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Clinical Cardiology logoLink to Clinical Cardiology
. 2009 Feb 3;24(4):286–290. doi: 10.1002/clc.4960240406

Endothelial dysfunction and decreased exercise tolerance in interferon‐alpha therapy in chronic hepatitis C: Relation between exercise hyperemia and endothelial function

Bonpei Takase 1,, Kimio Satomura 1, Fumitaka Ohsuzu 1, Akira Kurita 1, Facc, Akimi Uehata 2, Takahiro Fujioka 2, Toshio Kondo 2, Toshihiko Nishioka 2, Kazus1Ge Isojima 2
PMCID: PMC6654793  PMID: 11303695

Abstract

Background: We previously reported that reversible endothelial dysfunction is caused by interferon‐alpha therapy (IFN) in patients with chronic hepatitis C. In experimental studies, limb blood flow during exercise is reported to be dependent on endothelium‐derived nitric oxide.

Hypothesis: The purpose of this study was to confirm the effect of IFN on endothelial function and to investigate whether exercise hyperemia is dependent on endothelial function in humans.

Methods: We performed symptom‐limited exercise treadmill testing and measured flow‐mediated vasodilation (FMD, endothelium‐dependent vasodilation) and sublingual glyceryl‐trinitrate‐induced dilation (GTN‐D, 0.3 mg, endothelium‐independent vasodilation) in the brachial artery by using high‐resolution ultrasound in 10 patients with chronic active hepatitis C (age 53 ± 11 years, 2 men, 8 women) before and immediately after administration of recombinant interferon 2b (10 million U/day) for 4 weeks.

Results: There were no significant abnormal findings in any patients in routine studies of 24‐h ambulatory electrocardiogram monitoring, two‐dimensional echocardiography, and exercise treadmill testing both before and after treatment. Leg fatigue and exhaustion were the reasons for termination of exercise treadmill testing in each patient. Pressure rate product was calculated at rest and peak exercise. Interferonalpha therapy significantly (p<0.05) decreased FMD (6.8 ± 3.1 vs. 1.9 ± 2.6%), exercise treadmill testing tolerance time (437 ± 89 vs. 395 ± 62 s) and peak pressure rate product (283 ± 41 vs. 241 ± 47 mmHg · beats/min · 10−2), but not GTN‐D (13.4 ± 5.4 vs. 17.0 ± 5.5%). The change of FMD due to IFN significantly and highly correlated with exercise treadmill testing tolerance time (r = 0.86, p<0.001), but not with change of peak pressure rate product, suggesting that FMD is more closely related to the condition of the peripheral circulation than is cardiac performance.

Conclusion: These results suggest that IFN in patients with chronic hepatitis C impairs endothelial function and exercise tolerance, and that endothelial function might be at least partly involved in exercise hyperemia in humans.

Keywords: exercise physiology, endothelial function, interferon therapy, hepatitis C

