Cardiology/case reportStress-Induced Cardiomyopathy Caused by Heat Stroke
Introduction
Heat stroke is defined clinically by core body temperature exceeding 40°C (104°F), failure of thermoregulation, and central nervous system abnormalities such as delirium, convulsions, or coma. Heat stroke occurs during exposure to high environmental temperatures or during the performance of strenuous work and is classified as classic or exertional.1 Cooling, airway protection, supportive care, and management for complications are the mainstays of treatment. Mortality correlates with age and the degree of temperature increase, which affects the organs and the effectiveness of treatment.2
Heat stroke may cause multiorgan dysfunction syndromes. The myocardial injury of the heat stroke often presents with elevation of cardiac enzymes and electrocardiographic changes, which might act as diagnostic pitfalls.3, 4, 5 Such findings may lead to an erroneous diagnosis of acute myocardial infarction caused by coronary atherosclerosis subsequently followed by improper treatment. Wakino et al6 and Garcia-Rubira et al7 have described heat stroke patients with electrocardiographic ST-segment elevation diagnosed as acute myocardial infarction, in which transient coronary artery spasms or stress-induced cardiomyopathy was suspected; however, coronary angiography is necessary to make such diagnoses, yet these data were lacking in those studies. In addition, acute myocardial infarction from coronary artery occlusion should be ruled out before the diagnosis of coronary artery spasms or stress-induced cardiomyopathy is made. Coronary angiography was not performed in these cases, and acute coronary artery occlusive myocardial infarction was ruled out by indirect methods, including echocardiographic findings, the evolutional changes of ECG, the symptoms, and the physical signs.
We herein present another case of high core body temperature with hypotension and pulmonary edema. In addition, the laboratory data presented increased cardiac troponin I and ST-segment elevation at V4 to 6 by ECG. Echocardiogram revealed left ventricle systolic dysfunction with regional wall motion abnormality. Coronary angiography and left ventriculography were also performed, revealing patent coronary arteries, hence suggesting stress-induced cardiomyopathy. To the best of our knowledge, no previous studies have reported a direct method for ruling out myocardial infarction from coronary artery occlusion in patients with heat stroke and ST-segment elevation or provided direct evidence of stress-induced cardiomyopathy. Therefore, this is the first case report of coronary angiography displaying stress-induced cardiomyopathy in a patient with heat stroke.
Section snippets
Case Report
A 39-year-old male construction worker worked in an open field, with an ambient temperature of 35.6°C (96°F). After working for approximately 8 hours, he suddenly collapsed and was immediately sent to our emergency department. He presented with an infrared tympanic temperature on admission of 42.2°C (108°F) and rectal temperature was 43.1°C (109.6°F) and was determined to be 6 points on the Glasgow Coma Scale. Blood pressure was 98/50 mm Hg, pulse rate 160 beats/min, and respiratory rate 30
Discussion
ST-segment elevation is one of the ECG findings in patients with heat stroke.3, 4, 5, 6, 7 In addition, previous reports have indicated that patients with heat stroke and ST-segment elevation do not have symptoms of angina pectoris.6 Although echocardiography during the acute phase revealed segmental hypokinesis of the left ventricle, this condition resolved spontaneously in the absence of any specific treatment for acute coronary syndrome. In addition, ECG did not reveal Q waves in the
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2023, American Journal of MedicineCitation Excerpt :Similarly, in Japan26 the diagnosis of Takotsubo syndrome is made most commonly in summer and in early autumn. Furthermore, there are 2 case reports in the literature of Takotsubo syndrome as a complication of heatstroke.27,28 However, Takotsubo syndrome is often induced by various types of acute stress, and hypothermia has also been reported as a trigger.29
The Cardiovascular System in Heat Stroke
2022, CJC OpenCitation Excerpt :Data on coronary angiography in heat stroke are limited. Chen et al. reported a case of a 39-year-old man with exertional heat stroke, troponin elevation, and anterolateral ST elevation who had patent coronary arteries on coronary angiography and was diagnosed with stress-induced cardiomyopathy.22 Beyond this report, no robust studies have explored coronary angiography in heat stroke patients who have ST deviations or troponin elevations.
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2019, European Journal of Internal MedicineCitation Excerpt :In a retrospective cohort study, Yang et al. analyzes the data from 117 consecutive patients (86 survivors, 31 nonsurvivors) who has suffered an exertional heat stroke, at 48 Chinese hospitals between April 2003 and July 2015, which demonstrates that recurrent heat strokes could predispose to central nervous system injuries [6]. Heat stroke can cause multiple syndromes including bowel ischemia, [7] acute liver failure, [8] coagulopathy, [9] impaired renal function with electrolyte disturbances [10] and myocardial damage [11,12]. It is reported that patients who have suffered a heat stroke might have decreased left-ventricular end-diastolic volume, leading to a reduced cardiac stroke volume and decrease in coronary artery perfusion [13], resulting in ischemic heart disease (IHD).
High temperatures and nephrology: The climate change problem
2017, NefrologiaCitation Excerpt :The liver and the central nervous system are primarily affected and, vertigo, confusion, ataxia and coma may occur. In addition, the decrease in renal and splanchnic blood flow produced to achieve a greater blood supply to the skin impairs glomerular filtration and the already reduced liver function; intestinal and myocardial ischaemia may also appear.31 In these cases the prognosis depends on factors such as comorbidity, existence of organ damage (seizures, kidney failure, coagulopathy, elevated transaminases) and response to treatment with improvement of mental status when temperature falls below 40 °C.
Supervising editor: Deborah B. Diercks, MD
Funding and support: By Annals policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article as per ICMJE conflict of interest guidelines (see www.icmje.org). The authors have stated that no such relationships exist.
Publication date: Available online December 7, 2011.