Data in Brief 15 (2017) 30–39
Contents lists available at ScienceDirect
Data in Brief journal homepage: www.elsevier.com/locate/dib
Data Article
Data on exercise and cardiac imaging in a patient cohort with hypertrophic cardiomyopathy Lars A. Dejgaard a,b, Trine F. Haland a,b,c, Oyvind H. Lie a,b, Margareth Ribe a, Thea Bjune a, Ida Skrinde Leren a, Knut Erik Berge d, Thor Edvardsen a,b,c, Kristina H. Haugaa a,b,c,⁎ a Department of Cardiology and Center for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, Oslo, Norway b Institute for Clinical Medicine, University of Oslo, Oslo, Norway c Institute for Surgical Research, Oslo University Hospital, Rikshospitalet, Oslo, Norway d Unit for Cardiac and Cardiovascular Genetics, Department of Medical Genetics, Oslo University Hospital, Oslo, Norway
a r t i c l e i n f o
abstract
Article history: Received 7 July 2017 Received in revised form 4 August 2017 Accepted 24 August 2017 Available online 12 September 2017
Data presented in this paper are supplementary material to our study “Vigorous exercise in patients with hypertrophic cardiomyopathy” [1]. The current article presents supplementary data on collection and analyses of exercise parameters and genetic data in the original research article. & 2017 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
Keywords: Hypertrophic cardiomyopathy Exercise Genetics Arrhythmia
DOI of original article: http://dx.doi.org/10.1016/j.ijcard.2017.07.015 Corresponding author at: Department of Cardiology and Center for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, Oslo, Norway. E-mail address: [email protected] (K.H. Haugaa). ⁎
http://dx.doi.org/10.1016/j.dib.2017.08.018 2352-3409/& 2017 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
L.A. Dejgaard et al. / Data in Brief 15 (2017) 30–39
31
Specifications Table Subject area More specific subject area Type of data How data was acquired
Medicine Cardiology- cardiomyopathies Tables, images, questionnaire Survey (physical activity questionnaire), Echocardiography (Vivid 7 and Vivid E9 - GE Healthcare, Horten, Norway), Cardiac magnetic resonance (Magnetom Sonata and Magnetom Avanto Siemens, Erlangen, Germany), Holter Analyzed and raw material Statistical analysis with SPSS version 21.0, SPSS Inc., Chicago, IL, USA.
Data format Experimental factors Experimental Cross-sectional population study features Data source location Oslo, Norway Data accessibility Data is with this article Value of the data
Extensive clinical information and imaging data on study subjects. Extensive information on exercise habits and clinical endpoints in our hypertrophic cardiomyopathy study cohort.
Physical exercise questionnaire used in the survey Complete genetic information on all mutations in our hypertrophic cardiomyopathy study cohort, with potential for pooling of data and study mutation-specific variations in phenotypic expression.
1. Data The data presented in this article are supplementary material to our study on vigorous exercise in hypertrophic cardiomyopathy patients. [1]. Fig. A.1 displays study flowchart and A.2 and A.3 represent the letter and the physical activity questionnaire sent to study participants. Tables B.1 and B.2 are logistic regression models presenting markers of hypertrophic cardiomyopathy phenotype and ventricular arrhythmias. Table B.3 presents specific information on genetic mutations. Table B.4 contains clinical and imaging data related to hypertrophic cardiomyopathy phenotype and exercise status. Table B.5 shows additional exercise data.
2. Experimental design, materials and methods The study design was cross-sectional. Time of study inclusion was the first clinical evaluation and echocardiogram in the outpatient clinic, Unit for Genetic Cardiac Diseases, Department of Cardiology, Oslo University Hospital, Rikshospitalet, Norway (Fig. A.1). Hypertrophic cardiomyopathy genotype positive, phenotype negative (Genotypeþ LVH-) and hypertrophic cardiomyopathy phenotype positive (HCM LVHþ) patients were included. Inclusion commenced in 2001 and ended in 2015 [1]. In May 2015 we cross checked the HCM cohort against the Norwegian death registry and found 14 deaths, of which cause of death was documented for all cases in the medical journals, and is reproduced in Fig. A.1. During May 2015 we completed a physical activity survey via letter (A.2 and A.3) among the 260 live subjects enrolled in our HCM cohort. Non-responders were contacted by phone and offered the possibility of completing the physical activity questionnaire via structured interview (A.3).
32
L.A. Dejgaard et al. / Data in Brief 15 (2017) 30–39
Study participants who were actively participating in organized or competitive sports at study inclusion, were defined as competitive athletes.
Funding sources This work was supported by the Norwegian Research Council [203489/030].
Appendix A See Figs. A.1–A.3 here.
Fig. A.1. Study flow chart. HCM LVHþ ¼ Hypertrophic cardiomyopathy phenotype positive; Genotypeþ LVH- ¼Hypertrophic cardiomyopathy genotype positive, phenotype negative.
L.A. Dejgaard et al. / Data in Brief 15 (2017) 30–39
33
Fig. A.2. Letter sent to study participants together with physical activity questionnaire (A.3). Translated from Norwegian to English by the authors.
34
L.A. Dejgaard et al. / Data in Brief 15 (2017) 30–39
Fig. A.3. Physical activity questionnaire used in our survey. Translated from Norwegian to English by the authors.
