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Case Report
- Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy: Report of an autopsy case.
- Tae Yub Kim, Young Min Kim, Jae Gul Chung, Gyung Yub Gong, Su Kil Park, In Chul Lee, Joo Ryung Huh
- Korean J Pathol. 1997;31(11):1233-1236.
- 1,632 View
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Abstract
- A 35-year-old man was admitted with a 20 day history of generalized edema and muscular weakness of the lower extremities. He was alert with a pale puffy face and an ejection murmur was heard at the cardiac apex. The electrocardiogram disclosed low voltage, first degree atrioventricular block, and a right bundle branch block. During the hospitalization an intractable diastolic hypotension developed, which measured 0 mmHg at the lowest point. At that time the echocardiogram revealed a dilated, akinetic right ventricle. Eventually a multiorgan failure developed and an autopsy following his death presented a fibrofatty replacement of the right ventricular myocardium. This might be a case of an arrhythmogenic right ventricular dysplasia/cardiomyopathy, which is usually characterized clinically by a ventricular tachycardia and may cause a sudden death in young adults.
Original Articles
- Morphometric Study for Muscular and Microvascular Remodeling of Left Ventricular Free Wall and Interventricular Septum in Hypertrophic Cardiomyopathy.
- Young Jik Lee, Hyung Suk Kim, Jong Tae Park, Chang Soo Park
- Korean J Pathol. 1999;33(9):675-683.
- 1,602 View
- 17 Download
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Abstract
PDF - Hypertrophic cardiomyopathy (HCMP) is characterized myofiber hypertrophy and structural remodeling with changes in the proportion of the muscular, vascular, and interstitial compartments. A study was done to determine the structural remodeling patterns and the role of microvasculature of hearts in HCMP. Forty-two postmortem hearts were analyzed including 14 from patients who died of HCMP (group 1), 8 patients with HCMP but who died from extracardiac causes (group 2), 10 patients with ischemic heart disease (group 3), and 10 normal adult hearts (group 4). Macro- and microscopic examination, immunohistochemical study using CD34 antibody, and morphometric studies using image analyzer were performed. Mean cardiac weight and wall thickness were significantly higher in the HCMP group. Myocardial hypertrophy, and a variety of myocardial disarray and fibrosis involved the whole area of the left ventricles with HCMP. The percentage areas of microvessels were 6.40 0.7 in group 1, 5.90 0.6 in group 2, 4.98 0.3 in group 3, 4.85 0.4 in group 4, respectively, and the numbers of microvessels were 198.0 20.7 in group 1, 230.0 22.3 in group 2, 211.7 11.2 in group 3, and 236.4 11.4 in group 4, respectively (mean SE). The percentage area of microvessels was significantly higher in group 1 than in other groups. However, the number of microvessels in that group was lower than in the other groups, although it was statistically insignificant. Since flow-dependent vasodilation is preserved in HCMP, we considered flow-dependent vasodilation the cause of the discrepancy between the area and the number of microvessels. Ischemic changes observed in chronic HCMP and related heart failure were considesed to be due to the relative deficiency of the coronary flow compared to the increasing cardiac mass.
- Altered Expression of Tissue Inhibitor of Matrix Metalloproteinase-2 in Complicated Mice Heart Secondary to Experimentally Induced Viral Myocarditis.
- Sung Sook Kim, Dae Woon Eom, Yeong Ju Woo, Jae Hee Suh, Jooryung Huh, Young Me Hong, Inpyo Choi
- Korean J Pathol. 2001;35(3):196-200.
- 1,867 View
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Abstract
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- BACKGROUND
The pathogenesis of transition from viral myocarditis to dilated cardiomyopathy is elusive, although the incidence of dilated cardiomyopathy in human is increasing.
METHODS
To clarify the role of the tissue inhibitor of matrix metaloproteinase-2 (TIMP-2) in this event, we performed immunohistochemistry, immunoblotting and immunoassay of matrix metalloproteinase-9 (MMP-9) and TIMP-2 in the serum and heart tissue of mice, which were inoculated with 4000 plaque-forming units of coxsackie B virus.
RESULTS
The MMP-9 was expressed in damaged cardiomyocytes, and the TIMP-2 was expressed in mainly interstitial connective tissue between cardiac muscle bundles by immunohistochemistry. The level of serum MMP-9 was higher in the complicated than non-complicated group (p<0.001), but the level of TIMP-2 was much lower in complicated than non-complicated group (p<0.05). These findings were similar to the results of immunohistochemistry and immunoblotting in tissues.
CONCLUSIONS
These results suggest that an imbalance in the level of MMP-9 and its inhibitor might activate cardiac complication in viral myocarditis.
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