Relationship between left ventricular twist and circulating biomarkers of collagen turnover in hypertensive patients with heart failure


Aurora Cardiovascular Services, Aurora Sinai Medical Center, Aurora St. Luke's Medical Center


BACKGROUND: Left ventricular (LV) twist may be a compensatory mechanism to preserve ejection fraction (EF). In patients with hypertension, twist varies depending on the left ventricle's degree of remodeling and systolic function; it is increased in those with hypertension with normal EF (HTNEF) and diminished in those with hypertension with low EF (HTLEF). The ratio of collagen-degradation biomarkers in patients with hypertension is higher in those with low EFs than those with preserved EFs and may contribute to remodeling and systolic dysfunction.

METHODS: The aim of this study was to evaluate the relationship between these biomarkers and LV twist in 82 patients with hypertension, 41 with EFs < 50% (HTLEF group) and 41 with EFs ≥ 50% (HTNEF group). Net LV twist was measured using speckle-tracking echocardiography. Markers of collagen turnover, including serum concentrations of matrix metalloproteinase-1 (MMP1), tissue inhibitor of MMP1 (TIMP1), and the ratio of MMP1 to TIMP1, were measured.

RESULTS: Log TIMP1, log MMP1, and log MMP1/TIMP1 ratio levels were higher in the HTLEF group than the HTNEF group (12.3 ± 0.3 vs 11.8 ± 0.1 [P < .0001], 9.1 ± 0.3 vs 8.0 ± 0.2 [P < .0001], and -3.3 ± 0.3 vs -3.8 ± 0.2 [P < .0001], respectively). Net LV twist was lower in the HTLEF group than the HTNEF group (3.3 ± 1.1 vs 11.7 ± 0.7, P < .0001). An inverse correlation existed between log MMP1/TIMP1 and net LV twist after adjusting for age, EF, duration of heart failure, systolic blood pressure, LV mass index, and LV sphericity index at end-diastole (r = -0.43, P < .0001).

CONCLUSIONS: This inverse correlation between twist and loss of myocardial collagen scaffolding in patients with hypertension with heart failure suggests that the integrity of the extracellular matrix may play an important role in preserving myocardial deformation.

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