Attenuation by Nisoldipine of the Abnormal Response to Cold Pressor Stimulation in Patients with Ischaemia and Normal Coronary Arteries

  • S. O. Banim
  • J. L. Caplin
  • J. C. O’Keefe
  • D. S. Dymond
Conference paper


This study was designed to investigate the effect of nisoldipine, a calcium antagonist, on the left ventricular and peripheral haemodynamic response to cold pressor stimulation in 12 patients with angina and normal coronary arteries. All patients had chest pain, evidence of ischaemia on exercise electrocardiograms and abnormal responses to exercise on radionuclide angiography. Patients were imaged at rest and after 1 and 2.5 min of cold pressor stimulation, before and after 10 mg of oral nisoldipine. Radionuclide angiograms were performed using insother 195 Aum (half-life of 30.5 s). Before nisoldipine mean (SD) left ventricular ejection fraction fell from 61% (9%) at rest to 55% (9%) at 1 min of cold pressor stimulation and to 56% (8%) at 2.5 min cold pressor stimulation (both P < 0.01 vs rest). Ten patients showed an abnormal ejection fraction response to cold pressor (fall in ejection fraction of ≥ 5% ). Nisoldipine caused a rise in mean (SD) resting heart rate from 83 (12) to 92 (21) beats per min and a fall in resting systolic pressure from 145 (30) mmHg to 136 (25) mmHg. Both heart rate and systolic pressure rose significantly, however, from rest to both stages of cold pressor before and after nisoldipine. Moreover, the cold-induced increases in heart rate and systolic pressure from resting levels were not attenuated by nisoldipine at either stage. After nisoldipine, left ventricular ejection fraction was 63% (10%) at rest, 64% (9%) at 1 min cold pressor and 65% (6%) at 2.5 min cold pressor (not significantly different), and only three patients had an abnormal response. Left ventricular ejection fraction was significantly higher at each cold pressor stage as compared with pre-nisoldipine values (P < 0.001).

In conclusion an abnormal response to cold pressor stimulation is common in patients with ischaemic syndromes and normal coronary arteries; this response is largely blocked by nisoldipine; and this effect is not mediated by blocking the heart rate and systolic pressure responses to cold stimulation but is possibly related to inhibition of cold-induced coronary vasoconstriction.


Rest Heart Rate Cold Pressor Cold Pressor Test Normal Coronary Artery Abnormal Response 
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Copyright information

© Springer-Verlag Berlin Heidelberg 1987

Authors and Affiliations

  • S. O. Banim
  • J. L. Caplin
  • J. C. O’Keefe
  • D. S. Dymond

There are no affiliations available

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