Pulmonary Vascular Congestion Research Articles

Abstract 14117: Home Operated Ultrasound Exam for Detection of Worsening Heart Failure

Introduction: Acute Decompensated Heart Failure (ADHF) is associated with a high degree of morbidity and mortality. Dynamic lung ultrasound artifact called B-lines directly correlate with pulmonary vascular congestion (PVC) and can be seen on a limited lung ultrasound. Hypothesis: We assessed the ability of a recently hospitalized patient with ADHF to self-perform a lung ultrasound using a hand-held ultrasound and store images for physician interpretation. Methods: This was a prospective observational convenience sample of patients with known chronic heart failure admitted to an urban academic tertiary care center. The patient was educated on a 6 lung-zone image protocol, how to use the cloud archival system, and given a hand-held ultrasound transducer and iPad. The patients were asked to upload images three times a week, for 3 weeks. A B-line score for each interpretable lung zone was calculated. Results: Fifteen patients were enrolled, all of whom completed 7 or more scans. Average patient age was 60 years (range: 28- 86 years), 73% male, 60% white, and 47% obese. Five patients had ejection fraction >50%, and average length of hospital stay was 6.3 days. Of the 792 potential images, 784 were obtained (99%) and 637 (81%) were interpretable. The right upper zone was most often interpretable (97%), whereas the left lateral zone was least (70%). Median patient B line score when indexed to 6 interpretable scans was 3.00. Indexed B line scores are shown for all 15 patients (Figure 1). Patient survey data identified the left lateral zone as the most challenging to obtain. Conclusions: This pilot study shows that patients with ADHF can be taught how to use a hand-held portable ultrasound device and obtain and upload lung ultrasound images to a cloud. Compliance with the study protocol was excellent. Further studies are needed to determine if patient-performed lung ultrasound can be useful to clinicians to detect and manage PVC in this patient population.

Abstract 19052: Interferon B1A-Induced Dilated Cardiomyopathy

Introduction: Congestive heart failure is a leading causes of morbidity and mortality. Interferon therapy is a rare cause of dilated cardiomyopathy (DCM) and Heart Failure with Reduced Ejection Fraction (HFrEF). Specifically, interferon Alpha has been associated with cardiotoxicity. Here we describe a case of interferon B1A - induced HFrEF and DCM in a patient who took subcutaneous Interferon B1A for 11 years before developing clinical signs of heart failure. To our knowledge, only four other cases have been reported. Case Description: A 70-year-old man with a history of multiple sclerosis managed with Interferon B1A presented with shortness of breath, orthopnea, and lower extremity edema for 10 days. Physical examination revealed jugular venous distension and pitting edema. Brain natriuretic peptide (BNP) was 1580 pg/mL, troponin was 49 ng/L. Lipid panel, complete blood count, complete metabolic panel, Hemoglobin A1c, and thyroid stimulating hormone were within normal limits. Urine drug screen was negative. Chest X-ray revealed pulmonary vascular congestion and small pleural effusions bilaterally. A Transthoracic echocardiogram revealed mild aortic root dilatation (4.1cm), significant four-chamber dilatation, severely reduced left ventricular (LV) systolic function with an estimated ejection fraction of 20%, diastolic LV dysfunction, and moderately reduced systolic RV function, consistent with HFrEF and DCM (LVIDD 6.1cm). Coronary angiography showed normal coronary anatomy. The patient was started on guideline-directed medical therapy for HFrEF. Close follow-up was arranged to track improvement in systolic function after cessation of interferon b1a and consideration for Cardiac MRI and possible RV biopsy to evaluate for other causes of cardiomyopathy. Discussion/Conclusions: Due to the patient’s negative ischemic workup and absence of risk factors for cardiovascular disease, we strongly suspect that the patient’s cardiomyopathy was due to interferon B1A. With only 4 other cases of interferon B1A-induced DCM reported, it is a rare cause of medication-induced DCM. Interferon B1A should be considered a potential risk factor for developing heart failure, especially in high-risk patients.

Abstract 15913: Takotsubo Cardiomyopathy, is It Preventable?

Introduction: Takotsubo cardiomyopathy (TCM) is a reversible type of heart failure that occurs mostly in postmenopausal women. There are no definitive preventive measures in literature for this condition. Case: A 75-year-old female with a past medical history of hypertension presented with a new intermittent pressure-like chest pain and dyspnea right after a 1000-miles road trip. she reported that she had been feeling sad after her best friend died. Physical exam showed bilateral lower lung lobes crepitation and hypoxia. Lab work up revealed troponin of 1522 ng/L trending up to 2400 ng/L on serial measurements and elevated BNP. EKG showed ST changes and inverted T wave. Chest x-ray showed pulmonary vascular congestion and small bilateral pleural effusion. TTE showed LVEF 25-30% and mid and apical LV hypokinesis. Chest CT angiography was normal. Left heart catheter showed nonoccluded coronary arteries. LV angiogram portrayed mid and apical hypokinesis. Serology and PCR of EBV, Coxsackie B virus, CMV, HSV, influenza A and B, adenovirus and parvo virus were negative. She was started on a diuretic, a Beta blocker and an ACE inhibitor. Her symptoms improved. A follow up echocardiogram after 1 month showed improved ejection fraction and resolution of LV mid and apical hypokinesis. Recent combined emotional and physical stress of driving a long distance were thought to be the cause of stress cardiomyopathy. Discussion: Approximately 1-2% of patients presenting with symptoms of MI meet the criteria for TCM. A recent systematic review by Nyman et al on triggers of TCM found that physical factors are more common than emotional factors. However, some cases had both emotional and physical stressors. This patient had combined psychological and physical stressors, which may have precipitated TCM. postmenopausal women with recent emotional stressors should be advised to avoid physical stress until emotional issues have been resolved.

