San Antonio, TX. Introduction: ... This practice proved to be life-saving ... Rayan Yousefzai, Shiv Sab, Eric D. Adler, Victor D. Pretorius; UCSD, San Diego, CA.
The 20th Annual Scientific Meeting
•
HFSA
S129
Performance Improvement Initiatives/Case Studies 370
371
Entrapping a Giant Sleeping Killer: Successful Extraction of a Free-Floating Thrombus Archish Kataria, Ali J. Mehr; University of Texas Health Science Center at San Antonio, San Antonio, TX
High Output Heart Failure—A Reversible Cause Missed Again! Matthew Schaikewitz, Won Jun Park, Hugo Rosero, Sooraj Shah; Mount Sinai Beth Israel, New York, NY
Introduction: Free-floating thrombi (FFT) in the right heart are a rare occurrence with an unknown true prevalence. Mortality of 27.1% among treated patients to 100% if left untreated has been documented. FFT represent a medical therapeutic emergency as they can transform into pulmonary emboli leading to catastrophic consequences. Uniform consensus is lacking on the most appropriate management. Here we describe a case of this fatal disease which was successfully treated with interventional embolectomy and thrombolysis. Case Presentation: A 70 year old gentleman with a history of chronic kidney disease presented to the hospital with worsening shortness of breath, chest pain and two syncopal episodes. On exam, patient was afebrile with a blood pressure of 114/78 mm Hg, heart rate of 96/minute, respiratory rate of 22/ minute, signs of right heart failure and hypoxemia. Of note, the patient was recently admitted to the hospital with similar complaints and was found to have two vessel coronary artery disease on angiogram. He was discharged with a plan for a staged percutaneous coronary intervention (PCI) to avoid contrast induced nephropathy. On this admission, patient was diagnosed with a Non-ST elevation myocardial infarction and successfully underwent PCI as planned. A follow up transthoracic echocardiogram revealed a very large size, free-floating serpiginous echo-density in the dilated right atrium prolapsing into the enlarged hypokinetic right ventricle. There was no evidence of extension into the pulmonary vasculature .This finding, which was absent on the previous study was confirmed with a transesophageal echocardiogram (TEE). Due to the severity of the disease, a collective decision was taken by the cardiologists, surgeons and interventional radiologists to proceed with suction thrombectomy using AngioVac procedure. A large 22 cm intact clot, which had now travelled to the pulmonary vasculature, was aspirated under fluoroscopic and TEE guidance followed by catheter directed thrombolysis for remaining filling defects. Patient tolerated the procedure well and had an uneventful post operative course. He continues to remain stable on follow up visits. Conclusion: This case underlines the importance of considering pulmonary embolism as one of the potential etiologies of acute decompensated heart failure. The key to favorable outcome lies in prompt diagnosis and urgent intervention using a multi-disciplinary team approach. This practice proved to be life-saving in our case of FFT with exceptionally high mortality.
