Showed Sinus Bradycardia Research Articles

Mitral Annular Disjunction: A Diagnosis to Save Lives

Introduction Mitral annular disjunction (MAD) is caused by a variation in the attachment of posterior mitral valve (MV) leaflet causing a wide separation between the left atrial wall-MV junction and left ventricular (LV) wall. Longitudinal MAD distance from left atrial wall-MV junction to LV wall during end-systole in the echocardiographic parasternal long axis view should be in excess of 2mm to suspect MAD. Recent evidence suggests that MAD magnitude is linked to higher incidence of ventricular arrhythmias. We present a case of an individual presenting with unexplained syncope, MAD and multiple episodes of non sustained ventricular tachycardia (NSVT). Case description 68 year old male with history of hypertension presented to ER with syncope. Initial EKG showed sinus bradycardia without ischemic changes. His troponins were negative and electrolytes were normal. Exercise stress test for chronotropic competence revealed premature ventricular contractions (PVCs) and an episode of 9 beats NSVT. Patient continued to have multiple episodes of NSVT with significant PVC burden. Echo showed normal systolic-diastolic function, myxomatous MV, bileaflet mitral valve prolapse (MVP), mild mitral regurgitation and MAD with magnitude of 12mm. Myocardial perfusion imaging did not reveal any defects. Cardiac MRI (CMR) showed delayed enhancement of basal mid-lateral and mid-septal walls. He received a dual chamber implantable cardioverter defibrillator to decrease the risk of sudden cardiac death related to MAD. Discussion Papillary muscle fibrosis and MAD magnitude are markers for severe arrhythmic events. Both are commonly seen with bileaflet MVP. Typical findings seen on echocardiogram are curling motion of the basal lateral LV wall from hypercontraction of regional area which causes paradoxical increase in the MV annulus diameter during systole. It also causes myxomatous MV and myocardial stretch in the LV inferobasal segment eventually causing fibrosis as identified on CMR. MVP is associated with MAD but MAD can also occur without underlying MVP and should be considered an independent risk factor for arrhythmias. Physicians should consider MAD in patients with no apparent cause for PVCs and refer them for echocardiogram. There is currently no consensus regarding pharmacological or device therapy for MAD. Conclusion Identification and recognition of MAD, with or without MVP, as an independent arrhythmic risk factor should be routinely done by non invasive methods.

Hyperkalemic Cardiac Arrest in a Patient with Diabetic Ketoacidosis.

AimTo highlight the occurrence of cardiac arrest due to hyperkalemia in diabetic ketoacidosis (DKA).BackgroundDiabetic ketoacidosis is a commonly encountered condition. These patients can have normal or mildly elevated levels of potassium. Our patient had severe hyperkalemia due to DKA resulting in cardiac arrest. Her high potassium diet and use of angiotensin receptor blocker along with acute kidney injury (AKI) would have also contributed to hyperkalemia.Case descriptionA 58-year-old female, known case of diabetes mellitus on insulin therapy and hypertension on telmisartan, presented with nausea, vomiting, and abdominal pain. She was diagnosed to have DKA with AKI precipitated by missed insulin and urinary tract infection. She was also on high potassium diet. Her electrocardiogram showed sinus bradycardia with prolonged QRS interval. Her potassium levels were elevated. She soon went into asystole and cardiac arrest and was resuscitated. Diabetic ketoacidosis protocols were followed along with antibiotics, and the patient improved.ConclusionSevere hyperkalemia in DKA is uncommon, and this hyperkalemia resulting in cardiac arrest is an unreported scenario. Potassium correction along with DKA management protocol forms the mainstay of treatment.Clinical significanceMild to moderate elevation in serum potassium occurs frequently in DKA. However, severe hyperkalemia is uncommon and is likely to be the result of insulin deficiency, acidosis, hyperosmolality, severe dehydration, and renal potassium retention. Such elevated level of potassium requires urgent correction in order to prevent cardiac arrest.How to cite this articleManappallil RG, Nambiar J. Hyperkalemic Cardiac Arrest in a Patient with Diabetic Ketoacidosis. Indian J Crit Care Med 2020;24(8):737–738.

