Assessment of ventricular systolic rotation and deformation in premature ventricular contractions of different origins via three-dimensional speckle tracking imaging

Introduction

Premature ventricular contractions (PVCs) are among the most common types of arrhythmias. They originate below the bundle of His bifurcation and cause premature myocardial depolarization (1). Clinical manifestations of PVCs vary among patients, ranging from asymptomatic presentation to palpitations, chest tightness, and, in rare cases, syncope. Symptoms are not necessarily correlated with prognosis. Recent studies (2,3) have demonstrated that frequent PVCs in patients without structural heart disease may lead to ventricular enlargement and a decline in cardiac function, potentially resulting in PVC-induced cardiomyopathy. Pundi and Marcus (3) proposed that PVCs frequency, characteristics, and patient risk factors are key predictors of PVC-induced cardiomyopathy. In patients without structural heart disease, high-frequency PVC (typically >10,000 times/24 hours) can lead to left ventricular enlargement and reduced contractility, which can be significantly reversed after ablation therapy. Clinically, left ventricular ejection fraction (LVEF) is commonly used to assess overall left ventricular systolic function. However, most patients with frequent PVCs and no structural heart disease have LVEF within the normal range, which limits clinical evaluation. Therefore, identifying early diagnostic and prognostic markers for PVCs of different origins is crucial.

Strain is a parameter reflecting myocardial deformation and is defined as the percentage change in the length of a myocardial segment over time (4) as follows: strain = (L – L₀)/L₀ × 100%, where L₀ represents the initial myocardial segment length, and L is the length after deformation. Strain can be positive or negative, indicating myocardial elongation or shortening, respectively. Strain rate measures the rate of myocardial strain over time and is calculated as follows: strain rate = (V₁ – V₂)/L, where V₁ and V₂ are velocities of two points within a myocardial segment, and L is the distance between them. Strain and strain rate provide localized myocardial deformation information, offering advantages over conventional echocardiographic parameters as they are not influenced by myocardial wall thickness or cardiac motion, thereby accurately reflecting myocardial function in different segments and directions. Compared to traditional echocardiographic parameters, strain and strain rate allow for the early detection of myocardial dysfunction and contribute to disease diagnosis, severity assessment, treatment selection, and prognosis evaluation.

Two ultrasound imaging techniques are used to measure myocardial strain and strain rate: Doppler tissue imaging (DTI) and speckle-tracking imaging (STI). DTI utilizes the scattering principle of ultrasound waves to analyze tissue echoes, tracking the speckle signals formed by myocardial fibers. DTI filters out high-frequency blood flow signals while preserving low-frequency myocardial wall motion signals, displaying a color-coded two-dimensional (2D) image. However, DTI-based strain and strain rate measurements remain operator-dependent, requiring significant expertise, thus limiting their clinical application.

STI, on the other hand, captures high-frame-rate grayscale ultrasound images, tracking speckles formed by myocardial tissue scattering and reflection across consecutive frames. This technique provides global and regional myocardial displacement and motion information, allowing for strain and strain rate calculation (5). STI exhibits minimal intra- and interobserver variability, making it more widely used in clinical practice as compared to DTI. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2024-2627/rc).

Methods

Research objectives

This study aimed to use STI technology to quantitatively analyze myocardial motion during sinus beats, PVC beats, and compensatory beats in individual patients, as well as to compare different PVC origins. The overall goal was to identify the myocardial deformation characteristics of PVCs originating from different locations, thus providing insights for early disease recognition, clinical treatment, and long-term follow-up.

Participants, materials, and methods

Participants

A total of 91 patients diagnosed with PVCs and hospitalized for radiofrequency ablation at The First Affiliated Hospital, Zhejiang University School of Medicine, between September 2016 and July 2017 were included (28 males and 63 females; mean age 47.7±14.8 years). The inclusion criteria (I) included confirmation of successful ablation (PVCs disappeared immediately after ablation, no recurrence was observed after 20 minutes, isoproterenol infusion failed to induce PVCs, and 24-hour Holter monitoring postablation showed a >75% reduction or complete resolution of PVCs as compared to baseline); (II) monomorphic PVCs, with PVC origin determined by the ablation site; and (III) routine physical and laboratory examinations showing no abnormalities apart from PVCs.

