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Comparative Study
Journal Article
Impact of disease activity on left ventricular performance in patients with acromegaly.
American Heart Journal 2002 September
BACKGROUND: In patients with acromegaly, abnormalities of systolic and diastolic left ventricular (LV) performance, mostly associated with hypertension or LV hypertrophy, have been reported. We used 2-dimensional/Doppler echocardiographic methods and tissue Doppler imaging (TDI) to elucidate the impact of disease activity on LV function in patients with acromegaly.
METHODS: In a prospective study design, 15 patients with active acromegaly (AA group; mean age-adjusted serum insuline-like growth factor-I [IGF-I] level, 420 +/- 170 ng/mL, mean growth hormone nadir during 75-g oral glucose load, 12.3 +/- 30.1 microg/L), 18 patients with cured (n = 14, mean IGF-I level 205 +/- 115 ng/mL, mean growth hormone nadir during glucose load 0.72 +/- 0.34 microg/L) or well-controlled (n = 4, normal age-adjusted ranges of IGF-I levels with medication with somatostatin analogues 354 +/- 88 ng/mL) acromegaly (CA group), and 24 control subjects (control group) underwent 2-dimensional/Doppler echocardiographic measurements, including assessment of the Tei index (isovolumic contraction time and isovolumic relaxation time divided by ejection time). Systolic and diastolic mitral annular velocities (peak systolic velocity, peak early diastolic velocity [E'], peak late diastolic velocity [A'], E'/A' ratio) were derived from pulsed TDI.
RESULTS: No significant differences between study groups were observed with respect to muscle mass and systolic parameters, such as ejection fraction, fractional shortening, and peak systolic velocity. In patients with AA, E' and the E'/A' ratio were lower than in control and CA subjects (AA 6.8 +/- 1.7 cm/s, control 10.0 +/- 1.7 cm/s, CA 9.1+/- 3.0 cm/s, P <.01 AA vs control, P <.05 AA versus CA, AA 0.68 +/- 0.22, control 0.98 +/- 0.16, CA 0.89 +/- 0.37, P <.01 AA vs control and CA, respectively). In comparison with control subjects and patients with CA, patients with AA had a reduced mitral peak velocity of early/late filling ratio (AA 0.78 +/- 0.22 m/s, control 1.12 +/- 0.33 m/s, CA 1.11 +/- 0.36 m/s, P <.05 AA vs control and CA) and a prolonged deceleration time (AA 223 +/- 41 ms, control 188 +/- 26 ms, CA 185 +/- 25 ms, P <.05 AA vs control and CA). The Tei index was significantly elevated in patients with AA in comparison with control subjects and patients with CA (AA 0.54 +/- 0.13, control 0.40 +/- 0.09, CA 0.44 +/- 0.10, P <.05 AA vs control and CA). No significant differences were observed between control subjects and patients with CA with respect to mitral flow-derived variables, TDI parameters, and the Tei index.
CONCLUSION: Disease activity has a significant impact on LV performance in patients with acromegaly. In subjects with active disease, diastolic dysfunction and beginning impairment of overall LV performance are present. In patients with cured/well-controlled disease, systolic and diastolic function appear normal.
METHODS: In a prospective study design, 15 patients with active acromegaly (AA group; mean age-adjusted serum insuline-like growth factor-I [IGF-I] level, 420 +/- 170 ng/mL, mean growth hormone nadir during 75-g oral glucose load, 12.3 +/- 30.1 microg/L), 18 patients with cured (n = 14, mean IGF-I level 205 +/- 115 ng/mL, mean growth hormone nadir during glucose load 0.72 +/- 0.34 microg/L) or well-controlled (n = 4, normal age-adjusted ranges of IGF-I levels with medication with somatostatin analogues 354 +/- 88 ng/mL) acromegaly (CA group), and 24 control subjects (control group) underwent 2-dimensional/Doppler echocardiographic measurements, including assessment of the Tei index (isovolumic contraction time and isovolumic relaxation time divided by ejection time). Systolic and diastolic mitral annular velocities (peak systolic velocity, peak early diastolic velocity [E'], peak late diastolic velocity [A'], E'/A' ratio) were derived from pulsed TDI.
RESULTS: No significant differences between study groups were observed with respect to muscle mass and systolic parameters, such as ejection fraction, fractional shortening, and peak systolic velocity. In patients with AA, E' and the E'/A' ratio were lower than in control and CA subjects (AA 6.8 +/- 1.7 cm/s, control 10.0 +/- 1.7 cm/s, CA 9.1+/- 3.0 cm/s, P <.01 AA vs control, P <.05 AA versus CA, AA 0.68 +/- 0.22, control 0.98 +/- 0.16, CA 0.89 +/- 0.37, P <.01 AA vs control and CA, respectively). In comparison with control subjects and patients with CA, patients with AA had a reduced mitral peak velocity of early/late filling ratio (AA 0.78 +/- 0.22 m/s, control 1.12 +/- 0.33 m/s, CA 1.11 +/- 0.36 m/s, P <.05 AA vs control and CA) and a prolonged deceleration time (AA 223 +/- 41 ms, control 188 +/- 26 ms, CA 185 +/- 25 ms, P <.05 AA vs control and CA). The Tei index was significantly elevated in patients with AA in comparison with control subjects and patients with CA (AA 0.54 +/- 0.13, control 0.40 +/- 0.09, CA 0.44 +/- 0.10, P <.05 AA vs control and CA). No significant differences were observed between control subjects and patients with CA with respect to mitral flow-derived variables, TDI parameters, and the Tei index.
CONCLUSION: Disease activity has a significant impact on LV performance in patients with acromegaly. In subjects with active disease, diastolic dysfunction and beginning impairment of overall LV performance are present. In patients with cured/well-controlled disease, systolic and diastolic function appear normal.
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