Sage Journals: Discover world-class research

Abstract

Introduction

The present study was undertaken to investigate the prognostic value of the frontal QRS-T angle associated with adverse cardiac outcomes in patients with carbon monoxide (CO) poisoning in early stages in the emergency department.

Materials and methods

The data of 212 patients with CO poisoning who were admitted to the ED between January 2010 and May 2020 were retrospectively analyzed. The frontal QRS-T angle was obtained from the automatic reports of the EKG device.

Results

Compared to patients without myocardial damage, among patients with myocardial damage, statistically high creatinine, creatine kinase MB, cardiac troponin I, and frontal QRS-T angle values were found (p < 0.001 for all parameters), while the saturation of arterial blood pH and arterial oxygen values were found to be lower (p = 0.002 and p < 0.001, respectively). The frontal QRS-T angle values were correlated with creatine kinase, creatine kinase-MB, cardiac troponin I, and oxygen saturation (SpO₂) in arterial blood (r = 0. 232, p = 0.001; r = 0. 253, p = < 0.001; r = 0. 389, p = < 0.001; r = −0. 198, p = 0.004, respectively). The optimum cut-off value of the frontal QRS-T angle was found to be 44.5 (area under the curve: 0.901, 95% confidence interval: 0.814–0.988, sensitivity: 87%, specificity: 84%).

Conclusions

The frontal QRS-T angle, a simple and inexpensive parameter that can be easily obtained from 12-lead surface electrocardiography, can be used as an early indicator in the detection of myocardial damage in patients with CO poisoning.

Keywords

Carbon monoxide poisoning electrocardiography frontal QRS-T angle

Introduction

Background

Carbon monoxide (CO) is an odorless, tasteless, colorless, non-irritating gas emitted due to the incomplete combustion of organic compounds.¹ The clinical severity of CO poisoning depends on the amount of gas ventilation absorbed, the exposure time, the environmental concentrations of O₂ and CO, and the general health of the affected person.

Although CO poisoning is harmful to all the organs and systems, the primary target organ systems for CO poisoning are the central nervous system and heart, as they are the most dependent on oxygen.² Thus, effects of CO manifest through tissue hypoxia or/and direct cell damage. It has long been known that myocardial damage is related to CO poisoning, which subsequently leads to electrical, functional, and morphological changes in the heart. Therefore, left ventricular dysfunction and electrocardiography (ECG) changes are common in patients with CO poisoning.^3–6 However, cardiac damage due to CO poisoning may be silent in some patients.^7,8

The prognostic value of the frontal QRS-T angle, which is a useful ECG measure of the dispersion between depolarization (QRS axis) and repolarization (T axis), has recently become an area of research interest and has been studied extensively to assess the severity of cardiac damage in different populations.⁹ The frontal QRS-T angle as a useful ECG measure of the dispersion between depolarization (QRS axis) and repolarization (T axis) is crucial in assessing the severity of cardiac damage.

Moreover, an association between increased spatial QRS-T angle and higher mortality in the general population has been demonstrated. Although spatial QRS-T angle can be calculated based on specialized software from ECG, no special software is required to calculate the frontal QRS-T angle from a routine 12-lead ECG. As previously reported, frontal and spatial QRS-T angles are comparable, and there is a strong correlation between them.¹⁰ Recently, the frontal QRS-T angle has emerged as a powerful predictor of long-term mortality in patients with left ventricular systolic dysfunction after an acute myocardial infarction.^11–14

Although the increased frontal QRS-T angle predicts mortality in different populations with a higher risk of cardiovascular diseases, no previous studies investigate the association between adverse cardiac outcomes and increased frontal QRS-T angle in patients with acute CO poisoning.

Therefore, the present study was undertaken to investigate the prognostic value of the frontal QRS-T angle in patients suffering from acute CO poisoning during the early stages.

Patients and methods

Study design and setting

The data of 212 patients with acute CO poisoning admitted to the emergency department between January 2010 and May 2020 were retrospectively analyzed.

