Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a severe hereditary arrhythmia syndrome predominantly affecting children and young adults. It manifests through bidirectional or polymorphic ventricular arrhythmia, often culminating in syncope triggered by physical exertion or emotional stress which can lead to sudden cardiac death. Most cases stem from mutations in the gene responsible for encoding the cardiac ryanodine receptor (RyR2), or in the Calsequestrin 2 gene (CASQ2), disrupting the handling of calcium ions within the cardiac myocyte sarcoplasmic reticulum. Diagnosing CPVT typically involves unmasking the arrhythmia through exercise stress testing. This diagnosis emerges in the absence of structural heart disease by cardiac imaging and with a normal baseline electrocardiogram. Traditional first-line treatment primarily involves β-blocker therapy, significantly reducing CPVT-associated mortality. Adjunctive therapies such as moderate exercise training, flecainide, left cardiac sympathetic denervation and implantable cardioverter-defibrillators have been utilized with reasonable success. However, the spectrum of options for managing CPVT has expanded over time, demonstrating decreased rates of arrhythmic events. Furthermore, ongoing research into potential new therapies including gene therapies has the potential to further enhance treatment paradigms. This review aims to succinctly encapsulate the contemporary understanding of the clinical characteristics, diagnostic approach, established therapeutic interventions and the promising future directions in managing CPVT.

Thromboembolism-in-transit, specifically impending paradoxical embolism (IPDE), is a rare and life-threatening condition with limited reported cases. We present a case of a 51-year-old male with obstructive sleep apnea, initially diagnosed with deep vein thrombosis and pulmonary embolism. Further evaluation revealed a saddle pulmonary embolus extending into the right atrium, straddling a patent foramen ovale (PFO), confirmed by transesophageal echocardiogram. Despite a critical left anterior descending coronary artery stenosis, surgical thrombectomy, PFO closure, and coronary artery bypass grafting were successfully performed. Thromboembolism-in-transit poses diagnostic challenges, and there is a lack of consensus on the optimal treatment strategy. Surgical interventions, including embolectomy and PFO closure, have shown promise, while thrombolytic therapy remains controversial. This case underscores the importance of tailored management in the absence of standardized guidelines, emphasizing the need for further research to establish evidence-based protocols for this uncommon but potentially fatal condition.

We are presenting a case of a 78-year-old female with multiple comorbidities and history of neck surgery, who presented with acute dysphagia, odynophagia and neck pain that has been progressively getting worse over the course of 2 days, with no recent injury or infection. The patient was afebrile. There were no visible signs of infection on routine oropharyngeal examination. Initial workup was unremarkable except for elevated erythrocyte sedimentation rate, C-reactive protein and creatinine. CT of the cervical spine ruled out any fracture or cervical spine injury but showed an area of calcification, prevertebral oedema and fluid collection inferior to the anterior arch of C1. MRI of the cervical spine also showed prevertebral oedema and fluid collection in the retropharyngeal space from the skull base to the C3 level without abnormal surrounding enhancement that supported the diagnosis of acute calcific tendonitis of the longus colli muscle rather than an infectious process. There was significant improvement of symptoms 48 hours after initiating treatment with systemic steroids. The patient remains asymptomatic 6 months after treatment.

Myocardial bridging is an anatomical variant in which coronary arteries course within the myocardium rather than on the epicardial surface. Complete intramyocardial coronary systems are extremely rare and can lead to significant clinical consequences. An 18-year-old man with left ventricular noncompaction cardiomyopathy experienced chest pain and syncope while playing basketball, and was subsequently diagnosed with ST-segment elevation myocardial infarction. Coronary imaging revealed a completely intramyocardial coronary system. Despite medical management and placement of implantable cardioverter-defibrillator, he developed heart failure requiring heart transplant evaluation. This case underscores the complexity of managing extensive intramyocardial coronary anatomy, in which conventional revascularization strategies may not be viable and individualized, multidisciplinary approaches are essential. Extensive myocardial bridging involving the entire coronary system is a rare anatomical anomaly that can precipitate exertional ischemia, arrhythmias, and even sudden cardiac events. Management of complete intramyocardial coronary anatomy requires individualized, multidisciplinary assessment, as traditional revascularization strategies may be unfeasible.

BACKGROUND Ostial right coronary artery (RCA) involvement is a relatively uncommon location for coronary artery disease and requires consideration of anatomic factors (aortic root involvement) and potential increased recoil. This makes stent placement prone to a geographic miss, especially in the context of limitations associated with two-dimensional coronary angiography. Moreover, the design of newer stent generations, which allows for easier deliverability but with increased susceptibility to mechanical damage, may place them at increased risk for longitudinal deformity when deployed in the right coronary ostium. This report describes the case of a 79-year-old man with a history of ischemic heart disease presenting with RCA aorto-ostial stent deformity and restenosis. CASE REPORT The patient presented with acute-onset ischemic chest pain and was found to have non-ST-elevation myocardial infarction (NSTEMI). Coronary angiography revealed significant 2-vessel coronary artery disease involving the mid-portion of the left anterior descending artery and the ostium of the RCA. The latter was due to associated in-stent restenosis of an overhanging stent protruding into the aorta. The patient underwent coronary artery bypass graft surgery with removal of the displaced stent, which was found to have evidence of a longitudinal deformity in its middle portion. CONCLUSIONS This report highlights a rare but important complication of the use of coronary artery stents, particularly when used in the region of the RCA ostium, and the management of stent deformity and restenosis.