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A 26-year-old male with no significant medical history presented with hematochezia and was diagnosed with ulcerative colitis (UC) accompanied by immune thrombocytopenia (ITP) as an extraintestinal manifestation (EIM) of UC. This case report delves into the uncommon overlap between UC, a subtype of inflammatory bowel disease primarily affecting the colon and rectum, and ITP, an autoimmune condition leading to platelet destruction. The patient's atypical presentation and subsequent positive response to a treatment regimen targeting both UC and ITP underscores the necessity for a thorough and multifaceted diagnostic approach in individuals with UC, especially when faced with non-gastrointestinal symptoms like unexplained thrombocytopenia. The findings from this study enhance the understanding of UC's diverse manifestations and highlight its potential intersection with other autoimmune diseases, advocating for integrated care strategies in managing such intricate clinical cases.
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Epiploic appendages are fat-filled sacs that are generally located along the surface of the large intestine. In most cases, epiploic appendagitis (EA) is described as an ischemic infarction of an epiploic appendage as the result of torsion or spontaneous thrombosis of the central draining vein of the epiploic appendage. The patient described in this report presented with a sudden onset of diffuse abdominal pain, nausea, and fever. CT scan of the abdomen and pelvis with oral contrast revealed EA of the sigmoid colon. Along the course of the admission, the patient became septic with blood cultures growing E. coli. In this case, we present a rare presentation of E. coli sepsis in the setting of EA, a usually uncomplicated and self-resolving presentation of abdominal pain.
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Amyloidosis is characterized by depositing insoluble fibrillar proteins that misfold into beta-pleated sheets. This phenomenon occurs on a systemic or local level and may interfere with the function of various organs, including the heart, kidneys, and liver. Among those presenting with amyloidosis, hepatic, gastrointestinal, renal, cardiac, vitreous, and immunological involvement may occur. These manifestations are linked to several clinical presentations, varying from abdominal pain and hepatomegaly to restrictive cardiomyopathy and chronic renal failure. The two most common types of amyloid proteins are amyloid light chain (AL) and serum amyloid A (AA) proteins. AL produced by immunoglobulin light chains kappa and lambda (κ, λ) circulate systemically and accumulate in organs. At the same time, serum AA proteins are acute-phase reactants seen in infectious, chronic inflammatory states. In an immune-mediated infection such as COVID-19, serum AA levels may be a predictive factor of disease severity and a valuable biomarker to monitor the clinical course of COVID-19 patients. This report highlights a case in which infection with COVID-19 provoked an effective immune response that may have contributed to the accelerated progression of systemic amyloidosis with hepatic involvement. The study further investigates the involvement of AL and AA proteins in COVID-19 infections, including their role in synergistically exacerbating an already grueling clinical course.
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Background and Aim: Steroids have long been used in inducing remission of inflammatory bowel disease (IBD). Chronic use, defined as therapy greater than 3 months, has been implicated in complications including increased hospital length of stay (LOS), infections, and even death. In our retrospective study, we aim to identify the complications of chronic steroid use in patients with IBD. Methods: The fourth quarter of 2015-2019 National Inpatient Sample (NIS) was used in this study. International Classification of Diseases (ICD-10) codes were used to identify patients with a diagnosis of IBD and chronic steroid use. Adverse outcomes of chronic steroid use in IBD patients were analyzed, such as osteoporosis, opportunistic infections, mortality rate, and LOS. Cohorts were weighted using an algorithm provided by the NIS allowing for accurate national estimates. Results: A total of 283 970 patients had a diagnosis of IBD. Of those, 18 030 patients had concurrent chronic steroid use. Racial disparities existed, with 77.4% White, 12.7% Black, and 6.0% Hispanic. Patients with a history of IBD and chronic steroid use were found to have higher odds of developing osteoporosis, opportunistic infections, and acute thromboembolic events but did not have higher odds of mortality. Conclusion: There is much controversy about whether IBD patients should be on chronic steroids for maintenance therapy and this study highlights the importance of this decision as patients on chronic steroid use had higher odds of developing adverse effects. These results stress the importance of monitoring patients on steroids and avoiding chronic use.
