- Email: [email protected]
Rock at the LVAD Core: Inadvertent Calcified Apical Aneurysm during LVAD Implantation
The 23rd Annual Scientific Meeting HFSA Introduction: In CHF patients, medical therapy optimization (MTO) remains the mainstay of management. However, attaining MTO can be challenging in patients with advanced CHF due to their symptomatic and hemodynamic intolerance. We present a case of a patient with advanced CHF and rectal cancer in whom slowly cautious MTO succeeded in improving cardiac function and candidacy for cancer chemotherapy and surgery. Case: A 57-year-old male with a medical history of advanced nonischemic CHF (EF 10-15%), a-fib, and rectal well-differentiated adenocarcinoma stage IIA (diagnosed 1 month ago) with GI bleeding and defecation pain presented with dyspnea on minimal exertion and orthopnea. He also had dizziness with standing due to symptomatic hypotension. SBP was between 100-115 mmHg. MRI pelvis showed T3 rectal mass with no enlargement of lymph nodes. Further imaging showed no distant metastases. Due to his advanced CHF, the patient was considered at high risk for surgery or chemotherapy. Rectal palliative radiation therapy was performed. He agreed on hospice palliative care for symptomatic relief. From Cardiology stand of point, the decision was made to continue MTO aiming for myocardial recovery. Radical adjustment of regimen and initiation of medications at miniscule doses eventually led to myocardial recovery with EF of 51% (figure 1). Patient’s SOB and dizziness improved. Cancer progressed to stage IIIb. Due to his improvement, the patient became at lower cardiac risk for other cancer therapy options. As a result, Oncology plan changed to proceed with FOLFOX (5-FU/ Leucovorin/ Oxaliplatin) chemotherapy and surgery. Discussion: In our patient, advanced therapy with left ventricular assist device was not possible given his risk of worsening GI bleeding on anticoagulation. Heart transplantation was not an option given the risk of cancer progression on immunosuppressive therapy. In the context of the patient’s condition and comorbidities, the best option left was to proceed with cautious MTO with clinical and hemodynamic monitoring. MTO resulted in clinical and cardiac function improvement. This gave the patient the window to become a candidate for other cancer therapy options that were not available for him before. Conclusion: Medical therapy optimization in all patients with CHF should always be sought. Despite being challenging under certain circumstances, as seen in our patient, slow and cautious MTO can eventually result in significant improvement in clinical status, cardiac function, and candidacy for other therapy options for other comorbidities.
Figure 1. Demonstrates Patient’s Medical Therapy Optimization over Time. Newly Introduced Medications are in Green, Increased Doses are in Blue, and Cancer Diagnosis is in Red. Abbreviations: BID = Twice Daily, BP = Blood Pressure, EF = Ejection Fraction, HR = Heart Rate, LA = Left Atrial, LVIDd = Left Ventricular Internal Dimension at End Diastole, MUGA = Multigated Acquisition, NYHA = New York Heart Association, QD = Daily, RV = Right Ventricular, TTE = Transesophageal Echocardiogram.
