Why the study?
Does oral pirbuterol alter metabolic, hormonal, and hemodynamic parameters acutely and long-term in patients with severe heart failure?
Does oral pirbuterol alter metabolic, hormonal, and hemodynamic parameters acutely and long-term in patients with severe heart failure?
Oral pirbuterol provides sustained hemodynamic benefits in severe heart failure, with transient acute metabolic effects like hypokalemia that resolve with chronic use.
Pirbuterol may sustain hemodynamic gains in severe HF without persistent metabolic effects; this Level 3 cohort study leaves open randomized confirmation.
The metabolic, hormonal and haemodynamic effects of oral pirbuterol, a new beta 2-adrenoceptor agonist, were studied acutely (n = 19) and after 3 months treatment (n = 11) in patients with severe heart failure receiving chronic frusemide therapy. In the acute study fasted patients (n = 10) showed reductions in plasma K+ (P less than 0.005) and cortisol (P less than 0.01) and increases in plasma glucose (P less than 0.005), insulin (P less than 0.01), lactate (P less than 0.005) and pyruvate (P less than 0.0025). These acute changes were less in unfasted subjects (n = 9). Maximal increase in stroke volume occurred at approximately half the plasma pirbuterol concentration required for maximal effect on plasma insulin. Treatment with pirbuterol for 3 months was associated with sustained increases in stroke volume and fasting plasma glucose and insulin, but there was loss of all other acute metabolic effects. Despite concurrent frusemide and digoxin therapy acute hypokalaemia caused no adverse effects. Hypokalaemia did not occur with chronic pirbuterol administration.
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Canepa‐Anson et al. (1987) studied this question.
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