Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obesity can result in alterations in cardiac structure and function even in the absence of systemic hypertension and underlying organic heart disease. Increased total blood volume creates a high cardiac output state that may cause ventricular dilatation and ultimately eccentric hypertrophy of the left (and possibly the right) ventricle. Eccentric left ventricular (LV) hypertrophy produces diastolic dysfunction. Systolic dysfunction may ensue due to excessive wall stress if wall thickening fails to keep pace with dilatation. This disorder is referred to as obesity cardiomyopathy. The presence of systemic hypertension in obese individuals facilitates development of LV dilatation and hypertrophy. Congestive heart failure may occur in such individuals, and may be attributable to LV diastolic dysfunction or to combined LV diastolic and systolic dysfunction. The sleep apnea/obesity hypoventilation syndrome occurs in 5% of morbidly obese individuals and is potentially life-threatening. Treatment of obesity cardiomyopathy consists of weight loss, salt restriction, and diuretics. Digitalis and vasodilators may be useful in selected cases. Central obesity is probably a risk factor for the development of coronary heart disease. Alterations in lipid and insulin metabolism may facilitate development of coronary heart disease in obese patients.
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PMID:Obesity and the heart. 836 92

Atomic absorption spectrometry was used for red cell (MgRC) and plasma Mg (MgPL) measurement (mEq/L) in 24 normal individuals (Nls), aged 42.16 +/- 16 years, and 44 carefully selected consecutive patients (pts), aged 60.68 +/- 10 years with cor pulmonale. The results showed the following: (1) normal MgPL (1.69 +/- 0.19) and MgRC (4.22 +/- 0.32) in Nls; (2) decreased MgpL (1.56 +/- 0.23) and MgRC (2.85 +/- 0.54) in pts; (3) decreased FEV1 percent (37.56 +/- 13.1) in pts; (4) increased RVIDd (1.73 +/- 0.31 cm/m2) of the pts by M-mode echo; and (5) coexistence of decreased MgRC (2.55 +/- 0.33) and ECG arrhythmias-RBBB in 17/44 Pts (38.6 percent). We conclude the following; (1) red cell Mg concentration was more significantly decreased (p < 0.001) than plasma Mg concentration (p < 0.01); (2) there was no significant correlation coefficient (r) between red cell and plasma Mg concentration of pts (p > 0.05); (3) there was significant statistical difference between decreased red cell Mg levels in pts with and without ECG arrhythmias-RBBB (p < 0.01); (4) significant r between decreased red cell Mg concentration and aRVIDd (r = -0.43, p < 0.01), beta FEV1 percent (r = 0.47, p < 0.01); and (5) decreased red cell Mg levels of unknown origin have never been reported previously in the literature. Subsequently, could Mg salt intake attenuate pulmonary dysfunction and right ventricular dilatation in pts with chronic cor pulmonale?
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PMID:Red cell magnesium concentration in cor pulmonale. Correlation with cardiopulmonary findings. 844 63

Dilated cardiomyopathy (DCM) is a heart muscle disease characterized by ventricular dilatation and impaired systolic function. Patients with DCM suffer from heart failure, arrhythmia, and are at risk of premature death. DCM has a prevalence of one case out of 2500 individuals with an incidence of 7/100,000/year (but may be under diagnosed). In many cases the disease is inherited and is termed familial DCM (FDC). FDC may account for 20-48% of DCM. FDC is principally caused by genetic mutations in FDC genes that encode for cytoskeletal and sarcomeric proteins in the cardiac myocyte. Family history analysis is an important tool for identifying families affected by FDC. Standard criteria for evaluating FDC families have been published and the use of such criteria is increasing. Clinical genetic testing has been developed for some FDC genes and will be increasingly utilized for evaluating FDC families. Through the use of family screening by pedigree analysis and/or genetic testing, it is possible to identify patients at earlier, or even presymptomatic stages of their disease. This presents an opportunity to invoke lifestyle changes and to provide pharmacological therapy earlier in the course of disease. Genetic counseling is used to identify additional asymptomatic family members who are at risk of developing symptoms, allowing for regular screening of these individuals. The management of FDC focuses on limiting the progression of heart failure and controlling arrhythmia, and is based on currently accepted treatment guidelines for DCM. It includes general measures (salt and fluid restriction, treatment of hypertension, limitation of alcohol intake, control of body weight, moderate exercise) and pharmacotherapy. Cardiac resynchronization, implantable cardioverter defibrillators and left ventricular assist devices have progressively expanding usage. Patients with severe heart failure, severe reduction of the functional capacity and depressed left ventricular ejection fraction have a low survival rate and may require heart transplant.
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PMID:Cardiomyopathy, familial dilated. 1683 24