320 Non-Cirrhotic Intrahepatic Portal Hypertension Induced Pulmonary Arterial Hypertension: Is it More Prevalent than we Think? Sarine Beukian1, Ewelina Wojtaszek1, Lori A. Reyes1, Ramyashree Tummala2, Matthew I. Tomey1,3, Barry A. Love1,3, Johanna P. Contreras1,3, Maria G. Trivieri1,3; 1 Mount Sinai Hospital, New York, NY; 2Mount Sinai Beth Israel, New York, NY; 3 Icahn School of Medicine, New York, NY Introduction: Porto-Pulmonary Hypertension (PoPH) belongs to WHO group I, Pulmonary Arterial Hypertension (PAH). It has a prevalence of 0.5-5% and is potentially curable with liver transplant. Non-cirrhotic intrahepatic portal hypertension (NCIPH) is a rare cause of PoPH that shares clinical features of advanced right heart failure. Based on review of the literature and Pulmonary Hypertension (PH) registries, most studies report the prevalence of patients with the liver cirrhosis with little to no data on the incidence of PoPH amongst the non-cirrhotic patient population. In this report, we describe the two cases of “missed” NCIPH and PoPH who were diagnosed in our institution within the span of six months. Case Reports: The first patient was a 36 year old African American female who carried an initial diagnosis of SLE and ITP. She was on combination therapy with prostacyclin and endothelin receptor antagonist for the treatment of PAH. Her recurrent epistaxis from thrombocytopenia was refractory to therapy with prednisone, Rituximab, Romiplostim requiring multiple PRBC transfusions. Abdominal imaging revealed splenomegaly while liver biopsy demonstrated Nodular Regenerative Hyperplasia (NRH) without cirrhosis. The second patient, a 44 year old Chinese female, was initially diagnosed with idiopathic PAH. She was also identified to have ITP and showed no significant response to dexamethasone. On hospital admission, both patients presented with large volume ascites, splenomegaly and dependent edema. While in the ICU, they underwent RHC with assessment of Hepatic Venous Pressure Gradient (HVPG) demonstrating severely
S119
elevated pressures at 14 mmHg (Normally 5 mmHg) (Table 1). Liver biopsy was performed during the same procedure without complications. The pathology was consistent with NCIPH. Summary: Our report illustrates the importance of considering the diagnosis of NCIPH in patients with PH and refractory ITP, particularly in the setting of splenomegaly and lack of overt cirrhosis. Due to an estimated 50% of patients with NCIPH that go on to develop portal hypertension, it is important to consider this diagnosis when evaluating patients with PH as the treatment strategy differs from idiopathic and connective tissue disease-associated PAH. Given the limited risk of HVPG measurement as part of the evaluation of patients with PAH, our single center experience would suggest screening for NCIPH in select patients and embracing this etiology in the differential. Table 1.
Patient A Patient B
m Hepatic V Wedge
Hepatic Vein P
HVPG
28 28
14 14
14 14
321 Rock at the LVAD Core: Inadvertent Calcified Apical Aneurysm during LVAD Implantation Mohamad Khaled Soufi1, Loui A. Rejjal2, Kaitlyn S. Schaefer3, Tawnya R. Jackson3, Patrick T. Roughneen4, Ghannam A. Al-Dossari4, Jaime A. Hernandez-Montfort1; 1 Advanced Heart Failure and Transplant Cardiology, University of Texas Medical Branch, Galveston, TX; 2Department of Cardiology, University of Texas Medical Branch, Galveston, TX; 3Texas Transplant Center, University of Texas Medical Branch, Galveston, TX; 4Division of Cardiothoracic Surgery, Department of Surgery, University of Texas Medical Branch, Galveston, TX Introduction: Patients with ischemic cardiomyopathy (ICMP) and advanced CHF are at risk to develop calcified ventricular aneurysms as part of their ischemic remodeling over time. These aneurysms can significantly interfere with left ventricular assist device (LVAD) implantation. We present a case of a patient who had a calcified apical aneurysm that was preoperatively missed and inadvertently discovered during his LVAD surgery. Case: A 70 year-old male with a medical history of ICMP (EF 510%, NYHA II, Stage D) status post ICD placement on the heart transplant waiting list, CAD status post CABG (11 years ago), and a-fib presented for an elective LVAD implantation as a bridge to transplant due to worsening in his kidney function and declining in his myocardial oxygen consumption. The patient had CXR and TTE before his planned surgery as part of preoperative work up. During the operation, a calcified apical aneurysm was discovered and resected (figure 1). Afterward, the LVAD swing ring was fixed to the LV apical ventriculotomy followed by the LVAD inflow graft insertion. Thereafter, the operation was completed as planned. The patient recovered and was eventually discharged home. Discussion: Pre-LVAD identification of any calcified myocardial aneurysm is important especially when it is apical as the LVAD inflow graft cannot be sutured over calcified myocardial tissue. In our patient, CXR and TTE failed to identify his calcified apical aneurysm before surgery. Fortunately, the size of his calcified aneurysm was not very big and the surgeon was able to appropriately fix the LVAD swing ring on LV apical ventriculotomy after resecting the aneurysm. Retrospectively, our patient’s long history of ICMP, very low cardiac function, and dilated LV (end-diastolic diameter of 7.4 cm) were all unnoticed hints toward possible calcified aneurysmal formation that would have been
Figure 1. Demonstrates the Patient’s Calcified Apical Aneurysm (yellow Arrows) During its Resection.
