Relationships between QRS duration and left ventricular deformation in hypertrophic cardiomyopathy

Introduction

Hypertrophic cardiomyopathy (HCM) is the most common inheritable heart disease, with an incidence of approximately 1:500 (1). HCM is well known to be one of the most common causes of sudden cardiac death in clinical practice (2). However, left ventricular systolic dysfunction (LVSD) in HCM patients, which has a relatively low incidence, has long been underrecognized. A global HCM cohort study demonstrated that three-quarters of HCM patients with LVSD experienced relevant clinical events, and more than one-third of them experienced adverse heart failure outcomes, thus emphasizing the importance of risk stratification for cardiac function impairment (3). Early identification of LVSD is needed to provide necessary support for timely medical intervention and improve the long-term prognosis of HCM patients.

The prognosis of HCM is closely related to left ventricular (LV) morphology and function; however, the left ventricular ejection fraction (LVEF) often tends not to be impaired and slight increased at early stages of HCM (4,5). Cardiac magnetic resonance feature tracking (CMR-FT) is a promising non-invasive technology for assessing ventricular motion or cardiac function accurately and for detecting early ventricular dysfunction in preserved LVEF patients sensitively (6). The diagnostic and prognostic value of myocardial strain values in HCM patients has been reported in previous studies (7-12). Nonetheless, the high-cost burden for patients and the high professional requirements for physicians limit their popularization in general population screening and long-term follow-up, especially in developing countries.

Electrocardiography (ECG), which is a low-cost, widely available and reproducible testing method, still has irreplaceable value in the diagnosis and management of HCM patients (13). The typical ECG phenotype alternations in HCM patients are characterized as QRS abnormalities and pathological ST-T changes (14). Prolonged QRS duration was found to be an independent risk factor for new-onset heart failure and mortality among left ventricular hypertrophy (LVH) patients in a recent study (15,16). Nevertheless, the relationship between QRS duration and early LV function impairments with preserved LVEF is unclear.

The altered strain values are not included in the risk criteria in current HCM management guidelines (17,18). However, early detection of strain impairment can be useful for setting up a more accurate follow-up schedule and enabling proactive clinical management for better patient outcomes. In this study, we aimed to examine the correlations of QRS duration with CMR strain in both hypertrophic nonobstructive cardiomyopathy (HNCM) patients and hypertrophic obstructive cardiomyopathy (HOCM) patients, thus enhancing the risk stratification of patients with LV early myocardial deformation using routine ECG testing. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2024-2632/rc).

Methods

Study population

HCM patients with preserved LVEF were retrospectively enrolled in this study from March 2013 to February 2022 in the First Affiliated Hospital of Zhengzhou University. The inclusion criteria were as follows: (I) inpatients; (II) met the diagnostic criteria for HCM and had a LV thickness ≥15 mm, which cannot be explained solely by loading conditions (19); and (III) had a complete clinical assessment at baseline, including 12-lead ECG and CMR imaging data. The exclusion criteria were as follows: (I) LVH caused by metabolic disorders, mitochondrial cardiomyopathy, neuromuscular disease, malformation syndrome, or pressure overload; (II) ischaemic cardiomyopathy; (III) younger than 18 years; (IV) a reduced LVEF (LVEF <50%) (20). HCM patients who satisfied the eligibility criteria were enrolled and divided into HNCM and HOCM groups based on whether the left ventricular outflow tract pressure gradient (LVOTPG) was ≥30 mmHg (19). The patients in the two individual groups were subsequently exact-matched for sex, age, and body mass index (BMI), which could affect the distribution of the QRS duration and the results of the myocardial strain analysis. The Institutional Review Board (IRB) of the First Affiliated Hospital of Zhengzhou University approved the study protocol (No. 2022-KY-0698). The patients signed informed written consent for the publication of the study data. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments.

Clinical and ECG data collection

All analysed data in this study were collected at baseline. The ECG and CMR data were derived from the patients’ initial examinations at the First Affiliated Hospital of Zhengzhou University, whether these examinations were conducted in an outpatient or inpatient setting. The clinical characteristics, including demographic, echocardiography and biochemistry findings, were collected. The ECG data were selectively collected as close as possible to the date of CMR. Standard 12-lead ECGs were recorded and presented via a programmed digital procedure (ECG-2550, 25 mm/s speed, 10 mV/mm, Nihon Kohden^TM Japan, Tokyo, Japan). The QRS duration was determined from the system results of the automatic procedure, as described in a previous study (15). The ECG quality assessment and other electrophysiological parameters measurement were evaluated independently by two cardiology physicians. To provide better guidance to physicians in clinical practice, we divided patients into two groups based on the QRS duration. Patients with a QRS duration <110 ms were regarded as normal controls, and those with a QRS duration ≥110 ms were recognized as having QRS prolongation (21).

