Fluoropyrimidines-5-fluorouracil (5-FU) and capecitabine-have been implicated as cardiotoxic chemotherapy agents. This rare, albeit potentially serious toxicity has been described in nearly four decades of case reports, case series, and in vitro modeling; however, there is a paucity in clinical trials and prospective analyses focused on cardioprotective strategies and cardiotoxic surveillance of these agents. While much attention has focused on the well-known cardiac toxicity of anthracyclines and monoclonal antibody agents such as trastuzumab, fluoropyrimidines remain one of the most common causes of chemotherapy-associated cardiotoxicity. The introduction of capecitabine, an oral prodrug of 5-FU, has made the treatment of solid tumors more convenient along with a subsequent rise in documented cardiotoxic cases. This review discusses the symptomatology, clinical manifestations, and proposed molecular mechanisms that attempt to describe the heterogeneous spectrum of fluoropyrimidine-induced cardiotoxicity. Four case examples showcasing the varied manifestations of cardiotoxicity are presented. Finally, several proposed management strategies for cardiotoxicity and post-hospital course precautions are discussed.

BACKGROUND-Microvascular dysfunction (MVD) is a potential cause of chest pain in younger individuals. We hypothesized that non-elderly patients referred for computed tomography coronary angiography (CTA) but without significant stenosis would have a high prevalence of MVD by myocardial contrast echocardiography (MCE). Secondary aims were to test whether the presence of non-obstructive CAD or reduced brachial flow-mediated dilation (FMD) predicted MVD. METHODS-Subjects ≤60 years-of-age undergoing CTA were recruited if they had either no evidence of coronary plaque, or evidence of mild CAD (<50% stenosis) and at least one high-risk plaque feature. Subjects underwent quantitative MCE perfusion imaging at rest and during regadenoson vasodilator stress. Microvascular dysfunction was defined by global or segmental delay of microvascular refill (≥2 seconds) during regadenoson. FMD of the brachial artery was also performed.

Boerhaave syndrome, a rare yet frequently fatal diagnosis, is characterized by the spontaneous transmural rupture of the esophagus. The classic presentation of Boerhaave syndrome is characterized by Mackler's triad, consisting of chest pain, vomiting, and subcutaneous emphysema. However, Boerhaave syndrome rarely presents with all the features of Mackler's triad; instead, the common presentation of Boerhaave syndrome includes chest or epigastric pain, severe retching and vomiting, dyspnea, and shock. These symptoms are typically misdiagnosed as cardiogenic in origin. Due to its atypical presentation, rarity, and mimicry of emergent conditions, diagnosis of Boerhaave syndrome is often delayed, resulting in a high mortality rate at the time of diagnosis and with a subsequent exponential increase in mortality if treatment is delayed by greater than 48 hours. Here, we report two atypical presentations of Boerhaave syndrome presenting as tension hydropneumothorax and review ten previously reported cases of Boerhaave syndrome presenting as tension hydropneumothorax. This review serves to raise clinician awareness about the expansive and elusive ways by which esophageal perforation may present, and thereby facilitate timely and potentially life-saving diagnosis.