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Advisor(s)
Abstract(s)
Introdução: A hipertensão é o maior fator de risco prevenível de doenças cardiovasculares. A taxa de prevalência da hipertensão arterial (HTA) em Portugal situa-se nos (26.9%), sendo mais elevada no sexo feminino. A fibrose cardíaca é um fator comum na maioria das patologias cardíacas. Nas últimas duas décadas foram realizados muitos estudos sobre a fibrose cardíaca. Vamos rever a fisiopatologia, os métodos de diagnóstico e a terapêutica na fibrose cardíaca de sobrecarga de pressão induzida pela hipertensão.
Objetivos: Aprofundar o conhecimento atual sobre a fibrose cardíaca quando induzida pela hipertensão arterial.
Métodos: Foi efetuada uma pesquisa eletrónica nas bases de dados PubMed e B-on, utilizando as seguintes palavras-chave: "Cardiac fibrosis", "Hypertension", "Pressure overload fibrosis", com prioridade para artigos mais recentes. Foi também utilizada informação presente em diversos “websites”.
Conclusões: Uma grande causa de fibrose é a grande sobrecarga de pressão induzida pela hipertensão arterial, que é inicialmente associado com o aumento da rigidez muscular devido ao aumento de colagénio no miocárdio e consequente disfunção diastólica. Se esta pressão persistir pode ainda levar a uma dilatação do ventrículo surgindo disfunção sistólica através da ativação das metaloproteinas (MMP). Quanto mais fibrótico maior a probabilidade de ter arritmias e morte súbita. Vários processos estão presentes como a inflamação iniciada com a morte celular dos cardiomiócitos, a produção de espécies reativas de oxigénio (ROS), as ações inflamatórias do sistema Renina-angiotensina-aldosterona (RAAS) e regulada por quimiocinas (MCP-1/CCL2) e citocinas (TNF-a, o TGF-b, a IL-1b e a IL-6) que recrutam monócitos/macrófagos, mastócitos e progenitores-fibroblastos e ativam os fibroblastos, diferenciando-os para miofibroblástos aumentando as suas funções de produção de colagénio. Como métodos de diagnóstico são usados a biopsia por cateterismo, certos marcadores biológicos como o propéptido carboxiterminal do procolagénio tipo I (PIP) e a telepéptido carboxiterminal do colagénio tipo I (CITP) e mais recentemente a ressonância magnética que permite observar o tecido fibrótico de maneira precisa e não invasiva. Em relação à terapêutica neste momento não existem agentes anti fibróticos patenteadas para humanos. Algumas drogas anti hipertensoras são usadas como terapêutica, não só pela capacidade de regularem a pressão arterial mas pela eficácia com que interferem com fatores de produção de colagénio como a angiotensina II e o TGF-b. A terapêutica com inibidores da enzima conversora da angiotensina e o bloqueio do recetor AT1 tem mostrado melhorias significativas na redução da pressão arterial e fibrose cardíaca em modelos de ratos hipertensivos.
