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Heart failure and cardiomyopathies
ORIGINAL ARTICLE
Myocardial fibrosis progression on cardiac magnetic resonance in hypertrophic cardiomyopathy Hong-Mi Choi,1 Kyung-Hee Kim,2 Joo Myung Lee,1 Yeonyee E Yoon,1 Seung-Pyo Lee,1 Eun-Ah Park,3 Whal Lee,3 Yong-Jin Kim,1 Goo-Yeong Cho,1 Dae-Won Sohn,1 Hyung-Kwan Kim1 ▸ Additional material is published online only. To view please visit the journal online (http://dx.doi.org/10.1136/ heartjnl-2014-306555). 1
Department of Internal Medicine, Cardiovascular Center, Seoul National University College of Medicine, Seoul National University Hospital, Seoul, Republic of Korea 2 Department of Internal Medicine, Division of Cardiology, Sejong General Hospital 3 Department of Radiology, Cardiovascular Section, Seoul National University College of Medicine, Seoul National University Hospital, Seoul, Republic of Korea Correspondence to Professor Hyung-Kwan Kim, Division of Cardiology, Department of Internal Medicine, Seoul National University College of Medicine, 101 Daehak-ro, Jongno-gu, Seoul 110-744, Republic of Korea; [email protected] or [email protected] Received 22 July 2014 Revised 10 February 2015 Accepted 20 March 2015 Published Online First 20 April 2015
ABSTRACT Objective We hypothesised that, in hypertrophic cardiomyopathy (HCM), late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) is progressive and can be predicted by baseline CMR findings and HCM phenotype. Methods In this single-centre cohort study, 71 patients with HCM (59±13 years; 48 men) were prospectively enrolled with clinical, echocardiographic and CMR data. Two consecutive CMR scans were performed with a time interval of 582±174 days. The LGE extent was quantified as a proportion of total LV myocardium (%LGE). Results LGE was present in 65 patients (91.5%) at the first CMR (CMR-1). In all, LGE extent was significantly increased ( p5 SD than mean signal intensity of normal myocardium were defined as segments with LGE.9 10 LGE extent in each segment was expressed as the surface area showing LGE divided by the total area of the given myocardial segment, and then summation of the planimetered LGE areas in all short-axis slices yielded total LGE extent, which was subsequently expressed as a proportion of total LV myocardium (% LGE). LGE quantification of CMR-2 was performed without any information on the LGE extent measured at the CMR-1. LGE progression rate was calculated by the ratio between the %LGE increases and the time interval in months between the two CMR scans.
Statistical analysis Data are expressed as mean±SD or median with IQRs for continuous variables and as numbers ( percentages) for categorical variables, as appropriate. After assessing normality distribution Choi H-M, et al. Heart 2015;101:870–876. doi:10.1136/heartjnl-2014-306555
for continuous variables with Shapiro–Wilk test, two-sided Wilcoxon signed-rank test or paired t test was performed. The χ2 or Fisher’s exact test was conducted for non-continuous variables. Correlation was tested with Pearson’s correlation coefficient. LGE changes was separately analysed by two independent readers (H-MC and K-HK) and compared for interobserver agreement, and again confirmed by the independent third expert reader (E-AP). Intraobserver agreement was assessed by one observer (H-MC) at least three months apart. Four percentage of absolute LGE increase between the two CMR examinations was considered a meaningful LGE change. Technical and statistical backgrounds of selecting 4% as a meaningful change are described in detail in online supplementary table S1.