L.A. Dejgaard et al. / Data in Brief 15 (2017) 30–39
35
Appendix B See Tables B.1–B.5 here. Table B.1 Markers of hypertrophic cardiomyopathy phenotype positive (HCM LVH þ) (n ¼ 121) in 187 study participants. Markers of HCM LVH þ (n¼ 121) in 187 study participants
Athlete (yes vs. no) Age (years) Body mass index (kg/m2) Gender (male vs. female)
Univariate logistic regression
Multivariate logistic regression
OR, 95% CI
P
OR, 95% CI
P
0.78 (0.42–1.43) 1.08 (1.05–1.11) 1.17 (1.07–1.28) 2.76 (1.48–5.13)
0.42 o 0.001 0.001 0.001
0.73 (0.32–1.67) 1.07 (1.05–1.11) 1.06 (0.97–1.17) 4.17 (1.85–9.38)
0.46 o0.001 0.20 0.001
Values are odds ratio (OR) and p-values by univariate and multivariate logistic regression. CI ¼confidence interval; HCM LVHþ ¼ hypertrophic cardiomyopathy phenotype positive.
Table B.2 Markers of ventricular arrhythmia (n ¼28) in 121 hypertrophic cardiomyopathy phenotype positive. Markers of ventricular arrhythmia (n¼ 28) in 121 HCM LVHþ Univariate logistic regression
Multivariate logistic regression
OR, 95% CI
P
OR, 95% CI
P
Age (years) Athlete (yes vs. no) Body mass index (kg/m²) Gender (male vs. female)
0.99 (0.96–1.02) 0.85 (0.36–2.03) 1.02 (0.92–1.13) 1.24 (0.53–2.93)
0.34 0.71 0.68 0.62
0.72 (0.29–1.83)
0.50
Echocardiography Ejection fraction (%) Global longitudinal strain (%) Left atrium diameter (mm) Left atrium area index (cm²/m²) Left ventricular maximal wall thickness (mm) LVOT peak gradient (mmHg) LVOT peak gradient Z50 mmHg (yes vs. no)
0.93 (0.87–0.99) 1.21 (1.06–1.38) 0.96 (0.91–1.01) 0.91 (0.79–1.04) 1.16 (1.05–1.30) 0.99 (0.97–1.00) 3.3 (0.93–12.00)
0.03 0.005 0.14 0.15 0.006 0.07 0.07
1.16 (0.98–1.36)
0.08
1.08 (0.95–1.23)
0.23
Values are odds ratio (OR) and p-values by univariate and multivariate logistic regression. CI ¼confidence interval; HCM LVHþ ¼ hypertrophic cardiomyopathy phenotype positive; LVOT¼ left ventricular outlet tract.
36
Table B.3 Frequency of sarcomeric mutations (n ¼127) in the study cohort (n ¼ 187). Ref.seq
Amino Acid
c.DNA
Genomic_ref. data
rs
Affected individuals
MYBPC3 MYBPC3 MYH7 MYL2 MYBPC3 MYBPC3 MYL3 MYBPC3 MYBPC3 MYH7 MYBPC3 MYBPC3 MYBPC3 MYBPC3 MYBPC3 MYBPC3 MYH7 MYH7 MYH7 TINNI3 MYBPC3 MYBPC3 MYBPC3 MYBPC3 MYBPC3 MYBPC3 MYH7 MYH7 MYH7 MYH7 MYH7 MYH7 MYH7 MYH7 MYH7 TINNI3 TNNI3 TNNT2 TNNT2 TNNT2
NM_000256.3 NM_000256.3 NM_000257.2 NM_000432.3 NM_000256.3 NM_000256.3 NM_000258.2 NM_000256.3 NM_000256.3 NM_000257.2 NM_000256.3 NM_000256.3 NM_000256.3 NM_000256.3 NM_000256.3 NM_000256.3 NM_000257.2 NM_000257.2 NM_000257.2 NM_000363.4 NM_000256.3 NM_000256.3 NM_000256.3 NM_000256.3 NM_000256.3 NM_000256.3 NM_000257.2 NM_000257.2 NM_000257.2 NM_000257.2 NM_000257.2 NM_000257.2 NM_000257.2 NM_000257.2 NM_000257.2 NM_000363.4 NM_000363.4 NM_001001430.2 NM_001001430.2 NM_001001430.2
Splice mutation p.W792Vfs*41 p.R1420W p.R58* p.D770N p.R502W p.A57D p.G1249V p.E611K p.R442C p.W965* p.F271* p.K185Wfs*12 p.Q969* p.Y548Profs*19 p.I49del p.T1377M p.V606M p.D554E p.D196N p.Y237S p.L1238P p.Q998E p.P955Rfs*95) p.Y816* p.Y79* p.S1924Afs*9 p.R1818W p.R1696Q p.R1677H p.M982T p.I913_Q914delinsK p.R858C p.M849W p.A797T p.V147L p.A157V p.R278H p.K253R p.E195K
c.3190 þ 2T4G c.2373dupG c.4258C 4T c.172C 4T c.2308G 4A c.1504C 4T c.170C4A c.3746G 4T c.1831G4A c.1324C 4 T c.965G 4 A c.812_821 þ12del c.553-562del c.2905C 4T c.1641_1642del c.146_148del c.4130C 4T c.1816G4A c.1662C 4A c.586G 4 A c.710A 4C c.3713T4C c.2992C 4G c.2864_2865del c.2448C 4A c.237C 4G c.5769delG c.5452C 4T c.5090G 4A c.5030G 4A c.2945T 4C c.2738del c.2572C 4T c.2546T 4C c.2389G 4A c.439G 4 C c.470C4T c.833G4A c.758A 4G c.583G 4 A
