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. 2020 Apr 28;22(3):369–377. doi: 10.1177/1099800420921944

Exercise-Induced Premature Ventricular Contractions Are Associated With Myocardial Ischemia Among Asymptomatic Adult Male Firefighters: Implications for Enhanced Risk Stratification

Dillon J Dzikowicz 1,✉, Mary G Carey 1
PMCID: PMC7492778  PMID: 32342704

Abstract

Background:

Exercise-induced premature ventricular contractions (EI-PVCs) are associated with an increased risk of cardiovascular disease among asymptomatic adult males, but the underlying mechanisms remain understudied. Myocardial ischemia due to cardiovascular disease reduces coronary blood flow, may impair exercise performance, and initiates EI-PVCs; thus, EI-PVCs may be an early indicator of cardiovascular disease.

Objective:

The objective of this study was to determine whether EI-PVCs are associated with myocardial ischemia and reduced exercise performance among asymptomatic adult firefighters.

Methods:

Asymptomatic adult firefighters free of known cardiovascular disease underwent exercise treadmill testing. A 12-lead electrocardiography was placed on participants for 24 hr afterward to measure EI-PVCs in recovery. Univariate and multivariate binary logistic regression models were used to assess the odds of myocardial ischemia. Sensitivity and specificity analyses were conducted. Statistical significance was set at p < .05.

Results:

Participants comprised 86 asymptomatic adult males. The prevalence of myocardial ischemia was 30.8%. A single EI-PVC was associated with myocardial ischemia (χ2 = 8.98; p = .003). EI-PVC remained a significant predictor despite adjustment for other cardiovascular risks (odds ratio = 4.281, p = .038). Although not statistically significant, the EI-PVC group achieved lower total exercise time (11.4 ± 2.9 vs. 12.4 ± 3.0 min, p = .13), lower metabolic equivalent of tasks (METs; 11.6 ± 2.6 vs. 12.8 ± 2.3 METs, p = .06), and a lower maximum exercise speed (4.4 ± 0.7 vs. 4.7 ± 0.8 miles/hr, p = .07).

Discussion:

EI-PVCs are associated with myocardial ischemia among asymptomatic male firefighters, providing additional evidence of the association between EI-PVCs and myocardial ischemia and suggesting EI-PVCs as an early indicator of cardiovascular disease.

Keywords: electrocardiography, ventricular premature complexes/physiopathology, ischemia, coronary disease, exercise test

Exercise-induced premature ventricular contractions (EI-PVCs) are a common occurrence, with an estimated prevalence of 60% during exercise treadmill testing, yet their clinical significance remains underappreciated (Dewey et al., 2008). A number of meta-analyses and systematic reviews have reported worse clinical outcomes among asymptomatic patients with EI-PVCs (Ataklte et al., 2013; Kim et al., 2016; Lee et al., 2012; Lee et al., 2017). Specifically, EI-PVCs during exercise recovery are associated with worse prognoses, suggesting that they might indicate impaired myocardial recovery (Elhendy et al., 2002; Fejka et al., 2002; Lee et al., 2017; Meine et al., 2006). Some researchers have suggested that EI-PVCs be used for enhanced risk stratification purposes primarily among asymptomatic adults at high risk of cardiovascular death (Higgins & Higgins, 2007; Jouven & Ducimetière, 2001). However, there remains a lack of clarity on the causative agent or mechanism responsible for EI-PVCs. It is important to clarify the underlying pathological mechanisms responsible for EI-PVCs in order to increase clinical recognition and advance risk stratification considering past significant findings.

