RESUMEN
Cerebral small vessel disease (CSVD) is composed of several diseases affecting the small arteries, arterioles, venules, and capillaries of the brain, and refers to several pathological processes and etiologies. Neuroimaging features of CSVD include recent small subcortical infarcts, lacunes, white matter hyperintensities, perivascular spaces, microbleeds, and brain atrophy. The main clinical manifestations of CSVD include stroke, cognitive decline, dementia, psychiatric disorders, abnormal gait, and urinary incontinence. Currently, there are no specific preventive or therapeutic measures to improve this condition. In this review, we will discuss the pathophysiology, clinical aspects, neuroimaging, progress of research to treat and prevent CSVD and current treatment of this disease.
Asunto(s)
Enfermedades de los Pequeños Vasos Cerebrales/patología , Arterioloesclerosis/patología , Arterioloesclerosis/terapia , Angiopatía Amiloide Cerebral/patología , Angiopatía Amiloide Cerebral/terapia , Enfermedades de los Pequeños Vasos Cerebrales/clasificación , Enfermedades de los Pequeños Vasos Cerebrales/tratamiento farmacológico , Humanos , Imagen por Resonancia Magnética , Inhibidores de Agregación Plaquetaria/uso terapéutico , Accidente Cerebrovascular/prevención & control , Activador de Tejido Plasminógeno/uso terapéutico , Sustancia Blanca/diagnóstico por imagenRESUMEN
Arteriogenesis is a main defense mechanism to prevent heart and local tissues dysfunction in occlusive artery disease. TGF-ß and angiostatin have a pivotal role in arteriogenesis. We tested the hypothesis that aerobic training and l-arginine supplementation promotes cardiac and skeletal muscles arteriogenesis after myocardial infarction (MI) parallel to upregulation of TGF-ß and downregulation of angiostatin. For this purpose, 4 weeks after LAD occlusion, 50 male Wistar rats were randomly distributed into five groups: (1) sham surgery without MI (sham, n = 10), (2) control-MI (Con-MI, n = 10), (3) l-arginine-MI (La-MI, n = 10), (4) exercise training-MI (Ex-MI, n = 10), and (5) exercise and l-arginine-MI (Ex + La-MI). Exercise training groups running on a treadmill for 10 weeks with moderate intensity. Rats in the l-arginine-treated groups drank water containing 4 % l-arginine. Arteriolar density with different diameters (11-25, 26-50, 51-75, and 76-150 µm), TGF-ß, and angiostatin gene expression were measured in cardiac (area at risk) and skeletal (soleus and gastrocnemius) muscles. Smaller arterioles decreased in cardiac after MI. Aerobic training and l-arginine increased the number of cardiac arterioles with 11-25 and 26-50 µm diameters parallel to TGF-ß overexpression. In gastrocnemius muscle, the number of arterioles/mm(2) was only increased in the 11 to 25 µm in response to training with and without l-arginine parallel to angiostatin downregulation. Soleus arteriolar density with different size was not different between experimental groups. Results showed that 10 weeks aerobic exercise training and l-arginine supplementation promotes arteriogenesis of heart and gastrocnemius muscles parallel to overexpression of TGF-ß and downregulation of angiostatin in MI rats.
Asunto(s)
Arginina/uso terapéutico , Vasos Coronarios/fisiopatología , Suplementos Dietéticos , Músculo Esquelético/irrigación sanguínea , Infarto del Miocardio/rehabilitación , Neovascularización Fisiológica , Condicionamiento Físico Animal , Inductores de la Angiogénesis/uso terapéutico , Angiostatinas/antagonistas & inhibidores , Angiostatinas/genética , Angiostatinas/metabolismo , Animales , Arteriolas/fisiopatología , Arterioloesclerosis/dietoterapia , Arterioloesclerosis/fisiopatología , Arterioloesclerosis/terapia , Terapia Combinada , Regulación de la Expresión Génica , Corazón/fisiopatología , Miembro Posterior , Masculino , Actividad Motora , Músculo Esquelético/metabolismo , Músculo Esquelético/fisiopatología , Infarto del Miocardio/etiología , Infarto del Miocardio/metabolismo , Infarto del Miocardio/fisiopatología , Miocardio/metabolismo , Distribución Aleatoria , Ratas Wistar , Factor de Crecimiento Transformador beta/agonistas , Factor de Crecimiento Transformador beta/genética , Factor de Crecimiento Transformador beta/metabolismoRESUMEN
PURPOSE OF REVIEW: Atherosclerotic renal artery stenosis (ARAS) usually occurs in patients at high risk of vascular disease, and is associated with increased mortality. The primary goals of ARAS treatment include the control of blood pressure (BP), the improved renal function, and the benefit on cardiovascular events. Although medical therapy remains the standard approach to the management of ARAS, percutaneous transluminal renal angioplasty (PTRA) revascularization can be a therapeutic option under certain conditions. RECENT FINDINGS: Recent evidence confirms that ARAS increases cardiovascular risk, independent of BP and renal function. This suggests that revascularization might potentially improve overall prognosis, but no data are available currently. In cases of significant ARAS, the accepted indications for PTRA are uncontrollable hypertension, gradual or acute renal function decline with the use of agents blocking the renin-angiotensin-aldosterone system, and recurrent flash pulmonary edema. The key point of treatment success remains in all cases a careful patient selection. SUMMARY: Although the atherosclerotic lesions of the renal arteries tend to progress over time, the anatomical lesion progression is not always associated with changes in BP. Furthermore, a poor correlation was noted between the degree of anatomic stenosis and glomerular filtration rate. The high cardiovascular risk warrants aggressive pharmacological treatment to prevent progression of the generalized vascular disorder. Ongoing trials will show whether PTRA revascularization has added, long-term effects on BP, renal function, and cardiovascular prognosis. With or without PTRA revascularization, medical therapy using antihypertensive agents, statins, and aspirin is necessary in almost all cases.
Asunto(s)
Antihipertensivos/uso terapéutico , Arterioloesclerosis/tratamiento farmacológico , Presión Sanguínea , Hipertensión Renovascular/prevención & control , Obstrucción de la Arteria Renal/tratamiento farmacológico , Trombosis/tratamiento farmacológico , Anticolesterolemiantes/uso terapéutico , Arterioloesclerosis/terapia , Progresión de la Enfermedad , Humanos , Pronóstico , Obstrucción de la Arteria Renal/terapia , Sistema Renina-Angiotensina/efectos de los fármacos , Medición de Riesgo/métodos , Conducta de Reducción del Riesgo , Stents , Trombosis/terapiaRESUMEN
The history of a patient with calcific uremic arteriolopathy is discussed. The hypothetical pathogenesis and the therapeutic approach is revised.