Wave intensity as a useful modality for assessing ventilation–perfusion imbalance in subclinical patients with hypertension
Wave intensity (WI) is a novel noninvasive index of circulatory dynamics that reflects ventriculo-arterial coupling. It is calculated as the product of the first derivative of blood pressure and that of flow velocity measured by carotid echocardiography. This study aimed to clarify the clinical implications of WI and its relation with carbon dioxide production (VE/VCO2 slope). Twenty-one healthy volunteers (control group) and 21 patients with hypertension (HT group) underwent cardiopulmonary exercise testing (CPX) and exercise stress echocardiography. WI was assessed in the right carotid artery using an ultrasound system. The first peak of WI (W1) during the early ejection phase was measured at baseline and mitral annular velocity was assessed by tissue Doppler imaging. Ventilatory kinetics during exercise was assessed using the relation of minute ventilation to VE/VCO2 slope. VE/VCO2 slope, W1, and E/E′ were greater in the HT group than in the control group. PeakVO2 and VO2 at the anaerobic threshold were lower in the HT group than in the control group. VE/VCO2 slope was significantly correlated with W1 (r = 0.58, p < 0.01) and E/E′ (r = 0.44, p < 0.01). Stepwise multivariate analysis revealed that W1 was an independent determinant of VE/VCO2 slope (β = 0.43, p < 0.01). In conclusion, W1 might be able to predict the severity of heart failure without the need for CPX. Moreover, WI may be a useful modality in assessing heart failure pathophysiology based on ventriculo-arterial coupling.
KeywordsWave intensity Carotid echocardiography Exercise capacity
This study was supported by Professor Kiyomi Niki, Tokyo City University, and Motoaki Sugawara, Himeji Dokkyo University. The authors thank the technologists in the clinical laboratory at Tsukuba University Hospital for their help with the data collection.
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Conflict of interest
The authors have no conflict of interest directly relevant to the content of this article.
- 2.Rakebrandt F, Palombo C, Swampillai J, Schön F, Donald A, Kozàkovà M, Kato K, Fraser AG (2009) Arterial wave intensity and ventricular-arterial coupling by vascular ultrasound: rationale and methods for the automated analysis of forwards and backwards running waves. Ultrasound Med Biol 35:266–277CrossRefPubMedGoogle Scholar
- 5.Davies JE, Whinnett ZI, Francis DP, Manisty CH, Aguado-Sierra J, Willson K, Foale RA, Malik IS, Hughes AD, Parker KH, Mayet J (2006) Evidence of a dominant backward-propagating “suction” wave responsible for diastolic coronary filling in humans, attenuated in left ventricular hypertrophy. Circulation 113:1768–1778CrossRefPubMedGoogle Scholar
- 7.Balady GJ, Arena R, Sietsema K, Myers J, Coke L, Fletcher GF, Forman D, Franklin B, Guazzi M, Gulati M, Keteyian SJ, Lavie CJ, Macko R, Mancini D, Milani RV (2010) Interdisciplinary Council on Quality of Care and Outcomes Research. Clinician’s Guide to cardiopulmonary exercise testing in adults: a scientific statement from the American Heart Association. Circulation 122:191–225CrossRefPubMedGoogle Scholar
- 17.Schiller NB, Shah PM, Crawford M, DeMaria A, Devereux R, Feigenbaum H, Gutgesell H, Reichek N, Sahn D, Schnittger I (1989) Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr 2:358–367CrossRefPubMedGoogle Scholar
- 20.Niki K, Sugawara M, Uchida K, Tanaka R, Tanimoto K, Imamura H, Sakomura Y, Ishizuka N, Koyanagi H, Kasanuki H (1999) A noninvasive method of measuring wave intensity, a new hemodynamic index: application to the carotid artery in patients with mitral regurgitation before and after surgery. Heart Vessels 14:263–271CrossRefPubMedGoogle Scholar
- 31.Lele SS, Macfarlane D, Morrison S, Thomson H, Khafagi F, Frenneaux M (1996) Determinants of exercise capacity in patients with coronary artery disease and mild to moderate systolic dysfunction. Role of heart rate and diastolic filling abnormalities. Eur Heart J 17:204–212CrossRefPubMedGoogle Scholar