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Case report

Blunt chest trauma induced myocardial infarction with suggested coronary vasospasm

Elsayed, Yasser Mohammed Hassanain*

Author Information
The Egyptian Journal of Critical Care Medicine: August 2018 - Volume 6 - Issue 2 - p 57-59
doi: 10.1016/j.ejccm.2018.05.001
  • Open

Abstract

Abbreviations: STEMI, ST Segment Elevation Myocardial Infarction; AMI, Acute Myocardial Infarction; ACS, Acute Coronary Syndromes; ECG, Electrocardiogram; CVsp, Coronary Vasospasm; IHD, Ischaemic Heart Disease

1. Background

It is a usual to find an Acute ST Elevation Myocardial Infarction as complications to Traditional risk factors like diabetes, hypertension, and drug abuse. But an extremely rare to find an Acute ST Elevation Myocardial Infarction after the chest trauma.

2. Case presentation

A 50-year-old married Egyptian Farmer male, heavy smoker (about 60 cigarettes per day for about 20 years) presented to emergency room of chest hospital had complaining of severe burning pain in the chest. The condition started suddenly after exposure of his chest to strong smacker from his friend on joking together. Loss of consciousness for few seconds Suddenly had happened. After the patient regain his consciousness he started to sense of dizziness and severe central chest pain. The patient directed to Chest Hospital but an unfortunately, the Chest Physician managed the case as Gastroesophageal reflux disease, Specifically with Zantac injection. The patient left the hospital with no pain relive rather becoming more severe. The patient directed to my outpatient for more consultation for chest pain. The Patient denied any past history for Cardiac disease, or any other relevant diseases and any past similar conditions.

On examination, the patient was conscious. His vital signs were as follows: blood pressure 100/70 mmHg, pulse rate 62/minute, and temperature 36.6 °C. He was more pale with cold sweaty. No more relevant clinical data.

Urgent ECG (Fig. 1) in my outpatient show an acute ST-segment Elevation Myocardial Infarction (STEMI) in inferior (II, III, aVF) and lateral leads (V5,V6) and) ST depression changes in leads (V1,V2,V3) indicating Posterior Infarction with Reciprocal ST depression changes in leads (I, aVL). I had referred him to hospital for admission in the Intensive Care Unit. He was managed urgently in Intensive Care Unit essentially with Aspocid 75 mg chewing 4 tab. O2 inhalation, Pethidine injection and Streptokinase 1.5 million unit IVI over 60 min. He discharged 5 days later after stabilization on Aspocid 75 mg, Plavix 75 mg tab, Nitro Mack Retard cap, Ator 40 tab. In the hospital, his Hematological, Serological, and Biochemical investigations were found normal. Echocardiography report show: evidence of IHD: Regional wall motion abnormalities with Hypokinesia of Lateral and Inferior Wall with EF:55%.

Fig. 1.
Fig. 1.:
ECG 1 of Presentation, about 2 h of onset and 1 h before Streptokinase, showing an acute ST-segment Elevation Myocardial Infarction (STEMI) in inferior (II, III, aVF) and lateral leads (V5,V6) and) ST depression changes in leads (V1,V2,V3) indicating Posterior Infarction with Reciprocal ST depression changes in leads (I, aVL).

Eighteen days later, Pathological Q and fixed T-wave inversions follow infarction was seen in the Inferior leads (ECG-2: Fig. 2). Two weeks later, the patient had undergone to Coronary Catheterization which show: Absent Left Main Coronary Artery, Atherosclerotic Left Anterior Descending and Left Circumflex arteries without significant lesion, Atherosclerotic right coronary artery with 90% Ostial lesion and minimal Ectasia of Distal Segment of Left Anterior Descending artery.

Fig. 2.
Fig. 2.:
ECG 2:18 days of Presentation, showing Pathological Q and T wave inversion in Inferior leads (II, III, aVF) and taller T wave.

The patient is continuing on standard anti-ischemic drugs with no problem. He had refused any further coronary intervention.

Possible differential diagnosis of the case is an aortic dissection and musculoskeletal chest pain.

3. Discussion

Blunt chest trauma is among the most commonly seen problems in traumatology. Myocardial infarction and coronary artery thrombosis is implicated in its manifestations. Ischemic heart disease due to coronary artery dissection following blunt trauma is an extremely rare after ruling out preexisting coronary disease as the primary cause, myocardial infarction associated with blunt trauma should raise the suspicion of coronary artery injury [1].

A working diagnosis of myocardial infarction must first be made. Some patients present with less-typical symptoms, such as nausea/vomiting, shortness of breath, fatigue, palpitations or syncope. Timely diagnosis of STEMI is key to successful management [2]. Diagnosis of acute myocardial infarction (AMI) has to be made early in the emergency triage since maximal mortality occurs within first hour and the benefits of all interventions are greater once these are instituted early [3]. AMI has a mortality of 30% with half of deaths occurring before hospital arrival [4].

Acute myocardial infarction has traditionally been divided into ST elevation or non-ST elevation myocardial infarction [5], which are distinguished based on the findings from a diagnostic electrocardiogram (ECG) [6].

The ability to recognize the clinical presentation of AMI is a critical to achieving timely reperfusion and the reduction of mortality and morbidity associated with misdiagnosed AMIs [7]. Recognizing the signs and symptoms, such as chest pain or shortness of breath suggestive of an ACS, and obtaining an ECG as soon as possible (goal of less than 10 min following presentation of a patient) should be the standard of practice to manage this patient population [6].

Coronary vasospasm (CVsp) with transient ST-segment elevation can occur in diseased coronary arteries as Prinzmetal's variant angina. It may also occur in angiographically normal coronary arteries as so-called 'variant of the variant [8].

Cigarette smoking is a major risk factor for coronary spasm even without significant coronary narrowing [9]. Coronary artery spasm appears to be a multifactorial disease [10]. But the morbidity increases annually in lifestyle-related disease, such as hypertension, diabetes mellitus, and dyslipidemia [11]. CVsp plays an important role in the pathogenesis not only of variant angina but also of ischemic heart disease [8].

4. Conclusions

  • Chest Blunt Trauma may be complicated with Coronary vasospasm and subsequent Acute Myocardial Infarction.
  • This is a guide us to avoid any chest trauma as possible as especially in smoker one.
  • It's unknownly how is the blunt chest trauma induced Coronary vasospasm and subsequent Infarction? but it is suggested mechanisms.

Acknowledgement

My acknowledgement to the patient for his co-operation with me.

Conflicts of interest.

There are no conflicts of interest.

References

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[9] Sugiishi M, Takatsu F. Cigarette smoking is a major risk factor for coronary spasm. Circulation 1993;87:76-79. doi: https://doi.org/10.1161/01.CIR.87.1.76.
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[11] Ishii Masanobu, Kaikita Koichi, Sato Koji, et al. Changes in the risk factors for coronary spasm. IJC Heart Vasculature September 2016;12:85-87. doi: https://doi.org/10.1016/j.ijcha.2016.07.008doi:10.1016/j.ijcha.2016.07.008.
Keywords:

Chest trauma; Infarction; Vasospasm

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