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Effect of initial temperature changes on myocardial enzyme levels and cardiac function in acute myocardial infarction.
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PMID:  24944629     Owner:  NLM     Status:  Publisher    
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In the present study, the effect of initial body temperature changes on myocardial enzyme levels and cardiac function in acute myocardial infarction (AMI) patients was investigated. A total of 315 AMI patients were enrolled and the mean temperature was calculated based on their body temperature within 24 h of admission to hospital. The patients were divided into four groups according to their normal body temperature: Group A, <36.5°C; group B, ≥36.5°C and <37.0°C; group C, ≥37.0°C and <37.5°C and group D, ≥37.5°C. The levels of percutaneous coronary intervention, myocardial enzymes and troponin T (TNT), as well as cardiac ultrasound images, were analyzed. Statistically significant differences in the quantity of creatine kinase at 12 and 24 h following admission were identified between group A and groups C and D (P<0.01). A significant difference in TNT at 12 h following admission was observed between groups A and D (P<0.05), however, this difference was not observed with groups B and C. The difference in TNT between the groups at 24 h following admission was not statistically significant (P>0.05). Significant differences in lactate dehydrogenase at 12 and 24 h following admission were observed between groups A and D (P<0.05), however, differences were not observed with groups B and C (P>0.05). Significant differences in glutamic-oxaloacetic transaminase at 12 and 24 h following admission were observed between groups A and D (P<0.05), however, differences were not observed in groups B and C (P>0.05). However, no significant differences were identified in cardiac function index between all the groups. Therefore, the results of the present study indicated that AMI patients with low initial body temperatures exhibited decreased levels of myocardial enzymes and TNT. Thus, the observation of an initially low body temperature may be used as a protective factor for AMI and may improve the existing clinical program.
Authors:
Yuanyu Qian; Jie Liu; Jinling Ma; Qingyi Meng; Chaoying Peng
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-4-14
Journal Detail:
Title:  Experimental and therapeutic medicine     Volume:  8     ISSN:  1792-0981     ISO Abbreviation:  Exp Ther Med     Publication Date:  2014 Jul 
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Created Date:  2014-6-19     Completed Date:  -     Revised Date:  -    
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Nlm Unique ID:  101531947     Medline TA:  Exp Ther Med     Country:  -    
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Languages:  ENG     Pagination:  243-247     Citation Subset:  -    
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Journal Information
Journal ID (nlm-ta): Exp Ther Med
Journal ID (iso-abbrev): Exp Ther Med
Journal ID (publisher-id): ETM
ISSN: 1792-0981
ISSN: 1792-1015
Publisher: D.A. Spandidos
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open-access:
Received Day: 28 Month: 9 Year: 2013
Accepted Day: 30 Month: 1 Year: 2014
Print publication date: Month: 7 Year: 2014
Electronic publication date: Day: 14 Month: 4 Year: 2014
pmc-release publication date: Day: 14 Month: 4 Year: 2014
Volume: 8 Issue: 1
First Page: 243 Last Page: 247
PubMed Id: 24944629
ID: 4061241
DOI: 10.3892/etm.2014.1678
Publisher Id: etm-08-01-0243

Effect of initial temperature changes on myocardial enzyme levels and cardiac function in acute myocardial infarction
YUANYU QIAN
JIE LIU
JINLING MA
QINGYI MENG
CHAOYING PENG
Department of Emergency, Chinese PLA General Hospital, Beijing 100853, P.R. China
Correspondence: Correspondence to: Dr Yuanyu Qian, Department of Emergency, Chinese PLA General Hospital, 28 Fuxing Road, Beijing 100853, P.R. China, E-mail: yyqiancn@163.com

