No abstract

Background Ventricular tachycardia (VT) is often misdiagnosed as supraventricular tachycardia with aberrancy. Twelve-lead electrocardiogram remains a key diagnostic tool to differentiate them while providing insights to aid localization of VT. The use of Valsalva manoeuvre (VM) in terminating VT is not conventionally recommended due to lack of robust evidence of its effectiveness and poor understanding of its mechanism in terminating VT. Case summary A 74-year-old man with history of ischaemic heart disease was admitted with broad complex tachycardia. VT-1 was diagnosed following failed tachycardia termination by adenosine. Haemodynamic compromise necessitated synchronized cardioversion with successful reversion. However, a different VT-2 occurred after cardioversion. VM led to successful termination of VT-2. Subsequently, recurrent episodes of VT-2 occurred with consistent termination by VM. Transthoracic echocardiogram, cardiac magnetic resonance imaging, and a coronary angiogram were performed. Findings suggested that these are likely scar-related VT. VT-1 originated from an anteroseptal scar, whilst VT-2, responsive to VM, likely originated from the Purkinje fibres. Patient remained eurhythmic after Day 1 following amiodarone and beta-blocker initiation. An implantable cardioverter-defibrillator was implanted prior to discharge. Discussion VM is one of the vagal manoeuvres which are commonly used as initial management of supraventricular tachycardia. Its role in management of VT is obscure. Anecdotal case series recorded its successful use for managing particular VT. Exact mechanism remains elusive although postulated to involve change in cardiac size during strain and release of acetylcholine.

Background Myocardial infarction (MI) with non-obstructive coronary arteries presenting with ST-segment elevation can be challenging. Understanding the cardiac and non-cardiac causes aid in identifying the underlying diagnosis and deciding on the management. Neurological insult resulting in a mismatch of oxygen supply or demand to cardiomyocytes can lead to type 2 MI. Acute brain injury, such as intracranial haemorrhage, can induce cardiac dysfunction secondary to brain–heart interaction via hypothalamic–pituitary–adrenal axis and catecholamine surge. Case summary A 50-year-old Caucasian male who vaped cannabis presented with epileptic seizures. A Glasgow coma scale of 7/15 necessitated urgent intubation. Electrocardiogram showed ST-segment elevation in inferior leads. Computed tomography of the head suggested intracerebral haemorrhage. He was stabilized in the intensive care unit (ICU). Subsequent imaging confirmed anterior communicating cerebral artery aneurysm and haematoma. Echocardiogram showed severe left ventricular dysfunction and hypokinesia in the left circumflex (LCx) territory. After step down from ICU, cardiac magnetic resonance imaging revealed transmural MI and myocardial oedema at LCx territory. Coronary angiogram was normal. Patient was treated with Levetiracetam and heart failure regimen. A cardiac defibrillator was implanted for secondary prevention and he was scheduled for elective neurosurgical intervention. A follow-up outpatient echocardiogram was normal. Discussion Myocardial infarction with non-obstructive coronary arteries is uncommon. Though the majority is due to either plaque disruption or myocarditis, non-cardiac causes, such as acute neurological insults and substance use, should be considered. Scrutinizing the clinical presentation and using a meticulous approach with appropriate investigations are required to reach the correct diagnosis and appropriate management.

Background. Anticoagulation with warfarin remains the mainstay treatment for left ventricular thrombi. Although successful thrombus resolution has been reported with direct oral anticoagulants’ (DOACs’) recurrence/progression while resuming Apixaban therapy is yet to be reported. Case Presentation. This case report describes left ventricular thrombus progression/recurrence in a patient anticoagulated with Apixaban undergoing implantable cardioverter defibrillator to cardiac resynchronisation therapy with defibrillator upgrade procedure. He was thereafter changed to warfarin. Contrast echocardiogram at 6 months follow-up did not identify the previously demonstrated mural thrombus. Conclusion. Prospective randomised control trials should be conducted in patients with left ventricular thrombus to compare anticoagulants, assess the efficacy and safety of DOACs, and evaluate uninterrupted DOAC versus transient withdrawal for cardiac device procedures.

No abstract