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Primary hepatic undifferentiated pleomorphic sarcoma (UPS) is a rare malignant mesenchymal tumor with a nonspecific clinical and radiologic presentation. Primary hepatic UPS is often a diagnosis of exclusion made by multiple immunohistological testing that rules out hepatic, hematologic, neural, and epithelial origin. Stains for mesenchymal origin are usually the only positive stain and do not demonstrate evidence of specific mesenchymal cell differentiation. We report a case of a 56-year-old male with no significant past medical history that presented with complaint of epigastric abdominal pain of six months duration. A computed tomography (CT) scan of the abdomen and pelvis exhibited numerous hepatic masses involving right and left hepatic lobe. A CT-guided core needle biopsy discovered undifferentiated/pleomorphic sarcoma. Histomorphology showed spindle cell neoplasm without recognizable hepatic tissue. Immunohistochemistry (IHC) stains were positive for smooth muscle actin (SMA) but failed to establish a more specific histogenesis. Furthermore, IHC stains revealed spindle neoplastic cells with focal and patchy positive h-caldesmon (approximately 10-15% of neoplastic cells), and negative for desmin. Given these results, the diagnosis of undifferentiated/pleomorphic sarcoma was established. It is imperative to consider UPS in the differential diagnosis of large liver lesions without evidence of differentiation. Early identification of this rare tumor can prevent the possibility of distant metastasis and improve survival among patients.
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Nodular lymphoid hyperplasia (NLH) is characterized by the growth of multiple discrete small submucosal nodules specifically confined to the lamina propria and superficial submucosa layers of the intestinal wall. Gastric and rectal involvement of NLH is exceedingly rare. To date, few case reports have described diffuse NLH presenting with multiple submucosal lymphomatous polyposis occurring in the rectum. Our patient is a 39-year-old morbidly obese Hispanic female who presented to the gastroenterology clinic complaining of intermittent hematochezia for the past six months. Colonoscopy showed diffuse nodularity in the sigmoid colon and rectal mucosa, extending 20 cm from the rectal verge. Rectal biopsies revealed moderate active chronic inflammation predominantly of lymphoplasmacytic cells with areas of lymphoid hyperplasia and focal surface ulceration. Immunohistochemistry stains revealed reactive lymphoid hyperplasia (RLH). The NLH is a risk factor for extraintestinal and intestinal lymphomas. When encountering lymphoid hyperplasias, the possibility of malignancy must always be considered. It is crucial to monitor patients with NLH via capsule endoscopies, small bowel series, and colonoscopy for surveillance of new lesions in light of the potential for malignancy.
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Coronavirus disease 2019 (COVID-19) is known to primarily have respiratory tract involvement, but thromboembolic complications can occur as well, leading to increased overall mortality seen in these patients. We present a case of a patient infected with COVID-19 who then developed two simultaneous thrombotic events. Our patient is a 57-year-old male who presented to the emergency department with sudden onset dysarthria and left lower extremity weakness. Medical records indicated he recently tested positive for COVID-19 infection 10 days ago. Magnetic resonance imaging (MRI) of the brain revealed an acute right cerebellar infarction as well as acute bilateral thalamic infarcts. Later in the hospital course, computed tomography angiography (CTA) of the chest revealed a right lower lobe segmental pulmonary artery embolism. Patients with COVID-19 have been seen to develop a wide spectrum of thromboembolic manifestations, most commonly being venous thromboembolism. Arterial thrombosis and microvascular disease can be detected as well. Early diagnosis and treatment of clotting disease is essential and may decrease overall mortality in COVID-19-infected patients.
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Hypertriglyceridemia is a well-established cause of acute pancreatitis. Initial treatment for hypertriglyceridemia-induced pancreatitis has consisted of supportive measures; however, triglyceride levels can remain high, causing prolonged organ failure and sepsis. Plasmapheresis has been proposed as a treatment option to effectively reduce triglyceride levels. We present a patient case of hypertriglyceridemia-induced pancreatitis that was treated with standard acute pancreatitis interventions along with plasmapheresis, after which triglyceride levels reduced significantly. Further research is necessary to determine the clinical benefits of plasmapheresis in treating this type of pancreatitis.