The exclusion criteria were as follows: (I) presence of structural heart disease as indicated by echocardiography (e.g., congenital heart disease, cardiomyopathy, and valvular heart disease); (II) positive exercise stress test or coronary artery abnormalities detected via computed tomography or angiography or a history of ischemic heart disease; and (III) heart failure classified as New York Heart Association (NYHA) class III–IV or LVEF <50%.

Equipment

A Vivid E9 color Doppler ultrasound system (GE HealthCare, Chicago, IL, USA) was used with a 2D M5S probe (frequency 2.0–4.5 MHz; frame rate 50–70 frames/s). The EchoPAC workstation (GE HealthCare) was used for offline analysis.

Measurement methods

Patients were placed in the left lateral decubitus position under calm breathing, with simultaneous chest lead electrocardiographic (ECG) recording. 2D grayscale dynamic images were obtained from the apical long-axis, four-chamber, two-chamber, and short-axis views at the mitral valve and apical levels. Each sequence included four consecutive cardiac cycles, capturing sinus, PVC, and compensatory beats, and was stored digitally.

The EchoPAC workstation (version 110.1.2) was used to analyze 2D strain during PVCs, compensatory beats, and sinus beats. The endocardium of six left ventricular long-axis and short-axis dynamic images was manually delineated, with the system automatically segmenting the left ventricular wall into endocardial, midmyocardial, and epicardial layers, which was followed by speckle tracking analysis for each layer. The region of interest was manually adjusted to ensure satisfactory tracking. The system automatically divided the left ventricular basal, mid, and apical segments into the following six sections for a total of 18 segments: the lateral wall, posterior septum, anterior wall, inferior wall, posterior wall, and anterior septum. For each segment, the system displayed strain curves and values for central systolic pressure (CS) and left ventricular peak systolic strain (LPS) (Figure 1). The system also computed global CS and LPS values for each myocardial layer, generating bullseye maps and calculating the standard deviation of left ventricular myocardial strain peak time (PSD) (Figure 2). For torsion analysis, left ventricular short-axis images at the basal and apical levels were analyzed. End-systolic images were frozen, and the endocardium was manually traced. The software then automatically generated apical/basal rotation angle (RotB)-time curves and left ventricular twist angle (TwistLV)-time curves based on preset parameters. Peak values of TwistLV, RotB, and apical rotation angle (RotA) were obtained (Figure 3), and the absolute difference between the peak timing of basal and apical rotation (RDA-B) was calculated. Similarly, right ventricular free wall strain and global ventricular longitudinal strain (GLS) were measured with the same methodology.

Figure 1 Global longitudinal strain values and strain curves of the ENDO, MID, and EPI layers of the left ventricle during a PVC rhythm (A) and during normal sinus rhythm (B). ANT, anterior; ENDO, endocardial; EPI, epicardial; FR, filling rate; GLPS, global longitudinal peak strain; HR, heart rate; INF, inferior; LAT, lateral; MID, midmyocardial; POST, posterior; PSD, the standard deviation of left ventricular myocardial strain peak time; PVC, premature ventricular contraction; SEPT, septal.

Figure 2 Global circumferential strain values and strain curves of the ENDO, MID, and EPI layers at the basal segment of the left ventricle during a PVC rhythm (A) and during normal sinus rhythm (B). AVC, aortic valve closure; ENDO, endocardial; EPI, epicardial; GS, global strain; MID, midmyocardial; PVC, premature ventricular contraction.

Figure 3 Peak values of TwistLV, RotB, and RotA during a PVC rhythm (A) and during normal sinus rhythm (B). AVC, aortic valve closure; RotA, apical rotation angle; RotB, basal rotation angle; PVC, premature ventricular contraction; TwistLV, left ventricular twist angle.

