Highlights
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Cardiac magnetic resonance detected late gadolinium enhancement in 39% of patients with premature ventricular contractions or nonsustained ventricular tachycardia.
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Older age, male sex, heart failure, and polymorphic premature ventricular contractions independently predicted late gadolinium enhancement.
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Cardiac magnetic resonance improved diagnostic accuracy and risk stratification in this population.
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Targeted use of cardiac magnetic resonance may optimize evaluation of patients with high-risk ventricular arrhythmias.
Premature ventricular contractions (PVCs) and nonsustained ventricular tachycardia (NSVT) are common arrhythmias that may signal underlying structural heart disease (SHD). Cardiac magnetic resonance imaging (CMR) has emerged as a valuable tool for detecting myocardial abnormalities in this population. This study aimed to evaluate the diagnostic utility of CMR in patients with PVCs/NSVT and identify clinical predictors of pathologic late gadolinium enhancement (LGE). We retrospectively reviewed patients who underwent CMR for PVCs or NSVT between 2012 and 2023 at a single health system. The primary outcome was the presence of pathologic LGE. Clinical data were extracted using ICD-10 codes, and cardiac sarcoidosis (CS) was adjudicated by a multidisciplinary team using WASOG criteria. Among 553 patients (mean age 61.1 ± 14.6 years; 40.7% female), pathologic LGE was identified in 214 (38.6%). Patients with LGE were older and had a greater burden of comorbidities. On multivariable analysis, independent risk factors for LGE included age (aOR 1.04, p = 0.001), male sex (aOR 2.37, p < 0.001), heart failure (aOR 2.53, p < 0.001), and polymorphic PVCs (aOR 1.94, p = 0.015). Among patients with LGE, 12.6% had highly probable CS. Other diagnoses included nonischemic cardiomyopathy (53.7%), ischemic cardiomyopathy (11.7%), and idiopathic (34.6%). CMR frequently detects clinically significant myocardial abnormalities in patients with PVCs or NSVT, particularly in those with high-risk features. In this real-world study, nearly 40% of patients had LGE on CMR. An etiology was identified in one-third of these cases. These findings can inform patient selection for CMR in clinical practice to guide diagnosis, risk stratification, and management.
Premature ventricular contractions (PVCs) and nonsustained ventricular tachycardia (NSVT) are common forms of ventricular arrhythmias, often presenting significant diagnostic challenges in clinical practice due to significant heterogeneity in symptoms and clinical presentation. While many cases of PVC/NSVT are idiopathic, establishing the underlying etiology is crucial, particularly in the context of structural heart disease (SHD), where myocardial abnormalities may be present. This is partly because the presence of PVC/NSVT could signal significant underlying cardiac pathology, but also because their very presence portends a higher risk of sudden cardiac death (SCD).
Cardiac magnetic resonance imaging (CMR) is a modality often obtained during the evaluation of patients with PVC/NSVT, particularly when myocardial infarction (MI) or ischemic heart disease (IHD) have been excluded. Observational studies have shown a 15-30% incidence of CMR abnormalities among patients with PVC/NSVT, ,, further underscoring the importance of identifying diagnostic modalities most adept at providing answers to both patients and clinicians.
To-date, there are no prospective randomized trials demonstrating improvement in clinical outcomes with CMR. Additionally, performing routine CMR on all patients with PVC/NSVT is difficult due to high cost, limited accessibility and the expertise required for image interpretation. Therefore, properly selecting patients to undergo further advanced imaging can be challenging, and further guidance is certainly needed to avoid unnecessary routine imaging.
We conducted a study of patients undergoing CMR for PVC/NSVT, in hopes of further characterizing this patient cohort and identifying baseline characteristics and clinical variables associated with the identification of pathology on CMR, which could help guide clinicians in appropriately utilizing this imaging when needed.
Methods
Patient population and data collection
We retrospectively reviewed the electronic medical records (EMR) of patients seen in the Henry Ford Health System (Detroit, Michigan) between 2012 and 2023 who were diagnosed with PVCs or NSVT and subsequently underwent CMR. Patients were included if they had completed the CMR study with available data in the EMR for review. Patients were excluded if they had missing data, were unable to complete the CMR, or had uninterpretable results.
