CLINICAL STUDIES
Peak negative myocardial velocity gradient in early diastole as a noninvasive indicator of left ventricular diastolic function
Comparison with transmitral flow velocity indices
Yoshito Shimizu, MD*,
Masaaki Uematsu, MD, PhD ,
Hiromi Shimizu, MD*,
Ko Nakamura, MD*,
Masakazu Yamagishi, MD, PhD, FACC* and
Kunio Miyatake, MD, PhD, FACC*
* Cardiology Division of Medicine, National Cardiovascular Center, Suita, Osaka, Japan
Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Suita, Osaka, Japan
Manuscript received April 2, 1998;
revised manuscript received June 24, 1998,
accepted July 9, 1998.
Address for correspondence: Dr. Masaaki Uematsu, Cardiovascular Division, Osaka Police Hospital, 10-31 Kitayama-cho, Tennoji-ku, Osaka 543-0035, Japan (present address)
uematsu{at}hp-info.med.osaka-u.ac.jp
Objectives. We sought to assess the clinical significance of peak negative myocardial velocity gradient (MVG) in early diastole as a noninvasive indicator of left ventricular (LV) diastolic function.
Background. Peak systolic MVG has been shown useful for the quantitative assessment of regional wall motion abnormalities, but limited data exist regarding the diastolic MVG as an indicator of LV diastolic function.
Methods. Peak negative MVG was obtained from M-mode tissue Doppler imaging (TDI) in 43 subjects with or without impairment of systolic and diastolic performance: 12 normal subjects, 12 patients with hypertensive heart disease (HHD) with normal systolic performance and 19 patients with dilated cardiomyopathy (DCM), and was compared with standard Doppler transmitral flow velocity indices. In a subgroup of 30 patients, effects of preload increase on these indices were assessed by performing passive leg lifting. In an additional 11 patients with congestive heart failure at the initial examination, the measurements were repeated after 26 ± 16 days of volume-reducing therapy.
Results. Peak negative MVG was significantly depressed both in HHD (–3.9 ± 1.3/s, p < 0.01 vs. normal = –7.7 ± 1.5/s) and DCM (–4.4 ± 1.4/s, p < 0.01 vs. normal). In contrast, transmitral flow indices failed to distinguish DCM from normal due to the pseudonormalization. Transmitral flow velocity indices were significantly altered (peak early/late diastolic filling velocity [E/A] = 1.1 ± 0.5 to 1.5 ± 0.7, p < 0.01; E deceleration time = 181 ± 41 to 153 ± 38 ms, p < 0.01), while peak negative MVG remained unchanged (–5.3 ± 2.2 to –5.3 ± 2.0/s, NS) by leg lifting. Volume-reducing therapy resulted in the apparent worsening of the transmitral flow velocity pattern toward abnormal relaxation, as opposed to peak negative MVG, which improved by the therapy (p < 0.05).
Conclusions. Peak negative MVG derived from TDI may be a noninvasive indicator of LV diastolic function that is less affected by preload alterations than the transmitral flow velocity indices, and thereby could be used for the follow-up of patients with nonischemic LV dysfunction presenting congestive heart failure.
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Abbreviations and Acronyms
| | A | = peak late diastolic filling velocity | | DCM | = dilated cardiomyopathy | | DcT | = deceleration time of the early diastolic filling velocity | | E | = peak early diastolic filling velocity | | HHD | = hypertensive heart disease | | IRT | = isovolumic relaxation time | | LV | = left ventricular | | MVG | = myocardial velocity gradient | | TDI | = tissue Doppler imaging |
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