The inclusion criteria were patients ≥ 18 years of age who had complete ECG and laboratory investigations including the COHb level by using a CO-oximeter device; these patients were also diagnosed with acute CO poisoning based on the history of one CO source exposure and clinical manifestations during their first admission to the emergency department. The exclusion criteria included left ventricular systolic dysfunction, ventricular or atrial premature depolarization, presence of a pacemaker, electrolyte imbalance, moderate and severe heart failure, atrial fibrillation, chronic renal and hepatic failure, bundle branch block, atrioventricular block, and use of antiarrhythmic and vasodilator drugs (Figure 1)

Figure 1.

Flow chart of the patients admitted with acute carbon monoxide poisoning according to inclusion.

The frontal QRS-T angle was obtained from the automatic reports produced by the ECG device. The frontal QRS-T angle is a new marker of myocardial repolarization, defined as the angle between the directions of ventricular depolarization (QRS axis) and repolarization (T axis). Data describing the typical ranges of frontal QRS-T angle from digital ECG transformation methods varied. The absolute value of the difference between the frontal plane QRS and T axes was calculated as the frontal QRS-T angle in the current study. If such a difference was over 180°, the QRS-T angle was adjusted to the minimal angle as 360° minus the absolute value of the difference between the frontal plane QRS and T axes.

Acute CO poisoning diagnosis was based on the clinical manifestations, laboratory records (carboxyhemoglobin (COHb)), and ECGs of the patients with CO source exposure history. Based on troponin measurement, patients with acute CO poisoning were divided into 2 groups according to the presence of myocardial damage. Patients with cardiac troponin I (cTnI) value above 0.40 ng/mL were considered as Group 1 (presence of myocardial damage)¹⁵ and other patients with a cTnI value ≤ 0.40 ng/mL were considered as Group 2 (absence of myocardial damage). Also, based on the cut-off values in the receiver-operating characteristics (ROC) curve analysis for the frontal QRS-T angle, all patients were classified into two groups as Group 1 (1–44.5°) and Group 2 (> 44.5°). Clinical demographic and laboratory data were compared between the groups as appropriate.

All stages of this study have been carried out in compliance with the Helsinki Declaration on Research Projects. In addition, the study was reviewed and approved by the Ethical Committee of the Sivas Cumhuriyet University. Ethics approval for the study protocol (2020/06/13) was obtained from the Ethical Committee of the Sivas Cumhuriyet University (Sivas, Turkey)

Statistical Analyses

Statistical analyses were carried out on SPSS statistical software version 23.0 (SPSS Inc., Chicago, USA). Descriptive statistics, percentages, means, and standard deviations summarized patients’ demographic and laboratory characteristics. Differences in the characteristics between the two groups were assessed using the Mann–Whitney U test and chi-square test. Pearson correlation coefficients were used in comparing parameters. Next, logistic regression analysis was performed to assess independent variables associated with the QRS-T angle, using adjusted odds ratios and 95% confidence intervals (CI). The ROC curve and the area under the curve (AUC) were calculated with the frontal QRS-T angle on admission. All statistical tests were conducted at the 5% significance level.

Results

Of the 212 patients with acute CO poisoning included in the study, 122 (55.5%) were male, 90 (45.5%) were female, and the mean age was 68.9 ± 13.9 years.

As regards age and sex, no significant differences were found between patients with and without myocardial damage (p = 0.277 and p = 0.163, respectively) (Table 1).

Table 1.

Demographic features of patients with the carbon monoxide poisoning myocardial damage (−) patient group versus themyocardial damage (+) patient group.

Characteristic	Myocardial damage (+)	Myocardial damage (−)	p value
Characteristic	(n = 23, %)	(n = 189, %)	p value
Age, year (mean ± SD)	43.28 ± 12.53	40.03 ± 14.39	0.277^a
Gender
Male	9 (42.9)	113 (59.2)	0.163^b
Female	12 (57.1)	78 (40.8)

^aMann–Whitney U test

^bchi-square test.