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Background and Aims: We aimed to study the impact of acute myocardial infarction (AMI) in patients with celiac disease (CD). Methods: We used the National Inpatient Sample 2011-2018 to identify patients aged 18 years and older with a history of CD who presented with AMI using International Classification of Disease Nineth and Tenth Revision codes. Primary outcome of interest was mortality differences in AMI patients with and without CD. Secondary outcomes were in-hospital length of stay, hospital costs, and coronary revascularization. Results: A total of 2,287,840 weighted patients were included in this study with a principal diagnosis of AMI. Among this population, 183,027 weighted patients had a history of CD (0.08%), and 2,286,010 weighted patients had AMI without a history of CD (99.92%). Most AMI patients with and without CD were older (69.57 ± 13.21 vs 67.08 ± 13.87 years, respectively) and white (92.55% vs 75.39%, respectively). Patients with AMI and CD were more likely to be female than patients without CD (53.76% vs 38.47%; P < .05). In our study, we found that the difference in hospital charges (adjusted mean difference $2644.7) was lower among AMI and CD; however, length of stay was higher among patients with CD (adjusted mean difference 0.36 day) although they were not statistically significant (P > .05). Both cohorts had higher number of Medicare recipients and lower number of patients who self-pay. Our study also found that smoking was more prevalent among patients with CD, 12.14%, vs patients without CD, 2.51%. Moreover, patients with CD who developed AMI had a lower adjusted odds of mortality than those without CD (adjusted odds ratio [aOR] 0.41; P < .05). Patients with CD and AMI also had lower odds of coronary revascularization (aOR 0.80; P < .05). In addition, we found that adults with CD had a lower odds of developing AMI (aOR 0.78; P < .05). Conclusion: CD is a chronic disease leading to chronic inflammation and various nutrition-related problems which can lead to increased morbid conditions. However, we found lower odds of AMI among patients with CD, as well as lower mortality and comorbidities related to AMI, thus contradicting previous assumptions.
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Amlodipine is a dihydropyridine calcium channel blocker (CCB) commonly used to treat hypertension. In the United States, approximately 9,500 cases of CCB intoxication due to deliberate or inadvertent overdose were reported to poison centers in 2002. We present a case of a patient who presented with CCB overdose complicated by acute respiratory distress syndrome (ARDS) and recalcitrant shock all of which resolved with methylene blue therapy. We present a case of a 56-year-old African American woman who presented to the emergency department (ED) after intentional ingestion of large amounts of multiple pills likely consisting of cyclobenzaprine, amlodipine, losartan, and ibuprofen following an argument with her boyfriend. Treatment included insulin drip, 10% dextrose, and norepinephrine drip which was titrated up. First insulin drip and 10% dextrose were titrated up; however, vasopressor-resistant hypotension persisted, and the decision was made to administer methylene blue. Over 9,500 cases of CCB toxicity were reported to poison centers in the US in 2002. Although no definitive treatment is outlined, first-line therapy consists of IV calcium, high-dose insulin, and vasopressor support with either norepinephrine or epinephrine. Traditionally, methylene blue is used for methemoglobinemia and in cardiothoracic ICUs for post coronary artery bypass vasoplegia. It acts by selectively inhibiting nitric oxide-activated cyclic guanylate cyclase leading to decreased vasodilation of arteriolar smooth muscles improving vascular tone and systemic vascular resistance. In severe amlodipine overdose, experimental models demonstrate methylene blue improves HR and mean arterial pressure (MAP), improving survival rate. With few adverse side effects (green-tinged discoloration of urine, saliva, tears, and bodily fluids), methylene blue should be explored and implemented in the treatment of CCB overdose with refractory hypotension and ARDS.
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Infective endocarditis (IE), commonly caused by Staphylococcus aureus, can affect multiple cardiac structures and lead to significant morbidity and mortality. We present a case of IE with extensive mitral valve involvement causing perforation and hemodynamic compromise. A 66-year-old Caucasian female presented to the emergency department for progressive altered mental status and lethargy. The patient and family denied history of intravenous drug use (IVDU) on interview. Physical exam revealed tachypnea, tachycardia, lethargy, and fluctuance in the right antecubital fossa draining serous fluid. Initial studies revealed a urinary tract infection, patchy bilateral opacities on chest x-ray, hypoxic respiratory failure, elevated lactate and cardiac markers, leukocytosis, and positive urine toxicology for opioid and benzodiazepine. She was intubated and admitted to the ICU, and later developed acute respiratory distress syndrome with requirement for vasopressors. Antibiotics were started, and blood cultures ultimately grew methicillin-sensitive S. aureus. Coronavirus disease 2019 (COVID-19) results were negative. Cardiology was consulted for elevated cardiac markers that were due to myocardial injury in the setting of septic shock. A transthoracic echocardiogram showed a large mobile mass on the anterior mitral leaflet. Further evaluation with transesophageal echocardiogram revealed a large, mobile, and centrally necrotic vegetation on the medial portion of the mitral annulus extending to both the anterior and posterior leaflets. Doppler of the valve showed holosystolic retrograde ejection into the left atrium confirming a perforation. The patient was transferred urgently to a cardiothoracic surgery capable center for operative intervention on the mitral valve. IE is most commonly caused by S. aureus and seen in highest rates among patients with a prosthetic valve, congenital heart disease, and intracardiac device. However, roughly 50% of IE occurs in patients without any valvular disease. Other risk factors include IVDU, valvular disease, and prior history of endocarditis. Clinical diagnosis of IE is made using the Duke's criteria, with echocardiogram and bacteremia playing a major role. The initial management involves empiric antibiotics until a pathogen is identified. Surgical consult is also suggested, and indications for surgery include heart failure due to valve dysfunction, uncontrolled infection, prevention of embolism, and hemodynamic compromise. Prompt recognition and intervention is crucial in the prevention of mortality in patients with IE leading to mitral perforation and hemodynamic compromise.
