Electrocardiographic findings of methanol toxicity: a cross-sectional study of 356 cases in Iran.

BACKGROUND: Methanol is widely used in industry; however, methanol poisoning is not common. In this regard, a number of outbreaks have been recently reported due to inappropriate processing of alcoholic beverages. Shiraz, a city located in the southern part of Iran, faced one of such outbreaks in 2020 during COVID-19 pandemic. There is no sufficient literature on the electrocardiographic findings in methanol toxicity. This study aimed to address this gap in the literature. METHOD: A total of 356 cases with methanol toxicity referred to Shiraz University of Medical Science Tertiary Hospitals (Faghihi and Namazi) in March and April, 2020. The clinical findings of blindness and impaired level of consciousness, lab data such as arterial blood gas, electrolytes, and creatinine, and the most common findings from ECGs were collected. RESULTS: The most common ECG findings were J point elevation (68.8%), presence of U wave (59.2%), QTc prolongation (53.2% in males and 28.6% in females), and fragmented QRS (33.7%). An outstanding finding in this study was the presence of myocardial infarction in 5.3% of the cases. This finding, to the best of our knowledge, has only been reported in a few case reports. Brugada pattern (8.1%) and Osborn wave (3.7%) were the other interesting findings. In multivariate analysis, when confounding factors were adjusted, myocardial infarction, atrioventricular conduction disturbances, sinus tachycardia, and the prolonged QTC > 500 msecond were four independent factors correlated with methanol toxicity severity measured with arterial blood PH on arterial blood gas measurements, with odds ratios of 12.82, 4.46, 2.32 and 3.15 (P < 0.05 for all), respectively. CONCLUSION: Electrocardiographic variations during methanol intoxication are remarkable and well-correlated with poisoning severity. Myocardial infarction was an egregious and yet a common concerning finding in this sample, which need to be ruled out in methanol toxicity.

Electrocardiographic, cardiac enzymes, and magnesium in patients with severe acute pancreatitis.

Severe acute pancreatitis (SAP) can lead to multiple-organ dysfunction syndrome (MODS). Electrocardiographic (ECG), cardiac enzyme, and serum magnesium abnormalities occur after SAP. Electrocardiographic and cardiac enzyme abnormalities are described as variables in SAP patients, which contribute to the effects of MODS. Hypomagnesium is also closely associated with ECG abnormalities; therefore, hypomagnesium was also considered to be a variable in this study. A consecutive series of 54 patients admitted within 72 hours after SAP occurred was studied. A standard 12-lead ECG, cardiac enzyme, and serum magnesium measurement were routinely performed at admission. Linear correlation was used to analyze the relationship between hypomagnesemia and sinus tachycardia. The nonparametic binomial test was used to analyze dichotomized dependent variables (premature beat, atrial fibrillation, ST-segment depression, abnormal T wave, and long QT interval). Hypomagnesemia was present in 15 patients (28%), who subsequently had sinus tachycardia. There was a significant negative relationship (-1 < r <0) between hypomagnesemia and sinus tachycardia (p < .05). There were 14 (17%) premature beat, 7 (8%) atrial fibrillation, 21 (25%) ST-segment depression, 18 (21%) abnormal T wave, and 17 (31%) long QT-interval events in 54 SAP patients. Hypomagnesemia is a reason for ECG abnormalities. Electrocardiographic and cardiac enzyme abnormalities are considered to be transitory variables that are present in patients with SAP.

Cardiac responses to the intrapericardial delivery of metoprolol: targeted delivery compared to intravenous administration.

Anti-arrhythmic drugs have narrow therapeutic ranges and typically can engender harmful side effects. The intrapericardial (IP) delivery of anti-arrhythmic agents proposes to achieve higher myocardial levels while minimizing plasma concentrations, thus diminishing systemic side effects. Furthermore, IP delivery enables concentrations at the target site to be more precisely controlled. Our study objective was to compare the relative cardiac effects of intrapericardial administration of metoprolol to standard intravenous (IV) delivery in a swine surgical model. In order to answer the question of how IP metoprolol affects sinus tachycardia, atrial electrophysiology, and pharmacokinetics compared with IV delivery, a medial sternotomy was performed on 21 swine that were divided into three groups: (1) After inducing sinus tachycardia, metoprolol boluses were delivered IP (n = 4) or IV (n = 4); (2) metoprolol was administered either IP (n = 3) or IV (n = 3) with saline controls (n = 3), and electrophysiologic data were collected; (3) metoprolol levels were tracked both in the blood (IV, n = 2) and pericardial (IP, n = 2) fluid. After either IP or IV delivery of metoprolol, heart rates were lowered significantly to 70% and 73% of control rate, respectively. The therapeutic effect of IV-administered metoprolol was considerably reduced after 1 h but was sustained longer in the IP group. Additionally, ventricular contractility and mean arterial pressure parameters were significantly lower in IV-treated animals but were nearly unaffected in IP-treated animals. With IP administration, the elimination half-life of metoprolol in pericardial fluid was 14.4 min with negligible accumulations in the plasma, whereas with IV delivery, the elimination half-life in plasma was 11.1 min with negligible amounts found in the pericardial fluid. The targeted intrapericardial delivery of metoprolol effectively lowers heart rates for sustained periods of time, with minimal effect on either ventricular contractility or mean arterial pressure. We did not observe dramatic changes in induced atrial fibrillation times or refractory periods using this model.