As presented in Table 2, there was a statistically significant difference between the patients with and without myocardial damage in terms of creatine kinase, creatine kinase-MB, cTnI, level of hydrogen in arterial blood (pH), oxygen saturation in the arterial blood (SpO₂) and the frontal QRS-T angle. Creatine kinase (45 (346–877) vs 75.5 (42–113), p < 0.001), creatine kinase-MB (87 (70–116.5) vs 16 (10.5–21), p < 0.001) and troponin-I (4.8 ± 3.5 vs 0.003 ± 0.01, p < 0.001) values were significantly higher in patients with myocardial damage, while the level of hydrogen in arterial blood (pH) (7.3 ± 0.2 vs 7.4 ± 0.1, p = 0.002) and oxygen saturation (SpO₂) in arterial blood (87.8 ± 6.3 vs 94.8 ± 5.0, p < 0.001) were low. The frontal QRS-T angle was significantly higher in the patients with myocardial damage than in patients without myocardial damage (48.4 ± 4.0 vs 41.5 ± 3.9, p < 0.001) (Table 2). There was also a statistically significant difference between the groups of the frontal QRS-T angle concerning palpitation and chest pain (21.0% vs 36.0%, p = 0.027 and 9.9% vs 24.0, p = 0.012, respectively) (Table 3).

Table 2.

The mean values of blood parameters of patients with and without myocardial damage due to carbon monoxide poisoning.

Variable	Myocardial damage (+) (N = 23 mean ± SD)	Myocardial damage (−) (N = 189 mean ± SD)	p value (Mann–Whitney U test)
White blood cell (10³/μl)	8.3 ± 0.9	8.4 ± 2.3	0.866
Hemoglobin (g/dL)	13.6 ± 1.4	13.6 ± 1.6	0.929
Platelet (10³/μl)	251.7 ± 27.0	238.0 ± 36.1	0.080
Glucose (mg/dl)	124.8 ± 79.0	107.7 ± 26.2	0.312
BUN (mg/L)	13.8 ± 2.2	14.1 ± 5.9	0.563
Creatinine (mg/dL)	0.8 ± 0.3	0.7 ± 0.2	0.077
Creatine kinase (U/L) Median (%25–75)^a	456 (346–877)	75.5 (42–113)	< 0.001
Creatine kinase MB(U/L) median (%25–75)^a	87 (70–116.5)	16 (10.5–21)	< 0.001
Troponin-I (ng/dL)	4.8 ± 3.5	0.003 ± 0.01	< 0.001
Arterial blood pH	7.3 ± 0.2	7.4 ± 0.1	0.002
SpO₂ (%)	87.8 ± 6.3	94.8 ± 5.0	< 0.001
PaO₂ (mmHg)	101.2 ± 38.9	94.6 ± 17.2	0.432
PaCO₂ (mmHg)	34.7 ± 5.7	34.9 ± 12.7	0.951
% COHb	17.4 ± 13.1	15.5 ± 8.3	0.496
Frontal QRS-T angle	48.4 ± 4.0	41.5 ± 3.9	< 0.001

pH: power of hydrogen; SpO₂: oxygen saturation in the arterial blood; PaO₂: partial pressure of oxygen in the arterial blood; PaCO2: partial pressure of carbon dioxide in the arterial blood, Data p-value as median (25%–75% interquartile ranges).

^aBUN: blood urea nitrogen.

Table 3.

Clinical and cardiovascular characteristics in carbon monoxide–poisoned patients in relation to QRS-T angle (n = 212).

	FQRS-T angle
	Group 1 (1–44.5°)	Group 2 (> 44.5°)	p value^a
Characteristic	(n, %)	(n, %)
Palpitation
Present	34 (21.0)	18 (36.0)	0.027
Absent	128 (79.0)	32 (64.0)
Chest pain
Present	16 (9.9)	12 (24.0)	0.012
Absent	146 (90.1)	38 (76.0)
Pulse
> 100/min	15 (9.3)	7 (14.0)	0.238
60–100/min	147 (90.7)	43 (86.0)
Respiratory rate
> 20/min	74 (45.7)	22 (44.0)	0.483
12–20	88 (54.3)	28 (56.0)
Blood pressure
Hypertension	18 (11.1)	9 (18.0)	0.386
Normotension	143 (88.3)	41 (82.0)	0.363
Hypotension	1 (0.6)	0 (0.0)	0.176

^aMann–Whitney U test.

Correlation between the frontal QRS-T angle and variables in patients with CO poisoning are summarized in Table 4. The frontal QRS-T angle values correlated with creatine kinase, creatine kinase-MB, troponin-I, and oxygen saturation (SpO₂) in arterial blood (r = 0. 232, p = 0.001; r = 0. 253, p = < 0.001; r = 0. 389, p= < 0.001; r = −0. 198, p = 0.004, respectively).

