Abnormal ventricular conduction following dothiepin overdose simulating acute myocardial infarction

Abstract

Objective-To determine whether pharmacological stress leads to prolonged but reversible left ventricular dysfunction in patients with coronary artery disease, similar to that seen after exercise. Design-A randomised crossover study of recovery time of systolic and diastolic left ventricular function after exercise and dobutamine induced ischaemia. Subjects-10 patients with stable angina, angiographically proven coronary artery disease, and normal left ventricular function. Interventions-Treadmill exercise and dobutamine stress were performed on diVerent days. Quantitative assessment of systolic and diastolic left ventricular function was performed using transthoracic echocardiography at baseline and at regular intervals after each test. Results-Both forms of stress led to prolonged but reversible systolic and diastolic dysfunction. There was no diVerence in the maximum double product (p = 0.53) or ST depression (p = 0.63) with either form of stress. After exercise, ejection fraction was reduced at 15 and 30 minutes compared with baseline (mean (SEM), −5.6 (1.5)%, p < 0.05; and −6.1 (2.2)%, p < 0.01), and at 30 and 45 minutes after dobutamine (−10.8 (1.8)% and −5.5 (1.8)%, both p < 0.01). Regional analysis showed a reduction in the worst aVected segment 15 and 30 minutes after exercise (−27.9 (7.2)% and −28.6 (5.7)%, both p < 0.01), and at 30 minutes after dobutamine (−32 (5.3)%, p < 0.01). The isovolumic relaxation period was prolonged 45 minutes after each form of stress (p < 0.05). Conclusions-In patients with coronary artery disease, dobutamine induced ischaemia results in prolonged reversible left ventricular dysfunction, presumed to be myocardial stunning, similar to that seen after exercise. Dobutamine induced ischaemia could therefore be used to study the pathophysiology of this phenomenon further in patients with coronary artery disease. (Heart 2000;83:283-289)

Acute Myocardial Infarction Associated with Amitriptyline Overdose

“…ST segment elevation was reported in leads of DI, aVL, V1 and V2 mimicking a current of anteroseptal subepicardial injury after amitriptyline overdose, which persisted for four days. Serial cardiac enzyme estimates did not confirm an ischaemicevent Steeds & Muthusamy (2000) reported a case of dothiepin (sulphur‐containing analogue of amitriptyline) overdose with a symmetrical T wave repolarization; abnormalities appeared within 9 hr and mimicked acute anteroseptal myocardial infarction. ECG changes persisted for 6 weeks.…”

Myocardial infarction: a rare complication of dothiepin overdose

“…To our knowledge, there has been only one previous report of myocardial infarction due to a tricyclic antidepressant overdose [4]. Previous reports of transient QRS changes which mimic an acute myocardial infarction [5,6] may be either due to quinidine-like effect of dothiepin or to an alteration in membrane permeability rather than due to ischaemic changes of the myocardium itself.…”

Cardiac Troponin T and NT-proBNP as Biomarkers of Early Myocardial Damage in Amitriptyline-Induced Cardiovascular Toxicity in Rats

“…Electrocardiographic changes suggestive for myocardial infarction were described in the literature 17,19 in the acute poisoning with dothiepin, although Steeds considers that the cause was the blockade of potassium and rapid sodium channels rather than a real myocardial injury.…”

“…15,16 These cases were diagnosed using electrocardiographic records and elevated cardiac enzymes. Other studies reported either electrocardiographic signs of ischemia 17,18,19 or elevated myocardial cytolysis enzymes, 20 but none of these findings were associated with myocardial necrosis.…”