ABSTRACT
Aortix™ is a novel percutaneous mechanical circulatory support device designed to facilitate diuresis in patients with cardiorenal syndrome. We describe for the first time the development of end-organ hypoperfusion from excess blood acceleration at the nominal setting and demonstrate through temporal-perfusion marker curves, the potential for speed modulation to optimize results. This will inform future device development and investigation of patient-specific device titration.
ABSTRACT
Roemheld syndrome, also known as gastrocardiac syndrome, was first studied as a relationship between gastrointestinal and cardiovascular symptoms through the vagus nerve. Several hypotheses have attempted to explain the pathophysiology of Roemheld syndrome, but the underlying process remains unclear. We present a clinically diagnosed case of Roemheld syndrome in a patient with a hiatal hernia whose gastrointestinal and cardiac symptoms were successfully treated with robotic assisted hernia repair, esophagogastroduodenoscopy (EGD), and LINX magnetic sphincter augmentation. Our case is a 60-year-old male with a history of esophageal stricture and hiatal hernia who presented with complaints of gastroesophageal reflux disease (GERD) and related arrhythmias for five years. The patient did not have a history of cardiovascular disease other than hypertension. The cause of the hypertension was assumed to be primary, as workup for possible pheochromocytoma was negative. Cardiac work-up revealed arrhythmias that were characterized as supraventricular tachycardia with intermittent pre-ventricular contractions (PVC); however, testing was unable to determine a cause for the arrhythmias. High-resolution manometry showed low pressure in the lower esophageal sphincter with normal esophageal motility. Further evaluation included a 96-hour Bravo test and DeMeester score of 31 was recorded, confirming mild GERD; however, EGD was unremarkable. Surgeons elected to perform a robotic assisted hiatal hernia repair, EGD, and magnetic sphincter augmentation. Four months following surgery, the patient denied symptoms of GERD or episodes of palpitation and subsequently weaned off proton pump inhibitors with continual lack of symptoms. GERD is a common complaint among the primary care setting; however, ventricular dysrhythmias among this population and a clinical diagnosis of Roemheld syndrome is unique. One hypothesis may be that protrusion of the stomach into the chest cavity may exacerbate current reflux, and the anatomical relationship between a herniated fundus and anterior vagal nerve may cause direct physical stimulation that is a more potent risk factor for the development of arrythmias. However, Roemheld Syndrome is a unique diagnosis, and the pathophysiology is still yet to be understood.
ABSTRACT
As medicine advances to employ sophisticated anticancer agents to treat a vast array of oncological conditions, it is worth considering side effects associated with several chemotherapeutics. One adverse effect observed with several classes of chemotherapy agents is cardiotoxicity which leads to reduced ejection fraction (EF), cardiac arrhythmias, hypertension and Ischemia/myocardial infarction that can significantly impact the quality of life and patient outcomes. Research into possible mechanisms has elucidated several mechanisms, such as ROS generation, calcium overload and apoptosis. However, there is a relative scarcity of literature detailing the relationship between the exact mechanism of cardiotoxicity for each anticancer agent and observed clinical effects. This review comprehensively describes cardiotoxicity associated with various classes of anticancer agents and possible mechanisms. Further research exploring possible mechanisms for cardiotoxicity observed with anticancer agents could provide valuable insight into susceptibility for developing symptoms and management guidelines. Chemotherapeutics are associated with several side effects. Several classes of chemotherapy agents cause cardiotoxicity leading to a reduced ejection fraction (EF), cardiac arrhythmias, hypertension, and Ischemia/myocardial infarction. Research into possible mechanisms has elucidated several mechanisms, such as ROS generation, calcium overload, and apoptosis. However, there is a relative scarcity of literature detailing the relationship between the exact mechanism of cardiotoxicity for each anticancer agent and observed clinical effects. This review describes cardiotoxicity associated with various classes of anticancer agents and possible mechanisms. Further research exploring mechanisms for cardiotoxicity observed with anticancer agents could provide insight that will guide management.