ARRHYTHMIAS, PACING, ABLATIONC1 A DEPENDENT SYNCOPE

Abstract A 33-year-old man, ex drug addict on methadone therapy. He arrives to emergency department for syncope, reported by his wife reversion of the eyeballs and fine tremors with subsequent recovery of consciousness. A similar episode had happened a year ago. It was performed ECG: sinus bradycardia , 45 bpm, QT 600 msec, QTc 554 msec . Neurological examination performed: no motor deficits, negative Romberg. At brain CT no parenchymal tomodensitometric changes. Median line structures in axis. At the EEG: slight diffuse slow intercritical changes. Prescribed therapy with levetiracetam 500 mg. Cardiological examination and echocardiogram performed within the limits. Laboratory tests showed Trop HS 80 pg / ml. On the basis of the ECG and the slight increase of the troponin he was hospitalized in Cardiology and monitored. The following day, cardiac arrest due to torsade de pointes degenerated into ventricular fibrillation, DC shock was performed with the restoration of electrical and mechanical activity. Urgent coronary angiography was performed with evidence of coronary artery free from angiographically significant stenosis. SERT has been contacted: the patient had not been treated by them for some time and was using excessive doses of self-procuring methadone. In consideration of cardiac arrest from methadone long QT ventricular arrhythmia, ICD implantation was proposed, refused by the patient because he wanted to start detoxification therapy. During the hospitalization, progressive reduction of QT up to normalization in discharge. After a month new access to emergency department for presynopal episode, ECG showed sinus bradycardia with QTC 552 msec; the patient reports continuing to take excessive methadone doses and refuses treatment at a recovery center; considering that the ICD can be life-saving in this typ77e of patient (intractable addiction), we have re-proposed the ICD implant, rejected by the patient.

HIP INJURY- CROSS COUNTRY

HISTORY 18-year-old high school female cross-country runner presented with one week of left anterior hip pain. Denied a specific injury. Pain started during a late season meet causing her to finish at a slower pace. Pain progressively worsened requiring crutches to ambulate, despite no further activity. Max mileage was 40 miles/week, had tapered to 20 miles/week prior to injury. History of stress fracture 4 years prior. Initial x-ray of left hip revealed open epiphyseal plates, no other osseous abnormalities. Inquiring about menstrual history, she had yet to reach menarche. Per the patient’s mother, she had been trialed on growth hormone and is currently on estradiol patches. She has a known eating disorder for which she is not actively receiving help, despite multiple hospitalizations. PMHX Primary amenorrhea, followed by endocrinology. Lab work revealed low estradiol, LH, FSH with high alkaline phosphatase. Normal labs were thyroid studies, BMP, LFT, vitamin D and prolactin. Genetics showed 46XX. Multiple XR for bone age showed that of an 11-year-old. Cardiac work up showed sinus bradycardia on EKG and normal echo. Brain/pituitary MRI revealed normal pituitary and mild enlargement of ventricles, sulci, cerebellar folia. PHYSICAL EXAMINATION Patient stands 55 inches tall, weighing 61 pounds with a BMI of 14. She appears much younger than stated age. Hair is full, though fine. Breast tissue is not appreciated. On left hip exam, there is TTP along flexor tendon, lateral hip, and piriformis. She has pain with external rotation, weakness and pain with hip flexion, abduction, and adduction against resistance. She is unable to do a single leg hop due to groin pain. She is neurovascularly intact. DIFFERENTIAL DIAGNOSIS 1. Femoral neck stress fracture 2. Primary amenorrhea 3. Hip flexor strain 4. Relative Energy Deficiency in Sports syndrome 5. ASIS avulsion fracture TESTS/RESULTS MRI left hip 1. Partial thickness tear at attachment of left iliopsoas tendon to lesser trochanter with intramuscular hematoma 2. Minimal partial thickness tear of the left common hamstring origin FINAL DIAGNOSIS 1. Partial tear of left iliopsoas tendon and hamstring 2. RED-S TREATMENT/OUTCOMES 1. Shut down from all activities 2. Weightbearing as tolerated 3. Referral to gynecology for transvaginal ultrasound 4. Referral to Eating Recovery Center

