| pA2 online © Copyright 2004 The British Pharmacological Society |
188P
University of Newcastle Winter Meeting December 2004 |
Pulse wave analysis and the Framingham risk functions for cardiovascular risk assessment K. C. Williams, K. Rowland Yeo, C. Wilson & W. W. Yeo. Academic Unit of Clinical Pharmacology, University of Sheffield, Royal Hallamshire Hospital, Sheffield S10 2JF, UK. |
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Print abstractClinical guidelines recommend calculating coronary heart disease (CHD) or cardiovascular disease (CVD) risk using the Framingham algorithm. A possible limitation is that it is an indirect way of assessing arteries with silent atherosclerotic lesions, but it remains the clinical standard. Assessing vascular function and arterial stiffness involved in the pathology of CVD may prove useful. Pulse wave analysis (PWA) is a computer-based, non-invasive method of measuring arterial stiffness [1], with augmentation index (AIx) and pulse wave velocity (PWV) representing systemic vascular and central artery stiffness. Weexamined the relation between PWA and predicted CHD and CVD risks using original [2] and updated [3] Framingham functions.
One hundred men and women aged 18–80 years, with essential hypertension, attending the Sheffield Hypertension Clinic were recruited with ethics committee approval. Baseline data required for risk estimation were collected and patients had PWA at a single clinic visit. Table 1 shows the baseline characteristics and calculated risks. Performance of PWA as a diagnostic test for ‘high risk’ (CVD risk 
20% and CHD risk 15% over 10 years) was assessed using receiver operator characteristic (ROC) curves.
Table 1
Baseline characteristics in the primary and secondary prevention groups.
Prevention group |
Primary (n = 71) |
Secondary (n = 29) |
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Variable |
Men(n = 37) Mean ± SD |
Women ( n = 34) Mean ± SD |
Men (n = 22)
Mean ± SD |
Women(n = 7) Mean ± SD |
| Age (years) | 51 ± 13 |
54 ± 18 |
65 ± 9 |
66 ± 10 |
| BP (mmHg) | 148 ± 20/90 ± 10 |
141 ± 22/84 ± 9 |
161 ± 24/93 ± 10 |
151 ± 24/82 ± 9 |
AIx (%) |
19 ± 10 |
28 ± 11 |
24 ± 7 |
27 ± 7 |
| PWV (m s-1) | 8.9 ± 2.3 |
8.7 ± 2.8 |
11.7 ± 2.8 |
11.2 ± 3.1 |
| Initial 10 year CVD risk | 20.2 ± 16.0 |
15.5 ± 14.7 |
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Initial 10 year CHD risk |
14.2 ± 11.7 |
8.4 ± 8.0 |
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| Subsequent 2 year CHD risk | 9.4 ± 2.3 |
5.7 ± 4.3 |
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For primary prevention patients AIx was associated with CVD risk only (men r = 0.41, p < 0.05; women r = 0.46, p < 0.01). PWV was associated with CHD and CVD risks (CHD men r = 0.61, p < 0.001; women r = 0.64, p < 0.01; CVD men r = 0.75, p < 0.0001; women r = 0.60, p < 0.001). For secondary prevention patients the relation between PWV and subsequent CHD risk was weak in men and significant in women (men r = 0.19, p = 0.44; women r = 0.98, p < 0.001). The ROC curve for PWV as a diagnostic test for high CVD risk (10-year risk 20%) was 0.86 ± 0.05. PWA shows strong associations with predicted Framingham risks, and may provide added value in cardiovascular risk assessment.
1. O’Rourke MF, et al. Br J Clin Pharmacol 2001; 51: 507.
2. Anderson KM, et al. Am Heart J 1991; 121: 293.
3. D'Agostino RB, et al. Am Heart J 2000; 139 : 272.