Interaction Between the Haemodynamics of Coronary Flow and Aortic Valve Pathologies

  • Christopher J. BroydEmail author
  • Justin E. R. Davies


Pathological changes in the outflow tract of the left ventricle have a profound effect on coronary haemodynamics. This is evident as the production of myocardial ischaemia with worsening aortic valve disease, clinically represented as the onset of symptoms in advancing states. However, using modern investigative techniques, it is possible to classify the degree of ischaemia through more continuous scales to provide a more detailed quantification of the impact of aortic valve pathology and therefore a detailed insight into the mechanism by which they affect coronary haemodynamics. Aortic stenosis in particular leads to a disruption of normal coronary haemodynamics through two mechanisms. Firstly, there is an increasing force of ventricular contraction that is necessary to expel blood through a progressively increasing outflow tract obstruction. Secondly, the ventricle is inevitably forced to adapt through hypertrophic changes. These two features both have a significant influence on coronary haemodynamics and are the ultimate cause of myocardial ischaemia. Their effects on coronary physiology are complex, interacting and potentially oppositional. Delineating their representative contributions to the pathophysiology of this condition is therefore difficult but essential, initially for understanding the mechanistic processes involved but ultimately for providing bespoke and detailed patient risk stratification. The search for an appropriate tool to quantify the impact of these changes on coronary haemodynamics is long-standing. However, as many techniques are time-consuming or invasive, their employment is often limited, impairing our ability to understand the serial, continuous nature of this disease. Additionally, the complex interaction between left ventricular hypertrophy and outflow tract obstruction makes our recognition of the resultant measure fraught. However, as contemporary investigative approaches emerge that can document the interplay between aorta and myocardium in detail, it may ultimately be possible to separate out the pathophysiological effects of aortic stenosis to provide an accurate quantification of the burden imposed by aortic stenosis with the goal of therapeutic guidance.

To that end this chapter is used to detail the evidence for microvascular dysfunction and coronary haemodynamic disturbance in aortic stenosis. We go on to discuss the potential causes for these abnormalities and highlight those investigative modalities that may prove useful in the future for disease assessment.


Aortic stenosis Haemodynamics Wave-intensity analysis Microvascular dysfunction 


  1. 1.
    Lindroos M, Kupari M, Heikkila J, Tilvis R. Prevalence of aortic valve abnormalities in the elderly: an echocardiographic study of a random population sample. J Am Coll Cardiol. 1993;21:1220–5.PubMedCrossRefPubMedCentralGoogle Scholar
  2. 2.
    Ross J, Braunwald E. Aortic stenosis. Circulation. 1968;38:61.PubMedCrossRefGoogle Scholar
  3. 3.
    Leon MB, et al. Transcatheter aortic-valve implantation for aortic stenosis in patients who cannot undergo surgery. N Engl J Med. 2010;36:1597–607.CrossRefGoogle Scholar
  4. 4.
    Bonow RO, et al. Focused Update Incorporated Into the ACC/AHA 2006 Guidelines for the Management of Patients with Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee). Circulation. 2008;118:e523–661.PubMedGoogle Scholar
  5. 5.
    Rafique AM, et al. Meta-analysis of prognostic value of stress testing in patients with asymptomatic severe aortic stenosis. Am J Cardiol. 2009;104:972–7.PubMedCrossRefGoogle Scholar
  6. 6.
    Rajani R, Rimington H, Chambers JB. Treadmill exercise in apparently asymptomatic patients with moderate or severe aortic stenosis: relationship between cardiac index and revealed symptoms. Heart. 2010;96:689–95.PubMedCrossRefGoogle Scholar
  7. 7.
    Marechaux S, et al. Left ventricular response to exercise in aortic stenosis: an exercise echocardiographic study. Echocardiography. 2007;24:955–9.PubMedCrossRefGoogle Scholar
  8. 8.
    Rosenhek RM, et al. Natural history of very severe aortic stenosis. Circulation. 2010;121:151–6.PubMedCrossRefGoogle Scholar
  9. 9.
    Kitai T, et al. Clinical outcomes in non-surgically managed patients with very severe versus severe aortic stenosis. Heart. 2011;97:2029–32.PubMedCrossRefGoogle Scholar
  10. 10.
    Horstkotte D, Loogen F. The natural history of aortic valve stenosis. Eur Heart J. 1988;9:57–64.PubMedCrossRefGoogle Scholar
  11. 11.