EI-PVCs are early depolarizations of the myocardium initiated by the Purkinje fibers rather than the sinoatrial node in response to increased myocardial demands (i.e., increased exercise, excessive catecholamine release), myocardial irritation (i.e., myocardial ischemia, electrolyte changes), or noncardiac pathologies (Ahn, 2013). Increased myocardial demands from exercise in the presence of atherosclerosis and cardiovascular disease can induce myocardial ischemia, resulting in decreased exercise performance (Duncker & Bache, 2008; Meine et al., 2006). Over time, this repeated process can lead to dysregulation of the electrical and mechanical indices of the myocardium, leading to arrhythmia and death (Duncker & Bache, 2008). Therefore, EI-PVCs may be associated with myocardial ischemia and thus an early indicator of cardiovascular disease.

The purpose of the present study was to evaluate the associations between EI-PVCs and myocardial ischemia and exercise performance among a cohort of on-duty asymptomatic adult male firefighters. We specifically chose to study firefighters because cardiovascular death is the leading cause of on-duty mortality among this population (45% of all on-duty fatalities, based on observational data; Soteriades et al., 2011). Firefighting is a physically demanding job that is associated with myocardial ischemia due to atherosclerosis, hypercoagulation, and endothelial dysfunction (Al-Zaiti & Carey, 2015; Al-Zaiti et al., 2015; Hunter et al., 2017). Although firefighters must pass a physical examination to be hired, mandated annual exams thereafter are not required. An early indicator of cardiovascular disease is needed to enhance risk stratification among firefighters.

Method

This study was a secondary analysis of data from the cross-sectional National Institutes of Health-funded Surveying & Assessing Firefighters Fitness & Electrocardiogram (SAFFE) Study conducted in Western New York. The primary aim of SAFFE was to evaluate electrocardiogram (ECG) features among a sample of on-duty professional firefighters from seven firehouses using convenience sampling. All on-duty firefighters were eligible to participate in the SAFFE Study. Written consent was collected prior to data collection. The university institutional review board approved the study, and results have been previously reported (Al-Zaiti & Carey, 2015; Carey et al., 2011; Dzikowicz & Carey, 2019a, 2019b).

For this secondary analysis, we excluded firefighters if they were female, had received treatment for either cardiovascular or respiratory disease, or had a pacemaker. We excluded female firefighters for three reasons: (1) Women make up fewer than 5% of the firefighting force and did not enter the workforce until the 1980s; thus, female firefighters are much younger and healthier and not comparable to their older male peers. In the parent study, only four of the firefighters were female, and they were younger (35.8 ± 6.7 years vs. 43.3 ± 7.9 years, p = .06), had a lower body mass index (BMI; 25.1 ± 4.3 kg/m2 vs. 29.7 ± 4.1 kg/m2, p = .03), a lower diastolic blood pressure (DBP; 70.5 ± 7.7 mmHg vs. 82.1 ± 10.6 mmHg, p = .03), and a lower prevalence of myocardial ischemia (25% vs. 30%, p = .8) than their male colleagues. (2) Male sex is a significant risk factor for cardiovascular death among firefighters (Soteriades et al., 2011). (3) Men are more affected by EI-PVCs than women in that EI-PVCs are more prognostic of cardiovascular death and disease in men compared to women (Lee et al., 2012). Given these differences between male and female firefighters, we excluded females from this analysis.

Self-reported demographic data collected for the SAFFE Study included age, race (White/non-White), current smoker (yes/no), and history of sleep apnea (yes/no). A registered nurse obtained anthropometric measures including height, weight, and resting blood pressure (BP). Height was recorded using a tape measure, and weight was recorded once using a calibrated bathroom scale. BMI was categorized in accordance with the Centers for Disease Control and Prevention standard BMI range categories for adults (Calle et al., 1999). BP was measured with participants in the resting seated position. Investigators took two BP measurements 5 min apart and then averaged them together. BP categorization was performed in accordance with the 2017 American Heart Association guidelines (Whelton et al., 2018).