SUN-902 Bradycardia as a Presentation of Malignant Pheochromocytoma

IntroductionPheochromocytoma usually presents with tachycardia, hypertension and other symptoms related to catecholamine release. Bradycardia has been reported in up to 10% of patients and is due to an unusual reflex to cathecolamine surge.Case Report:57-year-old morbidly obese female with a history of COPD, hypertension, paroxysmal bradycardia, and urinary incontinence was referred to endocrinology clinic after an adrenal mass was found incidentally as part of a work-up for microscopic hematuria and urinary incontinence. CT abdomen showed unilateral 3.3 x 3.9 cm left lobular adrenal mass. Family history was negative for malignancies or pheochomocytoma. Patient denied substance abuse or ethanol use. Her medications include amlodipine, hydrochlorothiazide and albuterol. Physical exam was remarkable for a BMI of 51.6 and bradycardia of 50 bpm and well controlled blood pressure. On further review of her history, patient had prior visits to outpatient and emergency department for chronic headaches, insomnia, palpitations and sweating. Patient had a previous admission 13 years prior for chest pain and hypertensive urgency associated with headache and junctional bradycardia.Laboratory workup was significant for serum metanephrine levels of 749 pg/ml (normal <42), serum normetanephrine 185 pg/ml(normal <145), serum chromogranin A 130 ng/L(normal <39) and 24hr urine metanephrine of 1340 ug/24hr (normal <96) and urine normetanephrine of 357 ug/24hr (normal <80). Previous ECG showed sinus bradycardia. Echo-cardiogram revealed normal ejection fraction with left atrial enlargement.MIBG showed large focal area of intense radio-tracer accumulation in left mid abdomen and small focal lesions in the liver. Diagnosis of malignant pheochromocytoma was made and patient was referred to another institution for further management.Conclusion:Malignant pheochromocytoma is a rare neuroendocrine tumor that usually presents with tachycardia and hypertension. 10% of patients with malignant pheochromocytoma can debut with bradycardia due to sinus arrest. Although malignant and benign pheochromocytoma share the same clinical and histological features, the presence of metastasis is the main clue to differentiate them. Surgery remains the main treatment option even if complete debulking cannot be achieved. Nuclear radiation therapy or chemotherapy are two other therapeutic options that can be considered alone or in combination with surgery depending on the patients’ comorbidities. Lifetime surveillance is recommended as recurrence can occur up to 40 years after original resection. References-Chen H, Sippel RS, O’Dorisio MS, Vinik AI, Lloyd RV, Pacak K. The North American Neuroendocrine Tumor Society consensus guideline for the diagnosis and management of neuroendocrine tumors: pheochromocytoma, paraganglioma, and medullary thyroid cancer. Pancreas. 2010 Aug;39(6):775-83.

473 Chloroma: an unusual case with extensive cardiac involvement detected by echocardiography

Abstract Introduction Chloroma, also known as myeloid sarcoma, is a localized extramedullary tumour composed of malignant cells of the myeloid cell line, most frequently occurring in myelogenous leukemia. Heart involvement is exceptional, only about 20 cases have been reported in the literature. Case presentation A 38-year-old woman presenting with fatigue and pre-syncope was admitted to the hospital. The patient had a history of acute myeloid leukaemia diagnosed 2017, treated with chemotherapy and transplanted with allogenic bone-marrow the same year, remaining thereafter in clinical remission. Initial electrocardiogram showed sinus bradycardia and recurrent sinus arrests and therefore a pacemaker was implanted. An echocardiogram was performed which revealed multiple infiltrative masses with involvement of the superior vena cava extending to the right atrium, atrial septum, left atrium, mitral valve and aortic root. Magnetic resonance imaging was done confirming the echocardiographic results and showing even involvement of pulmonary veins, coronary arteries and myocardial infiltration. Chemoradiation was administered with initial response, however, disease progression led to the patients´death. Conclusion To our knowledge, this is the first case describing a chloroma with extensive involvement of cardiac walls, vessels and valves. This case also illustrates the value of echocardiography as a tool for early detection of cardiac masses. Abstract 473 Figure. Echo with contrast

Cardiogenic dementia improved after permanent pacemaker implantation: a case report

Background: Heart diseases are the most common diseases worldwide which cause significant morbidity and mortality. Bradycardia comes under the category of heart diseases and is more common in the elderly. Bradycardia is defined as “heart rate of less than 60 beats per minute (bpm)”. There is a wide range of causes of bradycardia and the road to diagnosis includes extensive investigations. Case Presentation: Here we present the case of a 71-year-old male who presented with a history of dizzy spells, easy fatigueability, syncopal attacks, and memory impairment for 3 months prior to admission. On investigation, his complete blood counts, liver function tests, renal function tests, serum electrolytes, and urine routine examination were normal. His thyroid function tests were also normal. Electrocardiogram showed sinus bradycardia with pauses. Echocardiography was also normal. Holter monitoring showed multiple sinus pauses of 3.15 seconds average. Conclusion: We made a diagnosis of cardiogenic dementia due to sinus node dysfunction. The patient underwent permanent pacemaker implantation therapy and his symptoms improved. Our case highlights the importance of early diagnosis of the culprit disease and early intervention to prevent further complications.