Table 4.

Correlation between the frontal QRS-T angle and some variables in all patients with monoxide poisoning (n = 212).

Variable	All patients
	R	p value
Creatine kinase (U/L)	0.232	0.001
Creatine kinase MB (U/L)	0.253	< 0.001
Troponin-I (ng/dL)	0.389	< 0.001
Arterial blood pH	−0.122	0.76
SpO₂ (%)	−0.198	0.004

The optimum cut-off value of the frontal QRS-T angle was determined by ROC analysis, the optimum cut-off value of the angle was found to be 44.5 ((AUC): 0.901, 95% CI: 0.814–0.988, sensitivity: 87%, specificity: 84%); optimum cut-off value of cTnI was found to be 0.27 ((AUC): 1.0, 95% CI: 1.0–1.0, sensitivity: 100%, specificity: 100%); optimum cut-off value of creatine kinase was found to be 168.5 ((AUC): 0.979, 95% CI: 0.956–1.0, sensitivity: 91%, specificity: 92%); optimum cut-off value of pH was found to be 7.33 ((AUC): 0.547, 95% CI: 0.393–0.701, sensitivity: 44%, specificity: 64%); optimum cut-off value of SpO₂ was found to be 99.6 ((AUC): 0.575, 95% CI: 0.419–0.731, sensitivity: 57%, specificity: 73%) (Table 5, Figures 2 and 3).

Table 5.

Cut-off value, sensitivity, specificity of the frontal QRS-T angle, cardiac troponin I, creatine kinase, pH, and SpO₂ for predicting myocardial damage in patients with carbon monoxide poisoning.

	Frontal QRS-T angle	Cardiac troponin I	Creatine kinase	pH	SpO₂
Cut-off value	44.5	0.27	168.5	7.33	99.6
Sensitivity	0.87	100	91	0.44	0.57
Specificity	0.84	100	92	0.64	0.73
PPV (95% CI)	86.96 (67.39–95.56)
NPV (95% CI)	84.13 (80.85–86.93)
AUC (95% CI)^a	0.901 (0.814–0.988)	1.0 (1.0–1.0)	0.979 (0.956–1.0)	0.547 (0.393–0.701)	0.575 (0.419–0.731)

PPV: positive predictive value; NPV: negative predictive value; CI: confidence interval; pH: hydrogen in arterial blood; SpO₂: oxygen saturation in the arterial blood.

^aAUC: area under the curve.

Figure 2.

Receiver-operating characteristic curve of the frontal QRS-T angle, cardiac troponin I, and creatine kinase for predicting myocardial injury in patients with acute carbon monoxide poisoning and exclusion criteria.

Logistic regression analysis was performed to explore associations with the frontal QRS-T and selected variables (creatine kinase, cTnI, arterial pH, and SpO₂) (Table 6). As shown in Table 6, only the cTnI was associated with the frontal QRS-T.

Figure 3.

Receiver-operating characteristic curve of power of hydrogen in arterial blood, oxygen saturation in the arterial blood angle for predicting myocardial injury in patients with acute carbon monoxide.

Table 6.

Logistic regression analysis of selected variables associated with the QRS-T angle (n = 212).

Variables	β	OR (95% CI)	p value
Creatine kinase	−0.846	0.43 (0.06, 3.06)	0.398
Cardiac troponin I	0.755	2.13 (1.47, 3.08)	<0.001
Arterial ph	−2780	0.06 (0.00, 3.33)	0.171
SpO₂	−0.008	0.99 (0.97, 1.01)	0.387

OR: odds ratio; CI: confidence interval; pH: potential of hydrogen; SpO₂: peripheral oxygen saturation.

Discussion

This study is the first in literature which determined the importance of a wide frontal QRS-T angle on the ECG in detecting myocardial damage among CO poisoning patients.