Abstract 17328: A Case of Reversible Severe Systolic Cardiomyopathy; Thinking Outside the Box

Introduction: Non-ischemic systolic cardiomyopathy is associated with significant morbidity and mortality. Prompt evaluation and timely removal of the potential insult may lead to reverse remodeling and recovery of the left ventricular (LV) systolic function. Case: A 39-year-old female with BMI 40 presented with dyspnea and bilateral lower extremity edema. Vital signs significant for mild tachycardia and hypertension. ECG showed sinus tachycardia. Physical exam revealed bibasilar crackles and 3+ pitting edema of the lower extremities. Laboratory significant for NTpro BNP 563 pg/dL and TSH <0.005 IU/mL with a free T4 of 2.73 ng/dL. Chest x-ray showed pulmonary vascular congestion. Echocardiogram showed severely reduced LV systolic function with ejection fraction (EF) of 27%, global LV hypokinesis and diastolic LV diameter of 6.85 cm. No significant atrial or ventricular arrhythmias noted on Telemetry. A CT angiography of the coronary arteries showed no evidence of calcification or obstructive coronary disease. Additional labs revealed severely elevated TSH receptor antibody and thyroid stimulating immunoglobulin. Diffuse thyroid enlargement noted on ultrasound. Patient was diagnosed with Grave’s disease (GD) with Burch-Wartofsky score of 30 indicating an impending thyroid storm. She was treated with Metoprolol and Methimazole. She underwent intravenous diuresis and was started on guideline-directed medical therapy for systolic cardiomyopathy. In follow-up after 6 months, her TSH had normalized. On repeat imaging, her LVEF improved to > 50% with diastolic LV diameter of 5.6 cm. Discussion: This patient was diagnosed with non-ischemic dilated systolic cardiomyopathy due to severe hyperthyroidism from GD. Thyrotoxicosis-induced systolic cardiomyopathy occurs in about 1% of patients with GD and is associated with increased morbidity and mortality. Excess thyroid hormones in thyrotoxicosis can affect multiple regulatory and structural genes of cardiac myocytes resulting in abnormal intracellular calcium regulation and impaired LV systolic and diastolic function. Our experience is consistent with literature demonstrating the importance of timely diagnosis and treatment of this reversible cause of systolic cardiomyopathy.

Neutralization of IL-1β and P-Selectin Inhibition Attenuate Organ Injury in Mice with Sickle Cell Disease

