Myocardial bridging in obstructive hypertrophic cardiomyopathy: a risk factor for myocardial fibrosis

Abstract

Background: Myocardial bridging (MB) is common in patients with hypertrophic cardiomyopathy (HCM). There are sparse data on the impact of MB on myocardial fibrosis in HCM. This study was designed to evaluate the relationship between MB and myocardial fibrosis in patients with obstructive HCM.

Methods: In this cohort study, retrospective data were collected from a high-volume HCM center. Patients with obstructive HCM who underwent septal myectomy and preoperative cardiac magnetic resonance (CMR) were screened from 2011 to 2018.

Results: Finally, 492 patients were included in this study, with an average age of 45.7 years. Of these patients, 76 patients had MB. MB occurred mostly in the left anterior descending artery (73/76). The global extent of late gadolinium enhancement (LGE) was correlated with the degree of systolic compression (r = 0.33, p = 0.003). Multivariable linear regression analysis revealed that the degree of systolic compression was an independent risk factor for LGE (β = 0.292, p = 0.007). The LGE fraction of basal and mid anteroseptal segments in patients with severe MB (compression ratio ≥ 80%) was significantly greater than that in patients with mild to moderate MB (compression ratio < 80%). During a median follow-up of 28 (IQR: 15-52) months, 15 patients died. Kaplan-Meier analysis did not identify differences in all-cause death (log-rank p = 0.63) or cardiovascular death (log-rank p = 0.72) between patients undergoing MB-related surgery and those without MB.

Conclusions: MB with severe systolic compression was significantly associated with a high extent of fibrosis in patients with obstructive HCM. Concomitant myotomy or coronary artery bypass grafting might provide excellent survival similar to that of patients without MB. Identification of patients with severe MB and providing comprehensive management might help improve the prognosis of patients with HCM.

Keywords: Fibrosis; Hypertrophic cardiomyopathy; Myocardial bridging; Survival.

Fig. 1

Flowchart of patient inclusion. Finally, 492 patients were enrolled in this analysis. CMR, cardiac magnetic resonance

Fig. 2

Myocardial fibrosis in a male patient with severe MB. Coronary angiography showed systolic compression of the left anterior descending coronary artery (LAD) (A, arrow) and almost complete recovery in diastole (B, arrow). Myocardial fibrosis is shown in the histological image (C, asterisk) and CMR images (D, arrow)

Fig. 3

Histopathological myocardial fibrosis in the MB group. The histopathological myocardial fibrosis ratio was significantly higher in the MB group (17.0 ± 9.1% versus 12.2 ± 5.3%; p = 0.001)

Fig. 4

Correlation between the extent of LGE and the characteristics of MB. The global extent of LGE was correlated with the degree of systolic compression (n = 76) (A), length of tunneled segment (n = 76) (B), and depth of myocardial mass overlying the tunneled artery (n = 18) (C)

Fig. 5

The distribution of LGE in this cohort. A The American Heart Association 16-segment model, 1 = basal anterior, 2 = basal anteroseptal, 3 = basal inferoseptal, 4 = basal lateral, 5 = basal inferolateral, 6 = basal anterolateral, 7 = mid anterior, 8 = mid anteroseptal, 9 = mid inferoseptal, 10 = mid inferior, 11 = mid inferolateral, 12 = mid anterolateral, 13 = apical anterior, 14 = apical septal, 15 = apical inferior, and 16 = apical lateral. B Distribution of the extent of LGE in patients with severe myocardial bridging. C Distribution of the extent of LGE in patients with mild to moderate myocardial bridging. D Distribution of the extent of LGE in patients without myocardial bridging

Fig. 6

Kaplan–Meier analysis of the relationship of MB with survival free from all causes and cardiovascular mortality. Kaplan–Meier analysis did not identify a difference in all-cause death (A) or cardiovascular death (B) between patients with MB and those without MB