Exercise Testing

Firefighters underwent standard Bruce protocol exercise treadmill testing (Bruce et al., 1973) using the X-Scribe™ stress-testing system (Mortara Instruments, Milwaukee, WI). The purpose of exercise treadmill testing was 3-fold: (1) determine which firefighters had myocardial ischemia and which firefighters did not, (2) compare exercise performance between firefighters with and without EI-PVCs, and (3) activate the sympathetic nervous system so 12-lead 24-hr Holter monitoring could record recovery. The firefighters were instructed to continue the exercise treadmill test even if they surpassed their maximum heart rate as long as they tolerated it and remained symptom free (symptom-limited exercise). Maximum heart rate was calculated as 220 − age in years. Diagnostic-quality 12-lead ECGs were obtained wirelessly from the X-Scribe system and displayed on a high-definition computer monitor. The system computes an average ST-T complex for each ECG lead and compares this value to a baseline collected prior to exercise, which allows for improved recognition of minor exercise-induced changes in ST segment and slope. The system also continuously measures BP and heart rate during exercise and recovery. Metabolic equivalent of task (MET) was calculated (Jetté et al., 1990). After semiautomatic annotation was performed, all ECGs were manually annotated by a blinded reviewer who was a PhD-prepared registered nurse. Myocardial ischemia was defined as horizontal ST-segment depression (≥1 mm) and/or T-wave inversion in two or more contiguous leads for at least 30 s during the peak of exercise or during the recovery from exercise, in accordance with current guidelines (Gibbons et al., 1997).

12-Lead 24-Hr Holter ECG Monitoring

After exercise treadmill testing, 12-lead 24-hr Holter ECG monitors were applied on the chest of the firefighters (H12+ Version 3.12; Mortara Instruments). The leads were placed on cleaned areas of the torso using the Mason-Likar lead configuration (Papouchado et al., 1987). Firefighters wore the monitor for 24 hr and were instructed not to exercise. After 24 hr, the firefighters removed the electrodes and returned the monitor. High-fidelity and high-resolution (1,000 samples/s) recordings with a frequency of 0.05–60 Hz were obtained and downloaded to a computer with H-Scribe Version 4 software (Mortara Instruments). After semiautomatic annotation was performed to filter noticeable artifacts, all ECGs were manually reviewed for quality assurance by a blinded reviewer who was a PhD-prepared registered nurse. Multiple measures of EI-PVCs were recorded and manually reviewed. EI-PVCs were defined as ectopic ventricular beats with a broad, premature, and prolonged (≥120 ms) QRS complex with abnormal morphology and discordance between the corresponding ST segment and T wave (Al-Khatib et al., 2018). The morphology and discordance of EI-PVCs were not quantified. The measures of EI-PVCs included in this analysis were as follows: at least one singlet EI-PVC (yes/no); at least one coupled EI-PVC (yes/no), ≥10 EI-PVCs/hr (yes/no), ≥3 continuous EI-PVCs (defined as nonsustained ventricular tachycardia [NSVT]; yes/no), number of NSVT events, and time (min) at which the NSVT events occurred (Al-Khatib et al., 2018). ST segments from the 24-hr recordings were not analyzed due to the risk of artifact.

Data Handling

After the completion of data collection, all data were double entered into a Statistical Package for Social Sciences (SPSS Version 25.0; IBM Corp., Armonk, NY) file by a blinded PhD-prepared registered nurse and a research nurse. Raw data were structured on a per-individual basis. Data were stored on a secure university-sponsored server that was fully encrypted and included a backup system. For the present study, a separate data set was created with only the variables of interest. Normality of the data was assessed (see Statistical Analysis section).

Secondary-Data Power Analysis

A power analysis was conducted to calculate the achieved power, given the Type I error, sample sizes, and estimated effect size using G*Power (Version 3.1.9.4). Assuming two-tailed two-group t tests with normal distributions and an expected effect size of Cohen’s d = 0.65, sample size 1 of 26, sample size 2 of 60, the calculated power is 0.80. Thus, the available data were suitable to draw a conclusion if the effect size was moderate.

