Introduction

Hypertrophic cardiomyopathy (HCM) is prone to myocardial heterogeneity and fibrosis, which are the substrate of ventricular arrhythmias (VAs).¹ Tissue tracking by cardiac magnetic resonance (CMR-TT) can quantitatively reflect the global and regional left ventricular strain from different directions.² It is uncertain whether myocardial strain by CMR-TT is associated with VAs.

Methods

We retrospectively included 93 HCM patients (38 with VAs and 55 without VAs) and 30 healthy cases. Routine left ventricular function, myocardial strain parameters and percentage of late gadolinium enhancement (%LGE) were evaluated.

Results

Global circumferential strain (GCS) and %LGE correlated moderately (r =0.51, P <0.001). HCM patients with VAs had worse left ventricular ejection fraction (LVEF), global radial strain (GRS), GCS and global longitudinal strain (GLS), and increased %LGE compared to those without VAs (P <0.01 for all). %LGE and GCS were indicators of VAs in HCM patients in the multivariate logistic regression analysis. HCM patients with %LGE >5.35% (AUC 0.81, 95% CI 0.70-0.91, P <0.001) and GCS <-14.73% (AUC 0.79, 95% CI 0.70-0.89, P <0.001) on CMR more frequently had VAs. %LGE + GCS were superior to detect HCM patients with VAs (AUC 0.87, 95% CI 0.79-0.95, P <0.001).

Discussion

In this study, we found that LVEF and SVI in HCM patients were significantly increased. At the same time, their LVESVI, GRS, GCS and GLS were obviously decreased, indicating that the changes in myocardial strain were much earlier than routine left ventricular systolic function. This is mainly related to the pathology that hypertrophic myocardium induced hyper-ejected status leads to normal or even higher LVEF and SVI.³ In fact, the disordered arrangement of hypertrophic cardiomyocytes and fibers caused sarcomeric systolic dysfunction. Myocardial strain could reflect the systolic function more accurately as the strain was not affected by the global movement and adjacent myocardium.^2,3 Therefore, myocardial strain is already reduced at an early stage in HCM patients. Furthermore, myocardial diastolic strain rates (GRSDr, GCSDr, GLSDr) were much lower when compared to healthy people, while LVEDVI was almost normal. This result further confirmed that the myocardial strain parameters have a higher sensitivity for detecting myocardial diastolic dysfunction.
In this study, %LGE in HCM patients with VAs was significantly higher than that of patients without VAs, but there was no significant difference in present LGE between the two groups. The results show that the extent of LGE is the risk factor of VAs in HCM patients, not the presence or absence of LGE. It suggest that %LGE is an independent risk factor for VAs in HCM patients, which can be used to identify whether there is VAs in HCM patients (AUC = 0.81). However, LGE can not be quantitatively evaluated in patients with contraindications or other reasons.
In this study, the myocardial strain parameters of HCM patients with VAs were significantly lower than those without VAs. Logistic regression analysis showed that reduced GCS was an independent risk factor for vas in HCM patients. uROC curve showed that HCM patients with GCS <-14.73% (AUC 0.79, 95% CI 0.70-0.89, P <0.001) on CMR more frequently had VAs. %LGE + GCS were superior to detect HCM patients with VAs (AUC 0.87, 95% CI 0.79-0.95, P <0.001).
In conclusion, CMR-TT, as a new technology, can quickly analyze the myocardial strain of HCM only based on the cine sequence. GCS is expected to become a new parameter to evaluate whether there is VAs in HCM patients, which may be useful for clinical diagnosis, treatment and prognosis.

Conclusions

Decreased GCS and increased %LGE were indicators of VAs in HCM. GCS may be a good potential predictor in identifying HCM patients with VAs, especially for those who can’t undergo the LGE scan.

Acknowledgements

No acknowledgement found.