A 58 year-old man who recently underwent a left superficial femoral artery thrombectomy presented with a three-day history of worsening exertional dyspnea and bilateral pedal edema. His past medical history is significant for coronary artery disease, myocardial infarction, and insulin dependent diabetes mellitus. The patient initially presented to an outside hospital where he developed ventricular tachycardia that warranted cardioversion three times. Initial electrocardiogram showed inferior lead ST segment elevations and lateral lead ST depression. The patient underwent a cardiac catheterization that showed triple vessel disease with total occlusion of the RCA, 90% occlusion of the LAD, and 50% to 60% occlusion of left circumflex. The patient had an echocardiogram (Figures 1 and 2) that showed severe left ventricular dysfunction with an ejection fraction of 10% and a large mobile thrombus occupying 60% of the left ventricular cavity and was diagnosed with a dilated cardiomyopathy. The patient underwent left ventricular thrombectomy (Figure 3), coronary artery bypass graft (i.e., a saphenous vein graft to LAD) and installation of a left ventricular assist device. The patient currently is doing well and is awaiting heart transplantation. DiscussionAn increased incidence of thromboembolism is seen in patients with left ventricular systolic dysfunction following myocardial infarction (MI).1 Following an acute MI, the formation of a left ventricular (LV) thrombus is a significant complication. LV thrombus occurs in up to one-third of patients with anterior wall MI and is much more frequent in patients with a large anterior MI and subsequent heart failure.2 The vast majority of LV thrombi are of the immobile mural type; unfortunately for our patient, he had the more rare mobile type which has a higher risk of embolism.3 LV thrombus has been associated with
A 69 year-old male presents to the Emergency Department with complaints of malaise, myalgias, rhinorrhea, increased congestion, and occasional fevers for one week. The symptoms have gradually worsened over the past week, and Tylenol has minimally alleviated his symptoms. He denies exacerbating factors. He denies any trauma, shortness of breath, chest pain, or recent weight change. He has no sick contacts or recent travel history.Past medical history is significant for coronary artery disease status post myocardial infarction and coronary artery bypass graft in 000, hypertension, hyperlipidemia, and atrial fibrillation. Medications on admission include amiodarone, aspirin, atorvastatin, docusate, losartan, metoprolol succinate (XL), and warfarin. He does not smoke, drink alcohol, or use illicit drugs.On admission, temperature was 99.7, blood pressure was 118/7, heart rate was 7, respiratory rate was 18, and oxygen saturation was 96% on room air. Physical examination was significant for dry mucosa and mild proximal muscle weakness. Initial labs on admission revealed an elevated creatinine of 1.9; CBC, UA, and LFTs were within normal limits. The patient was admitted with the diagnosis of upper respiratory tract infection with dehydration and started on intravenous fluids and supportive therapy for flu-like symptoms.Approximately days after admission, his rhinnorhea and congestion had resolved, but he complained of worsening myalgias. Physical exam at that time revealed worsening tenderness to palpation over his shoulder muscles and proximal lower extremities, as well as /5 muscle strength in his quadriceps and deltoids. He had difficulty standing from a seated position. Range of motion of all extremities was intact. At that time, it was revealed that his atorvastatin dose had been increased from 0 mg to 80 mg approximately 6 months ago as an outpatient. The CPK level drawn shortly thereafter was 5,17, supporting a diagnosis of statin-induced myositis, which is a form of drug-induced myopathy. Upon discontinuing his atorvastatin, his symptoms improved, and CPK trended down until it was within normal limits.
The patient is a 49 year-old female with past medical history of anxiety and hyperlipidemia who presented to an outside hospital with complaints of five hours of substernal chest pain followed by three episodes of syncope witnessed by her son. At presentation in the emergency department the patient denied any current chest pain or shortness of breath. She received 325 mg of aspirin en route to the hospital by EMS. Her vital signs were temperature 100° Fahrenheit, heart rate 60 beats/minute, blood pressure 101/50 mm Hg, respiratory rate 20 breaths/minute, and a pulse oxygenation of 98% on room air. The patient's EKG showed ST elevations in the inferior leads. The patient's laboratory studies were: white blood cell (wbc) count 14 B/L, hemoglobin 13.2 g/ dL, platelets 153 B/L, CKMB 32 U/L, troponin 8.27 ug/L, and CK 24.5 U/L. The patient was started on intravenous heparin and integrillin drips and transferred to Jefferson for emergent cardiac catheterization.The patient had left and right coronary angiography which showed no evidence of occlusive coronary disease. Left heart catheterization demonstrated moderate to severe inferoapical hypokinesis and a mildly depressed left ventricular ejection fraction (40%). During the procedure, the patient was noted to have 2:1 AV heart block with intraventricular conduction delay, and a temporary transvenous pacemaker was placed. The patient was then transferred to the cardiac care unit.In the cardiac care unit, the patient reported that she had no known drug allergies. Her only outpatient medication was a statin that was started six weeks ago. The patient denied any past surgical history. The patient consumed alcohol socially, had a 15 pack year history of smoking, and no history of illicit drug use. The patient's father died of a myocardial infarction at age 62, and the patient's mother was alive with a history of diabetes mellitus and arrhthymia. The patient noted that she had some nasal congestion for two days prior to the chest pain and syncope. The patient also reported working in her garden with rose bushes and was certain that she had a neck rash due to poison oak. Lastly, the patient reported decreased oral intake for the past two days due to "flu-like" disease.Overnight, the patient had multiple episodes of bradycardia that warranted venous pacing on telemetry. Significant laboratory studies were: wbc 4.3 B/L, AST 539 U/L, ALT 313 U/L, and troponin 14.7 ug/L. The patient underwent successful implantation of a dual chamber VDD pacemaker. A transthoracic echocardiogram demonstrated an ejection fraction of 60%, mild to moderate mitral regurgitation, and an inferior vena cava normal in size without inspiratory collapse. The patient was transferred to the telemetry floor service.On the third hospital day, the patient had no overnight complaints and wanted to be discharged home. Significant laboratory studies were a troponin of 16.5 and AST 299 U/L, and ALT 250 U/L. The patient had a CT of her head which showed no fracture or bleed. A CT of her chest demonstrated multifoca...
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