Advances in the clinical management of sickle cell disease (SCD) have significantly improved the life expectancy of patients. However, aging in SCD is worryingly associated with extensive end-organ damage, including nephropathy, hepatopathy, and pulmonary alterations. Continuous vaso-occlusive (VO) and inflammatory processes in the vasculature are most likely the principal cause of such lesions, and there is little evidence, to date, that long-term hydroxyurea therapy (the standard of care for SCD) reduces organ damage in SCD adults. Inhibition of P-selectin activity, using crizanlizumab, has shown some success for reducing VO crisis frequency in SCD. Furthermore, interleukin (IL)-1β blockade, in the form of canakinumab administration, was well tolerated in young patients with SCD and associated with inflammatory marker reduction. Exploring the hypothesis that a multi-target approach could potentiate the effects of biological agents such as crizanlizumab, we recently showed that acute neutralization of inflammasome-processed cytokines potentiated the effects of anti-P-selectin on tumor necrosis factor (TNF)-α-induced VO events in SCD mice. The aim of this study was to evaluate the effects of 6 weeks (wks) of anti-IL-1β and/or anti-P-selectin (CD62P) immunotherapy on inflammatory parameters and the organ histology of SCD mice. Transgenic Berkeley SCD mice (4-mo old) received ( i.p.) either anti-IL-1β monoclonal antibody (mAb) (01BSUR IgG2a; 7.5 mg/Kg; 2x/week), and/or anti-murine CD62P (RB40.34 IgG1; 30 µg/mouse; 3x/week), or an IgG1 mAb (30 µg/mouse; 3x/week) or saline (2x/week) for 6 wks (N=4-5 for each group). Prior dosing protocols determined the optimal mAb concentrations in SCD mice (data not shown). At two days after the last mAb administration, blood samples were analyzed by flow cytometry and serum stored for biomarker analysis (ELISA/colorimetric assays). Animals were then euthanized and organs were immediately collected and processed for staining with hematoxylin & eosin or Masson's trichrome (for collagen fiber staining). Histological analysis of 4 sections from each organ was performed blindly and alterations were scored qualitatively on a scale of 0 (absent) to 3 (severe). P-selectin inhibition, but not IL-1β blockade, for 6 wks resulted in inhibition (55.4 ± 6.4% inhibition, P=0.002) of the formation of circulating neutrophil-platelet (CD45 +Ly6G +CD41 +) aggregates in SCD mice, compared to non-specific IgG1, as did the combination of both anti-P-selectin/ anti-IL-1β administration (44.4 ± 5.2% inhibition, P=0.016). In contrast, IL-1β blockade, but not P-selectin inhibition, significantly reduced the circulating levels of TNF-α, compared to the saline/IgG1 controls, after 6 wks (40.4 ± 8.9% decrease, P=0.03). No significant alterations in serum biochemical markers (aspartate/alanine aminotransferase, total/direct/indirect bilirubins) were observed following any of the immunotherapies (P>0.05). With regard to effects on organ histology (see Figure): In the liver, P-selectin inhibition reduced tissue injury, while anti- IL-1β therapy significantly reduced sinusoidal congestion, injury and fibrosis, compared to saline/IgG1-treated SCD mice. In the kidney, anti-P-selectin therapy reduced renal congestion, while anti-IL-1β therapy ameliorated fibrosis, compared to saline/IgG1-treated SCD mice. In contrast, in the lungs, anti-P-selectin therapy reduced lung congestion and cell infiltrate, and significantly reduced bronchiole injury, while IL-1β immunotherapy and P-selectin/IL-1β inhibition combination therapy abrogated bronchiole injury/ fibrosis. As such, single immunotherapies had significant effects on multiple organs in SCD mice; P-selectin inhibition abrogated pulmonary bronchiole injury and vascular congestion, possibly mediated by reduced heterocellular aggregate formation, while IL-1β neutralization protected against liver and kidney alterations, and improved lung fibrosis, in association with reduced inflammatory cytokine production. Combination treatments, however, especially in the kidney and liver, had more complex effects. We suggest that future preclinical and clinical studies should investigate the potential of anti-inflammatory/adhesion approaches (alone or in combination) for preventing damage to multiple organs, in addition to preventing VO events.

Pediatric Pulmonary Hypertension in Left-Sided Heart Disease

Pulmonary hypertension (PH) from left-sided heart disease (group-II PH) is an increasingly recognized cause of PH in pediatrics. Group-II PH can result from obstruction at any level of the left heart, and can progress over time. Management can be particularly difficult, as targeted PH therapy in the setting of a fixed obstruction carries a risk of pulmonary vascular congestion and pulmonary edema. Based on existing evidence, the use of pulmonary vasodilators in group II PH is not recommended, and management centers around early identification and correction of the underlying left-sided lesion. In this review, we highlight the pathophysiology of group-II PH, the diagnostic evaluation of left heart pathology, and a general approach to both medical and surgical management, with particular attention to relevant left-sided lesions. Group-II PH is a multifaceted and progressive disease process that poses a difficult challenge to clinicians, and requires a thoughtful and individualized approach to management.

THU405 A Delicate Balance

Abstract Disclosure: N. Mohan: None. M.S. Shah: None. Introduction: Primary hyperparathyroidism is a disorder of excessive parathyroid hormone production causing increased calcium levels, usually due to a parathyroid adenoma. Commonly these cases are asymptomatic and detected incidentally on routine labs. They can be managed conservatively with sufficient fluid intake and avoiding dehydration. Congestive heart failure patients on diuretics with primary hyperparathyroidism require a delicate balance of their volume status to prevent exacerbation of either condition. We present a case of a woman with repeated hospitalizations due to poor volume status control. Clinical Case: An 82-year-old female with congestive heart failure (CHF), primary hyperparathyroidism (diagnosed 17 years ago), sick sinus syndrome with a pacemaker, and persistent atrial fibrillation presented to the emergency room with worsening b/l lower limb swelling for a few months. The remaining review of systems was largely negative. At home, she was on Losartan, Furosemide, and Carvedilol. Vitals were stable and physical exam revealed b/l lower extremity pitting edema. Chest x-ray showed cardiomegaly with mild pulmonary vascular congestion. Pertinent labs were NT pro-BNP 2190, Calcium 11.3 mg/dL, PTH 143 pg/mL, and Vit D, 25-hydroxy 48.6 ng/mL. The patient was started on IV diuretics and her home medications for CHF exacerbation. ECHO showed EF 39%, grade III diastolic dysfunction, severe pulmonary hypertension, mitral and tricuspid regurgitation. She was managed conservatively for her hypercalcemia and advised to maintain hydration at home. Spironolactone and Dapagliflozin were added to her regimen, and Furosemide was increased at discharge. The patient was re-admitted three weeks later with fatigue and decreased fluid intake. Vitals were stable and physical exam revealed dehydration. Pertinent labs were Calcium 13.4 mg/dL, Potassium 5.7 mmol/L, Creatinine 1.7 mg/dL (baseline 1.0), PTH 204 pg/mL, and Vit D 54.1 ng/mL. Repeat ECHO showed EF 15%. She was started on gentle 0.9% NS IV fluid to correct the hypercalcemia while preventing volume overload. Hypercalcemia and acute kidney injury improved with hydration. She was put on Cinacalcet 30 mg and home medications were modified for better volume control at discharge. Conclusion: This case highlights the complications of balancing the volume status with primary hyperparathyroidism and CHF. This patient’s primary hyperparathyroidism was well-controlled for more than fifteen years on adequate hydration. However, worsening CHF resulted in a higher requirement for diuretics, thereby worsening her hypercalcemia. Even though parathyroidectomy is an established treatment modality, she was not a suitable candidate due to age and comorbidities. Hence, to prevent such complications, parathyroidectomy must be considered early in patients with heart disease and even in asymptomatic hyperparathyroidism. Presentation: Thursday, June 15, 2023