P1602 An adult with mitochondrial cardiomyopathy

Abstract Introduction Mitochondrial diseases are a group of rare inherited disorders with diverse phenotypes that are caused by mutation in nuclear or mitochondrial DNA. The prevalence of mitochondrial disease is estimated to be one in 5000 livebirths. The heart depends mainly on the energy produced through aerobic respiration and hence cardiac involvement is common, progressive and its presence is an independent predictor of mortality in patients with mitochondrial disease and may occur as the principal clinical manifestation or part of a multisystem disease. Case report We present a 31 years old lady who was referred to our hospital with a newly diagnosed hypertension and non-specific ECG changes. The patient had no shortness of breath, no palpitation and no chest pain. She was overweight and had short stature. Her blood pressure was elevated 155/90. There was no signs of heart failure and no murmurs on auscultation of the heart and lung. Her ECG showed sinus bradycardia 55-60 b/min, ST segment elevation in the anterior chest leads with non-specific widespread t wave inversion. An Echocardiogram was done and showed concentric left ventricular hypertrophy (LVH) at 1.5 cm with speckling and granite-like appearance of the myocardium with no LV out flow tract (LVOT) obstruction and with normal systolic function and no significant valvular disease. A cardiac MRI was done and showed mildly dilated LV with normal geometry, normal systolic function, concentric LV hypertrophy with papillary muscles hypertrophy, relative sparing of the apical segments and with no LVOT flow acceleration and no late gadolinium enhancement. Our patient had mild hearing loss which is maternally inherited with her mother and her maternal uncle had cochlear implants. She also had borderline diabetes mellitus and she was also found to have the m.3243 &amp;gt; G mutation suggesting a mitochondrial disorder . A diagnosis of mitochondrial cardiomyopathy was made and the patient was started on an antihypertensive and planned to have regular cardiology clinic follow up. Conclusion Hypertrophic remodelling is the dominant pattern of cardiomyopathy in all forms of mitochondrial disease; occurring in up to 40% of patients and its presence is associated with higher mortality. The severity can vary from asymptomatic as in our patient to severe heart failure with acute decompensation that can occur with metabolic disorders or general illnesses. Treatment of mitochondrial disorders is mainly symptomatic with no curative therapy available. We aimed at increasing awareness of this rare disease. Abstract P1602 Figure.

Bradycardia in elderly patient: look at the body temperature

ABSTRACT&#x0D; We describe a case of a 83-year-old man who presented to the Emergency Department for bradycardia and reduced level of consciousness. His conditions had progressively worsened in the last few days and bradycardia induced his relatives to call on emergency team. He presented with hypoxia, cough, bradycardia and a reduced Glasgow Coma Scale value. The body temperature was not detected by standard thermometer and the electrocardiogram showed sinus bradycardia with prominent Osborne wave in the lateral precordial leads. His rectal temperature was 30.1 °C and the diagnostic work up showed a right lung pneumonia. He underwent active and passive rewarming treatment and sepsis treatment. Electrocardiographic abnormalities disappeared after rewarming and the patient was admitted to sub-intensive care unit.

1631 A Rare Case of Myxedema Ascites and Ischemic Colitis

INTRODUCTION: Myxedema is a severe form of hypothyroidism with various signs and symptoms. We present a rare case of myxedema ascites complicated with ischemic colitis (IC). CASE DESCRIPTION/METHODS: A 71-year-old female with a history of coronary artery disease and congestive heart failure (Ejective fraction 40%) presented with abdominal distention. Pertinent vitals included blood pressure of 100/54 mmHg and heart rate 38 beats/min. Pertinent labs included hematocrit of 28.2 %, albumin 3.1 g/dL, transaminases mildly elevated, alkaline phosphatase (ALP) 382 IU/L, thyroid stimulating hormone (TSH) 141 IU/mL, free triiodothyronine (T3) 1.26 pg/ml, total T3 45.30 ng/dL. Rest of the electrolytes, blood counts, including coagulation parameters, were normal. Electrocardiogram showed sinus bradycardia. She was started on levothyroxine for severe hypothyroidism. Abdominal ultrasound showed a large volume of ascites and normal liver contour. Paracentesis showed total nucleated cells of 2242, total protein 3.6 g/dL, lactate dehydrogenase 229, albumin 1.8 g/dL, serum ascites albumin gradient (SAAG) &lt; 1.1, and glucose 86 mg/dL. Ascitic fluid cultures were negative. Hence, the patient was diagnosed with neutrocytic ascites and treated with empiric antibiotics. Ascitic fluid was negative for malignancy and tuberculosis. She was managed with diuretics (furosemide and spironolactone) and therapeutic paracentesis. She later developed bloody diarrhea, and flexible sigmoidoscopy showed mild to moderate IC of the rectosigmoid colon. She was treated conservatively. Her transaminases normalized, but ALP remained elevated. She was discharged after a two-week hospital stay and six weeks follow up showed significant improvement in ascites and TSH of 10 IU/mL. DISCUSSION: Myxedema ascites is seen in only 4% of the patients with uncontrolled hypothyroidism. There are no case reports on IC in the setting of myxedema ascites thus far. It is a rare complication of myxedema megacolon; however, our patient had no signs of megacolon on repeated imaging. Therefore, our case is unique as it highlights a rare (ascites) and uncommon (IC) complication of severe hypothyroidism. Ascites with SAAG &lt; 1.1 should prompt physicians to consider hypothyroidism in the differential diagnosis for ascites especially when total ascitic fluid protein is &gt; 2.5 g/dL and other causes such as portal hypertension, malignancy, and infections are ruled out. It is easy to treat, can lead to complete resolution of ascites and decrease morbidity.