S120 Journal of Cardiac Failure Vol. 25 No. 8S August 2019 discovered with advanced imaging modalities such as computed tomography (CT) of the chest. Conclusion: Calcified apical aneurysms can develop in patients with ICMP and advanced CHF and should always be looked for before LVAD implantation. Advanced imaging techniques, such as CT of the chest, can help to identify such calcified aneurysms preoperatively and safely tailor surgical plans in these patients.
322 A Case Series of Biopsy-Proven Eosinophilic Myocarditis at a Tertiary Care Center Indra Bole1, Syed Z. Qamer2, Mark Hofmeyer1, Farooq H. Sheikh1, Selma F. Mohammed1; 1MedStar Heart and Vascular Institute, Washington, DC; 2Georgetown University, Washington, DC Background: There is limited published literature on acute eosinophilic myocarditis (EM), a rare form of acute myocarditis, wherein eosinophils invade the myocardium with wide-ranging clinical sequalae. We aim to describe our experience in the largest contemporary case series of histologically-proven EM. Methods: Two authors independently reviewed the surgical pathology and autopsy databases for acute EM (01/ 2009 to 12/2017). Only patients with endomyocardial biopsy/autopsy and clinical course consistent with acute EM were included. We abstracted demographic data, comorbidities, clinical diagnostics, and clinical outcomes. Results: Seven patients had acute EM (Table). The average age was 53-years and five subjects were women. The most common etiology of EM was idiopathic. Five patients had peripheral eosinophilia. Three patients had elevated pulmonary capillary wedge pressure and three patients had reduced cardiac output. Six patients were treated with steroids, four of whom received IV pulse dosed steroids. Two patients required intra-aortic balloon pump support, one of whom subsequently underwent durable left ventricular assist device implantation. Two patients died during index hospitalization, one of septic shock and one of refractory ventricular tachycardia. Conclusion: The etiologies, clinical presentation, and course of acute EM varied widely. Prompt diagnosis, treatment with immunosuppression, and circulatory support may reduce cardiovascular mortality in this population.
Postoperative (post-op) a-fib can develop in LVAD patients placing them at risk of developing cerebrovascular accident (CVA) from left atrial appendage (LAA) thrombus. We present a case of LVAD patient with a new post-op a-fib who developed embolic CVA from LAA thrombus despite having therapeutic INR. In addition, we discuss whether LAA should be precautionary closed during LVAD implantation to prevent such complication. Case: A 64-year-old female with a medical history of advanced ischemic HFrEF (EF 10-15%) status post-LVAD as DT, postoperative afib, uncontrolled DM II who presented with slurred speech and left-sided weakness. Last known well time was 16 hours ago. CT head showed hypodensity in the right centrum semiovale figure 1A. CT angiogram head showed a filling defect in the right middle cerebral artery figure 1B. The patient was diagnosed with acute embolic ischemic CVA. She did not have a-fib before her LVAD. However, during her postop day 2, she developed a new onset-afib requiring amiodarone and digoxin besides warfarin. She was maintained on therapeutic INR post-LVAD except for a period of sub-therapeutic INR of 14 days that was bridged with LMWH figure 1C. TEE revealed LAA thrombus figure 1D which was identified as the embolic source. Physical therapy (PT) worked with the patient in the hospital and after being discharged. She continued to follow up at the HF clinic with gradual functional improvement. Discussion: The patient’s LDH post-LVAD remained at its post-op range between 603 and 952 U/L without peaking, other acute hemolysis indices were negative, and LVAD did not give any alarm. All of that excluded LVAD thrombus as a culprit and confirmed that the LAA thrombus was the CVA source. It was felt that if LAA closure was done during the patient’s LVAD surgery, it would have prevented her CVA. However, the absence of previous a-fib, embolic CVA, or venous thromboembolic event at the time of surgery did not give the surgical team any hint to consider the LAA closure. Conclusion: Patients with LVAD and therapeutic INR remain at risk of forming a thrombus in the LAA and having cardio-embolic CVA. Pending further research focused on cardio-embolic profiling, the role of LAA closure during LVAD implantation surgery should be considered on a case-to-case basis.
