Perioperative myocardial infarction in a young adult after percutaneous nephrolithotomy.

The causes of myocardial infarction in a young adult can be divided into four groups: (1) atherosclerosis, (2) nonatherosclerosis, (3) hypercoagulable states, and (4) substance abuse. We present here a case of the 29-year-old male patient who developed myocardial infarction after undergoing percutaneous nephrolithotomy. Prompt diagnosis and timely intervention salvaged his myocardium. Copyright:

Introduction

Atherosclerotic coronary artery disease is the leading cause of morbidity and mortality in the developed countries, and the World Health Organization estimates that it will be the leading cause of death all over the world by the year 2020.[1] It primarily affects the ≥40 years population, but younger males and females can also be affected.[2] Perioperative myocardial infarction (PMI) is one of the most important predictors of short- and long-term morbidity and mortality associated with noncardiac surgery.

Case History

The 29-year-old male was admitted in the urology department with complaints of intermittent right-sided abdominal pain for 4 months. For pain, he was frequently taking tab dicyclomine hydrochloride. Ultrasonography showed a 33 mm size calculus in the right kidney. He was posted for right-sided percutaneous nephrolithotomy (PCNL). On preoperative evaluation, his pulse was 84 beats/minute, blood pressure 130/70 mmHg, weight 80 kg, height 165 cm, and body mass index 27.54 kg/m2. On airway examination, mouth opening was normal and it was Mallampati grade 2. His hemoglobin was 15.4 gm/dL and other laboratory investigations were within normal limits. He was a nonsmoker with no history of systemic illness. There was no family history of diabetes, hypertension, and ischemic heart disease. Informed written consent was obtained from the patient.

In operation theatre after securing intravenous access, a baseline parameter like non invasive blood pressure (NIBP), ECG, SpO2 were recorded. The patient was induced with fentanyl 2 μg/kg, propofol 2 mg/kg, and vecuronium 0.1 mg/kg. He was intubated with an 8-mm internal diameter cuffed endotracheal tube. Anesthesia was maintained in a mixture of oxygen, nitrous oxide, isoflurane, and the intermittent dose of vecuronium. In intraoperative period, he received intravenous fentanyl 50 μg, paracetamol 1 gm, and 2 L of ringer lactate. The total duration of surgery was approximately 1 hour and 30 min. Hemodynamic parameters were normal during the intraoperative period. The trachea was extubated at the end of surgery after the return of airway reflexes and reversal of the neuromuscular blocking agent.

After extubation, the patient was agitated and violent, and there was a decrease in SpO2 to 80% on oxygen by mask. Considering upper airway obstruction, positive pressure ventilation was applied and oxygen saturation improved to 99%. But he was still agitated and complained of chest pain. At that same time, ECG showed ST-segment elevation in lead II on the monitor. ECG was immediately taken which showed normal sinus rhythm with ST-segment elevation in leads II, III, and aVF, suggestive of inferior wall MI. Immediate cardiology consultation was taken. He was shifted to a coronary care unit (CCU). His heart rate was 100 beats/min, blood pressure 110/80 mmHg, and SpO2 99% on the face mask. There, he received tab sorbitrate 5 mg sublingually, aspirin 325 mg, clopidogrel bisulfate 300 mg, and rosuvastatin 40 mg along with oxygen by face mask. He was planned for angiography and informed written consent was taken. On angiography, after giving unfractionated heparin 5000 IU bolus, the left coronary system was found to be normal. The mid-portion of the right coronary artery showed 100% thrombus occlusion (grade 3) with distal thrombolysis in MI (TIMI)-3 flow [Figure 1]. The lesion was crossed with a soft floppy wire (BMW wire, Abbot Corporation, USA). Intravenous Gb2b/3a inhibitor tirofiban (25 mcg/kg IV infused over 5 min) bolus was given followed by intravenous infusion of 0.15 μg/kg/min for 18 h. After 3–4 min of infusion, the thrombus burden got reduced showing <50% blockage in the right coronary artery with distal TIMI-3 flow [Figure 2]. There was no residual lesion seen. So no balloon and stenting was done. By this time, the patient was pain-free. Postangiography ECG was taken in CCU that showed >50% resolution in ST segment and complete resolution of ST segment with T-wave inversion in inferior leads on day 3. Subcutaneous low-molecular-weight heparin was started twice daily after the completion of tirofiban infusion. Metoprolol succinate 25 mg once daily along with clopidogrel 75 mg and aspirin combination and tab rosuvastatin 40 mg once daily were added. He was monitored for bleeding from a surgical site. There was no increase in bleeding from the site. He was evaluated for coagulation factors and lipid profile, which were in normal limits. He was discharged on the 7th day uneventfully.

Figure 1

Angiogram of the right coronary artery showing thrombus in the mid of the right coronary artery

Figure 2

Angiography post BMW wire

Discussion

This is the unusual documentation of acute inferior wall ST-elevation MI in young adult undergoing PCNL. The etiologies of atherosclerosis coronary artery disease are associated with conventional risk factors like smoking, lipid abnormalities, diabetes, hyperhomocysteinemia, and lipoprotein (a). Nonatherosclerosis causes such as congenital coronary anomalies, spontaneous coronary dissection, myocardial bridge, coronary aneurysms, paradoxical embolization through foramen ovale, and septic vegetation embolization from infected valves may cause MI. Cocaine use and binge drinking of alcohol have been reported to cause MI in young. Central obesity, depicted by the waist to hip ratio, is an independent risk factor for CAD – even a modest increase in body fat with central distribution increases the risk further.

The majority of complications occurs in PCNL in intraoperative or in the early postoperative period.[3] Reported data showed that postoperative ST elevation occurred in <2% of postoperative ischemic events and was a rare cause of PMI.[4] Emergent coronary intervention, anticoagulants, or glycoprotein IIb/IIIa antagonists are rarely indicated in the immediate postoperative course and are hazardous because of the risk of bleeding unless ST elevation or intractable cardiogenic shock ensues.[5]

The cause of in-situ thrombosis formation in the coronary artery of our patient after PCNL may be plaque rupture or erosion that causes MI. Use of intracoronary thrombolytic agent may increase the chance of bleeding postoperatively, so it was avoided. As there was no obvious lesion seen, stenting was avoided. There is an elevation of creatine kinase in patients undergoing PCNL because of renal and skeletal muscle injury during operation, but this is not associated with elevation of troponins.[6] A recent study concluded that PMI has a markedly high mortality rate despite percutaneous intervention.[7]

PCNL is a well-tolerated procedure with a low risk of complication and death. Acute thrombotic occlusion of the right coronary artery without any conventional risk factors was seen in this young adult. Prompt diagnosis and timely intervention salvaged his myocardium.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.