Cardiac involvement is rare in inflammatory bowel disease (IBD) but can occur as a complication of either the disease itself or drug therapy. We describe an interesting clinical scenario of acute myopericarditis during Crohn’s flare-up. A 37-year-old patient with severe Crohn's disease started having multiple bloody bowel movements associated with abdominal pain. These symptoms were attributed to Crohn's disease flare-up, prompting the addition of steroids and an increase in the dose of mesalamine without any significant relief. Two weeks later, he presented to the emergency department with pleuritic chest pain. Electrocardiogram (EKG) revealed ST segments elevation in leads I and aVL. Laboratory work revealed elevated troponin I of 1.82 ng/mL, with increased erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) of 121 mm and 180.1 mg/L, respectively. Cardiac magnetic resonance imaging (MRI) revealed early gadolinium enhancement consistent with myocarditis. The patient was started on colchicine with an increase in the dose of steroids, resulting in clinical improvement. The patient reported having similar chest pain during a previous episode of Crohn's disease flare-up, suggesting underlying IBD as the likely etiology.
Serum troponin is a marker of cardiac myocyte damage that is typically used to assess for myocardial infarction in the setting of acute coronary syndrome. However, many conditions, including cardiomyopathy, pulmonary embolism, or myocarditis, can cause an elevation in serum troponin. The most common use of this tool is to determine whether acute coronary syndrome (ACS) is occurring, but other differentials include cardiomyopathy, pulmonary embolism, and even acute heart failure. We present the case of a patient who presented with symptoms consistent with viral myocarditis but ultimately was found to have severe coronary artery disease (CAD). A 33-year-old Caucasian male with no cardiac risk factors other than a five-pack year smoking history, presented with progressively worsening upper respiratory symptoms, including sore throat and a non-productive cough that began a few weeks ago. These symptoms were associated with fevers, and 24 hours prior to admission, he developed intermittent chest pain at rest, radiating to the back, worsening in the supine position. In the emergency room (ER), the patient was found to have an elevated serum troponin of 15.61 ng/L (normal <0.05 ng/L). The electrocardiogram (EKG) showed T-wave inversions in the lateral leads. Based on his presentation and age, there was a high suspicion of viral myocarditis. However, non-ST elevation myocardial infarction (NSTEMI) had not yet been ruled out and the patient was started on started on a heparin infusion per the ACS protocol. A transthoracic echocardiogram showed wall motion abnormalities with low-normal left ventricular ejection fraction. A coronary angiogram showed severe CAD and he underwent staged a percutaneous coronary intervention with the resolution of symptoms. CAD and viral myocarditis, at times, can share common presenting symptoms, EKG changes, and laboratory findings. Out of all possible diagnoses, an elevation in serum troponin correlates to an MI up to 60% of the time. Myocarditis is the second leading cause of troponin elevation and accounts for 25% of cases. We highlight this case to discuss the importance of maintaining a broad differential and pursuing complete work-up when treating younger patients with chest pain and elevated serum troponin who lack typical risk factors for CAD.
Introduction Coronary artery aneurysms (CAA) are not commonly seen in the general population, with an incidence of approximately 0.37% to 2.53%. Patients are typically asymptomatic but symptomatic presentation varies from dyspnea and angina to myocardial infarction or even sudden cardiac death. Methods We conducted a retrospective analysis using the National Inpatient Sample Healthcare Cost and Utilization Project (NIS-HCUP) database to query individuals with the diagnosis of CAA with the International Classification of Disease (ICD) code 414.11 in all discharge diagnoses for the years 2006-2014. History of Kawasaki disease was determined by ICD code 446.1. Results From 2006 to 2014, there were 23,033 patients identified with CAA, correlating to approximately one case per 10,000 patients or an incidence of close to 0.01%. Of this, 1,405 or approximately 6.1% of these patients had Kawasaki disease. The mortality rate of CAA was 1.79%. In terms of demographics, Caucasians were the most likely to develop CAA, with 73.8% of cases. The mean age was 61.2 years, with a mean length of stay of 5.1 days. The average cost of admission was $70892. The presence of perivascular disease (15.5% vs 4.5% p<0.05), hypertension (66.1% vs 39.1% p<0.05), chronic lung disease (20.2% vs 15.1% p<0.05), diabetes (21.7% vs 15% p<0.05), renal failure (11% vs 8.8% p<0.05), coagulopathy (6.2% vs 3.4% p<0.05), and obesity (13.1% vs 8.2% p<0.05) were all risk factors for CAA as compared to those without. It was noted that weight loss (3.28% vs 1.91% p<0.05), electrolyte abnormalities (18.2% vs 15.5% p<0.05), and blood loss (2.1% vs 0.9% p<0.05) were protective of CAA. Conclusion CAA risk factors appear to be similar to those of coronary artery disease risk factors, with hypertension, diabetes, perivascular disease, and renal failure. Additionally, obesity was noted to be a risk factor but weight loss appeared to be protective. Interestingly, Kawasaki disease was seen at almost similar rates as these cardiac risk factors. The incidence of CAA we found, of almost 0.01%, is much less than in the quoted literature, however, previous studies did not have as many cases as our study.
Vasospastic angina (VSA) is defined as spasm of the coronaries leading to transient constriction and eventual myocardial ischemia. VSA is treated typically with calcium-channel blockers (CCBs) and nitrates. However, there are times when the vasospasm is refractory to typical medications. When this occurs, unconventional treatment modalities may be employed for symptomatic relief. We present a case of a 48-year-old-male with a history of inferior ST-elevation myocardial infarction (STEMI) status post percutaneous coronary intervention (PCI) with drug-eluting stent (DES) to the distal right coronary artery (RCA), who presented with recurrent angina. The pain was described as pressure-like, substernal, radiating to both arms, and similar to his previous STEMI presentation. On presentation to the emergency room, he had an elevated serum troponin with no electrocardiogram (EKG) changes. He was taken to the cath lab where it was found that he revealed severe focal stenosis just proximal to the previously placed stent. Immediately after guidewire passage into the RCA, acute vasospasm developed, resulting in diffuse, severe stenosis, extending over previously normal segments to the proximal RCA, resolving with intracoronary nicardipine and nitroglycerin, including the initial focal stenosis. The patient was diagnosed with VSA. Unfortunately, despite optimal medical therapy, he developed refractory VSA, requiring the use of unconventional treatment methods. Our patient presented with a lesser-known phenomenon called refractory VSA, where intermittent vasospasm continues despite being on a combination of two medications. Treatment for VSA is well-documented, however, little data is available for refractory VSA.
A 50-year-old male presented to the hospital with an approximate three-week history of nausea, fever, and back pain. Upon initial evaluation he had an electrocardiogram with ischemic changes and initial labs significant for a troponin of >25.0 ng/ml (<0.30 ng/ml), pro b-type natriuretic peptide (proBNP) of 9884 pg/ml (<125 pg/ml), and a lactic acid of 4.3 mmol/L (0.5-1.9 mmol/L). There was a concern for an acute coronary syndrome presenting as cardiogenic shock, but the patient was unable to tolerate left heart catheterization. He had a rapid clinical decline and despite all efforts, he passed away. The initial cause of death was thought to be due to an acute myocardial infarction, however, autopsy results were consistent with acute myocarditis. This case highlights the presentation of acute myocarditis as an acute coronary syndrome with complete heart block.
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