ST-Segment Elevation Myocardial Infarction vs. Hypothermia-Induced Electrocardiographic Changes: A Case Report and Brief Review of the Literature

Salinski, Ellie; Worrilow, Charles C.

doi:10.1016/j.jemermed.2013.08.122

Cited by 11 publications

(5 citation statements)

References 10 publications

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“…We found 64 articles 4–67 comprising a total of 68 cases with a mean age of 55 years, out of which 79% were males. Cause of hypothermia were accidental in 38%, therapeutic hypothermia in 11%, sepsis in 11%, alcohol intoxication and endocrinal causes (including diabetic ketoacidosis and hypothyroidism) in 11%, head trauma and brain death in 9%, drug-induced in 5.5% and post-surgery and post-cardiac arrest in 3.6% each.…”

Section: Resultsmentioning

confidence: 99%

The correlation between the amplitude of Osborn wave and core body temperature

Omar

Camporesi

2014

European Heart Journal: Acute Cardiovascular Care

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Section: Resultsmentioning

confidence: 99%

The correlation between the amplitude of Osborn wave and core body temperature

Omar

Camporesi

2014

European Heart Journal: Acute Cardiovascular Care

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“…Temperature is known to unmask Brugada syndrome (Meggiolaro et al . ; Salinski & Worrilow, ). We characterized the temperature sensitivity of two mixed syndrome mutants, E1784K and R1193Q in the cardiac sodium channel Na V 1.5.…”

Section: Discussionmentioning

confidence: 99%

Differential thermosensitivity in mixed syndrome cardiac sodium channel mutants

Abdelsayed

Peters

Ruben

2015

The Journal of Physiology

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Key pointsr The E1784K mixed syndrome mutant of the cardiac voltage-gated sodium channel, Na V 1.5, responds differently to temperature changes compared to the R1193Q mutant and wild-type (WT) Na V 1.5.r In E1784K, elevated temperature causes a larger increase in persistent current; there is also an increase in use-dependent inactivation at 1 Hz, which is not apparent at 3 Hz.r WT Na V 1.5 and R1193Q channels respond similarly to temperature changes. r Action potential modelling (from extrapolated temperature coefficient (Q 10 )values) predicts the effects of differential temperature sensitivity on the cardiac action potential: greater attenuation of the epicardial action potential occurs in E1784K as temperature shifts from hypothermic to hyperthermic conditions, and when transient outward potassium currents are increased.r The results from the action potential model predict that, at febrile temperatures, E1784K channels results in a larger transmural voltage gradient.r Hyperthermia exacerbates the Brugada syndrome 1 (BrS1) phenotype, which may be arrhythmogenic in E1784K mutants.Abstract Cardiac arrhythmias are often associated with mutations in SCN5A the gene that encodes the cardiac paralogue of the voltage-gated sodium channel, Na V 1.5. The Na V 1.5 mutants R1193Q and E1784K give rise to both long QT and Brugada syndromes. Various environmental factors, including temperature, may unmask arrhythmia. We sought to determine whether temperature might be an arrhythmogenic trigger in these two mixed syndrome mutants. Whole-cell patch clamp was used to measure the biophysical properties of Na V 1.5 WT, E1784K and R1193Q mutants. Recordings were performed using Chinese hamster ovary (CHOk1) cells transiently transfected with the Na V 1.5 α subunit (WT, E1784K, or R1193Q), β1 subunit, and eGFP. The channels' voltage-dependent and kinetic properties were measured at three different temperatures: 10ºC, 22ºC, and 34ºC. The E1784K mutant is more thermosensitive than either WT or R1193Q channels. When temperature is elevated from 22°C to 34°C, there is a greater increase in late I Na and use-dependent inactivation in E1784K than in WT or R1193Q. However, when temperature is lowered to 10°C, the two mutants show a decrease in channel availability. Action potential modelling using Q 10 fit values, extrapolated to physiological and febrile temperatures, show a larger transmural voltage gradient in E1784K compared to R1193Q and WT with hyperthermia. The E1784K mutant is more thermosensitive than WT or R1193Q channels. This enhanced thermosensitivity may be a mechanism for arrhythmogenesis in patients with E1784K sodium channels.

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“…[164][165][166] Although mild hypothermia has been defined as a tar get body temperature of 32°C to 33°C and has been associated with improved neurological outcome and survival in this population, this degree of cooling slows impulse conduction through all cardiac tissue, result ing in prolongation of all electrocardiographic intervals and elevation of the J point, resulting in characteris tic Osborn waves, with the height of the Osborn wave proportional to the degree of hypothermia. [167][168][169] Addi tional changes on the ECG have also been recorded in response to both accidental and therapeutic hypother mia, including AF in up to 50% of patients, 170 STseg ment depression, 171 STsegment elevation, 170 Brugada syndrome morphology, 172 and QT prolongation. 81,82 All these findings may confuse interpretation of the ECG in patients treated with therapeutic hypothermia with core body temperatures <35°C.…”

Section: After MI Without Reperfusion or Revascularizationmentioning

confidence: 99%

Update to Practice Standards for Electrocardiographic Monitoring in Hospital Settings: A Scientific Statement From the American Heart Association

Sandau¹,

Funk²,

Auerbach³

et al. 2017

Circulation

207

214

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Background and Purpose: This scientific statement provides an interprofessional, comprehensive review of evidence and recommendations for indications, duration, and implementation of continuous electro cardiographic monitoring of hospitalized patients. Since the original practice standards were published in 2004, new issues have emerged that need to be addressed: overuse of arrhythmia monitoring among a variety of patient populations, appropriate use of ischemia and QT-interval monitoring among select populations, alarm management, and documentation in electronic health records. Methods: Authors were commissioned by the American Heart Association and included experts from general cardiology, electrophysiology (adult and pediatric), and interventional cardiology, as well as a hospitalist and experts in alarm management. Strict adherence to the American Heart Association conflict of interest policy was maintained throughout the consensus process. Authors were assigned topics relevant to their areas of expertise, reviewed the literature with an emphasis on publications since the prior practice standards, and drafted recommendations on indications and duration for electrocardiographic monitoring in accordance with the American Heart Association Level of Evidence grading algorithm that was in place at the time of commissioning. Results: The comprehensive document is grouped into 5 sections: (1) Overview of Arrhythmia, Ischemia, and QTc Monitoring; (2) Recommendations for Indication and Duration of Electrocardiographic Monitoring presented by patient population; (3) Organizational Aspects: Alarm Management, Education of Staff, and Documentation; (4) Implementation of Practice Standards; and (5) Call for Research. Conclusions: Many of the recommendations are based on limited data, so authors conclude with specific questions for further research.

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ST-Segment Elevation Myocardial Infarction vs. Hypothermia-Induced Electrocardiographic Changes: A Case Report and Brief Review of the Literature

Cited by 11 publications

References 10 publications

The correlation between the amplitude of Osborn wave and core body temperature

The correlation between the amplitude of Osborn wave and core body temperature

Differential thermosensitivity in mixed syndrome cardiac sodium channel mutants

Update to Practice Standards for Electrocardiographic Monitoring in Hospital Settings: A Scientific Statement From the American Heart Association

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