Echocardiographic findings and NT-proBNP level in type-2 diabetic patients with and without ischemic heart disease.

The aim of this study was to determine whether there are differences in echocardiographic findings or in the level of a biochemical marker (i.e. N-terminal probrain natriuretic peptide [NT-proBNP]) between controls and type-2 diabetic patients with or without ischemic heart disease. Echocardiography was used to assess left ventricular function and morphology. In addition, the plasma NT-proBNP concentration was measured. The prevalence of diastolic dysfunction was greater in diabetics without ischemic heart disease than in controls (88% vs. 74%, respectively; P< .001) and the NT-proBNP concentration was higher (350.6+/-197.8 vs. 281.7+/-190.4 fmol/mL; P< .001). Diabetics with ischemic heart disease had a higher NT-proBNP concentration than those without (720.4+/-278.1 vs. 350.6+/-197.8 fmol/mL, respectively; P< .001). An NT-proBNP concentration >490 fmol/mL had a sensitivity of 84% and a specificity of 75% for detecting ischemic heart disease in diabetics.

Estudio ecocardiográfico y de la concentración de NT-proBNP en pacientes diabéticos tipo 2 con y sin cardiopatía isquémica / Echocardiographic findings and NT-proBNP level in type-2 diabetic patients with and without ischemic heart disease

El objetivo de este trabajo es analizar posibles diferencias ecocardiográficas y bioquímicas (NT-proBNP) entre controles y pacientes diabéticos tipo 2 sin cardiopatía isquémica y con ella. El estudio ecocardiográfico comprendió la forma y la función ventricular izquierda. Además se determinaron las concentraciones plasmáticas de NT-proBNP. Los diabéticos sin cardiopatía isquémica presentaron mayor prevalencia de disfunción diastólica (el 88 frente al 74%; p < 0,001) y mayor concentración de NT-proBNP (350,6 ± 197,8 frente a 281,7 ± 190,4 fmol/ ml; p < 0,001) que los controles. Los diabéticos con cardiopatía isquémica mostraron concentraciones de NT-proBNP muy superiores a las de los diabéticos sin cardiopatía isquémica (720,4 ± 278,1 frente a 350,6 ± 197,8 fmol/ml respectivamente; p < 0,001). Una concentración de NT-proBNP > 490 fmol/ml tuvo el 84% de sensibilidad y el 75% de especificidad para detectar cardiopatía isquémica en pacientes diabéticos (AU)

The aim of this study was to determine whether there are differences in echocardiographic findings or in the level of a biochemical marker (i.e. N-terminal probrain natriuretic peptide [NT-proBNP]) between controls and type-2 diabetic patients with or without ischemic heart disease. Echocardiography was used to assess left ventricular function and morphology. In addition, the plasma NT-proBNP concentration was measured. The prevalence of diastolic dysfunction was greater in diabetics without ischemic heart disease than in controls (88% vs. 74%, respectively; P < .001) and the NT-proBNP concentration was higher (350.6±197.8 vs. 281.7±190.4 fmol/mL; P < .001). Diabetics with ischemic heart disease had a higher NT-proBNP concentration than those without (720.4±278.1 vs. 350.6±197.8 fmol/mL, respectively; P < .001). An NT-proBNP concentration >490 fmol/mL had a sensitivity of 84% and a specificity of 75% for detecting ischemic heart disease in diabetics (AU)

[Altered fibrillar collagen metabolism in hypertensive heart failure. Current understanding and future prospects]. / Alteraciones del metabolismo del colágeno fibrilar en la cardiopatía hipertensiva. Situación actual y perspectivas.

Arterial hypertension induces numerous alterations in the composition of cardiac tissue, which, in turn, result in structural remodeling of the myocardium. This remodeling is due to a range of pathologic mechanisms associated with mechanical, neurohormonal and cytokine processes that affect both cardiomyocyte and non-cardiomyocyte compartments of the myocardium. One of these processes involves disruption of the equilibrium between the synthesis and degradation of type-I and type-III collagen molecules. The result is excess accumulation of type-I and type-III collagen fibers in interstitial and perivascular spaces in the myocardium. The clinical significance of myocardial fibrosis lies in its contribution to the development of cardiac complications in hypertensive patients. This brief review focuses on the mechanisms of myocardial fibrosis and their clinical consequences. In addition, the techniques used for diagnosing myocardial fibrosis and the main therapeutic strategies for reducing fibrosis are also discussed.

Alteraciones del metabolismo del colágeno fibrilar en la cardiopatía hipertensiva. Situación actual y perspectivas / Altered fibrillar collagen metabolism in hypertensive heart failure. Current understanding and future prospects

La hipertensión arterial causa una serie de cambios en la composición del tejido cardiaco que dan lugar al remodelado estructural del miocardio. Dicho remodelado es la consecuencia de diversos procesos patológicos mediados por factores mecánicos, factores neurohormonales y citocinas que afectan al compartimento cardiomiocitario y no cardiomiocitario del miocardio. Uno de esos procesos está relacionado con la disrupción del equilibrio entre la síntesis y la degradación de las moléculas de colágeno tipo I y tipo III, que da lugar a una excesiva acumulación de fibras de colágeno tipo I y tipo III en el espacio intersticial y perivascular del miocardio. La relevancia clínica de la fibrosis miocárdica radica en que contribuye al desarrollo de complicaciones cardiacas en los pacientes hipertensos. Esta breve revisión está centrada en los mecanismos de la fibrosis miocárdica, así como en sus consecuencias clínicas. Además, se considerarán los métodos para su diagnóstico y las principales estrategias terapéuticas que facilitan su reducción

Arterial hypertension induces numerous alterations in the composition of cardiac tissue, which, in turn, result in structural remodeling of the myocardium. This remodeling is due to a range of pathologic mechanisms associated with mechanical, neurohormonal and cytokine processes that affect both cardiomyocyte and non-cardiomyocyte compartments of the myocardium. One of these processes involves disruption of the equilibrium between the synthesis and degradation of type-I and type-III collagen molecules. The result is excess accumulation of type-I and type-III collagen fibers in interstitial and perivascular spaces in the myocardium. The clinical significance of myocardial fibrosis lies in its contribution to the development of cardiac complications in hypertensive patients. This brief review focuses on the mechanisms of myocardial fibrosis and their clinical consequences. In addition, the techniques used for diagnosing myocardial fibrosis and the main therapeutic strategies for reducing fibrosis are also discussed