All data were manually abstracted from the EMR by the research team. The study was approved by the institutional review board (IRB), with a waiver for patient informed consent based on the retrospective nature of the investigation.
Definitions and outcomes
The primary endpoint was presence of pathologic late gadolinium enhancement (LGE) on CMR. Anterior and inferior right ventricular insertion point LGE in isolation was excluded. The presence or absence of LGE was gathered from the CMR report at the time of study completion.
Past medical history diagnoses were quantified based on ICD-10 codes in the EMR during initial data abstraction and were present prior to the index CMR. As sarcoidosis is always part of the differential diagnosis in patients with PVC/NSVT undergoing CMR, each case of extracardiac sarcoidosis was adjudicated by the research team, with identification of radiographic evidence of sarcoidosis, pathologic diagnosis by biopsy, or on active treatment.
Cardiac sarcoidosis (CS) was assessed retrospectively by the treatment team, with application of the World Association of Sarcoidosis and Other Granulomatous Diseases (WASOG) definitions: highly probable (>90% probability of CS), probable (50-90% probability of CS), and possible (<50% probability of CS).
Arrhythmia information was gathered from documentation, or if not documented, the research team confirmed the presence of cardiac monitor that first identified the arrhythmia. PVC morphology was adjudicated by cardiovascular medicine specialist on the research team.
Statistical analysis
All statistical analyses were performed using SPSS software (IBM, Armonk, NY, USA). Categorical variables were reported as frequency rates (n) and percentages (%); data was analyzed using the chi-square test or Fisher’s exact test, for parametric or nonparametric variables, respectively. Continuous variables were reported as medians with interquartile range (IQR); data was analyzed by the t-test or Mann-Whitney U test, for parametric or nonparametric continuous variables, respectively. Univariate analysis of risk factors associated with pathologic LGE was performed, followed by multivariable logistic regression analysis, with presence of LGE as the dependent variable, to identify independent risk factors associated with the primary endpoint. The model included all risk factors with a p-value of < 0.10 from 2-sided alpha testing. Multicollinearity was tested, and no variables met the threshold for exclusion. The Hosmer-Lemeshow test was applied to assess the goodness of fit of the model.
Results
Of the 819 patients assessed, 553 (67.5%) were included in the final analysis. 64 patients were excluded due to technical issues with completing the CMR (7.8%) while others were excluded for missing/uninterpretable data (24.6%). 214 patients (38.6%) of patients met the primary endpoint.
Baseline demographics and clinical characteristics
The mean (SD) age of the cohort was 61.1 (14.6) years, with 59.3% male, and a median (IQR) BMI of 29.8 (25.3-34.2) kg/m 2. Past medical history included diabetes mellitus (21%), hypertension (55.7%), prior MI (9.6%), heart failure (35.6%) with a baseline left ventricular ejection fraction (LVEF) of 40.0% (30.0-48.0), and smoking (25.3%). 27 (4.9%) patients had previously diagnosed sarcoidosis prior to CMR, the vast majority being pulmonary involvement. 38.5% of patients were on a beta blocker, 4.2% on a class 1 or 3 antiarrhythmic, and 16.1% on a nondihydropyridine calcium channel blocker prior to CMR acquisition. Patients with pathologic LGE were older (p < 0.001), with a higher prevalence of males (p < 0.001), diabetes (p = 0.017), hypertension (p < 0.001), prior MI (p < 0.001), heart failure (p < 0.001), and active tobacco use (p = 0.003).
