INTRODUCTION
Concomitant acute ischemic stroke and acute myocardial infarction (AMI), also known as cardio-cerebral infarction (CCI), is a rare medical emergency, with a reported incidence of 0.0009%.[1] The low incidence rate may be due to underreporting, given the diagnostic difficulty of this condition.[1] There is a wide spectrum of potential causes, and treatment of both conditions is time critical.[1]
We herein report case of a patient in a deep coma for whom a diagnosis proved difficult.
CASE REPORT
The patient was a 69-year-old man who called an ambulance due to dyspnea in the middle of the night. He had diabetes mellitus and lived alone. His family history was unknown. When the ambulance arrived at his house, emergency medical technicians found that he had collapsed into a deep coma in front of his house. He was transported to our hospital at 70 min from the first call.
On arrival, he remained in a deep coma (Glasgow Coma Scale of 3 and National Institutes of Health Stroke Scale of 42), with a blood pressure of 124/62 mmHg, heart rate of 65 beats per minute, respiratory rate of 20 breaths per minute, SpO2 of 77% under 10 L/min of oxygen, and body temperature of 36.2°C. An arterial blood gas analysis under 10 L/min of oxygen showed a pH of 7.063, PCO2 of 70.9 mmHg, PO2 of 44.0 mmHg, HCO3− of 19.3 mmol/L, base excess of −12.3 mmol/L, and lactate of 8.1 mmol/L. He was snoring, and auscultation revealed bilateral moist rales in the lung fields. A venous route was secured, and tracheal intubation was performed.
An electrocardiogram showed ST elevation at the II, III, and arteriovenous fistula leads with complete atrioventricular block [Figure 1]. Chest roentgen showed bilateral butterfly shadow in the lung fields [Figure 2]. Cardiac ultrasound at the emergency department revealed ejection fraction of 30% with diffuse hypokinesis, no significant valvular heart disease, and no large thrombus in any cardiac chambers. Head computed tomography (CT) showed dense middle cerebral artery sign and loss of cortical ribbon in the left temporal lobe [Figure 3]. However, these minute early cerebral ischemic signs were initially overlooked. Truncal CT suggested bilateral lung edema and aspiration without aortic dissection. The results of a biochemical analysis of blood are shown in Table 1.
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Figure 1: Electrocardiogram on arrival at 80 min (upper) and transcutaneous coronary angiography at 140 min (lower) from the first call. The electrocardiogram showed ST elevation at II, III, and AVF leads with complete atrioventricular block. Transcutaneous coronary angiography on arrival showed obstruction of the middle segment of the right coronary artery (arrow). AVF: Arteriovenous fistula
Figure 2: Chest roentgen on arrival at 90 min from the first call. Chest roentgen showed bilateral butterfly shadow in the lung fields
Figure 3: Head computed tomography (CT) on arrival at 100 min (upper) and on the 2nd hospital day at 17 h (lower) from the first call. CT showed a dense middle cerebral artery sign (arrow) and loss of cortical ribbon in the left temporal lobe (triangles). However, these minute signs were initially overlooked. The second CT showed diffuse low-density areas in the bilateral frontal lobe and left temporoparietal lobes with left-to. CT: Computed tomography
Table 1: Laboratory data at the time of deterioration
At this time, he received diagnosis of AMI, and his unconsciousness was attributed to acute respiratory failure induced by acute left ventricular failure and aspiration, renal failure, and glucose intolerance. He underwent urgent transcutaneous coronary angiography, which showed obstruction of the middle segment of the right coronary artery and severe stenosis of the left anterior descending (LAD) artery [Figure 1]. His cardiac rhythm spontaneously became sinus rhythm following catheterization, so we continued reperfusion therapy without the use of temporary pacing. The obstruction was reopened by implanting a drug-eluting stent. He had decompensated heart failure with Killip III and severe stenosis in the LAD artery, so we placed an intra-aortic balloon pump (IABP) to decrease the cardiac afterload and preserve the coronary blood flow, thus finishing percutaneous coronary intervention. He was admitted to the intensive care unit treated with continuous infusion of nicorandil and heparin, intermittent infusion of sulbactam, intermittent subcutaneous injection of insulin, and tube administration of 3.75 mg of prasugrel, 4 mg of pitavastatin, 10 mg of dapagliflozin, 20 mg of teneligliptin, and 5 mg of enalapril. On the 2nd day, after improvement of his acute respiratory failure, sedation was ceased. However, he remained in a coma state and demonstrated anisocoria. Repeated head CT showed diffuse low-density areas in the bilateral frontal lobe and left temporoparietal lobes with left-to-right midline shift [Figure 3].
Because there were no relatives with him, decompressive craniotomy was not performed. He died on the 5th day.