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Vasculitis, by definition, causes changes in the walls of blood vessels, including thickening, weakening, narrowing, and scarring, leading to inflammation and necrosis of the blood vessel walls. Small-vessel vasculitis is commonly associated with anti-neutrophil cytoplasmic antibodies (ANCA), which activate cytokine-primed neutrophils and monocytes that express ANCA antigens proteinase 3 (PR3) and myeloperoxidase (MPO) on their surface. The continuous injury and inflammation of these small vessels characterized by circulating immune complexes and antinuclear antibodies result in clinical features standard in all types of vasculitis. When a 59-year-old male with a history of heart failure, hypertension (on hydralazine 100 mg every eight hours for more than ten years), diabetes mellitus, and dyslipidemia presented to the hospital, he was complaining of hematuria, intermittent periumbilical abdominal pain, and 40-lb weight loss over four months. Initial evaluation showed symptomatic anemia and large blood cells with proteinuria on urine analysis. During his clinical course, the patient developed a new diffuse purpuric rash. Imaging showed systemic involvement with ground-glass opacities, diffuse alveolar hemorrhage, and peripancreatic inflammatory changes, consistent with small-vessel vasculitis. Immunological tests confirmed ANCA-associated vasculitis, and kidney biopsy showed ANCA-mediated pauci-immune glomerulonephritis supported by the salvage technique used by pronase immunofluorescence, which provides evidence against the glomerular disease of the complex immune type in the setting of MPO-ANCA seropositivity. Despite the withdrawal of hydralazine and prompt initiation of immunosuppressive therapy and alternating sessions of plasmapheresis, the patient succumbed to acute massive pulmonary hemorrhage and subsequent demise. We recommend that patients on the common antihypertensive, hydralazine, should be monitored with non-specific inflammatory markers and, if warranted, with qualitative and quantitative assessment tools to measure inflammatory disease activity for possible complications of hydralazine drug-induced vasculitis or hydralazine ANCA-associated vasculitis (HAAV). Furthermore, cumulative dosages may be a predisposing factor for HAAV to present as a pulmonary-renal syndrome, which can be fulminant and fatal, despite aggressive efforts. Therefore, screening, revisiting therapy, early diagnosis, and prompt discontinuation of the drug are imperative.
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We aim to study the impact of pulmonary hypertension on acutely exacerbated chronic obstructive pulmonary disease (AECOPD). We used the 2016 and 2017 National Readmission Database with an inclusion criterion of AECOPD as a primary and pulmonary hypertension as a secondary diagnosis using ICD 10-CM codes. Exclusion criteria were age under 18 years, non-elective admission, and discharge in December. The primary outcome was in-hospital mortality during the index admission. Secondary outcomes were 30-day readmission rate, resource utilization, and instrument utilization including intubation, prolonged invasive mechanical ventilation >96 h (PIMV), tracheostomy, chest tube placement, and bronchoscopy during the index admission. A total of 627,848 patients with AECOPD were included in the study, and 68,429 (10.90%) patients had a diagnosis of pulmonary hypertension. Pulmonary hypertension was more common among females (61.14%) with a mean age of 71 ± 11.66, Medicare recipients (79.5%), higher Charlson comorbidity index, and treatment in an urban teaching hospital. Pulmonary hypertension was associated with greater mortality (adjusted odds ratio (aOR) 1.89, p < 0.001), higher 30-day readmission (aOR 1.24, p < 0.001), higher cost (adjusted mean difference (aMD) $2785, p < 0.01), length of stay (aMD 1.09, p < 0.001), and higher instrument utilization including intubation (aOR 199, p < 0.001), PIMV (aOR 2.12, p < 0.001), tracheostomy (aOR 2.1, p < 0.001), bronchoscopy (aOR 1.46, p = 0.007), and chest tube placement (aOR 1.39 p < 0.004). We found that pulmonary hypertension is related to higher in-hospital mortality, length of stay, increased instrument utilization, readmission, and costs. Our study aims to shed light on the impact of pulmonary hypertension on AECOPD in hopes to improve future management.