    Kennedy KD, Nishimura RA, Holmes DR, Bailey KR. Natural history of moderate aortic stenosis. J Am Coll Cardiol. 1991;17:313–9.PubMedCrossRefGoogle Scholar
  12. 12.
    Otto CM, et al. Prospective study of asymptomatic valvular aortic stenosis: clinical, echocardiographic, and exercise predictors of outcome. Circulation. 1997;95:2262–70.PubMedCrossRefGoogle Scholar
  13. 13.
    Rosenhek R, et al. Mild and moderate aortic stenosis: natural history and risk stratification by echocardiography. Eur Heart J. 2004;25:199–205.PubMedCrossRefGoogle Scholar
  14. 14.
    Kang DH, et al. Early surgery versus conventional treatment in asymptomatic very severe aortic stenosis. Circulation. 2010;121:1502–9.PubMedCrossRefGoogle Scholar
  15. 15.
    Vahanian A, et al. Guidelines on the management of valvular heart disease. Eur Heart J. 2007;28:230–68.PubMedGoogle Scholar
  16. 16.
    Fallen EL, Elliott WC, Gorlin RI. Mechanisms of angina in aortic stenosis. Circulation. 1967;36:480–8.PubMedCrossRefGoogle Scholar
  17. 17.
    Griggs DM, Chen CC, Tchokoev VV. Subendocardial anaerobic metabolism in experimental aortic stenosis. Am J Phys. 1973;224:607–12.CrossRefGoogle Scholar
  18. 18.
    Kupari M, et al. Exclusion of coronary artery disease by exercise thallium-201 tomography in patients with aortic valve stenosis. Am J Cardiol. 1992;70:635–40.PubMedCrossRefGoogle Scholar
  19. 19.
    Scheler S, Motz W, Strauer BE. Transient myocardial ischaemia in hypertensives: missing link with left ventricular hypertrophy. Eur Heart J. 1992;13:62–5.PubMedCrossRefGoogle Scholar
  20. 20.
    Julius BK, et al. Angina pectoris in patients with aortic stenosis and normal coronary arteries: mechanisms and pathophysiological concepts. Circulation. 1997;95:89–8.CrossRefGoogle Scholar
  21. 21.
    Marcus ML, Doty DB, Hiratzka LF, Wright CB, Eastham CL. Decreased coronary reserve – a mechanism for angina pectoris in patients with aortic stenosis and normal coronary arteries. N Engl J Med. 1982;307:1362–6.PubMedCrossRefGoogle Scholar
  22. 22.
    Hildick-Smith DJ, Shapiro LM. Coronary flow reserve improves after aortic valve replacement for aortic stenosis: an adenosine transthoracic echocardiography study. J Am Coll Cardiol. 2000;36:1889–96.PubMedCrossRefGoogle Scholar
  23. 23.
    Kume T, et al. Mechanisms of impaired coronary flow reserve in patients with aortic stenosis: transthoracic Doppler echocardiographic study. J Cardiol. 2004;43:173–8.PubMedGoogle Scholar
  24. 24.
    Eberli FR, et al. Coronary reserve in patients with aortic valve disease before and after successful aortic valve replacement. Eur Heart J. 1991;12:127–38.PubMedCrossRefGoogle Scholar
  25. 25.
    Meimoun P, et al. Factors associated with noninvasive coronary flow reserve in severe aortic stenosis. J Am Soc Echocardiogr. 2012;25:835–41.PubMedCrossRefGoogle Scholar
  26. 26.
    Isaaz K, Bruntz JF, Paris D, Ethevenot G, Aliot E. Abnormal coronary flow velocity pattern in patients with left ventricular hypertrophy, angina pectoris, and normal coronary arteries: a transesophageal Doppler echocardiographic study. Am Heart J. 1994;128:500–10.PubMedCrossRefGoogle Scholar
  27. 27.
    Omran H, Fehske W, Rabihieh R. Relationship between symptoms and profile of coronary artery blood flow velocities in patients with aortic valve stenosis: a study using transoesophageal echocardiography. Heart. 2011;75:377–83.CrossRefGoogle Scholar
  28. 28.
    Galiuto L, et al. Impaired coronary and myocardial flow in severe aortic stenosis is associated with increased apoptosis: a transthoracic Doppler and myocardial contrast echocardiography study. Heart. 2006;92:208–12.PubMedCrossRefGoogle Scholar
  29. 29.