Table 1
Baseline characteristics of recruited patients with HCM n=71
Patient characteristics Age at study enrolment (years) Age at diagnosis (years) Male (%) Rate pressure product Hypertension, n (%) Diabetes mellitus, n (%) Smoking, n (%) Current smoker Ex-smoker Non-smoker Cerebrovascular accident, n (%) NYHA class at enrolment, n (%) I II II IV Types of HCM Apical Septal Diffuse/mixed Echocardiographic parameters LVEF (%) Left atrial size (mm) LVOT pressure gradient >30 mm Hg SCD risk factors Prior cardiac arrest or sustained ventricular tachycardia Family history of sudden death Unexplained syncope History of non-sustained ventricular tachycardia Maximal wall thickness > 30 mm Abnormal blood pressure response during exercise test Number of SCD risk factors 0 1 ≥2 Medications Beta–blocker Calcium channel blocker RAS blockade Diuretics
59.0±13.4 53.7±14.6 48 (67.6) 8275.2±1463.1 36 (50.7) 10 (14.1) 9 (12.7) 6 (8.5) 56 (78.9) 4 (5.6) 31 (43.7) 35 (49.3) 5 (7.0) 0 (0) 19 (26.8) 30 (42.3) 22 (31.0) 66.5±7.0 45.4±6.4 17 (23.9) 0 (0.0) 13 (18.3) 9 (12.7) 5 (7.0) 4 (5.6) 3 (4.2) 35 (49.3) 23 (32.4) 13 (18.3) 36 (50.7) 28 (39.4) 23 (32.4) 6 (8.5)
HCM, hypertrophic cardiomyopathy; LVOT, LV outflow tract; NYHA, New York Heart Association; RAS, renin–angiotensin system; SCD, sudden cardiac death.
871
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Heart failure and cardiomyopathies Table 2 Changes in CMR parameters
CMR parameters LV end-diastolic volume (mL) LV end-systolic volume (mL) LVEF (%) Maximal end-diastolic thickness (mm) LV mass index (g/m2) LGE Presence of LGE LGE extent (%) Median (IQR)
CMR-1
CMR-2
p Value
149.5±32.5 50.7±16.9 66.9±5.7 22.3±4.8
147.7±32.7 49.3±17.3 67.2±6.2 22.7±4.9
0.55 0.28 0.57 0.007
106.0±30.5
104.9±29.3
0.57
65 (91.5) 7.0±6.5 5.9 (1.9, 10.8)
65 (91.5) 9.4±8.9 6.5 (2.5, 15.5)
1.00
Heart failure and cardiomyopathies
ORIGINAL ARTICLE
Myocardial fibrosis progression on cardiac magnetic resonance in hypertrophic cardiomyopathy Hong-Mi Choi,1 Kyung-Hee Kim,2 Joo Myung Lee,1 Yeonyee E Yoon,1 Seung-Pyo Lee,1 Eun-Ah Park,3 Whal Lee,3 Yong-Jin Kim,1 Goo-Yeong Cho,1 Dae-Won Sohn,1 Hyung-Kwan Kim1 ▸ Additional material is published online only. To view please visit the journal online (http://dx.doi.org/10.1136/ heartjnl-2014-306555). 1
Department of Internal Medicine, Cardiovascular Center, Seoul National University College of Medicine, Seoul National University Hospital, Seoul, Republic of Korea 2 Department of Internal Medicine, Division of Cardiology, Sejong General Hospital 3 Department of Radiology, Cardiovascular Section, Seoul National University College of Medicine, Seoul National University Hospital, Seoul, Republic of Korea Correspondence to Professor Hyung-Kwan Kim, Division of Cardiology, Department of Internal Medicine, Seoul National University College of Medicine, 101 Daehak-ro, Jongno-gu, Seoul 110-744, Republic of Korea; [email protected] or [email protected] Received 22 July 2014 Revised 10 February 2015 Accepted 20 March 2015 Published Online First 20 April 2015
ABSTRACT Objective We hypothesised that, in hypertrophic cardiomyopathy (HCM), late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) is progressive and can be predicted by baseline CMR findings and HCM phenotype. Methods In this single-centre cohort study, 71 patients with HCM (59±13 years; 48 men) were prospectively enrolled with clinical, echocardiographic and CMR data. Two consecutive CMR scans were performed with a time interval of 582±174 days. The LGE extent was quantified as a proportion of total LV myocardium (%LGE). Results LGE was present in 65 patients (91.5%) at the first CMR (CMR-1). In all, LGE extent was significantly increased ( p5 SD than mean signal intensity of normal myocardium were defined as segments with LGE.9 10 LGE extent in each segment was expressed as the surface area showing LGE divided by the total area of the given myocardial segment, and then summation of the planimetered LGE areas in all short-axis slices yielded total LGE extent, which was subsequently expressed as a proportion of total LV myocardium (% LGE). LGE quantification of CMR-2 was performed without any information on the LGE extent measured at the CMR-1. LGE progression rate was calculated by the ratio between the %LGE increases and the time interval in months between the two CMR scans.