Statistical Analysis

All analyses were conducted using SPSS (Version 25.0). Statistical significance was set at p < .05. Normality was assessed using the Shapiro–Wilk test and by visually assessing the distribution. Outliers, defined as values >3 standard deviations (SD) from the mean, were also assessed and removed if necessary. For this analysis, no transformations were performed and no outliers were removed.

Categorical variables are provided as % (n) and continuous variables as mean ± SD. To assess the difference in demographics and exercise performance measures between the group with EI-PVCs and the group without EI-PVCs, two-tailed t tests were conducted. When statistical tests were repeated multiple times, such as for evaluating BP over exercise, the Bonferroni correction was used to correct the critical p value. χ2 analysis was conducted to evaluate the association of EI-PVCs with myocardial ischemia. Due to the smaller and uneven sample sizes, Fisher’s exact test was used to determine whether there was a nonrandom association between the presence of EI-PVC and the presence of myocardial ischemia. Specificity, sensitivity, and relative risk (RR) analyses were conducted based on the sample disease prevalence. To assess the odds ratio (OR) between the presence of EI-PVCs and the presence of myocardial ischemia, logistic regression models were computed on the univariate level and after adjustment for known confounding cardiovascular risk factors including BMI, resting systolic blood pressure (SBP), resting DBP, mean heart rate, and current smoking (yes/no; Simpson et al., 2002; von Rotz et al., 2017). Model fit was measured using Nagelkerke R 2, Cox & Snell R 2, and for multivariate modeling, the Hosmer and Lemeshow test.

Results

The sample for this secondary analysis included 86 asymptomatic males, the majority of whom were overweight or obese (90.7%, n = 78) and hypertensive (73.3%, n = 63). Nearly one in three (30.2%, n = 26) participants had myocardial ischemia. The majority of participants had at least one EI-PVC during the 24-hr recording session (80.2%, n = 60), and these EI-PVCs were mostly characterized as isolated singlet EI-PVCs, though some participants had coupled EI-PVCs as well (7.0%, n = 6). Only three (3.5%) participants experienced more than 10 EI-PVCs per hour for at least 20 hr. No participants experienced NSVT during the 24-hr recording session. Figure 1 provides an example 12-lead ECG snapshot recorded after exercise treadmill testing and showing normal sinus rhythm at a rate of 80 bpm with ventricular trigeminy.

Figure 1.

Figure 1.

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Example 12-lead electrocardiogram (ECG) showing normal sinus rhythm at 80 bpm with unifocal premature ventricular contractions in an initial trigeminal pattern.

Table 1 presents a cross tabulation of the presence/absence of myocardial ischemia and EI-PVCs. Among the present sample, the prevalence of myocardial ischemia was 30.23%, 95% CI [20.79, 41.08]. χ2 analysis and cross tabulation demonstrated that EI-PVCs were significantly associated with myocardial ischemia (χ2 = 8.98; p = .003). The RR of myocardial ischemia with the presence of an EI-PVC was 1.54 (95% CI [1.22, 1.95]). The Fisher’s exact test was also statistically significant (p = .002), indicating a nonrandom association between EI-PVCs and myocardial ischemia with a small and uneven sample. The likelihood ratio of association was 10.54 (p = .001), indicating that it is very likely that the EI-PVCs were due to myocardial ischemia. The results of sensitivity, specificity, and negative and positive predictive value analyses are shown in Table 2.

Table 1.

Presence of Myocardial Ischemia With and Without EI-PVCs in Asymptomatic Adult Male Firefighters.

Ischemia No EI-PVCs Present n (%) EI-PVCs Present n (%)
No ischemia present 24 (92) 36 (60)
Ischemia present 2 (8) 24 (40)
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Note. N = 86. EI-PVCs = exercise-induced premature ventricular contractions.

Table 2.

Sensitivity and Specificity Analysis of Exercise-Induced Premature Ventricular Contractions.

