Hiroko Kobayakawa1, Nobuyuki Ohte2, Kazuaki Wakami1, Hidekatsu Fukuta1, Toshihiko Goto1, Tomomitsu Tani1, Hitomi Narita1, Genjiro Kimura1. 1. Department of Cardio-Renal Medicine and Hypertension, Nagoya City University Graduate School of Medical Sciences, Mizuho-cho, Mizuho-ku, Nagoya, 467-8601, Japan. 2. Department of Cardio-Renal Medicine and Hypertension, Nagoya City University Graduate School of Medical Sciences, Mizuho-cho, Mizuho-ku, Nagoya, 467-8601, Japan. ohte@med.nagoya-cu.ac.jp.
Abstract
BACKGROUND: It is acknowledged that expansion of the remote normal region of the left ventricle causes remodeling after myocardial infarction (MI). However, the characteristics of that region have not been fully elucidated. METHODS: We studied 13 patients with atypical chest pain (controls) and 15 patients with a prior anterior MI who underwent cardiac catheterization. With Doppler strain imaging, we measured the peak radial myocardial systolic strain and peak radial early diastolic strain rate at the posterior wall of the left ventricle. None of the patients with atypical chest pain exhibited significant stenosis of the three major coronary arteries or left ventricular (LV) wall motion abnormality in cardiac catheterization. The patients with a prior anterior MI had single anterior descending artery disease without wall motion abnormality in the LV inferoposterior wall. LV ejection fraction and the LV relaxation time constant were also measured. RESULTS: The LV ejection fraction was significantly smaller in patients with a prior MI compared to controls. The peak radial systolic strain in the LV posterior wall was not significantly different between the patients with a prior MI and controls (125 ± 49 vs. 122 ± 29%). In contrast, the peak radial early diastolic strain rate in the same area was significantly lower in the patients with a prior MI than in controls (-7.4 ± 2.7 vs. -13.2 ± 4.0 s(-1), p < 0.001). Peak early diastolic radial strain rate was significantly correlated with the LV relaxation time constant in all patients (r = 0.69, p < 0.001). CONCLUSION: LV remodeling after an MI impairs local early diastolic myocardial function in the remote normal region and it is related to global LV diastolic dysfunction.
BACKGROUND: It is acknowledged that expansion of the remote normal region of the left ventricle causes remodeling after myocardial infarction (MI). However, the characteristics of that region have not been fully elucidated. METHODS: We studied 13 patients with atypical chest pain (controls) and 15 patients with a prior anterior MI who underwent cardiac catheterization. With Doppler strain imaging, we measured the peak radial myocardial systolic strain and peak radial early diastolic strain rate at the posterior wall of the left ventricle. None of the patients with atypical chest pain exhibited significant stenosis of the three major coronary arteries or left ventricular (LV) wall motion abnormality in cardiac catheterization. The patients with a prior anterior MI had single anterior descending artery disease without wall motion abnormality in the LV inferoposterior wall. LV ejection fraction and the LV relaxation time constant were also measured. RESULTS: The LV ejection fraction was significantly smaller in patients with a prior MI compared to controls. The peak radial systolic strain in the LV posterior wall was not significantly different between the patients with a prior MI and controls (125 ± 49 vs. 122 ± 29%). In contrast, the peak radial early diastolic strain rate in the same area was significantly lower in the patients with a prior MI than in controls (-7.4 ± 2.7 vs. -13.2 ± 4.0 s(-1), p < 0.001). Peak early diastolic radial strain rate was significantly correlated with the LV relaxation time constant in all patients (r = 0.69, p < 0.001). CONCLUSION: LV remodeling after an MI impairs local early diastolic myocardial function in the remote normal region and it is related to global LV diastolic dysfunction.
Authors: A Gimelli; J Schneider-Eicke; D Neglia; G Sambuceti; A Giorgetti; G Bigalli; G Parodi; R Pedrinelli; O Parodi Journal: J Am Coll Cardiol Date: 1998-02 Impact factor: 24.094