摘要
Aims: Dilated cardiomyopathy often shows left ventricular systolic dysfunction, although histologically it always exhibits non-specific abnormality. We hypothesized that myocyte sound speed might be altered due to incomplete protein accumulation in cells. Methods and Results: Ninety eight biopsied samples were obtained from 49 patients comprising 43 with clinical dilated cardiomyopathy and 6 with hypertrophic cardiomyopathy. Sound speed was evaluated in deparaffinized 10 μm thick sections using an acoustic microscope (frequency range: 50 - 105 MHz). Conventional histology revealed 7 cases of persistent myocarditis derived from clinical dilated cardio- myopathy samples. Histology of the remaining dilated cardiomyopathy patients indicated non-specific abnormality. All hypertrophic cardiomyopathy cases exhibited myocardial disarray. Ten normal autopsied hearts were compared as controls. The sound speed of controls was 1627 ± 30m/sec. The sound speed in dilated cardiomyopathy samples (1700 ±51m/sec) was 1.045-fold faster compared to controls. The sound speed in hypertrophic cardiomyopathy samples (1734 ±51m/sec, 1.066-fold compared to controls) was faster than that of the myocarditis group (1672 ±30m/sec, 1.028-fold) (P = 0.0218). Furtheremore, desmin expression was evaluated as extent of emergence (grading 0 - 4). The desmin expression score in hypertrophic cardiomyopathy samples (2.7 ± 0.8) was significantly higher than in other groups (dilated 2.0 ± 1.4, myocarditis 1.6 ± 1.5 vs., controls 0, P ≤ 0.0001, 0.0001, 0.0129, respectively). Conclusion: Cardio-myopathy enhanced the sound speed, which correlated with the elasticity of myocytes, following the impaired compliance of left ventricle, despite the absence of histological changes. The elevation of sound speed of myocytes may be linked to cytoskeletal changes. Myocyte sound speed may be a new diagnostic tool for diagnosis of idiopathic cardiomyopathy independently of conventional histological diagnosis.
Aims: Dilated cardiomyopathy often shows left ventricular systolic dysfunction, although histologically it always exhibits non-specific abnormality. We hypothesized that myocyte sound speed might be altered due to incomplete protein accumulation in cells. Methods and Results: Ninety eight biopsied samples were obtained from 49 patients comprising 43 with clinical dilated cardiomyopathy and 6 with hypertrophic cardiomyopathy. Sound speed was evaluated in deparaffinized 10 μm thick sections using an acoustic microscope (frequency range: 50 - 105 MHz). Conventional histology revealed 7 cases of persistent myocarditis derived from clinical dilated cardio- myopathy samples. Histology of the remaining dilated cardiomyopathy patients indicated non-specific abnormality. All hypertrophic cardiomyopathy cases exhibited myocardial disarray. Ten normal autopsied hearts were compared as controls. The sound speed of controls was 1627 ± 30m/sec. The sound speed in dilated cardiomyopathy samples (1700 ±51m/sec) was 1.045-fold faster compared to controls. The sound speed in hypertrophic cardiomyopathy samples (1734 ±51m/sec, 1.066-fold compared to controls) was faster than that of the myocarditis group (1672 ±30m/sec, 1.028-fold) (P = 0.0218). Furtheremore, desmin expression was evaluated as extent of emergence (grading 0 - 4). The desmin expression score in hypertrophic cardiomyopathy samples (2.7 ± 0.8) was significantly higher than in other groups (dilated 2.0 ± 1.4, myocarditis 1.6 ± 1.5 vs., controls 0, P ≤ 0.0001, 0.0001, 0.0129, respectively). Conclusion: Cardio-myopathy enhanced the sound speed, which correlated with the elasticity of myocytes, following the impaired compliance of left ventricle, despite the absence of histological changes. The elevation of sound speed of myocytes may be linked to cytoskeletal changes. Myocyte sound speed may be a new diagnostic tool for diagnosis of idiopathic cardiomyopathy independently of conventional histological diagnosis.
