Allergic myocardial ischemia causing reversible hemodynamic collapse during gastroscopy.

This case report details the development of an acute heart dysfunction during gastroscopy under sedation in a patient with normal coronary arteries. The early diagnosis by echocardiography and aggressive management allowed us to prevent a serious and fatal outcome. We spot on the diagnosis of allergic cardiogenic shock based on our clinical and laboratory finding.

INTRODUCTION

Symptoms of myocardial ischemia accompanying allergic reaction are defined in the literature as Kounis syndrome.[1] Acute reversible left ventricular (LV) dysfunction due to myocardial stunning is a known phenomenon during acute myocardial infarction (MI), coronary angiography, and coronary angioplasty or after coronary artery bypass surgery.

Early and aggressive management of myocardial dysfunction by inotropic drugs, intra-aortic balloon pump, or LV assist devices could restore LV function. We report a case of reversible stunned myocardium during gastroscopy under sedation.

CASE REPORT

A 54-year-old woman with a height of 170 cm and weight of 68 kg, not known to have any drug allergy and a heavy smoker with no other coronary risk factor, was operated 2 years ago for bilateral cataract extraction under local anesthesia and breast augmentation associated with abdominoplasty under general anesthesia without any known complications. She presented to our center for screening gastroscopy and colonoscopy under sedation indicated for exploration of occult anemia. No premedication was given to the patient (especially anticholinergic medications were not used). After the standard parameter monitoring (noninvasive blood pressure [NIBP], SPO2, and electrocardiogram [EKG]), oxygen was supplemented through the nasal cannula at 4 L/min. A baseline vital signs was normal [NIBP=112/65, heart rate = 72 beats/min, respiratory rate = 12 per minute, saturation SPO2 = 100% on room air]. The patient was sedated with 50 mg meperidine, 2 mg midazolam, and 40 mg propofol intravenously. Gastroscopy started without any problem. After 10 min, the patient developed a bradycardia, without hypoxia [SPO2 = 97%], which was converted to asystole [premature ventricular contraction without P wave and bizarre QRS wave] and undetectable blood pressure; there was no evidence of skin rash. Patient received immediately 60 mg xylocaine, a total of 2 mg atropine, 0.01 mg epinephrine, and 250 mg hydrocortisone intravenously; 100% face mask ventilation was applied. She responded to the treatment with sinus tachycardia (heart rate = 112 beats/ min) and slight improvement in the systemic blood pressure [NIBP=70/42 mmHg] on spontaneous breathing without dyspnea [respiratory rate = 8 per minute]. Few minutes later, the patient regained consciousness with acute chest pain, pulmonary edema, dyspnea and hypoxia [SPO2 = 60%]. The procedure was aborted, and the patient was transferred to intensive care unit where an EKG was not indicative and chest X-ray showed diffuse bilateral infiltrations. An immediate transthoracic echocardiography, performed by the cardiologist, showed a global hypokinesia and ejection fraction estimated to be 20–29% associated with respiratory acidosis on ABGs [PH 7.31, PO2 43.5, PCO2 51.5, SBE 0.5, and HCO3 23.2]. At this time, we confirm an acute LV dysfunction with pulmonary edema. Treatment was started with intravenous bolus dose of Lasix 80 mg, and continuous dobutamine at a rate of 15 mcg/kg/min. Two hours later, the patient improved clinically, and the saturation picked up to 95% under noninvasive ventilation with bilevel positive airway pressure ventilation [BiPAP]. The patient improved completely after 24 h, and the weaning of dobutamine was started. Hence, the troponin level upon admission to the intensive care unit and at 12 and 18 h later was 0.08, 0.54, and 0.58, respectively. Serial EKGs did not show any evolving changes. Twenty-four hours later, a coronary angiography was performed and revealed no significant coronary stenosis. The patient fully recovered, 48 h later, with no cardiac symptoms, and she was weaned and discontinued from the BiPAP and the inotropic support. By the fourth day, an echocardiography showed improved LV function with no regional wall motion abnormality and EF estimated at 68%; chest x-ray showed no evidence of pulmonary edema. She was discharged on carvedilol and rabeprazole sodium and was doing well at three months’ follow-up.

DISCUSSION

This 54-year-old woman with no significant coronary risk factor developed cardiogenic shock during gastroscopy under sedation. This case was characterized by an acute severe LV dysfunction in a previously normal heart with the normal LV function. She developed a transient arrhythmia followed by hypotension and pulmonary edema. The EKG did not show any acute modification on ST segment, and there was a mild elevation of the cardiac enzyme level. The fact that myocardial contractility improved rapidly with inotropic support shows that the myocardium was metabolically active. Stunned myocardium is characterized by a reversible contractile dysfunction, when the myocardial blood flow is fully or almost fully restored. In this condition, no metabolic deterioration occurs during inotropic stimulation.

The recovery of biventricular function in our patient within four days would not have been compatible with untreated massive pulmonary embolism.