1772 Novel Use of Low Dose Amitriptyline in the Prevention of Deglutition Syncope: A Case Report

INTRODUCTION: Deglutition syncope is a rare entity with approximately 100 reported cases. It is a subtype of neurocardiogenic syncope triggered by deglutition secondary to organic and functional esophageal pathology. There are limited treatment options, and here we report a case of using low-dose amitriptyline (10 mg) for deglutition syncope. CASE DESCRIPTION/METHODS: A 58 year old male with hypertension, diabetes mellitus, and peripheral neuropathy presented to gastroenterology clinic with a diagnosis of deglutition syncope. Over the preceding year, he experienced four syncopal episodes while eating, described as lightheadedness before losing consciousness for a minute. Electroencephalogram, electrocardiogram, and echocardiography were unremarkable. Tile-table test showed reflex vasovagal syncope with systolic vasodepression (63 mm Hg) without cardioinhibition. Continuous telemetry showed sinus bradycardia (50 bpm) followed by three sinus pauses up to 4 seconds and return to normal sinus rhythm during episodes of dysphagia and lightheadedness. Evaluation for dysphagia with esophagogastroduodenoscopy (EGD) was unremarkable. Esophagram showed tertiary contractions in the mid-distal esophagus. Esophageal manometry was unremarkable for dry swallows with premature contractions possibly suggestive of distal esophageal spasm (Figure 1). Patient refused repeat EGD. A diagnosis of deglutition syncope with combined cardioinhibition and vasodepression secondary to esophageal spasm was made. Pacemaker implantation was recommended for syncopal symptoms from cardioinhibition; however, the patient declined due to potential persistence of symptoms from vasodepression. Initial recommendations of dietary changes and avoidance of triggering medications were made. Calcium channel blockers and nitrates were limited by bradycardia and hypotension. Hyoscyamine provided partial relief, but pre-syncopal symptoms persisted. Low-dose amitriptyline was initiated for the potential underling etiology of esophageal spasm. After a year, the patient reported resolution syncopal symptoms and dysphagia. DISCUSSION: Deglutition syncope due to cardioinhibition and vasodepression secondary to underlying esophageal spasm was diagnosed with tilt-table testing, continuous telemetry, and esophageal manometry. Amitriptyline was chosen for its anticholinergic effects and esophageal neuromodulator properties. Low-dose amitriptyline may be considered as a preventative treatment for resistant deglutition syncope.

HYPERCALCEMIC CRISIS CAUSED BY CALCIUM-ALKALI SYNDROME REQUIRING URGENT HEMODIALYSIS

SESSION TITLE: Wednesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Hypercalcemic crisis is a rare, life-threatening event secondary to decompensated hypercalcemia leading to renal failure and altered mental status. Primary hyperparathyroidism and hypercalcemia of malignancy are the majority of cases. However, hypercalcemia resulting from increased consumption of calcium supplement as part of the calcium-alkali syndrome should be considered. CASE PRESENTATION: An 88-year-old male presented to the ED with a history of increased confusion for 2 days. His past medical history was significant for chronic kidney disease stage 3. There was no family history of kidney stone disease, hyperparathyroidism or hypercalcemia. Vital signs were stable. Physical examination was remarkable only for dry oral mucosa and confusion. His medications did not include diuretics. His wife reported that he had been taking 10-12 tablets daily of Tums (calcium carbonate 1000mg/tablet, equivalent to 400mg of elemental calcium/tablet) recently due to worsening acid reflux. Initial electrolytes revealed serum total calcium 15.2 mg/dL, BUN 80 mg/dL, Creatinine 8.2 mg/dL, and bicarbonate 33 mmol/L. The parathyroid hormone-related peptide and 25(OH)D were normal. He had normal liver function tests, thyroid function test, Prostate-Specific Antigen, and hemoglobin. Multiple myeloma was ruled out based on normal serum and urine immunofixation studies. Electrocardiogram showed sinus bradycardia with normal corrected QT interval. A CT scan of the brain revealed no evidence of stroke. Renal ultrasound showed no renal stones or hydronephrosis. Chest x-ray did not show evidence of mass or lymphadenopathy. Hypercalcemia and renal failure failed to improve despite medical management with intravenous fluids and Calcitonin. The next day the patient received one session of hemodialysis. There was a gradual improvement in the patient’s mental status, calcium level, and renal function over the next week. DISCUSSION: The diagnosis of calcium-alkali syndrome is made based on history and metabolic abnormalities. The classic triad consists of hypercalcemia, varying degrees of renal failure, and metabolic alkalosis. The clinical presentation varies depending upon the severity of hypercalcemia. Patients may be relatively asymptomatic or may present with symptoms of nausea, vomiting, and altered mental status. In asymptomatic patients, initial management with aggressive hydration and induced diuresis with either calcitonin or bisphosphonates is recommended. However, in symptomatic or failed medical management patients, one session of hemodialysis to reduce hypercalcemia is recommended. Patients should have a close serial follow-up to rule out occult malignancy for the next 6 months. CONCLUSIONS: Due to the increasing use of calcium carbonate for dyspepsia and osteoporosis, patients should be educated and made aware of these severe, potentially life-threatening adverse effects. Reference #1: Ziegler R. Hypercalcemic crisis. J Am Soc Nephrol 2001; 12 (Suppl 17): S3–S9 Reference #2: Patel AM, Goldfarb S. Got calcium? Welcome to the calcium- alkali syndrome. J Am Soc Nephrol 2010; 21: 1440–1443 DISCLOSURES: No relevant relationships by Meily Arevalo, source=Web Response No relevant relationships by Cinthya Carrasco Barcenas, source=Web Response No relevant relationships by John Makram, source=Web Response No relevant relationships by Haneen Mallah, source=Web Response No relevant relationships by Myrian Vinan Vega, source=Web Response No relevant relationships by Wasawat Vutthikraivit, source=Web Response