Dyspnoea in liver cirrhosis: beyond the ordinary cardiopulmonary cause

BackgroundDyspnoea is a common presentation to the casualties, attributed mostly to cardiopulmonary diseases. Approach to dyspnoea consists of initial acute management to ensure airway patency, respiratory support, and hemodynamic stability, followed by identification of the underlying disease for a definite management to reduce short-term inpatient morbidity and mortality, and rehospitalization in long term. Awareness of the patient’s pre-existing medical conditions is a crucial clue to guide the attending doctor to the primary cause. Dyspnea in chronic liver disease can be due to concomitant cardiopulmonary diseases as well as pulmonary vascular congestion or abnormality associated with portal hypertension such as hepatopulmonary syndrome.Case presentationA 59-year-old man presented with a syncopal attack associated with breathlessness after physical exertion. He had alcohol associated liver cirrhosis for 2 years with a 6-month duration of platypnea and reduced effort tolerance. His physical examination revealed a cyanosed man with normal blood pressure and heart rate, without evidence of systemic and pulmonary fluid congestions. Chest radiography and computed tomography showed no evidence of pulmonary embolism and parenchymal disease and a normal echocardiography ruled out any cardiogenic cause. A diagnosis of hepatopulmonary syndrome was made after the appearance of microbubbles over left atrium at fourth to fifth cardiac cycle demonstrated by a transthoracic contrast-enhanced echocardiography to suggest an extracardiac intrapulmonary shunt.ConclusionsHPS is not an uncommon complication of chronic liver disease. Usual manifestation of HPS is platypnea which needs to be differentiated from orthopnoea associated with cardiopulmonary disease. Nevertheless, there is no effective therapeutic approach of HPS besides liver transplantation.

P211 BLEEDING AND THROMBOSIS: A MULTIDISCIPLINARY SLALOM

Abstract GG is a 75 kg and 75 years old smoker man with metabolic syndrome, potus, OSAS and LBBB. In 1/2022 the echo imaging showed EF 35%, high dissincrony and PVCs so a myocardial SPECT had been recommended but not carried out by the patient. In 6/2022 new exertional dyspnea, orthopnea and peripheral oedema lead the patient to the Emergency Department: the ECG indicated new onset AF 75 bpm, at laboratory tests creatinine 1.8 mg/dL and NTproBNP 6200 pg/ml and echocardiography confirmed hypokinetic cardiopathy with EF 35%, mild–moderate mitral and tricuspidal regurgitation with pulmonary hypertension and vascular congestion. Admitted for heart failure and new onset AF, diuretic and levosimendan ev, MRA, BB and LMWH started with benefit. At the end of inotropic therapy, ARNI, SGLT2 and inhaled cortisone began. Myocardial SPECT proved moderate fixed inferior wall hypoperfusion. Hospitalization was complicated by ecchymoses and hematomas of abdomen superficial soft tissues during LMWH and proximal saphenous vein and III middle left thigh thrombophlebitis, so apixaban 5mg BID and elastic stockings started with resolution. The onset of paresthesias, pain and left leg progressive hyposthenia led to diagnosis of a partial hematoma of the ilio–psoas muscle resulting in a complete left femoral nerve lesion and severe obturator nerve and left lumbosacral trunk suffering plus further right iliac and rectus abdominis muscles hematomas. Discontinued apixaban, after 72 hours the hematoma was surgically removed without complications and fast recovery thanks to FKT. 9 days later left leg DVT recurrence was observed: in absence of absolute contraindications to anticoagulant therapy and blood count stability, without evident new bleedings, heparin infusion was set with maintenance of the aPTT values at the lower therapeutic range limits. One week later radiological imaging demonstrated reduction of left retroperitoneal hematoma so dabigatran 150 mg BID was initiated. Control echo showed EF 42%, mild MR and TR. Regular the subsequent rehabilitation course: the patient was discharged with dabigatran 110 mg twice daily to limit long–term bleeding risk. The thrombotic/bleeding risks require a complex therapeutic modulation in a multidisciplinary teamwork.

Histopathological Study to Evaluate the Effect of Aqueous Extract of Portunuspelagicus and Mebendazole on Hydatid Cysts in Mice.