Table. Clinical Characteristics and Outcomes in Patients with Histologically-Proven Acute Eosinophilic Myocarditis
Figure 1. A: CT Head Showing Hypodensity in the Right Centrum Semiovale (Yellow Arrows) Including Acute Ischemic CVA. B: CT Angiography Head Showing a Filling Defect Extending from Right ICA to Right MCA (yellow Arrows) Indicating Thrombotic Occlusion. C: Patient’s INR Levels Between LVAD and CVA, Period of low INR Extending from 11/5 to 11/21 was Bridged with SC LMWH. D: TEE Veiw Showing LAA Thrombus (Asteric) E: Repeated CT Head (after 3 Months) Showing Evolved Hypodensity in the Right Centrum Semiovale Indicating Chronic Ischemic CVA (yellow Arrows). Abbreviations: ACA = Anterior Cerebral Artery, CR = Coumadin Ridge, ICA = Internal Carotid Artery, L = Left, LUPV = Left Upper Pulmonary Vein, LV = Left Ventricle, MCA = Middle Cerebral Artery, PCA = Posterior Cerebral Artery. R = Right, S = Smoke, VA = Vertebral Artery.
324 323 Cerebrovascular Accident in a Patient with Left Ventricular Assist Device and Therapeutic INR: Should Left Atrial Appendage Be Routinely Closed? Mohamad Khaled Soufi1, Patrick T. Roughneen2, Ghannam A. Al-Dossari2, Jaime A. Hernandez-Montfort1; 1Advanced Heart Failure and Transplant Cardiology, University of Texas Medical Branch, Galveston, TX; 2Division of Cardiothoracic Surgery, Department of Surgery, University of Texas Medical Branch, Galveston, TX Introduction: Left ventricular assist device (LVAD) as a destination therapy (DT) is considered one of the main therapeutic strategies in patients with end-stage CHF.
A Novel Clinical Decision Support System for Diagnosis and Treatment of Heart Failure: Concordance with Expert Decision Demir Baykal1, Gorica Malisanovic2, Nirav Raval3; 1Eastside Medical Center, Snellville, GA; 2University of Novi Sad Faculty of Medicine, Novi Sad, Serbia; 3AdventHealth Transplant Institute, Orlando, FL Objectives: Conundrum health care providers and institutions face is how to deliver evidence-based medical care at lower cost to an ever expanding portion of society in need. Translation of clinical studies to daily practice and adoption of national and international guidelines have not met expectations. This disappointing shortfall stems primarily from lack of interface between ever growing and changing vast medical literature and individual patient profile. Concurrently, threats of penalties for
Figure 1. Demonstrates Patient’s Medical Therapy Optimization over Time. Newly Introduced Medications are in Green, Increased Doses are in Blue, and Cancer Diagnosis is in Red. Abbreviations: BID = Twice Daily, BP = Blood Pressure, EF = Ejection Fraction, HR = Heart Rate, LA = Left Atrial, LVIDd = Left Ventricular Internal Dimension at End Diastole, MUGA = Multigated Acquisition, NYHA = New York Heart Association, QD = Daily, RV = Right Ventricular, TTE = Transesophageal Echocardiogram.
