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. 2015 Oct;8(5):1194-200.
doi: 10.1161/CIRCEP.115.003047. Epub 2015 Aug 21.

Abnormal Left Ventricular Mechanics of Ventricular Ectopic Beats: Insights Into Origin and Coupling Interval in Premature Ventricular Contraction-Induced Cardiomyopathy

Jonathan Potfay  1 , Karoly Kaszala  1 , Alex Y Tan  1 , Adam P Sima  1 , John Gorcsan 3rd  1 , Kenneth A Ellenbogen  1 , Jose F Huizar  2
Affiliations

Abnormal Left Ventricular Mechanics of Ventricular Ectopic Beats: Insights Into Origin and Coupling Interval in Premature Ventricular Contraction-Induced Cardiomyopathy

Jonathan Potfay et al. Circ Arrhythm Electrophysiol. 2015 Oct.

Abstract

Background: Left ventricular (LV) dyssynchrony caused by premature ventricular contractions (PVCs) has been proposed as a mechanism of PVC-induced cardiomyopathy. We sought to understand the impact of different PVC locations and coupling intervals (prematurity) on LV regional mechanics and global function of the PVC beat itself.

Methods and results: Using our premature pacing algorithm, pentageminal PVCs at coupling intervals of 200 to 375 ms were delivered from the epicardial right ventricular apex, RV outflow tract, and LV free wall, as well as premature atrial contractions, from the left atrial appendage at a coupling interval of 200 ms in 7 healthy canines. LV short-axis echocardiographic images, LV stroke volume, and dP/dtmax were obtained during all ectopic beats and ventricular pacing. LV dyssynchrony was assessed by dispersion of QRS-to-peak strain (earliest-last QRS-to-peak strain) between 6 different LV segments during each of the aforementioned beats (GE, EchoPac). LV dyssynchrony was greater during long-coupled rather than short-coupled PVCs and PVCs at 375 ms compared with rapid ventricular pacing at 400 ms (P<0.0001), whereas no difference was found between PVC locations. Longer PVC coupling intervals were associated with greater stroke volume and dP/dtmax despite more pronounced dyssynchrony (P<0.001).

Conclusions: PVCs with longer coupling intervals demonstrate more pronounced LV dyssynchrony, whereas PVC location has minimal impact. LV dyssynchrony cannot be attributed to prematurity or abnormal ventricular activation alone, but rather to a combination of both. This study suggests that late-coupled PVCs may cause a more severe cardiomyopathy if dyssynchrony is the leading mechanism responsible for PVC-induced cardiomyopathy.

Keywords: cardiomyopathies; heart ventricles; stroke volume; ventricular dysfunction, left; ventricular premature contraction.

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Conflict of interest statement

Conflict of Interest Disclosures: Dr. Kaszala receives research support from Medtronic, Inc. Dr. Tan receives research support from Boston Scientific Corp. and Biotronik, Inc. Dr. Ellenbogen receives research support from Boston Scientific Corp., Biosense Webster, Medtronic, Inc., St. Jude Medical and NIH; he is a consultant for Boston Scientific Corp., St. Jude Medical., Atricure, and also receives honoraria from Medtronic, Inc., Boston Scientific Corp., Biotronik, Inc., Biosense Webster and Atricure. Dr. Gorcsan III receives research support from GE, Medtronic, and Biotronik. Dr. Huizar received research support from Boston Scientific Corp., Biotronik, Inc. and St. Jude Medical.

Figures

Figure 1
Figure 1
(a) LV dyssynchrony (QRS-to-Peak LV radial strain), (b) stroke volume, and (c) dP/dtmax in premature ventricular beats (PVC) by different coupling intervals (200, 250,300, 375ms) and rapid ventricular paced beats (400ms) from RV, RVOT and LV free wall, as well as premature atrial beats (PACs) at 200ms (R-R interval 290–430ms). RV= RV apex, RVOT= RV outflow tract, LV = LV free wall.
Figure 2
Figure 2
(a) LV dyssynchrony (QRS-to-Peak LV radial strain), (b) stroke volume and (c) dP/dtmax in premature ventricular beats (PVC) arranged by different origin (RV, RVOT and LV) at 200, 250, 300 and 375ms and rapid pacing (RP) at 400ms, in addition to premature atrial beats (PAC) at 200ms (R-R interval 290–340ms). RV= RV apex, RVOT= RV outflow tract, LV = LV free wall.
Figure 3
Figure 3
Segmental LV radial strain during a (a) short-coupled LV PVC at 200ms, (b) long-coupled LV PVC at 375ms, (c) LV rapid VP at 400ms, (d) PAC at 200ms, (e) normal intrinsic beat. Direct visualization of contraction and radial strain in a short-coupled PVC (Panel a) demonstrate those segments near the origin of an early or short-coupled PVCs (LV free wall in green and light blue) have their peak maximum contraction immediately after peak contraction of the preceding intrinsic beat, which appears as a long fused peak contraction between intrinsic and PVC beat in segments near PVC origin. Few milliseconds later, the peak contraction of segments away from PVC origin (septal segments in red and dark blue) is noted while the first segments (near PVC origin) start relaxation (Supplemental Video 1). In contrast, segments near the origin of a late-coupled PVC (Panel b) have their peak radial strain after relaxation of the preceding intrinsic beat is almost completed, causing dyskinesia of the opposite segments, while the segments away from PVC origin have their peak contraction when the segments near PVC origin have already completed relaxation, leading to a visually apparent LV dyssynchrony (Supplemental Video 2). Yellow dot marks QRS of a normal intrinsic beat with a peak radial strain (yellow arrow) that occurs at least around 250ms after beginning of QRS. Red arrow marks QRS initiation of LV PVC in panel “a” and “b” (200, 375ms coupling interval) and PAC (200ms) in panel “d”. White arrow in panel “c” denotes the initiation of VP beat at 400ms. White dotted line marks dispersion of QRS-to-peak strain in all panels. Left lower quadrant in all panels is a representation of radial strain in all 6 segments (Y axis) plotted by time (X axis), with red color representing the peak radial strain (contraction) and blue color indicating the lowest radial strain (greatest relaxation).
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