Statistical analysis Data are expressed as mean±SD or median with IQRs for continuous variables and as numbers ( percentages) for categorical variables, as appropriate. After assessing normality distribution Choi H-M, et al. Heart 2015;101:870–876. doi:10.1136/heartjnl-2014-306555
for continuous variables with Shapiro–Wilk test, two-sided Wilcoxon signed-rank test or paired t test was performed. The χ2 or Fisher’s exact test was conducted for non-continuous variables. Correlation was tested with Pearson’s correlation coefficient. LGE changes was separately analysed by two independent readers (H-MC and K-HK) and compared for interobserver agreement, and again confirmed by the independent third expert reader (E-AP). Intraobserver agreement was assessed by one observer (H-MC) at least three months apart. Four percentage of absolute LGE increase between the two CMR examinations was considered a meaningful LGE change. Technical and statistical backgrounds of selecting 4% as a meaningful change are described in detail in online supplementary table S1.
Table 1
Baseline characteristics of recruited patients with HCM n=71
Patient characteristics Age at study enrolment (years) Age at diagnosis (years) Male (%) Rate pressure product Hypertension, n (%) Diabetes mellitus, n (%) Smoking, n (%) Current smoker Ex-smoker Non-smoker Cerebrovascular accident, n (%) NYHA class at enrolment, n (%) I II II IV Types of HCM Apical Septal Diffuse/mixed Echocardiographic parameters LVEF (%) Left atrial size (mm) LVOT pressure gradient >30 mm Hg SCD risk factors Prior cardiac arrest or sustained ventricular tachycardia Family history of sudden death Unexplained syncope History of non-sustained ventricular tachycardia Maximal wall thickness > 30 mm Abnormal blood pressure response during exercise test Number of SCD risk factors 0 1 ≥2 Medications Beta–blocker Calcium channel blocker RAS blockade Diuretics
59.0±13.4 53.7±14.6 48 (67.6) 8275.2±1463.1 36 (50.7) 10 (14.1) 9 (12.7) 6 (8.5) 56 (78.9) 4 (5.6) 31 (43.7) 35 (49.3) 5 (7.0) 0 (0) 19 (26.8) 30 (42.3) 22 (31.0) 66.5±7.0 45.4±6.4 17 (23.9) 0 (0.0) 13 (18.3) 9 (12.7) 5 (7.0) 4 (5.6) 3 (4.2) 35 (49.3) 23 (32.4) 13 (18.3) 36 (50.7) 28 (39.4) 23 (32.4) 6 (8.5)
HCM, hypertrophic cardiomyopathy; LVOT, LV outflow tract; NYHA, New York Heart Association; RAS, renin–angiotensin system; SCD, sudden cardiac death.
871
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Heart failure and cardiomyopathies Table 2 Changes in CMR parameters
CMR parameters LV end-diastolic volume (mL) LV end-systolic volume (mL) LVEF (%) Maximal end-diastolic thickness (mm) LV mass index (g/m2) LGE Presence of LGE LGE extent (%) Median (IQR)
CMR-1
CMR-2
p Value
149.5±32.5 50.7±16.9 66.9±5.7 22.3±4.8
147.7±32.7 49.3±17.3 67.2±6.2 22.7±4.9
0.55 0.28 0.57 0.007
106.0±30.5
104.9±29.3
0.57
65 (91.5) 7.0±6.5 5.9 (1.9, 10.8)
65 (91.5) 9.4±8.9 6.5 (2.5, 15.5)
1.00