Hydatid disease is a parasitic infestation by a tapeworm of the genus Echinococcus sp., which has a global distribution. The current study was conducted to evaluate the effectiveness of the crustacean aqueous extract of Portunuspelagicus for 2 weeks of treatment compared to mebendazole on hydatid cyst in laboratory mice male Balb / C strain. Mice were infected intraperitoneally with 2000 protoscolices. After 12 weeks of infection, each mouse was treated with mebendazole (50mg/kg) and the hot aqueous extract of p. pelagicus (8, 16 g/kg). Samples of infected organs (liver, spleen, and lungs) were examined under a microscope to evaluate the morphological and histopathological changes of hydatid cysts and tissues. The study confirmed macroscopically that there were a number of hydatid cysts of different sizes in the liver, spleen, and lungs, splenomegaly, and congestion of the lungs of the positive control group. The histological changes in the organs of the group treated with the crustacean extract were represented by the vacuolation of hepatocytes in the centrilobular area of the liver. At the same time, the lungs show intensive peri-bronchiolar inflammation, pulmonary vascular congestion, and in the spleen, the deposition of amyloid-like material in the white pulp, extramedullary hematopoiesis, While the histopathological changes in the organs of mice treated with mebendazole, were represented by the presence in the mild liver vacuolation of the centrilobular area. In contrast, the lungs show mild pulmonary vascular congestion and emphysema, and the spleen shows normal white pulp, the normal red pulp of mice. The aqueous extract Portunuspelagicus and mebendazole are effective in controlling the contamination in the intermediate hosts.

Quercetin ameliorates acute lung injury in a rat model of hepatopulmonary syndrome

BackgroundCommon bile duct ligation (BDL) is a rat experimental model to induce biliary cirrhosis. Lung fibrosis and pulmonary vascular angiogenesis and congestion are the most common complications of biliary cirrhosis that is known as hepatopulmonary syndrome. The aim of the present work is to investigate the acute lung injury in a BDL model and to investigate the possible protective effect of quercetin on this injury.MethodsTwenty-four adult male albino rats of the Wister strain (weighing 150–250 g). Animals were divided into 3 groups, with 8 rats each: Group I: Sham-operated group (control). Group II: Bile duct ligation group (BDL) sacrificed after 28 days from the surgery. Group III: Quercetin-treated bile duct ligation group (Q-BDL) was given orally by gastric gavage in a dose of 50 mg/kg/day, starting from the 4th day of the operation until the 28th day. At the end of the experiment, at day 28, all rats were sacrificed. Lung specimens were processed to measure Endothelin B receptor gene expression by PCR, lung surfactant by ELISA, “eNO” s by immunohistochemistry. Histological assessment was done using; H&E, Masson’s trichrome, PAS, toluidine blue-stained semi-thin sections, transmission electron microscope. Histomorphometric and statistical studies were done.ResultsBDL group showed significant increase in lung index together with mononuclear cellular infiltration denoting lung inflammatory state. Also, the significant increase in pulmonary endothelial nitric oxide synthase ("eNO" s) area percent and endothelin B receptor (ETB) gene expression indicates enhanced angiogenesis. Pulmonary surfactant concentration was significantly decreased together with thickening of interalveolar septa denoting lung injury and fibrosis. Quercetin led to significant decrease in lung index, pulmonary "eNO" s area percent, ETB gene expression and significant increase in pulmonary surfactant concentration. Quercetin treatment improved histological changes and morphometric measurements, limited mononuclear cellular infiltration and decreased perivascular and perialveolar collagen deposition.ConclusionQuercetin ameliorates the hepatopulmonary syndrome-induced lung injury through its anti-inflammatory, antioxidative and antifibrotic effects.

Abstract 9991: Index Case of Prosthetic Mitral Valve Dehiscence Secondary to SARS CoV 2 Virus: Histopathologic Evidence of T-cell Mediated Injury

Introduction: SARS-Cov-2 virus has been shown to inflict damage on native cardiac valvular tissue. We present the index case of prosthetic mitral valve (MV) dehiscence secondary to SARS-Cov-2 virus as evidenced by histopathologic analysis of peri-valvular annular tissue . Case: 63-year-old male with history of MV replacement 2 years ago presented with complaint of dyspnea for 2 weeks. He was asymptomatic on a cardiology appointment a month ago and had an unremarkable transthoracic echocardiography (TTE) at that time. On arrival, he was hypoxic to 80% on room air and chest exam revealed bibasilar crackles. Complete blood count and electrolytes were within normal ranges. He tested positive for SARS-Cov-2 virus RNA and had a recent family history of COVID-19. Chest X-ray revealed bilateral pulmonary vascular congestion. He was given supplemental oxygen through nasal cannula with improvement in pulse oximetry. Repeat TTE revealed mitral paravalvular leak with suspicion for prosthetic dehiscence. Transesophageal echocardiogram showed multiple jets of severe paravalvular regurgitation and disruption of the MV apparatus. No vegetations were detected on echocardiography. He underwent a pre-operative right heart catheterization which confirmed severe MV regurgitation with pulmonary artery (PA) capillary wedge pressure of 45mmHg (Normal: <12) and a PA pressure of 40mmHg (Normal:<20). Intra-operatively, we found near-complete dehiscence of prosthetic MV with surrounding annular calcifications. Our patient underwent surgical MV replacement with a biosynthetic valve. Histopathologic analysis of the annular tissue revealed myxomatous degeneration and an inflammatory infiltrate of CD4 T helper cells consistent with subacute to chronic inflammation. Of note, neutrophils were not detected which usually signify acute bacterial endocarditis. Tissue and blood cultures remained sterile. Our patient improved hemodynamically after MV replacement and was discharged home in stable condition. Conclusion: We propose that SARS-Cov-2 virus may cause prosthetic MV dehiscence through CD4 T cell-mediated damage to annular tissue. Such cases would require surgical valve replacement to manage the resulting hemodynamic compromise.

