Troponin Leak Research Articles

A CARDIOVASCULAR COMPLICATION OF COVID-19: DELAYED PRESENTATION OF ACUTE MYOPERICARDITIS

SESSION TITLE: Medical Student/Resident Cardiovascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: “SARS CoV-2” is an enveloped non segmented positive-sense RNA virus,. In December 2019, SARS CoV-2 started as a pandemic in Wuhan city of China and spread to the rest of the world. The classical clinical picture of COVID-19 is variable ranging from asymptomatic, a flu-like syndrome of mild severity, to interstitial pneumonia and a variable degree of respiratory failure with elevation of cardiac troponin I (cTnI) levels and arrhythmia in most cases. In here we present a case of delayed presentation of acute Viral Myopericarditis by COVID 19 even after the patient had recovered from infection. CASE PRESENTATION: A previously healthy 29 year old female presented with acute chest pressure of 5 hour duration, 10/10 in intensity, located at left sternal border. It was worsened with lying flat, and deep breathing and better with sitting up and bending forward. Forty five days before this presentation, she had cough, fever and fatigue and was diagnosed with COVID 19. After 14 days, patient was cleared by the state health department. Physical examination including the CVS and respiratory systems was normal. Laboratory tests showed on elevated troponin-1 level of 0.5 µg/L, which peaked to 8.09 µg/L the following day, (ESR) elevated at 35mm/hr, lactate dehydrogenase (LDH) elevated at 244U/L, C-reactive protein (CRP) elevated at 19.2mg/L. and D-dimer elevated at 561 FEUng/m. Two repeat SARS CoV-2 testing were negative. Electrocardiogram showed some non-specific T wave inversions in leads V3 with normal sinus rhythm at a rate of 87 beats per minute. Transthoracic echocardiography performed which did not demonstrate wall motion abnormalities or pericardial effusion. Chest CTA was negative for acute pulmonary embolism. The patient was diagnosed with viral myopericarditis caused by COVID 19. The patient was managed with pain medications, ibuprofen, and colchicine and was discharged in 2 days. DISCUSSION: Viral myopericarditis is the most common cause of myopericarditis. The exact mechanism COVID 19 causing cardiac injury is not clear. It could be either due to direct invasion of the cardiac myocytes or through immune mediated which is more likely in our patient. The cardiac manifestation of COVID 19 ranges from patients having asymptomatic troponin leak, acute CHF exacerbation due to dilated cardiomyopathy and arrhythmias. The treatment at this time is mainly supportive with medications such as remdesivir, favipivir, protease inhibitors under trial. CONCLUSIONS: A thorough history and physical for previous history and timing of exposure, and also help establish diagnosis and exclusion for acute coronary syndrome, to avoid delay in anti-inflammatory therapy and unnecessary testing. Post-viral acute myopericardial damage should be suspected even in the absence of residual viral genome Reference #1: Management of Acute and Recurrent Pericarditis. J Am Coll Cardiol 2020;75:76-92. Chiabrando JG, Bonaventura A, Vecchié A, et al. DISCLOSURES: No relevant relationships by Navya Akula, source=Web Response No relevant relationships by Miluska Mejia Trebejo, source=Web Response No relevant relationships by tausif syed, source=Web Response

Prevalence of a postoperative troponin leak in patients with cardiac risk factors undergoing knee and hip arthroplasty in a South African population.

