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Diffuse myocardial fibrosis resulting from the excessive deposition of collagen fibres through the entire myocardium is encountered in a number of chronic cardiac diseases. This lesion results from alterations in the regulation of fibrillary collagen turnover by fibroblasts, facilitating the excessive deposition of type I and type III collagen fibres within the myocardial interstitium and around intramyocardial vessels. The available evidence suggests that, beyond the extent of fibrous deposits, collagen composition and the physicochemical properties of the fibres are also relevant in the detrimental effects of diffuse myocardial fibrosis on cardiac function and clinical outcomes in patients with heart failure. In this regard, findings from the past 20 years suggest that various clinicopathological phenotypes of diffuse myocardial fibrosis exist in patients with heart failure. In this Review, we summarize the current knowledge on the mechanisms and detrimental consequences of diffuse myocardial fibrosis in heart failure. Furthermore, we discuss the validity and usefulness of available imaging techniques and circulating biomarkers to assess the clinicopathological variation in this lesion and to track its clinical evolution. Finally, we highlight the currently available and potential future therapeutic strategies aimed at personalizing the prevention and reversal of diffuse myocardial fibrosis in patients with heart failure.

Los niveles circulantes de la proteína de unión del factor de crecimiento de tipo insulina 2 (IGFBP2) aumentan en la insuficiencia renal crónica (IRC), y se asocian con un mayor riesgo de mortalidad en la miocardiopatía dilatada. Dado que la IRC se asocia con una mayor mortalidad en la insuficiencia cardiaca (IC), hemos investigado si, en pacientes con IC de distinta etiología, IGFBP2 se asocia con la IRC, y si la IRC modifica el valor pronóstico de esta proteína.

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The chronic hemodynamic load imposed by hypertension on the left ventricle leads to lesions in the myocardium that result in structural remodeling, which provides support for alterations in cardiac function, perfusion, and electrical activity that adversely influence the clinical evolution of hypertensive heart disease. Management must include detecting, reducing, and reversing left ventricular hypertrophy, as well as the detection and repair of microscopic lesions responsible for myocardial remodeling. Reducing the burden associated with hypertensive heart disease can be targeted using personalized treatment. The noninvasive, biomarker-mediated identification of subsets of patients with hypertensive heart disease is essential to provide personalized treatment.

Cardiotrophin-1 (CT-1) induces hypertrophic growth and contractile dysfunction in cardiomyocytes. This cross-sectional study was aimed to analyze CT-1 associations with echocardiographically assessed left ventricular systolic properties taking into account the influence of left ventricular growth i.e. left ventricular hypertrophy (LVH) and inappropriate left ventricular mass (iLVM) in asymptomatic hypertensive patients.

Abstract: Hypertensive heart disease, here defined by the presence of pathologic left ventricular hypertrophy in the absence of a cause other than arterial hypertension, is characterized by complex changes in myocardial structure including enhanced cardiomyocyte growth and non-cardiomyocyte alterations that induce the remodeling of the myocardium, and ultimately, deteriorate left ventricular function and facilitate the development of heart failure. It is now accepted that a number of pathological processes mediated by mechanical, neurohormonal, and cytokine routes acting on the cardiomyocyte and the non-cardiomyocyte compartments are responsible for myocardial remodeling in the context of arterial hypertension. For instance, cardiotrophin-1 is a cytokine member of the interleukin-6 superfamily, produced by cardiomyocytes and non-cardiomyocytes in situations of biomechanical stress that once secreted interacts with its receptor, the heterodimer formed by gp130 and gp90 (also known as leukemia inhibitory factor receptor beta), activating different signaling pathways leading to cardiomyocyte hypertrophy, as well as myocardial fibrosis. Beyond its potential mechanistic contribution to the development of hypertensive heart disease, cardiotrophin-1 offers the opportunity for a new translational approach to this condition. In fact, recent evidence suggests that cardiotrophin-1 may serve as both a biomarker of left ventricular hypertrophy and dysfunction in hypertensive patients, and a potential target for therapies aimed to prevent and treat hypertensive heart disease beyond blood pressure control.

To analyze whether genetic variants of PPARAare associated with the development of stage C heart failure.

La insuficiencia cardiaca es un síndrome complejo y una de las principales causas de morbilidad y mortalidad en los países occidentales. A pesar del enorme esfuerzo realizado en los últimos años, todavía existen importantes limitaciones en la prevención y el tratamiento de la insuficiencia cardiaca, por lo que se impone un nuevo enfoque conceptual y práctico. En este contexto se inscribe la aplicación de las ciencias «ómicas» a la insuficiencia cardiaca. La incorporación de la metodología «ómica» al estudio de las enfermedades humanas ha modificado sustancialmente el enfoque biológico y ha estimulado enormemente la investigación de nuevos mecanismos, así como de biomarcadores y dianas terapeúticas. La aplicación de la genómica, la proteómica y la metabonómica al estudio de la insuficiencia cardiaca puede facilitar la comprensión del origen y el desarrollo de las distintas entidades que configuran dicho síndrome, con lo que se propiciaría el establecimiento de perfiles diagnósticos y patrones terapéuticos diferenciales que pueden mejorar el mal pronóstico que la insuficiencia cardiaca conlleva. En esta breve revisión se definen brevemente aspectos básicos sobre las ciencias «ómicas» y se evalúa el estado actual de la aplicación de estas nuevas tecnologías a la investigación de la insuficiencia cardiaca humana, centrándose principalmente en los análisis de microarraysde expresión génica en el campo de la genómica y los estudios de electroforesis bidimensional acoplada a espectrometría de masas en el ámbito de la proteómica.

To investigate whether the glycoprotein (gp130)-mediated survival pathway, which protects cardiomyocytes from apoptosis, is depressed in left ventricular hypertrophy hypertensive patients with chronic heart failure.

Previous studies have shown that as well as left ventricular hypertrophy, myocardial fibrosis develops early in rats with spontaneous hypertension (SHR). The present study was designed to investigate whether chronic treatment with the angiotensin II type 1 (AT1) receptor antagonist losartan modifies collagen type I metabolism and reverses left ventricular fibrosis in young SHR with left ventricular hypertrophy.