Abstract 14545: Extramedullary Plasmacytoma of Tonsil Presenting as Cardiac Amyloidosis

Introduction: AL amyloidosis is a systemic disease characterized by the deposition of misfolded immunoglobulin light chains produced from clonal plasma cells in multiple organs of the body causing its dysfunction. We present you an unusual case of AL cardiac amyloidosis in a patient with extramedullary plasmacytoma of the tonsils. Case Presentation 61-year-old female presented with dyspnea on exertion with NT-proBNP elevated to 1439 pg/ml. CXR showed increased pulmonary vascular congestion. The patient was started on IV furosemide 40 mg BID with good urine output. Transthoracic echocardiogram revealed left ventricular hypertrophy with an ejection fraction of 60-65% with a global longitudinal strain of -9.0% and regional longitudinal strain reduced in the basal and mid-left ventricular segment but preserved in apical segment consistent with infiltrative cardiomyopathy. The patient underwent a nuclear (nuclear technetium pyrophosphate) scan of the heart consistent with cardiac amyloid deposition. She also was noted to have increased tonsillar mass which was biopsied. In the hospital, the patient had a cardiac arrest with the initial rhythm being ventricular fibrillation. The patient received 6 rounds of shock, and multiple injections of epinephrine, amiodarone, and bicarbonate push. The patient died despite all efforts of resuscitation. Histopathology results of tonsillar mass were consistent with plasmacytoma with amyloid deposition on Congo-red stain. Lambda: Kappa ratio was 70:1. Discussion: In cardiac amyloidosis, light chain deposits between cardiac myocytes disrupt cell-cell interaction. It can present as restrictive cardiomyopathy, conduction system abnormalities, or sudden cardiac death. It is essential to diagnose cardiac amyloidosis earlier. If untreated, the median survival of patients with cardiac AL amyloidosis is 6 months from the onset of heart failure. Conclusion: Our case was unusual in which a rare tumor of tonsils had plasma cell tumor which led to cardiac amyloidosis

USE OF POINT-OF-CARE ULTRASONOGRAPHY (POCUS) TO PREVENT DILTIAZEM-INDUCED CARDIOGENIC SHOCK

USE OF POINT-OF-CARE ULTRASONOGRAPHY (POCUS) TO PREVENT DILTIAZEM-INDUCED CARDIOGENIC SHOCK

ANTI-JO-1 ANTIBODY-ASSOCIATED CLINICALLY AMYOPATHIC DERMATOMYOSITIS WITH RAPIDLY PROGRESSIVE INTERSTITIAL LUNG DISEASE

ANTI-JO-1 ANTIBODY-ASSOCIATED CLINICALLY AMYOPATHIC DERMATOMYOSITIS WITH RAPIDLY PROGRESSIVE INTERSTITIAL LUNG DISEASE

MYXEDEMA COMA: A LIFE-THREATENING DIFFERENTIAL OF ALTERED MENTAL STATUS

MYXEDEMA COMA: A LIFE-THREATENING DIFFERENTIAL OF ALTERED MENTAL STATUS

Bilateral Pulmonary Embolism Masked by New-Onset Atrial Fibrillation with Rapid Ventricular Rate: The Role of Mechanical Thrombectomy

Patient: Male, 70-year-old Final Diagnosis: Atrial fibrillation • pulmonary embolism Symptoms: Dyspnea Medication: — Clinical Procedure: — Specialty: Cardiology Objective: Unusual clinical course Background:Management of atrial fibrillation (AF) with rapid ventricular rate in the setting of submassive pulmonary emboli (PE) has not been well defined in the literature. It is challenging as the hemodynamics caused by a PE can change the management of AF. We report a case of bilateral PE masked by new-onset AF with rapid ventricular rate that was treated pharmaceutically and mechanically, with thrombectomy.Case Report:An 85-year-old man presented with gradual dyspnea and was found to be in AF with rapid ventricular rate (~160–180 bpm). The patient had tachypnea and hypoxia requiring oxygen administration. On physical examination, he had euvolemia. Chest X-ray did not reveal pulmonary vascular congestion. He was started on standard AF management with atrioventricular nodal blockers. Laboratory tests revealed a normal troponin level but mildly elevated B-type natriuretic peptide and lactate. Because his dyspnea was out of proportion to the physical examination, radiographic, and laboratory findings, a D-dimer level was obtained and was elevated. Computed tomography with pulmonary angiogram showed extensive bilateral PE. An echocardiogram (TTE) showed evidence of right ventricular failure. The patient underwent mechanical thrombectomy with clot retrieval, deterring the risk of hemodynamic collapse that would have ensued with atrioventricular nodal blockers monotherapy. On repeat TTE, right ventricular dysfunction was completely resolved and the remaining hospitalization was uneventful.Conclusions:In patients with concomitant AF with rapid ventricular rate and submassive PE, the use of mechanical thrombectomy, in addition to the standard AF management, could be beneficial in deterring the risk of hemodynamic collapse.