Right Ventricular Infarction Associated with Pulmonary Embolism.

Background:Since the introduction of heparin as part of the management of acute coronary syndrome, the occurrence of pulmonary embolism (PE) as a complication of myocardial infarction (MI) have somewhat been unheard of. Given this rarity, its recognition is now a formidable challenge.Case Description:We present a case of a previously well 56-year-old male who presented with typical chest pain radiating to the left arm and dizziness. Initial vital signs revealed a blood pressure of 95/65 mmHg and his heart rate was 42 bpm. Physical exam revealed a middle-aged male in no acute distress with cool extremities, normal heart sounds, no murmurs and flat neck veins. His chest was clear to auscultation, abdomen benign and clinically, he was euvolemic. His first electrocardiogram (EKG) was significant for bradycardia with heart block and junctional escape rhythm and ST depressions in the anteroseptal leads. Subsequent right sided EKG showed sinus bradycardia with ST segment elevations in leads II, III and aVF. Troponin I was 0.95 ng/L [normal <0.04 ng/L] and initial transthoracic echo (TTE) was unremarkable with an ejection fraction (EF) of 55–60%. He was given loading doses of aspirin and clopidogrel, heparin drip initiated, and he proceeded to cardiac catheterization which revealed a 60 % stenotic lesion of the mid LAD and a large filling defect with 100% stenosis of the mid RCA consistent with thrombus. Post procedure TTE revealed an EF of 40%, septal and posterior hypokinesis, right ventricular regional wall motion abnormality of the basal and mid free wall with apical hypercontractility (McConnell’s sign) suggestive of PE. CT pulmonary angiography revealed bilateral pulmonary emboli and anticoagulation therapy was initiated.Conclusion:This case illustrates that pulmonary embolism is a potential complication of RV infarction and its early identification is critical for implementation of anticoagulation therapy for this potentially fatal condition if left undiagnosed and untreated.

First case report of inducible heart block in Lyme disease and an update of Lyme carditis

BackgroundLyme disease (LD), is the most common vector-borne illness in the US and Europe, with predominantly cutaneous, articular, cardiac and neuro-psychiatric manifestations. LD affects all layers of the heart and every part of the conducting system. Carditis is a less common manifestation of LD. Heart block (HB) as the initial and sole manifestation of LD is rare. Inducible HB has never been reported in LD. We report a case of heart block (HB) inducible with exercise and reversible with rest.Case presentationA 37-year-old male presented to the emergency department after experiencing two episodes of syncope while at work. He presented, with a heart rate of 57 bpm, and the ECG showed sinus bradycardia with first degree AV block. The PR interval was 480 ms (NL 120–200 ms). Physical exam was unremarkable. The cardiologist’s initial impression was vaso-vagal attack. He developed high degree AV block during a stress test for the initial work up, which resolved on cessation of exercise. A similar episode while walking in the hallway, resolved at rest. The high degree AV block appeared inducible with exercise and reversible with rest. His Lyme serology was strongly positive. He was treated with ceftriaxone and doxycycline. After completing treatment, the patient had a normal ECG and returned to work without limitations, doing manual labor.ConclusionsManifestations of Lyme carditis (LC) vary from asymptomatic and symptomatic electrocardiographic changes and heart block (HB) reversible with treatment, to sudden death. HB as the sole and initial presentation of LC is rare. There have been no reports of inducible HB in LD. Here we present a case of inducible and reversible high degree HB in a case of LC and an update of literature. Exercise and stress testing should be avoided in suspected cases of LC until resolution of carditis. Lyme carditis should be suspected in individuals with cardiac manifestations in an endemic area, particularly in the younger patients with no other etiology evident.

SUN-586 A Case Of Myxedema Coma With A Surprising Twist of SubAcute Infarct In The Frontal Lobe.

