Key result
Normal-thickness myocardium in HCM shows impaired radial diastolic peak strain rates versus healthy controls.
Why the study?
Myocardial strain is a sensitive indicator of mechanical changes in hypertrophic cardiomyopathy, but myocardial mechanics in segments of normal wall thickness (< 12 mm) have not been well studied.
Does cardiac magnetic resonance-tissue tracking detect diastolic dysfunction in normal-thickness wall segments of patients with hypertrophic cardiomyopathy compared to controls?
Case-Control (n=93)
No
Does cardiac magnetic resonance-tissue tracking detect diastolic dysfunction in normal-thickness wall segments of patients with hypertrophic cardiomyopathy compared to controls?
Absolute Event Rate: -2.43% vs -2.67%
p-value: p=0.002
CMR tissue tracking reveals that diastolic mechanical dysfunction precedes morphological thickening and systolic dysfunction in normal-thickness myocardial segments of patients with hypertrophic cardiomyopathy.
May indicate preclinical diastolic dysfunction in HCM; hypothesis-generating and requires prospective validation before clinical use.
OBJECTIVES: Myocardial strain is reported to be a sensitive indicator of myocardial mechanical changes in patients with hypertrophic cardiomyopathy (HCM). The changes in the mechanics of the myocardium of normal wall thickness (< 12 mm) have yet to be well studied. This study aimed to evaluate the function of myocardial segments of normal thickness in patients with HCM. METHODS: Sixty-three patients with HCM and 30 controls were retrospectively enrolled in this retrospective study. Cine imaging, native and post-contrast T1 maps, T2 maps, and late gadolinium enhancement were performed. In addition, regional myocardial strain was assessed by cardiac magnetic resonance-tissue tracking. Strain parameters were compared between the controls and HCM patients with segments of the myocardium of normal thickness. Subgroup analysis was conducted in obstructive and non-obstructive HCM. Lastly, p < 0.05 was considered statistically significant. RESULTS: In normal-thickness myocardial segments of HCM (n = 716), diastolic peak strain rates (PSRs) were significantly lower than in the control group (n = 480) (radial, - 2.43 [- 3.36, - 1.78] vs. - 2.67 [- 3.58, - 1.96], p = 0.002; circumferential, 1.28 [1.01,1.60] vs. 1.39 [1.14, 1.78], p < 0.001; and longitudinal, 1.16 [0.75,1.51] vs. 1.28 [0.90, 1.71], p < 0.001). The normal-thickness segments showed no significant difference in systolic PSRs between HCM and the controls. In the subgroup analysis, significantly decreased diastolic PSRs were noted in both obstructive and non-obstructive HCM, compared with the controls (p < 0.05). CONCLUSIONS: Diastolic changes in myocardial mechanics were observed in normal-thickness segments of HCM, occurring before morphological remodeling and systolic dysfunction developed. This finding contributed to a better understanding of the mechanical pathophysiology of HCM with preserved left ventricular ejection fraction. It may potentially aid in predicting disease progression and risk stratification.
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Qiao et al. (2023) conducted a case-control in Hypertrophic cardiomyopathy (n=93). Hypertrophic cardiomyopathy vs. Healthy controls was evaluated on Radial diastolic peak strain rate (1/s) in normal-thickness myocardial segments (p=0.002). In normal-thickness myocardial segments of patients with hypertrophic cardiomyopathy, radial diastolic peak strain rates were significantly impaired compared to healthy controls (-2.43 vs. -2.67, p=0.002).
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