320 Non-Cirrhotic Intrahepatic Portal Hypertension Induced Pulmonary Arterial Hypertension: Is it More Prevalent than we Think? Sarine Beukian1, Ewelina Wojtaszek1, Lori A. Reyes1, Ramyashree Tummala2, Matthew I. Tomey1,3, Barry A. Love1,3, Johanna P. Contreras1,3, Maria G. Trivieri1,3; 1 Mount Sinai Hospital, New York, NY; 2Mount Sinai Beth Israel, New York, NY; 3 Icahn School of Medicine, New York, NY Introduction: Porto-Pulmonary Hypertension (PoPH) belongs to WHO group I, Pulmonary Arterial Hypertension (PAH). It has a prevalence of 0.5-5% and is potentially curable with liver transplant. Non-cirrhotic intrahepatic portal hypertension (NCIPH) is a rare cause of PoPH that shares clinical features of advanced right heart failure. Based on review of the literature and Pulmonary Hypertension (PH) registries, most studies report the prevalence of patients with the liver cirrhosis with little to no data on the incidence of PoPH amongst the non-cirrhotic patient population. In this report, we describe the two cases of “missed” NCIPH and PoPH who were diagnosed in our institution within the span of six months. Case Reports: The first patient was a 36 year old African American female who carried an initial diagnosis of SLE and ITP. She was on combination therapy with prostacyclin and endothelin receptor antagonist for the treatment of PAH. Her recurrent epistaxis from thrombocytopenia was refractory to therapy with prednisone, Rituximab, Romiplostim requiring multiple PRBC transfusions. Abdominal imaging revealed splenomegaly while liver biopsy demonstrated Nodular Regenerative Hyperplasia (NRH) without cirrhosis. The second patient, a 44 year old Chinese female, was initially diagnosed with idiopathic PAH. She was also identified to have ITP and showed no significant response to dexamethasone. On hospital admission, both patients presented with large volume ascites, splenomegaly and dependent edema. While in the ICU, they underwent RHC with assessment of Hepatic Venous Pressure Gradient (HVPG) demonstrating severely
S119
elevated pressures at 14 mmHg (Normally 5 mmHg) (Table 1). Liver biopsy was performed during the same procedure without complications. The pathology was consistent with NCIPH. Summary: Our report illustrates the importance of considering the diagnosis of NCIPH in patients with PH and refractory ITP, particularly in the setting of splenomegaly and lack of overt cirrhosis. Due to an estimated 50% of patients with NCIPH that go on to develop portal hypertension, it is important to consider this diagnosis when evaluating patients with PH as the treatment strategy differs from idiopathic and connective tissue disease-associated PAH. Given the limited risk of HVPG measurement as part of the evaluation of patients with PAH, our single center experience would suggest screening for NCIPH in select patients and embracing this etiology in the differential. Table 1.
Patient A Patient B
m Hepatic V Wedge
Hepatic Vein P
HVPG
28 28
14 14
14 14
321 Rock at the LVAD Core: Inadvertent Calcified Apical Aneurysm during LVAD Implantation Mohamad Khaled Soufi1, Loui A. Rejjal2, Kaitlyn S. Schaefer3, Tawnya R. Jackson3, Patrick T. Roughneen4, Ghannam A. Al-Dossari4, Jaime A. Hernandez-Montfort1; 1 Advanced Heart Failure and Transplant Cardiology, University of Texas Medical Branch, Galveston, TX; 2Department of Cardiology, University of Texas Medical Branch, Galveston, TX; 3Texas Transplant Center, University of Texas Medical Branch, Galveston, TX; 4Division of Cardiothoracic Surgery, Department of Surgery, University of Texas Medical Branch, Galveston, TX Introduction: Patients with ischemic cardiomyopathy (ICMP) and advanced CHF are at risk to develop calcified ventricular aneurysms as part of their ischemic remodeling over time. These aneurysms can significantly interfere with left ventricular assist device (LVAD) implantation. We present a case of a patient