Biventricular thrombi in a patient with methamphetamine induced dilated cardiomyopathy

A 39-year-old male with a 20-year history of cannabis and methamphetamine abuse presented to the ER with progressive shortness of breath, orthopnea, and bilateral leg swelling.Temperature 36.8°C, pulse 116/min, blood pressure 125/89 mmHg, respiratory rate 18/min, oxygen saturation 93% on room air. He had 2+ bilateral pitting pedal edema, elevated JVD, and S3. He had elevated BNP and creatinine, low magnesium, and potassium. UDS was positive for Amphetamine and THC (Marijuana) but normal Ethanol level. EKG was sinus rhythm, PVCs, and non-specific T wave changes; CXR showed cardiomegaly with pulmonary vascular congestion. CT chest revealed an indeterminate well-circumscribed filling defect in the right ventricle’s apex concerning for a thrombus versus neoplastic nodule. Transthoracic Echocardiography (TTE) findings of biventricular dilatation, global hypokinesis, right and left apical thrombus, a 5 X 3.2 cm mass in the right ventricle, Left Ventricular Ejection Fraction (LVEF) of 15 to 20%, grade 2 diastolic dysfunction, and Pulmonary Artery Systolic Pressure (PASP) of 40 mmHg (Figure 1a & 1b). He had widely patent coronary arteries on left heart catheterization, but Right heart catheterization showed elevated pulmonary capillary wedge pressure. Thrombophilia screen was negative, and there was no Deep Venous Thrombus (DVT) on lower extremity venous Doppler ultrasound.

ACUTE RESPIRATORY DISTRESS: A RARE PRESENTATION OF URETERAL RUPTURE

TOPIC: Signs and Symptoms of Chest Diseases TYPE: Medical Student/Resident Case Reports INTRODUCTION: Cardiorespiratory disorders usually present with acute respiratory distress; likewise, ureteral rupture usually presents as an acute abdomen [1]. We report a case of ureteral rupture presenting with acute respiratory distress leading to a delayed diagnosis. CASE PRESENTATION: An 82 y/o M with a history of congestive heart failure (CHF), chronic obstructive pulmonary disease, chronic renal failure and recently diagnosed COVID -19 pneumonia, was admitted for progressive dyspnea and abdominal discomfort for 2 days. Arterial blood gas showed hypercapnic hypoxic respiratory failure. Chest computed tomographic (CT) scan without contrast showed moderate right-sided pleural effusion but pulmonary embolism (PE) could not be ruled out. He also had a left leg deep venous thrombosis with worsening renal function and B-type natriuretic peptide (BNP) of 139pg/ml.His symptoms were thought to be due to acute decompensated CHF, COVID-19 pneumonia and possible PE. He failed to improve with intravenous furosemide, bilevel positive airway pressure ventilation and empiric anticoagulation. Due to worsening renal function and abdominal pain, an abdominal CT was done which showed right ureteral rupture with retroperitoneal collection and multiple non-obstructing renal calculi. The patient had placement of a double J stent with prompt resolution of respiratory distress. DISCUSSION: There are very few case reports of ureteral rupture occurring spontaneously and causing marked dyspnea. Respiratory distress may occur if the extravasated urine leads to an urinothorax or abdominal compartment syndrome [1]. Suspicion of non-cardiorespiratory causes of acute dyspnea in patients with underlying congestive heart failure includes respiratory distress disproportionate to the size of pleural effusion, unilateral effusions or effusions of markedly disparate size, absence of pulmonary vascular congestion and cardiomegaly, worsening renal function, ascites, urinary retention or anuria, abdominal pain, failure of the effusion to respond to management of heart failure, fever or pleuritic chest pain, and low or near-normal natriuretic peptides [2,3].When there are concerns for non-cardiorespiratory causes of respiratory distress, the diagnosis can be made with thoracentesis and imaging such as abdominal ultrasound, or CT [2]. CONCLUSIONS: This case illustrates a rare presentation of ureteral rupture causing respiratory distress and the key points that should elicit high clinical suspicion for non-cardiorespiratory causes of acute respiratory distress. When these findings are present, appropriate investigations and urgent intervention may be life-saving. REFERENCE #1: Choi SK, Lee S, Kim S, et al. A rare case of upper ureter rupture: ureteral perforation caused by urinary retention. Korean J Urol. 2012;53(2):131-133. doi:10.4111/kju.2012.53.2.131 REFERENCE #2: Leonidas Laskaridis, Spyridon Kampantais, Chrysovalantis Toutziaris, Basileios Chachopoulos, Ioannis Perdikis, Anastasios Tahmatzopoulos, Georgios Dimitriadis, "Urinothorax—An Underdiagnosed Cause of Acute Dyspnea: Report of a Bilateral and of an Ipsilateral Urinothorax Case", Case Reports in Emergency Medicine, vol. 2012, Article ID 395653, 3 pages, 2012. https://doi.org/10.1155/2012/395653 REFERENCE #3: Porcel JM. Pleural effusions from congestive heart failure. Semin Respir Crit Care Med. 2010 Dec;31(6):689-97. DOI: 10.1055/s-0030-1269828. Epub 2011 Jan 6. PMID: 21213200. DISCLOSURES: No relevant relationships by sharmela Brijmohan, source=Web Response No relevant relationships by Angelica Medina-Pena, source=Web Response No relevant relationships by Noura Semreen, source=Web Response