Chr11(GRCh37):g.47355106A 4C Chr11(GRCh37):g.47359281dup Chr14(GRCh37):g.23886807G 4A Chr12(GRCh37):g.111352092G 4A Chr11(GRCh37):g.47360071C4 T Chr11(GRCh37):g.47364249G 4 A Chr3(GRCh37):g.46902303G 4T Chr11(GRCh37):g.47353691C 4A Chr11(GRCh37):g.47362755C4T Chr14(GRCh37):g.23898247G4A Chr11(GRCh37):g.47367883C4 Chr11(GRCh37):g.47369396_47369417del Chr11(GRCh37):g.47371417_47371426del Chr11(GRCh37):g.47356593G4A Chr11(GRCh37):g.47363690_47363691del Chr11(GRCh37):g.47372934_47372936del Chr14(GRCh37):g.23887458G 4A Chr14(GRCh37):g.23896866C 4T Chr14(GRCh37):g.23897020G 4 T Chr19(GRCh37):g.55663249C 4 T Chr11(GRCh37):g.47370037T4 G Chr11(GRCh37):g.47353724A4 G Chr11(GRCh37):g.47355475G 4 C Chr11(GRCh37):g.47356633_47356634del Chr11(GRCh37):g.47359096G4 Chr11(GRCh37):g.47372845G 4 C Chr14(GRCh37):g.23882989del Chr14(GRCh37):g.23884311G 4A Chr14(GRCh37):g.23884905C 4 T Chr14(GRCh37):g.23884965C 4 T Chr14(GRCh37):g.23892910A 4G Chr14(GRCh37):g.23893298_23893300del Chr14(GRCh37):g.23894085G 4A Chr14(GRCh37):g.23894111A 4G Chr14(GRCh37):g.23894525C 4T Chr19(GRCh37):g.55665508C 4 G Chr19(GRCh37):g.55665477G4A Chr1(GRCh37):g.201328372C 4T Chr1(GRCh37):g.201330429T 4C Chr1(GRCh37):g.201331147C 4T
rs113358486 rs397515963 rs145213771 rs756671869 rs36211723 rs375882485 rs139794067 rs727504259 rs730880555 rs148808089
21 21 15 6 5 5 5 3 3 3 2 2 2 2 2 2 2 2 2 2 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1
rs397515992 rs398123279 rs781207661 rs397516201 rs121913627 rs750828477 rs104894727 rs397516070 rs730880702 rs11570112 rs397515990 rs730880698 rs763073072 rs766831916 rs730880914 rs145532615 rs2754158 rs397516156 rs3218716 rs777782551 rs397516353 rs397516484 rs3730238 rs150008205
L.A. Dejgaard et al. / Data in Brief 15 (2017) 30–39
Sarcomeric mutation
Table B.4 Clinical and cardiac imaging characteristics of 187 study participants, grouped according to phenotype and exercise status (competitive athletes vs. subjects not fulfilling competitive athlete definition). Genotype þ LVH−(n ¼ 66)
HCM LVH þ(n ¼ 121) Not fulfilling definition of competitive athlete (n¼ 110)
Competitive athlete (n¼ 11)
Age, years Atrial fibrillation, n (%) Betablocker therapy, n (%) Body mass index, kg/m² Female, n (%) Hypertension, n (%) Implantable cardiac defibrillator, n (%) Primary prevention, n (%) Secondary prevention, n (%)
41 7 15 0 8 (16) 24 7 4.4 33 (66) 3 (6) 0
27 7 10 0 0 23 7 2.8 9 (56) 0 0
55 7 14 19 (17) 89 (81) 27 7 4 45 (41) 12 (11) 15 (14) 12 (80) 3 (20)
48 7 15 0 7 (64) 25 7 4 2 (18) 0 1 (9) 1 (100) 0
Lifetime vigorous exercise, hours Sarcomere protein mutation, n (%) Ventricular arrhythmias, n (%) Cardiac arrest, n (%) NSVT, n (%)
1396 (0- 10208) 50 (100) 0
5706 (2689- 10384) 16 (100) 0
1464 (0- 35776) 53 (48) 25 (23) 3 (3) 22 (20)
7940 (2527- 13993) 8 (73) 3 (27) 0 3 (27)
Vigorous exercise age 7- 20 years, hours Vigorously exercising at study inclusion, n (%)
999 (0- 8752) 20 (40)
3400 (65- 8663) 16 (100)
549 (0- 10067) 23 (21)
1986 (728- 8489) 11 (100)
1.5 7 0.6 10.8 7 0.3 7.0 7 2.6 61 7 6 -21.5 7 2.2 8.5 7 2 34 7 6 8.7 7 3 48 7 4 27 7 3 85 7 26
1.9 7 0.5 14.4 7 0.2 5.4 7 0.9 58 7 4 -21.2 7 2.3 8.4 7 1 34 7 3 9.5 7 2 51 7 3 27 7 2 118 7 29
1.3 7 0.7 5.9 7 3 15 7 9 62 7 7 -16.5 7 3.5 16.9 7 0.4 43 7 8 12.5 7 3 47 7 6 24 7 4 81 7 29
