Download PDF
Thorac Cardiovasc Surg 2002; 50(4): 216-222
DOI: 10.1055/s-2002-33092
Original Cardiovascular
Original Paper
© Georg Thieme Verlag Stuttgart · New York

Myocardial Collagen Type I and Impaired Left
Ventricular Function under Exercise in Hypertrophic Cardiomyopathy

M.  Mundhenke1 , B.  Schwartzkopff1 , P.  Stark1 , H.  D.  Schulte2 , B.  E.  Strauer1
  • 1Department of Cardiology, Pulmology and Angiology; Medical School of the Heinrich Heine University,
    Düsseldorf, Germany
  • 2Department of Cardiothoracic Surgery, Medical School of the Heinrich Heine University, Düsseldorf, Germany
This paper is dedicated to the 65th anniversary of Prof. Hagen D. Schulte
Further Information

Publication History

Publication Date:
07 August 2002 (online)

    Permissions and Reprints All articles of this category

Abstract

Background: Transaortic subvalvular myectomy (TSM) reduces left ventricular outflow tract gradient and improves symptoms and working capacity in patients with hypertrophic obstructive cardiomyopathy (HOCM). Nevertheless, TSM does not completely restore normal ventricular function, and some patients complain of symptoms despite optimal surgical results. Abnormal myocardial collagen structure in hypertrophic cardiomyopathy might be an indicator of impaired cardiac function. Methods: Nine patients with HOCM were investigated. Myocytic diameter, collagen volume fraction and light absorbance of immunohistochemically stained collagen subtype I and its product (Coll Iprod) were measured quantitatively in myectomy specimens. Patients underwent symptom-limited bicycle exercise testing with equilibrium radionuclide angiocardiography to determine ejection fraction (EF). Right heart catheterization was performed simultaneously in order to measure pulmonary capillary wedge pressure (PCWP) as a parameter of global ventricular diastolic filling and cardiac index (CI) as a parameter of functional capacity. Results: Postoperatively, CI increased from 3.1 ± 0.4 to 5.7 ± 1.3 l/min/m2 under exercise. EF was normal at rest (64 ± 9 %) but did not increase significantly under exercise (66 ± 14 %). Coll Iprod (13.62 ± 7.35 Vv%prod) correlated inversely with EF under exercise (r = - 0.64; p = 0.05). PCWP increased under exercise from 8 ± 2 mmHg at rest to 22 ± 9 mmHg (p = 0.01). Coll Iprod correlated with PCWP under exercise (r = 0.90; p = 0.001). Conclusions: Increased collagen subtype I is a predictor of diastolic as well as systolic dysfunction under exercise in patients with HCM after successful TSM.