In CO intoxications, it competes with oxygen and forms carboxyhemoglobin (COHb) with 200 times greater affinity than oxygen. Displacement of oxygen reduces oxygen-carrying capacity. CO also stabilizes the Hb quaternary state and reduces oxygen release and delivery to tissues. However, the toxic effects of CO cannot be explained by this event alone. Due to the increase in the binding of CO to enzymes and proteins (cytochrome P-450 and myoglobin) at the cellular level, the resultant effect is a cellular damage caused by the reduction of energy production in the mitochondria of the cells mainly due to the binding of cytochrome aa3. With these effects occurring in the myocardium, anaerobic respiration begins, Adenosine triphosphate (ATP) production is interrupted, and lactate accumulates with free radicals at the cellular level. Relaxation of vascular smooth muscles with increased inflammation and thrombotic tendency, myocardial damage, and clinical complications are observed. As a result, the cardiotoxic effects of CO occur¹⁶ in the early stages of CO poisoning; the oxygen requirement of the myocardium increases with compensatory tachyarrhythmias that develop due to systemic hypoxia, after which the diffusion of CO in the myocardium is accelerated; thus, the hypoxic damage is further increased.¹⁷

Electrocardiography alterations are described in many studies. The alterations after acute CO intoxication can be reversed or prolonged according to the severity of the intoxication and can occur due to the repolarization disturbances (e.g., ischemic changes and QT interval prolongation).¹⁸

In patients who were presented with CO poisoning, estimating the risk of myocardial damage can help determine both immediate and short-term treatment strategies. Patients suspected of exposure to CO should be screened for myocardial damage. One of the indications for hyperbaric O₂ treatment of CO poisoning is myocardial ischemia.¹⁹ It has been shown that cardiotoxicity-related morbidity and mortality rates can be reduced with appropriate treatment.²⁰

While myocardial damage due to severe CO poisoning can predict short-term undesirable bad results²¹ in patients with moderate-to-severe CO poisoning, it was a significant predictor of mortality.²² Therefore, emergency room physicians should always identify myocardial damage after CO poisoning with an ECG, cardiac markers (B-type natriuretic peptide), etc. and imaging (echocardiography or coronary angiography) tests.¹⁶

Cardiac biomarkers are of great importance due to the fact that they indicate myocardial damage in systemic or cardiac diseases. Primary cardiac causes of myocardial damage and other systemic diseases play an essential role in the patient’s morbidity and mortality. Elevated troponin levels predict short-term (sepsis, pulmonary embolism, and ischemic stroke)^23–25and long-term mortality (in critical patients, end-stage kidney disease, and major vascular surgery cases).^26–29

Cardiac biomarkers have also been used to determine myocardial damage in CO poisonings.^30,22

Cardiac dysfunction due to CO exposure can be indicated by chest pain, ECG changes, dyspnea, and low blood pressure measurement.³¹ Most importantly, CO-induced myocardial damage can also occur in the absence of cardiac symptoms,³² and ST-T changes in ECG can be a misleading indicator of severity in CO poisoning.³³

Electrocardiography is a noninvasive and prognostic diagnostic tool commonly used for cardiac damage in emergency departments. The frontal QRS-T angle is defined as the angle between the main electrical axes of ventricular depolarization and repolarization.¹⁴ Evaluating QRS-T in the frontal plane is simple and can be easily calculated and included in the output results with automatic interpretation features to the ECG devices.

Pavri et al. demonstrate that a frontal QRS-T angle > 90° was a significant predictor of adverse outcomes in non-ischemic cardiomyopathic patients. They evaluated the groups with the endpoint for death, appropriate implantable cardioverter-defibrillator (ICD) shock, or resuscitated cardiac arrest. Relative risk was associated with a near doubling of the risk of death, appropriate ICD shock, or resuscitated cardiac arrest.^34*

In addition, Zhang et al. found the frontal QRS-T angle to be significant for predicting the incidence of coronary heart disease and total mortality among women. Similarly, a study of atherosclerosis risk in communities involving 9498 patients found that the frontal and spatial QRS-T angle was a marker that predicted silent myocardial ischemia.¹⁰