1.5 7 0.6 8.5 7 3 10 7 6 60 7 5 -17.6 7 3.2 14.4 7 0.4 40 7 8 12.0 7 3 51 7 6 26 7 3 103 7 40
Echocardiography E/A e', cm/s E/e' Ejection fraction, % Global longitudinal strain, % Interventricular septal diameter, mm Left atrium diameter, mm Left atrium area index, cm²/m² LV end-diastolic diameter, mm LV end-diastolic diameter index, mm/m² LV end-diastolic volume, cm³
37
Competitive athlete (n¼ 16)
L.A. Dejgaard et al. / Data in Brief 15 (2017) 30–39
Not fulfilling definition of competitive athlete (n¼ 50)
38
Table B.4 (continued ) Genotype þ LVH−(n ¼ 66)
Stroke volume, cm³ Stroke volume index, cm³/m² Cardiac magnetic resonance, n (%) Ejection fraction, % LGE, n (%) # LGE, % of LV mass # LV mass, g LV mass index, g/m² Maximal wall thickness, mm
Not fulfilling definition of competitive athlete (n¼ 50)
Competitive athlete (n¼ 16)
Not fulfilling definition of competitive athlete (n¼ 110)
Competitive athlete (n¼ 11)
47 7 12 31 7 4 17 7 2 34 7 11 19 7 5 131 7 34 72 7 16 7.7 7 1
60 7 13 34 7 4 18 7 2 50 7 16 25 7 7 142 7 30 73 7 13 7.6 7 1
0 8.6 14 (28) 14 (100) 0
0 8.6 1 (6) 1 (100) 0
41 7 13 28 7 6 15 7 3 31 7 14 16 7 6 255 7 91 132 7 46 10.2 7 2 14 (2- 128) 56 (4- 166) 44 (40) 19.1 76 (69) 46 (61) 26 (34)
52 7 16 32 7 5 16 7 1 40 7 14 22 7 7 262 7 106 130 7 41 10.4 7 2 4 (2- 47) 41 (16- 65) 1 (9) 16.4 3 (27) 3 (100) 0
0
0
4 (5)
0
52 7 17 29 7 8 n¼0
68 717 35 7 8 n ¼0
50 7 17 25 7 8 n ¼ 69 (63) 70 7 9 41 (60) 0 (0- 23) 231 7 93 119 7 46 22.6 7 6
64 7 27 31 7 12 n ¼7 (64) 61 7 6 4 (57) 0 (0-17) 198 7 72 97 7 29 17.8 7 3
Values are mean 7 SD or n (%) or median (range). Genotype þ LVH- ¼hypertrophic cardiomyopathy genotype positive, phenotype negative; HCM LVH þ ¼hypertrophic cardiomyopathy phenotype positive; LGE ¼late gadolinium enhancement; LV ¼ left ventricle; LVOT ¼left ventricular outlet tract; NSVT ¼non-sustained ventricular tachycardia. § n ¼ 36. # n¼ 74.
L.A. Dejgaard et al. / Data in Brief 15 (2017) 30–39
LV end-diastolic volume index, cm³/m² LV end-systolic diameter, mm LV end-systolic diameter index, mm/m² LV end-systolic volume, cm³ LV end-systolic volume index, cm³/m² LV mass, g LV mass index, g/m² LV posterior wall diameter, mm LVOT max gradient, rest/Valsalva, mmHg LVOT max gradient, stress-echo, mmHg § LVOT max gradient Z 50 mmHg, n (%) Maximal wall thickness, mm Mitral regurgitation, n (%) Mild regurgitation, n (%) Moderate regurgitation, n (%) Severe regurgitation, n (%)
HCM LVH þ(n ¼ 121)
L.A. Dejgaard et al. / Data in Brief 15 (2017) 30–39
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Table B.5 Frequency of types of main sport conducted in 187 study participants. Type of sport
Frequency
Percent
No exercise history Cycling Running Soccer Calisthenics Cross country skiing Handball Swimming Aerobics Dancing Field hockey Basketball Athletics Gymnastics Karate Pingpong Archery Badminton Figure skating Speed skating Alpine skiing Indoor cycling Tennis Total
46 27 25 15 13 10 9 9 5 5 4 4 2 2 2 2 1 1 1 1 1 1 1 187
24.6 14.4 13.4 8.0 7.0 5.3 4.8 4.8 2.7 2.7 2.1 2.1 1.1 1.1 1.1 1.1 0.5 0.5 0.5 0.5 0.5 0.5 0.5 100
Transparency document. Supplementary material Supplementary data associated with this article can be found in the online version at http://dx.doi. org/10.1016/j.dib.2017.08.018.
Reference [1] L.A. Dejgaard, T.F. Haland, O.H. Lie, M. Ribe, T. Bjune, I.S. Leren, K.E. Berge, T. Edvardsen, K.H. Haugaa, Vigorous exercise in patients with hypertrophic cardiomyopathy, Int. J. Cardiol. (2017), in press.