    Vinten-Johansen J, Weiss HR. Oxygen consumption in subepicardial and subendocardial regions of the canine left ventricle. The effect of experimental acute valvular aortic stenosis. Circ Res. 1980;46:139–45.PubMedCrossRefGoogle Scholar
  30. 30.
    Miyagawa S, et al. Coronary microcirculatory dysfunction in aortic stenosis: myocardial contrast echocardiography study. Ann Thorac Surg. 2009;87:715–9.PubMedCrossRefGoogle Scholar
  31. 31.
    Rajappan K, et al. Assessment of left ventricular mass regression after aortic valve replacement – cardiovascular magnetic resonance versus M-mode echocardiography. Eur J Cardiothorac Surg. 2003;24:59–65.PubMedCrossRefGoogle Scholar
  32. 32.
    Rajappan K, et al. Mechanisms of coronary microcirculatory dysfunction in patients with aortic stenosis and angiographically normal coronary arteries. Circulation. 2002;105:470–6.PubMedCrossRefPubMedCentralGoogle Scholar
  33. 33.
    Burwash IG, et al. Myocardial blood flow in patients with low-flow, low-gradient aortic stenosis: differences between true and pseudo-severe aortic stenosis. Results from the multicentre TOPAS (Truly or Pseudo-Severe Aortic Stenosis) study. Heart. 2008;94:1627–33.PubMedCrossRefPubMedCentralGoogle Scholar
  34. 34.
    O’Gorman DJ, Thomas P, Turner MA, Sheridan DJ. Investigation of impaired coronary vasodilator reserve in the Guinea pig heart with pressure induced hypertrophy. Eur Heart J. 1992;13:697–703.PubMedCrossRefPubMedCentralGoogle Scholar
  35. 35.
    Rajappan K, et al. Functional changes in coronary microcirculation after valve replacement in patients with aortic stenosis. Circulation. 2003;107:3170–5.PubMedCrossRefPubMedCentralGoogle Scholar
  36. 36.
    Spaan JA, Breuls NP, Laird JD. Diastolic-systolic coronary flow differences are caused by intramyocardial pump action in the anesthetized dog. Circ Res. 1981;49:584–93.PubMedCrossRefPubMedCentralGoogle Scholar
  37. 37.
    Davies JE, et al. Arterial pulse wave dynamics after percutaneous aortic valve replacement: fall in coronary diastolic suction with increasing heart rate as a basis for angina symptoms in aortic stenosis. Circulation. 2011;124:1565–72.PubMedCrossRefGoogle Scholar
  38. 38.
    Sun YH, Anderson TJ, Parker KH, Tyberg JV. Effects of left ventricular contractility and coronary vascular resistance on coronary dynamics. Am J Physiol Heart Circ Physiol. 2004;286:1590–5.CrossRefGoogle Scholar
  39. 39.
    Lockie TP, et al. Synergistic adaptations to exercise in the systemic and coronary circulations that underlie the warm-up angina phenomenon. Circulation. 2012;126:2565–74.PubMedCrossRefGoogle Scholar
  40. 40.
    Mattace-Raso FU, et al. Arterial stiffness and risk of coronary heart disease and stroke: the Rotterdam study. Circulation. 2006;113:657–63.PubMedCrossRefGoogle Scholar
  41. 41.
    O’Rourke MF, Staessen JA, Vlachopoulos C, Duprez D, Plante GE. Clinical applications of arterial stiffness; definitions and reference values. Am J Hypertens. 2002;15:426–44.PubMedCrossRefGoogle Scholar
  42. 42.
    Briand M, et al. Reduced systemic arterial compliance impacts significantly on left ventricular afterload and function in aortic stenosis: implications for diagnosis and treatment. J Am Coll Cardiol. 2005;46:291–8.PubMedCrossRefGoogle Scholar
  43. 43.
    Sunagawa K, Maughan WL, Burkhoff D, Sagawa K. Left ventricular interaction with arterial load studied in isolated canine ventricle. Am J Phys. 1983;245:773–80.Google Scholar
  44. 44.
    Chemla D, Antony I, Lecarpentier Y, Nitenberg A. Contribution of systemic vascular resistance and total arterial compliance to effective arterial elastance in humans. Am J Physiol Heart Circ Physiol. 2003;285:614–20.CrossRefGoogle Scholar
  45. 45.