Cardiac magnetic resonance (CMR) acquisition and feature tracking analysis

CMR scanning was performed on a 3-T scanner (Ingenia 3.0T CX, Philips Health care, Best, The Netherlands). CMR image acquisition, including 3 single long-axis and 8 short-axis cine images from the basis to the apex, was conducted via a standard steady-state free precession (SSFP) sequence with breath holding. Late gadolinium enhancement (LGE) images were captured 10 to 15 minutes following an intravenous injection of 0.2 mmol/kg gadolinium-diethylene triamine pentaacetic acid (DTPA), utilizing a breath-held phase-sensitive segmented inversion-recovery sequence. The views matched those used for the cine images.

The LGE, CMR-FTs and myocardial deformation were quantified via CVI42 (version 5.0, Circle Cardiovascular Imaging, Inc., Calgary, Canada). LV global and regional (basal, mid and apical) strain and the strain rate (SR) in the circumferential, radial and longitudinal directions were measured via long-axis and short-axis cine images. The peak values of strain (PS), systolic SR (PSSR), and diastolic SR (PDSR) were defined as the highest strain irrespective of time during systole/diastole. The segmental strain parameters were partitioned based on the recommendations of the American Heart Association 16-segment model (22). Two experienced radiologists who were blinded to the study design and clinical data measured the CMR strain values separately.

Statistical analysis

The categorical variables were presented as counts and percentages, and the continuous variables were expressed as the means ± standard deviations or as the medians with [interquartile ranges (IQRs)] according to the variable distribution. Differences between groups were compared via Student’s t-test or the Mann-Whitney U test, depending on the variable distribution. The categorical variables were analysed via the Chi-squared test or Fisher’s exact test. Data correlation coefficients among variables were calculated via Pearson correlation analysis and adjusted by LGE level. The statistical significance was set as a two-sided P value <0.05. Statistical analysis was performed with SPSS software version 21 (SPSS Inc., IBM Company, Chicago, Illinois, USA) and R packages.

Results

Baseline characteristics of HNCM and HOCM patients

A total of 45 HNCM patients and 81 HOCM patients were enrolled in our study and matched based on sex, age, and BMI. Compared with that in HNCM patients, interventricular septum (IVS) thickness (16.62±6.00 vs. 18.70±5.09 mm, P=0.042) and LVOTPG (5.46±19.73 vs. 73.64±44.75 mmHg, p<0.001) were significantly higher in the HOCM group (Table 1). According to the ECG findings, the QTc (429.41±37.34 vs. 448.81±48.27 ms, P=0.024) and QRS duration (100.71±28.18 vs. 113.80±25.60 ms, P=0.009) were prolonged in the HOCM group. A total of 12 HNCM patients (26.67%) and 46 HOCM patients (56.79%) experienced QRS prolongation. There were no statistically significant intergroup differences in LVEF, end-systolic volume index (ESVI), end-diastolic volume index (EDVI), or multidirectional myocardial deformation parameters including global circumferential strain (GCS), global radial strain (GRS), and global longitudinal strain (GLS). The baseline biochemistry variable levels were also similar between these two groups. In summary, the differences in baseline clinical characteristics and LV function were subtle between the HNCM and HOCM groups.

Relationships between QRS duration and global strain/SR in different groups

Typical ECGs from HCM patients with prolonged QRS durations and their CMR-FTs are shown in Figure 1. Considering that the LV myocardial strain values differ intrinsically between HNCM and HOCM (23,24), we analysed the relationships between QRS duration and global strain/SR in the HNCM and HOCM groups separately. The correlation curves between QRS duration and global LV myocardial strain parameters in HNCM and HOCM patients are shown in Figure 2. In the HNCM group, the results of the Pearson correlation analysis indicated that GCS (r=0.386, P=0.013), GRS (r=−0.374, P=0.016) and GLS (r=0.346, P=0.026) were significantly correlated with the QRS duration. Similarly, GCS (r=0.253, P=0.036) and GRS (r=−0.257, P=0.033) were also correlated with QRS duration in HOCM patients, while no significant correlation coefficient between GLS (r=0.134, P=0.272) and QRS duration was found.

