Trends in Cardiovascular Medicine
Volume 16, Issue 8 , Pages 273-279 , November 2006

Mechanisms of Diastolic Dysfunction in Heart Failure

  • Barry A. Borlaug

      Affiliations

    • Division of Cardiology, Department of Medicine, The Mayo Clinic College of Medicine, Rochester, MN, 55905 USA
  • ,
  • David A. Kass

      Affiliations

    • Division of Cardiology, Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, MD, 21205 USA
    • Corresponding Author InformationAddress correspondence to: David A. Kass, MD, Johns Hopkins Medical Institutions, Ross 835, 720 Rutland Avenue, Baltimore, MD 21205, USA. Tel.: (+1) 410-9557153; fax: (+1) 410-5022558.

References 

  1. Ahmed SH, Clark LL, Pennington WR, et al. Matrix metalloproteinases/tissue inhibitors of metalloproteinases. Relationship between changes in proteolytic determinants of matrix composition and structural, functional, and clinical manifestations of hypertensive heart disease. Circulation. 2006;113:2089–2096
  2. Asif M, Egan J, Vasan S, et al. An advanced glycation endproduct cross-link breaker can reverse age-related increases in myocardial stiffness. Proc Natl Acad Sci U S A. 2000;97:2809–2813
  3. Badenhorst D, Maseko M, Tsotetsi OJ, et al. Cross-linking influences the impact of quantitative changes in myocardial collagen on cardiac stiffness and remodelling in hypertension in rats. Cardiovasc Res. 2003;57:632–641
  4. Baicu CF, Zile MR, Aurigemma GP, et al. Left ventricular systolic performance, function, and contractility in patients with diastolic heart failure. Circulation. 2005;111:2306–2312
  5. Borlaug BA, Melenovsky V, Shively L, et al. Impaired systolic and vasodilator reserve in patients with heart failure and a normal ejection fraction. Circulation. 2005;112:2841
  6. Borlaug BA, Melenovsky V, Marhin T, et al. Sildenafil inhibits beta-adrenergic-stimulated cardiac contractility in humans. Circulation. 2005;112:2642–2649
  7. Carson P, Massie BM, McKelvie R, et al. The irbesartan in heart failure with preserved systolic function (I-PRESERVE) trial: rationale and design. J Card Fail. 2005;11:576–585
  8. Dauterman K, Pak PH, Maughan WL, et al. Contribution of external forces to left ventricular diastolic pressure. Implications for the clinical use of the Starling law. Ann Intern Med. 1995;122:737–742
  9. Del Monte F, Harding SE, Dec GW, et al. Targeting phospholamban by gene transfer in human heart failure. Circulation. 2002;105:904–907
  10. Diez J, Querejeta R, Lopez B, et al. Losartan-dependent regression of myocardial fibrosis is associated with reduction of left ventricular chamber stiffness in hypertensive patients. Circulation. 2002;105:2512–2517
  11. Frank KF, Bolck B, Brixius K, et al. Modulation of SERCA: implications for the failing human heart. Basic Res Cardiol. 2002;97:I72–I78(suppl 1)
  12. Fukuta H, Sane DC, Brucks S, et al. Statin therapy may be associated with lower mortality in patients with diastolic heart failure: a preliminary report. Circulation. 2005;112:357–363
  13. Granzier H, Labeit S. Cardiac titin: an adjustable multi-functional spring. J Physiol. 2002;541:335–342
  14. Hasenfuss G, Schillinger W, Lehnart SE, et al. Relationship between Na+–Ca2+-exchanger protein levels and diastolic function of failing human myocardium. Circulation. 1999;99:641–648
  15. He KL, Dickstein M, Sabbah HN, et al. Mechanisms of heart failure with well preserved ejection fraction in dogs following limited coronary microembolization. Cardiovasc Res. 2004;64:72–83
  16. Higashi M, Shimokawa H, Hattori T, et al. Long-term inhibition of Rho-kinase suppresses angiotensin II-induced cardiovascular hypertrophy in rats in vivo: effect on endothelial NAD(P)H oxidase system. Circ Res. 2003;93:767–775
  17. Hoshijima M, Ikeda Y, Iwanaga Y, et al. Chronic suppression of heart-failure progression by a pseudophosphorylated mutant of phospholamban via in vivo cardiac rAAV gene delivery. Nat Med. 2002;8:864–871
