PURPOSE: To prospectively investigate the relationship between myocardial contractile impairment and left ventricular (LV) hypertrophy measured at cardiac magnetic resonance (MR) imaging in patients with hypertrophic cardiomyopathy (HCM) caused by the substitution of aspartic acid 175 with asparagine (ie, Asp175Asn mutation) in the alpha-tropomyosin gene (TPM1). MATERIALS AND METHODS: The study protocol was approved by the hospital ethics committee, and all subjects gave written informed consent. LV mass, maximal LV wall thickness, and myocardial fractional thickening during systole were measured at cine MR imaging in 24 subjects (11 male, 13 female; mean age, 42 years; age range, 17-68 years) with the Asp175Asn mutation in TPM1 and in 17 healthy volunteers (eight men, nine women; mean age, 38 years; age range, 23-60 years). The proportion of hypokinetic LV segments was calculated as the number of LV segments with fractional thickening of less than 30% divided by the total number of segments measured. Anthropometric and biochemical correlates of LV hypertrophy were determined. Univariate and multiple linear regression analyses were used to investigate the association of the proportion of hypokinetic segments and other correlates of LV hypertrophy with LV mass and maximal wall thickness. RESULTS: The proportion of hypokinetic segments was higher in patients with HCM than in control subjects (37% +/- 20 [standard deviation] vs 12% +/- 12, P < .001). In stepwise multiple regression analysis, the proportion of hypokinetic segments accounted for 42% (P < .001); the LV end-diastolic volume, for 24% (P = .003); and male sex, for 10% (P = .014) of the variability in LV mass in patients with HCM. The proportion of hypokinetic LV segments, which accounted for 48% of the variability in LV maximal wall thickness (P < .001), was the only variable significantly associated with maximal wall thickness. CONCLUSION: The extent of myocardial contractile impairment is strongly and independently related to LV mass and maximal wall thickness in patients with HCM attributable to the Asp175Asn mutation in TPM1.
PURPOSE: To prospectively investigate the relationship between myocardial contractile impairment and left ventricular (LV) hypertrophy measured at cardiac magnetic resonance (MR) imaging in patients with hypertrophic cardiomyopathy (HCM) caused by the substitution of aspartic acid 175 with asparagine (ie, Asp175Asn mutation) in the alpha-tropomyosin gene (TPM1). MATERIALS AND METHODS: The study protocol was approved by the hospital ethics committee, and all subjects gave written informed consent. LV mass, maximal LV wall thickness, and myocardial fractional thickening during systole were measured at cine MR imaging in 24 subjects (11 male, 13 female; mean age, 42 years; age range, 17-68 years) with the Asp175Asn mutation in TPM1 and in 17 healthy volunteers (eight men, nine women; mean age, 38 years; age range, 23-60 years). The proportion of hypokinetic LV segments was calculated as the number of LV segments with fractional thickening of less than 30% divided by the total number of segments measured. Anthropometric and biochemical correlates of LV hypertrophy were determined. Univariate and multiple linear regression analyses were used to investigate the association of the proportion of hypokinetic segments and other correlates of LV hypertrophy with LV mass and maximal wall thickness. RESULTS: The proportion of hypokinetic segments was higher in patients with HCM than in control subjects (37% +/- 20 [standard deviation] vs 12% +/- 12, P < .001). In stepwise multiple regression analysis, the proportion of hypokinetic segments accounted for 42% (P < .001); the LV end-diastolic volume, for 24% (P = .003); and male sex, for 10% (P = .014) of the variability in LV mass in patients with HCM. The proportion of hypokinetic LV segments, which accounted for 48% of the variability in LV maximal wall thickness (P < .001), was the only variable significantly associated with maximal wall thickness. CONCLUSION: The extent of myocardial contractile impairment is strongly and independently related to LV mass and maximal wall thickness in patients with HCM attributable to the Asp175Asn mutation in TPM1.
Authors: Petri Sipola; Jarkko Magga; Minna Husso; Pertti Jääskeläinen; Keijo Peuhkurinen; Johanna Kuusisto Journal: Eur Radiol Date: 2011-01-28 Impact factor: 5.315
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Authors: Mika Tarkiainen; Petri Sipola; Mikko Jalanko; Tiina Heliö; Pertti Jääskeläinen; Kati Kivelä; Mika Laine; Kirsi Lauerma; Johanna Kuusisto Journal: Sci Rep Date: 2019-04-11 Impact factor: 4.379
Authors: Pertti Jääskeläinen; Jagadish Vangipurapu; Joose Raivo; Teemu Kuulasmaa; Tiina Heliö; Katriina Aalto-Setälä; Maija Kaartinen; Erkki Ilveskoski; Sari Vanninen; Liisa Hämäläinen; John Melin; Jorma Kokkonen; Markku S Nieminen; Markku Laakso; Johanna Kuusisto Journal: ESC Heart Fail Date: 2019-02-18
Authors: Mika Tarkiainen; Petri Sipola; Mikko Jalanko; Tiina Heliö; Mika Laine; Vesa Järvinen; Kaisu Häyrinen; Kirsi Lauerma; Johanna Kuusisto Journal: J Cardiovasc Magn Reson Date: 2016-06-04 Impact factor: 5.364