    Lancellotti P, et al. Impact of global left ventricular afterload on left ventricular function in asymptomatic severe aortic stenosis: a two-dimensional speckle-tracking study. Eur J Echocardiogr. 2010;11:537–43.PubMedCrossRefGoogle Scholar
  46. 46.
    Rieck ÅE, et al. Global left ventricular load in asymptomatic aortic stenosis: covariates and prognostic implication (the SEAS trial). Cardiovasc Ultrasound. 2012;10:43.PubMedPubMedCentralCrossRefGoogle Scholar
  47. 47.
    Hachicha Z, Dumesnil JG, Pibarot P. Usefulness of the valvuloarterial impedance to predict adverse outcome in asymptomatic aortic stenosis. J Am Coll Cardiol. 2009;54:1003–11.PubMedCrossRefGoogle Scholar
  48. 48.
    Lancellotti P, et al. Risk stratification in asymptomatic moderate to severe aortic stenosis: the importance of the valvular, arterial and ventricular interplay. Heart. 2010;96:1364–71.PubMedCrossRefGoogle Scholar
  49. 49.
    Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med. 1990;322:1561–6.PubMedCrossRefGoogle Scholar
  50. 50.
    Haider AW, Larson MG, Benjamin EJ, Levy D. Increased left ventricular mass and hypertrophy are associated with increased risk for sudden death. J Am Coll Cardiol. 1998;32:1454–9.PubMedCrossRefPubMedCentralGoogle Scholar
  51. 51.
    Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP. Left ventricular mass and incidence of coronary heart disease in an elderly cohort. The Framingham Heart Study. Ann Intern Med. 1989;110:101–7.PubMedCrossRefGoogle Scholar
  52. 52.
    Koren MJ, Devereux RB, Casale PN, Savage DD, Laragh JH. Relation of left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension. Ann Intern Med. 1991;114:345–52.PubMedCrossRefPubMedCentralGoogle Scholar
  53. 53.
    Verdecchia P, et al. Left ventricular hypertrophy as an independent predictor of acute cerebrovascular events in essential hypertension. Circulation. 2001;104:2039–44.PubMedCrossRefGoogle Scholar
  54. 54.
    Wicker P, Tarazi RC, Kobayashi K. Coronary blood flow during the development and regression of left ventricular hypertrophy in renovascular hypertensive rats. Am J Cardiol. 1983;51:1744–9.PubMedCrossRefPubMedCentralGoogle Scholar
  55. 55.
    Sato F, Isoyama S, Takishima T. Normalization of impaired coronary circulation in hypertrophied rat hearts. Hypertension. 1990;16:26–34.PubMedCrossRefPubMedCentralGoogle Scholar
  56. 56.
    Kingsbury M, Mahnke A, Turner M, Sheridan D. Recovery of coronary function and morphology during regression of left ventricular hypertrophy. Cardiovasc Res. 2002;55:83–96.PubMedCrossRefPubMedCentralGoogle Scholar
  57. 57.
    Nunez E, Hosoya K, Susic D, Frohlich ED. Enalapril and losartan reduced cardiac mass and improved coronary hemodynamics in SHR. Hypertension. 1997;29:519–24.PubMedCrossRefPubMedCentralGoogle Scholar
  58. 58.
    Brilla CG, Janicki JS, Weber KT. Cardioreparative effects of lisinopril in rats with genetic hypertension and left ventricular hypertrophy. Circulation. 1991;83:1771–9.PubMedCrossRefGoogle Scholar
  59. 59.
    Motz W, Strauer BE. Improvement of coronary flow reserve after long-term therapy with enalapril. Hypertension. 1996;27:1031–8.PubMedCrossRefGoogle Scholar
  60. 60.
    Xu R, et al. Relationship between regression of hypertensive left ventricular hypertrophy and improvement of coronary flow reserve. Zhonghua Yi Xue Za Zhi. 2003;83:658–61.PubMedGoogle Scholar
  61. 61.
    Mizuno R, Fujimoto S, Saito Y, Okamoto Y. Optimal antihypertensive level for improvement of coronary microvascular dysfunction: the lower, the better? Hypertension. 2012;60:326–32.PubMedCrossRefGoogle Scholar
  62. 62.
