O papel do acúmulo de colágeno no interstício miocárdico na sobrevida dos pacientes com cardiomiopatia dilatada idiopática e chagásica / The role of storage of interstitial myocardial collagen on the overlife rate of patients with idiopathic and chagasic dilated cardiomyopathy

OBJETIVO: Avaliar a correlação entre um marcador estrutural do miocárdio e a sobrevida dos pacientes com cardiomiopatia dilatada. MÉTODOS: Mediante realização da biópsia endomiocárdica e exame ecocardiográfico foram estudados 9 indivíduos sem doença estrutural miocárdica (controle) e 45 pacientes com cardiomiopatia dilatada grave de etiologia idiopática (MCDI) e chagásica (MCDC). Foi analisada a correlação entre a quantidade de colágeno miocárdico intersticial (FVCI) e a sobrevida desses pacientes, se a FVCI diferia entre as etiologias, e se a fibrose interferia na função e geometria do miocárdio. RESULTADOS: Foi observado que a FVCI foi 15 vezes maior nos cardiomiopatas em relação ao grupo-controle, mas não diferiu em relação às MCDI e MCDC (*p < 0,001). Não houve correlação da FCVI com a sobrevida dos pacientes com cardiomiopatias (MCDI p = 0,249 e na MCDC p = 0,587) e apenas na MCDI a fração de ejeção do ventrículo esquerdo teve correlação com a FVCI. O diâmetro diastólico final do ventrículo esquerdo não se correlacionou com a FCVI nas duas etiologias. CONCLUSÃO: A fibrose miocárdica não diferiu entre as duas etiologias, não se correlacionou com o prognóstico das MCDC e MCDI e apenas na MCDI ela se correlacionou com a FEVE.

OBJECTIVE: To find out whether there is a correlation between a myocardial structural marker and the overlife rate of patients with dilated cardiomyopathy. METHODS: Using endomyocardial biopsy and 2D-echocardiogram, we studied nine patients with no changes in myocardial structure (control) and 45 patients with severe dilated cardiomyopathy of idiopathic etiology (IDCM) and of Chagasic etiology (CDCM). We analyzed the correlation between the quantity of interstitial myocardial collagen (ICVF) and the overlife rates of these patients. We also evaluated the difference in ICVF between these groups and whether fibrosis interfered on the geometry and function of the myocardium. RESULTS: We observed that ICVF was 15 times higher in cardiomyopathy patients than in the control group, but there was no difference in ICVF between CDCM and IDCM (*p < 0.001) patients. There was no correlation between ICVF and the overlife rate in cardiomyopathy patients (IDCM p = 0.249, and CDCM p = 0.587). We observed a significant correlation between ICVF and left ventricular ejection fraction (LVEF) only for IDCM. There was no correlation between ICVF and left ventricular diastolic diameter in either etiology. CONCLUSION: There was no difference in myocardial fibrosis between patients with CDCM or IDCM, and there was no correlation between fibrosis and the prognosis either for IDCM or CDCM. There was a correlation between myocardial fibrosis and LVEF only for IDCM.

Endomyocardial fibrosis is associated with selective deposition of type I collagen.

BACKGROUND: Endomyocardial fibrosis is a distinct form of heart disease leading to restrictive ventricular filling and cardiac failure. The disease is characterized by a marked thickening of the endocardium due to the deposition of dense fibrous tissue composed of wavy bundles of collagen. Changes in collagen composition and an abnormal increase in its concentration result in a stiffer myocardium and ventricular diastolic dysfunction. The nature of cardiac collagens and the relative proportions of collagen types in endomyocardial fibrosis have not been documented in the literature. METHODS AND RESULTS: This study analyzed collagen composition in the cardiac tissues of 13 patients with endomyocardial fibrosis and 6 individuals who were the victims of traffic accidents or suicidal deaths and did not have any heart disease. We estimated the relative proportions of types I and III collagen after pepsin digestion of the tissue and separation of the emerging peptides by sodium dodecyl sulfate polyacrylamide gel electrophoresis. The mean type I:III collagen ratio was 0.51+/-0.06 in normal individuals, and 0.93+/-0.43 in patients with endomyocardial fibrosis (p<0.05). The alteration in the type I:III collagen ratio was due to a disproportionate increase in type I collagen. CONCLUSIONS: The results indicate that a selective increase in type I collagen may contribute to the impaired diastolic distension of the ventricles in patients with endomyocardial fibrosis.

Digoxin and membrane sodium potassium ATPase inhibition in cardiovascular disease.

Kerala has a high incidence of mucoid angiopathy, metabolic syndrome X and endomyocardial fibrosis. Magnesium deficiency has been reported in these disorders even though the Keralite diet has adequate magnesium. A possible cause of magnesium deficiency is the increased digoxin, a potent inhibitor membrane Na(+)-K+ ATPase which can lead to magnesium depletion. Digoxin is known to be synthesised by the hypothalamus and other tissues and can also be obtained from plant sources in the diet. Inhibition of Na(+)-K+ ATPase can cause intracellular magnesium depletion and increase in intracellular calcium. In view of these, a study has been carried out on the activity of membrane Na(+)-K+ ATPase, using RBC membrane, serum digoxin, magnesium and glycosaminoglycan levels in patients of mucoid angiopathy, endomyocardial fibrosis and syndrome X. Significant decrease in the membrane Na(+)-K+ ATPase was observed in patients while serum digoxin levels showed an increase. Serum magnesium was significantly lower while glycosaminoglycan levels were increased. The inhibition of Na(+)-K+ ATPase activity may be due to increase in endogenous and/or exogenous digoxin. This inhibition leads to depletion of intracellular magnesium and an increase in intracellular calcium load. The role of underlying magnesium-related insulin resistance and the consequence of this intracellular magnesium and calcium alteration in the pathogenesis of these disorders is discussed.