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Alterations in the Pattern of Collagen Deposition May Contribute to the Deterioration of Systolic Function in Hypertensive Patients With Heart Failure

Begoña López, PhD^_*, Arantxa González, PhD^_*, Ramón Querejeta, MD, PhD, Mariano Larman, MD and Javier Díez, MD, PhD^_*,,_*

^_* Division of Cardiovascular Sciences, Centre for Applied Medical Research, School of Medicine, University of Navarra, Pamplona, Spain
Division of Cardiology, Donostia University Hospital, San Sebastián, Spain
Division of Hemodynamics, Guipúzcoa Polyclinics, San Sebastián, Spain
Department of Cardiology and Cardiovascular Surgery, University Clinic, University of Navarra, Pamplona, Spain

View larger version (48K): [in a new window]   Figure 1 Endomyocardial tissue from one hypertensive patient with heart failure. Sections were stained with picrosirius red and collagen fibers were identified in red (x40). Collagen tissue was seen as thin bands surrounding individual cardiomyocytes or groups of cardiomyocytes (mysial collagen, left panel), as large strands localized around intramyocardial vessels (perivascular collagen, middle panel), and as masses or scars diffusely localized within the interstitium (scar collagen, right panel).

View larger version (18K): [in a new window]   Figure 2 (A) Representative Western blot autoradiogram of the 52-kDa MMP-1 protein and the 28-kDa TIMP-1 protein. Autoradiograms include endomyocardial samples from one normotensive patient, one hypertensive patient with diastolic heart failure, and one hypertensive patient with systolic heart failure. (B) Bars represent mean + SEM of the ratio of MMP- to TIMP-1, calculated in endomyocardial samples from the three groups of subjects. DHF = diastolic heart failure; HT = hypertensive; MMP = matrix metalloproteinase; NT = normotensive; SHF = systolic heart failure; TIMP = tissue inhibitor matrix metalloproteinase.

View larger version (101K): [in a new window]   Figure 3 Endomyocardial tissue from one normotensive patient (A and D), one hypertensive patient with diastolic heart failure (B and E), and one hypertensive patient with systolic heart failure (C and F). Sections were immunostained with an antibody anti-MMP-1 (A, B, and C) or an antibody anti-TIMP-1 (D, E, and F), and these molecules were identified in brown within the cardiomyocytes. Arrows highlight specific points. (Magnification: x100.) Abbreviations as in Figure 2.

View larger version (16K): [in a new window]   Figure 4 (A) Direct correlation (y = 0.03x + 4.75) between left ventricular end-systolic circumferential wall stress and MMP-1 measured in peripheral vein blood in all subjects. (B) Direct correlation (y = 5.28x – 1.93) between log amino-terminal pro-brain natriuretic peptide and MMP-1 measured in peripheral vein blood in all subjects. LV = left ventricular; NT-proBNP = amino-terminal pro-brain natriuretic peptide; other abbreviations as in Figure 2.

View larger version (15K): [in a new window]   Figure 5 (A) Inverse correlation (y = –33.39x + 49.97) between the ratio of MMP-1 to TIMP-1 (log MMP-1:TIMP-1) measured in peripheral vein blood and ejection fraction in all subjects. (B) Direct correlation (y = 1.98x + 5.50) between log MMP-1:TIMP-1 measured in peripheral blood and left ventricular end-diastolic diameter in all subjects. EF = ejection fraction; LVEDD = left ventricular end-diastolic diameter; other abbreviations as in Figure 2.