Differential left atrial function in hypertensive and sarcomeric left ventricular hypertrophy

Abstract Funding Acknowledgements Type of funding sources: Public hospital(s). Main funding source(s): Emili Letang - Josep Font research contract fund. Introduction Left ventricular (LV) hypertrophy is a common finding in clinical practice that can be caused by multiple conditions. Left atrial (LA) dysfunction is common due to abnormalities in LV distensibility and impairment in LV filling. In patients with sarcomeric LV hypertrophy, primary cardiomyopathy disease might also involve the atria. Purpose To evaluate if there are differences in left atrial function between arterial hypertension (HT) and hypertrophic cardiomyopathy (HCM) patients. Methods 37 patients with HCM (according to ESC guidelines criteria) and 36 patients with HT (under treatment with ≥1 hypertensive drug for ≥3 months) underwent an echocardiography to assess LA function with strain analysis and LV diastolic function. Continuous normally distributed variables were compared with T-student test, accepting as significant a p-value <0.05. Results HCM patients were slightly younger and showed thicker LV walls as compared to HT patients (48.7±17 vs. 55±5.9 y.o., and 17.7±5.8 vs. 12.4±2.2 mm, respectively, p<0.05 for both). LA volumes were larger in the HCM patients (82.4±37.4 vs. 62.8±20 ml, p<0.05). Also, HCM patients showed significantly lower LA contractile, conduit and reservoir strain as compared to HT patients (12.1±5.9% vs. 17.4±4.5%, 12.9±6.5% vs. 15.6±4, 25.2±10.4 vs. 33.1±6.8, all with p<0.05). Mitral annular velocities were lower (medial e` 7±2.7 vs. 8.2±1.86 and medial a` 8.4±3 vs. 10.2±2, both with p<0.05) and E/A ratio was slightly higher (1.32±0.65 vs. 1.02±0.26, p<0.05) in the HCM as compared to the HT group. In the subgroup of patients with moderately severe LV hypertrophy (<15mm, n=39; HCM=12, HT=27), LA contractile strain was lower in HCM as compared to HT patients (12.5±6.1% vs. 16.7±4%, p<0.05) (Figure 1), despite being younger; no differences in mitral annular velocities, E/A ratio or in LA volume were noted between HCM and HT etiologies in this subgroup of patients. Conclusions Our study shows that LA strain is more impaired in HCM patients as compared to HT patients, especially the LA contractile strain, that remains lower even in those with moderately severe LV hypertrophy, despite having similar LV diastolic function and LA size. This finding could suggest the direct involvement of atrial cardiomyocites in sarcomeric disease and might help in the etiological differential diagnosis of moderately to severe LV hypertrophy. In the setting of a moderately severe hypertrophy of unknown origin, the presence of an abnormally reduced LA contractility strain could be suggestive of HCM.