    Davies JE, et al. Evidence of a dominant backward-propagating ‘suction’ wave responsible for diastolic coronary filling in humans, attenuated in left ventricular hypertrophy. Circulation. 2006;113:1768–78.PubMedCrossRefGoogle Scholar
  63. 63.
    Breisch EA, White FC, Nimmo LE, Bloor CM. Cardiac vasculature and flow during pressure-overload hypertrophy. Am J Physiol Heart Circ Physiol. 1986;251:1031–7.CrossRefGoogle Scholar
  64. 64.
    Mueller TM, et al. Effect of renal hypertension and left ventricular hypertrophy on the coronary circulation in dogs. Circ Res. 1978;42:543–9.PubMedCrossRefGoogle Scholar
  65. 65.
    Bishop SP, et al. Coronary vascular morphology in pressure-overload left ventricular hypertrophy. J Mol Cell Cardiol. 1996;28:141–54.PubMedCrossRefGoogle Scholar
  66. 66.
    Ecker T, et al. Decreased cardiac concentration of cGMP kinase in hypertensive animals. An index for cardiac vascularization? Circ Res. 1989;65:1361–9.PubMedCrossRefGoogle Scholar
  67. 67.
    Rakusan K, Flanagan MF, Geva T, Southern J, Van Praagh R. Morphometry of human coronary capillaries during normal growth and the effect of age in left ventricular pressure-overload hypertrophy. Circulation. 1992;86:38–46.PubMedCrossRefGoogle Scholar
  68. 68.
    Villari B, et al. Regression of coronary artery dimensions after successful aortic valve replacement. Circulation. 1992;85:972–8.PubMedCrossRefGoogle Scholar
  69. 69.
    Schwartzkopff B, et al. Morphometric investigation of human myocardium in arterial hypertension and valvular aortic stenosis. Eur Heart J. 1992;13:17–23.PubMedCrossRefGoogle Scholar
  70. 70.
    Monrad ES, et al. Time course of regression of left ventricular hypertrophy after aortic valve replacement. Circulation. 1988;77:1345–55.PubMedCrossRefGoogle Scholar
  71. 71.
    Gould KL, Carabello BA. Why angina in aortic stenosis with normal coronary arteriograms? Circulation. 2003;107:3120–3.CrossRefGoogle Scholar
  72. 72.
    Carpeggiani C, et al. Coronary flow reserve in severe aortic valve stenosis: a positron emission tomography study. J Cardiovasc Med. 2008;9:893–8.CrossRefGoogle Scholar
  73. 73.
    Kupari M, Turto H, Lommi J. Left ventricular hypertrophy in aortic valve stenosis: preventive or promotive of systolic dysfunction and heart failure? Eur Heart J. 2005;26:1790–6.PubMedCrossRefPubMedCentralGoogle Scholar
  74. 74.
    Zhu YH, Zhu YZ, Spitznagel H, Gohlke P, Unger T. Substrate metabolism, hormone interaction, and angiotensin-converting enzyme inhibitors in left ventricular hypertrophy. Diabetes. 1996;45:59–65.CrossRefGoogle Scholar
  75. 75.
    Just H, Frey M, Zehender M. Calcium antagonist drugs in hypertensive patients with angina pectoris. Eur Heart J. 1996;17:20–4.PubMedCrossRefGoogle Scholar
  76. 76.
    Anversa P, Ricci R, Olivetti G. Coronary capillaries during normal and pathological growth. Can J Cardiol. 1986;2:104–13.PubMedPubMedCentralGoogle Scholar
  77. 77.
    Paulus WJ, Heyndrickx GR, Nellens P, Andries E. Impaired relaxation of the hypertrophied left ventricle in aortic stenosis: effects of aortic valvuloplasty and of postextrasystolic potentiation. Eur Heart J. 1988;9:25–30.PubMedCrossRefPubMedCentralGoogle Scholar
  78. 78.
    Antony I, Nitenberg A, Foult JM, Aptecar E. Coronary vasodilator reserve in untreated and treated hypertensive patients with and without left ventricular hypertrophy. J Am Coll Cardiol. 1993;22:514–20.PubMedCrossRefPubMedCentralGoogle Scholar
  79. 79.
    Brush JE, et al. Angina due to coronary microvascular disease in hypertensive patients without left ventricular hypertrophy. N Engl J Med. 1988;319:1302–7.PubMedCrossRefPubMedCentralGoogle Scholar
  80. 80.
