Hypertrophic Cardiomyopathy Complicated with Cardiac Amyloidosis.

Kohno, Isao; Komori, Sadayoshi; Yamamoto, Kimio; Sano, Shuichi; Ishihara, Tsukasa; Umetani, Ken; Sawanobori, Takao; Ijiri, Hiroshi; Tamura, Kohji

doi:10.2169/internalmedicine.39.637

Cited by 3 publications

(3 citation statements)

References 14 publications

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“…The hypertrophy is considered a protective and adaptive response. However, further hypertrophy leads to severe and irreversible cardiomyopathy, eventually resulting in heart failure (24)(25)(26).…”

Section: Myocardial Responses To Environmental Toxicantsmentioning

confidence: 99%

Molecular and cellular mechanisms of cardiotoxicity.

Kang

2001

Environ Health Perspect

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Cardiotoxicity resulting from detrimental environmental insults has been recognized for a long time. However, extensive studies of the mechanisms involved had not been undertaken until recent years. Advances in molecular biology provide powerful tools and make such studies possible. We are gathering information about cellular events, signaling pathways, and molecular mechanisms of myocardial toxicologic responses to environmental toxicants and pollutants. Severe acute toxic insults cause cardiac cell death instantly. In the early response to mild environmental stimuli, biochemical changes such as alterations in calcium homeostasis occur. These may lead to cardiac arrhythmia, which most often is reversible. Prolonged stimuli activate transcription factors such as activator protein-1 through elevation of intracellular calcium and the subsequent activation of calcineurin. Upregulation by activated transcription factors of hypertrophic genes results in heart hypertrophy, which is a short-term adaptive response to detrimental factors. However, further development of hypertrophy will lead to severe and irreversible cardiomyopathy, and eventually heart failure. From cardiac hypertrophy to heart failure, myocardial cells undergo extensive biochemical and molecular changes. Cardiac hypertrophy causes tissue hypoperfusion, which activates compensatory mechanisms such as production of angiotensin II and norepinephrine. Both further stimulate cardiac hypertrophy and, importantly, activate counterregulatory mechanisms including overexpression of atrial natriuretic peptide and b-type natriuretic peptide, and production of cytokines such as tumor necrosis factor-alpha. This counterregulation leads to myocardial remodeling as well as cell death through apoptosis and necrosis. Cell death through activation of mitochondrial factors and other pathways constitutes an important cellular mechanism of heart failure. Our current knowledge of cardiotoxicity is limited. Further extensive studies are warranted for a comprehensive understanding of this field.

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Section: Myocardial Responses To Environmental Toxicantsmentioning

confidence: 99%

Molecular and cellular mechanisms of cardiotoxicity.

Kang

2001

Environ Health Perspect

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“…CA is usually associated with low blood pressure, and, with CA, primary hypertension can sometimes "cure" naturally. The reason may be related to amyloidosis of vessels, hypoadrenalism or hypothyroidism evoked by autonomic nervous system [23] . It is easy to identify left ventricular hypertrophy caused by valvular heart disease on the basis of morphology and function of valves of the patients.…”

Section: Echocardiographic Differential Diagnosismentioning

confidence: 99%

“…Tissue Doppler imaging (TDI) at the mitral annulus is a well-established method for the estimation of regional myocardial velocities [6][7][8][9][10] , and the indexes may be more sensitive in reflecting cardiac functions than routinely used indicators. This study retrospectively analyzed the characteristics of conventional echocardiographs and TDI indexes of CA and reviewed related literatures [11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28] in order to increase the awareness of this disease among physicians.…”

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confidence: 99%

The value of conventional echocardiographic and tissue doppler imaging in the diagnosis of cardiac amyloidosis

Zhang

Xie

Wang

et al. 2008

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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Transthoracic echocardiographic characteristics of 17 cases of cardiac amyloidosis (CA), a rare disease in China, were analyzed in order to improve the understanding of the disease. Seventeen cases of biopsy-proven CA, admitted to Wuhan Union Hospital from June 1994 to September 2008 were retrospectively reviewed. Twenty normal volunteers served as control group. Left atrial and ventricular functions and mitral inflow velocity were measured by two-dimensional, and Doppler echocardiography, and tissue Doppler imaging (TDI)-derived peak systolic wall motion velocities (Sv), peak early diastolic wall motion velocities (Ev), and peak late diastolic wall motion (Av) were measured at the septum, lateral, inferior and anterior corners of mitral annulus from the apical 4- and 2 chamber views. Compared with the control group, the interventricular septal thickness (IVSd), the left ventricular posterior wall (LVPWd), right ventricular transverse diameter (RVTDd) near the end of diastole and the interauricular septum thickness (IASs), left atrial anteroposterior diameter (LAADs), right atrial transverse diameter (RATDs) near the end of systole were increased significantly (all P<0.05) and left ventricular ejection fraction (LVEF) decreased (P<0.05) in the CA group. Compared with the control group, Sv, Ev at each wall and Av at almost all walls were significantly decreased in the CA group. In the CA group, Myocardial echoes of interventricular septum and free wall of left ventricle were enhanced evidently and distributed unevenly. The echoes presented as ground glass-like images, with some spotty hyper echoes. Both atria were enlarged, and LVEF decreased, with diastolic function impaired, and mild-moderate hydropericardium found in the CA group. It was concluded that echocardiography was a relatively sensitive and highly specific non-invasive method for the diagnosis of CA.

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Left ventricular hypertrophy: diagnostics pitfalls

Bonvini

Camenzind²

2004

Swiss Med Wkly

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Hypertrophic Cardiomyopathy Complicated with Cardiac Amyloidosis.

Cited by 3 publications

References 14 publications

Molecular and cellular mechanisms of cardiotoxicity.

Molecular and cellular mechanisms of cardiotoxicity.

The value of conventional echocardiographic and tissue doppler imaging in the diagnosis of cardiac amyloidosis

Left ventricular hypertrophy: diagnostics pitfalls

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