Statistical analysis

Statistical analyses were performed with SPSS 23.0 (IBM Corp., Armonk, NY, USA). Data are expressed as the mean ± standard deviation. Paired t-tests were used for within-participant comparisons, while one-way analysis of variance (ANOVA) and post hoc least significant difference (LSD) tests were employed for intergroup comparisons. A P value <0.05 was considered statistically significant.

Ethical considerations

This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments and was approved by the Clinical Research Ethics Committee of Shengzhou People’s Hospital (Shengzhou Branch of The First Affiliated Hospital, Zhejiang University School of Medicine) (No. 2024019). Informed consent was obtained from all participants.

Results

Distribution of PVC origin sites

Among the 91 included cases, 60 had origins from the right ventricular outflow tract (RVOT), including 12 from the suprapulmonary valve, 34 from the septal region, and 14 from the free wall. Thirteen cases had origins from the left ventricular outflow tract (LVOT). Other origins were found in 18 cases, including 5 from the left ventricular conduction system (3 from the left bundle of His, 1 from the left anterior fascicle, and 1 from the left posterior fascicle), 1 from the right ventricular conduction system (1 from the right bundle of His), 5 from the left ventricular papillary muscle (4 from the left anterior papillary muscle and 1 from the left posterior papillary muscle), 1 from the right ventricular papillary muscle (1 from the moderator band), 3 from the mitral annulus, and 3 from the tricuspid annulus (Figure 4).

Figure 4 Distribution of PVC origins of the included cases. LV, left ventricular; LVOT, left ventricular outflow tract; PVC, premature ventricular contraction; RVOT, right ventricular outflow tract.

Comparison of conventional echocardiographic parameters among sinus beat, PVC, and compensatory beat

At the sinus beat, the left ventricular internal diastolic diameter (LVIDd), E/A ratio, lateral wall e’, and E/e’ were 4.77±0.46 cm, 1.30±0.77, 0.15±0.15 m/s, and 7.32±2.50, respectively.

Except for left end-diastolic volume (LEDV), which showed significant differences between sinus beat and PVC as well as between PVC and compensatory beat, none of the parameters, including left ventricular end-systolic volume (LVESV), stroke volume (SV), LVEF, left ventricular Tei index (LVTei), right ventricular fractional area change (RVFAC), and tricuspid annular plane systolic excursion (TAPSE) showed significant differences among the three beats (Table 1).

Comparison of STI parameters across the three beats in the whole sample

Apart from the peak rotational angle of the left ventricular basal segment between sinus beat and compensatory beat (–5.36±4.51° vs. –5.40±4.58°, respectively; P=0.820), the time-to-peak difference between the left ventricular basal and apical rotations across the three beats (0.4±20.3 vs. –9.5±95.2 vs. 3.1±22.0 ms, respectively; P=0.142), and the peak radial strain of the left ventricular apex between sinus beat and PVC (18.6%±11.1% vs. 18.1%±12.6%, respectively; P=0.777), all STI parameters demonstrated statistically significant differences across the three beats (Table 2).

Comparison of STI parameters among the different origin groups at sinus beat

At sinus beat, significant differences between origin groups were observed only in peak rotational angle of the left ventricular apex (P=0.021), overall peak rotational angle of the left ventricle (P=0.043), and peak radial strain of the left ventricular apex (P<0.001) (Table 3).

Comparison of STI parameters among different origin groups at PVC

At PVC, significant differences between origin groups were observed only in peak radial strain of the left ventricular basal segment (P<0.001), standard deviation of the time to peak myocardial strain of the left ventricle (P=0.019), and overall peak longitudinal strain of the right ventricle (P=0.013) (Table 4).

Comparison of STI parameters among different origin groups at compensatory beat

At compensatory beat, significant differences between origin groups were observed only in mean peak circumferential strain of the left ventricular basal segment (P=0.021), peak circumferential strain of the left ventricular basal epicardium (P=0.023), and peak radial strain of the left ventricular apex (P=0.008) (Table 5).