Contents lists available at ScienceDirect
Data in Brief journal homepage: www.elsevier.com/locate/dib
Data Article
Data on exercise and cardiac imaging in a patient cohort with hypertrophic cardiomyopathy Lars A. Dejgaard a,b, Trine F. Haland a,b,c, Oyvind H. Lie a,b, Margareth Ribe a, Thea Bjune a, Ida Skrinde Leren a, Knut Erik Berge d, Thor Edvardsen a,b,c, Kristina H. Haugaa a,b,c,⁎ a Department of Cardiology and Center for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, Oslo, Norway b Institute for Clinical Medicine, University of Oslo, Oslo, Norway c Institute for Surgical Research, Oslo University Hospital, Rikshospitalet, Oslo, Norway d Unit for Cardiac and Cardiovascular Genetics, Department of Medical Genetics, Oslo University Hospital, Oslo, Norway
a r t i c l e i n f o
abstract
Article history: Received 7 July 2017 Received in revised form 4 August 2017 Accepted 24 August 2017 Available online 12 September 2017
Data presented in this paper are supplementary material to our study “Vigorous exercise in patients with hypertrophic cardiomyopathy” [1]. The current article presents supplementary data on collection and analyses of exercise parameters and genetic data in the original research article. & 2017 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
Keywords: Hypertrophic cardiomyopathy Exercise Genetics Arrhythmia
DOI of original article: http://dx.doi.org/10.1016/j.ijcard.2017.07.015 Corresponding author at: Department of Cardiology and Center for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, Oslo, Norway. E-mail address: [email protected] (K.H. Haugaa). ⁎
http://dx.doi.org/10.1016/j.dib.2017.08.018 2352-3409/& 2017 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
L.A. Dejgaard et al. / Data in Brief 15 (2017) 30–39
31
Specifications Table Subject area More specific subject area Type of data How data was acquired
Medicine Cardiology- cardiomyopathies Tables, images, questionnaire Survey (physical activity questionnaire), Echocardiography (Vivid 7 and Vivid E9 - GE Healthcare, Horten, Norway), Cardiac magnetic resonance (Magnetom Sonata and Magnetom Avanto Siemens, Erlangen, Germany), Holter Analyzed and raw material Statistical analysis with SPSS version 21.0, SPSS Inc., Chicago, IL, USA.
Data format Experimental factors Experimental Cross-sectional population study features Data source location Oslo, Norway Data accessibility Data is with this article Value of the data
Extensive clinical information and imaging data on study subjects. Extensive information on exercise habits and clinical endpoints in our hypertrophic cardiomyopathy study cohort.
Physical exercise questionnaire used in the survey Complete genetic information on all mutations in our hypertrophic cardiomyopathy study cohort, with potential for pooling of data and study mutation-specific variations in phenotypic expression.
1. Data The data presented in this article are supplementary material to our study on vigorous exercise in hypertrophic cardiomyopathy patients. [1]. Fig. A.1 displays study flowchart and A.2 and A.3 represent the letter and the physical activity questionnaire sent to study participants. Tables B.1 and B.2 are logistic regression models presenting markers of hypertrophic cardiomyopathy phenotype and ventricular arrhythmias. Table B.3 presents specific information on genetic mutations. Table B.4 contains clinical and imaging data related to hypertrophic cardiomyopathy phenotype and exercise status. Table B.5 shows additional exercise data.
2. Experimental design, materials and methods The study design was cross-sectional. Time of study inclusion was the first clinical evaluation and echocardiogram in the outpatient clinic, Unit for Genetic Cardiac Diseases, Department of Cardiology, Oslo University Hospital, Rikshospitalet, Norway (Fig. A.1). Hypertrophic cardiomyopathy genotype positive, phenotype negative (Genotypeþ LVH-) and hypertrophic cardiomyopathy phenotype positive (HCM LVHþ) patients were included. Inclusion commenced in 2001 and ended in 2015 [1]. In May 2015 we cross checked the HCM cohort against the Norwegian death registry and found 14 deaths, of which cause of death was documented for all cases in the medical journals, and is reproduced in Fig. A.1. During May 2015 we completed a physical activity survey via letter (A.2 and A.3) among the 260 live subjects enrolled in our HCM cohort. Non-responders were contacted by phone and offered the possibility of completing the physical activity questionnaire via structured interview (A.3).
32
L.A. Dejgaard et al. / Data in Brief 15 (2017) 30–39
Study participants who were actively participating in organized or competitive sports at study inclusion, were defined as competitive athletes.
Funding sources This work was supported by the Norwegian Research Council [203489/030].
Appendix A See Figs. A.1–A.3 here.
Fig. A.1. Study flow chart. HCM LVHþ ¼ Hypertrophic cardiomyopathy phenotype positive; Genotypeþ LVH- ¼Hypertrophic cardiomyopathy genotype positive, phenotype negative.
L.A. Dejgaard et al. / Data in Brief 15 (2017) 30–39
33
Fig. A.2. Letter sent to study participants together with physical activity questionnaire (A.3). Translated from Norwegian to English by the authors.
34
L.A. Dejgaard et al. / Data in Brief 15 (2017) 30–39
Fig. A.3. Physical activity questionnaire used in our survey. Translated from Norwegian to English by the authors.
