Comprehensive cardiac magnetic resonance imaging in patients with idiopathic premature ventricular contractions: role of feature-tracking strain and T1/T2 mapping in detecting subclinical myocardial dysfunction

Introduction

Premature ventricular contractions (PVCs) are common both in individuals with and those without structural heart disease (1-4). Although frequent occurrence of PVCs is associated with an elevated risk of sudden and total cardiac death even in the absence of demonstrable underlying disease (5-9), whether an underlying structural substrate is present in these patients—and its characteristics—remains unclear (10-13).

Evaluation of patients with PVCs typically begins with transthoracic echocardiography (TTE), as recommended by major societal guidelines (14-19). However, conventional TTE has limited sensitivity for detecting subtle arrhythmogenic substrates, leaving a controversy as whether advanced imaging is needed in select cases (16). Cardiac magnetic resonance (CMR), particularly late gadolinium enhancement (LGE), has proven invaluable for identifying focal scar and stratifying arrhythmic risk (12,20). However, a significant proportion (54–85%) of patients experiencing PVCs show no LGE or obvious structural abnormalities on routine imaging (21-24).

Comprehensive CMR extends beyond LGE, incorporating techniques for the quantification of diffuse tissue pathology through native T1 and T2 mapping, which can detect interstitial fibrosis and edema (25). Although these techniques show promise in the characterization of the arrhythmic substrate in known structural heart disease (26-28), their role for idiopathic PVCs remains less defined. Similarly, CMR feature-tracking (FT) strain analysis offers a sensitive measure of systolic function but remains underinvestigated in the context of ventricular arrhythmias (VAs) (13,29-32).

Given the potential of comprehensive CMR to detect early tissue alterations, we conducted a systematic evaluation in patients with idiopathic PVC and normal CMR findings. This exploratory study aimed to determine whether advanced CMR parameters can reveal subtle myocardial abnormalities and to investigate their potential association with PVC burden. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1190/rc).

Methods

Ethical considerations

This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments and was approved by the Ethics Review Committee of Shanghai General Hospital (No. 2023364). The requirement for informed consent was waived due to the retrospective nature of the study.

Participant population and study design

In this single-center, retrospective study conducted at Shanghai General Hospital, eligible patients (October 2017–December 2024) were identified through a systematic query of the institutional electronic medical records. The search encompassed a broad spectrum of patients evaluated at our tertiary center, which included both referred individuals and those presenting directly for evaluation. The inclusion criteria were (I) documented PVCs on 24-hour Holter monitoring and (II) CMR examination performed within 7 days of Holter monitoring. Meanwhile, the exclusion criteria were as follows: (I) any form of structural heart disease (including but not limited to cardiomyopathies, significant valvular heart disease, congenital heart disease, or any other cardiac structural abnormality), ischemic cardiomyopathy, and mild-to-severe coronary atherosclerosis (any coronary artery stenosis ≥25%), or left ventricular ejection fraction (LVEF) <50%; (II) myocarditis or pericardial disease; (III) any systemic diseases that could affect the heart, such as hypertension, diabetes mellitus, connective tissue disease, and hyperthyroidism; (IV) electrocardiogram findings of multifocal PVC or atrioventricular blocks; (V) delayed myocardial contrast enhancement in CMR imaging; (VI) structural or functional abnormalities detected by cardiac ultrasound; (VII) previous administration of radiofrequency or alcohol ablation; (VIII) poor or incomplete images; and (IX) a family history of cardiomyopathy or premature sudden death or a history of prior cardiac arrest or persistent ventricular tachycardia. Based on these classification criteria, 72 adult patients were included in the final analysis. The patients were divided into three groups based on the number of PVCs within a 24-hour period (<500 PVCs, 500–10,000 PVCs, and >10,000 PVCs). The control group comprised 25 individuals who underwent CMR (e.g., for evaluation of atypical chest pain or palpitations) and were confirmed to have completely normal cardiac structure, function, absence of LGE, and normal T1/T2 mapping values. Moreover, none of the controls demonstrated evidence of PVCs on 24-hour Holter monitoring or met any of the study’s exclusion criteria.