who had a calcified apical aneurysm that was preoperatively missed and inadvertently discovered during his LVAD surgery. Case: A 70 year-old male with a medical history of ICMP (EF 510%, NYHA II, Stage D) status post ICD placement on the heart transplant waiting list, CAD status post CABG (11 years ago), and a-fib presented for an elective LVAD implantation as a bridge to transplant due to worsening in his kidney function and declining in his myocardial oxygen consumption. The patient had CXR and TTE before his planned surgery as part of preoperative work up. During the operation, a calcified apical aneurysm was discovered and resected (figure 1). Afterward, the LVAD swing ring was fixed to the LV apical ventriculotomy followed by the LVAD inflow graft insertion. Thereafter, the operation was completed as planned. The patient recovered and was eventually discharged home. Discussion: Pre-LVAD identification of any calcified myocardial aneurysm is important especially when it is apical as the LVAD inflow graft cannot be sutured over calcified myocardial tissue. In our patient, CXR and TTE failed to identify his calcified apical aneurysm before surgery. Fortunately, the size of his calcified aneurysm was not very big and the surgeon was able to appropriately fix the LVAD swing ring on LV apical ventriculotomy after resecting the aneurysm. Retrospectively, our patient’s long history of ICMP, very low cardiac function, and dilated LV (end-diastolic diameter of 7.4 cm) were all unnoticed hints toward possible calcified aneurysmal formation that would have been
Figure 1. Demonstrates the Patient’s Calcified Apical Aneurysm (yellow Arrows) During its Resection.
S120 Journal of Cardiac Failure Vol. 25 No. 8S August 2019 discovered with advanced imaging modalities such as computed tomography (CT) of the chest. Conclusion: Calcified apical aneurysms can develop in patients with ICMP and advanced CHF and should always be looked for before LVAD implantation. Advanced imaging techniques, such as CT of the chest, can help to identify such calcified aneurysms preoperatively and safely tailor surgical plans in these patients.
322 A Case Series of Biopsy-Proven Eosinophilic Myocarditis at a Tertiary Care Center Indra Bole1, Syed Z. Qamer2, Mark Hofmeyer1, Farooq H. Sheikh1, Selma F. Mohammed1; 1MedStar Heart and Vascular Institute, Washington, DC; 2Georgetown University, Washington, DC Background: There is limited published literature on acute eosinophilic myocarditis (EM), a rare form of acute myocarditis, wherein eosinophils invade the myocardium with wide-ranging clinical sequalae. We aim to describe our experience in the largest contemporary case series of histologically-proven EM. Methods: Two authors independently reviewed the surgical pathology and autopsy databases for acute EM (01/ 2009 to 12/2017). Only patients with endomyocardial biopsy/autopsy and clinical course consistent with acute EM were included. We abstracted demographic data, comorbidities, clinical diagnostics, and clinical outcomes. Results: Seven patients had acute EM (Table). The average age was 53-years and five subjects were women. The most common etiology of EM was idiopathic. Five patients had peripheral eosinophilia. Three patients had elevated pulmonary capillary wedge pressure and three patients had reduced cardiac output. Six patients were treated with steroids, four of whom received IV pulse dosed steroids. Two patients required intra-aortic balloon pump support, one of whom subsequently underwent durable left ventricular assist device implantation. Two patients died during index hospitalization, one of septic shock and one of refractory ventricular tachycardia. Conclusion: The etiologies, clinical presentation, and course of acute EM varied widely. Prompt diagnosis, treatment with immunosuppression, and circulatory support may reduce cardiovascular mortality in this population.