    Rodriguez-Porcel M, et al. Functional and structural remodeling of the myocardial microvasculature in early experimental hypertension. Am J Physiol Heart Circ Physiol. 2006;290:978–84.CrossRefGoogle Scholar
  81. 81.
    Crabos M, et al. Reduced basal NO-mediated dilation and decreased endothelial NO-synthase expression in coronary vessels of spontaneously hypertensive rats. J Mol Cell Cardiol. 1997;29:55–65.PubMedCrossRefGoogle Scholar
  82. 82.
    McGoldrick RB, Kingsbury M, Turner MA, Sheridan DJ, Hughes AD. Left ventricular hypertrophy induced by aortic banding impairs relaxation of isolated coronary arteries. Clin Sci. 2007;113:473–8.PubMedCrossRefGoogle Scholar
  83. 83.
    Kingsbury MP, Turner MA, Flores NA, Bovill E, Sheridan DJ. Endogenous and exogenous coronary vasodilatation are attenuated in cardiac hypertrophy: a morphological defect? J Mol Cell Cardiol. 2000;32:527–38.PubMedCrossRefGoogle Scholar
  84. 84.
    McAinsh AM, et al. Cardiac hypertrophy impairs recovery from ischaemia because there is a reduced reactive hyperaemic response. Cardiovasc Res. 1995;30:113–21.PubMedCrossRefGoogle Scholar
  85. 85.
    Koyanagi S, Eastham CL, Harrison DG, Marcus ML. Increased size of myocardial infarction in dogs with chronic hypertension and left ventricular hypertrophy. Circ Res. 1982;50:55–62.PubMedCrossRefGoogle Scholar
  86. 86.
    Mihaljevic T, Paul S, Cohn LH, Wechsler A. Pathophysiology of aortic valve disease cardiac surgery in the adult. New York: McGraw-Hill; 2003. p. 791–810.Google Scholar
  87. 87.
    Kalkman EA, et al. Determinants of coronary reserve in rats subjected to coronary artery ligation or aortic banding. Cardiovasc Res. 1996;32:1088–95.PubMedCrossRefGoogle Scholar
  88. 88.
    Tomanek RJ, Wangler RD, Bauer CA. Prevention of coronary vasodilator reserve decrement in spontaneously hypertensive rats. Hypertension. 1985;7:533–40.PubMedCrossRefGoogle Scholar
  89. 89.
    Opherk D, et al. Reduction of coronary reserve: a mechanism for angina pectoris in patients with arterial hypertension and normal coronary arteries. Circulation. 1984;69:1–7.PubMedCrossRefGoogle Scholar
  90. 90.
    Ishihara K, et al. Coronary blood flow after the regression of pressure-overload left ventricular hypertrophy. Circ Res. 1992;71:1472–81.PubMedCrossRefGoogle Scholar
  91. 91.
    Ito N, Isoyama S, Takahashi T, Takishima T. Coronary dilator reserve and morphological changes after relief of pressure-overload in rats. J Mol Cell Cardiol. 1993;25:3–14.PubMedCrossRefGoogle Scholar
  92. 92.
    Barone-Rochette G, et al. Prognostic significance of LGE by CMR in aortic stenosis patients undergoing valve replacement. J Am Coll Cardiol. 2014;64:144–54.PubMedCrossRefPubMedCentralGoogle Scholar
  93. 93.
    Davies JE, et al. Arterial pulse wave dynamics after percutaneous aortic valve replacement/clinical perspective. Circulation. 2011;124:1565–72.PubMedCrossRefGoogle Scholar
  94. 94.
    Broyd CJ, Rigo F, Nijjer S, Sen S, Petraco R, Al-Lamee R, Foin N, Chuwuemeka A, Anderson J, Parker J, Malik IS, Mikhail GW, Francis DP, Parker K, Hughes AD, Mayet J, Davies JE. Regression of left ventricular hypertrophy provides additive physiological benefit following treatment of aortic stenosis: Insights from serial coronary wave intensity analysis. Acta Physiologica. 2018;224:e13109.PubMedCrossRefGoogle Scholar

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© Springer-Verlag GmbH Austria, part of Springer Nature 2019

Authors and Affiliations

  1. 1.Bart’s Heart Centre, St Bartholomew’s HospitalLondonUK
  2. 2.International Centre for Circulatory HealthLondonUK

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