Paradoxical Shock and Management of a Post-percutaneous Mechanical Thrombectomy Device in a Morbidly Obese Patient With a Submassive Pulmonary Embolism.

A submassive pulmonary embolism (PE) is a type of PE where the pulmonary artery is partially obstructed. It is categorized as an intermediate risk when compared to massive PE, which presents as a complete obstruction of the pulmonary artery, therefore placing it in the high-risk category. In either case, if not promptly assessed and treated, it can prove to be fatal. We report the case of a morbidly obese middle-aged female who presented with a submassive PE. Based on the evaluation of the patient's pre-existing conditions, risk factors, clinical severity, imaging, and lab findings, it was concluded that percutaneous mechanical thrombectomy (PMT) was essential to promptly alleviate the clot burden. Following the procedure, it was observed that the patient became hemodynamically unstable, accompanied by hypoxemia and respiratory acidosis. With the assistance of pressors and later the placement of a right ventricular Impella device, the patient was successfully stabilized and, several days later, discharged from the hospital. This report explores the potential factors that may have contributed to the patient's hemodynamic instability and acute right ventricular failure after the PMT procedure. These factors can be attributed to pre-existing changes in the right ventricle (RV) as a result of morbid obesity, as well as possible associations with obstructive sleep apnea or obesity hypoventilation syndrome. Furthermore, it is important to highlight that patients exhibiting submassive PE can be considered suitable candidates for PMT, with careful consideration of the patient's medical history, clinical severity of symptoms, and diagnostic findings. It is worth noting that PMT intervention in this patient demonstrated a favorable outcome.

BRASH Syndrome Presenting With Idioventricular Escape Rhythm in a Patient With Trifascicular Block.

Bradycardia, renal failure, atrioventricular (AV) nodal disease, shock, and hyperkalemia (BRASH) syndrome is a well-recognized constellation of distinct clinicopathologic entities comprising bradycardia, renal failure, AV nodal disease, shock, and hyperkalemia. Our patient is an 89-year-old female with a past medical history significant for hypertension and diabetes, who was newly started on labetalol and had recent gastroenteritis; she presented to our Emergency Department with bradycardia and shock. Upon presentation, she showed physical signs of volume depletion, and her blood pressure was 50 mmHg systolic and heart rate was 25 beats per minute. The initial electrocardiogram showed an idioventricular rhythm. The laboratory workup revealed hyperkalemia. The patient was given repeated doses of atropine with no significant response. She was resuscitated with isotonic fluids. The patient improved clinically, her blood pressure stabilized, her potassium level, renal function, and heart rate were normalized, and normal sinus rhythm was restored with a narrow QRS complex. A diagnosis of BRASH syndrome was made retrospectively. Overall, the treatment of this syndrome is largely symptomatic. Hemodynamic support with fluid and treatment of hyperkalemia remains the goal of care. The overall prognosis is good if identified early and managed appropriately.

A Rare Case of Vasospastic Angina Presenting with Inferior Lead ST-segment Elevation and Ventricular Fibrillation in the Absence of Coronary Obstruction: A Case Report.

Vasospastic angina (VSA) is a variant form of angina pectoris, which occurs at night or at rest, with transient electrocardiogram modifications and preserved exercise capacity. Its association with stable angina, sudden cardiac death, acute coronary syndrome, arrhythmia, and syncope has previously been established. Its presentation can occur with or without existing coronary artery disease and may present with focal or diffuse alteration and dysfunction of the coronary vasculature. VSA diagnosis involves patient response to nitrates, transient ischemic electrocardiogram (ECG) changes, and coronary artery spasms. The mechanisms proposed to constitute the substrate for susceptibility to VSA include vascular smooth muscle cell hyperreactivity, endothelial dysfunction, magnesium deficiency, low-grade inflammation, altered autonomic nervous system response, hypothyroidism, and oxidative stress. Herein, we present the rare case of a patient with ST-segment elevation in the inferior leads, increased troponin, and an episode of ventricular fibrillation initially thought to be due to lateral wall ST-elevation myocardial infarction (STEMI), although it was revealed to be vasospastic angina. We will also review the literature. Vasospastic angina remains underdiagnosed and a timely diagnosis is crucial to prevent major cardiac events. In patients with diffuse ST-segment elevation on ECG (independently of angiographic findings), VSA should be considered as one of the differential diagnoses and treated if found to be the cause of pathological changes.

ST-Segment Elevation Myocardial Infarction with Acute Stent Thrombosis Presenting as Intractable Hiccups: An Unusual Case.

BACKGROUND Acute coronary syndrome (ACS) can present with atypical chest pain or symptoms not attributed to heart disease, such as indigestion. Hiccups, a benign and self-limited condition, can become persistent or intractable with overlooked underlying etiology. There are various causes of protracted hiccups, including metabolic abnormalities, psychogenic disorders, malignancy, central nervous system pathology, medications, pulmonary disorders, or gastrointestinal etiologies. It is rarely attributed to cardiac disease. CASE REPORT We report a case of intractable hiccups in a 51-year-old male with cocaine related myocardial infarction (MI) before and after stent placement. Coronary angiogram showed in-stent thrombosis of the initial intervention. Following thrombectomy, balloon angioplasty, and stent, the patient recovered well without additional episodes of hiccups. Although hiccups are not known to present with a predilection for a particular cause of myocardial ischemia, this case may additionally be explained by the sympathomimetic effects of cocaine, which lead to vasoconstriction of coronary arteries. CONCLUSIONS Hiccups associated with cardiac enzyme elevation and EKG ST-segment elevation before and after percutaneous coronary intervention (PCI) maybe a manifestation of acute MI with or without stent. The fact that this patient was a cocaine user may have contributed to the unique presentation.

Treatment of symptomatic vascular rings in the elderly.

A 76-year-old woman presented with respiratory failure that was later determined to be a result of a right aortic arch with an aberrant left brachiocephalic artery. This vascular ring compressed the trachea, requiring operative intervention. A median sternotomy gave access for an aorta-to-left brachiocephalic artery bypass and division of the vascular ring. This is a unique case, because vascular rings rarely present in elderly patients with such acute life-threatening symptoms. To our knowledge, this is the oldest and heaviest patient ever reported with symptomatic presentation and one of only 4 patients over the age of 50. The current literature on vascular rings of the thoracic aorta in adults is reviewed.

Aborted sudden cardiac death (SCD) in a patient with hypertrophic cardiomyopathy (HCM) with low-risk factors for SCD.

Remarkable advancements have been made in understanding the pathophysiology of hypertrophic cardiomyopathy (HCM), since the first implantable cardioverter defibrillator (ICD) was placed in a human, more than 25 years ago to prevent sudden cardiac death (SCD). ICD has become the cornerstone in the management of HCM, with an ability to change the natural course of this complex disease. American College of Cardiology/American Heart Association guidelines have been charted out to help risk stratify asymptomatic or minimally symptomatic adults with HCM, in order to prevent SCD in such individuals. Our patient with left ventricular outflow tract gradient <30 mm Hg, left ventricular wall thickness < 30 mm, negative medical history of syncope and no family history of SCD, would have been at low risk for SCD.