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CLINICAL RESEARCH: HEART RHYTHM DISORDER

Extracellular Matrix Alterations in Patients With Paroxysmal and Persistent Atrial Fibrillation

Biochemical Assessment of Collagen Type-I Turnover

Eleftherios M. Kallergis, MD^_*, Emmanuel G. Manios, MD^_*, Emmanuel M. Kanoupakis, MD^_*, Hercules E. Mavrakis, MD^_*, Dimitris A. Arfanakis, MD^_*, Niki E. Maliaraki, MD, Chrisovalantis E. Lathourakis, MD^_*, Gregory I. Chlouverakis, PhD^_* and Panos E. Vardas, MD, PhD, FESC, FACC^_*,_*

^_* Department of Cardiology, University Hospital of Heraklion, Crete, Greece
Laboratory of Biochemistry, University Hospital of Heraklion, Crete, Greece.

Manuscript received October 29, 2007; revised manuscript received February 13, 2008, accepted March 18, 2008.

^_* Reprint requests and correspondence: Dr. Panos E. Vardas, Department of Cardiology, Heraklion University Hospital, 71100, Heraklion, Crete, Greece. (Email: cardio{at}med.uoc.gr).

Objectives: We investigated whether the serum markers of collagen turnover differed in various forms of atrial fibrillation (AF) and in sinus rhythm (SR) in humans.

Background: Structural alterations and fibrosis have been implicated in the generation and perpetuation of AF.

Methods: Serum C-terminal propeptide of collagen type-I (CICP), C-terminal telopeptide of collagen type-I (CITP), matrix metalloproteinase-1, and tissue inhibitor of matrix metalloproteinases-1 were measured as markers of collagen synthesis and degradation in 70 patients with AF and 20 healthy control subjects in SR.

Results: C-terminal propeptide of collagen type-I and CITP were significantly higher in AF patients than in control subjects (91 ± 27 ng/ml vs. 67 ± 11 ng/ml, p < 0.001 and 0.38 ± 0.20 ng/ml vs. 0.25 ± 0.08 ng/ml, p < 0.001, respectively). Persistent AF patients had higher levels of CICP (105 ± 28 ng/ml vs. 80 ± 21 ng/ml, p < 0.001), but not CITP, compared with those with paroxysmal AF. Patients with persistent AF had lower levels of matrix metalloproteinase-1 but increased levels of tissue inhibitor of matrix metalloproteinases-1 compared with patients with paroxysmal AF (11.90 ± 4.79 ng/ml vs. 14.98 ± 6.28 ng/ml, p = 0.03 and 155 ± 45 ng/ml vs. 130 ± 38 ng/ml, p < 0.001, respectively). Tissue inhibitor of matrix metalloproteinases-1 levels were significantly lower in control subjects compared with those in both paroxysmal and persistent AF patients (102 ± 15 ng/ml vs. 130 ± 38 ng/ml vs. 155 ± 45 ng/ml, respectively, p < 0.001).

Conclusions: Serum markers of collagen type-I turnover differed significantly between patients with AF and SR. Furthermore, these markers also differed significantly between paroxysmal and persistent AF patients, suggesting that the intensity of the extracellular synthesis and degradation of collagen type-I may be related to the burden or type of AF.

Key Words: atrial fibrillation • collagen • fibrosis

Abbreviations and Acronyms   AF = atrial fibrillation   CICP = C-terminal propeptide of collagen type-I   CITP = C-terminal telopeptide of collagen type-I   LA = left atrial   LVEF = left ventricular ejection fraction   MMP = matrix metalloproteinase   SR = sinus rhythm   TIMP = tissue inhibitor of matrix metalloproteinase

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