Introduction: Myxedema Coma is a rare life threatening condition with a high mortality rate ranging from 25-60%. It results from longstanding, poorly controlled or undiagnosed hypothyroidism triggered by different precipitating factors including infections, cerebrovascular disease, myocardial infarction, and trauma or drug therapy. Hypothyroidism has a clear influence on atherosclerotic risk factors which may lead to cerebrovascular disease; however there is insufficient evidence to prove the relationship between these two distinct diseases. We present a case of myxedema coma with a surprising twist of sub-acute infarct in the frontal lobe. Case Presentation:61 year old female with history of diabetes mellitus and hypothyroidism due to non-adherence with thyroid hormone after total thyroidectomy for thyroid cancer presented with altered mental status. She was found after three days of no contact with her family, covered in her feces and urine. Physical exam showed hypothermia 86,3o F, bradycardia 41 beats/min and puffiness of hands and face. Her laboratory showed elevated TSH 71.7 IU/ml, Free T4 0.22ng/dl, free T3 188pg/dl, high cortisol 33 UG/dl. EKG showed sinus bradycardia. Head CT noted for 1,6 by 1.5 hypodense lesions in frontal lobe concerning for sub-acute infarction. Myxedema coma was diagnosed with precipitating factor being stroke in the state of hypothyroidism and medication noncompliance and self-neglect due to frontal lobe sub-acute infarction. Admitted to ICU and started on intravenous Levothyroxyne , Liothyronine and cortisone. Due to worsening hypotension and respiratory status she was intubated and pressors -support was initiated. With clinical improvement on day three she was extubated and thyroid hormone replacement transitioned to oral regimen with good clinical outcome. Discussion: Myxedema refers to thickened, non-pitting edematous changes to the soft tissues of patients in a markedly hypothyroid state. With Hemodynamic instability, patient often progress into myxedema comatose state, which can be a life threatening condition if not treated quickly.Treatment involves intravenous administration of levothyroxine and Liothyronine supplements and often requires stress doses of steroids until adrenal insufficiency is excluded. We suspect that our patient developed self-neglect most likely due to her frontal lobe ischemia leading to further medication non-compliance which most likely precipitated the myxedema state given her thyroxin dependent state. Conclusion: Diagnosis of myxedema coma should always prompt inquiry into the possible precipitating factors and cerebrovascular accident especially with behavioral changes. Prompt recognition and supportive measures are extremely important in this endocrine emergency state.

SAT-623 Acute Bradycardia Secondary to Worsening of Hypothyroidism Post-Iodine Contrast

BACKGROUNDPatient with history or risk of developing thyroid disorder can develop worsening of overt hypothyroidism after exposure to iodine containing contrast. We report a case of bradycardia requiring CCU treatment due to worsening of hypothyroidism due to iodine contrast.CASE DETAILSA 68 years old female with history of heart failure, coronary artery disease, hypertension, diabetes mellitus and hypothyroidism presented to ED for chest pain and dyspnea. She was taking L-thyroxine 100mcg with other medications at home. CT angiography was negative and coronary angiogram was unremarkable. Her symptoms were alleviated and she was discharged home next day. Her discharge vitals included heart rate within normal limit. After 3 days she presented to ED for dizziness and weakness. Her vitals included heart rate of 51 and BP of 105/50. EKG showed sinus bradycardia. She was not taking medications that could potentially cause bradycardia, including beta-blockers. She was discharged next day without change in medications. She again presented to the hospital next day due to dizziness, fatigue and bradycardia. Vitals signs showed BP of 91/48 with heart rate of 37. She was admitted to CCU and treated with dopamine drip. Her TSH was 11.90(0.35-5.5 uIU/ml) and free T4 0.69(0.76-1.46ng/dl). She was started on 125mcg of L-thyroxine and was discharged home on this dose. After 2 days of discharge patient again presented to ED for the 4th time for dizziness and bradycardia. EMS details regarding vitals and EKG were not available but document did include atropine given en route, suggesting likely bradycardia of <40. On arrival to ED, Heart rate was 52 with BP 120/59. TSH done this visit was reported 26.40. Patient confided not taking 125mcg of L-thyroxine but continuing 100mcg, the dose she was on before first admission. Patient was again started on 125mcg of levothyroxine in hospital and observed for 3 days. Patient’s symptoms were resolved, and her heart rate was >60/min on the day of discharge.DISCUSSION Association of iodine contrast with hypothyroidism has been less studied compared to that with hyperthyroidism. Risk factors such as pre-existing sub-clinical hypothyroidism and hashimoto thyroiditis has been identified in some studies. It is postulated that in presence of excess iodine, iodine internalization into the thyrocyte and iodine organification is suppressed, also known as Wolff-Chaikoff effect. In most of the reported cases and studies, transient changes in thyroid function after exposure to iodine contrast rarely resulted change in management. Our case is unique in the sense that patient needed treatment in cardiac critical care including chronotropic agent. As use of iodine contrast in acute care setting has been on rise since last few decades, a hospital clinician needs to be vigilant about this phenomenon.

