Title: Central Pulse Pressure: Is It Really an Independent Predictor of Cardiovascular Risk?
Abstract: HomeHypertensionVol. 52, No. 1Central Pulse Pressure: Is It Really an Independent Predictor of Cardiovascular Risk? Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBCentral Pulse Pressure: Is It Really an Independent Predictor of Cardiovascular Risk? Grzegorz Kopeć and Piotr Podolec Grzegorz KopećGrzegorz Kopeć Department of Cardiac and Vascular Diseases, Jagiellonian University, John Paul II Hospital, Kraków, Poland and Piotr PodolecPiotr Podolec Department of Cardiac and Vascular Diseases, Jagiellonian University, John Paul II Hospital, Kraków, Poland Originally published26 May 2008https://doi.org/10.1161/HYPERTENSIONAHA.108.115121Hypertension. 2008;52:e4Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: May 26, 2008: Previous Version 1 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.4The 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.5Until 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 FundingThis research was supported by the Ministry of Science and Higher Education grant 2-P05B-150-30.DisclosuresNone.1 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.LinkGoogle Scholar2 Wilkinson IB, Franklin SS, Cockcroft JR. Nitric oxide and the regulation of large artery stiffness: from physiology to pharmacology. Hypertension. 2004; 44: 112–116.LinkGoogle Scholar3 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.CrossrefMedlineGoogle Scholar4 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.CrossrefMedlineGoogle Scholar5 Podolec P, Kopeć G, Podolec J, Wilkołek P, Krochin M, Rubiś P, Cwynar M, Grodzicki T, Zmudka K, Tracz W. Aortic pulse wave velocity and carotid – femoral pulse wave velocity: similarities and discrepancies. Hypertens Res. 2007; 30: 1151–1158.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Akashi R, Koga S, Yonekura T, Ikeda S, Kawano H and Maemura K (2021) Cardio-ankle vascular index is associated with coronary plaque composition assessed with iMAP-intravascular ultrasound in patients with coronary artery disease, Journal of Cardiology, 10.1016/j.jjcc.2021.05.015, 78:6, (502-508), Online publication date: 1-Dec-2021. Selwaness M, van den Bouwhuijsen Q, Mattace-Raso F, Verwoert G, Hofman A, Franco O, Witteman J, van der Lugt A, Vernooij M and Wentzel J (2014) Arterial Stiffness Is Associated With Carotid Intraplaque Hemorrhage in the General Population, Arteriosclerosis, Thrombosis, and Vascular Biology, 34:4, (927-932), Online publication date: 1-Apr-2014. Güngör B, Yılmaz H, Ekmekçi A, Özcan K, Tijani M, Osmonov D, Karataş B, Taha Alper A, Mutluer F, Gürkan U and Bolca O (2014) Aortic stiffness is increased in patients with premature coronary artery disease: A tissue Doppler imaging study, Journal of Cardiology, 10.1016/j.jjcc.2013.08.008, 63:3, (223-229), Online publication date: 1-Mar-2014. Kopeć G, Moertl D, Jankowski P, Tyrka A, Sobień B and Podolec P (2013) Pulmonary Artery Pulse Wave Velocity in Idiopathic Pulmonary Arterial Hypertension, Canadian Journal of Cardiology, 10.1016/j.cjca.2012.09.019, 29:6, (683-690), Online publication date: 1-Jun-2013. Kopeć G, Podolec P, Podolec J, Rubiś P, Żmudka K and Tracz W (2009) Atherosclerosis progression affects the relationship between endothelial function and aortic stiffness, Atherosclerosis, 10.1016/j.atherosclerosis.2008.09.003, 204:1, (250-254), Online publication date: 1-May-2009. Jankowski P and Kawecka-Jaszcz K (2008) Response to Central Pulse Pressure: Is It Really an Independent Predictor of Cardiovascular Risk?, Hypertension, 52:1, (e5-e5), Online publication date: 1-Jul-2008. July 2008Vol 52, Issue 1 Advertisement Article InformationMetrics https://doi.org/10.1161/HYPERTENSIONAHA.108.115121PMID: 18504318 Originally publishedMay 26, 2008 PDF download Advertisement SubjectsChronic Ischemic Heart DiseaseEpidemiologyMechanismsPathophysiology