Author + information
- Received August 17, 1982
- Revision received January 4, 1983
- Accepted January 5, 1983
- Published online June 1, 1983.
- Samuel Z. Goldhaber, MD*,
- Harvey D. White, MB, ChB,
- B. Leonard Holman, MD, FACC,
- Richard W. Nesto, MD,
- Gilbert H. Mudge Jr., MD, FACC,
- James E. Muller, MD, FACC,
- Joseph Kozlowski, RT and
- Joshua Wynne, MD, FACC
- ↵*Address for reprints: Samuel Z. Goldhaber, MD, 55 Pond Avenue, Brookline, Massachusetts 02146.
To examine the effects of nifedipine on changes in ventricular function produced by cold, the cold pressor test was administered to eight patients with angiographically documented coronary artery disease. Radionuclide ventriculograms were obtained at baseline and during the cold pressor stimulus both before and after administration of nifedipine, 10 mg buccally; thus, four serial radionuclide ventriculograms were obtained per patient.
The cold pressor stimulus did not produce any significant difference in the mean (± standard deviation) peak rate-pressure product during the control or nifedipine test (10,900 ± 3,390 versus 10,600 ± 3,700). However, the increase in systolic blood pressure (p = 0.05) and the peak systolic blood pressure achieved (p < 0.001) were greater during the control (134 ± 19 to 160 ± 25 mm Hg) than during the nifedipine (125 ± 18 to 145 ± 21 mm Hg) cold pressor test. The mean global left ventricular ejection fraction decreased during the control cold pressor test from a baseline value of 0.60 ± 0.08 to 0.52 ± 0.08 (p = 0.004). After nifedipine, this variable did not change during the repeat cold pressor test (0.63 ± 0.09) compared with the repeat baseline value (0.63 ± 0.11). Therefore, the difference in left ventricular ejection fraction response during control versus nifedipine cold pressor testing was highly significant (p < 0.0001).
In patients with obstructive coronary artery disease, nifedipine abolished the decrease in left ventricular ejection fraction observed during the control cold pressor test and may be of value to protect patients from cold-induced left ventricular dysfunction. The mechanism may be a combination of coronary artery vasodilation and systolic unloading of the left ventricle.
This study was supported, in part, by Grant HL24241 from the U.S. Public Health Service, Bethesda, Maryland. Dr. Goldhaber was supported by National Service Research Award HL07049 of the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. Dr. White was supported by the National Heart Foundation of New Zealand, Auckland, New Zealand. Dr. Wynne was supported by a Young Investigatorship Award of the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland
- Received August 17, 1982.
- Revision received January 4, 1983.
- Accepted January 5, 1983.
- American College of Cardiology Foundation