Test Value [95% CI]
Specificity 92.31% [74.87, 99.05]
Sensitivity 40.00% [27.56, 53.46]
Positive likelihood ratio 1.54 [1.22, 1.95]
Negative likelihood ratio 0.19 [0.05, 0.75]
Disease prevalence 30.23% [20.79, 41.08]
Positive predictive valuea 40.00% [34.53, 45.74]
Negative predictive valuea 92.31% [75.36, 97.92]
Accuracya 55.81% [44.70, 66.52]
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a Values based on the calculated disease prevalence (i.e., myocardial ischemia) of 30.23%.

Differences in demographic and cardiovascular risk factors were assessed between those with EI-PVCs (69.8%, n = 60) and those without EI-PVCs (31.1%, n = 28; see Table 3). The only variable that differed significantly between the two groups was age, with men with EI-PVCs more likely to be older (44.6 ± 7.3 years vs. 39.7 ± 8.0 years, p = .007).

Table 3.

Demographic Characteristics and Cardiovascular Risk Factors for Asymptomatic Adult Male Firefighters.

Variable No EI-PVCs (n = 26) EI-PVCs (n = 60) p Value
Demographic
 Race
  White 20 (76.9) 49 (81.7) .61
  Non-White, Other 6 (23.1) 11 (18.3) .61
 Age (years) 39.7 ± 8.0 44.6 ± 7.3 .007
 Height (m) 1.79 ± 0.7 1.77 ± 0.7 .472
 Weight (kg) 95.0 ± 13.2 93.4 ± 13.7 .620
 BMI (kg/m2) 29.9 ± 4.1 29.6 ± 4.2 .887
 Obesity classification
  Normal (BMI 18.5–24.9) 2 (7.7) 6 (10.0) .74
  Overweight (BMI 25.0–29.9) 13 (50.0) 29 (48.3) .89
  Obese Class I (BMI 30.0–34.9) 9 (34.6) 21 (35.0) .97
  Obese Class II (BMI 35.0–39.9) 1 (3.8) 2 (3.3) .91
  Obese Class III (BMI ≥ 40.0) 1 (3.8) 2 (3.3) .91
 Waist circumference >100 cm 14 (53.8) 35 (58.3) .70
Risk factor
 Current smoker 2 (7.7) 8 (13.3) .46
 Sleep apnea 1 (3.8) 2 (3.3) .91
 Hypertension classification
  Normal 8 (30.8) 10 (16.7) .14
  Prehypertension 1 (3.8) 4 (6.7) .60
  Hypertension Stage I 10 (38.5) 26 (43.3) .68
  Hypertension Stage II 7 (26.9) 20 (33.3) .56
 Smoking (pack/day) 0.55 ± 0.6 1.04 ± 0.6 .349
 Blood pressure (mmHg)
  Systolic at rest (mmHg) 127.7 ± 16.3 130.6 ± 11.9 .358
  Diastolic at rest (mmHg) 80.0 ± 10.0 83.0 ± 7.2 .224
 Heart rate at rest (bpm) 78.6 ± 7.3 76.0 ± 9.7 .223
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Note. N = 86. Values are n (%) for categorical variables or mean ± SD for continuous variables. BMI = body mass index; EI-PVCs = exercise-induced premature ventricular contractions.

Table 4 shows differences in exercise treadmill testing parameters between the two groups. In summary, although the differences were not statistically significant, the EI-PVC group achieved a lower mean total exercise time, exercise expenditure, and maximum exercise speed than the no-EI-PVC group. Differences between the two groups in dynamic changes in heart rate were assessed, but no statistically significant differences were found for before exercise (EI-PVC 76.0 ± 9.7 bpm, no EI-PVC 78.6 ± 7.3 bpm, p = .22), maximum obtained heart rate (EI-PVC 166.6 ± 18.5 bpm, no EI-PVC 171.1 ± 15.8 bpm, p = .28), or 1-min postexercise (EI-PVC 136.6 ± 20.1 bpm, no EI-PVC 140.0 ± 15.8 bpm, p = .45). Figure 2 and Table 5 show the dynamic changes in SBP and DBP over the course of the exercise. Compared to subjects without EI-PVCs, those with EI-PVCs had a significantly lower postexercise SBP; however, the SBP recovery was comparable between groups. After Bonferroni correction, the difference in postexercise SBP was no longer significant (new critical p < .006). In general, a deviation in SBP occurred between the two groups, with the EI-PVC group achieving a lower pressure.