PVCs/NSVT were diagnosed with ECG (40.9%), Holter Monitor (35.8%), Telemetry (19.0%), Event Monitor (9.9%), or Implantable Loop Recorder (1.8%). Monomorphic PVC morphology was most prevalent overall (86.3%), although patients with pathologic LGE demonstrated a higher percentage of polymorphic PVCs (p = 0.001). Overall, 62% of the identified PVCs appeared to originate from the right ventricular outflow tract (RVOT), while 31% originated from the left ventricular outflow tract (LVOT). These percentages are based solely on PVCs captured and reviewed using EKG, Holter monitoring, and implantable loop recorder data. It is important to note that a more comprehensive analysis of PVC morphology was limited, as some episodes were only documented through telemetry and other monitoring systems, which did not allow for detailed characterization.
Table 1 highlights baseline clinical characteristics. Figure 1 highlights the various modalities used to diagnose PVCs/NSVT.
Table 1
Baseline characteristics
|
Entire cohort
( N = 553) |
LGE
( n = 214) |
No LGE
( n = 339) |
p value | |
|---|---|---|---|---|
| Demographics | ||||
| Age– years | 61.1 (14.6) | 67.0 (57.0– 73.8) | 61.0 (48.9– 69.8) | < 0.001 |
| Male Sex | 328 (59.3) | 156 (72.9) | 172 (50.7) | < 0.001 |
| Body mass index– kg/m 2 | 29.8 (25.3– 34.2) | 30.0 (25.4– 33.3) | 30.0 (25.3– 35.4) | 0.738 |
| Past medical history | ||||
| Diabetes | 116 (21.0) | 56 (26.2) | 60 (17.7) | 0.017 |
| Hypertension | 308 (55.7) | 141 (65.9) | 167 (49.3) | < 0.001 |
| Prior myocardial infarction | 53 (9.6) | 33 (15.4) | 20 (5.9) | < 0.001 |
| Heart failure | 197 (35.6) | 109 (50.9) | 88 (26.0) | < 0.001 |
| Baseline LVEF | 40.0 (30.0– 48.0) | 35.0 (25.0– 45.0) | 44.0 (32.0– 50.5) | 0.005 |
| Smoker | 140 (25.3) | 69 (32.2) | 71 (20.9) | 0.003 |
| Noncardiac sarcoidosis | 27 (4.9) | 10 (4.7) | 16 (4.7) | 0.980 |
| Pulmonary | 26 (4.7) | 10 (4.7) | 16 (4.7) | |
| Ophthalmologic | 2 (0.4) | 2 (0.9) | 0 (0.0) | |
| Cutaneous | 3 (0.5) | 1 (0.5) | 2 (0.6) | |
| Neuro | 3 (0.5) | 2 (0.9) | 1 (0.3) | |
| Splenic | 1 (0.2) | 0 (0.0) | 1 (0.3) | |
| Medications prior to CMR | ||||
| Beta-blocker | 213 (38.5) | 97 (45.3) | 116 (34.2) | 0.009 |
| Class 1 or 3 antiarrhythmic | 23 (4.2) | 5 (2.3) | 18 (5.3) | 0.088 |
| Nondihydropyridine CCB | 89 (16.1) | 25 (11.7) | 64 (18.9) | 0.025 |
| Arrhythmia information | ||||
| Method of PVC/NSVT diagnosis | ||||
| ECG | 226 (40.9) | 86 (40.2) | 140 (41.3) | 0.796 |
| Holter monitor | 198 (35.8) | 68 (31.8) | 130 (38.3) | 0.117 |
| Event monitor | 55 (9.9) | 14 (6.5) | 41 (12.1) | 0.034 |
| Implantable loop recorder | 10 (1.8) | 8 (3.7) | 2 (0.6) | 0.007 |
| Telemetry | 105 (19.0) | 53 (24.8) | 52 (15.3) | 0.006 |
| PVC morphology | 0.018 | |||
| Monomorphic | 481 (87.0) | 172 (80.4) | 309 (91.2) | |
| Right bundle | 270 (49.0) | 101 (47.2) | 173 (51.0) | |
| Left bundle | 211 (38.0) | 71 (33.2) | 136 (40.2) | |
| Polymorphic | 72 (13.0) | 42 (19.6) | 30 (8.8) | |
| Electrophysiology consulted prior to CMR | 282 (50.9) | 117 (54.9) | 165 (48.7) | 0.319 |
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