J Echocardiogr (2010) 8:112–117 DOI 10.1007/s12574-010-0057-6
ORIGINAL INVESTIGATION
Left ventricular remodeling after myocardial infarction impairs early diastolic, but not systolic, function in the radial direction in the remote normal region Hiroko Kobayakawa • Nobuyuki Ohte • Kazuaki Wakami • Hidekatsu Fukuta Toshihiko Goto • Tomomitsu Tani • Hitomi Narita • Genjiro Kimura
•
Received: 18 March 2010 / Revised: 10 June 2010 / Accepted: 28 June 2010 / Published online: 31 July 2010 Ó Japanese Society of Echocardiography 2010
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
H. Kobayakawa N. Ohte (&) K. Wakami H. Fukuta T. Goto T. Tani H. Narita G. Kimura Department of Cardio-Renal Medicine and Hypertension, Nagoya City University Graduate School of Medical Sciences, Mizuho-cho, Mizuho-ku, Nagoya 467-8601, Japan e-mail:
[email protected]
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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. Keywords Diastolic function Myocardial infarction Remodeling Strain Strain rate
Introduction It is acknowledged that one of several causes of heart failure secondary to myocardial infarction (MI) is due to structural alterations that occur in the remote normal myocardium [1–3]. As a consequence of acute MI, changes occur in left ventricular (LV) size, shape, and thickness that involve the infarct and non-infarct (remote normal) regions of the left ventricle; these changes are referred to as ‘‘LV remodeling’’ [1–3]. A substantial manifestation of LV remodeling is the combination of LV dilatation and hypertrophy of the residual remote normal myocardium [1–3]. We previously reported that, in the chronic stage of MI, the remote normal region of the dilated left ventricle exhibited impairments in myocardial oxidative metabolism and LV systolic function in the longitudinal direction [4]. However, it remains unidentified whether changes occur in myocardial function in the radial direction in the remote normal region, which plays a key role in ejecting blood into the aorta [5]. Accordingly, we investigated this issue in patients that had experienced a prior anterior MI.
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medicine as a patient with hypercholesterolemia. Medicine that study patients were taking is also shown in Table 2.
Methods Subjects
Doppler echocardiography We studied 15 patients who had had a prior anterior MI and were angiographically proven to have single anterior descending artery disease. Percutaneous coronary intervention for reperfusion of the occluded vessel had been performed in the acute phase; follow-up coronary angiography was performed 6–14 months after the onset of the MI and we confirmed the involved artery was open and that the other two major coronary arteries exhibited no significant stenosis. The mean time interval from the onset of MI to Doppler echocardiographic examination was 11.4 months. Left ventriculography showed no wall motion abnormality in their inferoposterior wall. Mitral regurgitation more than Sellers’ grade II was not observed in patients with a prior MI. As a normal control group, we studied 13 patients who had no significant stenosis of the three major coronary arteries and no LV wall motion abnormality in cardiac catheterization, but had had atypical chest pain. Mitral regurgitation more than Sellers’ grade I was not observed in this group. Doppler echocardiography showed that none of the patients in the both groups had a significant valvular disease. Incidences of hypertension, diabetes mellitus, and hypercholesterolemia in each group are indicated in Table 1. A patient who met the criteria that systolic blood pressure was at least 140 mmHg and/or diastolic blood pressure was at least 90 mmHg or who took antihypertensive drugs was diagnosed as a patient with hypertension. Diabetes mellitus was diagnosed by the blood glucose level at fasting exceeding 126 mg/dl in each patient or by the finding that a patient took blood glucose-lowering medicine. We regarded a patient who had LDL-cholesterol level exceeding 140 mg/dl or who took cholesterol-lowering
Table 1 Comparisons of clinical characteristics and hemodynamic data between controls and patients with a prior anterior myocardial infarction