CMR studies

A standardized CMR protocol was maintained throughout the study period to ensure technical consistency. All examinations were performed on a 3.0-T Ingenia scanner (Philips Healthcare, Amsterdam, the Netherlands) with a dStream torso coil and vector-electrocardiographic gating. The protocol included (I) cine imaging for ventricular function and strain analysis; (II) native T1 and T2 mapping for tissue characterization; and (III) LGE for focal fibrosis assessment. Cine images were acquired with a balanced steady-state free precession (SSFP) sequence during repeated breath-holds at end expiration, which covered the long-axis (two-, three-, and four-chamber) and short-axis (stacked from base to apex) planes. The typical sequence parameters were as follows: slice thickness =8 mm, repetition time/echo time =2.8–3.2/1.4–1.5 ms, flip angle =45°; matrix size =[160–176]×[138–192], field of view =300×300 to 350×350 mm², and temporal resolution =15–25 ms. For LGE imaging, acquisitions commenced 10–15 minutes after intravenous administration of 0.2 mmol/kg of gadopentetic acid with a phase-sensitive inversion recovery sequence. Native T1 mapping was performed precontrast with a modified Look-Locker inversion recovery sequence in short-axis views. T2 mapping was acquired with a T2-prepared SSFP sequence with T2-preparation times of 0, 30, and 55 ms.

All image analyses were performed via CVI42 software version 5.17.1 (Circle Cardiovascular Imaging, Calgary, Canada) by an experienced observer blinded to clinical data. Left ventricular (LV) volumes, ejection fraction, and mass were quantified from short-axis cine stacks. For FT strain analysis, endocardial and epicardial contours were semiautomatically traced on cine images, with manual adjustments being applied as needed. Global and segmental peak systolic strain parameters (longitudinal, circumferential, and radial) were derived in two-dimensional (2D) and three-dimensional (3D). For tissue characterization, T1 and T2 maps were generated, and values were automatically sampled from the 16 American Heart Association segments (excluding the apex), with global and regional (basal, mid, and apical) averages calculated for analysis.

Inter- and intraobserver reproducibility

To assess interobserver reproducibility, 20 randomly selected participants (10 patients and 10 controls) were reanalyzed by a second blinded observer. To assess intraobserver reproducibility, the primary observer reanalyzed the same 20 participants after a washout period of at least 4 weeks.

Statistical analysis

Statistical analyses were performed with SPSS version 25 (IBM Corp., Armonk, NY, USA). Missing data for specific parameters were handled via exclusion of cases on an analysis-by-analysis basis; each test was performed with all available data for the relevant variables. Normally distributed continuous data are presented as the mean ± standard deviation, nonnormally distributed data as the median with interquartile range, and categorical data as frequencies (percentages). Group comparisons were performed via one-way analysis of variance or the Kruskal-Wallis test, as appropriate, with a two-tiered approach to control for multiple comparisons: first, false-discovery rate (FDR) correction was applied to P values from omnibus tests within prespecified parameter families (strain parameters and T1/T2 mapping parameters), with an FDR-corrected P value (Q value) <0.05 being considered significant. Second, for parameters surpassing this threshold, post hoc pairwise comparisons were conducted via the Tukey test (parametric) or Dunn test with Bonferroni adjustment (nonparametric). Associations between PVC burden and CMR parameters were assessed with Spearman rank correlation and partial correlation analyses (with adjustments for age, sex, and LV volumes); meanwhile, burden-dependent trends were evaluated with the Jonckheere-Terpstra test, with a two-sided P value (or Q value) <0.05 being considered statistically significant.

Results

Patient demographics

Among the 288 patients who initially met the inclusion criteria, 216 were excluded base on the predefined criteria, resulting in a final cohort of 72 patients with idiopathic PVC and 25 controls (Figure 1). The baseline characteristics are summarized in Table 1. Groups were well-balanced in terms of age, sex, and clinical comorbidities. The only exception was LV end-systolic volume (ESV), which was significantly higher in both the medium- (10,000–500 PVC/24 h) and high-burden (>10,000 PVC/24 h) groups than in the control group (P<0.05). Consistent with this, Spearman correlation analysis indicated weak positive correlations between PVC burden and both LV-ESV (r=0.258) and LV end-diastolic volume (EDV; r=0.261) (Figure S1).

Figure 1 Patient flowchart. The flowchart shows the enrollment of patients and healthy controls. CMR, cardiac magnetic resonance; PVC, premature ventricular contraction.