Case 262.

History A 17-year-old white male adolescent was re-evaluated for a withheld cardiac condition initially detected during prenatal imaging at an outside institution. He had previously experienced intermittent episodes of shortness of breath, chest pain, and palpitations with exertion, but more recently he had been asymptomatic. He had no other comorbidities and no family history of congenital heart disease, cardiomyopathy, arrhythmia, or sudden cardiac death. At physical examination, the patient had a grade II/IV rumbling systolic murmur best heard at the left upper sternal border. Otherwise, cardiovascular and other physical examination findings were normal. An electrocardiogram showed sinus bradycardia and nonspecific T wave changes. A graded exercise stress test was normal. Cardiac MRI was performed without and with gadolinium-based contrast material ( Figs 1 - 3 ). Multiple echocardiograms obtained since birth, cardiac MR images obtained 2 and 4 years earlier ( Fig 4 ), and nongated CT images obtained with iodinated contrast material to evaluate trauma 8 years prior ( Fig 5 ) showed findings similar to those of the current examination. Prior chest radiographs (not shown) were normal, and angiography performed when the patient was 4 years old revealed normal coronary arteries. [Figure: see text][Figure: see text][Figure: see text][Figure: see text][Figure: see text][Figure: see text][Figure: see text].

Cope's sign and complete heart block in a 78-year-old patient with biliary colic

IntroductionAcute cholecystitis and biliary colic may have signs and symptoms similar to those of Acute Coronary Syndrome(ACS) along with ischemic ECG changes. Cholecystitis and/or biliary colic have been both reported as trigger factors for bradyarrhythmia in the literature. Case ReportA 78-year-old male patient was admitted to our Emergency Department (ED) due to acute abdominal pain. The ECG on admission showed sinus bradycardia with a rate of 40 beats per minute (bpm) without signs of acute ischemia and a brief period (7 s) of complete atrioventricular (AV) block. He was initially treated with analgesics. After the remission of the pain, a subsequent ECG was performed which showed sinus bradycardia of 55 bpm. The AV block terminated one hour after the patient’s admission. The patient remained hemodynamically stable during the episode. He underwent an ultrasound of the abdomen in the ED which revealed sludge and one stone in the gallbladder without signs of inflammation. Laboratory test results for D-dimer and troponin were negative, while the coronary angiography showed coronary vessels without significant lesions. ConclusionBiliary colic can cause severe reversible reflex bradycardia (Cope’s Sign), even complete heart block. Pain relief is very important in the management of such cases.

Unusual digoxin toxicity with myocardial injury

A 38-year-old healthy male presented with vomiting and profuse diarrhea, associated with blurry and yellow coloration of the vision (xanthopsia). Laboratory workup was unremarkable, except for hyperkalemia (K 5.2 mEq/L) and mildly elevated troponin level 0.11 ng/mL (cut-off value 0.08). An electrocardiogram showed sinus bradycardia with deep scooping of the T waves. Although the patient denied intake of any drugs, herbs, consumption of plants, a digoxin level was drawn and was significantly elevated >5ng/mL (therapeutic range 0.8–2.0). Further questioning revealed that the patient was a pharmacist mixing raw material to fabricate medication, and that he could have incidentally ingested contaminated water. His symptoms improved with parallel improvement in the electrocardiogram T wave abnormalities. An echocardiogram was normal. The positive troponin was felt to be secondary to severe digoxin toxicity. Review of the literature however showed no report of elevated troponin in the setting of digoxin toxicity.

Catecholaminergic polymorphic ventricular tachycardia associated with sinus node dysfunction and junctional rhythm: Case report and literature review

We report the case of a 38-year-old woman with history of syncope and polymorphic ventricular tachycardia; tachycardia was inducible at exercise stress test, not at electrophysiologic study. Phases of QT prolongation were found at ambulatory electrocardiogram monitoring.The woman came to our attention for periodic control of implantable loop recorder. Rest electrocardiogram at admission unexpectedly showed sinus bradycardia, junctional rhythm, and ventricular premature beats. Furthermore, loop recorder control revealed a short run of bidirectional tachycardia, not associated with syncope.Final diagnosis was catecholaminergic polymorphic ventricular tachycardia, and the patient was implanted with an ICD. We therefore report an unusual case of bidirectional ventricular tachycardia associated with sinus node dysfunction and junctional escape rhythm. We hypothesize that a diffuse dysfunction of cardiac conduction system, presumably based on diffuse disorder of calcium handling, may be responsible for both sinus node failure and ventricular tachycardia.