Central Pulse Pressure: Is It Really an Independent Predictor of Cardiovascular Risk?
To the Editor:
We read with interest the article by Jankowski et al1 about the cardiovascular risk associated with central aortic pulse pressure (aPP). Because the measurement of aPP by invasive methods is impractical for the risk stratification and as a means of monitoring the effectiveness of antihypertensive therapy, the authors highlighted in the discussion to the article that the important value of their findings seems to be “the understanding of the nature of relationship between pressure wave and atherosclerosis complications development.” However, it is a matter of debate whether the current study gives the reader any additional knowledge about the mechanisms of how aPP influences the progression of atherosclerosis. It is generally known that increased aPP is a consequence of aortic stiffening, thus it reflects all of the processes and risk factors that lead to aortic stiffening, such as aging, endothelial dysfunction,2 and atherosclerosis.3 The same processes are responsible for the majority of cardiovascular events. On the other hand, the pulsatile blood flow may reduce NO bioavailability and enhance endothelial dysfunction.4
The question now arises whether aPP only reflects the pathological processes that lead to aortic stiffening and potentially to the damage of other arterial beds or whether aPP adds additional cardiovascular risk independent of the risk reflected by aortic stiffness. To answer this question, another cohort study would be required in which pulse pressure or its derivatives would be accounted for indices of aortic stiffness. We believe that simultaneous invasive measurement of aPP and aortic pulse wave velocity (aPWV) using the method described recently would be a suitable tool for the study.5
Until results of such a study are available, some preliminary conclusions can be drawn from our cross-sectional analysis of 206 (126 male) consecutive patients (59.6±8.6 years) with stable angina in which we assessed aPP and aPWV simultaneously during cardiac catheterization. The values of both parameters were compared between patients with ≥1 significant (≥50%) coronary artery stenosis (CAS+) and patients without significant coronary artery stenosis (CAS−). Compared with CAS− group, the CAS+ group had significantly higher values of both aPWV (9.6±2.6 versus 7.8±1.7 m/s; P<0.0001) and aPP (71.6±20.5 versus 62.0±18.6 mm Hg; P=0.001). In 2 separate stepwise logistic regression analysis models in which aPWV or aPP, as well as main cardiovascular disease risk factors, height, medication, and central mean blood pressure, were used as independent variables, the only independent predictors of significant CAS were male sex, cigarette smoking (current or previous), and aPWV or aPP. However, when aPWV and aPP were included in the regression model together, aPP was no longer an independent predictor of significant CAS. The institutional ethics committee approved the protocol for the study, and informed consent was obtained from each included patient.
Source of Funding
This research was supported by the Ministry of Science and Higher Education grant 2-P05B-150-30.
Jankowski P, Kawecka-Jaszcz K, Czarnecka D, Brzozowska-Kiszka M, Styczkiewicz K, Loster M, Kloch-Badełek M, Wilińskí J, Curyło AM, Dudek D, on behalf of the Aortic Blood Pressure and Survival Study Group. Pulsatile but not steady component of blood pressure predicts cardiovascular events in coronary patients. Hypertension. 2008; 51: 848–855.
Wilkinson IB, Franklin SS, Cockcroft JR. Nitric oxide and the regulation of large artery stiffness: from physiology to pharmacology. Hypertension. 2004; 44: 112–116.
Silacci P, Desgeorges A, Mazzolai L, Chambaz C, Hayoz D. Flow pulsatility is a critical determinant of oxidative stress in endothelial cells. Hypertension. 2001; 38: 1162–1166.
Giannattasio C, Failla M, Emanuelli G, Grappiolo A, Boffi L, Corsi D, Manciaet G. Local effects of atherosclerotic plaque on arterial distensibility. Hypertension. 2001; 38: 1177–1180.