L.A. Dejgaard et al. / Data in Brief 15 (2017) 30–39
35
Appendix B See Tables B.1–B.5 here. Table B.1 Markers of hypertrophic cardiomyopathy phenotype positive (HCM LVH þ) (n ¼ 121) in 187 study participants. Markers of HCM LVH þ (n¼ 121) in 187 study participants
Athlete (yes vs. no) Age (years) Body mass index (kg/m2) Gender (male vs. female)
Univariate logistic regression
Multivariate logistic regression
OR, 95% CI
P
OR, 95% CI
P
0.78 (0.42–1.43) 1.08 (1.05–1.11) 1.17 (1.07–1.28) 2.76 (1.48–5.13)
0.42 o 0.001 0.001 0.001
0.73 (0.32–1.67) 1.07 (1.05–1.11) 1.06 (0.97–1.17) 4.17 (1.85–9.38)
0.46 o0.001 0.20 0.001
Values are odds ratio (OR) and p-values by univariate and multivariate logistic regression. CI ¼confidence interval; HCM LVHþ ¼ hypertrophic cardiomyopathy phenotype positive.
Table B.2 Markers of ventricular arrhythmia (n ¼28) in 121 hypertrophic cardiomyopathy phenotype positive. Markers of ventricular arrhythmia (n¼ 28) in 121 HCM LVHþ Univariate logistic regression
Multivariate logistic regression
OR, 95% CI
P
OR, 95% CI
P
Age (years) Athlete (yes vs. no) Body mass index (kg/m²) Gender (male vs. female)
0.99 (0.96–1.02) 0.85 (0.36–2.03) 1.02 (0.92–1.13) 1.24 (0.53–2.93)
0.34 0.71 0.68 0.62
0.72 (0.29–1.83)
0.50
Echocardiography Ejection fraction (%) Global longitudinal strain (%) Left atrium diameter (mm) Left atrium area index (cm²/m²) Left ventricular maximal wall thickness (mm) LVOT peak gradient (mmHg) LVOT peak gradient Z50 mmHg (yes vs. no)
0.93 (0.87–0.99) 1.21 (1.06–1.38) 0.96 (0.91–1.01) 0.91 (0.79–1.04) 1.16 (1.05–1.30) 0.99 (0.97–1.00) 3.3 (0.93–12.00)
0.03 0.005 0.14 0.15 0.006 0.07 0.07
1.16 (0.98–1.36)
0.08
1.08 (0.95–1.23)
0.23
Values are odds ratio (OR) and p-values by univariate and multivariate logistic regression. CI ¼confidence interval; HCM LVHþ ¼ hypertrophic cardiomyopathy phenotype positive; LVOT¼ left ventricular outlet tract.
36
Table B.3 Frequency of sarcomeric mutations (n ¼127) in the study cohort (n ¼ 187). Ref.seq
Amino Acid
c.DNA
Genomic_ref. data
rs
Affected individuals
MYBPC3 MYBPC3 MYH7 MYL2 MYBPC3 MYBPC3 MYL3 MYBPC3 MYBPC3 MYH7 MYBPC3 MYBPC3 MYBPC3 MYBPC3 MYBPC3 MYBPC3 MYH7 MYH7 MYH7 TINNI3 MYBPC3 MYBPC3 MYBPC3 MYBPC3 MYBPC3 MYBPC3 MYH7 MYH7 MYH7 MYH7 MYH7 MYH7 MYH7 MYH7 MYH7 TINNI3 TNNI3 TNNT2 TNNT2 TNNT2
NM_000256.3 NM_000256.3 NM_000257.2 NM_000432.3 NM_000256.3 NM_000256.3 NM_000258.2 NM_000256.3 NM_000256.3 NM_000257.2 NM_000256.3 NM_000256.3 NM_000256.3 NM_000256.3 NM_000256.3 NM_000256.3 NM_000257.2 NM_000257.2 NM_000257.2 NM_000363.4 NM_000256.3 NM_000256.3 NM_000256.3 NM_000256.3 NM_000256.3 NM_000256.3 NM_000257.2 NM_000257.2 NM_000257.2 NM_000257.2 NM_000257.2 NM_000257.2 NM_000257.2 NM_000257.2 NM_000257.2 NM_000363.4 NM_000363.4 NM_001001430.2 NM_001001430.2 NM_001001430.2
Splice mutation p.W792Vfs*41 p.R1420W p.R58* p.D770N p.R502W p.A57D p.G1249V p.E611K p.R442C p.W965* p.F271* p.K185Wfs*12 p.Q969* p.Y548Profs*19 p.I49del p.T1377M p.V606M p.D554E p.D196N p.Y237S p.L1238P p.Q998E p.P955Rfs*95) p.Y816* p.Y79* p.S1924Afs*9 p.R1818W p.R1696Q p.R1677H p.M982T p.I913_Q914delinsK p.R858C p.M849W p.A797T p.V147L p.A157V p.R278H p.K253R p.E195K
c.3190 þ 2T4G c.2373dupG c.4258C 4T c.172C 4T c.2308G 4A c.1504C 4T c.170C4A c.3746G 4T c.1831G4A c.1324C 4 T c.965G 4 A c.812_821 þ12del c.553-562del c.2905C 4T c.1641_1642del c.146_148del c.4130C 4T c.1816G4A c.1662C 4A c.586G 4 A c.710A 4C c.3713T4C c.2992C 4G c.2864_2865del c.2448C 4A c.237C 4G c.5769delG c.5452C 4T c.5090G 4A c.5030G 4A c.2945T 4C c.2738del c.2572C 4T c.2546T 4C c.2389G 4A c.439G 4 C c.470C4T c.833G4A c.758A 4G c.583G 4 A