The frontal QRS-T angle is a strong predictor of cardiovascular events in different patient populations. Lown et al. investigated the survival of 1843 patients admitted with acute coronary syndromes, and they were stratified by the frontal QRS-T angle. A frontal QRS-T angle age-risk (FAAR) score was constructed according to their age and the frontal QRS-T angle. The FAAR score offered good discriminative performance for 30-day and 2-year mortality.³⁵ The frontal QRS-T angle at admission and after the percutaneous procedure was found to be a marker of in-hospital mortality, and 78 from 128 STEMI patients who had successful thrombolysis had a lower frontal QRS-T angle measured at 90 min compared to the failed thrombolysis group.³⁶ Blood pressure has a diurnal rhythm and decreases approximately 10% during sleep. A lack of blood pressure fall during the night is called a non-dipping blood pressure pattern and is associated with cardiovascular risk. A study conducted in hypertensive patients without left ventricular hypertrophy found that the frontal QRS-T angle predicted a non-dipper state.³⁷

Diabetes mellitus damages the autonomic nerve fibers in the heart, resulting in abnormalities in heart rate control and vascular dynamics. May et al. conducted a study in diabetic patients and observed 153 patients for 21.5 years. They concluded that the abnormal frontal QRS-T angle (QRS-T angle ≥ 73° in men and ≥ 67° in women), similar to cardiovascular autonomic neuropathy, independently predicted long-term mortality due to all causes.³⁸ Repolarization and depolarization abnormalities are commonly seen during heart failure with preserved ejection fraction clinical state. Increased frontal QRS-T angle was found to predict impaired left and right ventricular function, adverse cardiac remodeling, and undesirable cardiac events in patients with heart failure with a preserved ejection fraction.³⁹

In our study, the frontal QRS-T angle in the group of patients who developed myocardial damage after CO intoxication was greater, compared to the group who did not develop myocardial damage, and this is a strong predictor of cardiovascular events, as in previous studies (Table 2).^9,40,41

It should be kept in mind that the COHb level does not correlate with clinical status, and the toxicity threshold can show individual differences. A correlation between COHb levels and ECG changes following acute or chronic CO exposure may not be observed.¹⁸ In our study, COHb percentage levels were not significant between two groups with and without myocardial damage (Table 2). Since the COHb level does not provide information about myocardial damage, myocardial damage can be predicted by calculating the frontal QRS-T angle on the ECG, a cost-free and straightforward study.

In addition, our study also showed that the frontal QRS-T angle could be used to detect myocardial damage with high sensitivity and specificity with cut-off values above 44.5 (Table 3).

Strengths and limitations

Our work has some limitations. The first and most important limitation is that it is a retrospective study with a relatively small group of patients with myocardial damage and was not supported by echocardiographic and coronary angiography. Also, patients could not be monitored for possible complications and consequences after pain.

Conclusions

CO causes myocardial damage and tissue hypoxia with its direct and indirect effects. In order to prevent cardiovascular risks and other complications in CO poisoning we must select the right oxygen administration way and time. The frontal QRS-T angle is a simple and inexpensive parameter that can be easily obtained from ECG and can affect our management. Our study shows that this simple ECG parameter may have an essential role in determining the risk of myocardial damage, regardless of COHb levels, in patients with CO poisoning.

Footnotes

Author contributions

The concept and design of the study; the acquisition, analysis, and interpretation of data for work; drafting of the work and the critical revision for important intellectual content; and final approval of the article was made by YKT. The drafting of the study and its critical revision for important intellectual content was performed by NN. GT, İK, and SY made the analysis and interpretation of data for the study.

Declaration of conflicting interests

The author(s) declared no potential conflicts of interest for 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: The author(s) received no financial support for the research, authorship, and/or publication of this article.

Ethical approval

The institutional ethics committee approved the Sivas Cumhuriyet University study protocol (2020–06/13).

Informed consent

The medical authorities of our hospital authorized this study, and patients were informed and signed their consent to their data collection.

Data availability

The data were retrieved from the Clinical Data Analysis and Reporting System, the Clinical Management System, and the Electronic Patient Record System of the Hospital Authority, Sivas.

ORCID iD

Yusuf K Tekin

References

Rose

Wang

, et al. Carbon monoxide poisoning: pathogenesis, management, and future directions of therapy. Am J Respir Crit Care Med 2017; 195(5): 596–606.

Gozubuyuk

Dag

Kacar

, et al. Epidemiology, pathophysiology, clinical evaluation, and treatment of carbon monoxide poisoning in child, infant, and fetus. North Clin Istanbul 2017; 4(1): 100–107.

Lippi

Rastelli

Meschi

, et al. Pathophysiology, clinics, diagnosis and treatment of heart involvement in carbon monoxide poisoning. Clin Biochem 2012; 45(16–17): 1278–1285.