  18. Hundley WG, Kitzman DW, Morgan TM, et al. Cardiac cycle-dependent changes in aortic area and distensibility are reduced in older patients with isolated diastolic heart failure and correlate with exercise intolerance. J Am Coll Cardiol. 2001;38:796–802
  19. Kass DA. Assessment of diastolic dysfunction. Invasive modalities. Cardiol Clin. 2000;18:571–586
  20. Kass DA, Solaro RJ. Mechanisms and use of calcium-sensitizing agents in the failing heart. Circulation. 2006;113:305–315
  21. Kass DA, Midei M, Brinker J, et al. Influence of coronary occlusion during PTCA on end-systolic and end-diastolic pressure–volume relations in humans. Circulation. 1990;81:447–460
  22. Kass DA, Wolff MR, Ting CT, et al. Diastolic compliance of hypertrophied ventricle is not acutely altered by pharmacologic agents influencing active processes. Ann Intern Med. 1993;119:466–473
  23. Kass DA, Bronzwaer JG, Paulus WJ. What mechanisms underlie diastolic dysfunction in heart failure?. Circ Res. 2004;94:1533–1542
  24. Kawaguchi M, Hay I, Fetics B, et al. Combined ventricular systolic and arterial stiffening in patients with heart failure and preserved ejection fraction: implications for systolic and diastolic reserve limitations. Circulation. 2003;107:714–720
  25. Kitzman DW, Little WC, Brubaker PH, et al. Pathophysiological characterization of isolated diastolic heart failure in comparison to systolic heart failure. JAMA. 2002;288:2144–2150
  26. Kuwahara F, Kai H, Tokuda K, et al. Transforming growth factor-beta function blocking prevents myocardial fibrosis and diastolic dysfunction in pressure-overloaded rats. Circulation. 2002;106:130–135
  27. Labeit D, Watanabe K, Witt C, et al. Calcium-dependent molecular spring elements in the giant protein titin. Proc Natl Acad Sci U S A. 2003;100:13716–13721
  28. Lahmers S, Wu Y, Call DR, et al. Developmental control of titin isoform expression and passive stiffness in fetal and neonatal myocardium. Circ Res. 2004;94:505–513
  29. Leite-Moreira AF, Correia-Pinto J. Load as an acute determinant of end-diastolic pressure–volume relation. Am J Physiol Heart Circ Physiol. 2001;280:H51–H59
  30. Little WC, Zile MR, Kitzman DW, et al. The effect of alagebrium chloride (ALT-711), a novel glucose cross-link breaker, in the treatment of elderly patients with diastolic heart failure. J Card Fail. 2005;11:191–195
  31. Liu CP, Ting CT, Lawrence W, et al. Diminished contractile response to increased heart rate in intact human left ventricular hypertrophy. Systolic versus diastolic determinants. Circulation. 1993;88:1893–1906
  32. MacKenna DA, Omens JH, McCulloch AD, et al. Contribution of collagen matrix to passive left ventricular mechanics in isolated rat hearts. Am J Physiol. 1994;266:H1007–H1018
  33. Marx SO, Reiken S, Hisamatsu Y, et al. PKA phosphorylation dissociates FKBP12.6 from the calcium release channel (ryanodine receptor): defective regulation in failing hearts. Cell. 2000;101:365–376
  34. Matsumoto T, Wada A, Tsutamoto T, et al. Chymase inhibition prevents cardiac fibrosis and improves diastolic dysfunction in the progression of heart failure. Circulation. 2003;107:2555–2558
  35. Melenovsky V, Borlaug BA, Hay I, et al. Atrial dilation/dysfunction: a defining feature of heart failure with normal ejection fraction (HFnEF). Circulation. 2005;112:3535
  36. Miyamoto MI, Del Monte F, Schmidt U, et al. Adenoviral gene transfer of SERCA2a improves left-ventricular function in aortic-banded rats in transition to heart failure. Proc Natl Acad Sci U S A. 2000;97:793–798
  37. Netticadan T, Temsah RM, Kawabata K, et al. Sarcoplasmic reticulum Ca(2+)/Calmodulin-dependent protein kinase is altered in heart failure. Circ Res. 2000;86:596–605
  38. Neumann J. Altered phosphatase activity in heart failure, influence on Ca2+ movement. Basic Res Cardiol. 2002;97:I91–I95(suppl 1)
  39. Oh JK, Hatle L, Tajik AJ, et al. Diastolic heart failure can be diagnosed by comprehensive two-dimensional and Doppler echocardiography. J Am Coll Cardiol. 2006;47:500–506
