This study examined LA mechanics in LVH secondary to HTN and HCM and analyzed if LA remodeling was associated with the extent of LV hypertrophy and fibrosis in HCM. The results provide several notable insights into LA function. We could demonstrate that LA mechanics is globally decreased in either HTN or HCM. Particularly, LA function is significantly impaired in HCM, in relation to HTN (Table 2, Figure 1).. The best discriminators of HCM were LA-SRs and LA-SRa with an AUC of 0.8. LA ɛe had the highest specificity (94%) and LA ɛa the highest sensitivity (95%) (Table 3).. Furthermore, we could demonstrate a moderate correlation between LA mechanics and the degree of fibrosis assessed by CMR in HCM, namely, LA-SRe and extension of LGE (Table 4)..
LA reservoir function impairment is accompanied by deterioration of LV function, with greater LA dysfunction in HCM than in HTN. The reduction in LA reservoir function in HCM is related to the LV longitudinal dysfunction, due to a reduction in the systolic descent of LV base, which leads to an impaired LA relaxation and stiffness7,18.
Although LA conduit function is associated to LV systolic function, namely ventricular desynchrony, it is less related to the extent of hypertrophy2,18. In our study, LA-SRe was the parameter that correlated better with the extent of fibrosis. This is probably explained by reduction of LV compliance due to myocardial fibrosis, with accompanying reduction of the atrial conduit function in HCM.
LA contractile phase was also impaired in HCM, which is somewhat inconsistent with previous reports that showed a trend toward increased LA contractile booster pump function in HCM with absent LV fibrosis (although not statistically significant)2. This might be related to the fact that 87% of our HCM patients already presented with LGE on CMR, so LA contractile function might already be compromised.
When evaluating diastolic dysfunction in HCM versus HTN, we noted that LAVi and mitral E and A velocities did not vary between groups. E/E’ ratio, albeit varying significantly between groups, was not a good discriminator between groups and was not correlated to the extent of myocardial fibrosis in HCM. LA mechanics appear as a more discriminator factor between LVH groups and is related to the degree of myocardial fibrosis in HCM. This suggests that LA mechanics might be an earlier marker of both atrial and myocardial dysfunctions. Furthermore, in HTN patients with significant LVH, in which excluding HCM might be challenging, the evaluation of LA mechanics might be useful, since the three phases are not very impaired in this group. In our study, albeit being statistically inferior from HCM, the IVS thickness values of our HTN cohort were still high (mean of 14.3±3.6 mm).
Our study has several limitations. First, we only included 60 HCM patients and 60 HTN patients, which may have influenced the statistical power of the analysis. Second, this was not an outcome-based study, so we could not draw any conclusions about the prognostic value of LA strain rate in this population. Nevertheless, this study attempted to clarify the LA deformation mechanics in LVH secondary to HCM and to HTN. Future studies with large sample size are warranted to clarify the prognostic value of LA strain rate in LVH.
In this study, we have demonstrated that LA strain and strain rate were potential discriminators between HCM and HTN, not only in physiologic response to LVH, but also to the determinants of dysfunction. This represents an important finding of our study, since the LAVi, E/E’ ratio, and even IVS thickness were not sufficient reliable to do so (Tables 2 and 3).. In addition, LA mechanics was moderately correlated to fibrosis extension in HCM, which can potentially become a marker of severity and prognosis in earlier stages or doubtful cases.