Experiencia inicial con la válvula aórtica percutánea de muy bajo perfil SAPIEN 3 / Initial experience with the low-profile percutaneous aortic valve SAPIEN 3

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Effect of candesartan on coronary flow reserve in patients with systemic hypertension.

BACKGROUND: Patients with hypertension have structural and functional changes in conductance and resistance vessels. In the absence of coronary stenosis the coronary microvascular function can be analysed by studying the coronary reserve. The aim of this study was to evaluate, non-invasively, the effect of candesartan on coronary microvascular function in hypertensive patients. METHODS: Twenty-two hypertensive patients (> 40 years) without clinical coronary disease (age 63.86 +/- 10.3 years; women, 59.1%) were studied. In addition to blood pressure (BP), measurement of carotid intima-medial thickness (IMT), left ventricle mass index (LVMI) and the coronary flow reserve (CFR) were evaluated with echography at the beginning, and after 3 months of treatment with 16 mg/day of candesartan. Twelve hypertensive controls (64.50 +/- 10.8 years; women, 58.4%) completed the same study without any change in treatment. RESULTS: A 15% improvement in CFR (3.10 +/- 1.02 to 3.56 +/- 1.06; P = 0.001) was observed simultaneously with the BP reduction. There was no change in CFR in the control group (2.9 +/- 1.1 to 3.01 +/- 0.9; P = 0.23). The IMT was not modified significantly at the end of the follow-up (0.86 +/- 0.1 to 0.83 +/- 0.1 mm; P = 0.103). CONCLUSION: Candesartan improves the CFR in hypertensive patients. The improvement was not related to BP control or LVMI regression. Patients with a lower CFR show a better response to candesartan. This fact can be demonstrated non-invasively with echography after 3 months of therapy.

Prevención de la fibrilación auricular en los pacientes con insuficiencia cardiaca / Prevention of atrial fibrillation in patients with heart failure

La insuficiencia cardiaca promueve la aparición de fibrilación auricular y ésta agrava la insuficiencia cardiaca. La fibrilación auricular puede afectar en cualquier momento a un gran porcentaje de los pacientes con insuficiencia cardiaca. La manifestación y presentación clínica cambia con el paso del tiempo y depende de cada paciente. Empeora la sintomatología de los pacientes, como una complicación más de su enfermedad, y causa frustración tanto a los pacientes como a los médicos. Se estima que hasta un 50% de los pacientes con insuficiencia cardiaca presentan fibrilación auricular en algún momento de su evolución, por lo que son necesarias medidas tanto para la prevención de la embolia como para el alivio de los síntomas. La interferencia farmacológica con señales específicas de las vías de transducción es prometedora. Hasta ahora, los agentes más efectivos son los inhibidores de la enzima de conversión de la angiotensina y los antagonistas de los receptores de la angiotensina II, que reducen el estrés oxidativo, restauran las concentraciones de óxido nítrico, inhiben la formación de tejido fibroso y pueden reducir la ectopia de las venas pulmonares. El desenmascaramiento de factores genéticos implicados aún no conocidos puede tener gran repercusión. Es necesario un mejor conocimiento de la fisiología molecular. Esto puede ayudar a desarrollar nuevos regímenes de tratamiento o terapia híbrida con combinación de fármacos «antiarrítmicos» y «no antiarrítmicos» para aumentar la eficacia del tratamiento (AU)

The presence of heart failure increases the risk of atrial fibrillation, a condition which in turn aggravates heart failure. At any point in time, a large percentage of patients with heart failure are affected by atrial fibrillation. Its clinical characteristics change over time and vary according to the individual patient. It worsens patients’ symptoms, adds a further a complication to their illness, and is problematic for both patients and physicians. It is estimated that 50% of patients with heart failure will experience atrial fibrillation, and will require treatment to prevent embolism and relieve symptoms. The ability of drugs to interfere with specific signal transduction pathways is promising. To date, the most effective agents appear to be angiotensin-converting enzyme inhibitors and angiotensin-II receptor antagonists. These compounds reduce oxidative stress, restore the nitric oxide level, inhibit the formation of fibrous tissue, and can ameliorate pulmonary vein ectopy. Uncovering the, as yet unknown, genetic factors involved could have significant implications. Better understanding of the relevant molecular biology is essential. This could lead to new treatment regimes or to hybrid therapy with a combination of antiarrhythmic and non-antiarrhythmic drugs, which could improve treatment effectiveness (AU)