Clinical features and treatment options for mitral regurgitation in elderly inpatients.

OBJECTIVE: To summarize clinical characteristics and treatment strategy of Chinese elderly mitral regurgitation (MR) inpatients under the current guidelines, and to identify factors related to treatment options in them. METHODS: A single center retrospective study was conducted in which patients hospitalized in Fuwai hospital from May 1st of 2014 to April 30 of 2015 with moderate to severe MR assessed by transthoracic echocardiography were enrolled consecutively (n = 1741). Patients > 60 years old were grouped as elderly group (n = 680) and patients < 60 years were grouped as control group (n = 1061). The elderly group was categorized into two subgroups based on surgical status. RESULT: s The mean age of the elderly group was 66.98 ± 5.94 years. The most common reason of MR in elderly group was degenerative MR (41.18%). Atherosclerotic risk factors such as hypertension, diabetes or hyperlipidaemia were more commonly observed in elderly group than the control group (45.44% vs. 25.17%, P < 0.001; 19.56% vs. 8.48%, P < 0.001; 35.29% vs. 19.51%, P < 0.001). Elderly group had higher EuroscoreIIscore (5.54 ± 2.42 vs. 3.15 ± 1.66), greater left ventricular end diastolic diameter (LVEDD) (57.72 ± 12.3 vs. 57.33 ± 10.19 mm) and a lower surgery rate (54.71% vs. 63.91%); P < 0.05. Age, left ventricular ejection fraction (LVEF), regurgitation grade, EuroScore-II high risk stratification and having diabetes were identified as factors associated with therapy decisions in elderly MR patients. CONCLUSIONS: Valve surgery was denied in 45.29% of elderly MR inpatients. Older age, impaired LVEF, lower regurgitation grade, EuroScore-II high risk stratification, and having diabetes were factors most significantly associated with surgery denial among elderly Chinese inpatients with MR.

Progress in Molecular Genetic Study of Mitochondrial Cardiomyopathy.

Mitochondria plays a key role in providing ATP for the energy-consuming cardiac tissues. Mitochondrial cardiomyopathy is a myocardial condition characterized by abnormal heart structure and/or function secondary to genetic defects involving the mitochondrial respiratory chain. The typical cardiac manifestations of mitochondrial cardiomyopathy include hypertrophic and dilated cardiomyopathy,while left ventricular myocardial noncompaction is less common. Recent research has suggested that most mitochondrial diseases result from mitochondrial DNA mutation,which can be found in genes that encode ancillary proteins needed for genetic transcription (tRNA),in genes that encode subunits of the electron transport chain complexes,or in genes that control the activities of the mitochondria called D-loop zone. However,the exact physiological mechanisms remain unclear. This review summarizes the recent advances in the molecular mechanism of mitochondrial cardiomyopathy.

Advances in Diagnosis and Management of Mitochondrial Cardiomyopathy.

Mitochondrial cardiomyopathy (MCM) is a series of myocardial conditions characterized by abnormal heart-muscle structure,function,or both,secondary to genetic defects involving the mitochondrial respiratory chain,in the absence of concomitant coronary artery disease,hypertension,valvular disease,or congenital heart disease. MCM patients typically have hypertrophic or dilated cardiomyopathy. Arrhythmias and left ventricular myocardial noncompaction are less common,and heart failure may occur as the first symptom in some patients. Since MCM patients often have symptoms of multiple organ involvement,the symptoms are not specific and the diagnosis can be difficult. Thus,awareness of this disease must be increased in clinical settings. Treatments for MCM are mostly supportive and nonspecific. In this review,we summarize new advances in the diagnosis and management of MCM,with an improve the clinical management of this disease.

A comparison of apoptosis levels in keloid tissue, physiological scars and normal skin.

Apoptosis is a process of programmed cell death that occurs in multicellular organisms. The mitochondrial pathway plays a paramount role in apoptosis. In this study, the expression levels of key factors in the mitochondrial pathway and the cell proliferation factor (PCNA) were measured to evaluate the level of apoptosis and proliferation in keloid scars, physiological scars and normal skin tissue. Thirty samples were taken from 30 patients: 10 keloid patients, 10 physiological scar patients and 10 patients without obvious scarring. All 30 patients were selected randomly from the Department of Plastic Surgery at Peking Union Medical College Hospital from June 2016 to December 2016. Hematoxylin and eosin staining and Masson staining were used to observe the differences in histology and fiber tissue content. Mitochondrial pathway factors (caspase-3, caspase-8, caspase-9, Bcl-2, Bax, cytochrome-c) and PCNA expression levels were detected by immunohistochemistry and were analyzed as the percentage of positively stained cells in the epidermis and dermis. Relative protein expression levels were measured by western blotting. Compared with physiological scars and normal skin tissue, keloid tissue had an increase in fiber number and decrease in cell content. In our immunohistochemical and western blot analyses, all tissue types showed similar expression levels of the mitochondrial pathway factors. However, the percentage of PCNA-positive cells and the relative protein expression level of PCNA were significantly higher in keloid tissue. Keloid has a similar apoptosis level as physiological scars and normal skin but has a higher expression of PCNA, indicating that keloid scars have high levels of proliferation and normal apoptosis.