Figure 1 Representative ECG data indicating QRS prolongation and CMR-FT images of LV deformation in HNCM and HOCM. (A) Typical ECG data indicating QRS prolongation (QRS duration =128 ms); (B) typical CMR-FT image of strain analysis in HNCM; Red circle: Left ventricular cavity (blood pool); Green circle: Left ventricular myocardial wall; (C) bull’s eye plots of the peak circumferential strain (%); (D) bull’s eye plots of the peak radial strain (%); (E) bull’s eye plots of the peak longitudinal strain (%); (F) typical CMR-FT image of strain analysis in HOCM; Red circle: Left ventricular cavity (blood pool); Green circle: Left ventricular myocardial wall; (G) bull’s eye plots of the peak circumferential strain (%); (H) segmental peak circumferential strain curves in HOCM patients. AHA, American Heart Association; avF, augmented voltage foot; avL, augmented voltage left arm; avR, augmented voltage right arm; CMR-FT, cardiac magnetic resonance feature-tracking; ECG, electrocardiography; HNCM, hypertrophic nonobstructive cardiomyopathy; HOCM, hypertrophic obstructive cardiomyopathy; LV, left ventricular.

Figure 2 The Pearson correlations between the QRS duration and global strain values in HNCM (left) and HOCM (right). GCS, global circumferential strain; GLS, global longitudinal strain; GRS, global radial strain; HOCM, hypertrophic obstructive cardiomyopathy; HNCM, hypertrophic nonobstructive cardiomyopathy; ns, not significant.

The global circumferential PS (−15.02%±5.72% vs. −19.60%±5.68%, P=0.034), radial (17.03%±8.74% vs. 30.69%±12.74%, P=0.003) and longitudinal PS (−6.37%±4.11% vs. −10.25%±6.38%, P=0.008) were all reduced in HNCM patients with a QRS duration ≥110 ms than in patients with a normal QRS duration (Table 2). In addition, the global radial PSSR (1.07±0.47 vs. 1.96±0.92 s⁻¹, P=0.006) and PDSR (−0.90±0.49 vs. −1.71±0.78 s⁻¹, P=0.004) were also lower in HNCM patients with QRS prolongation. In the HOCM group, the global circumferential PS (−15.88%±3.65% vs. −18.44%±3.65%, P=0.006) and radial PS (25.33%±10.81% vs. 31.70%±13.46%, P=0.036) was impaired in patients who had a QRS duration ≥110 ms. In addition, the global circumferential PSSR (−0.95±0.19 vs. −1.10±0.21 s⁻¹, P=0.004) and PDSR (0.71±0.20 vs. 0.85±0.28 s⁻¹, P=0.020) were decreased in HOCM patients with prolonged QRS. The differences in other global LV myocardial parameters were not significant between the QRS prolongation group and the normal QRS duration group in HNCM and HOCM patients.

Relationships between QRS duration and regional strain/SR in the HNCM group

The correlation coefficients between the 16 independent segment myocardial variables and the QRS duration in HNCM patients were calculated via Pearson correlation analysis. The segments with significant correlation coefficients are highlighted with different colours according to the P values in Figure 3. The correlation curves between the QRS duration and the regional PS, PSSR and PDSR in the circumferential, radial and longitudinal directions at the basal, mid and apical levels are presented in Figures S1-S3. Three directions of PS all presented significant correlation with QRS duration at three segment levels (Figure S1). The radial PSSR also correlated with the QRS duration at different segment level (Figure S2). The QRS duration tended to had stronger correlation with strain or SR in apex, especially with PS and PDSR (Figure S3).

Figure 3 Relationships between QRS duration and strain values in different segments in HNCM patients. Light blue represents the P values of Pearson correlation analysis <0.05; dark blue represents P values <0.01; grey represents P values >0.05. HNCM, hypertrophic nonobstructive cardiomyopathy.

The deformation differences in strain and SR in HNCM with a QRS duration ≥110 ms, which were compared with those in HNCM with a normal QRS duration, are shown in Figure 4. Except for circumferential PSSR, every segmental strain and SR was impaired to varying degrees. Most strain variables exclude circumferential and longitudinal PSSR were all reduced at apex segments in HNCM with QRS prolongation. In contrast, basal segments for strain and SR differences were less significant in HNCM with prolonged QRS duration. It suggested that the prolonged QRS would indicate the regional PS impairments, and particularly the apical segments for strain/SR reduction in HNCM patients.

