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Rev Med Inst Mex Seguro Soc. 2017;55(Suppl. 2):S195-200.

Left ventricular hypertrophy, fibrosis heart, and diastolic dysfunction in chronic kidney disease

[Article in Spanish; Abstract available in Spanish from the publisher]

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Servicio de Cardiología, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Ciudad de México, México Correo electrónico:


in English, Spanish

Cardiovascular diseases occur 75 to 80% as causes of morbidity and mortality in patients with chronic kidney disease. In epidemiological studies the causes of cardiovascular deaths are sudden death, arrhythmias, heart failure, coronary arteries disease and myocardial infarction. Heart failure and cardiac arrhythmias are caused mainly by left ventricular hypertrophy and cardiac fibrosis. Pathophysiological factors involved in left ventricular hypertrophy ventricular hypertrophy have been divided into 3 categories: related to afterload, related to preload and not related to afterload or preload. Myocardial hypertrophy induces the activation of cellular apoptosis signals and activates metabolic pathways able to increase extracellular matrix production up to fibrosis. Fibrosis leads to progressive impairment in contractility with stiffening of myocardial wall, diastolic and systolic dysfunction and finally dilated cardiomyopathy with congestive heart failure. The main of this review is to understand the pathophysiology of left ventricular hypertrophy, cardiac fibrosis and diastolic dysfunction.


Renal Insufficiency, Chronic; Hypertrophy, Left Ventricular; Endomyocardial Fibrosis


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