P319 Evidence for abnormal deformational reserve in hypertrophic cardiomyopathy on exercise: is it a game-changer?
Authors: Halmai L , Ward M , Wong J , Nemes A , Forster T , Pantazis A 
Published: January 2020

Funding Acknowledgements

None

Hypertrophic obstructive cardiomyopathy (HOCM) is characterized by muscle hypertrophy and fibrosis, interfering with force generation and relaxation. Abnormal ventricular (LV) myocardial deformation have been demonstrated in patients with HOCM at rest, but there is lack of data regarding the deformational mechanics in exercise. AIMS: We wanted to assess the adaptability of LV deformational behaviour to physical exercise in HCM patients as compared to healthy control subjects.

METHODS

24 obstructive HOCM (age 51.2 ± 14.2yrs; 16 men, LVOT-obstruction 56 ± 19mmHg at rest or on Valsalva maneuver) and 32 control subjects (50.9 ± 6.8 yrs, 19 men from the MAGYAR-PATH Registry) underwent supine bicycle stress echocardiography (ESE) with measurements of 2D- and Doppler, 2D-Speckle Tracking Tracking Imaging and 3D-Full Volume Analysis. Beyond conventional LV/RV functional measurements; peak longitudinal (LS), circumferential (CS) Strain values; peak Twist and Torsion angles; post-systolic shortening index (PSS) and diastolic phase indices (Untwisting time - UTT and rate - UTR) calculated; the UTR/Twist ratio was given as "coupling index". The LV/RV-EF calculated by 3D-Full Volume Analysis off-line by TomTec Arena™ software both at rest and on submaximal ESE.

RESULTS

The HOCM group had lower resting LS (-14.6 ± 4.5 vs 18.4 ± 2.6%, p &lt; 001) but higher CS (-32.9 ± 5.1 vs 28.8 ± 2.3%, p &lt; 0.001) and Twist angles (9.9 ± 2.6 vs 6.1 ± 2.2º, p &lt; 0.01) than control subjects. Exercise induced an increase in all strains in control subjects, but much less in HOCM (LS: -21.4 ± 3.5 vs 15.1 ± 3.0% and CS: -33.9 ± 3.6 vs 34.1 ± 4.2% in HOCM, p &lt; 0.02 in controls, NS in HOCM); the increase of Twist angle was minimal in HOCM (Δ1.2 ± 1.2 vs Δ3.6 ± 2.3º in controls, p &lt; 0.01). The PSS was more pronounced on ESE in HOCM than in controls (46.6 ± 12 vs 21.2 ± 9.6% in controls, p &lt; 0.001). Peak UTR was slower (118 ± 2.1 vs 133.1 ± 14.1 º/s) during ESE and occured later (141 ± 19 vs 121 ± 9.1% of systolic time, p &lt; 0.02) in HOCM than in controls. There was significant relationship between the Twist and UTR in control subjects (β=-0.0807, p &lt; 0.001), but not in HOCM (β=-0.0046, p = 0.05). The UTR/Twist ratio diminished only in HOCM but not in controls (-8.0 ± 0.6 vs -13.1 ± 2.5 1/s, p &lt; 0.02).

CONCLUSIONS

The HOCM patients had significantly impaired strain-adaptability; developed post-systolic shortening and no LV Torsional reserve was found on exercise. Also, I detected decreased and delayed UTR indices in the HOCM group. These findings support evidence for reduced systolic-diastolic coupling efficiency, assessed by Twist-Untwist mechanics in HOCM patients, which can contribute to the development of exercise-related symptoms and the dynamic LVOT-obstruction. This unique pattern of deformational behaviour to exercise can help in the differential diagnostic workup in patients with LV hypertrophy of unknown aetiology and also would hold additional value in the risk stratification process for patients with HCM-phenotypes.