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Aortic Compliance and Left Ventricular Diastolic Function – Do Endovascular Repairs for Aortic Aneurysm Alter Aortic Stiffness? – Hideaki Kanzaki, MD

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Aortic Compliance and Left Ventricular Diastolic Function – Do Endovascular Repairs for Aortic Aneurysm Alter Aortic Stiffness? – Hideaki Kanzaki, MD Circulation Journal EDITORIAL Official Journal of the Japanese Circulation Society http://www.j-circ.or.jp Aortic Compliance and Left Ventricular Diastolic Function – Do Endovascular Repairs for Aortic Aneurysm Alter Aortic Stiffness? – Hideaki Kanzaki, MD ndovascular aortic repair or endovascular aneurysm re- tole. In diastole, the elastic forces of the aorta propel this volume pair (EVAR) is a type of endovascular surgical treat- to the peripheral circulation, thereby converting the pulsatile E ment for abdominal aortic aneurysm (AAA) or tho- arterial blood flow into a nearly continuous peripheral blood racic aortic aneurysm (TAA). The procedure for treating TAA is flow.4 The interaction between the ejected blood volume and specifically termed TEVAR (thoracic endovascular aortic/aneu- the compliance of large elastic arteries is referred to as the rysm repair). Ruptured AAA has a mortality rate of approxi- Windkessel effect (Figure). The Windkessel function of the mately 90%; however, elective AAA repair is associated with a aorta influences not only on the peripheral circulation, but also mortality rate of <5%.1 Aortic aneurysm is a life-threatening heart. The extension of the aortic wall reduces LV afterload, condition that necessitates consideration of repair, and patients and the blood volume stored within the distended aortic wall at high risk for open surgery are EVAR candidates, making augments coronary perfusion.4 preoperative risk stratification important.2 Takeda et al demon- The stiffness of the aorta, which resists its systolic distension, strated that EVAR increases vascular stiffness and induces left increases with aging, hypertension, diabetes, abdominal visceral ventricular (LV) diastolic dysfunction, concluding that EVAR fat, and smoking.5 Aging plays a major role in the process of can worsen exercise tolerance, especially in patients with low aortic degenerative disease. Pathologically, fragmentation and LV distensibility.3 loss of elastic fibers of the aortic wall cause dilatation of the vessel. Subsequent repair involving replacement fibrosis with Article p 322 stiffer collagen increases wall stiffness. Concomitant hyperten- sion and accelerated atherosclerosis may also contribute to both The aorta is an elastic artery with regular elastic laminae development of aortic aneurysm and decreased aortic compli- between layers of smooth muscle cells in the tunica media. By ance.6 Hypertension and arterial stiffness interact with each acting as an elastic buffering chamber behind the heart, the aorta other in a bidirectional manner and are closely associated with stores approximately 50% of the LV stroke volume during sys- age. Reduced aortic compliance reportedly induces LV hyper- Figure. Windkessel is a German word meaning air chamber. When water is pumped into the chamber, the water both com- presses the air in the enclosed room and pushes water back out of the chamber. The effect is to transform the pulsatile water output of pump into an almost continuous flow. The compressibility of the air in the chamber simulates the extensibility and elastic- ity of the aorta. The opinions expressed in this article are not necessarily those of the editors or of the Japanese Circulation Society. Received December 15, 2013; accepted December 15, 2013; released online December 27, 2013 Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Japan Mailing address: Hideaki Kanzaki, MD, FJCC, Department of Cardiovascular Medicine, Heart Failure Division, National Cerebral and Cardiovascular Center, 5-7-1 Fujishiro-dai, Suita 565-8565, Japan. E-mail: [email protected] ISSN-1346-9843 doi: 10.1253/circj.CJ-13-1520 All rights are reserved to the Japanese Circulation Society. For permissions, please e-mail: [email protected] Circulation Journal Vol.78, February 2014 308 KANZAKI H trophy.7 The exact etiology of aortic aneurysm is unclear, but tion as well as aortic aneurysm, repair may aggravate or even smoking, atherosclerosis, hypertension and aging are thought cause the clinical syndrome of heart failure in the long term. to be risk factors, which are almost common features of pa- tients with diastolic heart failure. LV hypertrophy and arterial References stiffening could influence LV diastole by increasing the sys- 1. Katzen BT, Dake MD, MacLean AA, Wang DS. Endovascular repair tolic load to prolong relaxation, compromise filling, and in- of abdominal and thoracic aortic aneurysms. Circulation 2005; 112: crease end-diastolic pressure.8 1663 – 1675. 