Table 4.

Exercise Treadmill Performance by Presence or Absence of Exercise-Induced Premature Ventricular Contraction (EI-PVC).

Parameter No EI-PVCs (n = 26)
Mean ± SD 		EI-PVC (n = 60)
Mean ± SD 		p Value [95% CI]
Total exercise time (min) 12.4 ± 3.0 11.4 ± 2.9 .13 [−0.32, 2.38]
Treadmill maximum speed achieved (mph) 4.7 ± 0.8 4.4 ± 0.7 .07 [−0.02, 0.66]
Treadmill maximum incline achieved 17.5 ± 2.2 17.0 ± 4.4 .60 [−1.3, 2.3]
METs achieved 12.8 ± 2.3 11.6 ± 2.6 .06 [−0.06, 2.3]
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Note. N = 86. METs = metabolic equivalent of tasks.

Figure 2.

Figure 2.

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Differences in systolic blood pressure (SBP) and diastolic blood pressure (DBP) over exercise duration between asymptomatic adult male firefighters with exercise-induced premature ventricular contraction (EI-PVC; n = 60) and those without (n = 26). *Statistically significant finding at p < .05. There were no statistically significant differences post-Bonferroni adjustment, with p < .006.

Table 5.

Differences in SBP and DBP Over Exercise Duration Between Asymptomatic Adult Male Firefighters With Exercise-Induced Premature Ventricular Contraction (EI-PVC) and Without EI-PVC.

Phase of Exercise No EI-PVCs (n = 26)
Mean ± SD 		EI-PVCs (n = 60)
Mean ± SD 		p Value [95% CI]
SBP (mmHg)
 Preexercise 130.2 ± 17.6 130.5 ± 15.3 .94 [−7.9, 7.3]
 Maximum 175.5 ± 31.4 165.7 ± 25.8 .14 [−3.3, 22.9]
 2-Min postexercise 162.3 ± 21.0 149.8 ± 24.8 .03* [3.4, 26.4]
 2-Min recovery 14.8 ± 25.9 17.8 ± 24.8 .67 (−14.4, 10.4)
DBP (mmHg)
 Preexercise 78.2 ± 11.6 78.5 ± 12.0 .91 [−5.9, 5.3]
 Maximum 76.8 ± 15.0 76.5 ± 14.1 .93 [−6.5, 7.2]
 2-Min postexercise 72.0 ± 17.1 75.3 ± 16.1 .41 [−11.3, 4.7]
 2-Min recovery 4.9 ± 16.9 0.9 ± 12.7 .27 [−3.1, 10.9]
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Note. N = 86. *Statistically significant finding at p < .05. There were no statistically significant differences post-Bonferroni adjustment, with p < .006. SBP = Systolic blood pressure; DBP = diastolic blood pressure.

