Perioperative myocardial infraction following video-assisted thoracic surgery: A case report and review.

Perioperative myocardial infarction (PMI) during video-assisted thoracoscopy (VAT) surgery is rarely reported in the literature. ST-segment-elevated myocardial infarction (STEMI) is rare in the perioperative period. We report a case of STEMI, following VAT surgery, complicated by acute coronary syndrome. A 53-year male, admitted with recurrent left-sided pneumothorax, an intercostal chest drain was inserted and planned for VAT and lung resection. The intra-operative period was stable, minimal lung resection, and excision of bullae was done. Just before extubation, patient had acute myocardial infarction and cardiogenic shock. An immediate percutaneous coronary intervention (PCI) angiogram showed 90% blockage of the right coronary artery with thrombus. Export thrombectomy and balloon angioplasty was done. Weaned off from inotropes and ventilator. He was transferred to ward from there by day 12, discharged home on double antiplatelet therapy. The PMI can occur earlier than it is commonly thought, and in our patient, it was STEMI, which is rare and occurred during VAT Surgery. In our patient early detection and earlier PCI may have resulted in better outcome.

INTRODUCTION

Perioperative myocardial infarction (PMI) is one of the most feared complications in anesthesia practice, fortunately rare but leads to devastating perioperative outcome.

The numbers of noncardiac surgeries are increasing, due to recent advances and better treatment of cancer and arthritis leading to a better quality of life.[1] There are various patient and surgical risk factors for the development of PMI, but can occur without any risk factors. Early recognition and appropriate therapy will decrease the morbidity and mortality of this cardiac emergency. We report a case of PMI, following video-assisted thoracoscopy (VAT) surgery, complicated by acute coronary syndrome diagnosed early and managed successfully.

Illustrated case

A 53-year old male, heavy smoker and a known case of carcinoma esophagus operated 2 years back. Admitted with recurrent left-sided pneumothorax, due to ruptured lung bullae; an intercostal chest drain was inserted and planned for video-assisted thoracoscopy (VAT). He was slightly dehydrated but not malnourished (BMI of 20). Preoperative ECG was normal and echocardiogram showed left ventricular ejection fraction 58%, no wall movement abnormality and right ventricular systolic pressure of 29 mmHg. His ASA physical status was 2; he was premedicated with midazolam, induction of anesthesia was with propofol, and maintained with fentanyl and cisatracurium infusions. The patient was intubated with double lumen tube with the left-lung collapse. The intraoperative period was uneventful, minimal lung resection and excision of bullae was done. Just before reversal and extubation patient had bradycardia (40–45 beats/min) and hypotension (80–82 mmHg systolic) with ST segment elevation in inferior leads.

Immediately resuscitated with atropine and added dopamine infusion to maintain the blood pressure. Immediate 12 lead ECG showed ST segment elevation in inferior leads [Figure 1] echocardiogram revealed, severe left ventricular dysfunction with ejection fraction 32%, Hypokinetic inferior and posterior wall.

Figure 1

ECG showing ST segment changes

He was shifted to intensive care unit (ICU); his cardiac biomarkers were raised (CK-MB, troponin I and T), and [Graph 1], remained on ionotropic and ventilatory support. Aspirin and clopidogrel were given through the nasogastric tube, and continued on intravenous fluid. He was immediately taken for percutaneous coronary intervention (PCI); angiogram showed 90% blockage of the right coronary artery with thrombus. Export thrombectomy and balloon angioplasty was done. Postprocedure integrillin and heparin infusions were continued for 6 and 24 h, respectively. He was continued on aspirin, clopidogrel, and enteral feeding, weaned off from dopamine by day 3, weaned from the ventilator and extubated on day 4. He was awake, obeying commands, and hemodynamically stable. On day 6 he was transferred to the ward, from there discharged home by day 12, on double antiplatelet therapy. A month later follow-up coronary angiogram was essentially normal.

Graph 1

Cardiac biomarkers in our case

DISCUSSION

ST-segment elevated myocardial infarction (STEMI) in the perioperative period is rare. Perioperative myocardial infarction (PMI) in VAT surgery is rarely reported in the literature.[2] Although our patient was not known to have cardiac co-morbidities but has risk factors (smoking, dehydration, and intra-thoracic surgery) that might have been contributed for PMI and acute coronary syndrome.

The incidence of PMI is rare and varies depending on patient's cardiac co-morbidity, and type of surgery. It is reported to be 0.6% of all noncardiac surgeries. The incidence will increase to 2% in veterans and significantly higher if patient had history of coronary artery disease (CAD).[3] The main risk factors for PMI are, poor cardiac status, diabetes mellitus, chronic renal insufficiencies, cerebrovascular disease, hypertension, smoking, dyslipidemia, anemia, major surgeries, significant intraoperative blood loss and blood transfusion, peri-operative hypotension,[4] recent PCI and stent implantation, Improper perioperative analgesia.[5]

It is commonly believed that most of the PMI occurs after three postoperative days, but recently it was found that PMI occurs earlier and most of them occurs on the day of surgery or first postoperative day.[6]

The exact pathophysiology of PMI is not clearly understood. Understanding from the postmortem studies about PMI is that it is evenly distributed, etiologically either due to oxygen supply/demand mismatch or plaque rapture [Figure 2].[6] From perioperative Holter and hemodynamic monitoring it was realized that ST segment depression myocardial infarction is 40 times more frequent than that with ST segment elevation. ST segment elevated PMI occurs only in less than 3% of total patients.[7]