There are a number of reversible causes of acute myocardial dysfunction. These include transient ischemia-related causes, such as coronary vasoconstriction, transient thrombotic occlusion, and high-output states,[2] some of which may lead to stunning and/or hibernating myocardium, myocarditis, sepsis, pulmonary embolism, exposure to drugs or toxin anaphylaxis, subarachnoid hemorrhage, cathecholamine-induced cardiomyopathy, and postcardiopulmonary bypass.

Adequate investigation to identify LV dysfunction is important for the detection of potentially reversible myocardial dysfunction.[3] In our case, LV dysfunction was diagnosed early using echocardiography, and the etiology was immediately related to a hidden CAD because of age [54 years] and clinical findings [acute chest pain and dyspnea raised up lately after resuscitation]. However, coronary angiography 24 h later was found to be normal. Other etiologies should have been responsible for the acute LV dysfunction.

Severe cardiac arrhythmias, including ventricular tachycardia and fibrillation, as well as sudden death related to vasospastic coronary may be associated with acute MI.[4] Although responses to various vasoconstrictor substances, including catecholamines, serotonin, endothelin, thromboxane A2, and arginine vasopressin, are greater in spastic segment of coronary arteries; hypersensitivity to vasoconstrictor stimuli also occurs throughout the entire coronary trees in the patient with vasospastic angina.[5] In our case, transit vasospastic coronary arteries might be a logical reason for these symptoms. This situation increases the idea of an allergic release of inflammatory mediators inducing a hyperadrenergic state with acute coronary vasospasm.

Although it was believed generally that coronary arteries were not involved primarily in the hemodynamic derangement associated with anaphylaxis, recent observations indicate that coronary blood flow can be impaired during anaphylaxis.[6]

The coincidental occurrence of chest discomfort with characteristic clinical symptoms, signs, and laboratory findings of angina pectoris, together with acute or chronic allergic processes, constitutes a new clinical entity, which is named allergic MI or “Kounis syndrome”.[78]

Kounis syndrome has been defined as a coronary syndrome that manifests with unstable vasospastic or nonvasospastic angina and even as acute MI triggered by the release of inflammatory mediators following an allergic insult. There are currently two variants of Kounis syndrome.[4910] The first is observed in patients with no cardiovascular risk factor and with healthy coronary arteries in which the inflammatory cascade triggered by the allergic insult causes a coronary vasospasm accompanied by elevated levels of markers of myocardial damage. The second is observed in patients with pre-existing atheromatous disease in whom the release of these mediators would also produce a coronary vasospasm, which occurs with normal cardiac enzymes or rupture of the atheromatous plaque, manifesting as acute MI.

Many case reports are published describing allergic reaction to some medication as Kounis syndrome.[891112]

Triggiani[13] described the pathogenesis of heart anaphylaxis showing that mast cells are more abundant and produce more mediators in hearts with ischemic cardiomyopathy. Atherosclerotic lesions make coronary arteries more susceptible to the effects of mast cell and basophile-derived mediators. Exposure to the allergen evokes a transient, profound drop in contractility and rhythm disturbances as sinus tachycardia, atrioventricular blocks, ventricular tachycardia, or idioventricular rhythm.[14] In in vitro experiments, antigen administration into coronary circulation triggers histamine release. Similar changes occur after parenteral application of antigen in vivo.[12] Our patient developed a bradycardia, which was converted to premature ventricular contraction without P wave and bizarre QRS wave. The release of mast cell and basophile-derived mediators usually occurs within minutes, triggering cardiovascular manifestation of anaphylaxis, including hypotension and shock, cardiac arrhythmias, ventricular dysfunction, and cardiac arrest.[15]

However, catecholamine release may be present during upper gastrointestinal endoscopy by airway obstruction, gastric or salivary aspiration, direct pressure on the diaphragm, air insufflations, and stress anxiety contributing to cardiac arrhythmias. The distension and collapse of hollow abdominal viscera during the procedure might be another factor accounting for the electrocardiographic abnormalities.[16]

Elevated serum tryptase levels are useful in the diagnosis of anaphylactic reaction because this is one of the main markers of this condition.[17] The blood sample should be taken between the first and second hour after the onset of symptoms. Unfortunately, in our case, we did not measure the serum tryptase level; the diagnosis of allergic angina was not present at this time.

Most probably, our patient developed an allergic reaction to one of the medications received during the procedure. Hence, after reviewing the old anesthesia chart, only meperidine was not present, which is not sufficient to make it the suspected drug. Unfortunately, the patient refused to undergo an allergic screening to identify the responsible agent. For this reason, only clinical findings and improvement as well as coronary angiography and echocardiography modification were taken in consideration to suspect the diagnosis of Kounis syndrome.

The manifestation of drug-induced allergic angina can be completely atypical and, therefore, causes diagnostic confusion. Our case highlights the fact that the diagnosis of allergic ischemic heart should be taken into consideration in the differential diagnosis of ischemic heart disease. Kounis syndrome should be present in mind upon encountering patients with no cardiovascular risk factors who experience acute coronary syndrome with symptoms of anaphylaxis.