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21 Progressive vasculo-ventricular remodelling in persistent asymptomatic left ventricular diastolic dysfunction and links with immune-inflammatory biochemical markers
  1. V Voon1,
  2. K McDonald1,
  3. M Ledwidge1,
  4. C Watson2,
  5. J Baugh2
  1. 1St. Vincent’s University Hospital, Dublin, Ireland
  2. 2University College Dublin, Ireland


Background The natural history of persistent asymptomatic left ventricular diastolic dysfunction (ALVDD) is not fully understood. Altered immune-inflammatory markers have been linked to extracellular matrix remodelling of myocardial interstitium and perivasculature in hypertensive animal models. We aimed to evaluate the link between immune-inflammatory markers and vasculo-ventricular remodelling in ALVDD.

Methods 91 asymptomatic hypertensive patients from the community were consecutively enrolled and subjected to guideline-based management at a dedicated Blood Pressure Unit. Demographics, Doppler-echocardiography and serum biomarkers were measured at baseline and routine 12 month follow-up. Patients with ALVDD (left atrial volume index (LAVi) > 34 ml/m2, n = 22) and Comparators (LAVi < 34 ml/m2, n = 44) were propensity matched to age in 1:2 ratio at baseline. From this cohort, patients with persistent ALVDD (at both timepoints, n = 10) were observed against others (n = 56).

Results ALVDD was associated with higher serum natriuretic peptide, matrix metalloproteinase (MMP)-2, LAVi and left ventricular mass index versus Comparators at baseline. All patients had mean ejection fraction (EF) 67 ± 8%.

Over the follow-up duration, persistent AVLDD was associated with greater increase in monocyte chemoattractant protein-1 (924.6 ± 2420.3 vs 198.5 ± 239.4 pg/ml) and aortic root diameter (0.27 ± 0.45 vs 0.06 ± 0.27 cm) with reduction in EF (-5.4 ± 5.2 vs -0.2 ± 7.0%) versus others; all p < 0.05. Despite within-group reductions in LAVi in both groups supported by increase in anti-hypertensives with blood pressure and MMP-2 lowering, there was a significant increase in interleukin-8 and tumour necrosis factor-alpha over follow-up.

Conclusion Persistent ALVDD is associated with progressive vascular and ventricular remodelling not optimally negated by conventional anti-hypertensive therapies. These changes are linked to altered immune-inflammatory markers. The impact of inhibiting these markers requires further evaluation.

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