Acute myocardial infarction in yellow oleander poisoning.

Self-harm by consuming yellow oleander seeds has become more frequent in South Asian countries, especially Sri Lanka and in southern parts of India. Yellow oleander poisoning usually presents with gastrointestinal, cardiovascular, and neurological manifestations as well as electrolyte abnormalities. Cardiac effects can manifest as nearly any type of dysrhythmia and sudden death with very few premonitory signs. To our knowledge yellow oleander poisoning related acute myocardial infarction has not yet been reported. We report a 37-year-old man with yellow oleander poisoning who had normal sinus rhythm at presentation but within few hours developed acute ST-segment myocardial infarction.

Introduction

Consumption of yellow oleander (Thevetia peruviana) is becoming a more frequent cause of intentional self-harm in South India.[1] Entire plant is poisonous, but the kernel contains the highest concentration and is most poisonous. It contains cardiac glycosides, and its consumption has effects similar to digitalis poisoning. Cardiac arrhythmias and electrolyte abnormalities may sometimes be life-threatening.[2] The cardiotoxicity does not correlate with the number of seeds consumed. The absorption of yellow oleander is reported to be erratic. The time course for progression and resolution of cardiotoxicity is variable. To the best of our knowledge, there are no case reports in literature of yellow oleander poisoning presenting with acute myocardial infarction.

Case Report

A 37-year-old man with no known comorbidities presented to our ED with alleged history of consumption of yellow oleander seed. He had consumed a single crushed yellow oleander seed mixed with water. Initially, he was asymptomatic for 4 h, following which, he developed vomiting and dizziness. He presented to our ED 16 h after ingestion. On arrival, he was conscious, oriented, and his vital signs were pulse rate of 63 beats/min, blood pressure of 140/80 mm of Hg, and SpO2 of 98% at room air. His initial electrocardiogram (ECG) [Figure 1] showed normal sinus rhythm with PR interval of 0.16 ms, QTc interval 336 ms, and QRS duration 0.10 ms without any evidence of digitalis effect [Figure 1]. Routine blood investigations and blood for serum cardiac glycoside concentration were sent. Ondansetron 4 mg was given parenterally for emesis. He was kept under observation with continuous cardiac monitoring. His laboratory work is shown in Table 1.

Figure 1

Baseline electrocardiogram showing normal sinus rhythm

Table 1

Laboratory values of this patient

Laboratory investigations	Values
Random blood glucose	117 mg/dL
Urea	39 mg/dL
Creatinine	1.2 mg/dL
Serum sodium	140 mEq/L
Serum potassium	4.6 mEq/L
Total calcium	8.6 mg/dL
Magnesium	2.1 mg/dL
Serum cardiac glycoside concentration	3.7 ng/mL

After 2 h of observation, he developed profound lightheadedness and vomiting. His vital signs now were pulse rate of 40 beats/min and blood pressure of 60/40 mm of Hg. Resuscitation was started with IV crystalloids, after 1000 ml of normal saline bolus blood pressure improved to 90/60 mm of Hg. Repeat ECG showed ST-segment elevation in leads II, III, aVF, V5R, V6R with complete heart block [Figure 2a and b]. Cardiac enzymes and baseline echocardiography were not performed for this patient because of time constraints. The patient was immediately transferred to cardiac cath laboratory for primary coronary intervention (PCI). Since the patient had hemodynamically unstable bradycardia, temporary pacemaker implantation (TPI) was done before angiography. His angiography revealed single vessel disease involving the right coronary artery (RCA) (total occlusion of mid-RCA due to thrombus) [Figure 3a]; hence PCI to RCA with drug-eluting stent 3 × 24 mm ultimaster was performed [Figure 3b and c]. Post procedure, patient's cardiac rhythm improved and TPI was removed. His echocardiogram on day 2 did not show any regional wall motion abnormality. Rest of the inhospital course was uneventful. He was discharged on day 5 and advised to follow-up after a month.

Figure 2

(a) Electrocardiogram showing ST-segment elevation in leads II, III, aVF with reciprocal changes and with complete heart block (b) Electrocardiogram showing ST-segment elevation in right-sided leads (V3R, V4R, V5R, V6R) suggestive of right ventricular infarction

Figure 3

(a) Coronary angiography showing total occlusion of mid-right coronary artery. (b) Coronary angiography showing placement of drug-eluting stent into the right coronary artery. (c) Poststenting coronary angiography showing restoration of blood flow to right coronary artery

Discussion

Consumption of yellow oleander (T. peruviana) is a common method of intentional self-harm in South India.[1] It contains cardiac glycosides, and its consumption has effects similar to digitalis poisoning. The primary pharmacological effect of these glycosides is to inhibit the Na+/K+ ATPase channel that extrudes sodium and imports potassium into cardiomyocytes. Inhibition causes buildup of sodium, which increases intracellular calcium, which in turn induces further calcium release from the sarcoplasmic reticulum. The myocardium becomes irritable and arrhythmogenic. In addition, increased vagal tone causes bradycardia.[3] Ventricular tachycardia and fibrillation seen in cardiac glycoside toxicity are usually resistant to defibrillation.[3]

Patients may develop arrhythmias and become hypotensive. Hypotension interferes with intracellular production of ATP through glycolysis, as lactate (produced due to anaerobic metabolism) inhibits the rate-limiting enzyme phosphofructokinase. This in turn will further reduce the activity of Na+/K+ ATPase resulting in a vicious cycle.[4]