Chr11(GRCh37):g.47355106A 4C Chr11(GRCh37):g.47359281dup Chr14(GRCh37):g.23886807G 4A Chr12(GRCh37):g.111352092G 4A Chr11(GRCh37):g.47360071C4 T Chr11(GRCh37):g.47364249G 4 A Chr3(GRCh37):g.46902303G 4T Chr11(GRCh37):g.47353691C 4A Chr11(GRCh37):g.47362755C4T Chr14(GRCh37):g.23898247G4A Chr11(GRCh37):g.47367883C4 Chr11(GRCh37):g.47369396_47369417del Chr11(GRCh37):g.47371417_47371426del Chr11(GRCh37):g.47356593G4A Chr11(GRCh37):g.47363690_47363691del Chr11(GRCh37):g.47372934_47372936del Chr14(GRCh37):g.23887458G 4A Chr14(GRCh37):g.23896866C 4T Chr14(GRCh37):g.23897020G 4 T Chr19(GRCh37):g.55663249C 4 T Chr11(GRCh37):g.47370037T4 G Chr11(GRCh37):g.47353724A4 G Chr11(GRCh37):g.47355475G 4 C Chr11(GRCh37):g.47356633_47356634del Chr11(GRCh37):g.47359096G4 Chr11(GRCh37):g.47372845G 4 C Chr14(GRCh37):g.23882989del Chr14(GRCh37):g.23884311G 4A Chr14(GRCh37):g.23884905C 4 T Chr14(GRCh37):g.23884965C 4 T Chr14(GRCh37):g.23892910A 4G Chr14(GRCh37):g.23893298_23893300del Chr14(GRCh37):g.23894085G 4A Chr14(GRCh37):g.23894111A 4G Chr14(GRCh37):g.23894525C 4T Chr19(GRCh37):g.55665508C 4 G Chr19(GRCh37):g.55665477G4A Chr1(GRCh37):g.201328372C 4T Chr1(GRCh37):g.201330429T 4C Chr1(GRCh37):g.201331147C 4T
rs113358486 rs397515963 rs145213771 rs756671869 rs36211723 rs375882485 rs139794067 rs727504259 rs730880555 rs148808089
21 21 15 6 5 5 5 3 3 3 2 2 2 2 2 2 2 2 2 2 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1
rs397515992 rs398123279 rs781207661 rs397516201 rs121913627 rs750828477 rs104894727 rs397516070 rs730880702 rs11570112 rs397515990 rs730880698 rs763073072 rs766831916 rs730880914 rs145532615 rs2754158 rs397516156 rs3218716 rs777782551 rs397516353 rs397516484 rs3730238 rs150008205
L.A. Dejgaard et al. / Data in Brief 15 (2017) 30–39
Sarcomeric mutation
Table B.4 Clinical and cardiac imaging characteristics of 187 study participants, grouped according to phenotype and exercise status (competitive athletes vs. subjects not fulfilling competitive athlete definition). Genotype þ LVH−(n ¼ 66)
HCM LVH þ(n ¼ 121) Not fulfilling definition of competitive athlete (n¼ 110)
Competitive athlete (n¼ 11)
Age, years Atrial fibrillation, n (%) Betablocker therapy, n (%) Body mass index, kg/m² Female, n (%) Hypertension, n (%) Implantable cardiac defibrillator, n (%) Primary prevention, n (%) Secondary prevention, n (%)
41 7 15 0 8 (16) 24 7 4.4 33 (66) 3 (6) 0
27 7 10 0 0 23 7 2.8 9 (56) 0 0
55 7 14 19 (17) 89 (81) 27 7 4 45 (41) 12 (11) 15 (14) 12 (80) 3 (20)
48 7 15 0 7 (64) 25 7 4 2 (18) 0 1 (9) 1 (100) 0
Lifetime vigorous exercise, hours Sarcomere protein mutation, n (%) Ventricular arrhythmias, n (%) Cardiac arrest, n (%) NSVT, n (%)
1396 (0- 10208) 50 (100) 0
5706 (2689- 10384) 16 (100) 0
1464 (0- 35776) 53 (48) 25 (23) 3 (3) 22 (20)
7940 (2527- 13993) 8 (73) 3 (27) 0 3 (27)
Vigorous exercise age 7- 20 years, hours Vigorously exercising at study inclusion, n (%)
999 (0- 8752) 20 (40)
3400 (65- 8663) 16 (100)
549 (0- 10067) 23 (21)
1986 (728- 8489) 11 (100)
1.5 7 0.6 10.8 7 0.3 7.0 7 2.6 61 7 6 -21.5 7 2.2 8.5 7 2 34 7 6 8.7 7 3 48 7 4 27 7 3 85 7 26
1.9 7 0.5 14.4 7 0.2 5.4 7 0.9 58 7 4 -21.2 7 2.3 8.4 7 1 34 7 3 9.5 7 2 51 7 3 27 7 2 118 7 29
1.3 7 0.7 5.9 7 3 15 7 9 62 7 7 -16.5 7 3.5 16.9 7 0.4 43 7 8 12.5 7 3 47 7 6 24 7 4 81 7 29
