ADVERTISEMENT
Ascending Aortic Hemodynamics and One-Year Clinical Events
Following Percutaneous Coronary Intervention
October 2004
Large vessel arterial compliance declines with advancing age and with atherosclerotic coronary artery disease.1-7 While compliance can be measured in a detailed manner using hi-fidelity hemodynamics,8 pulse pressure (aortic systolic pressure – aortic diastolic pressure) can be used to estimate arterial compliance accurately.9,10 Increased pulse pressure is likely to reflect, at least in part, a loss of compliance due to atherosclerotic damage to arterial walls.11 This loss of vascular compliance has been demonstrated to correlate with diminished coronary flow,12,13 and with the development of left ventricular hypertrophy.14 The loss of compliance has been demonstrated to independently contribute to an increased risk of congestive heart failure,15 myocardial infarction1,6,17 and mortality.17-23
Although higher coronary artery perfusion pressure associated with intra-aortic balloon counter pulsation appears to increase short-term coronary artery patency following acute myocardial infarction,24 higher pulse pressure over time has been shown to be a predictor of deleterious arterial remodeling and intimal thickening.25
There have been two small studies that suggest that higher pulse pressure, or higher fractional pulse pressure (defined as the pulse pressure divided by the mean arterial pressure)26 measured immediately prior to percutaneous coronary balloon angioplasty was associated with an increased risk of restenosis.26,27 The total number of subjects studied (140) has been small, and the contribution of pulse pressure or fractional pulse pressure, has not been evaluated when intracoronary stenting is performed with PTCA. We sought to determine the value of pulse pressure and fractional pulse pressure for the prediction of restenosis and recurrent events in a general population undergoing PTCA with stenting.
Methods
A retrospective review was conducted of all subjects who presented for percutaneous coronary stenting at our institution from January 1998 to July 2001. For a direct comparison to previous studies, subanalysis was performed excluding those patients with left-ventricular ejection fraction of less than 0.50, serum creatinine greater than 2.0 mg per deciliter, systolic blood pressure less than 90 mmHg at the time of diagnostic angiography or presentation with acute myocardial infarction.
Hemodynamic measurements were performed using a fluid-filled catheter in the ascending aorta. We compared tracings of systolic, diastolic, mean and pulse pressures in patients with and without restenosis. Fractional pulse pressure (PPf) was defined as the ratio of pulse pressure to mean pressure. The primary outcome was the 1-year occurrence of major adverse cardiac events (MACE) [defined as death, myocardial infarction or revascularization] compared to the PP and PPf measured as continuous variables in the total population. A secondary outcome was the occurrence of MACE compared to PP and PPf in the subset of patients previously described. These subjects were selected for comparison to those prior studies of PP and PPf in PTCA patients without stenting.26,27 Myocardial infarction was defined as a creatinine kinase MB isoform (CKMB) level greater than 2-fold the upper limit of normal or a CKMB-index greater than 5 that was not associated with a revascularization procedure.
Categorical variables are presented as percentages. Continuous variables are presented as means ± standard deviations. Student’s t-test was used for comparison of normally distributed continuous variables. Chi-squared test was used for categorical variables. Statistical analysis was performed using StatView, Version 5 (SAS Institute Inc., Cary, North Carolina). P values were considered significant when
1. Franklin SS, Gustin Wt, Wong ND, et al. Hemodynamic patterns of age-related changes in blood pressure. The Framingham Heart Study. Circulation 1997;96:308–315.
2. Lehmann ED, Gosling RG, Sonksen PH. Arterial wall compliance in diabetes. Diabet Med 1992;9:114–119.
3. Whelton P, He J, Klag M. Blood pressure in westernized populations. In: Swales J, ed. Textbook of Hypertension. Oxford: Blackwell Scientific Productions. 1994:11–21.
4. Stefanadis C, Stratos C, Boudoulas H, et al. Distensibility of the ascending aorta: comparison of invasive and non-invasive techniques in healthy men and in men with coronary artery disease. Eur Heart J 1990;11:990–996.
5. Gatzka CD, Cameron JD, Kingwell BA, et al. Relation between coronary artery disease, aortic stiffness, and left ventricular structure in a population sample. Hypertension 1998;32:575–578.
6. Hirai T, Sasayama S, Kawasaki T, et al. Stiffness of systemic arteries in patients with myocardial infarction. A noninvasive method to predict severity of coronary atherosclerosis. Circulation 1989;80:78–86.