Pirasath and Arulnithy[10] also reported that the toxicity was not related to the number of intake of yellow oleander seeds. In their study, the patients (69%) who have taken less seeds[123] had developed more cardiotoxic manifestations than those who have taken more seeds.[56789] They suggested that this might be due to the effect of intake of more seeds on forced and frequent vomiting by the patients.[10]

Cardiac manifestations were attributed to both increased vagotonia and direct cardiac glycoside toxicity. Arrhythmias occur due to depression or blockade of conduction and/or enhanced impulse formation. Enhanced impulse formation appears in the form of atrial, junctional, or ventricular arrhythmias. Conduction blocks occur in the sinus and atrioventricular (AV) nodes. Interference with sinus node conduction manifests as sinus bradycardia, sinus arrest, or sinoatrial block. Significant depression of AV nodal conduction presents as second- and third-degree AV block. Second-degree block usually manifests as a Wenckebach's phenomenon. Mobitz type II AV block though uncommon in digoxin toxicity has been reported in yellow oleander toxicity. Early toxicity may present with PR interval prolongation, decreased QT interval, scooping of ST segments, and T-wave flattening or inversion. Atrial tachycardia with heart block is caused by both disturbances in conduction and enhanced impulse formation. Certain tachyarrhythmias are characteristic of digoxin intoxication such as atrial tachycardia with variable AV block, accelerated junctional rhythms, and fascicular tachycardia.[5]

Hyperkalemia exacerbates cardiac glycoside-induced cardiac arrhythmias and is a marker of a poor outcome in cardiac glycoside poisoning. Serum cardiac glycoside concentration was seen to correlate with the severity of yellow oleander toxicity.

Management starts with assessment of severity of toxicity, continuous hemodynamic and cardiac monitoring, and measurement of serum creatinine; electrolytes such as sodium, potassium, calcium, magnesium, and serum cardiac glycoside levels. Digoxin-specific Fab fragments are an effective treatment of acute intoxication. Treatment of hyperkalemia is controversial, largely due to limited data.[6] Atropine antagonizes cardiac glycoside-induced vagal activation, increasing the heart rate. Doses of 0.6–1 mg are used first line. Isoprenaline (isoproterenol) infusions are not recommended for the treatment of bradycardia due to its potency to precipitate ventricular ectopy.[7] Cardiac pacing can be used in the presence of severe bradycardia, thus ensuring adequate cardiac output. Pacing is usually indicated if heart rate < 40/min, any form of sick sinus syndrome, or heart block. Tachyarrhythmias have a poor prognosis because they are more difficult to treat. Use of antiarrhythmic drugs in yellow oleander poisoning has not been studied. Lidocaine is the preferred antiarrhythmic agent. Electrical cardioversion may also result in ventricular fibrillation or asystole. Hence, it may be used only in resistant cases; using low energy levels.[8]

Anti-digoxin Fab fragments reverse toxicity by binding digoxin in extracellular fluid, causing a decrease in the effective free extracellular drug concentration. The concentration promotes release of digoxin from receptor sites. They are now considered as first-line therapy for severe digoxin poisoning in patients with life-threatening arrhythmias, cardiogenic shock, and hyperkalemia.[9]

To our knowledge no case report of yellow oleander poisoning presenting with acute myocardial infarction. In our patient, though he presented with a normal sinus rhythm, his serum cardiac glycoside concentration was 3.7 ng/mL. He developed acute ST-segment elevation myocardial infarction, 18 h after consuming single crushed yellow oleander seed. The pathophysiology behind the development of acute MI in this patient is not clear. He did not have any risk factor identified for coronary artery disease. His angiography revealed single vessel disease involving the RCA (total occlusion of mid-RCA due to thrombus). Whether his preexisting cardiac lesion was exacerbated by yellow oleander induced myocardial toxicity remains a dilemma.

An animal study done in mice showed that administration of aqueous extract of the seed kernel of T. peruviana increased the acetylcholine esterase (AChE) activity and the ceruloplasmin levels. Increased AChE activity indirectly reflects a reduced concentration of Ach and increase in the local and systemic inflammation. Ceruloplasmin is a serum α2-globulin considered as an acute phase reactant, where its serum concentration increases during infection, tissue injury, and other pathological states. And also, histological preparations of the heart tissue of mice showed leukocyte infiltrates and necrotic areas in myocardium, consistent with infarcts. The increased levels of AChE and the heart tissue infiltrative lesions induced by the aqueous seed kernel extract of T. peruviana explain in part the poisoning caused by this plant, which can be related to an inflammatory process.[11]

Furthermore, management guidelines for acute coronary syndrome in yellow oleander poisoning are not clear. In our patient, we managed with standard ACC/AHAACS-STEMI protocol and the patient recovered uneventfully. His echocardiogram on day 2 did not show any regional wall motion abnormality.

Conclusion

Yellow oleander poisoning related acute myocardial infarction has not yet reported. Further case reports will help establish whether yellow oleander poisoning can precipitate acute myocardial infarction and clarify the underlying pathophysiology of acute myocardial infarction due to an acute thrombotic episode. Management guidelines of yellow oleander poisoning presenting with acute myocardial infarction need to be established.

Declaration of patient consent

The authors certify that appropriate patient consent was obtained.

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Conflicts of interest

There are no conflicts of interest.