Notably, the four patients in the high-burden group who were on antiarrhythmic medication at the time of assessment still exhibited a high PVC burden, indicating ineffective control. Following CMR, 2 patients in the medium-burden group and 21 in the high-burden group underwent a cardiac electrophysiological examination. Analysis of available Holter records (n=54) indicated that PVCs predominantly presented with a left bundle branch block morphology (43/54, 79.6%), consistent with a right ventricular origin. In the subgroup with electrophysiological data (n=23), the right ventricular outflow tract (RVOT) was the most common site of origin (16/23, 69.6%).

Global and segmental strain analysis in patients with PVC and healthy controls

As shown in Figure 2 and Table S1, comprehensive strain analysis revealed a distinctive pattern of myocardial dysfunction in patients with a high PVC burden (>10,000 PVC/24 h). After FDR correction, significant impairments were first identified at the global level, with this group exhibiting reduced 2D global radial strain (GRS), 2D global circumferential strain (GCS), and 3D-GCS compared to both the control group (P<0.01) and the low-burden (<500 PVC/24 h) group (P<0.05). Segmental analysis further localized the most prominent alterations to the apical segments, with 2D apical radial strain (ARS) and 2D apical circumferential strain (ACS) were being reduced (P<0.01 and P<0.001, respectively), highlighting the apex as a key region of myocardial involvement.

Figure 2 Comparison of 2D left ventricular strain parameters. (A) GRS; (B) BRS; (C) MRS; (D) ARS; (E) GCS; (F) BCS; (G) MCS; (H) ACS; (I) GLS; (J) BLS; (K) MLS; (L) ALS. Data are shown for healthy controls and groups stratified by PVC burden (<500, 500–10,000, >10,000 PVC/24 h). *, P<0.05; **, P<0.01; ***, P<0.001 (Jonckheere-Terpstra test). ACS, apical circumferential strain; ALS, apical longitudinal strain; ARS, apical radial strain; BCS, basal circumferential strain; BLS, basal longitudinal strain; BRS, basal radial strain; GCS, global circumferential strain; GLS, global longitudinal strain; GRS, global radial strain; MCS, mid-circumferential strain; MLS, mid-longitudinal strain; MRS, mid-radial strain; PVC, premature ventricular contraction.

The biological relevance of these findings was strongly supported by a consistent, burden-dependent decrease across the vast majority of strain parameters, as evidenced by significant Jonckheere-Terpstra tests (P values ranging from <0.001 to <0.05). This trend was also present in several longitudinal strain parameters [e.g., 2D global longitudinal strain (GLS) and 3D-GLS], which while not meeting the significance threshold for specific intergroup comparisons after FDR correction, demonstrated a clear progression of worsening function with increasing PVC burden.

Spearman correlation and partial correlation analyses investigated the association between global and partial correlation parameters and PVC burden. The results of the simple correlation analysis indicated a moderate correlation (correlation coefficient >0.3) between 2D-GRS, 2D-ARS, 2D-GCS, 2D-ACS, 2D-GLS, 3D-GCS, 3D basal circumferential strain (BCS), 3D mid-circumferential strain (MCS), and PVC burden. This correlation remained significant after age and sex were controlled for. When the EDV and ESV related to PVC burden were excluded, the correlation coefficients were slightly reduced; however, 2D-ARS, 2D-ACS, 3D-GCS, and 3D-BCS still exhibited a moderate significant correlation with PVC burden (Figure 3 and Figure S1).

Figure 3 Simple and partial Spearman correlation between strain parameters and PVC burden. (A) Simple correlation coefficients. (B,C) Partial correlation coefficients. *, P<0.05; **, P<0.01; ***, P<0.001. 2D, two-dimensional; ACS, apical circumferential strain; ALS, apical longitudinal strain; ARS, apical radial strain; BCS, basal circumferential strain; BLS, basal longitudinal strain; BRS, basal radial strain; EDV, end-diastolic volume; ESV, end-systolic volume; GCS, global circumferential strain; GLS, global longitudinal strain; GRS, global radial strain; MCS, mid-circumferential strain; MLS, mid-longitudinal strain; MRS, mid-radial strain; PVC, premature ventricular contraction.

Global and segmental LV myocardial native T1 and T2 values

Native T1 values were available for 48 patients with PVC, while T2 values were available for 55 patients with PVC. The mean global and segmental LV myocardial T1 and T2 values are presented in Tables 2,3 and Figure 4. The bull’s-eye plots in Figure 5 illustrate the average septal and free-wall segments of the LV myocardial T1 and T2 values, while Figure 6 presents a typical example.