Correlation between coupling interval and STI parameters

Coupling interval showed a strong positive correlation with overall peak longitudinal strain of the left ventricle (r=0.732), mean peak circumferential strain of the left ventricular basal segment (r=0.605), overall peak rotational angle of the left ventricle (r=0.557), and peak radial strain of the left ventricular basal segment (r=0.515) (all P values <0.001) (Table 6).

Discussion

PVCs are a common type of cardiac arrhythmia observed both in individuals without structural heart disease and in those with various underlying cardiac conditions. Epidemiological studies indicate that in routine ECG screenings, approximately 1% of the general population exhibit PVCs, while long-term Holter monitoring records PVCs in 70–75% of the population (6). The prevalence of PVCs is age-dependent, with an incidence of less than 1% in children under 11 years old (7), rising to over 69% in individuals older than 75 years (8). It is widely acknowledged that PVCs in patients with structural heart disease increase the risk of sudden cardiac death. Previously, frequent PVCs in individuals without structural heart disease were considered benign (6). However, recent studies (3) suggest that frequent PVCs may contribute to the development of an idiopathic form of dilated cardiomyopathy (9), as radiofrequency catheter ablation (RFCA) of PVCs has been shown to reverse some cases of unexplained dilated cardiomyopathy and improve cardiac function. Pundi and Marcus (3) proposed that PVC-induced cardiomyopathy is a subtype of secondary dilated cardiomyopathy, characterized by reversible heart function after ablation surgery.

Jose et al. (10) were the first to demonstrate improvement in LVEF in four patients with dilated cardiomyopathy and frequent PVCs (>20,000 PVCs/24 hours, origin unspecified) after antiarrhythmic therapy. The LVEF of these patients improved significantly from 27%±10% to 49%±17%, with one patient treated with β-blockers and three with amiodarone. Subsequent studies have shown similar LVEF improvements following RFCA in such patients (11). In 2010, Blaauw et al. (12) reported that in a study of patients with dilated cardiomyopathy undergoing RFCA for PVCs, the PVC burden decreased from 33%±14% to 1.9%±4.4% within 24 hours after ablation; simultaneously, LVEF improved from 35%±9% to 54%±10%. Notably, in five patients in whom ablation was unsuccessful, antiarrhythmic drug therapy (three with amiodarone) resulted in an increase in LVEF from 34%±4% to 47%±9%. Another comparative study reported that among 22 patients with dilated cardiomyopathy, RFCA successfully eliminated PVCs in 18 patients. After 6 months of follow-up, their LVEF improved from 35%±13% to 59%±7%, whereas those in whom ablation was unsuccessful and control patients showed no improvement in left ventricular function.

Long-term frequent PVCs can lead to structural cardiac changes, reduced cardiac output, and impaired myocardial contractility, ultimately resulting in PVC-induced cardiomyopathy. This significantly impacts long-term prognosis and quality of life. Therefore, accurate assessment of the impact of PVCs on cardiac function and early intervention and follow-up are crucial. ECG plays a key role in evaluating cardiac structure and function. Emerging technologies such as velocity vector imaging (VVI) and STI (12) can detect early PVC-induced myocardial dysfunction, assist in localizing ectopic pacemaker sites, guide RFCA, and predict long-term prognosis in individuals with PVC. Lan et al. (13) found that both speckle-tracking stratified strain and MW measurement may sensitively detect the impairment of left ventricular myocardial function at an early stage for patients with heart failure with preserved ejection fraction.

The precise mechanism by which frequent PVCs in patients without structural heart disease leads to cardiomyopathy remains unclear, although studies suggest a strong correlation between PVCs burden, location, and PVC-related cardiomyopathy (14). It is not yet well-established which patients with frequent PVCs, in the absence of structural heart disease, require pharmacological or RFCA therapy to prevent PVC-induced cardiomyopathy. Conventional echocardiographic assessments may not adequately reflect cardiac dysfunction in these patients. Identifying a sensitive and effective method for evaluating myocardial damage in patients with PVC is thus of paramount importance. This study employed three-dimensional (3D)-STI and PVC coupling intervals to quantitatively analyze myocardial function in patients with frequent PVCs, aiming to identify reliable indicators for detecting high-risk patients susceptible to PVC-induced cardiomyopathy and optimizing clinical management.

