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Eur J Cardiothorac Surg 2006;29:637
© 2006 Elsevier Science NL

Letter to the Editor

Comparison of mast cell properties and myocardial structure in dilated and ischemic hearts under mechanical circulatory support

Ahmet Akgul a , * , George P Noon b

a Yuksek Ihtisas Hospital, Department of Cardiovascular Surgery, Ankara, Turkey
b Michael E. DeBakey Department of Surgery, Division of Transplantation and Assist Devices, Baylor College of Medicine, Houston, TX, USA

Received 1 January 2006; accepted 16 January 2006.

* Corresponding author. Address: Mahmut Esat Bozkurt Caddesi, No: 17/7, Incesu 06600, Ankara, Turkey. Tel.: +90 312 431 45 17; fax: +90 312 431 94 13. (Email: aakgul{at}hotmail.com).

Key Words: Cardiomyopathy • Mast cell • Re-remodeling • Collagen • bFGF • Left ventricular assist device

We read the excellent study of Ibaraki et al. [1] with great interest. They found that both tryptase-positive mast cells (MCT) and tryptase- and chymase-positive mast cells (MCTC) counts in the border lung cancer region, where microvessels counts higher, were higher than in the central region. The ratio of MCTC to MCT in the border region was significantly higher than that in the normal region. They concluded that MCTC might be involved in the pathogenesis of angiogenesis in lung cancer.

Although our studies were not related to lung disease, mast cells and their products in the heart remain the base of our investigations.

As the cellular bases of myocardial remodeling, progression of myocardial failure, and re-remodeling, recovery, still remain unclear, we have looked into grade and distribution of interstitial fibrosis, mast cell density, mast cell phenotypes, and fibroblast activity [2] and relation of mast cells and fibrosis [3] in the failing myocardiums.

We compared the differences in mast cell properties and composition in dilated and ischemic myopathic hearts following left ventricular assist device (LVAD) implantation.

Paired myocardial tissue samples were obtained from 12 patients with end-stage cardiomyopathy (6 dilated, 6 ischemic patients) at the time of LVAD implantation and removal and from donor hearts (n = 4). Tissue sections were stained and quantified for MCTC and for myocardial fibrosis. The expression of basic fibroblast growth factor (bFGF) was determined as the intensity of a given band on the Western blot. Immunostaining was performed to express the decrease in bFGF level and its relation with mast cells and fibrosis.

There was an increase in MCTC in both dilated and ischemic myopathic tissues when compared with normal myocardium (p < 0.01); however, a significant decrease in MCTC density occurred in myocardium after long-term mechanical support, furthermore, in dilated hearts, the decrease in MCTC density is higher (12.6 ± 1.1 SEM cells/10 fields) when compared with the ischemic ones (20.3 ± 2 SEM cells/10 fields) following LVAD-implantation (p < 0.01). This was significant correlated with decreased expression of bFGF and decreased interstitial fibrosis in the same patient tissues (p < 0.01).

As a conclusion, mechanical unloading contributes to a decrease in MCTC density. The decrease in numbers is correlated with the duration of support and with the type of the myopathy. Dilated myopathy has higher potential for recovery when compared with the ischemic ones. There was also a concurrent decrease in bFGF levels in these LVAD-treated heart tissues, which contribute to reducing fibrosis and increasing improvement in diastolic function.

These new findings and our previous studies [2,3] demonstrate that chymase-positive mast cells were associated with increased fibrosis. In Nagaya et al.'s [4] study, they showed that transplantation of mesenchymal stem cells improved cardiac function of dilated cardiomyopathy through induction of angiogenesis and inhibition of fibrosis.

We would be glad to understand how the chymase-positive mast cells might be involved only in angiogenesis, not in the fibrosis. If both remodeling occurs, how can two reverse mechanisms (fibrosis and angiogenesis) come together in the same tissue?

References

  1. Ibaraki T, Muramatsu M, Takai S, Jin D, Maruyama H, Orino T, Katsumata T, Miyazaki M. The relationship of tryptase- and chymase-positive mast cells to angiogenesis in stage I non-small cell lung cancer. Eur J Cardiothorac Surg 2005;28:617-621.[Abstract/Free Full Text]
  2. Akgul A, Skrabal CA, Thompson LO, Loebe M, Lafuente JA, Noon GP, Youker KA. Role of mast cells and their mediators in failing myocardium under mechanical ventricular support. J Heart Lung Transplant 2004;23(6):709-715.[CrossRef][Medline]
  3. Akgul A, Youker KA, Noon GP, Loebe M. Quantitative changes in mast cell populations after left ventricular assist device implantation. ASAIO J 2005;51(3):275-280.[CrossRef][Medline]
  4. Nagaya N, Kangawa K, Itoh T, Iwase T, Murakami S, Miyahara Y, Fujii T, Uematsu M, Ohgushi H, Yamagishi M, Tokudome T, Mori H, Miyatake K, Kitamura S. Transplantation of mesenchymal stem cells improves cardiac function in a rat model of dilated cardiomyopathy. Circulation 2005;112(8):1128-1135.[Abstract/Free Full Text]




This Article
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