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We aimed to study the impact of Hepatic Cirrhosis (HC) on chronic obstructive pulmonary disease (COPD). Our study is a retrospective cohort study using the 2016-2017 National Readmission Database (NRD). NRD is part of the Healthcare Cost and Utilization Project (HCUP), organized and supported by means of the Agency for Healthcare Research and Quality (AHRQ). Patients were included if they were 18 years or older and had a principal diagnosis of COPD based on International Classification of Diseases, Tenth Revision (ICD-10- CM) codes and had a secondary diagnosis of HC. A total of 505,004 patients were included in the study with a diagnosis of COPD, 6196 (1.23%) of whom had HC. HC was found to be more common amongst male patients between the ages of 50 and 65 years. Medicare beneficiaries with high comorbidity burden, lower socioeconomic status, and those who received treatment in a large urban teaching hospital also had higher rates of HC. Patients with HC and COPD correlated to an increase of in-hospital mortality (adjusted odds ratio (aOR: 2.21, p<0.001) and 30-day hospital readmission rate (aOR: 1.23, p<0.001) compared with patients without HC. The in-hospital mortality rate was higher during readmission compared with index admissions (5.01% versus 2.16%; p<0.001). In addition, HC was associated with higher morbidity including prolonged mechanical ventilation (aOR: 1.39, p<0.001), resource utilization with prolong length of stay (LOS) (adjusted mean difference (aMD: 0.51, p<0.001), higher total hospitalization charges (aMD: 4967, p<0.001), and costs (aMD: 1200, p<0.001). Both patient groups had similar odds of being intubated (aOR: 1.18, p-0.13), tracheostomy (aOR: 0.81, p-069) and bronchoscopy rates (aOR: 1.27, p-0.36). The most common causes of hospital readmission were found to be COPD with acute exacerbation (19.7%), sepsis, unspecified organism (6.0%, acute and chronic respiratory failure with hypoxia (4.2%), acute on chronic systolic heart failure (3.9%), and hepatic failure, unspecified coma (3.1%). Various autonomous prognosticators of readmission were sex (particularly female), alcohol dependence, LOS greater than 7 days, lower comorbidity burden, and discharge to short term hospital or against medical advice. On the other hand, males, patients without a history of alcohol dependence, greater comorbidity burden, and LOS fewer than 3 days, were less likely to be readmitted. We found that HC is related to higher in-hospital mortality, LOS, increased mechanical ventilation, resource utilization with prolonged LOS, hospital costs, odds of intubation, and tracheostomy and bronchoscopy rates. Our study aims to shed light on the impact of HC on COPD in hopes to improve future management.
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Wallenberg syndrome is the most common stroke of the posterior circulation. Diagnosis of Wallenberg syndrome is often overlooked as initial MRI may show no visible lesion. We present an atypical case of Wallenberg syndrome in which the initial MRI of the brain was normal. Our patient is a 65-year-old male who was brought in by emergency medical services complaining of right-sided facial droop, slurred speech, and left-sided weakness for one day. Physical examination showed decreased left arm and leg strength compared to the right side, decreased left facial temperature sensations, decreased left arm and leg temperature sensations, and difficulty sitting upright with an associated leaning towards the left side. An initial magnetic resonance imaging (MRI) of the brain with and without contrast revealed no abnormality. In light of such a high suspicion for stroke based on the patient's neurologic deficits, a repeat MRI of the brain was performed three days later and exposed a small focus of bright signal (hyperintensity) on T2-weighted fluid-attenuated inversion recovery and diffusion-weighted imaging (DWI) in the left posterior medulla. Wallenberg syndrome, also known as lateral medullary syndrome or posterior inferior cerebellar artery syndrome, is a constellation of symptoms caused by posterior vascular accidents. The neurological deficits associated with this disease are due to damage of the lateral medulla, inferior cerebellar peduncle, nucleus of trigeminal nerve, nucleus and fibers of vagus and glossopharyngeal nerves, descending sympathetic tract, spinothalamic tract, and/or vestibular nuclei. MRI with DWI is the gold standard to confirm the diagnosis. Wallenberg syndrome has the potential to leave patients extremely debilitated. Early detection, management, and rehabilitation are critical for improving post-stroke recovery.
