,
Takao Nishizawa, MD*,
Ryoji Ishiki, MD, PhD,
Fuji Somura, MD,
Kohzo Nagata, MD, PhD,
Satoshi Isobe, MD and
Akiko Noda, PhD
* Cardiovascular Division, Department of Clinical Pathophysiology, Nagoya, Japan
First Department of Internal Medicine, Nagoya University, Graduate School of Medicine, Nagoya, Japan
Nagoya University School of Health Sciences, Nagoya, Japan
Manuscript received January 29, 2001;
revised manuscript received April 16, 2001,
accepted April 26, 2001.
Reprint requests and correspondence: Dr. Mitsuhiro Yokota, Department of Clinical Laboratory Medicine, Nagoya University Hospital, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8560, Japan
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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Abbreviations and Acronyms
| | 201Tl | = thallium 201 | | ANOVA | = analysis of variance | | ECG | = electrocardiogram | | EDD | = end-diastolic dimension | | ESD | = end-systolic dimension | | HCM | = hypertrophic cardiomyopathy | | HR | = heart rate | | LV | = left ventricular | | LV dP/dtmax | = the maximum first derivative of LV pressure | | LVEDP | = left ventricular end-diastolic pressure | | SPECT | = single-photon emission computed tonography | | T1/2 | = LV pressure half-time |
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