Author + information
- Received May 10, 2019
- Revision received June 28, 2019
- Accepted July 8, 2019
- Published online August 26, 2019.
- Julio A. Chirinos, MD, PhDa,b,∗ (, )
- Patrick Segers, PhDc,
- Timothy Hughes, PhDd and
- Raymond Townsend, MDb,e
- aDivision of Cardiovascular Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania
- bUniversity of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania
- cBiofluid, Tissue, and Solid Mechanics for Medical Applications, IBiTech Ghent, University of Ghent, Ghent, Belgium
- dWake Forest School of Medicine, Winston-Salem, North Carolina
- eDivision of Nephrology and Hypertension, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania
- ↵∗Address for correspondence:
Dr. Julio A. Chirinos, South Tower, Room 11-138, Perelman Center for Advanced Medicine, 3400 Civic Center Blvd. Philadelphia, Pennsylvania 19104.
• LAS is an important determinant of CV health and target organ damage.
• LAS is an independent predictor of CV risk and may aid in clinical decision making in various clinical scenarios.
• Multiple mechanisms can lead to LAS, but further research is required to identify key molecular determinants of LAS in humans.
• LAS represents a high-priority therapeutic target to ameliorate the global burden of CV disease.
A healthy aorta exerts a powerful cushioning function, which limits arterial pulsatility and protects the microvasculature from potentially harmful fluctuations in pressure and blood flow. Large-artery (aortic) stiffening, which occurs with aging and various pathologic states, impairs this cushioning function, and has important consequences on cardiovascular health, including isolated systolic hypertension, excessive penetration of pulsatile energy into the microvasculature of target organs that operate at low vascular resistance, and abnormal ventricular-arterial interactions that promote left ventricular remodeling, dysfunction, and failure. Large-artery stiffness independently predicts cardiovascular risk and represents a high-priority therapeutic target to ameliorate the global burden of cardiovascular disease. This paper provides an overview of key physiologic and biophysical principles related to arterial stiffness, the impact of aortic stiffening on target organs, noninvasive methods for the measurement of arterial stiffness, mechanisms leading to aortic stiffening, therapeutic approaches to reduce it, and clinical applications of arterial stiffness measurements.
- arterial stiffness
- heart failure
- liver disease
- matrix gla protein
- renal disease
- systolic hypertension
- vascular calcification
Dr. Chirinos is supported by NIH grants R01 HL 121510-01A1, R61-HL-146390, R01-AG058969, 1R01HL104106, P01HL094307, and R56 HL136730; has served as a consultant for Sanifit, Bayer, Bristol-Myers Squibb, OPKO Healthcare, Ironwood, Akros Pharma, Merck, Pfizer, Edwards Lifesciences, Microsoft, and Fukuda-Denshi; has received research grants from the National Institutes of Health, American College of Radiology Network, Fukuda-Denshi, Bristol-Myers Squibb, and Microsoft; and is named as inventor in University of Pennsylvania patent applications for the use of inorganic nitrates/nitrites for the treatment of Heart Failure and Preserved Ejection Fraction, novel methods of pulse wave analysis and neoepitope-based collagen biomarkers of tissue fibrosis in heart failure. All other authors have reported that they have no relationships relevant to this paper to disclose.
Listen to this manuscript's audio summary by Editor-in-Chief Dr. Valentin Fuster on JACC.org.
- Received May 10, 2019.
- Revision received June 28, 2019.
- Accepted July 8, 2019.
- 2019 American College of Cardiology Foundation
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