Doppler echocardiography was performed within 2 h prior to the follow-up cardiac catheterization. All ultrasound examinations were performed with a commercially available echocardiograph (Aplio80TM, Toshiba Medical Systems, Tokyo, Japan) and a 3-MHz transducer. Patients were examined at rest, lying in the left lateral decubitus position. After standardized screening for cardiac disorders, digital cine loops were acquired with two-dimensional tissue Doppler imaging (velocity imaging) during two cardiac cycles at the papillary muscle level in the parasternal shortaxis view. We used frame rates in the range of 60–80 s-1. Myocardial strain and strain rate were analyzed offline with an echo image analyzer (EchoAgentTM, Toshiba Medical Systems). All analyses were performed by the same observer, who was blinded to the cardiac catheterization data. Transmural myocardial strain and strain rate profiles in the radial direction on the short-axis image were computed from myocardial velocity data as follows: the center of contraction in the LV short-axis image was visually and manually established at the end of diastole, and Doppler angle correction was used to instantaneously calculate myocardial velocities toward and away from the center throughout a cardiac cycle. The center defined at the end of diastole was applied throughout the cardiac cycle. Myocardial velocity data sets in the cardiac cycle were then converted to myocardial displacement data sets with a tissue tracking method. Myocardial displacement data were differentiated on the basis of myocardial distance throughout the cardiac cycle and converted to myocardial strain data sets. For measurements of radial strain with the Lagrangian method [6], we used a 3-mm length for the
Characteristic
Control (n = 13)
Male/female
9/4
15/0
Age (years)
61.1 ± 10.7
66.8 ± 7.4
0.11
Heart rate (beats/min)
68.9 ± 10.5
69.3 ± 12.5
0.93
Mean blood pressure (mmHg)
94.4 ± 16.6
88.9 ± 13.4
0.34
36.6 ± 1.7
47.4 ± 8.5
\0.001
72.9 ± 4.7
55.0 ± 12.1
\0.001
2
LV left ventricular, s time constant of LV relaxation, MI myocardial infarction
p value
s (ms) LV ejection fraction (%) Data are presented as mean ± SD
Prior anterior MI (n = 15)
LV end-diastolic volume index (ml/m )
73.0 ± 10.9
92.2 ± 26.6
\0.05
LV end-systolic volume index (ml/m2)
19.8 ± 4.6
42.5 ± 18.2
\0.001
Hypertension
54%
60%
0.74
Diabetes mellitus
7.7%
13%
0.88
Hypercholesterolemia
31%
80%
\0.01
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initial differential distance. For measurements of radial strain rate, we used a fixed differential distance of 3 mm throughout the cardiac cycle. We obtained transmural strain and strain rate profiles along the 4-mm-wide M-mode sampling cursor that was aligned perpendicular to the LV posterior wall on the short-axis view. Strain and strain rate images were recorded throughout the cardiac cycle. We measured peak radial systolic strain and peak radial early diastolic strain rate on each M-mode strain and strain rate transmural profile, as shown in Fig. 1. Table 2 Comparison of prevalence in medication between controls and patients with a prior anterior myocardial infarction Medicine
Control (%)
Prior anterior MI (%)
p value
Antiplatelets
38
87
0.63
b-blockers
12.5
53
\0.01
Calcium channel blockers ACEIs or ARBs
15 62
40 53
0.22 0.66
Statins
23
53
0.10
Cardiac catheterization LV pressure waves were measured with a catheter-tipped micromanometer (SPC-454D, Millar Instrument Co., Houston, TX) and recorded on a polygraph system (RMC3000, Nihon Kohden Inc., Tokyo, Japan) and on a digital data recorder (NR-2000, Keyence, Osaka, Japan), as described elsewhere [7–9]. From the recorded pressure waves, a monoexponential curve with zero asymptote was fitted to the LV pressure decay curve to compute the time constant, s, of the fall in LV pressure [10]. LV end-systolic and end-diastolic volumes were measured with biplane left ventriculography according to the method proposed by Chapman et al. [11]. The volumes were corrected for individual body surface area and were expressed as endsystolic and end-diastolic volume indices. Statistical analysis
ACEIs angiotensin-converting enzyme inhibitors, ARBs angiotensin type-1 receptor blockers
Statistical software (SPSS Version 17.0, SPSS Inc, Chicago, IL) was used for all statistical analyses. Data are presented as the mean ± standard deviation (SD). Parameters between two groups were compared with the unpaired
Fig. 1 Representative measurements of peak radial systolic strain (a) and peak radial early diastolic strain rate (b) in the left ventricular posterior wall. a The point of peak radial strain at end-systole was searched and obtained on the M-mode transmural strain profile at the intersection of the time-strain (x-axis) and the myocardial wall
depth-strain (y-axis) as a point with peak color intensity. The respective individual curves are shown below the x-axis and to the right of the M-mode image. b The point of peak radial early diastolic strain rate was also searched and obtained on the M-mode transmural strain rate profile similarly
123
-1
a 200
Peak radial systolic strain (%)
115 Peak radial early diastolic strain rate (s )
J Echocardiogr (2010) 8:112–117
NS
150
100
50
0
Control
Anterior MI
b 5.0
*
p
