Pulmonary hypertension is a contraindication to β-blockade in patients with severe mitral stenosis

Abstract Intravenous atenolol was given to 31 patients just before balloon mitral valvotomy to assess the hemodynamic efficacy and safety of β-blockade in mitral stenosis complicated by pulmonary hypertension. Hemodynamic response in patients with pulmonary resistance >600 dynes · sec · cm −5 (group 2, n = 17) was compared with those (group 1, n = 14) with a resistance below this value. In addition to a higher pulmonary arterial resistance (by design), patients in group 2 had a higher systemic resistance, lower cardiac index, and smaller mitral valve area compared with those in group 1. After atenolol infusion, transmitral gradient and left atrial pressure improved similarly. In spite of the decline in left atrial pressure, pulmonary vascular resistance increased in both groups, more in group 2 (847 ± 398 dynes · sec · cm −5 to 1135 ± 648 dynes · sec · cm −5 ) than in group 1 (291 ± 149 dynes · sec · cm −5 to 363 ± 200; p p = 0.027 for group effect by two-way analysis of variance). Cardiac index declined similarly from 2.77 ± 0.51 L/min/m 2 to 2.37 ± 0.37 L/min/m 2 in group 1 and from 2.33 ± 0.58 L/min/m 2 to 1.92 ± 0.54 L/min/m 2 in group 2. Systemic pressure tended to decline only in group 2 (mean aortic pressure, 89 ± 12 mm Hg to 89 ± 12 mm Hg in group 1 and 90 ± 9 mm Hg to 83 ± 12 mm Hg in group 2; p = 0.06 for group effect). Two patients in group 2 required fluids and cardioactive drugs for severe hypotension (aortic systolic pressures, 50 and 60 mm Hg) after atenolol doses of 10 and 1.5 mg, respectively; and in three other patients in group 2 (who received doses of 10, 10, and 6 mg), mean aortic pressure fell to −5 to 2455 ± 487 dynes · sec · cm −5 ) and in group 1 (1617 ± 349 dynes · sec · cm −5 to 1824 ± 414 dynes · sec · cm −5 ) an inappropriate decline in systemic resistance was observed in these five patients (2002 ± 444 dynes · sec · cm −5 to 1851 ± 530 dynes · sec · cm −5 ; p = 0.05 for group effect). The only baseline hemodynamic marker of a hypotensive response to atenolol was a higher right atrial pressure (> 10 mm Hg in three of five patients). Thus β-blockade given to patients with pulmonary hypertension and right heart failure complicating mitral stenosis may produce hypotension as a result of a reduction in cardiac output with an inappropriate fall in systemic vascular resistance.