Clinical, electrocardiographic, and laboratory findings in children with amitriptyline intoxication.

BACKGROUND: Amitriptyline is one of the major tricyclic antidepressants, and the data on amitriptyline poisoning in children are limited. OBJECTIVES: To present our experiences with amitriptyline poisoning in children, particularly with regard to its effects on electrocardiogram (ECG) and relation with clinical status. METHODS: Clinical, laboratory, and electrocardiographic findings in 52 children admitted with amitriptyline poisoning were reviewed. Patients were divided into 2 groups according to age, as 6 years or younger (group A) and older than 6 years (group B). RESULTS: Mean age was 4.6 +/- 3.0 years. Thirty-one patients were male, and 41 were 6 years or younger. Ingested amitriptyline dose was known in 23 patients (range, 2.3 mg/kg-27 mg/kg). The most frequent findings were lethargy (76.9%), sinus tachycardia (57.7%), and coma (48.1%). Four patients had a history of convulsion. The most common laboratory abnormalities were hyponatremia (26.9%) and leukocytosis (25%). Elevated transaminase levels were observed in 4 patients. In ECG, 11 (22.4%) patients had QTc prolongation and in 4 (8.2%) of them, it was significant. In 4 patients (8.2%), the QRS duration was 100 ms or longer and in 15 patients, the R wave in aVR was 3 mm or longer. The frequencies of clinical, laboratory, and electrocardiographic findings were similar between the 2 age groups (P > 0.05). No clinically apparent arrhythmias were observed. The positive predictive value of a widened QRS was 100% in terms of coma. None of the patients with an R wave in aVR of less than 3 mm developed convulsion; thus, the negative predictive value of an R wave in aVR of 3 mm or longer was 100% in terms of convulsion. CONCLUSIONS: Amitriptyline poisoning may result in severe toxicity. Frequencies of clinical, laboratory, and ECG findings were similar in the 2 age groups. Amitriptyline overdose results in some ECG changes that can possibly help to predict the results of poisoning. Absence of an R wave in aVR of 3 mm or longer predicts seizures with a high negative predictive value, and a QRS duration of 100 or longer ms predicts coma with a high positive predictive value.

Troponin I and risk stratification of patients with acute nonmassive pulmonary embolism.

The assessment of risk and appropriate treatment of patients with acute pulmonary embolism (PE) remains a challenge. The prognostic performance of cardiac troponin I (cTnI) in predicting 30-day all-cause mortality was prospectively assessed in consecutive haemodynamically stable patients with PE. The present study included 318 haemodynamically stable patients with PE. During the 30-day study period, 23 (7%) patients died. cTnI was elevated (>or=0.1 ng x mL(-1)) in 102 (32%) patients. An age >65 yrs, systolic blood pressure <120 mmHg and severity of illness assessed using the PE severity index (PESI) were significantly associated with an increased risk for mortality, but no significant association was found between elevation of cTnI and 30-day mortality in a logistic regression analysis. When only fatal PE was considered, multivariate analysis showed that severity of illness using the PESI and an elevated cTnI (odds ratio 3.7, 95% confidence interval (CI) 1.1-12.8) were associated with a significant increase in the risk for death. The negative predictive value (95% CI) of a negative cTnI for mortality was 93 (90-97)%. In conclusion, in haemodynamically stable patients with acute pulmonary embolism, cardiac troponin I was not an independent predictor of 30-day all-cause mortality, although it did predict fatal pulmonary embolism.

Difference in elevation of N-terminal pro-BNP and conventional cardiac markers between patients with ST elevation vs non-ST elevation acute coronary syndrome.

BACKGROUND: N-terminal pro-B-type natriuretic peptide (NT-proBNP) is elevated in patients with acute coronary syndrome (ACS), and is a powerful predictor of long-term mortality. Differences in the clinical utility and pathophysiological implication of NT-proBNP and conventional cardiac markers in patients with ST elevation (STE) vs non-STE (NSTE) ACS were investigated in the present study. METHODS AND RESULTS: Ninety consecutive patients admitted with acute chest pain and a diagnosis of unstable angina or acute myocardial infarction were analyzed. Patients with >or=Killip class II were excluded to focus on the effect of myocardial ischemia on the release of cardiac markers. The markers were measured on admission and analyzed according to the time from onset. Conventional cytosolic marker (creatine kinase-MB) and myofibril marker (troponin T: TnT) were both significantly higher in STE-ACS patients compared with NSTE-ACS patients. Conversely, NT-proBNP was significantly higher in NSTE-ACS patients than STE-ACS especially within 3 h of onset, suggesting a larger ischemic insult despite the smaller extent of myocardial necrosis compared with STE-ACS patients. There was no significant correlation between NT-proBNP level and left ventricular ejection fraction (LVEF) obtained at acute-phase echocardiography in either NSTE-ACS patients (LVEF 57.7+/-11.2%) or STE-ACS patients (LVEF 55.1+/-12.7%). Comparison between NT-proBNP and TnT levels revealed a marked difference of elevations, with significantly augmented elevation of NT-proBNP (p<0.001) in NSTE-ACS patients as compared with prominent elevation of TnT in STE-ACS patients. CONCLUSIONS: NT-proBNP is an early sensitive marker of myocardial ischemia that rises much higher in the earlier phase as compared with conventional markers of myocardial damage, especially in NSTE-ACS patients.

