Relation between plasma amino-terminal propeptide of procollagen type III and left ventricular longitudinal strain in

S H Poulsen1, N H Andersen, L Heickendorff

  • 1Department of Cardiology, Skejby Hospital, Aarhus University Hospital, DK-8200 Aarhus N, Denmark. steen.hvitfeldt@dadlnet.dk

Insights

Essential hypertension is linked to myocardial fibrosis, which impairs left ventricular systolic function. This study found a significant association between fibrosis markers and reduced contractility in hypertensive patients.

Area of Science:

  • Cardiology
  • Hypertension Research
  • Cardiac Imaging

Background:

  • Essential hypertension can lead to cardiac structural changes.
  • Myocardial fibrosis is an indicator of cardiac remodeling.
  • Assessing fibrosis non-invasively is crucial for understanding hypertensive heart disease.

Purpose of the Study:

  • To determine the relationship between non-invasively assessed myocardial fibrosis and left ventricular (LV) longitudinal systolic function.
  • To investigate markers of fibrosis in patients with essential hypertension.
  • To correlate cardiac function with serological fibrosis markers.

Main Methods:

  • The study included 40 hypertensive patients and 30 controls with normal LV ejection fraction.
  • Tissue Doppler echocardiography assessed LV longitudinal systolic strain.
  • Plasma concentrations of amino-terminal propeptide of type III procollagen (PIIINP) were measured.

Main Results:

  • Hypertensive patients showed significantly reduced mean LV longitudinal strain and elevated plasma PIIINP levels compared to controls.
  • A significant negative correlation was observed between mean strain and PIIINP (r = -0.56, p < 0.001).
  • Patients with abnormal diastolic filling exhibited further reductions in strain and higher PIIINP levels.

Conclusions:

  • Myocardial fibrosis is significantly associated with impaired LV longitudinal contractility in essential hypertension.
  • Non-invasive assessment of fibrosis may provide insights into cardiac dysfunction in hypertensive individuals.
  • These findings highlight the impact of fibrosis on systolic function in hypertension.
Abstract

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