7. O'Rourke M, Kelly R, Avolio A. The Arterial Pulse. Philadelphia, PA: Lea and Febiger, 1992.
8. Liu Z, Brin KP, Yin FC. Estimation of total arterial compliance: an improved method and evaluation of current methods. Am J Physiol 1986;251:H588–600.
9. Stergiopulos N, Segers P, Westerhof N. Use of pulse pressure method for estimating total arterial compliance in vivo. Am J Physiol 1999;276:H424–428.
10. Chemla D, Hebert JL, Coirault C, et al. Total arterial compliance estimated by stroke volume-to-aortic pulse pressure ratio in humans. Am J Physiol 1998;274:H500–505.
11. Dart AM, Kingwell BA. Pulse pressure--a review of mechanisms and clinical relevance. J Am Coll Cardiol 2001;37:975–984.
12. Kass DA, Saeki A, Tunin RS, et al. Adverse influence of systemic vascular stiffening on cardiac dysfunction and adaptation to acute coronary occlusion. Circulation 1996;93:1533–1541.
13. Watanabe H, Ohtsuka S, Kakihana M, et al. Coronary circulation in dogs with an experimental decrease in aortic compliance. J Am Coll Cardiol 1993;21:1497–1506.
14. Pannier B, Brunel P, el Aroussy W, et al. Pulse pressure and echocardiographic findings in essential hypertension. J Hypertens 1989;7:127–132.
15. Chae CU, Pfeffer MA, Glynn RJ, et al. Increased pulse pressure and risk of heart failure in the elderly. J Am Med Assoc 1999;281:634–639.
16. Millar JA, Lever AF, Burke V. Pulse pressure as a risk factor for cardiovascular events in the MRC Mild Hypertension Trial. J Hypertens 1999;17:1065–1072.
17. Verdecchia P, Schillaci G, Borgioni C, et al. Ambulatory pulse pressure: a potent predictor of total cardiovascular risk in hypertension. Hypertension 1998;32:983–988.
18. Franklin SS. Cardiovascular risks related to increased diastolic, systolic and pulse pressure. An epidemiologist's point of view. Pathol Biol (Paris) 1999;47:594–603.
19. Franklin SS, Khan SA, Wong ND, et al. Is pulse pressure useful in predicting risk for coronary heart Disease? The Framingham heart study. Circulation 1999;100:354–360.
20. Lee ML, Rosner BA, Weiss ST. Relationship of blood pressure to cardiovascular death: The effects of pulse pressure in the elderly. Ann Epidemiol 1999;9:101–107.
21. Benetos A, Safar M, Rudnichi A, et al. Pulse pressure: A predictor of long-term cardiovascular mortality in a French male population. Hypertension 1997;30:1410–1415.
22. Domanski MJ, Mitchell GF, Norman JE, et al. Independent prognostic information provided by sphygmomanometrically determined pulse pressure and mean arterial pressure in patients with left ventricular dysfunction. J Am Coll Cardiol 1999;33:951–958.
23. Domanski MJ, Davis BR, Pfeffer MA, et al. Isolated systolic hypertension: Prognostic information provided by pulse pressure. Hypertension 1999;34:375–380.
24. Ohman EM, George BS, White CJ, et al. Use of aortic counterpulsation to improve sustained coronary artery patency during acute myocardial infarction. Results of a randomized trial. The Randomized IABP Study Group. Circulation 1994;90:792–799.
25. Boutouyrie P, Bussy C, Lacolley P, et al. Association between local pulse pressure, mean blood pressure, and large-artery remodeling. Circulation 1999;100:1387–1393.
26. Nakayama Y, Tsumura K, Yamashita N, et al. Pulsatility of ascending aortic pressure waveform is a powerful predictor of restenosis after percutaneous transluminal coronary angioplasty. Circulation 2000;101:470–472.
27. Lu TM, Hsu NW, Chen YH, et al. Pulsatility of ascending aorta and restenosis after coronary angioplasty in patients >60 years of age with stable angina pectoris. Am J Cardiol 2001;88:964–968.
28. Schwartz RS, Topol EJ, Serruys PW, et al. Artery size, neointima, and remodeling: time for some standards. J Am Coll Cardiol 1998;32:2087–2094.