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References

  • 1. Maxwell AJ, Schauble E, Bernstein D, Cooke JP: Limb blood flow during exercise is dependent on nitric oxide. Circulation 1998; 98: 369–374 [DOI] [PubMed] [Google Scholar]
  • 2. Uehata A, Lieberman EH, Gerhard MD, Anderson TJ, Ganz P, Polak JF, Creager MA, Yeung AC: Non‐invasive assessment of endothelium‐dependent flow‐mediated dilation of brachial arteries. Vasc Med 1997; 2: 87–92 [DOI] [PubMed] [Google Scholar]
  • 3. Celermajer DS, Sorensen KE, Gooch VM, Spiegelhalter DJ, Miller OI, Sullivan ID, Lloyd JK, Deanfield JE: Non‐invasive detection of endothelial dysfunction in children and adults at risk of atherosclerosis. Lancet 1992; 340: 1111–1115 [DOI] [PubMed] [Google Scholar]
  • 4. Ross R: Atherosclerosis‐an inflammatory disease. N Engl J Med 1999; 340: 115–126 [DOI] [PubMed] [Google Scholar]
  • 5. Uehata A, Takase B, Nagai T, Hakamata N, Kastushika S, Nishioka T, Isojima K: Reversible endothelial dysfunction caused by interferon alpha therapy in chronic hepatitis C patients. Circulation 1997; 96 (suppl‐I): I–728 [Google Scholar]
  • 6. Hakozaki Y, Shirahama T, Katou M, Nakagawa K, Oba K, Yoshii O, Matsumoto T, Kuwabara N, Mitamura K: Long‐term prognosis of chronic hepatitis C after treatment with interferon alpha 2b and characterization of incomplete responders. Am J Gastroenterol 1996; 10: 2144–2149 [PubMed] [Google Scholar]
  • 7. Friesel R, Kowiriya A, Maciag T: Inhibition of endothelial cell proliferation by gamma interferon. J Cell Biol 1987; 104: 689–696 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8. Wakelee‐Lynch J: Interferon may offer first drug therapy for diabetic retinopathy. New research showing that alpha‐interferon blocked new blood vessel formation in the iris of monkeys may point the way to new treatment for diabetes retinopathy. Diabetes Care 1992; 15: 300–301 [DOI] [PubMed] [Google Scholar]
  • 9. Creutzig A, Freund M, Caspary L, Alexander K: Microangiopathy in patients with chronic myelogenous leukemia treated with interferon. Microvasc Res 1996: 52: 288–292 [DOI] [PubMed] [Google Scholar]
  • 10. Sonnenblick M, Rosin A: Cardiotoxicity of interferon: A review of 44 cases. Chest 1991; 99: 557–561 [DOI] [PubMed] [Google Scholar]
  • 11. Friess GG, Brown TD, Wrenn RC: Cardiovascular rhythm effects of gamma recombinant DNA interferon. Invest New Drugs 1989; 7: 275–280 [DOI] [PubMed] [Google Scholar]
  • 12. Cohen MC, Huberman MS, Nesto RW: Recombinant alpha2 inter‐feron‐related cardiomyopathy. Am J Cardiol 1988; 85: 549–551 [DOI] [PubMed] [Google Scholar]
  • 13. Teragawa H, Hondo T, Amano H, Hino F, Ohbayashi M: Adverse effects of interferon on the cardiovascular system in patients with chronic hepatitis C. Jpn Heart J 1996; 37: 905–915 [DOI] [PubMed] [Google Scholar]
  • 14. Teragawa H, Hondo T, Amano H, Watanabe H, Ohe H, Hattori N, Watanabe Y, Hino F, Ohbayashi M: Cardiogenic shock following recombinant alpha‐2b interferon therapy for chronic hepatitis C. Jpn Heart J 1996; 37: 137–142 [DOI] [PubMed] [Google Scholar]
  • 15. Tanaka H, Yamakado T, Emi Y, Nabeshima K, Itoh S, Nakano T: Interferon‐induced coronary vasospasm: A case history. Angiology 1995; 46: 1139–1143 [DOI] [PubMed] [Google Scholar]
  • 16. Kugiyama K, Yasue H, Okumura K, Ogawa H, Fujimoto K, Nakao K, Yoshimura M, Motoyama T, Inobe Y, Kawano H: Nitric oxide activity is deficient in spasm arteries of patients with coronary spastic angina. Circulation 1996; 94: 266–272 [DOI] [PubMed] [Google Scholar]
  • 17. Celermajer DS, Sorensen KE, Bull C, Robinson J, Deanfield JE: Endothelium‐dependent dilation in the systemic arteries of asymptomatic subjects relates to coronary risk factors and their interaction. J Am Coll Cardiol 1994; 24: 1468–1474 [DOI] [PubMed] [Google Scholar]
  • 18. Watts RP, Johnson PC: Metabolism and vasodilatation In Vasodilation (Eds. Vanhoutte PM, Leusen I.), pp. 52–65. New York: Raven Press, 1981. [Google Scholar]
  • 19. Fleg JL, Schulman S, O'Connor F, Becker LC, Gerstenblith G, Clulow JF, Renlund DG, Lakatta EG: Effects of acute 8‐adrenergic receptor blockade on age‐associated changes in cardiovascular performance during dynamic exercise. Circulation 1994; 90: 2333–2341 [DOI] [PubMed] [Google Scholar]
  • 20. Myers J, Froelicher VF: Hemodynamic determinants of exercise capacity in chronic heart failure. Ann Intern Med 1991; 115: 377–386 [DOI] [PubMed] [Google Scholar]
  • 21. Endo T, Imaizumi T, Tagawa T, Shiramoto M. Ando S, Takeshita A: Role of nitric oxide in exercise‐induced vasodilation of the forearm. Circulation 1994; 90: 2886–2890 [DOI] [PubMed] [Google Scholar]
  • 22. Wilson JR, Kapoor S: Contribution of endothelium‐derived relaxing factor to exercise‐induced vasodilation in humans. J Appl Physiol 1993; 75: 2740–2744 [DOI] [PubMed] [Google Scholar]
  • 23. Gilligan DM, Panza JA, Kilcoyne CM, Waclawiw MA, Casino PR, Quyyumi AA: Contribution of endothelium‐derived nitric oxide to exercise‐induced vasodilation. Circulation 1994; 90: 2853–2858 [DOI] [PubMed] [Google Scholar]
  • 24. Dyke CK, Proctor DN, Dietz NM, Joyner MJ: Role of nitric oxide in exercise hyperaemia during prolonged rhythmic handgripping in humans. J Physiol 1995; 488.1: 259–265 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 25. Takase B, Uehata A, Akima T, Nagai T, Nishioka T, Hamabe A, Satomura K, Ohsuzu F, Kurita A: Endothelium‐dependent flow‐mediated vasodilation in coronary and brachial arteries in suspected coronary artery disease. Am J Cardiol 1998; 82: 1535–1539 [DOI] [PubMed] [Google Scholar]
  • 26. Anderson TJ, Uehata A, Gerhard MD, Meredith IT, Knab S, Delagrange D, Lieberman EH, Ganz P, Creager MA, Yeung AC, Selwyn AP: Close relation of endothelial function in the human coronary and peripheral circulation. J Am Coll Cardiol 1995; 26: 1235–1241 [DOI] [PubMed] [Google Scholar]
  • 27. Elias LA: Tumor necrosis factor interacts with interleukin‐1 and interferons to inhibit fibroblast proliferation via fibroblast prostaglandin‐dependent and ‐independent mechanisms. Am Rev Respir Dis 1988; 138: 652–658 [DOI] [PubMed] [Google Scholar]
  • 28. Hoffman T, Lizzio EF, Ting A, Marshall LA, Bonvini E, Jennings MK: Release of arachidonic acid metabolites by human monocytes or lymphocytes: Effect of treatment with interferon on stimulation by phorbol ester or calcium ionophore. Clin Immunol Immunopathol 1987; 44: 82–92 [DOI] [PubMed] [Google Scholar]

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