PVCs and left ventricular torsion

Left ventricular torsion refers to the rotational movement of the entire left ventricle, defined as the sum of the absolute values of apical and basal rotation. In normal individuals, left ventricular torsion is characterized by the counterclockwise rotation of the apex and clockwise rotation of the base during systole when viewed from the apex to the base. The left ventricular twist-displacement loop forms a characteristic figure-8 pattern (15). The helical arrangement of myocardial fibers is a key determinant of left ventricular torsion (16). With advances in myocardial mechanics research and the introduction of the myocardial band theory, the 3D architecture of myocardial fibers and the mechanisms governing left ventricular torsion have become increasingly well understood. The rotational movement of the left ventricular apex plays a crucial role in overall left ventricular torsion, likely related to the helical organization of myocardial fibers. Takeuchi et al. (17) used 2S STI to assess left ventricular torsion in myocardial infarction patients, demonstrating significantly reduced left ventricular torsion compared to normal controls, with a close correlation between left ventricular torsion indices, LVEF, and end-systolic left ventricular volume. Liu et al. (18) found that in patients with coronary artery disease (CAD), even those with normal LVEF, left ventricular torsion was already impaired, suggesting that left ventricular torsion abnormalities precede detectable reductions in LVEF and are associated with the extent and severity of ischemia. Wang et al. (19) applied STI to evaluate left ventricular torsion and untwisting under different pacing modes, showing that atrial pacing-ventricular pacing (APVP) reduced LVEF, decreased peak left ventricular apical rotation, increased the time delay between peak rotations of the basal and apical segments, and impaired untwisting. These findings suggest that APVP disrupts physiological left ventricular torsion and untwisting as compared to native atrioventricular (AV) conduction. Individuals with frequent PVCs exhibit similar characteristics to those with APVP pacing. Multiple studies (3,20) have demonstrated that frequent PVCs, even in individuals without structural heart disease, can lead to left ventricular dilation, impaired contractility, and ultimately PVC-induced cardiomyopathy (20). Pundi and Marcus (3) proposed that PVC load has a dose-effect relationship with cardiomyopathy, indicating that PVC frequency >24% is a high-risk predictor of cardiomyopathy and patients that without structural heart disease can also develop this condition. In our study found that, compared to sinus beats, PVCs resulted in significantly reduced peak left ventricular rotation angles; decreased circumferential, longitudinal, and radial strain; and prolonged standard deviation of time to peak myocardial strain. These findings confirm that frequent PVCs impair left ventricular torsion and untwisting, cause asynchronous basal-apical rotation, and diminish apical rotation capacity. Consequently, persistent frequent PVCs may induce left ventricular contraction dyssynchrony, systolic dysfunction, and ultimately PVC-induced cardiomyopathy.

Potential mechanisms of heart failure induced by frequent PVCs

The precise mechanisms by which frequent PVCs lead to cardiac dysfunction remain unclear. However, they may share similarities with the pathophysiological changes observed in patients with chronic right ventricular apical pacing. Frequent PVCs can cause both interventricular and intraventricular contraction dyssynchrony, leading to ventricular remodeling and impairing both systolic and diastolic function (21). Studies suggest that shortened coupling intervals and contraction dyssynchrony result in myocardial energy depletion, an imbalance in the endocardial-to-epicardial blood flow ratio, and relative myocardial ischemia (22,23), all of which may contribute to the development of heart failure.