Çiftçi

Günday

Çaliskan

, et al. Mild carbon monoxide poisoning impairs left ventricular diastolic function. Indian J Crit Care Med 2013; 17(3): 148–153.

Ozyurt

Karpuz

Yucel

, et al. Effects of acute carbon monoxide poisoning on ECG and echocardiographic parameters in children. Cardiovasc Toxicol 2017; 17(3): 326–334.

Park

Seo

Choi

, et al. Various echocardiographic patterns of left ventricular systolic dysfunction induced by carbon monoxide intoxication. Cardiovasc Toxicol 2016; 16(4): 361–369.

Gandini

Castoldi

Candura

, et al. Carbon monoxide cardiotoxicity. J Toxicol Clin Toxicol 2001; 39(1): 35–44.

Zhang

Rautaharju

Prineas

, et al. Electrocardiographic QRS-T angle and the risk of incident silent myocardial infarction in the atherosclerosis risk in communities study. J Electrocardiol 2017; 50(5): 661–666.

Yamazaki

Froelicher

Myers

, et al. Spatial QRS-T angle predicts cardiac death in a clinical population. Heart Rhythm 2005; 2(1): 73–78.

10.

Zhang

Prineas

Case

, et al. Comparison of the prognostic significance of the electrocardiographic QRS/T angles in predicting incident coronary heart disease and total mortality (from the Atherosclerosis Risk In Communities Study). Am J Cardiol 2007; 100(5): 844–849.

11.

Macfarlane

. The frontal plane QRS-T angle. Europace 2012; 14(6): 773–775.

12.

Aro

Huikuri

Tikkanen

, et al. QRS-T angle as a predictor of sudden cardiac death in a middle-aged general population. Europace 2012; 14(6): 872–876.

13.

Oehler

Feldman

Henrikson

, et al. QRS-T Angle: a Review. Ann Noninvasive Electrocardiol 2014; 19(6): 534–542.

14.

Raposeiras-Roubín

Virgós-Lamela

Bouzas-Cruz

, et al. Usefulness of the QRS-T angle to improve long-term risk stratification of patients with acute myocardial infarction and depressed left ventricular ejection fraction. Am J Cardiol 2014; 113(8): 1312–1319.

15.

Antman

Tanasijevic

Thompson

, et al. Cardiac-specific troponin I levels to predict the risk of mortality in patients with acute coronary syndromes. New Engl J Med 1996; 335(18): 1342–1349.

16.

Szponar

Kołodziej

Majewska

, et al. Myocardial injury in the course of carbon monoxide poisoning. Przeglad lekarski 2012; 69(8): 528–534.

17.

Chiew

Buckley

. Carbon monoxide poisoning in the 21st century. Crit Care 2014; 18: 221.

18.

Carnevali

Omboni

Rossati

, et al. Electrocardiographic changes in acute carbon monoxide poisoning. Minerva Med 1987; 78(3): 175–178.

19.

Gülbay

Önen

. Carbon monoxide poisoning. Turkiye Klinikleri J Surg Med Sci 2006; 2: 109–112.

20.

Adir

Merdler

Ben Haim

, et al. Effects of exposure to low concentrations of carbon monoxide on exercise performance and myocardial perfusion in young healthy men. Occup Environ Med 1999; 56(8): 535–538.

21.

Kao

Lien

Kou

, et al. Assessment of myocardial injury in the emergency department independently predicts the short-term poor outcome in patients with severe carbon monoxide poisoning receiving mechanical ventilation and hyperbaric oxygen therapy. Pulm Pharmacol Ther 2009; 22(6): 473–477.

22.

Henry

Satran

Lindgren

, et al. Myocardial injury and long-term mortality following moderate to severe carbon monoxide poisoning. JAMA 2006; 295(4): 398–402.

23.

Spies

Haude

Fitzner

, et al. Serum cardiac troponin T as a prognostic marker in early sepsis. Chest 1998; 113(4): 1055–1063.

24.

Giannitsis

Müller-Bardorff

Kurowski

, et al. Independent prognostic value of cardiac troponin T in patients with confirmed pulmonary embolism. Circulation 2000; 102(2): 211–217.

25.

