Ventricular preexcitation-induced subclinical LV dysfunction: Insights from pressure-strain loop imaging
Mingxia Li1, Fen Chen2, Jing Yao2
1Department of Ultrasound Medicine, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, Nanjing, Jiangsu, 210008, China.
Background:
Ventricular preexcitation causes subclinical LV dysfunction despite preserved LVEF. Pressure-strain loop (PSL) analysis, a novel method, sensitively quantifies myocardial work to assess such functional alterations. This study evaluated global and segmental myocardial work alterations by PSL in these patients.MethodsSeventy-seven patients with ventricular preexcitation (stratified into right-AP [n = 33], left-AP [n = 16], and septal-AP [n = 28] groups) and 25 controls underwent speckle-tracking echocardiography. Global longitudinal strain (GLS) and mechanical dyssynchrony indices-the standard deviation of time-to-peak strain (PSD) and maximal temporal difference (ΔT)-were quantified. PSL analysis derived myocardial work parameters (work efficiency [WE], constructive work [CW], wasted work [WW]) at global, basal-apex, and segmental levels, with focused assessment of six basal LV segments.
Results:
Septal AP and right AP demonstrated significantly increased global and basal-middle ventricular WW along with reduced WE compared to controls (all P < 0.01). Additionally, the GLS in right AP was mildly less negative than in controls (P < 0.05). PSD and ΔT were significantly elevated in the basal-middle ventricular levels of septal and right AP compared to controls (P < 0.05). Furthermore, PSD exhibited a moderate negative correlation with GWE (r = -0.59, P < 0.001). Multivariate linear regression analysis identified PSD as an independent factor associated with increased GWW (β = 1.71, P = 0.03), decreased GWE (β = -0.136, P < 0.001), and reduced GCW (β = -7.93, P < 0.001).
Conclusion:
PSL analysis effectively identifies subclinical left ventricular dysfunction in ventricular preexcitation patients with preserved LVEF, particularly pronounced in right-sided and septal accessory pathway subgroups. Ventricular mechanical dyssynchrony emerges as a key mechanistic contributor to these functional impairments, highlighting its pivotal role in early-stage electromechanical uncoupling.