Figure 2

Etiopathology of perioperative myocardial infarction

Diagnosis is a challenging aspect of PMI, as most of PMI are silent, low incidence of chest pain and if at all pain is there it will be easily masked by analgesia and residual perioperative anesthesia. Although PMI occurs in the monitored patients [Table 1], but the ECG changes are not typical and the diagnostic abilities of two lead continuous ECG to detect ST segment trends of ischemia is poor, it will be able to detect ischemia in only 3% of high risk patients. As most of ischemic events occurs in lead V2-4 and not in lead V5 or II, which are commonly monitored.[8] Moreover, the initial ECG after MI is diagnostic in 50% of the patients, normal in 10% and abnormal but not diagnostic in 40% of the MI patients.[9] The cardiac biomarker rise and fall is a significant diagnostic and prognostic finding in PMI patients. Creatinine myocardial branch (CK-MB) is a traditional cardiac biomarker, CK-MB/CK >5% in first three postoperative days are strongly suggestive of PMI.[7] The newer cardiac biomarkers (troponin I and T) are highly sensitive and specific, as they are released into the circulation, after injury to the cardiac myocytes. Troponins are not only elevated in AMI, but also in patients with severe sepsis, septic shock and pulmonary embolism; hence, an echocardiogram and CT angiogram is essential to differentiate these conditions from acute myocardial infraction.[7]

Table 1

Differences between non-surgical MI and perioperative MI

According to World health organization (WHO) at least two of the following criteria are required to diagnose PMI, (i) typical chest pain (ii) rise and fall of cardiac biomarkers (iii) typical ECG changes and (iv) echocardiographic wall movement abnormalities.[10] The type of surgery is of vital importance in evaluating cardiac risk; hence, adding to the cardiac risk, the type of surgeries and abnormal preoperative ECG (atrial fibrillations, right or left bundle branch block, LVH, pacemaker rhythm, or ventricular ectopic) will improve the predicative value for the cardiac complications.[11] Apart from the routine laboratory risk indicators for myocardial infarction (serum creatinine, fasting blood sugar, and lipid profile), raised plasma pro-type B natriuretic peptides (ProBNP) and glycosylated hemoglobin levels are found to be strong predictors of perioperative adverse cardiac events.[12] Plasma proBNP levels are raised in heart failure, aortic stenosis and myocardial ischemia patients. Diabetes mellitus is known to increase the perioperative cardiac adverse events, the preoperative glycosylated hemoglobin levels in these patients’ correlates with the perioperative cardiac outcome.[13] If a patient has an increased perioperative cardiac risk or presence of coronary artery disease, in these circumstances further cardiac tests will be needed. The most practical, simple, cost-effective cardiac imaging is a resting echocardiogram for evaluation of the left ventricular systolic, diastolic functions, and valulvar lesions. Presence of aortic stenosis is related to fivefold increase in perioperative cardiac events.[14]

The initial therapy in non-ST segment elevated myocardial infraction (NSTEMI) [Figures 3 and 4] is medical stabilization, whereas for ST segment elevated myocardial infraction (STEMI), fibrinolysis or percutaneous coronary interventions (PCI) are therapy of choice. In PMI treatment options are limited due to the risk of bleeding.

Figure 3

Management of perioperative myocardial Infraction

Figure 4

Diagnosis and management of perioperative myocardial infarction

Apart from maintaining a tight hemodynemic, pain control, correction of anaemia, and hypoxia [Figures 3 and 4]. Keeping serum electrolyte within normal range, following medical therapy may be beneficial in the management of PMI.

The advantage of β-blocker is blunting the cardiovascular sympathetic surge; hence, causing decrease in cardiac oxygen consumption, decreasing the cardiac rate, arrhythmia, and gives a protection against reinfarction and sudden cardiac death.[15]

In patients with myocardial infarction (MI) and high risk patients β-blockers causes a decrease in mortality by 28%, at first week and maximum benefits were obtained in first 48 hours of therapy, as reinfarction and cardiac arrest were reduced by 18 and 15% respectively. In high risk vascular patients on β-blocker therapy, there is 10 fold reduction in incidence of PMI and perioperative death compared to patients not on β-blocker therapy.[15]

A small study showed use of clonidine, reduces perioperative myocardial infarction and 2-year mortality.[16] Statins should be continued in perioperative period, as sudden withdrawal may lead to plaque destabilization and fatal MI. Statins are shown to reduce PMI and mortality by 50%, as well as reduction in perioperative as well as long term complications.[17]

It is a common practice to discontinue aspirin 5 to 7 days before any surgical procedure, although there is evidence of mild increase in bleeding with aspirin but also no clear beneficial effect of continuing aspirin in non-cardiac surgical patients. Patients on dual antiplatelet therapy (aspirin and clopidogrel) are at greater risk of bleeding if continued in the perioperative period and if stopped much higher risk of thrombosis of coronary stent. Hence it is mandatory to continue dual antiplatelet therapy for at least 4 weeks after metallic stent implantation and a year after drug eluding stent implantation. All elective surgeries should be discouraged during this period, as there is adverse relationship between time after PCI and major adverse cardiac events.[18]

Fibrinolytic therapy in perioperative period is feared due to the risk of major bleeding. In patients with ST segment elevated myocardial infarction (STEMI) and/or cardiogenic shock [Figures 3 and 4], an immediate coronary angiogram and direct angioplasty or thrombolysis/extraction thrombectomy is feasible and safe, it improves survival by 65% even in cardiogenic shock patients.[19]

To conclude, PMI can occur earlier than it is commonly thought, and in our patient, it was STEMI, and occurred during VAT surgery, which is rare. Early detection and an earlier PCI may have resulted in better outcome.