Logistic regression models were used to adjust OR with demographic variables and other cardiovascular risk factors. At the univariate level, EI-PVCs were a significant predictor of myocardial ischemia (OR = 5.11; p = .015; 95% CI [1.38, 18.9]; Cox & Snell R 2 = .085; Nagelkerke R 2 = .121). In Model 2, demographic characteristics and cardiovascular risk factors including age (B = 0.069; OR = 1.07; p = .098; 95% CI [0.987, 1.162]), race (B = 0.158; OR = 1.171; p = .814; 95% CI [0.315, 4.353]), BMI (B = −0.038; OR = 0.963; p = .548; 95% CI [0.850, 1.090]), resting SBP (B = 0.017; OR = 1.017; p = .487; 95% CI [0.969, 1.068]), resting DBP (B = −0.013; OR = 0.987; p = .657; 95% CI = [0.930, 1.047]), resting mean 24-hr heart rate (B = −0.012; OR = 0.988; p = .680; 95% CI [0.935, 1.045]), and current smoking (B = −0.747; OR = 0.474; p = .414; 95% [CI 0.079, 2.838]) were corrected, and EI-PVCs remained a statistically significant predictor of myocardial ischemia (95% CI [1.087, 16.862]; B = 1.454; Cox & Snell R 2 = .140; Nagelkerke R 2 = .198; OR = 4.281; p = .038). The Hosmer and Lemeshow test was not statistically significant, indicating adequate model fit (χ2 = 5.285; df = 8; p = .727).

Discussion

In the present study, EI-PVCs were associated with myocardial ischemia among asymptomatic male firefighters without known cardiovascular disease. In addition, we found evidence suggestive of associations between EI-PVCs and reduced exercise performance and potentially lower postexercise SBP. EI-PVC was a strong predictor of myocardial ischemia even after adjustment for demographic and cardiovascular risk factors. Age was the only statistically significant demographic characteristic that differed significantly between men with and without EI-PVCs, with the group experiencing EI-PVC being older. Additionally, those with EI-PVC had, on average, a lower maximum SBP and a lower postexercise SBP, indicating reduced cardiac contractility during exercise and impaired vascular recovery response. This evidence supports the proposition that EI-PVCs are indicative of myocardial ischemia and are a potential early indicator of cardiovascular disease specifically among high-risk asymptomatic male firefighters. EI-PVCs may be able to aid in risk stratification, especially in high-risk, but asymptomatic, populations (Higgins & Higgins, 2007).

EI-PVCs reflect spontaneous electrical activity of the ventricles in a site below the atrioventricular node in response to exercise. The physiological mechanisms responsible for the induction of EI-PVCs include reentry circuits, triggered activity, and enhanced automaticity (Antzelevitch & Burashnikov, 2011). Enhanced automaticity occurs when pacemaker cells in the heart are surrounded by ischemic, infarcted, or otherwise compromised tissues that permit spontaneous beat generation (Antzelevitch & Burashnikov, 2011). This electrical activity is characterized by EI-PVCs with variable coupling intervals and can induce ventricular arrhythmias (Antzelevitch & Burashnikov, 2011). In adults with a structurally normal heart, as in the adults sampled in this study, the most common mechanism of EI-PVCs is enhanced automaticity, which can occur due to exercise, isoproterenol (in the electrophysiology laboratory), or hormonal changes in females (e.g., pregnancy, menses, menopause; Antzelevitch & Burashnikov, 2011; Simpson et al., 2002). Factors that increase the risk of enhanced automaticity include male sex, advanced age, African American race, hypertension and underlying cardiovascular disease, low educational attainment, high pack-years of smoking, high waist-to-hip ratio, and electrolyte deficiencies (Simpson et al., 2002; von Rotz et al., 2017). In our multivariate analysis, age, race, hypertension, smoking, and BMI were adjusted to address these potential confounding factors.

The association between EI-PVCs and ischemia may be due to an exacerbated mismatch between myocardial blood supply and exercise-related increases in cardiac demands. Poor coronary blood flow due to cardiovascular disease may contribute to myocardial ischemia, leading to enhanced automaticity and EI-PVCs (Elhendy et al., 2002; Fejka et al., 2002; Meine et al., 2006). Meine and colleagues (2006) studied EI-PVCs during recovery among patients who underwent cardiac catheterization within 180 days of a treadmill stress test with radionuclide perfusion imaging. They reported that those with EI-PVCs during recovery were more likely to be older Caucasian males with three-vessel coronary artery disease and have a history of hypertension and coronary artery bypass grafting.