Introduction: High output heart failure is a rare but often reversible condition in adults. Current guidelines do not suggest screening for high output in heart failure patients unless it is suggested by history or physical exam. We describe here an unusual case of heart failure secondary to renal A-V malformation discovered incidentally. Case Presentation: A 74 year old woman with hypertension, hyperlipidemia, and chronic systolic heart failure due to nonischemic cardiomyopathy diagnosed over a year ago presented with acute exacerbation to the emergency department. Her echocardiogram revealed dilated cardiomyopathy with ejection fraction of 30%. During work up for her abdominal pain at this hospitalization, an ultrasound and a CT scan revealed an incidental large cavernous right renal arteriovenous malformation with a dilated right renal artery (2.3 cm) feeding into a nidus of vessels. Right heart catheterization revealed cardiac output of 8.3 L/min. In absence of any other reason for her high output heart failure, vascular surgery was consulted and the renal A-V malformation was successfully embolized. Three months later, the patient was seen at a follow up visit with complete resolution of her symptoms. At that visit, the echocardiogram revealed normalization of EF (55–60%) and chamber sizes. Cardiac output measured by echocardiography was 5.2 L/min. Discussion: Over 25% of heart failure patients have idiopathic cardiomyopathy. Attempts to find a reversible cause are vital as otherwise the prognosis is poor with high morbidity and mortality. Cardiac output can be measured noninvasively during a routine echocardiography, avoiding need for an invasive test such as cardiac catheterization. In cases of idiopathic cardiomyopathy leading to heart failure, detecting high output through a noninvasive test may lead to establishment of a reversible cause. Some of the causes of high output heart failure are A-V fistulas, anemia, hyperthyroidism, and sepsis. Beriberi can also cause high output heart failure but it is rare in adults in developed countries. Echocardiography can help not only in diagnosis but also in follow up after treatment to monitor change in cardiac output. Thus a routine noninvasive test, if used properly, could provide significant information that can alter the course of the patient’s disease. Conclusion: In cases of idiopathic heart failure, measuring cardiac output through echocardiography is safe and inexpensive. Detection of high cardiac output should ignite the search for a potentially reversible etiology. Echocardiography can also be used to monitor efficacy of treatment.
372 Auto-Transplantation in Cardiac Sarcoma Rayan Yousefzai, Shiv Sab, Eric D. Adler, Victor D. Pretorius; UCSD, San Diego, CA Background: Primary cardiac tumors are rare with a reported incidence of 0.017– 0.019.Undifferentiated pleomorphic sarcoma is extremely rare with controversial therapeutic options. Case: 20 years old female with no significant past medical history and 6 weeks pregnant, presents with atrial fibrillation.Echocardiogram showed multilobulated mass in left atrium prolapsing to mitral annulus and extended to left pulmonary veins with several satellite nodules at mitral annulus (Fig. 1).She underwent unsuccessful tumor resection and was referred to our institution.MRI (Fig. 2) showed large tumor in left atrium with infiltration of left atrium, left pulmonary vein and left lung.Pathology (Fig. 3) was consistent with high-grade undifferentiated pleomorphic sarcoma.After pregnancy termination, she underwent cardiac auto-transplantation with cardiac explanation, ex-vivo resection of left atrial tumor, resection of left atrium (Fig. 4), left pneumonectomy and re-implantation of native heart.Patient was discharged with plan to adjunct chemotherapy 6 weeks post-op. Discussion: High-grade undifferentiated pleomorphic sarcoma is frequently located at left atrium and mainly reported in young adult women with median age in the fourth decade.Therapeutic options remain challenging and controversial due to the rarity and aggressive nature of this tumor; without surgery the life expectancy is 9 to 12 months despite any radiotherapy and chemotherapy.There is a survival benefit for complete resection (6 vs 25 months), which is only possible with auto-transplantation approach due to the posterior location of the left atrium.
S130 Journal of Cardiac Failure Vol. 22 No. 8S August 2016
373 Case Report of Multiembolic Cerebrovascular Event Associated with Ramp Study Echocardiogram Brian Butera, Luanda Grazette, Tracy Lawrence, Michael Bowdish, Andrew J. Yoon; University of Southern California, Los Angeles, CA Case Presentation: A 64-year old male with ischemic CM and Type B aortic dissection received a HeartMate II LVAD as destination therapy. 35 months after implantation, he had an asymptomatic internal pump thrombus diagnosed by an elevated LDH level of 1027 u/L in the setting of a subtherapeutic INR. The LDH rapidly returned to baseline after IV Heparin therapy, and the patient continued Aspirin and Warfarin with therapeutic INRs on subsequent testing (target INR 2.2–2.7). Five months later, the patient presented to an outside hospital in fluid overload and respiratory distress. He was intubated and transferred to our hospital emergently. Sputum was positive for Influenza A, and antiviral therapy was started; Blood cultures were negative. Initial INR = 2.9, LDH = 1429 units/L, and haptoglobin