Patients undergoing arthroplasty may have comorbidities that put them at risk of myocardial injury after non-cardiac surgery (MINS). MINS, a new clinical concept that has a different pathophysiology from conventional myocardial infarction, is related to a supply-demand mismatch ischaemia in the perioperative setting. MINS is often a silent event, and the diagnosis relies on cardiac biomarker testing such as troponin T. The incidence is estimated at 40%, with a fourfold increase in morbidity and mortality risk 1 year post surgery. To determine the prevalence of postoperative troponin leak in a single-centre arthroplasty unit in patients with various cardiac risk factors undergoing hip or knee arthroplasty and investigate the differences in troponin T levels between comorbidities and different types of arthroplasty, i.e. total hip replacement (THR), total knee replacement (TKR) and neck of femur (NoF) fracture hip replacement. A prospective, cross-sectional study of patients with one or more cardiac risk factors undergoing replacement surgery was conducted from October 2017 to April 2018. Troponin levels of all included patients were recorded on days 1 and 3 post surgery using a high-sensitivity cardiac troponin T assay (Roche hs-cTnT). A level of >15 ng/L is considered abnormal and termed a positive troponin leak, while >100 ng/L is considered suspected acute coronary syndrome (ACS). One hundred and sixty patients (n=66 THR, n=55 NoF hip replacement, n=39 TKR) were included. Sixty-eight patients (42%) had a positive troponin leak, and in 6 of these cases ACS was suspected. The highest prevalence of troponin leak was recorded in patients undergoing NoF hip replacement (62%), followed by TKR (46%) and then THR (24%). Sixty-two patients (38%) had positive troponin levels on day 1 and 53 patients (33%) had positive levels on day 3. Important patient cardiac risk factors were identified in the presence of a positive troponin leak, with ischaemic heart disease, hypertension, diabetes, renal disease, age >65 years and atrial fibrillation being statistically most likely. Postoperative troponin surveillance is an inexpensive and reliable way to identify patients at risk of MINS and subsequently enhance early detection, medical optimisation and referral strategies. Simple interventions may improve outcomes and contribute to lower ACS rates and the timeous prevention of other complications. The prevalence of MINS in orthopaedic-specific patients in South Africa (SA) and other resource-constrained developing countries is unknown. Our finding of 42% positive troponin leaks raises awareness of this issue, and we recommend routine postoperative troponin surveillance for all arthroplasty units in SA.

Update on a no-cost epilepsy gene panel for seizure onset between 2 and 4 years of age: Results from 682 tests

A young child presented with severe ventricular dysfunction and troponin leak in the setting of coronavirus disease-2019. He developed intermittent, self-resolving, and hemodynamically insignificant episodes of complete heart block that were diagnosed on telemetry and managed conservatively. This report is the first description of coronavirus disease-2019–induced transient complete heart block in a child. (Level of Difficulty: Intermediate.)

EXPRESS: Myocardial Bridge - An Unrecognized Cause of Chest Pain in Pulmonary Arterial Hypertension.

Pulmonary arterial hypertension (PAH) is characterized by an increased pulmonary vascular resistance resulting in progressive right ventricular hypertrophy and failure. While dyspnea on exertion is the leading symptom at diagnosis, the occurrence of chest pain, although less frequently observed, is an alarming symptom that requires immediate diagnostic work-up.Here we report the case of a 44-year-old woman with severe end-stage group 1 PAH who had repetitive occurrences of chest pain that led to frequent emergency room visits with documented signs of myocardial ischemia on EKG and troponin leaks. A computed tomography (CT) angiogram of the coronary arteries revealed the presence of a myocardial bridge (MB). An invasive coronary angiogram confirmed a MB over the left anterior descending (LAD) artery compressing the lumen of the LAD. As the patient was deteriorating on maximal medical PAH therapy, she was listed for, and subsequently received, a bilateral lung transplantation. Recognizing that the MB would pose a significant risk for ischemia during surgery as well as continuing source for chest pain after lung transplantation, the MB was surgically “unroofed” during the transplant surgery. The patient did well after surgery and did not complain of any residual chest pain.In conclusion, a MB compressing a segment of the coronary artery could be an under-diagnosed, but potentially not so rare cause of recurrent chest pain in PAH patients, which requires specialized diagnostic evaluation and treatment

Carbon monoxide poisoning can act as a stress test to reveal underlying coronary artery disease: case report

Carbon monoxide (CO) poisoning presents with many different cardiac effects, but one important presentation is its effect as a CO stress test to reveal underlying coronary artery disease (CAD). There are a limited number of publications detailing this phenomenon, but after CO intoxication it is important to suspect CAD in association with mild troponin leak or non-ST segment elevation myocardial infarction (NSTEMI) shown on electrocardiogram (EKG). We recently treated three patients with CO poisoning who had underlying CAD. In the first case a man presented to the emergency department with CO toxicity and an ST segment elevation myocardial infarction (STEMI), resulting in emergent angioplasty and the discovery of severe CAD. The second case involved an individual who presented with CO poisoning with rising troponin levels. An angioplasty discovered a stable 90% occlusion. The third case was a patient with CO poisoning and transient inferior T wave inversion EKG with borderline troponin elevation. Angioplasty showed only 30% occlusion, so the patient's presentation was likely due to direct CO cardiac toxicity. These cases demonstrate the varied presentations that CO poisoning can have on patients with underlying heart disease.