Introduction: Hypertension is the greatest preventable risk factor of cardiovascular diseases. The prevalence of hypertension (HTA) in Portugal is around (26.9%), while the prevalence is higher on females. Myocardial fibrosis is a typical factor on the majority of myocardial pathologies, contributing to myocardial hypertrophy and diastolic dysfunction. On the last two decades were realized many studies about myocardial fibrosis. We will review the pathophysiology, diagnostic methods and therapy of cardiac fibrosis due to hypertension. Objectives: Deepen the actual knowledge about cardiac fibrosis when induced by hypertension Methods: An electronic research was made on the databases PubMed and B-on, using the following keywords: "Cardiac fibrosis", "Hypertension", "Pressure overload fibrosis", giving priority to recent articles. Information on diverse websites and an Internal Medicine book were also used. Conclusions: A great cause of fibrosis is the pressure overload induced by Hypertension, which is initially associated with the increase in muscular stiffness due to the increase of collagen on myocardium and diastolic dysfunction. If this pressure persists it can lead to a dilation of the ventricle creating a systolic dysfunction due to metalloproteases (MMP). The increase of fibrotic tissue on myocardium leads to a higher probability of arrhythmias and sudden death. Several processes are present like inflammation, initiated with cellular death of cardio myocytes, the production of reactive oxygen species (ROS), the inflammatory actions of renin–angiotensin–aldosterone system (RAAS), and regulated by chemokines (MCP-1/CCL2), and cytokines (TNF-a, o TGF-b, a IL-1b e a IL-6) which recruit monocytes/macrophages, mast cells, fibroblasts progenitors and activate the fibroblasts, which get differentiated to myofibroblasts increasing their collagen production functions. The diagnostic methods used are the biopsy with a catheter, biological markers like PIP and CITP, and more recently the magnetic resonance which allow the evaluation of the fibrotic tissue in a precise and noninvasive manner. On this day they are still no certified anti fibrotic drugs for humans. Some anti-hypertensive drugs are used as therapeutic, not only for their capacity regulating the arterial pressure but their efficacy interfering with fibrotic factors such as angiotensin II and TGF-b. Therapeutic action with inhibitors of angiotensin converting enzyme and blockade of receptor of AT1 have showed improvements on the reduction of arterial pressure and myocardial fibrosis on studies in hypertensive rats.
Introduction: Hypertension is the greatest preventable risk factor of cardiovascular diseases. The prevalence of hypertension (HTA) in Portugal is around (26.9%), while the prevalence is higher on females. Myocardial fibrosis is a typical factor on the majority of myocardial pathologies, contributing to myocardial hypertrophy and diastolic dysfunction. On the last two decades were realized many studies about myocardial fibrosis. We will review the pathophysiology, diagnostic methods and therapy of cardiac fibrosis due to hypertension. Objectives: Deepen the actual knowledge about cardiac fibrosis when induced by hypertension Methods: An electronic research was made on the databases PubMed and B-on, using the following keywords: "Cardiac fibrosis", "Hypertension", "Pressure overload fibrosis", giving priority to recent articles. Information on diverse websites and an Internal Medicine book were also used. Conclusions: A great cause of fibrosis is the pressure overload induced by Hypertension, which is initially associated with the increase in muscular stiffness due to the increase of collagen on myocardium and diastolic dysfunction. If this pressure persists it can lead to a dilation of the ventricle creating a systolic dysfunction due to metalloproteases (MMP). The increase of fibrotic tissue on myocardium leads to a higher probability of arrhythmias and sudden death. Several processes are present like inflammation, initiated with cellular death of cardio myocytes, the production of reactive oxygen species (ROS), the inflammatory actions of renin–angiotensin–aldosterone system (RAAS), and regulated by chemokines (MCP-1/CCL2), and cytokines (TNF-a, o TGF-b, a IL-1b e a IL-6) which recruit monocytes/macrophages, mast cells, fibroblasts progenitors and activate the fibroblasts, which get differentiated to myofibroblasts increasing their collagen production functions. The diagnostic methods used are the biopsy with a catheter, biological markers like PIP and CITP, and more recently the magnetic resonance which allow the evaluation of the fibrotic tissue in a precise and noninvasive manner. On this day they are still no certified anti fibrotic drugs for humans. Some anti-hypertensive drugs are used as therapeutic, not only for their capacity regulating the arterial pressure but their efficacy interfering with fibrotic factors such as angiotensin II and TGF-b. Therapeutic action with inhibitors of angiotensin converting enzyme and blockade of receptor of AT1 have showed improvements on the reduction of arterial pressure and myocardial fibrosis on studies in hypertensive rats.
Description
Keywords
Fibrose Cardíaca Fibrose de Sobrecarga de Pressão Hipertensão Remodelação Cardíaca