Incremental prognostic value of C-reactive protein and N-terminal proB-type natriuretic peptide in acute coronary syndrome.

BACKGROUND: Cardiac biomarkers, including high-sensitivity C-reactive protein (hs-CRP), N-terminal proB-type natriuretic peptide (NT-proBNP) and cardiac troponin-I (Tn-I), have been associated with an adverse outcome in patients with acute coronary syndrome (ACS). Thus, in the present study the incremental prognostic value of these cardiac biomarkers was evaluated for risk stratification of ACS. METHODS AND RESULTS: The baseline levels of hs-CRP, NT-proBNP and Tn-I were measured in 215 patients (140 males; 65+/-46 years) with ACS: ST-elevation myocardial infarction (STEMI): 56; non-ST-elevation myocardial infarction (NSTEMI): 98; unstable angina (UA): 61. The patients were retrospectively followed up for a mean of 246 days. There were 24 cardiac events: STEMI: 1, NSTEMI: 6, UA: 6, chronic heart failure: 1, death: 10. The baseline levels of hs-CRP and NT-proBNP were significantly higher in the patients with cardiac events than in those without events. After adjustment for major clinical prognostic factors, hs-CRP and NT-proBNP remained significantly independent predictors for cardiac events. Patients with hs-CRP level >3.5 mg/L and NT-proBNP level >500 pg/ml had an 11-fold higher risk for cardiac events than those with hs-CRP level

Relationship between coronary hemodynamic changes and the phasic events of rapid eye movement sleep.

Previous studies in dogs showed dramatic increases in coronary blood flow associated with episodes of sinus tachycardia during rapid eye movement (REM) sleep. The present study demonstrates that 90% of these surges in heart rate and coronary flow are concentrated during periods of phasic REM sleep and only 10% in tonic REM sleep. Intensely phasic REM was distinguished from moderately phasic REM sleep by the degree of phasic eye movement. The surges were three times more frequent during intensely phasic REM than in moderately phasic REM sleep. However, the magnitudes of heart rate (37% +/- 3%) and coronary flow (25% +/- 3%) surges were unaffected by the specific substage of REM sleep. The incidence of surge events was almost eleven times greater in epochs of phasic REM that also contained a muscle twitch than in those that did not. During REM sleep, muscle twitches accompanying surges were not associated with any additional elevations in coronary flow or myocardial demand. Our data indicate that the sinus tachycardia-associated surges in coronary flow represent integrated autonomic responses intrinsic to phasic periods of REM sleep in dogs.

Supraventricular tachycardia treated with continuous infusions of propranolol.

Because oral therapy is often contraindicated in hospitalized patients we assessed the safety and efficacy of continuous intravenous propranolol infusions in nine patients with refractory supraventricular tachycardia. Standard pharmacokinetic formulas predicted a loading dose (52.2 +/- 38.3 micrograms/kg), steady-state plasma concentration, and the initial maintenance dose (16.1 +/- 16.2 micrograms/kg/hr; range 6.1 to 56.0 micrograms/kg/hr) to control heart rate. Subsequent maintenance doses (3.9 to 74.9 micrograms/kg/hr) were determined by clinical response. Heart rate decreased from 146 +/- 22 to 98 +/- 16 beats/min (p less than 0.0001). This decrease persisted throughout the infusion. Measured propranolol levels (28 +/- 21 ng/ml) did not differ significantly from the predicted levels (23 +/- 17 ng/ml). The duration of the infusion averaged 97 +/- 77 hours. A side effect, transient wheezing, occurred in only one patient. This resolved when the infusion rate was decreased. We conclude that continuous propranolol infusions appear safe and effective in treating these patients with supraventricular tachycardia.

Conjunctival oxygen monitoring: relationship to ventricular arrhythmias.

The results of conjunctival oxygen monitoring in a critically ill patient whose cardiac rhythm changed from sinus tachycardia to ventricular tachycardia and ventricular fibrillation and back to sinus tachycardia are described. Monitoring revealed a significant decrease in conjunctival oxygen tension 2 minutes before ventricular tachycardia was manifested by continuous electrocardiography, and an immediate rise in conjunctival oxygen tension was seen with the resumption of sinus tachycardia. This monitoring modality may be a useful adjunct in the hemodynamic evaluation of critically ill patients.