1. ¹Department of Pharmacological Sciences, Medical School, University of Tampere, Tampere, Finland
2. ²Department of Internal Medicine, Tampere University Hospital, Tampere, Finland
3. ³Department of Internal Medicine, Päijät-Häme Central Hospital, Lahti, Finland
4. ⁴Department of Clinical Physiology, Tampere University Hospital, and Medical School, University of Tampere, Tampere, Finland
5. ⁵Heart Center, Department of Cardiology, Pirkanmaa Hospital District, Tampere, Finland
6. ⁶Ragnar Granit Institute, Tampere University of Technology, Tampere, Finland
7. ⁷Laboratory of Atherosclerosis Genetics, Department of Clinical Chemistry, Tampere University Hospital, Tampere, Finland
8. ⁸Centre for Laboratory Medicine, Medical School, University of Tampere, Tampere, Finland
9. ⁹Tampere Polytechnic, Tampere, Finland

Correspondence: Dr T Nieminen, Department of Pharmacological Sciences, Medical School, FI-33014 University of Tampere, Lääketieteen Laitos, Tampere, Finland. E-mail: tuomo.nieminen@iki.fi

Received 20 September 2007; Revised 8 April 2008; Accepted 13 April 2008; Published online 29 May 2008.

Abstract

We tested the hypothesis that the change from the peak to recovery values of systolic arterial pressure (SAP_recovery) and rate–pressure product (RPP_recovery) can be used to predict all-cause and cardiovascular mortality, as well as sudden cardiac death (SCD) in patients referred to a clinical exercise stress test. As a part of the Finnish Cardiovascular Study (FINCAVAS), consecutive patients (n=2029; mean ageSD=5713 years; 1290 men and 739 women) with a clinically indicated exercise test using a bicycle ergometer were included in the present study. Capacities of attenuated SAP_recovery, RPP_recovery and heart rate recovery (HRR) to stratify the risk of death were estimated. During a follow-up (means.d.) of 4713 months, 122 patients died; 58 of the deaths were cardiovascular and 33 were SCD. In Cox regression analysis after adjustment for the peak level of the variable under assessment, age, sex, use of -blockers, previous myocardial infarction and other common coronary risk factors, the hazard ratio of the continuous variable RPP_recovery (in units 1000 mm Hg b.p.m.) was 0.85 (95% CI: 0.73–0.98) for SCD, 0.87 (0.78–0.97) for cardiovascular mortality, and 0.87 (0.81 to 0.94) for all-cause mortality. SAP_recovery was not a predictor of mortality. The relative risks of having HRR below 18 b.p.m., a widely used cutoff point, were as follows: for SCD 1.28 (0.59–2.81, ns), for cardiovascular mortality 2.39 (1.34–4.26) and for all-cause mortality 2.40 (1.61–3.58). In conclusion, as a readily available parameter, RPP_recovery is a promising candidate for a prognostic marker.