REFRACTORY HYPOXEMIA IN A NONAGENARIAN WITH PATENT FORAMEN OVALE MANAGED MEDICALLY

TOPIC: Pulmonary Vascular Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: Patent foramen ovale (PFO) is a cardiac defect with a prevalence of 25-30%, which notably decreases with age. A study done in 2018 showed an increased incidence of PFO in patients with pulmonary hypertension (pHTN). It is suggested that the presence of PFO in these individuals is a reflection of dilated and dysfunctional right atrium and ventricles, leading to an increased right to left gradient, stretching open a communication between the two atria. CASE PRESENTATION: We present a 96 year old female with heart failure with preserved ejection fraction, chronic respiratory failure secondary to moderate persistent asthma, on 4L of O2 at baseline, recurrent venous thromboembolic disease on apixaban, severe untreated OSA, initially admitted for septic shock due to acute cholecystitis requiring percutaneous cholecystostomy and broad spectrum antibiotics. On admission she also had significant hypoxia with cyanosis requiring intubation. The level of hypoxia was discordant with the clinical picture, with chest x-ray only showing atelectasis. She was extubated to high flow nasal cannula five days later, however we faced challenges in weaning her oxygen requirements. She received systemic steroids, anticoagulation and diuresis without improvement. Subsequently, the patient underwent an echocardiogram that showed a pulmonary artery systolic pressure (PASP) of 79mmHg (previously 47 mmHg in a study done 8 months ago). Given the degree of hypoxia and associated increase in PASP, intracardiac shunting was suspected. A repeat TTE with bubble study confirmed the presence of a small PFO. We discussed surgical closure, however invasive measures were deferred given her advanced age. Instead, the patient was treated with short acting diltiazem every 6 hours and furosemide daily with the goal of reducing pulmonary pressures and R to L shunting of deoxygenated blood. Although diltiazem is associated with negative outcomes in patients with heart failure, there was no evidence of pulmonary vascular congestion, and the immediate benefit outweighed the risk. Many days after initiating our plan, her oxygen requirements suddenly dropped from 60L/min to 4L/min and we were able to discharge her successfully. DISCUSSION: It is postulated that sepsis can lead to pHTN from elevated pulmonary vascular resistance through various mechanisms. Opening of PFO in severe pHTN is a common occurrence - resulting in resistive hypoxemia. Although we lack definitive evidence without right heart catheterization, we were able to exclude other etiologies of hypoxia through trial and error, strengthening our theory that PFO was the main driver of the clinical presentation. CONCLUSIONS: To summarize, hypoxia due to intracardiac shunting is an important cause of hypoxia, not to be missed on our list of differential diagnoses, with timely identification and appropriate therapy being the key to positive outcomes. REFERENCE #1: Sharan L, Stackhouse K, Awerbach JD, Bashore TM, Krasuski RA. Effect of Patent Foramen Ovale in Patients With Pulmonary Hypertension. Am J Cardiol. 2018 Aug 1;122(3):505-510. doi: 10.1016/j.amjcard.2018.04.014. Epub 2018 May 1. PMID: 30201113. REFERENCE #2: William J. Sibbald, NigelA.M. Paterson, Ronald L. Holliday, Richard A. Anderson, Trevor R. Lobb, John H. Duff, Pulmonary Hypertension in Sepsis: Measurement by the Pulmonary Arterial Diastolic-Pulmonary Wedge Pressure Gradient and the Influence of Passive and Active Factors, Chest, Volume 73, Issue 5, 1978, Pages 583-591, ISSN 0012-3692, https://doi.org/10.1378/chest.73.5.583. REFERENCE #3: Islam S, Masiakos P, Schnitzer JJ, Doody DP, Ryan DP. Diltiazem reduces pulmonary arterial pressures in recurrent pulmonary hypertension associated with pulmonary hypoplasia. J Pediatr Surg. 1999 May;34(5):712-4. doi: 10.1016/s0022-3468(99)90361-5. PMID: 10359169. DISCLOSURES: No relevant relationships by Maryam Ahmed, source=Web Response No relevant relationships by Robert McDonald, source=Web Response