James

Ellis

Whitlock

, et al. Relation between troponin T concentration and mortality in patients presenting with an acute stroke: observational study. BMJ 2000; 320(7248): 1502–1504.

26.

Landesberg

Shatz

Akopnik

, et al. Association of cardiac troponin, CK-MB, and postoperative myocardial ischemia with long-term survival after major vascular surgery. J Am Coll Cardiol 2003; 42(9): 1547–1554.

27.

Dierkes

Domröse

Westphal

, et al. Cardiac troponin T predicts mortality in patients with end-stage renal disease. Circulation 2000; 102(16): 1964–1969.

28.

Apple

Murakami

Pearce

, et al. Predictive value of cardiac troponin I and T for subsequent death in end-stage renal disease. Circulation 2002; 106(23): 2941–2945.

29.

Khan

Hemmelgarn

Tonelli

, et al. Prognostic value of troponin T and I among asymptomatic patients with end-stage renal disease. Circulation 2005; 112(20): 3088–3096.

30.

Yang

, et al. Striatal dopamine transporter binding for predicting the development of delayed neuropsychological sequelae in suicide attempters by carbon monoxide poisoning: a SPECT study. Psychiatry Res Neuroimaging 2011; 194(3): 219–223.

31.

Diltoer

Colle

Hubloue

, et al. Reversible cardiac failure in an adolescent after prolonged exposure to carbon monoxide. Eur J Emerg Med 1995; 2(4): 231–235.

32.

Marius-Nunez

. Myocardial infarction with normal coronary arteries after acute exposure to carbon monoxide. Chest 1990; 97(2): 491–494.

33.

McMeekin

Finegan

. Reversible myocardial dysfunction following carbon monoxide poisoning. Can J Cardiol 1987; 3(3): 118–121.

34.

Pavri

Hillis

Subačius

, et al. Prognostic value and temporal behavior of the planar QRS-T angle in patients with nonischemic cardiomyopathy. Circulation 2008; 117(25): 3181–3186.

35.

Lown

Munyombwe

Harrison

, et al. Association of frontal QRS-T angle-age risk score on admission electrocardiogram with mortality in patients admitted with an acute coronary syndrome. Am J Cardiol 2012; 109(3): 307–313.

36.

Colluoglu

Tanriverdi

Unal

, et al. The role of baseline and post-procedural frontal plane QRS-T angles for cardiac risk assessment in patients with acute STEMI. Ann Noninvasive Electrocardiol : official J Int Soc Holter Noninvasive Electrocardiol Inc 2018; 23(5): e12558.

37.

Tanriverdi

Unal

Eyuboglu

, et al. The importance of frontal QRS-T angle for predicting non-dipper status in hypertensive patients without left ventricular hypertrophy. Clin Exp Hypertens 2018; 40(4): 318–323.

38.

May

Graversen

Johansen

MØ

, et al. The prognostic value of the frontal QRS-T angle is comparable to cardiovascular autonomic neuropathy regarding long-term mortality in people with diabetes. a population based study. Diabetes Res Clin Pract 2018; 142: 264–268.

39.

Selvaraj

Ilkhanoff

Burke

, et al. Association of the frontal QRS-T angle with adverse cardiac remodeling, impaired left and right ventricular function, and worse outcomes in heart failure with preserved ejection fraction. J Am Soc Echocardiogr 2014; 27(1): 74–e2.

40.

de Torbal

Kors

van Herpen

, et al. The electrical T-axis and the spatial QRS-T angle are independent predictors of long-term mortality in patients admitted with acute ischemic chest pain. Cardiology 2004; 101(4): 199–207.

41.

Malik

Hnatkova

Batchvarov

. Post infarction risk stratification using the 3-D angle between QRS complex and T-wave vectors. J Electrocardiol 2004; 37: 201–208.

Frontal QRS-T angle as a predictive marker for myocardial damage in acute carbon monoxide poisoning

Abstract

Introduction

Materials and methods

Results

Conclusions

Keywords

Introduction

Background

Patients and methods

Study design and setting

Statistical Analyses

Results

Discussion

Strengths and limitations

Conclusions

Footnotes

Author contributions

Declaration of conflicting interests

Funding

Ethical approval

Informed consent

Data availability

ORCID iD

References