Hypertensive crisis-induced electrocardiographic changes: a case series

Abstract

IntroductionMyocardial injury is one of the most notorious complications of a hypertensive crisis. Key electrocardiograph signs used to detect cardiac injury such as ST segment changes and cardiac arrhythmias usually indicate acute ongoing end-organ damage. Lack of early signs to predict end-organ damage might lead to a delay in the initiation of therapy and selection of the incorrect therapeutic strategy.Case presentationWe describe five cases of tall, hyper acute symmetrical T-waves alone or accompanied by other electrocardiograph abnormalities in five healthy participants: three women aged 52, 60 and 62-years and two men aged 49 and 66-years, during a tyramine-monoamine oxidase-inhibitor interaction, phase I clinical trial. T-wave changes appeared early during the course of the hypertensive crisis and were attributed to subendocardial ischemia. The changes were transient and reverted to baseline in parallel with a fall in blood pressure.ConclusionRecognition of tall symmetrical T-waves in early phases of hypertensive crisis heralds commencement of myocardial damage. This calls for prompt medical intervention to avoid an impending irreversible myocardial injury. It is our belief that these findings will add new insight into the management of hypertensive crisis and will open avenues of further investigation.

Extended resuscitative endovascular balloon occlusion of the aorta (REBOA)-induced type 2 myocardial ischemia: a time-dependent penalty

“…These data agree with prior reports12–14 on the effects of abrupt significant increases in afterload on the heart. The results reported in our experiments likely represent the best case scenario, a non-diseased animal with a healthy heart and compliant aorta who experiences REBOA with dramatically reduced preload, which likely attenuates the afterload response from REBOA.…”

“…This metric was specifically chosen as changes in T-wave amplitude have been shown to be an early ECG feature of myocardial ischemia. This is related to decreased action potential durations via ATP-sensitive K + channels 14 25…”

“…Whereas animal models10 11 of cardiac arrest have shown the benefit of AO on coronary perfusion and increased rates of return of spontaneous circulation, the tolerance and effect of AO on the non-arrested heart are less well described. A severe abrupt increase in afterload alone has been described to cause type 2 myocardial ischemia/injury, such as with cases of hypertensive emergency related to pheochromocytomas, medication side effects, and during aortic cross-clamping 12–14. Others15 have demonstrated that there is a significantly attenuated afterload response to AO with decreased preload (hemorrhage) in a swine model which may result in a cardioprotective effect; however, this has not been well characterized.…”

Chest pain: The importance of serial ECGs

“…Serial ECGs can help identify myocardial ischemia and monitor response to blood pressure treatment. 3 The de Winter syndrome The de Winter syndrome is reported in 2% of patients with anterior myocardial infarction and should not be missed. 1 In initial reports in the literature, the ECG changes noted in de Winter syndrome were static and did not progress to ST-segment elevation.…”

Rethinking, reducing, and refining the classical oral tyramine challenge test of monoamine oxidase (MAO) inhibitors

“…As a consequence, SBP excursions very much above 30 mm Hg may occur in an uncontrolled manner, exposing study participants to a potential risk. A case report referred to hypertensive episodes of more than 60 mm Hg over baseline in 35 of 179 participants (20%) in an oral tyramine challenge study, observed after oral tyramine doses in the range of 100–500 mg. 13 In 5 of these 35 subjects, subendocardial ischemia was reported, presenting as tall, hyper‐acute symmetrical T‐waves, with or without other electrocardiograph abnormalities or angina symptoms, with prolonged PR interval and a 20‐fold increase of troponin T level over the normal reference level in one subject. Cantarini et al reported sinus bradycardia and a third‐degree heart block in one subject out of a group of 12 study participants receiving systemically delivered tyramine.…”