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      DNA Repair Gene Polymorphism and the Risk of Mitral Chordae Tendineae Rupture

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          Abstract

          Polymorphisms in Lys939Gln XPC gene may diminish DNA repair capacity, eventually increasing the risk of carcinogenesis. The aim of the present study was to evaluate the significance of polymorphism Lys939Gln in XPC gene in patients with mitral chordae tendinea rupture (MCTR). Twenty-one patients with MCTR and thirty-seven age and sex matched controls were enrolled in the study. Genotyping of XPC gene Lys939Gln polymorphism was carried out using polymerase chain reaction- (PCR-) restriction fragment length polymorphism (RFLP). The frequencies of the heterozygote genotype (Lys/Gln-AC) and homozygote genotype (Gln/Gln-CC) were significantly different in MCTR as compared to control group, respectively (52.4% versus 43.2%, p = 0.049; 38.15% versus 16.2%, p = 0.018). Homozygote variant (Gln/Gln) genotype was significantly associated with increased risk of MCTR (OR = 2.059; 95% CI: 1.097–3.863; p = 0.018). Heterozygote variant (Lys/Gln) genotype was also highly significantly associated with increased risk of MCTR (OR = 1.489; 95% CI: 1.041–2.129; p = 0.049). The variant allele C was found to be significantly associated with MCTR (OR = 1.481; 95% CI: 1.101–1.992; p = 0.011). This study has demonstrated the association of XPC gene Lys939Gln polymorphism with MCTR, which is significantly associated with increased risk of MCTR.

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          Apoptosis in myocytes in end-stage heart failure.

          B Khaw, U Schmidt, T DiSalvo … (1996)
          Heart failure can result from a variety of causes, including ischemic, hypertensive, toxic, and inflammatory heart disease. However, the cellular mechanisms responsible for the progressive deterioration of myocardial function observed in heart failure remain unclear and may result from apoptosis (programmed cell death). We examined seven explanted hearts obtained during cardiac transplantation for evidence of apoptosis. All seven patients had severe chronic heart failure: four had idiopathic dilated cardiomyopathy, and three had ischemic cardiomyopathy. DNA fragmentation (an indicator of apoptosis) was identified histochemically by in situ end-labeling as well as by agarose-gel electrophoresis of end-labeled DNA. Myocardial tissues obtained from four patients who had had a myocardial infarction one to two days previously were used as positive controls, and heart tissues obtained from four persons who died in motor vehicle accidents were used as negative controls for the end-labeling studies. Hearts from all four patients with idiopathic dilated cardiomyopathy and from one of the three patients with ischemic cardiomyopathy had histochemical evidence of DNA fragmentation. All four myocardial samples from patients with dilated cardiomyopathy also demonstrated DNA laddering, a characteristic of apoptosis, whereas this was not seen in any of the samples from patients with ischemic cardiomyopathy. Histological evidence of apoptosis was also observed in the central necrotic zone of acute myocardial infarcts, but not in myocardium remote from the infarcted zone. Rare isolated apoptotic myocytes were seen in the myocardium from the four persons who died in motor vehicle accidents. Loss of myocytes due to apoptosis occurs in patients with end-stage cardiomyopathy and may contribute to progressive myocardial dysfunction.
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            Reperfusion injury induces apoptosis in rabbit cardiomyocytes.

            K Burleson, R Kloner, B Babior … (1994)
            The most effective way to limit myocardial ischemic necrosis is reperfusion, but reperfusion itself may result in tissue injury, which has been difficult to separate from ischemic injury. This report identifies elements of apoptosis (programmed cell death) in myocytes as a response to reperfusion but not ischemia. The hallmark of apoptosis, nucleosomal ladders of DNA fragments (approximately 200 base pairs), was detected in ischemic/reperfused rabbit myocardial tissue but not in normal or ischemic-only rabbit hearts. Granulocytopenia did not prevent nucleosomal DNA cleavage. In situ nick end labeling demonstrated DNA fragmentation predominantly in myocytes. The pattern of nuclear chromatin condensation was distinctly different in reperfused than in persistently ischemic tissue by transmission electron microscopy. Apoptosis may be a specific feature of reperfusion injury in cardiac myocytes, leading to late cell death.
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              Clinical outcome of mitral regurgitation due to flail leaflet.

              James B Seward, A Tajik, Joseph K. Bailey … (1996)
              Mitral regurgitation due to flail leaflet is difficult to manage, because it is frequently asymptomatic yet carries a high risk of left ventricular dysfunction and because the natural history of the condition is poorly defined. We obtained clinical follow-up data through 1994-1995 in 229 patients with isolated mitral regurgitation due to flail leaflet; this condition was first diagnosed by echocardiography between 1980 and 1989. The 86 patients who were treated medically had a mortality rate significantly higher than expected (6.3 percent yearly, P=0.016 for the comparison with the expected rate in the U.S. population according to the 1990 census). Independent determinants of mortality were an older age, the presence of symptoms, and a lower ejection fraction. Patients who were even transiently in New York Heart Association functional class III or IV had a high mortality rate (34 percent yearly), but the rate was also notable (4.1 percent yearly) among those in class I or II. At 10 years, the mean (+/- SE) rates of heart failure, atrial fibrillation, and death or surgery were 63 +/- 8, 30 +/- 12, and 90 +/- 3 percent, respectively. In a multivariate analysis, surgical correction of mitral regurgitation (performed in 143 patients) was associated with a reduced mortality rate (hazard ratio, 0.29; 95 percent confidence interval, 0.15 to 0.56; P<0.001). When treated medically, mitral regurgitation due to flail leaflet is associated with excess mortality and high morbidity. Surgery is almost unavoidable within 10 years after the diagnosis and appears to be associated with an improved prognosis; this finding suggests that surgery should be considered early in the course of the disease.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Dis Markers
                Journal ID (iso-abbrev): Dis. Markers
                Journal ID (publisher-id): DM
                Title: Disease Markers
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 0278-0240
                ISSN (Electronic): 1875-8630
                Publication date (Print): 2015
                Publication date (Electronic): 28 October 2015
                Volume: 2015
                Electronic Location Identifier: 825020
                Affiliations
                1Department of Medical Biology and Genetics, Faculty of Medicine, Sakarya University, 54290 Sakarya, Turkey
                2Department of Cardiology, Faculty of Medicine, Sakarya University, 54290 Sakarya, Turkey
                3Department of Biostatistics, Faculty of Medicine, Sakarya University, 54290 Sakarya, Turkey
                4Department of Anatomy, Faculty of Medicine, Sakarya University, 54290 Sakarya, Turkey
                Author notes

                Academic Editor: Gad Rennert

                Article
                DOI: 10.1155/2015/825020
                PMC ID: 4641204
                SO-VID: 5f3d20a4-c147-4e88-a7fa-4d811d02d9a9
                Copyright © Copyright © 2015 Aysel Kalayci Yigin et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 24 July 2015
                Date revision received : 21 September 2015
                Date accepted : 22 September 2015
                Categories
                Subject: Research Article

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