1.5 7 0.6 8.5 7 3 10 7 6 60 7 5 -17.6 7 3.2 14.4 7 0.4 40 7 8 12.0 7 3 51 7 6 26 7 3 103 7 40
Echocardiography E/A e', cm/s E/e' Ejection fraction, % Global longitudinal strain, % Interventricular septal diameter, mm Left atrium diameter, mm Left atrium area index, cm²/m² LV end-diastolic diameter, mm LV end-diastolic diameter index, mm/m² LV end-diastolic volume, cm³
37
Competitive athlete (n¼ 16)
L.A. Dejgaard et al. / Data in Brief 15 (2017) 30–39
Not fulfilling definition of competitive athlete (n¼ 50)
38
Table B.4 (continued ) Genotype þ LVH−(n ¼ 66)
Stroke volume, cm³ Stroke volume index, cm³/m² Cardiac magnetic resonance, n (%) Ejection fraction, % LGE, n (%) # LGE, % of LV mass # LV mass, g LV mass index, g/m² Maximal wall thickness, mm
Not fulfilling definition of competitive athlete (n¼ 50)
Competitive athlete (n¼ 16)
Not fulfilling definition of competitive athlete (n¼ 110)
Competitive athlete (n¼ 11)
47 7 12 31 7 4 17 7 2 34 7 11 19 7 5 131 7 34 72 7 16 7.7 7 1
60 7 13 34 7 4 18 7 2 50 7 16 25 7 7 142 7 30 73 7 13 7.6 7 1
0 8.6 14 (28) 14 (100) 0
0 8.6 1 (6) 1 (100) 0
41 7 13 28 7 6 15 7 3 31 7 14 16 7 6 255 7 91 132 7 46 10.2 7 2 14 (2- 128) 56 (4- 166) 44 (40) 19.1 76 (69) 46 (61) 26 (34)
52 7 16 32 7 5 16 7 1 40 7 14 22 7 7 262 7 106 130 7 41 10.4 7 2 4 (2- 47) 41 (16- 65) 1 (9) 16.4 3 (27) 3 (100) 0
0
0
4 (5)
0
52 7 17 29 7 8 n¼0
68 717 35 7 8 n ¼0
50 7 17 25 7 8 n ¼ 69 (63) 70 7 9 41 (60) 0 (0- 23) 231 7 93 119 7 46 22.6 7 6
64 7 27 31 7 12 n ¼7 (64) 61 7 6 4 (57) 0 (0-17) 198 7 72 97 7 29 17.8 7 3
Values are mean 7 SD or n (%) or median (range). Genotype þ LVH- ¼hypertrophic cardiomyopathy genotype positive, phenotype negative; HCM LVH þ ¼hypertrophic cardiomyopathy phenotype positive; LGE ¼late gadolinium enhancement; LV ¼ left ventricle; LVOT ¼left ventricular outlet tract; NSVT ¼non-sustained ventricular tachycardia. § n ¼ 36. # n¼ 74.
L.A. Dejgaard et al. / Data in Brief 15 (2017) 30–39
LV end-diastolic volume index, cm³/m² LV end-systolic diameter, mm LV end-systolic diameter index, mm/m² LV end-systolic volume, cm³ LV end-systolic volume index, cm³/m² LV mass, g LV mass index, g/m² LV posterior wall diameter, mm LVOT max gradient, rest/Valsalva, mmHg LVOT max gradient, stress-echo, mmHg § LVOT max gradient Z 50 mmHg, n (%) Maximal wall thickness, mm Mitral regurgitation, n (%) Mild regurgitation, n (%) Moderate regurgitation, n (%) Severe regurgitation, n (%)
HCM LVH þ(n ¼ 121)
L.A. Dejgaard et al. / Data in Brief 15 (2017) 30–39
39
Table B.5 Frequency of types of main sport conducted in 187 study participants. Type of sport
Frequency
Percent
No exercise history Cycling Running Soccer Calisthenics Cross country skiing Handball Swimming Aerobics Dancing Field hockey Basketball Athletics Gymnastics Karate Pingpong Archery Badminton Figure skating Speed skating Alpine skiing Indoor cycling Tennis Total
46 27 25 15 13 10 9 9 5 5 4 4 2 2 2 2 1 1 1 1 1 1 1 187
24.6 14.4 13.4 8.0 7.0 5.3 4.8 4.8 2.7 2.7 2.1 2.1 1.1 1.1 1.1 1.1 0.5 0.5 0.5 0.5 0.5 0.5 0.5 100
Transparency document. Supplementary material Supplementary data associated with this article can be found in the online version at http://dx.doi. org/10.1016/j.dib.2017.08.018.
Reference [1] L.A. Dejgaard, T.F. Haland, O.H. Lie, M. Ribe, T. Bjune, I.S. Leren, K.E. Berge, T. Edvardsen, K.H. Haugaa, Vigorous exercise in patients with hypertrophic cardiomyopathy, Int. J. Cardiol. (2017), in press.