Introduction

Coronary heart disease is currently a serious threat to human health. The extent of myocardial infarction (MI) is important when assessing the therapeutic strategy and evaluating the prognosis for acute MI (AMI) patients (13). Positron emission tomography (PET) is regarded as the gold standard for identifying viable myocardia. However, there are disadvantages associated with PET, including the requirement for expensive specialist equipment and the complexity of continuous detection and popularization. Thus, a simple and inexpensive method for the continuous detection of the degree of MI is required. As MI is an inflammatory process and body temperature is an inflammatory indicator that is easily obtained in clinical practice, the initial change in body temperature in AMI patients may be a potential indication of the degree of MI (46). An animal study conducted using mice demonstrated that genetic background, gender, age (but not in imprinting control regions mice), body temperature and arterial blood pH exhibit considerable effects on infarction size (7). However, clinical studies have only determined the ambient temperature as a risk factor. An additional study demonstrated that no association existed between the daily ambient temperature and the prognosis of AMI, with and without adjusting for PM10, NOx, O3, age and gender (8). Furthermore, an additional study demonstrated that exposure to cold temperatures increased the risk of acute MI (9) and acute aortic dissection (10), whereas heat exposure increased the risk of mortality following AMI (9).

The present study was conducted with hospitalized AMI patients to investigate the changes in myocardial enzyme levels and cardiac function in association with differing body temperature gradients.


Patients and methods
Patients

A total of 385 AMI patients were admitted to the Chinese PLA General Hospital (Beijing, China) between 2001 and 2010. The patient group comprised 315 males (81.8%) and 70 females (18.2%). The age of the subjects ranged between 27 and 68 years with a mean age of 49.25±7.45 years. Body temperature was measured within 24 h of admission at intervals of 4 h and the mean temperature was calculated. Subjects were divided into four groups based on their normal body temperature: Group A, <36.5°C; group B, ≥36.5°C and <37.0°C; group C, ≥37.0°C and <37.5°C and group D, ≥37.5°C.

The sample sizes of groups A–D were 83 (males, 62; females, 21), 153 (males, 133; females, 20), 963 (males, 72; females, 24) and 53 (males, 48; females, 5), respectively. The age ranges of groups A–D were 28–65, 27–68, 27–67 and 27–68 years, respectively, with the mean age of groups A–D being 51.21±3.4, 49.86±3.1, 50.48±3.3 and 50.44±3.1 years, respectively. The present study was conducted in accordance with the Declaration of Helsinki and with approval from the Ethics Committee of the Chinese PLA General Hospital. Written informed consent was obtained from all participants.

Diagnostic criteria

Inclusion criteria were determined based on the diagnostic criteria of MI, including: i) Chest pain that persisted for >30 min; ii) an electrocardiogram that exhibited elevation of the last two connected precordial ST-segments; iii) serum enzyme levels indicating that the creatine kinase-MB fraction (CK-MB) was significantly higher than normal levels; and iv) the patient had no history of MI. The exclusion criteria were: i) Onset of AMI >24 h prior to admission and ii) the patient exhibited a co-infection, malignant disease or severe liver or kidney failure. The blood flow index, vascular recanalization index and the degree of symptom relief was based on the Seventh American College of Chest Physicians Conference on antithrombotic and thrombolytic therapy. A total of 315 patients were included in the present study.

Data collection

The body temperature of each patient was measured within 24 h of admission to hospital at intervals of 4 h. The mean axillary temperature was calculated and the patients were assigned to different groups based on their normal body temperature. Information was collected from each patient, including age, gender and risk factors of coronary heart disease (smoking, hypertension, diabetes and hypercholesterolemia). At 12 and 24 h following admission, the blood samples obtained from the patients were tested for CK, CK-MB, cardiac troponin T (TNT), lactate dehydrogenase (LDH) isoenzyme and glutamic-oxaloacetic transaminase (GOT). The myocardial enzyme levels were tested using a Roche test kit (Roche Ltd.; Shanghai, China). At 24 h and one week following admission, the patients were examined using Vivid 7 Dimension color Doppler flow imaging (General Electric Company, Schenectady, NY, USA) and the cardiac function indexes were observed.

Statistical analysis

The mean and SD were calculated to analyze the measured data and comparisons between the groups were tested using analysis of variance and χ2 tests, whereas the count data were analyzed with ratios. Pearson’s correlation analysis was used to analyze the correlations between body temperature and the corresponding index. The data were cleaned and analyzed using SPSS 11.0 (SPSS, Inc., Chicago, IL, USA). P<0.05 was considered to indicate a statistically significant difference.


