1,721,128 research outputs found

    Pathophysiological role of heart rate: from ischaemia to left ventricular dysfunction

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    Myocardial ischaemia results from imbalance between myocardial oxygen demand and supply. An increase in heart rate (HR) will raise both demand and supply. HR is the most important determinant of myocardial oxygen consumption and of cardiac energy demand. HR reduction improves myocardial perfusion by increasing the fraction of the cardiac cycle occupied by diastole, which accounts for 80% of coronary flow. Besides these physiological characteristics, HR is also linked to the progression of atherosclerosis, at least in animals, and an increase in HR is associated with plaque rupture in humans. The symptom of chest pain in stable angina is almost always triggered by elevated HR owing to physical or emotional stress. Equally, an increased HR precedes an episode of asymptomatic or silent myocardial ischaemia. Therefore, it is not surprising that the efficacy of some anti-anginal drugs such as b-blockers and non-dihydropyridine calcium antagonists has been related to their effectiveness in reducing HR. In many studies, multivariate analysis has shown HR to be an independent predictor of mortality and of hospitalization for heart failure. A relationship has been found between HR reduction and mortality in patients with congestive heart failure treated with b-blockers. Thus HR is an important therapeutic target for ischaemia and left ventricular dysfunction or congestive heart failure, and it seems likely that relatively high HR is both causative and indicative of important pathophysiological processes: HR is a risk factor for cardiovascular morbidity and mortality throughout the cardiovascular continuu

    Skeletal muscle myosin heavy chains expression in rats with monocrotaline-induced cardiac hypertrophy and failure. Relation to blood flow and degree of muscle atrophy

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    Background: In congestive heart failure (CHF) the skeletal muscle of the lower limbs develops a myopathy characterised by atrophy and shift from the slow to the fast type fibres. The mechanisms responsible for these changes are not clear yet. Objectives: We investigated the influence of blood flow and degree of muscle atrophy on the myosin heavy chains (MHC) composition of the soleus and extensor digitorum longus (EDL) of rats with right ventricle hypertrophy and failure. Methods: CHF was induced in 16 rats by injecting 30 mg/kg monocrotaline. Eight animals had the same dose of monocrotaline but resulting in compensated right ventricle hypertrophy. Two age- and diet- matched groups of control animals (nine and five respectively) were also studied. The relative percentage of MHC1 (slow isoform), MHC2a (fast oxidative) and MHC2b (fast glycolytic) was determined by densitometric scan after electrophoretic separation. The relative weights of soleus and EDL (muscle weight/body weight) were ..
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