Comparison of the effects of adenosine and nifedipine in pulmonary hypertension

Abstract

The hemodynamic effects of intravenously administered adenosine, a potent vasodilator, were examined in 15 patients with pulmonary hypertension. All patients were given adenosine, 50 micrograms/kg per min, increased by 50 micrograms/kg per min at 2 min intervals to a maximum of 500 micrograms/kg per min or until the development of untoward side effects. The patients were then given oral nifedipine, 20 mg every hour, until a greater than or equal to 20% decrease in pulmonary vascular resistance or systemic hypotension occurred. The administration of maximal doses of adenosine, 256 +/- 46 micrograms/kg per min, produced a 2.4% reduction in pulmonary artery pressure (p = NS), a 37% decrease in pulmonary vascular resistance (p less than 0.001) and a 57% increase in cardiac index (p less than 0.001). The administration of maximally effective doses of nifedipine (91 +/- 36 mg) produced a 15% reduction in the mean pulmonary artery pressure (p less than 0.05), a 24% decrease in pulmonary vascular resistance (p less than 0.01) and an 8% increase in cardiac index (p = NS). There was a significant correlation (r = 0.714, p = 0.01) between the reduction in pulmonary vascular resistance that resulted from adenosine administration and that achieved with the administration of nifedipine. Six patients had substantial reductions in pulmonary vascular resistance with adenosine but not with nifedipine. Thus, adenosine is an effective vasodilator in patients with pulmonary hypertension and can be used for safe and rapid assessment of vasodilator reserve in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Iloprost for pulmonary vasodilator testing in idiopathic pulmonary arterial hypertension

“…The cardiac frequency and the transcutaneous arterial oxygen saturation were monitored continuously. [4,7]. Haemodynamic parameters and blood gases were monitored during adenosine administration.…”

“…epoprostenol and i.v. adenosine often cause systemic hypotension and other intolerable adverse effects when their dosages are incrementally increased to higher levels [7,10,11]. Inhaled NO has been advocated as an effective way of identifying acute haemodynamic responses but the use of inhaled NO requires complicated administration and monitoring devices, and its acute withdrawal can lead to dangerous rebound pulmonary hypertension [12,13].…”

“…Currently, three shortacting agents are widely recommended in these guidelines for acute pulmonary vasoreactivity testing: intravenous epoprostenol [5,6], i.v. adenosine [4,7], and inhaled nitric oxide (NO) [8,9]. However, both i.v.…”

Acute Vasoreactivity Testing With Nicardipine in Patients With Pulmonary Arterial Hypertension

“…Acute vasoreactivity testing is most commonly performed using inhaled iNO (10), intravenous epoprostenol (11), or intravenous adenosine (12). However, several investigators have also pointed out a problem with these agents: it is important to consider that these agents have different mechanisms of action and diverse hemodynamic effects, and their use may therefore not be interchangeable (13,23).…”

“…Although acute vasoreactivity testing is most commonly performed using inhaled nitric oxide (iNO) (10), intravenous epoprostenol (11), or intravenous adenosine (12), there are uncertainties regarding the choice of vasodilator (13).…”