Heart failure (HF) has been classically defined as a condition in which the heart is unable to deliver sufficient oxygen to match the needs of the metabolizing tissues. Dr Paul… Click to show full abstract
Heart failure (HF) has been classically defined as a condition in which the heart is unable to deliver sufficient oxygen to match the needs of the metabolizing tissues. Dr Paul Wood was the first to state that ‘heart failure can be defined as a state in which the heart fails to maintain an adequate circulation for the needs of the body despite a satisfactory venous filling pressure’ in his classic textbook Diseases of the Heart and Circulation, published in 1956.1 Dr Eugene Braunwald later modified this definition to ‘a pathophysiological state in which the heart is unable to pump blood at a rate commensurate with the requirements of the metabolizing tissues or can do so only from an elevated filling pressure’.2 In the present issue of this journal, Adamo et al. publish a retrospective analysis designed to determine the prevalence of elevated lactate levels in stable patients with advanced HF.3 The authors used a single peripheral lactate measurement as a surrogate for the balance between oxygen supply and metabolic demand. The study included 96 HF patients who underwent evaluation for a left ventricular assist device (LVAD) with right heart catheterization. Lactate was measured within 24 h of LVAD placement in a single sample of peripheral venous blood collected on ice. The arterio–venous oxygen (a–vO2) difference was above the upper limit of normal (>5 mL/100 mL) in 93% of these patients. Lactate levels were normal (<2.1 mmol/L) in ∼75% of the patients. There was no correlation between cardiac index and peripheral lactate level. The authors conclude: ‘Lactate levels were normal in ∼75% of the patients with advanced HF and a widened a–vO2 difference, suggesting that the cardiac output was sufficient to meet the metabolic needs of the peripheral metabolizing tissues. Given that ∼4% of HF patients are in NYHA class IV, these findings suggest that the classic definition of HF pertains to ∼1% of patients with HF.’3 Few studies have assessed resting lactate levels in patients with severe HF. The data from the present study3 are therefore
               
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