Figure 4 Global and segmental native T1 and T2 values of LV. (A) Line charts of native T1 values. (B) Line charts of T2 values. (C) Bar charts of native T1 values. (D) Bar charts of T2 values. Lines represent mean values and error bars represent standard deviation. *, P<0.05; **, P<0.01; ***, P<0.001. LV, left ventricular.

Figure 5 Bull’s-eye plots displaying the mean regional LV myocardial T1 and T2 values for the control and PVC cohorts. The native T1 values (ms) are shown in red, while the native T2 values are in blue. The plots include the septal and free-wall regions of the basal (outer ring), mid-cavity (middle ring), and apical (central ring) planes. LV, left ventricular; PVC, premature ventricular contraction.

Figure 6 CMR mapping and measurement. Top row: a healthy control (a 61-year-old female patient). Bottom row: a patient with PVCs (a 66-year-old female patient; burden 25%; 34,510/24 h). (A,E) T1 mapping. (B,F) Bull’s-eye plots of T1 mapping. (C,G) T2 mapping. (D,H) Bull’s-eye plots of T2 mapping. CMR, cardiac magnetic resonance; PVC, premature ventricular contraction.

Patients with >10,000 PVC/24 h exhibited a statistically significant increase in LV global T1 values (P<0.001). Furthermore, segmental analysis of LV T1 values indicated a statistically significant increase across all segments, with the exception of the interventricular apical segments. Notably, within the interventricular basal segments, the T1 values in the high-burden group showed a significant increase compared to both the control and low-burden groups (both P values <0.01). Similarly, LV global myocardial T2 values exhibited a significant increase, with robust statistical significance (P<0.001). Segmental analysis of T2 values indicated a statistically significant increase in the basal and mid-segments, covering both septal and free wall segments (P=0.002–0.020).

The Jonckheere-Terpstra test indicated a significant upward tendency in both T1 and T2 values with increased PVC frequency (P≤0.011 for global, basal, and midventricular segments). Apical segments showed a similar but weaker tendency (P=0.015–0.045).

Data reproducibility

All measures of strain and mapping demonstrated moderate-to-excellent reliability for intra-and interobserver variability [intraclass correlation coefficient (ICC) 0.626–0.993]. Table S2 summarizes the ICC values for both intra- and interobserver reproducibility.

Discussion

This study identified a novel, burden-dependent myocardial phenotype in patients with idiopathic PVCs and normal CMR findings. The phenotype is characterized by (I) impaired LV strain, most consistently in global/apical circumferential and radial directions; and (II) elevated native T1 and T2 values, predominantly in the basal and midventricular segments. Collectively, these patterns suggest that the observed alterations may represent concomitant subclinical systolic dysfunction and interstitial changes.

CMR-FT-based strain parameters

Research on the association between CMR-FT strain analysis and PVCs remains limited and inconclusive. A previous study involving 42 patients with PVCs (>10/h) or nonsustained ventricular tachycardia (NSVT) and structurally normal hearts reported altered segmental radial and circumferential strains in the basal and mid-LV segments, alongside reduced longitudinal strain in the mid-LV segments (32). Another CMR-FT analysis reported impaired LV GRS and GCS in patients with frequent PVCs (≥500/24 h) or NSVT, although no statistically significant differences in LV GLS were observed between patients and controls (13). The heterogeneity in these findings likely stems from differences in the patient selection criteria and the multifactorial nature of myocardial strain alterations. Our study sought to clarify this picture by implementing rigorous inclusion criteria and stratifying patients based on 24-hour PVC burden, consistent with established clinical guidelines (4,18).

In this context, our findings both confirm and extend previous observations. We found impaired global LV 2D strain (2D-GRS and GCS) and 3D strain (3D-GCS) in patients with >10,000 PVC/24 h than in controls, which aligns with previous findings of GRS and GCS impairment in patients with frequent PVCs (13). A key point of consistency is the relative sparing of GLS, for which we also observed no significant differences between groups, only a tendency toward a decrease, consistent with previous work (33). This recurring pattern across studies suggests a particular susceptibility of patients with circumferential and radial deformation to PVC-induced dyssynchrony. The mechanism underlying this relationship may involve the intrinsic mechanics of ventricular contraction. In the normal heart, the majority of the myocardium exhibits relatively low longitudinal deformation (34). It has been proposed that asynchronous electrical activation, such as that from PVCs, could introduce disproportional alterations in the timing and pattern of wall thickening and shortening, potentially affecting circumferential and radial strains to a greater extent than longitudinal strains (35-37). Therefore, while strain analysis broadly demonstrates an ability to detect subtle contractile impairments in high-burden PVC patients, the choice of specific strain parameters is critical.