Figure 4 Regional differences in radial, circumferential, and longitudinal strain and strain rates between HNCM patients with normal and prolonged QRS durations. (A) Violin plots of differences in radial, circumferential, and longitudinal peak strain at the basal, mid and apical levels between HNCM patients with normal and prolonged QRS durations. (B) Differences in radial, circumferential, and longitudinal peak strain in 16 segments between HNCM patients with normal and prolonged QRS durations. (C) Violin plots of differences in radial, circumferential, and longitudinal peak systolic strain rates at the basal, mid and apical levels between HNCM patients with normal and prolonged QRS durations. (D) Differences in radial, circumferential, and longitudinal peak systolic strain rates in 16 segments between HNCM patients with normal and prolonged QRS durations. (E) Violin plots of differences in radial, circumferential, and longitudinal peak diastolic strain rates at the basal, mid and apical levels between HNCM patients with normal and prolonged QRS durations. (F) Differences in radial, circumferential, and longitudinal peak diastolic strain rates in 16 segments between HNCM patients with normal and prolonged QRS durations. *, P<0.05; **, P<0.01; ***, P<0.001. HNCM, hypertrophic nonobstructive cardiomyopathy.

Relationships between QRS duration and regional strain/SR in the HOCM group

The same presentation scheme was applied to perform the significance of the correlation coefficients between QRS duration and different strain variables in HOCM patient group (Figure 5). Apparently, the imaging patterns of the correlation between QRS duration and myocardial strain variables were quite different in HNCM and HOCM group. Comparatively, the segmental circumferential strain and SR had relatively strong correlation with QRS duration, whereas this correlation was weak in other directions without any significance. The circumferential PS and PSSR were all correlated with QRS duration at apical (PS: r=0.365, P=0.002; PSSR: r=0.482, p<0.001), mid (PS: r=0.301, P=0.013; PSSR: r=0.304, P=0.012) and basal (PS: r=0.325, P=0.007; PSSR: r=0.379, P=0.002) level, and the circumferential PDSR at mid segment (r=−0.285, P=0.019) also had a significant correlation with QRS duration (Figure S4).

Figure 5 Relationships between QRS duration and strain values in different segments in HOCM patients. Light blue represents the P values of Pearson correlation analysis <0.05; dark blue represents P values <0.01; grey represents P values >0.05. HOCM, hypertrophic obstructive cardiomyopathy.

The circumferential PS and PSSR were all reduced from the basal to apical segments in HOCM patients with QRS duration ≥110 ms (Figure 6A). Besides, the circumferential PS, PSSR and PDSR in basal inferoseptal segment were all impaired in HOCM patients with prolonged QRS (Figure 6B). In summary, the QRS prolongation tended to reflect the reduction of LV global and regional circumferential strain and SR.

Figure 6 Regional differences in circumferential strain and strain rates between HOCM patients with normal and prolonged QRS durations. (A) Violin plots of differences in circumferential peak strain, peak systolic strain rate and peak diastolic strain rate at the basal, mid and apical levels between HOCM patients with normal and prolonged QRS durations. (B) Differences in circumferential peak strain, peak systolic strain rate and peak diastolic strain rate in 16 segments between HOCM patients with normal and prolonged QRS durations. HOCM, hypertrophic obstructive cardiomyopathy.

Discussion

In this study, we first demonstrated the relationship between QRS duration and myocardial deformation in both HNCM and HOCM patients. To minimize confounding factors and to specifically identify the relationship between electrophysiological abnormalities and LV morphology at the early hypertrophy stage, we not only matched patients based on sex (25), age (23) and BMI (26) but also selectively enrolled HCM patients with preserved LVEF. Additionally, on the basis of the heterogeneous strain patterns in HNCM and HOCM, we established this relationship in these two HCM subtypes to better illustrate the correlations and differences. According to the results of global strain analysis, the GCS, GRS and GLS impairments were associated with QRS prolongation in the HNCM group, and radial PSSR/PDSR reduction can also be found in HNCM patients with a QRS duration ≥110 ms. The GCS and GRS, along with the circumferential PSSR/PDSR, were impaired in HOCM patients with prolonged QRS duration. The results of the regional and segmental analyses revealed that the apical segment for strain and SR had a more significant relationship with QRS prolongation in HNCM. The major myocardial deformation in HOCM patients with a QRS duration ≥110 ms, however, was related mainly to regional circumferential strain and SR impairments.