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Benign proliferations of smooth muscle cells are known as leiomyomas; these proliferations can occur in the colon and are typically found incidentally. Colonic leiomyomas are very rare and are most commonly found in the descending or sigmoid colon. A 59-year-old Hispanic female presented to the gastroenterology clinic for surveillance colonoscopy. The biopsy showed a submucosal microscopic leiomyoma in the transverse colon. The treatment of choice for most colonic leiomyomas is surgical excision. This rare case favors the notion that endoscopic polypectomy may be superior to surgical excision, ultimately providing a less-invasive and less-costly procedure without complications or recurrence.
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Clozapine is a Food and Drug Administration-approved, second-generation antipsychotic used to treat treatment-resistant schizophrenia. Known for its benefits in reducing extrapyramidal symptoms typically seen with antipsychotics, this drug carries a risk of agranulocytosis and, to a lesser-known extent, myocarditis. A 49-year-old patient, who was initially admitted to psychiatry with a primary diagnosis of schizophrenia, was started on clozapine. After three weeks of being on clozapine, the patient developed fevers and was admitted under internal medicine for further workup of presumed systemic inflammatory response syndrome due to noninfectious etiology. The patient was also asymptomatic. He was subsequently found to have elevated cardiac markers and C-reactive protein levels as well as decreased left ventricular ejection fraction and findings consistent with myocarditis using echocardiography. Clozapine was discontinued and the patient was transferred to the cardiology service for guideline-directed medical management of myocarditis and heart failure with reduced ejection fraction. The overall mechanism of clozapine cardiotoxicity is not well understood. Proposed hypotheses include IgE-mediated acute hypersensitivity and cardiac myocyte damage via the release of proinflammatory cytokines. However, when suspecting myocarditis after initiating clozapine, continuous monitoring and cessation of the medication are crucial in preventing permanent damage to the myocardium. Given the cardiac risk of medication and potential lethality of myocarditis via progression to heart failure, it is important to observe physical examination findings as well as symptoms of the condition when initiating a patient on clozapine.
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Dual left anterior descending artery (LAD) is a rare phenomenon that occurs in less than one percent of the population. To date, 12 variants have been identified. Proper identification of coronary vessels is crucial in emergent situations that require prompt action, such as percutaneous coronary intervention (PCI). We propose that our case highlights a novel 13th (type XIII) variant. We present the case of a 57-year-old African American woman with a past medical history of hypertension, glaucoma, cerebral vascular accident, dyslipidemia who presented to the ED complaining of atypical chest pain for one day duration. Electrocardiography showed normal sinus rhythm at 60 beats per minute (bpm), normal axis, normal intervals, no acute ischemic changes, and an isolated T wave inversion in DIII. Cardiac markers were within normal limits. The patient was started on aspirin 81mg, atorvastatin 40mg, and restarted on amlodipine 5mg. Echocardiography showed a left ventricular ejection fraction (LVEF): 65%, normal right ventricular size and systolic function, mild mitral valve regurgitation, and mild aortic regurgitation. Computed tomographic (CT) angiography showed a novel subtype of dual LAD, the left circumflex and right coronary arteries were patent. The patient was discharged once stabilized and advised to follow up with cardiology. Dual LAD describes a rare anatomic variant in which two coronary branches, known as short and long LAD arteries, supply the territory normally supplied by the solitary LAD artery. To date, 12 variants of dual LAD, classified by origin and course of the short and long LAD arteries, have been described in the literature. To the best of our knowledge, the current case describes a novel subtype of dual LAD, variant XIII. The LAD originates as usual from the left main coronary artery (LMCA) and initially runs in the anterior interventricular groove for a short course before bifurcating into two long LADs which both leave the interventricular groove and course out to the apex. One of the vessels courses laterally and the other courses medially of the interventricular groove. It is pertinent to identify the coronary vessels accurately before certain interventions are taken. Acknowledgement of this phenomenon can help guide accurate management in the future for patients with this condition.