Our analysis identified two potential pathways through which PVC burden may influence myocardial strain. First, we observed that higher PVC burden was weakly correlated with increased LV volume (EDV and ESV), and this volumetric change appeared to contribute to a generalized reduction in myocardial strain. Second, and more notably, the correlation between PVC burden and certain strain parameters—particularly global strains and apical radial/circumferential strain (ARS and ACS)—remained significant after LV volumes were accounted for. This indicates a direct relationship between PVC burden and myocardial dysfunction that is independent of gross structural remodeling. The most pronounced impairments were consistently localized to the apical segment, a region of complex mechanics that may be uniquely vulnerable to the dyssynchronous activation patterns of PVCs, due to its shape, curvature, and fiber architecture (38-40).

Myocardial tissue characteristics of patients with PVCs

In patients with a high PVC burden, the observed reduction in strain accompanied by increased ventricular volumes suggests the presence of subclinical myocardial injury. Such impaired cardiac function has previously been linked to increased myocardial stiffness (41,42). Although LV myocardial replacement fibrosis, detectable by LGE, is a recognized marker of maladaptive remodeling (43), our study focused on the earlier, diffuse tissue changes that precede overt scar formation. Myocardial fibrosis and inflammatory edema are interrelated processes that drive LV remodeling and dysfunction (44). Although elevated T1 or T2 mapping values have been associated with VA in established cardiomyopathies (27,28), the myocardial tissue characteristics in patients with idiopathic PVCs but otherwise normal hearts remain largely unexplored.

In our study, patients with >10,000 PVC/24 h exhibited higher native T1 and T2 values, particularly in the basal segments, as compared to healthy controls. In the context of normal conventional imaging, these variations are consistent with the presence of myocardial interstitial pathology, such as edema or fibrosis. Thus, beyond functional strain analysis, CMR mapping provides preliminary evidence that myocardial involvement in patients with a high burden of PVCs might extend to the microstructural level, potentially revealing subclinical interstitial changes. Although this interpretation requires validation through future studies incorporating histological correlation or ECV measurement, our findings highlight the potential of CMR mapping to identify a novel tissue phenotype in this patient population. The myocardial interstitium, a dynamic compartment comprising stromal cells and extracellular matrix, is critical to postinjury repair. Both reparative and reactive myocardial interstitial fibrosis contribute to cardiac dysfunction and poor outcomes in individuals with nonischemic disease (45). Despite further investigation and histopathological validation being needed to determine the exact nature of the underlying tissue change, our findings nevertheless demonstrate the presence of a quantifiable interstitial abnormality.

Limitations

This study involved several limitations that should be addressed. First, we employed a retrospective, single-center design and vendor-specific methodology, which may limit the generalizability of the findings and require external validation. Second, although the stringent patient selection enhanced the internal validity of the study, the resulting cohort and modest subgroup sizes may not fully represent the broader PVC population. Third, the absence of postablation CMR data precluded assessment of causality, and the potential influence of PVC origin could not be examined due to limited mapping data. Finally, the modest sample size led us to employ partial correlation rather than more complex multivariable models for adjusting confounders. Although this approach supports independence, the stability of more comprehensive models requires validation in larger cohorts.

Conclusions

This exploratory study identified a novel, burden-dependent myocardial phenotype among patients with idiopathic PVCs, characterized by CMR-derived strain impairment and elevated native T1/T2 values. The robust dose-response relationship is consistent with the subclinical myocardial involvement directly related to PVC burden. Given the study’s limitations, including its sample size, the findings are inherently hypothesis-generating. Future longitudinal studies with histological correlation are essential to definitively establish the clinical and prognostic significance of this phenotype.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1190/rc

Data Sharing Statement: Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1190/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-2025-1190/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 study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. This study received approval from the Ethics Review Committee of Shanghai General Hospital (No. 2023364) and was exempt from the requirement for informed consent due to the retrospective nature of the study.

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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