Key words

Hypertrophic cardiomyopathy - Collagen - Ventricular function

References

  • 1 Maron B J. Hypertrophic cardiomyopathy.  Lancet. 1997;  350 127-133
    CrossrefPubMedGoogle Scholar
  • 2 Sutton M GStJ, Lie J T, Anderson K R, O'Brien P C, Frye R L. Histopathological specificity of hypertrophic obstructive cardiomyopathy.  Br Heart J. 1980;  44 433-443
    PubMedGoogle Scholar
  • 3 Tanaka M, Fujiwara H, Onodera T, Wu D-J, Hamashima Y, Kawai C. Quantitative analysis of myocardial fibrosis in normals, hypertensive hearts, and hypertrophic cardiomyopathy.  Br Heart J. 1986;  55 575-581
    PubMedGoogle Scholar
  • 4 Factor S M, Butany J, Sole M J, Wigle E D, Williams W C, Rojkind M. Pathologic fibrosis and matrix connective tissue in the subaortic myocardium of patients with hypertrophic cardiomyopathy.  J Am Coll Cardiol. 1991;  17 1343-1351
    PubMedGoogle Scholar
  • 5 Mundhenke M, Schwartzkopff B, Strauer B E. Structural analysis of arteriolar and myocardial remodelling in the subendocardial region of patients with hypertensive heart disease and hypertrophic cardiomyopathy.  Virchows Arch. 1997;  431 265-273
    CrossrefPubMedGoogle Scholar
  • 6 Wigle E D, Rakowski H, Kimball B P, Williams W G. Hypertrophic cardiomyopathy: clinical spectrum and treatment.  Circulation. 1995;  92 1680-1692
    CrossrefPubMedGoogle Scholar
  • 7 Schwartzkopff B, Mundhenke M, Strauer B E. Alterations of the architecture of subendocardial arterioles in patients with hypertrophic cardiomyopathy and impaired coronary vasodilator reserve: a possible cause for myocardial ischemia.  J Am Coll Cardiol. 1998;  31 1089-1096
    CrossrefPubMedGoogle Scholar
  • 8 Chikamori T, Counihan P J, Doi Y L, Takata J, Stewart J T, Frenneaux M P, McKenna W J. Mechanisms of exercise limitation in hypertrophic cardiomyopathy.  J Am Coll Cardiol. 1992;  19 507-512
    PubMedGoogle Scholar
  • 9 Wigle E D, Wilansky S. Diastolic dysfunction in hypertrophic cardiomyopathy.  Heart failure. 1987;  3 82-93
    PubMedGoogle Scholar
  • 10 Boerrigter G, Mundhenke M, Stark P, Schulte H D, Strauer B E, Schwartzkopff B. Immunohistochemical video-microdensitometry of myocardial collagen type I and type III.  Histochem J. 1998;  30 783-791
    PubMedGoogle Scholar
  • 11 Schulte H D, Bircks W H, Lösse B, Godehardt E AJ, Schwartzkopff B. Prognosis of patients with hypertrophic obstructive cardiomyopathy after transaortic myectomy.  J Thorac Cardiovasc Surg. 1993;  106 709-717
    PubMedGoogle Scholar
  • 12 Schulte H D, Borisov K, Gams E, Gramsch-Zabel H, Lösse B, Schwartzkopff B. Management of symptomatic hypertrophic obstructive cardiomyopathy - long-term results after surgical therapy.  Thorac Cardiovasc Surg. 1999;  47 213-218
    PubMedGoogle Scholar
  • 13 Schwartzkopff B, Stark P, Schulte H D, Mundhenke M, Klein R M, Lösse B, Vester E G, Strauer B E. Early changes in systolic and diastolic function at rest and under exercise in patients with hypertrophic cardiomyopathy after myectomy.  Z Kardiol. 1997;  86 438-449
    CrossrefPubMedGoogle Scholar
  • 14 Brilla C G, Matsubara L, Weber K T. Advanced hypertensive heart disease in spontaneously hypertensive rats. Lisinopril mediated regression of myocardial fibrosis.  Hypertension. 1996;  28 269-275
    PubMedGoogle Scholar
  • 15 Villari B, Campbell S E, Hess O M, Mall G, Vassalli G, Weber K T, Krayenbuehl H P. Influence of collagen network on the left ventricular systolic and diastolic function in aortic valve disease.  J Am Coll Cardiol. 1993;  22 1477-1484
    PubMedGoogle Scholar
  • 16 Frenzel H, Schwartzkopff B, Reinecke P, Kamino K, Lösse B. Evidence for muscle fiber hyperplasia in the septum of patients with hypertrophic obstructive cardiomyopathy.  Z Kardiol. 1987;  76 (Suppl 3) 14-19
    PubMedGoogle Scholar
  • 17 Brutsaert D, Sys S U, Gillebert T C. Diastolic failure: pathophysiology and therapeutic implications.  J Am Coll Cardiol. 1993;  22 318-325
    PubMedGoogle Scholar
  • 18 Vikstrom K L, Bohlmeyer T, Factor S M, Leinwand L A. Hypertrophy, pathology, and molecular markers of cardiac pathogenesis.  Circ Res. 1998;  82 773-778
    PubMedGoogle Scholar
  • 19 Nagueh S F, Lakkis N M, Middleton K J, Killip D, Zoghbi W A, Quinones M A, Spencer W H3. Changes in left ventricular diastolic function 6 months after nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy.  Circulation. 1999;  99 344-347
    PubMedGoogle Scholar
  • 20 Frenneaux M P, Porter A, Caforio A LP, Odawara H, Counihan P J, McKenna W J. Determinants of exercise capacity in hypertrophic cardiomyopathy.  J Am Coll Cardiol. 1989;  13 1521-1526
    PubMedGoogle Scholar

1 This paper is dedicated to the 65th anniversary of Prof. Hagen D. Schulte

MD Bodo Schwartzkopff

Division of Cardiology, Medical School of the Heinrich Heine University, Düsseldorf

Moorenstrasse 5

40225 Düsseldorf

Germany

Phone: +49 211 811 88 00

Fax: +49 211 811 95 20

Email: schwartk@uni-duesseldorf.de