Results
Distribution of MI areas

Tables I and II show the general distribution of the MI areas that were observed in each group. In total, 315 patients received interventional examinations within 4 h of admission to hospital. A total of 144 cases of single coronary artery lesion, 116 cases of double branch and 125 cases of triple branch artery lesions were reported. The predominant areas of MI were the anterior descending artery and the right coronary artery; the anterior descending artery lesion was mainly observed in the proximal and middle branches. Thus, the anterior descending artery lesion was the main type of MI, followed by the right coronary artery and the circumflex artery. The patients received stent implantations and the distribution of the MI areas in the four groups was estimated using a χ2 test. The comparability for the other variables was reasonable as no significant differences were observed between the groups.

Body temperature changes

Body temperature was measured within 24 h of admission to hospital at intervals of 4 h. Among the four groups, the majority of patients were in groups B and C, thus, body temperature predominantly ranged between 35.5 and 37.0°C (Table III).

Myocardial enzyme changes

Myocardial enzyme levels in each group were measured and compared at 12 and 24 h following admission to hospital. With regard to the CK level at 12 h following admission, significant differences were identified between group A and groups C and D (P<0.01), as well as between group B and groups C and D (P<0.05). However, no significant differences were observed between groups A and B (P>0.05) or between groups C and D (P>0.05). With regard to the CK level at 24 h following admission, significant differences were observed between group A and groups C and D (P<0.01), as well as between group B and groups C and D (P<0.05). No significant differences were identified between groups A and B (P>0.05) or between groups C and D (P>0.05; Table IV).

With regard to the CK-MB level at 12 h following admission, significant differences were observed between group A and groups C and D (P<0.01), as well as between group B and groups C and D (P<0.05). However, no significant differences were identified between groups A and B (P>0.05) or between groups C and D (P>0.05). With regard to the CK-MB level at 24 h following admission, significant differences were observed between group A and groups C and D (P<0.01), as well as between group B and groups C and D (P<0.05). However, no significant differences were observed between groups A and B (P>0.05) or between groups C and D (P>0.05; Table IV).

The difference in TNT at 12 h following admission was significant between groups A and D (P<0.05), however, was not significant between group A and groups B and C. The difference in TNT at 24 h following admission among the four groups was not identified to be statistically significant (P>0.05; Table IV).

Significant differences in LDH at 12 h following admission were observed between groups A and D (P<0.05), however, were not observed between group A and groups B and C (P>0.05). Significant differences in LDH at 24 h following admission were observed between groups A and D (P<0.05), but not between group A and groups B and C (P>0.05; Table IV).

Significant differences in GOT at 12 h following admission were observed between groups A and D (P<0.05), but not among other groups (P>0.05). Significant differences in GOT at 24 h following admission were observed between groups A and D (P<0.05), but similarly were not observed among the other groups (P>0.05; Table IV).

Changes in cardiac function

All 315 AMI patients were examined via cardiac ultrasound at 24 h and one week following admission. Table V shows the comparisons between the main cardiac function indexes. No statistically significant differences were identified between the groups, indicating that initial body temperature changes in AMI did not effect cardiac function.


Discussion

The initial phase of AMI is the ischemic state, where ischemic myocardial cells maintain vitality, but gradually die over time. A greater quantity of ischemic myocardial cells survive when acute myocardial ischemia reperfusion therapy is conducted at an earlier stage, regardless of intravenous thrombolysis or interventional therapy. However, few AMI patients are able to receive thrombolytic and interventional therapy in a timely manner and the majority of patients receive reperfusion therapy after 3 h of chest pain (11). Therefore, protection from myocardial ischemia and delaying myocardial necrosis are essential. MI is an inflammatory process and body temperature is an inflammatory indicator that is easily acquired in clinical practice. The initial changes in body temperature in AMI patients may be positively associated with the degree of MI (2). The correlation between initial body temperature in AMI and the MI area has been increasingly investigated in previous years (12,13); however, the present study analyzed the effect of initial temperature on AMI in association with myocardial enzyme reactions.