Shortened coupling intervals of PVCs

The coupling interval is the time interval between a premature beat and the preceding normal sinus beat. In patients with frequent PVCs, shortened coupling intervals lead to reduced diastolic filling time, decreased ventricular preload, and subsequently, diminished cardiac output. Additionally, a shortened diastolic period reduces coronary perfusion time, leading to decreased myocardial blood flow, myocardial ischemia, sympathetic nervous system excitation, and activation of the renin-angiotensin-aldosterone system (RAAS), which collectively contribute to myocardial hypertrophy, fibrosis, and abnormal ventricular wall stress. During PVCs, there is an excessive accumulation of calcium within the sarcoplasmic reticulum, leading to increased calcium efflux and intracellular calcium overload. This results in persistent myocardial activation, known as diastolic spasm, which impairs ventricular diastolic function (24). An experimental study in canine models, in which pacemakers were implanted to simulate frequent PVCs, demonstrated increased myocardial apoptosis, mitochondrial dysfunction, and progressive myocardial fibrosis upon long-term follow-up (10). Our study also found a strong positive correlation between coupling intervals and several key parameters of left ventricular function, including global peak longitudinal strain, basal circumferential strain, overall rotational peak angle, and basal radial strain. Since myocardial strain is directly related to myocardial contractility, it provides a highly sensitive measure of regional myocardial function. Moreover, it can detect subclinical left ventricular dysfunction that may not be evident using conventional assessment methods. Wijnmaalen et al. (25) used 2D-STI to evaluate ventricular function in 49 patients with frequent PVCs and preserved LVEF. Their study revealed that frequent PVCs could induce subclinical systolic dysfunction, characterized by reduced strain in both the left and right ventricles. In another study, compared to LVEF and conventional wall motion scoring, left ventricular longitudinal strain was found to be a more sensitive marker for detecting early myocardial dysfunction (26). Our findings further confirm that shorter coupling intervals are associated with lower global peak longitudinal strain values, indicating more severe left ventricular systolic dysfunction. Therefore, shortening of the coupling interval may be one of the key mechanisms by which PVCs contribute to myocardial contractile impairment.

Left ventricular contraction dyssynchrony

Under normal physiological conditions, cardiac conduction originates from the sinoatrial (SA) node and propagates through the AV node, the His-Purkinje system, and into both ventricles, resulting in synchronized left and right ventricular contraction. However, during PVCs, an ectopic pacemaker located within the ventricle or interventricular septum discharges prematurely, triggering ventricular depolarization. This disrupts the normal sequence of myocardial activation and conduction, leading to ventricular contraction dyssynchrony and hemodynamic abnormalities. Akoum et al. (27) conducted an experimental study in which cardiac pacemakers were implanted in dogs to simulate frequent PVCs. After a 4-week follow-up, they observed a significant increase in left ventricular end-diastolic diameter and a marked reduction in LVEF as compared to baseline. Research has shown that contraction dyssynchrony can lead to reduced myocardial perfusion near the ectopic pacemaker site while increasing perfusion in areas of delayed depolarization (28). Prolonged ventricular contraction dyssynchrony may result in asymmetric myocardial hypertrophy, with myocardial thinning near the ectopic pacemaker site and thickening in areas of delayed depolarization (10). Long-term follow-up studies of patients with chronic right ventricular apical pacing have demonstrated that persistent ventricular contraction dyssynchrony leads to increased left ventricular end-diastolic diameter and a significant reduction in LVEF over time. Similarly, frequent PVCs can cause abnormal electrical activity and ventricular dyssynchrony, ultimately leading to ventricular remodeling, left ventricular dilation, and impaired cardiac function. The impact of PVCs on cardiac ejection function varies depending on their site of origin, as different activation sequences result in different hemodynamic effects. This study confirmed that compared to sinus beats, PVCs are associated with a significant reduction in peak left ventricular rotational angle, as well as decreases in circumferential, longitudinal, and radial strain. Additionally, the standard deviation of time-to-peak myocardial strain was markedly prolonged. These findings indirectly confirm that PVCs lead to ventricular contraction dyssynchrony and that persistent frequent ectopic electrical activity contributes to left ventricular structural remodeling and impaired systolic function.

