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  • Open Access

Increased extracellular volume and altered mechanics are associated with left ventricular hypertrophy in hypertensive heart disease, not hypertension alone

  • 1,
  • 1,
  • 3,
  • 1,
  • 3,
  • 1,
  • 1, 2 and
  • 1, 3
Journal of Cardiovascular Magnetic Resonance201416 (Suppl 1) :P393

https://doi.org/10.1186/1532-429X-16-S1-P393

  • Published:

Keywords

  • Hypertensive Patient
  • Left Ventricular Hypertrophy
  • Circumferential Strain
  • Extracellular Volume
  • Hypertensive Heart Disease

Background

Study purpose

To detect differences in extracellular volume (ECV) and systolic strain in hypertensive patients with LVH as compared to hypertensive patients without LVH and age-matched controls. Background: Increased ECV due to diffuse myocardial fibrosis in hypertensive patients may be an underlying mechanism contributing to increased cardiovascular risk. Moreover HTN patients with left ventricular hypertrophy (LVH) are at higher risk of cardiovascular morbidity and mortality when compared to HTN Non-LVH subjects. We compared levels of ECV and systolic strain between HTN LVH, HTN Non-LVH and control subjects.

Methods

T1 mapping was performed in 21 HTN LVH (55 ± 11 years), 12 HTN Non-LVH (60 ± 14 years) and 21 control (52 ± 9) subjects on a Siemens 1.5T Avanto using 3-5 MOLLI (11 heart beats, 2 inversions, 3 recovery beats, 8 images). Patients with known coronary disease, significant valvular disease, and other causes of LVH were excluded. MOLLI sequence parameters included: echo time/repetition time/flip angle 1.1 ms/2.5 ms/35°, field of view 340 × 260, resolution 1.8 mm × 1.8 mm, thickness 8 mm. T1 was determined pre-contrast and 10,15 and 20 minutes following injection of 0.15 mmol/kg Gd-DTPA. T1 maps were generated using an in-house MATLAB program. Partition Coefficient (λ) was determined from the slope of a plot of 1/T1 of the myocardium versus 1/T1 of the blood. Volume of distribution (Vd) was calculated as λ*(1-Hematocrit). LV mass and function was assessed by SSFP cine imaging. Circumferential strain measurements were performed using cine DENSE. Values were compared between groups using one-way ANOVA.

Results

HTN LVH subjects had significantly higher BP, LV mass and were on more anti-hypertensive medications when compared to HTN Non-LVH subjects and controls (Table 1). HTN LVH subjects had higher levels of ECV, as measured by λ and Vd, when compared to HTN Non-LVH and control subjects (Table 1 and Figure 1). Peak mid-wall circumferential strain was significantly reduced in HTN LVH subjects as compared to HTN Non-LVH subjects and controls (-0.12 ± 0.02 vs. -0.16 ± 0.03, p = 0.006 and -0.17 ± 0.03, p < 0.001, respectively).

Table 1

 

Age-matched controls (n = 21)

Hypertensive Non-LVH (n = 12)

Hypertensive LVH (n = 21)

Sex

15 females; 6 males

6 females; 6 males

13 females; 8 males

Age (yrs)

52 ± 9

60 ± 14

55 ± 11

Systolic BP (mm Hg)

120 ± 16

136 ± 13^

156 ± 21*^

Diastolic BP (mm Hg)

69 ± 10

77 ± 12

88 ± 14^

Heart Rate

72 ± 12

72 ± 12

73 ± 16

Number of HTN meds

0

2.0 ± 1.3^

3.0 ± 1.5^

LV Mass (g)

75 ± 20

85 ± 23

147 ± 40*^

LVMI

41 ± 8

41 ± 9

71 ± 16*^

Partition Coefficient

0.43 ± 0.02

0.45 ± 0.02

0.48 ± 0.04*^

Volume of Distribution

0.26 ± 0.02

0.26 ± 0.02

0.28 ± 0.02*^

Mid-CircumferentialStrain

-0.17 ± 0.03

-0.16 ± 0.03

-0.12 ± 0.02*^

[* = p < 0.05 vs. Non-LVH groups. ^ = p < 0.05 vs. controls.]

Figure 1
Figure 1

Partition Coefficient (left) and Volume of distribution (right) among all three groups.

Conclusions

HTN LVH patients had higher ECV and associated reduction in mid-wall circumferential strain when compared to HTN Non-LVH and control subjects. Increased ECV as a surrogate for diffuse fibrosis in HTN LVH subjects may explain the increased cardiovascular morbidity and mortality seen in HTN LVH as compared to other HTN subtypes.

Funding

AHA 10SDG2650038.

Authors’ Affiliations

(1)
Cardiology, University of Virginia Medical Center, Charlottesville, Virginia, USA
(2)
Radiology, University of Virginia Health System, Charlottesville, Virginia, USA
(3)
Biomedical Engineering, University of Virginia Health System, Charlottesville, Virginia, USA

Copyright

© Kuruvilla et al.; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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