In this case report, we describe a case of an 84-year-old woman, was brought to the emergency department (ED) by ambulance with symptoms of occasional chest tightness occurring over the previous 4 years, and recurrent over the preceding 2 days, sudden chest tightness persisting for 1 hour and without relief. And the patient was shifted to the Medical Intensive Care Unit (MICU). On admission, she had AMI for worsening heart failure, with previous medical history significant for more than 20 years of hypertension (grade 3, very high-risk group), dyslipidemia, coronary artery disease (CAD) and twice percutaneous coronary intervention (PCI) and two stents placement surgery history. And she has a long-term oral thiazide diuretics history for chronic renal insufficiency (CRI) elevated creatinine and oliguria. And she was suffering chronic constipation (CC) in the past 1 year, and had a long-term oral rhubarb soda tablets. And she had a positive history for nitroglycerin, penicillin, and cephalosporin. On physical examination, low heart sound and pulmonary wet rales were heard on auscultation, ambiguous and with a pained expression. Her electrocardiogram (ECG) demonstrated monomorphic VT, 168 beats per minute (bpm) and irregular, 37 breaths per minute (bpm), blood pressure (BP) was 80/60 mmHg, and blood oxygen saturation (SpO2) was 96–99%.
Defibrillation using 200J was immediately performed with restoration of sinus rhythm (70 bpm), with an elevated blood pressure present, and the patient appeared drowsy, with a Glasgow Coma Scale (GCS) score of 13 (E3V5M5). Then she was received clopidogrel and aspirin for oral administration, low molecular weight heparin (LMWH) subcutaneous injection, dopamine infusion to maintain blood pressure, lansoprazole to inhibit of gastric acid secretion, and the ECG monitor displayed, BP 117/75 mmHg, HR 64 bpm (sinus rhythm), R 19 bpm.
She was assessed as Killip IV-grade. Her troponin I level was elevated at 11.871 ng/ml (normal 0-0.04 ng/ml), and brain natriuretic peptide (BNP) concentration was 1348.8 pg/ml (normal < 100 pg/ml). A 12-lead ECG revealed sine-wave pattern and ST elevation with features of low cardiac output. On transthoracic echocardiography, the left atrium (LA) and left ventricle (LV) diameter was 35 mm and 65 mm, respectively. The ventricular septum was 60 mm, and the posterior wall of the left ventricle was 60 mm, and the activity of them was reversed and the wall motion exhibited globally severe hypokinesis with an LV ejection fraction (LVEF) of 13%.
The patient was monitored in the MICU while experiencing unconsciousness, shallow breathing, hypotension, and hypoperfusion of end organs (cool extremities, low urine output and heart rate of 50–75 bpm) and supported with dopamine, the urine volume was 1299 ml within the first 24 hours.
After defibrillation, a 12-lead ECG depicted normal sinus rhythm, premature ventricular contractions, first-degree atrioventricular block, ST-T segment changed in leads Ⅰ, Ⅱ, Ⅲ, aVL, aVF, V4 through V9, T-wave changed in leads V2-V4, suggested old myocardial infarction.
The results of complete blood count indicated a rise in leukocyte and neutrophil counts, and serum concentrations of electrolytes were normal, creatinine 387umol/L (45-84umol/L), and liver function tests were ALT 1190 U/L (0–40 U/L), AST 1578.4 U/L (0–35 U/L), TBA 22.2umol/L (0.5-10umol/L), LDH 1776 U/L (120–250 U/L). Coagulation function showed D-DI 26.3ug/mL (< 0.5ug/mL).
On hospital day 2, the patient developed a recurrent wide complex QRS that transitioned into sustained monomorphic ventricular tachycardia (SMVT), requiring electrical defibrillation. After defibrillation, the patient's QRS interval normalized, SMVT occurred again, just 6 minutes after defibrillation, then after 3 times of defibrillation, antiarrhythmic treatment with amiodarone was initiated immediately, we administered an intravenous infusion of 150 mg amiodarone, followed by a continuous infusion (1 mg/min) as a maintenance volume for 6 hours. But this also failed to terminate the occurrence of arrhythmia, SMVT occurred repeatedly, with a total of 9 ventricular arrhythmias rapidly degenerating to ventricular tachycardia with hypotension within 8 hours, fortunately, electrical defibrillation could restore the sinus rhythm, and the interval was extended with the amiodarone maintenance. Over the next 12 hours, each SMVT could be converted to sinus rhythm through one or two doses of intravenous amiodarone (150 mg each, intravenously) without defibrillation, and since had no documented episodes of ventricular tachycardia. Her non-invasive blood pressure (NBP) varied between 65/42 mmHg and 151/90 mmHg, and his pulse ranged from 99 to 182 bpm, with a stable respiratory rate from 12 to 20 bpm.
A post-cardioversion ECG confirmed sinus rhythm. She was continuous amiodarone with 0.5 mg/min infusion for 2 days after first 6 hours with 1 mg/min. After defibrillation and amiodarone infusion, the ECG changes began to normalize gradually, contractility of the heart also improved. On the next days in hospital, her mental status returned to her baseline, and her GCS score was 15. And several daily ECGs during hospitalization depicted normal sinus rhythm. The patient was discharged her 10th day in the hospital with clinically stable and medically asymptomatic.
The patient remained free from sustained ventricular arrhythmia during the six-month follow-up.