Abstract
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.
Highlights
Genetic cardiomyopathy is one of the causes of systolic and diastolic heart failure based on abnormality of proteins which comprise intra-myocyte architecture
All in the persistent myocarditis group exhibited inflammatory cells infiltrated into the interstitium without necrosis of myocytes
The present manuscript has demonstrated that the sound speed of myocytes associated with cardiomyopathy was escalated compared to that of normal myocytes
Summary
Genetic cardiomyopathy is one of the causes of systolic and diastolic heart failure based on abnormality of proteins which comprise intra-myocyte architecture. Degeneration of myocytes with/without fibrosis leads to a diminished ejection performance and reduced ventricular elasticity. Developments in molecular technology have allowed characterization of many gene mutations related to cardiomyopathy. Even hypertrophic cardiomyopathy is not confirmed as a gene mutation in all cases [1,2,3,4]. Because cardiomyopathies exhibit several phenotypes and a varied pathogenesis with few characteristic findings, it is quite difficult to obtain a precise diagnosis. For this reason, the diagnosis of cardiomyopathy “is confused”, some Societies have made a statement
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