Postoperative (post-op) a-fib can develop in LVAD patients placing them at risk of developing cerebrovascular accident (CVA) from left atrial appendage (LAA) thrombus. We present a case of LVAD patient with a new post-op a-fib who developed embolic CVA from LAA thrombus despite having therapeutic INR. In addition, we discuss whether LAA should be precautionary closed during LVAD implantation to prevent such complication. Case: A 64-year-old female with a medical history of advanced ischemic HFrEF (EF 10-15%) status post-LVAD as DT, postoperative afib, uncontrolled DM II who presented with slurred speech and left-sided weakness. Last known well time was 16 hours ago. CT head showed hypodensity in the right centrum semiovale figure 1A. CT angiogram head showed a filling defect in the right middle cerebral artery figure 1B. The patient was diagnosed with acute embolic ischemic CVA. She did not have a-fib before her LVAD. However, during her postop day 2, she developed a new onset-afib requiring amiodarone and digoxin besides warfarin. She was maintained on therapeutic INR post-LVAD except for a period of sub-therapeutic INR of 14 days that was bridged with LMWH figure 1C. TEE revealed LAA thrombus figure 1D which was identified as the embolic source. Physical therapy (PT) worked with the patient in the hospital and after being discharged. She continued to follow up at the HF clinic with gradual functional improvement. Discussion: The patient’s LDH post-LVAD remained at its post-op range between 603 and 952 U/L without peaking, other acute hemolysis indices were negative, and LVAD did not give any alarm. All of that excluded LVAD thrombus as a culprit and confirmed that the LAA thrombus was the CVA source. It was felt that if LAA closure was done during the patient’s LVAD surgery, it would have prevented her CVA. However, the absence of previous a-fib, embolic CVA, or venous thromboembolic event at the time of surgery did not give the surgical team any hint to consider the LAA closure. Conclusion: Patients with LVAD and therapeutic INR remain at risk of forming a thrombus in the LAA and having cardio-embolic CVA. Pending further research focused on cardio-embolic profiling, the role of LAA closure during LVAD implantation surgery should be considered on a case-to-case basis.
Table. Clinical Characteristics and Outcomes in Patients with Histologically-Proven Acute Eosinophilic Myocarditis
Figure 1. A: CT Head Showing Hypodensity in the Right Centrum Semiovale (Yellow Arrows) Including Acute Ischemic CVA. B: CT Angiography Head Showing a Filling Defect Extending from Right ICA to Right MCA (yellow Arrows) Indicating Thrombotic Occlusion. C: Patient’s INR Levels Between LVAD and CVA, Period of low INR Extending from 11/5 to 11/21 was Bridged with SC LMWH. D: TEE Veiw Showing LAA Thrombus (Asteric) E: Repeated CT Head (after 3 Months) Showing Evolved Hypodensity in the Right Centrum Semiovale Indicating Chronic Ischemic CVA (yellow Arrows). Abbreviations: ACA = Anterior Cerebral Artery, CR = Coumadin Ridge, ICA = Internal Carotid Artery, L = Left, LUPV = Left Upper Pulmonary Vein, LV = Left Ventricle, MCA = Middle Cerebral Artery, PCA = Posterior Cerebral Artery. R = Right, S = Smoke, VA = Vertebral Artery.
324 323 Cerebrovascular Accident in a Patient with Left Ventricular Assist Device and Therapeutic INR: Should Left Atrial Appendage Be Routinely Closed? Mohamad Khaled Soufi1, Patrick T. Roughneen2, Ghannam A. Al-Dossari2, Jaime A. Hernandez-Montfort1; 1Advanced Heart Failure and Transplant Cardiology, University of Texas Medical Branch, Galveston, TX; 2Division of Cardiothoracic Surgery, Department of Surgery, University of Texas Medical Branch, Galveston, TX Introduction: Left ventricular assist device (LVAD) as a destination therapy (DT) is considered one of the main therapeutic strategies in patients with end-stage CHF.
A Novel Clinical Decision Support System for Diagnosis and Treatment of Heart Failure: Concordance with Expert Decision Demir Baykal1, Gorica Malisanovic2, Nirav Raval3; 1Eastside Medical Center, Snellville, GA; 2University of Novi Sad Faculty of Medicine, Novi Sad, Serbia; 3AdventHealth Transplant Institute, Orlando, FL Objectives: Conundrum health care providers and institutions face is how to deliver evidence-based medical care at lower cost to an ever expanding portion of society in need. Translation of clinical studies to daily practice and adoption of national and international guidelines have not met expectations. This disappointing shortfall stems primarily from lack of interface between ever growing and changing vast medical literature and individual patient profile. Concurrently, threats of penalties for