Myocardial ischemia also hinders exercise performance and dampens the contractile force of the ventricles, which were both demonstrated in this study in a previous analysis of this data set, we reported impaired ventricular stretch during exercise due to myocardial ischemia, and hypertrophy may also be related to a widened QRST angle, a measure of heterogeneity in the action potential increasing the susceptibility to dysrhythmias (Dzikowicz & Carey, 2019b). Frolkis et al. (2003) assessed the ejection fraction by either echocardiogram or contrast ventriculography among asymptomatic adults undergoing exercise testing and found that a significantly higher percentage of patients with EI-PVCs had undiagnosed left ventricular (LV) dysfunction. Moreover, those patients with impaired LV function had an increased risk of death. In contrast, Morshedi-Meibodi et al. (2004) studied community-dwelling asymptomatic individuals from the Framingham Offspring Study and found that frequent EI-PVCs were associated with neither an ischemic ECG response nor reduced LV function assessed by fractional shortening in ECG during exercise testing.

A number of considerations need to be taken into account when interpreting the results of this analysis. First, echocardiography to evaluate for structural heart disease and cardiac performance was not performed. Echocardiography would have been useful for determining if firefighters with EI-PVCs had diminished myocardial contractility that might have contributed to lower postexercise SBP. Lower postexercise SBP can be due to heart disease, as postulated, or due to other pathological conditions that cause higher preload (e.g., hypertension) or simply due to aging. Without echocardiography, it is difficult to discern the exact cause of this finding. Although other studies have associated EI-PVCs with myocardial ischemia, some researchers have suggested other causes including hypertension, LV hypertrophy, increase in sympathetic activation, and autonomic instability (Jouven & Ducimetière, 2001; Kim et al., 2016). In our multivariate regression analysis, we controlled for these other possibilities and maintained a statistically significant relationship between myocardial ischemia and EI-PVCs. We suspect cardiovascular disease, specifically atherosclerotic disease, to be the most likely mechanism of myocardial ischemia because of the high reported prevalence among male firefighters; however, other possible causes of myocardial ischemia include hypercoagulation, endothelial dysfunction, epicardial coronary spasm, and inflammatory conditions (Pepine, 2015; Soteriades et al., 2011). In the present study, the unit of measurement for an EI-PVC was dichotomous; we aim to quantify the number and patterning (i.e., bigeminy, trigeminy) of EI-PVCs in future research to determine whether these values relate to the severity of myocardial ischemia.

This study adds evidence to support multiple observational studies and meta-analyses findings associating EI-PVCs with cardiovascular disease. Nurses, who play important roles in risk reduction and promotion of health behaviors, can use the present research to inform future studies and develop new interventions aimed at enhancing risk stratification and risk reduction among high-risk but asymptomatic adults such as firefighters (Wimberley, 2016). In the fire service, the majority of firefighters have other cardiovascular risk factors including hypertension, obesity, depression, and stress, all of which can be modified with intervention. In cardiac settings, nurses can use this information to execute treatment plans and address risk factors, thus leading to an improvement in the patient’s overall recovery.

Acknowledgments

The authors would like to acknowledge Sigma Theta Tau Epsilon Xi, University of Rochester School of Nursing Chapter, for recognizing this work at the local chapter. The results of this study were presented at the American Heart Association Scientific Sessions 2018 in Chicago, IL, USA.

Footnotes

Author Contributions: Dillon J. Dzikowicz contributed to conception, design, analysis, and interpretation; drafted the manuscript; critically revised the manuscript; gave final approval; and agreed to be accountable for all aspects of work ensuring integrity and accuracy. Mary G. Carey contributed to design and analysis, critically revised the manuscript, gave final approval, and agreed to be accountable for all aspects of work ensuring integrity and accuracy.

Declaration of Conflicting Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding: The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This study was supported by a grant from the National Institutes of Health, R21 NR-011077 (M. G. C.).

ORCID iD: Dillon J. Dzikowicz Inline graphic https://orcid.org/0000-0001-7230-1927

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