QRS prolongation has been found to be a risk factor for heart failure in dilated cardiomyopathy and ischaemic cardiomyopathy clinical cohorts (27). According to previous HCM studies, the QRS duration could be an important predictor of malignant ventricular arrhythmias and sudden cardiac death (28) and increase mortality risk (29). The potential mechanism of QRS prolongation could be explained by anatomical structure abnormalities within cells and intercellular electrical activity (30). Disrupted conduction in the ventricular myocardium is one of the typical features of the arrhythmogenic substrate in the HCM pathological process, and slower activation of the ventricles (ventricular depolarization) leads to a longer QRS complex duration. In HCM, myocardial disarray, interstitial fibrosis and Purkinje fibre network dysfunction may also be present during the disease course (31).

As noted above, the present study is the first to report a significant and interesting relationship between QRS prolongation and apical segment deformation in nonobstructive HCM patients. In a previous report of HCM patients who developed an LV apical aneurysm, the QRS duration was prolonged at the latest examination compared with the condition at their first enrolment (32). A decrease in apical myocardial contraction function often tends to be the initial manifestation and gradually worsens during the chronic course of apical aneurysm formation (33). The potential pathophysiological mechanism for the formation of apical aneurysms is that distal coronary perfusion decreases, and myocardial ischaemia occurs at the apex (34). The density of the Purkinje fibre network is relatively high in the apex myocardium (35). The prolonged QRS duration tested by standard 12-lead ECGs can reflect the destruction of regional Purkinje fibre bundles, abnormal depolarization of locally necrotic cardiomyocytes, and slow activation caused by chronic ischaemia at apical segments in HCM pathogenesis (16). Combining the findings of previous studies with our findings, QRS prolongation could not only be an effective predictor of the risk of developing apical aneurysms but also an early indicator of slight degeneration of myocardial compliance and systolic dysfunction in HNCM patients.

In HOCM patients, septal hypertrophy, subendocardial fibrosis and fibre reorientation often cause longitudinal strain impairment at the early stage. The circumferential and radial strains, however, are increased to maintain normal LV cardiac function at this stage (36). As the disease progresses, myocardial disarray and fibrosis replacement gradually extend to the mid wall and subepicardial layers. The circumferential and radial strains are subsequently affected as a result (37). Our results suggested that global and regional circumferential strain and the SR were the main myocardial deformation phenotypes in the prolonged QRS duration group of HOCM patients, whereas the longitudinal strain values were not significantly different between the two QRS groups. Additionally, the circumferential strain in the basal inferoseptal segment, where typical septal hypertrophy occurs, was impaired even more significantly in HOCM patients with QRS prolongation. Thus, the prolongation of QRS in these HOCM patients could serve as an important indicator of the pathohistological progress of septal hypertrophy involvement and myocardial deformation in the mid wall of the LV.

Study limitations

This was a retrospective study, and selection bias was not avoidable. Although there was a statistically significant effect, the correlation between QRS duration and strain values was moderate. In addition, owing to the strict inclusion and exclusion criteria, the size of the study population was limited, and multivariable adjustment was not performed in this study. The strain values of most patients were not available during their follow-up. Thus, we focused on the specific relationship between QRS duration and LV deformation at the early hypertrophy stage when patients still have a preserved LVEF in a cross-sectional study. Repeated CMR examinations of patients in the cohort based on their wishes and actual needs will be conducted to obtain more valuable clinical information and establish a more accurate association between prolonged QRS duration and deterioration of strain values. The necessity for establishing risk stratification and management strategies for LVSD in HCM patients based on QRS prolongation by routine ECG testing still needs further clarification.

Conclusions

QRS prolongation is associated with LV myocardial deformation in HCM. QRS prolongation is not only correlated with the apical strain and SR impairments in HNCM patients but also correlated with the decrease in circumferential strain in the HOCM population. These results highlight the importance of QRS duration in identifying mild LV morphology abnormalities and cardiac dysfunction in HCM patients. Prolonged QRS duration may serve as a prediction tool in HCM risk stratification in the future.

Acknowledgments

The authors appreciate the understanding and support of the patients and families who have made this work possible.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-2024-2632/rc

Data Sharing Statement: Available at https://qims.amegroups.com/article/view/10.21037/qims-2024-2632/dss

Funding: This study was funded by National High Level Hospital Clinical Research Funding, Elite Medical Professionals Initiative of China-Japan Friendship Hospital (No. ZRJY2025-GG04), Program for Science and Technology Development of Henan Province (No. 212102310210), National Natural Science Foundation of China (No. 82102654 and No. 82500446) and The Beijing Natural Science Foundation (No. 2024BZR-7242126).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2024-2632/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 Institutional Review Board (IRB) of the First Affiliated Hospital of Zhengzhou University approved the study protocol (No. 2022-KY-0698). The patients signed informed written consent for the publication of the study data. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments.

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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