Tobacco smoking is a chief cause of preventable deaths worldwide, accounting for various cancers, cardiovascular and respiratory diseases. Tobacco smoking accounts for more than seven million deaths every year. Worldwide statistics show that about 1.1 billion active smokers exist; 80% live in low- and middle-income countries. Nicotine is the addictive ingredient with the least harm compared to other active ingredients in tobacco, albeit not completely benign. Nicotine acts on the nicotinic cholinergic receptors (nAChRs) and produces the release of neurotransmitters. The mechanism by which it affects the cardiovascular system involves endothelial dysfunction by reducing nitrogen monoxide production, pro-thrombotic conditions, and activating inflammatory routes. These factors, along with the increased amounts of coronary atherosclerosis, have addictive adverse effects. Smoking has been shown to cause increased amounts of coronary atherosclerosis which may be responsible for the increased risk of hypertension, coronary heart disease, and atrial fibrillation, potentially contributing to the association of current smokers with a higher incidence of heart failure. This has led to worsened burdens and outcomes of cardiovascular disease among smokers. Smoking cessation has been associated with a reduction in cardiovascular mortality. This ranges from the reduction in the incidence of hypertension, type 2 diabetes, and heart failure. As regards behavioral and mental health, smoking cessation reduces the risk of cardiovascular disease in people experiencing mental illness. The prevalence of smoking continues to trend downward over the past couple of decades. Despite this downtrend, cigarette smoking is responsible for approximately half a million deaths per year in the United States and billions of dollars spent in healthcare. This buttresses the need to explore the various effects of smoking cessation on cardiovascular health and suggest ways to curb the disease burden.

Hemophagocytic lymphohistiocytosis (HLH) is a rare and life-threatening syndrome of excessive inflammation and tissue destruction secondary to abnormal immune activation. The term macrophage activation syndrome (MAS) is used when HLH develops in the setting of systemic juvenile idiopathic arthritis (SJIA; formerly known as Still's disease), adult-onset Still's disease, or any other rheumatologic disorder. We present a case of a 21-year-old female with a known history of SJIA who presented to the hospital with fever, chills, myalgia, nausea, vomiting, and hypotension. Initial evaluation at the time of presentation suggested sepsis likely due to acute pyelonephritis, and the patient was started on antibiotics and intravenous fluid hydration. However, further workup suggested that her symptoms were non-infectious and were likely due to MAS, a rare complication of SJIA. We promptly diagnosed her, and she received a course of steroids and made an uneventful recovery.

We report a 58-year-old female with severe throat pain, difficulty swallowing, choking on solid meals, coughing, and hoarseness. CT angiography of the chest revealed vascular compression of the esophagus by an aberrant right subclavian artery (ARSA). The patient underwent thoracic endovascular aortic repair (TEVAR) and revascularization to address the ARSA. The patient experienced significant improvement in her symptoms following the surgical intervention.Dysphagia lusoria is a rare condition involving compression of the esophagus and airway by an ARSA. While medical management is the first line of treatment for mild symptoms, surgical intervention is often necessary for severe cases or those unresponsive to conservative management. TEVAR with revascularization is a feasible and minimally invasive option for treating symptomatic non-aneurysmal ARSA, potentially resulting in favorable outcomes.

Sudden cardiac death (SCD) is one of the leading causes of cardiovascular mortality, and it is caused by a diverse array of conditions. Among these is commotio cordis, a relatively infrequent but still significant cause, often seen in young athletes involved in competitive or recreational sports. It is known to be caused by blunt trauma to the chest wall resulting in life-threatening arrhythmia (typically ventricular fibrillation). The current understanding pertains to blunt trauma to the precordium, with an outcome depending on factors such as the type of stimulus, the force of impact, the qualities of the projectile (shape, size, and density), the site of impact, and the timing of impact in relation to the cardiac cycle.In the management of commotio cordis, a history of preceding blunt chest trauma is usually encountered. Imaging is mostly unremarkable except for ECG, which may show malignant ventricular arrhythmias. Treatment is focused on emergent resuscitation with the advanced cardiac life support protocol algorithm, with extensive workup following the return of spontaneous circulation. In the absence of underlying cardiovascular pathologies, implantable cardiac defibrillator insertion is not beneficial, and patients can even resume physical activity if the workup is unremarkable. Proper follow-up is also key in the management and monitoring of re-entrant ventricular arrhythmias, which are amenable to ablative therapy. Prevention of this condition involves protecting the chest wall against blunt trauma, especially with the use of safety balls and chest protectors in certain high-risk sporting activities.This study aims to elucidate the current epidemiology and clinical management of SCD with a particular focus on a rarely explored etiology, commotio cordis.