2. Yamamoto K, Fukui T, Matsuyama S, Tabata M, Aramoto H, Aortic pulse wave velocity (PWV) provides information re- Takanashi S. Prior cardiac and thoracic aortic surgery as a complica- garding the time taken for a pressure wave to travel a known tion risk factor for abdominal aortic aneurysm repair. Circ J 2012; 76: distance. A higher aortic PWV denotes increased aortic stiffness. 1380 – 1384. PWV is calculated on the basis of the Moens–Korteweg formula 3. Takeda Y, Sakata Y, Ohtani T, Tamaki S, Omori Y, Tsukamoto Y, under the assumption that there are no significant changes in the et al. Endovascular aortic repair increases vascular stiffness and alters cardiac structure and function. Circ J 2014; 78: 322 – 328. vessel cross-sectional area or wall thickness along the arterial 4. Belz GG. Elastic properties and Windkessel function of the human segment.9 In patients with aortic aneurysm, PWV values gener- aorta. Cardiovasc Drugs Ther 1995; 9: 73 – 83. ally increase10–13 after the repair, but interpretation of this find- 5. Sutton-Tyrrell K, Newman A, Simonsick EM, Havlik R, Pahor M, ing requires caution. PWV is defined as: E R, where Lakatta E, et al. Aortic stiffness is associated with visceral adiposity ×h/2×ρ× in older adults enrolled in the study of health, aging, and body com- E is Young’s modulus of the arterial wall, h is wall thickness, R position. Hypertension 2001; 38: 429 – 433. is arterial radius at the end of diastole, and ρ is blood density. 6. Payne RA, Wilkinson IB, Webb DJ. Arterial stiffness and hyperten- In cases of aortic aneurysm, however, dilatation of the aortic sion: Emerging concepts. Hypertension 2010; 55: 9 – 14. radius obviously violates the assumption. Thus, to begin with, 7. Ioannou CV, Morel DR, Katsamouris AN, Katranitsa S, Startchik I, Kalangos A, et al. Left ventricular hypertrophy induced by reduced PWV may not represent the true degree of aortic stiffness in such aortic compliance. J Vasc Res 2009; 46: 417 – 425. cases. The restored radius of the aorta by aortic repair may in- 8. Leite-Moreira AF, Correia-Pinto J, Gillebert TC. Afterload induced fluence PWV. And, because the aortic arch contributes approxi- changes in myocardial relaxation: A mechanism for diastolic dysfunc- mately 50% of total arterial compliance,7 EAVR for AAA may tion. Cardiovasc Res 1999; 43: 344 – 353. 9. Oliver JJ, Webb DJ. Noninvasive assessment of arterial stiffness and differ from TEAVR regarding the increase in aortic stiffness. In risk of atherosclerotic events. Arterioscler Thromb Vasc Biol 2003; contrast, there is also a report that brachial–ankle PWV (baPWV) 23: 554 – 566. is less influenced by the presence of AAA. The baPWV can be 10. Iwahashi T, Obitsu Y, Koizumi N, Shiraishi Y, Shigematsu H. Clinical conveniently measured using pressure cuffs on the 4 extremities comparison of two different types of bifurcated graft for postopera- and is a measurement of aortic mechanical properties between tive baPWV and ABI. Int Angiol 2009; 28: 232 – 237. 11. Lantelme P, Dzudie A, Milon H, Bricca G, Legedz L, Chevalier JM, the brachial artery and ankle artery. But the length of an AAA et al. Effect of abdominal aortic grafts on aortic stiffness and central may represent only a small fraction of the virtual traveling dis- hemodynamics. J Hypertens 2009; 27: 1268 – 1276. tance between the brachial and ankle arteries.14 12. Tzilalis VD, Kamvysis D, Panagou P, Kaskarelis I, Lazarides MK, However that may be, the Windkessel effect could be attenu- Perdikides T, et al. Increased pulse wave velocity and arterial hyper- tension in young patients with thoracic aortic endografts. Ann Vasc ated by EVAR, because the elastic properties of the aortic media Surg 2012; 26: 462 – 467. are absent in the arterial segment that is replaced, especially if 13. Kadoglou NP, Moulakakis KG, Papadakis I, Ikonomidis I, Alepaki noncompliant stent-grafts are extensively used. Normalcy of LV M, Lekakis J, et al. Changes in aortic pulse wave velocity of patients systolic function in 50% of patients with heart failure implicates undergoing endovascular repair of abdominal aortic aneurysms. J Endovasc Ther 2012; 19: 661 – 666. diastolic dysfunction as the probable etiology, whereas most 14. Lee CW, Sung SH, Chen CK, Chen IM, Cheng HM, Yu WC, et al. patients with isolated LV diastolic dysfunction do not have the Measures of carotid-femoral pulse wave velocity and augmentation clinical features of heart failure.15 Decreased aortic compliance index are not reliable in patients with abdominal aortic aneurysm. J following EVAR may result in increased LV afterload and wall Hypertens 2013; 31: 1853 – 1860. 15. Goto T, Ohte N, Fukuta H, Wakami K, Tani T, Kimura G. Relationship stress, predisposing to LV hypertrophy. And, LV diastolic fill- between effective arterial elastance, total vascular resistance, and ing and subendocardial blood flow may be deteriorated. Conse- augmentation index at the ascending aorta and left ventricular dia- quently, especially in patients who have LV diastolic dysfunc- stolic function in older women. Circ J 2013; 77: 123 – 129. Circulation Journal Vol.78, February 2014.
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