DISCUSSION
We reported a rare case of CCI with a fatal outcome. Recently, Ng et al. reviewed 44 cases of CCI using meta-analysis method.[1] Based on their reports, the average age was 58 years, with male dominance (66%). Concerning cardiovascular risk factors, hypertension (31.8%), smoking history (27.3%), atrial fibrillation (18.1%), diabetes mellitus (15.9%), dyslipidemia (11.4%), history of stroke (11.4%), and history of myocardial infarction (9.1%), percutaneous intervention (9.1%), and aortic dissection (6.8%) were noted. Rarer causes included cancer, essential thrombocythemia, genetic thrombophilia, and antiphospholipid antibody syndrome. The present case was old, male, and had diabetes mellitus, similar to the main findings of the previous report.
The two main mechanisms reported for CCI are embolic and hypotensive etiologies.[1] Atherosclerotic processes in the cerebrovascular and cardiovascular systems heighten the risk of simultaneous infarctions when there is a fall in systemic blood pressure, such as in the case of arrhythmias or myocardial infarction. However, hypotension in the present case was not documented. Left atrium or ventricular thrombus, which can embolize in the whole body, including the brain, can result from regional wall motion abnormalities, caused by blood stasis and procoagulant states. As the present case showed diffuse hypokinetic wall motion, which is not typical of AMI, and was initially able to summon an ambulance for himself, AMI followed by cerebral infarction deteriorated by hypoxia, based on the embolic etiology, was considered a reasonable cause of the CCI in the present case.[1,2] We could not exclude the possibility of iatrogenic stroke due to the procedures during coronary reperfusion, such as percutaneous coronary intervention and IABP implantation. However, the fact that the coma occurred before hospital arrival and there had been signs of early cerebral infarction on CT at hospital arrival suggested that the stroke had occurred before hospital arrival.
Correctly and promptly diagnosing CCI remains a clinical problem. If a patient demonstrates both typical signs of AMI, such as chest pain, and acute cerebral infarction, such as hemiplegia or dysarthria, under clear consciousness, an early diagnosis of CCI may be obtained using an electrocardiogram, biochemical analysis of the blood, and head magnetic resonance imaging (MRI).[3–6] The present case initially demonstrated dyspnea, probably due to acute heart failure, and AMI in the present case was easily and correctly diagnosed by an initial electrocardiogram on arrival. However, our patient was in a deep coma state on arrival and thus failed to demonstrate focal cerebral ischemic signs.
We experienced a suggestive case of AMI with deep coma that may have been combined with fatal cerebral infarction as CCI. The acute cerebral infarction in the present case was overlooked on initial head CT, which had already shown early CT signs of ischemic stroke, and would have been easily diagnosed if diffusion-weighted MRI had been applied.[4] However, MRI is a time-consuming method to perform for the diagnosis of ischemic stroke.[7] Use of MRI might result in failure to treat AMI within the golden time frame from the onset.[8] Accordingly, the ideal early diagnostic methods for acute cerebral ischemia or occlusion of major cerebral vessels in the present case might have been CT cerebral perfusion and CT Willis ring as well as a carotid angiogram or aortogram, none of which have been reported useful for diagnosing CCI before.
If the diagnosis of CCI had been made correctly in the present case, endovascular thrombectomy for carotid artery might have been the ideal treatment after percutaneous coronary intervention was finished.[9] Thrombolytic drug therapy was most frequently used in the cases reported by Ng et al.; however, this treatment is not useful for cerebral large-vessel occlusion.[1,10]
Finally, professional societies have recommended insulin therapy as the cornerstone of inpatient pharmacological management, and clinical guidelines recommend stopping oral antidiabetes drugs during hospitalization.[11] Accordingly, the administration of oral antidiabetes drugs in the present case might not have been necessary. However, in some countries, the continuation of oral antidiabetes drugs is common in patients with type 2 diabetes admitted to the hospital, and findings from clinical trials have suggested that noninsulin drugs, alone or in combination with basal insulin, can be used to achieve appropriate glycemic control in select populations.[11]
CONCLUSION
We experienced a suggestive case of AMI with deep coma that may have been combined with fatal cerebral infarction as CCI. In cases of AMI with a deep coma state, it might be best to check for cerebral perfusion or occlusion of major cerebral vessels using enhanced CT or an aortogram if percutaneous coronary intervention is performed.
Research quality and ethics statement
The authors followed applicable EQUATOR Network (http://www.equator-network.org/) guidelines, notably the CARE guideline, during the conduct of this report.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
This work was supported in part by a Grant-in-Aid for Special Research in Subsidies for ordinary expenses of private schools from The Promotion and Mutual Aid Corporation for Private Schools of Japan.
Conflicts of interest
There are no conflicts of interest.
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