Previous clinical studies have identified differences in the expression of myocardial enzymes in patients at different body temperatures. CK level in AMI patients increases between 4 and 8 h after MI and subsequently decreases over 4–5 days (14). In the present study, the CK and CK-MB levels in patients were significantly lower in group A than those observed in group D. In addition, the other indexes were lower in groups A–C when compared with those in group D. Thus, an increase in body temperature was shown to be associated with mean levels of myocardial enzymes. Patients with lower body temperatures exhibited lower levels of myocardial enzymes and had an improved clinical prognosis, whereas patients with higher body temperatures received a poor prognosis. Elevated body temperature may be a manifestation of the inflammatory reaction following myocardial necrosis. The inflammatory reaction has an adverse effect on left ventricular remodeling (15). However, in a study of 171 AMI patients, in which only 17 patients exhibited a peak body temperature of >37.5°C, no significant correlation was identified between the peak body temperature and the predetermined inflammatory response markers (16). Although an elevated temperature is a natural reaction in the process of repair, it may be associated with increased activation of the immune system, which promotes left ventricular remodeling (17). Body temperature has a marked effect on oxygen consumption. Oxygen demand increases with increasing body temperature, thus, a fever may affect the infarction area. An association between elevated body temperature and elevated CK levels was determined in the present study. A study of 357 AMI patients showed that the anterior wall of the MI area significantly narrowed in AMI patients with a lower body temperature, which was accompanied by low CK-MB levels and an increased left ventricular ejection fraction. By contrast, the treatment outcomes were unaffected by low body temperatures observed in the control group (18,19).

Previous studies have identified that numerous factors affect the prognosis of AMI patients. Body temperature monitoring is a simple method with the ability to estimate risks and the prognosis of AMI patients. The effect of low body temperature on AMI is currently being investigated via animal experimentation (20). Data indicate that hypothermia exhibits a protective effect on the myocardial ischemia model. A previous study investigated whether the use of warm or cold blood cardioplegia resulted in superior myocardial protection. Reduced cardiac enzyme release and improved postoperative cardiac indexes were observed in the warm cardioplegia group, however, similar short-term mortality was identified with no differences observed in the clinical outcomes (21). The application of this measure in clinical practice is currently difficult predominantly due to the lack of effective safety methods to cool the heart (2224). In addition, clinical studies have identified that numerous factors affect body temperature. Thus, full consideration of the confounding factors is required and cases that include bias factors should be excluded.

In conclusion, few studies have investigated the effect of body temperature in AMI patients on MI recovery in China. To the best of our knowledge, this is the first study to investigate whether hypothermia therapy reduces the MI area, inflammatory reaction and immune response; therefore, these areas may be the subject of future investigations.