  40. Pak PH, Maughan L, Baughman KL, et al. Marked discordance between dynamic and passive diastolic pressure–volume relations in idiopathic hypertrophic cardiomyopathy. Circulation. 1996;94:52–60
  41. Paolocci N, Tavazzi B, Biondi R, et al. Metalloproteinase inhibitor counters high-energy phosphate depletion and AMP deaminase activity enhancing ventricular diastolic compliance in subacute heart failure. J Pharmacol Exp Ther. 2006;317:506–513
  42. Senzaki H, Fetics B, Chen CH, et al. Comparison of ventricular pressure relaxation assessments in human heart failure: quantitative influence on load and drug sensitivity analysis. J Am Coll Cardiol. 1999;34:1529–1536
  43. Senzaki H, Paolocci N, Gluzband YA, et al. Beta-blockade prevents sustained metalloproteinase activation and diastolic stiffening induced by angiotensin II combined with evolving cardiac dysfunction. Circ Res. 2000;86:807–815
  44. Stroud JD, Baicu CF, Barnes MA, et al. Viscoelastic properties of pressure overload hypertrophied myocardium: effect of serine protease treatment. Am J Physiol Heart Circ Physiol. 2002;282:H2324–H2335
  45. Takemoto Y, Barnes ME, Seward JB, et al. Usefulness of left atrial volume in predicting first congestive heart failure in patients > or = 65 years of age with well-preserved left ventricular systolic function. Am J Cardiol. 2005;96:832–836
  46. Takimoto E, Soergel DG, Janssen PM, et al. Frequency- and afterload-dependent cardiac modulation in vivo by troponin I with constitutively active protein kinase A phosphorylation sites. Circ Res. 2004;94:496–504
  47. Takimoto E, Champion HC, Li M, et al. Chronic inhibition of cyclic GMP phosphodiesterase 5A prevents and reverses cardiac hypertrophy. Nat Med. 2005;11:214–222
  48. Vahebi S, Kobayashi T, Warren CM, et al. Functional effects of rho-kinase-dependent phosphorylation of specific sites on cardiac troponin. Circ Res. 2005;96:740–747
  49. VanHeerebeek L, Borbely A, Niessen HW, et al. Myocardial structure and function differ in systolic and diastolic heart failure. Circulation. 2006;113:1966–1973
  50. Wang TJ, Levy D, Benjamin EJ, et al. The epidemiology of “asymptomatic” left ventricular systolic dysfunction: implications for screening. Ann Intern Med. 2003;138:907–916
  51. Wolska BM, Vijayan K, Arteaga GM, et al. Expression of slow skeletal troponin I in adult transgenic mouse heart muscle reduces the force decline observed during acidic conditions. J Physiol. 2001;536:863–870
  52. Wu Y, Cazorla O, Labeit D, et al. Changes in titin and collagen underlie diastolic stiffness diversity of cardiac muscle. J Mol Cell Cardiol. 2000;32:2151–2162
  53. Wu Y, Bell SP, Trombitas K, et al. Changes in titin isoform expression in pacing-induced cardiac failure give rise to increased passive muscle stiffness. Circulation. 2002;106:1384–1389
  54. Yamamoto K, Masuyama T, Sakata Y, et al. Myocardial stiffness is determined by ventricular fibrosis, but not by compensatory or excessive hypertrophy in hypertensive heart. Cardiovasc Res. 2002;55:76–82
  55. Yamasaki R, Wu Y, McNabb M, et al. Protein kinase A phosphorylates titin's cardiac-specific N2B domain and reduces passive tension in rat cardiac myocytes. Circ Res. 2002;90:1181–1188
  56. Yu CM, Lin H, Yang H, et al. Progression of systolic abnormalities in patients with “isolated” diastolic heart failure and diastolic dysfunction. Circulation. 2002;105:1195–1201
  57. Yusuf S, Pfeffer MA, Swedberg K, et al. Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction: the CHARM-Preserved Trial. Lancet. 2003;362:777–781
  58. Zile MR, Baicu CF, Gaasch WH. Diastolic heart failure—abnormalities in active relaxation and passive stiffness of the left ventricle. N Engl J Med. 2004;350:1953–1959

PII: S1050-1738(06)00090-9

doi: 10.1016/j.tcm.2006.05.003

Trends in Cardiovascular Medicine
Volume 16, Issue 8 , Pages 273-279 , November 2006