Application of 2D-STI in the assessment of cardiac function in patients with PVC

There is currently a lack of specific clinical indicators for predicting heart failure in patients with PVCs. Therefore, early assessment and long-term follow-up of cardiac function in these patients are crucial. Although most patients with frequent PVCs have a normal LVEF, this is not a sensitive indicator for detecting early left ventricular systolic dysfunction and may not accurately reflect the impact of frequent PVCs on left ventricular contractility (29). Myocardial strain is a direct and objective measure of myocardial contractility, as it quantifies myocardial deformation rather than displacement, making it independent of passive stretching and a reliable reflection of regional myocardial function. Two dimensional STI is an advanced echocardiographic technique that tracks speckle patterns in the myocardium over sequential frames of 2D ultrasound images. By selecting a region of interest within the myocardial wall, the software automatically tracks grayscale speckles over the cardiac cycle, comparing their positions frame by frame to calculate myocardial strain in different segments. Since speckle-tracking technology is not dependent on Doppler frequency shifts, it is unaffected by the angle between the ultrasound beam and myocardial motion, eliminating angle dependency. This feature renders 2D-STI particularly useful in detecting the subtle, subclinical myocardial dysfunction caused by frequent PVCs. Zhang et al. (30) used 2D-STI to evaluate the impact of PVCs on cardiac function in 60 patients with PVCs originating from different sites and 30 healthy controls. They analyzed myocardial strain during sinus rhythm and PVC beats separately. Although there was no significant difference between the PVCs and control groups during sinus rhythm, strain values were significantly lower during PVC beats. Furthermore, patients with PVCs originating from the aortic sinus had lower strain values in the basal anterior septum, posterior septum, and inferior wall as compared to those with PVCs from the RVOT or tricuspid annulus. Wijnmaalen et al. (25) applied 2D-STI to assess ventricular function in 49 patients with frequent PVCs and normal LVEF. They found that frequent PVCs led to subclinical ventricular dysfunction, primarily characterized by decreased left and right ventricular strain. After successful RFCA, these impaired strain indices improved to normal levels. Nie et al. (31) investigated the effects of RFCA on patients with frequent PVCs and preserved LVEF using 2D-STI. Among 32 patients who underwent successful RFCA, postprocedural follow-up showed a significant reduction in PVC burden. Although there was no substantial change in LVEF or left ventricular end-diastolic diameter, left ventricular short-axis, long-axis, and circumferential strain improved significantly compared to preablation levels. These findings suggest that 2D-STI can help detect early, subclinical myocardial dysfunction in patients with PVC and assist in evaluating RFCA outcomes, guiding appropriate treatment and follow-up strategies.

This study further demonstrated that 3D-STI provides a quantitative assessment of myocardial motion in patients with frequent PVCs. Compared to conventional parameters such as LVEF, left ventricular torsion and strain-related indices obtained from 3D-STI are more sensitive in the detection of early myocardial dysfunction in patients with PVC. These advanced imaging techniques may facilitate the early identification of subclinical myocardial impairment, optimize RFCA treatment assessment, and guide clinical management and follow-up strategies.

Conclusions

• Compared to sinus beat, both left and right ventricular systolic function are impaired during PVC, while compensatory beats demonstrate better systolic function than do sinus beats.
• Peak longitudinal strain of the left ventricle, peak radial strain of the left ventricular basal segment, standard deviation of the time to peak myocardial strain of the left ventricle, and overall peak longitudinal strain of the right ventricle serve as early sensitive indicators of PVC-induced myocardial dysfunction.
• The coupling interval is strongly positively correlated with overall peak longitudinal strain of the left ventricle, mean peak circumferential strain of the left ventricular basal segment, overall peak rotational angle of the left ventricle, and peak radial strain of the left ventricular basal segment, suggesting that a shortened coupling interval may be a critical risk factor for PVC-induced heart failure.
• 3D-STI can provide quantitative analysis of myocardial motion in patients PVC, aiding in the early detection of myocardial dysfunction and guiding treatment and follow-up strategies.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-2024-2627/rc

Data Sharing Statement: Available at https://qims.amegroups.com/article/view/10.21037/qims-2024-2627/dss

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2024-2627/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The trial was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the clinical research ethics committee of Shengzhou People’s Hospital (Shengzhou Branch of TheFirst Affiliated Hospital, Zhejiang University School of Medicine) (No.2024019), and informed consent was taken from all individual participants.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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