References
1. Ibrahim T,Nekolla SG,Hörnke M,et al. Quantitative measurement of infarct size by contrast-enhanced magnetic resonance imaging early after acute myocardial infarction: Comparison with single-photon emission tomography using Tc99m-sestamibiJ Am Coll Cardiol45544552Year: 200515708702
2. Singh RB,Pella D,Neki NS,et al. Mechanisms of acute myocardial infarction study (MAMIS)Biomed Pharmacother58Suppl 1S111S115Year: 200415754848
3. Dinarello CA. Infection, fever, and exogenous and endogenous pyrogens: some concepts have changedJ Endotoxin Res10201222Year: 200415373964
4. Hale SL,Kloner RA. Ischemic preconditioning and myocardial hypothermia in rabbits with prolonged coronary artery occlusionAm J Physiol276H2029H2034Year: 199910362684
5. Schwartz DS,Bremner RM,Baker CJ,et al. Regional topical hypothermia of the beating heart: preservation of function and tissueAnn Thorac Surg72804809Year: 200111565662
6. Hale SL,Kloner RA. Myocardial temperature in acute myocardial infarction: protection with mild regional hypothermiaAm J Physiol273H220H227Year: 19979249493
7. Guo Y,Flaherty MP,Wu WJ,et al. Genetic background, gender, age, body temperature, and arterial blood pH have a major impact on myocardial infarct size in the mouse and need to be carefully measured and/or taken into account: results of a comprehensive analysis of determinants of infarct size in 1,074 miceBasic Res Cardiol107288Year: 201222864681
8. Wichmann J,Rosengren A,Sjöberg K,Barregard L,Sallsten G. Association between ambient temperature and acute myocardial infarction hospitalisations in Gothenburg, Sweden: 1985–2010PLoS One8e62059Year: 201323646115
9. Madrigano J,Mittleman MA,Baccarelli A,et al. Temperature, myocardial infarction, and mortality: effect modification by individual- and area-level characteristicsEpidemiology24439446Year: 201323462524
10. Verberkmoes NJ,Soliman Hamad MA,Ter Woorst JF,Tan ME,Peels CH,van Straten AH. Impact of temperature and atmospheric pressure on the incidence of major acute cardiovascular eventsNeth Heart J20193196Year: 201222328355
11. Dave RH,Hale SL,Kloner RA. Hypothermic, closed circuit pericardioperfusion: a potential cardioprotective technique in acute regional ischemiaJ Am Coll Cardiol3116671671Year: 19989626849
12. Hale SL,Kloner RA. Myocardial hypothermia: a potential therapeutic technique for acute regional myocardial ischemiaJ Cardiovasc Electrophysiol10405413Year: 199910210504
13. Felberg RA,Krieger DW,Chuang R,Persse DE,Burgin WS,Hickenbottom SL,et al. Hypothermia after cardiac arrest: feasibility and safety of an external cooling protocolCirculation10417991804Year: 200111591617
14. Behringer W,Safar P,Wu X,et al. Veno-venous extracorporeal blood shunt cooling to induce mild hypothermia in dog experiments and review of cooling methodsResuscitation548998Year: 200212104113
15. Reis SE,Holubkov R,Conrad Smith AJ,et al. WISE InvestigatorsCoronary microvascular dysfunction is highly prevalent in women with chest pain in the absence of coronary artery disease: results from the NHLBI WISE studyAm Heart J141735741Year: 200111320360
16. Kacprzak M,Kidawa M,Zielińska M. Fever in myocardial infarction: is it still common, is it still predictive?Cardiol J19369373Year: 201222825897
17. Klaiman JM,Fenna AJ,Shiels HA,Macri J,Gillis TE. Cardiac remodeling in fish: strategies to maintain heart function during temperature changePLoS One6e24464Year: 201121915331
18. Mehta RH,Rathore SS,Radford MJ,Wang Y,Wang Y,Krumholz HM. Acute myocardial infarction in the elderly: differences by ageJ Am Coll Cardiol38736741Year: 200111527626
19. Granger CB,Goldberg RJ,Dabbous O,et al. Global Registry of Acute Coronary Events InvestigatorsPredictors of hospital mortality in the global registry of acute coronary eventsArch Intern Med16323452353Year: 200314581255
20. Eagle KA,Lim MJ,Dabbous OH,et al. GRACE InvestigatorsA validated prediction model for all forms of acute coronary syndrome: estimating the risk of 6-month postdischarge death in an international registryJAMA29127272733Year: 200415187054
21. Abah U,Garfjeld Roberts P,Ishaq M,De Silva R. Is cold or warm blood cardioplegia superior for myocardial protection?Interact Cardiovasc Thorac Surg14848855Year: 201222402501
22. Boersma E,Pieper KS,Steyerberg EW,et al. Predictors of outcome in patients with acute coronary syndromes without persistent ST-segment elevation. Results from an international trial of 9461 patients The PURSUIT InvestigatorsCirculation10125572567Year: 200010840005
23. Rich MW. Treatment of acute myocardial infarctionAm J Geriatr Cardiol10328336Year: 200111684917
24. Tresch DD,Alla HR. Diagnosis and management of myocardial ischemia (angina) in the elderly patientAm J Geriatr Cardiol10337344Year: 200111684918

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Keywords: acute myocardial infarction, body temperature, myocardial enzyme, cardiac function.

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