LEGIONELLA MICDADEI: A CASE OF CULTURE NEGATIVE NATIVE MITRAL VALVE ENDOCARDITIS

SESSION TITLE: Monday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/21/2019 02:30 PM - 03:15 PM INTRODUCTION: Legionella is a Gram-negative bacteria that is most commonly associated with pneumonia. We describe a rare case of native valve endocarditis caused by a Legionella isolated from mitral valve tissue. CASE PRESENTATION: A 29-year-old male with a history of stroke with no residual deficits and Mitral valve (MV) endocarditis presented with slurred speech and left facial droop which lasted for 30 seconds after which it resolved completely. Prior to admission, he reported fevers, chills, and night sweats. Medical history was notable for lupus nephritis diagnosed one year ago on azathioprine and mycophenolate. He denied any intravenous drug use. A grade 2/6 holosystolic murmur was heard at the left lower sternal border to the apex. He was febrile to 101.2 F, heart rate of 114 bpm, blood pressure 106/62 mm Hg. Labs were significant for a small troponin leak. Blood cultures were sterile. CT head showed mild encephalomalacia on the left insula. Transthoracic echocardiogram showed severely dilated left atrium and new mobile echo density located laterally on the mitral annulus and transesophageal echocardiogram showed MV dehiscence. He was started on empirical coverage for culture-negative endocarditis and was transferred to surgery. He underwent Redo sternotomy and redo mitral valve replacement with a St. Jude’s mechanical prosthesis. The valve tissue appeared very friable, possibly infected and it was debrided and sent to microbiology for culture and polymerase chain reaction [PCR]. PCR was positive for Legionella micdadei. He was discharged with appropriate antibiotics. DISCUSSION: This case is another example of culture-negative legionella endocarditis diagnosed using infected valve tissue. Extrapulmonary manifestations of Legionella infections (septic arthritis, myocarditis, pericarditis, and endocarditis) often occur in immunocompromised patients and are most often treated with fluoroquinolones. Diagnostic tests for culture-negative endocarditis include special culturing techniques, molecular techniques e.g., PCR and serologic assays, and histopathology evaluation of valvular tissue when surgical excision is performed. CONCLUSIONS: Legionella species should be considered in the differential diagnosis of culture-negative endocarditis in both immunocompetent and immunocompromised patients. Reference #1: Pearce, M. M., Theodoropoulos, N., Noskin, G. A., Flaherty, J. P., Stemper, M. E., Aspeslet, T., ... Reed, K. D. (2011). Native valve endocarditis due to a novel strain of Legionella. Journal of Clinical Microbiology, 49(9), 3340-3342. Reference #2: Park D, Pugliese A, Cunha BA. Legionella micdadei prosthetic valve endocarditis. Infection. 1994;22(3):213–215. Reference #3: Chen TT, Schapiro JM, Loutit J. Prosthetic valve endocarditis due to Legionella pneumophila. J Cardiovasc Surg. 1996;37(6):631–633 DISCLOSURES: No relevant relationships by Mohammed Essa, source=Web Response No relevant relationships by Karthik Gonuguntla, source=Web Response No relevant relationships by Gaurav Manek, source=Web Response No relevant relationships by Shivaraj Patil, source=Web Response

GIANT CELL MYOCARDITIS: A SILENT BUT DEADLY KILLER

SESSION TITLE: Cardiovascular Cases SESSION TYPE: Med Student/Res Case Report PRESENTED ON: 10/22/2019 3:45 PM - 4:45 PM INTRODUCTION: Giant cell myocarditis (GCM) usually affects previously healthy adults and is a rapidly progressive and frequently fatal disease, accounting for approximately 17% of all myocarditis fatalities. Early diagnosis is critical, with evidence showing rapidly instituted cyclosporine-based immunosuppression can improve transplant-free survival. CASE PRESENTATION: A 56 year old male with a history of Type 2 Diabetes presented with 1 week of exertional dyspnea and lightheadedness. Initial exam and tests were remarkable for a mild Troponin leak. EKG revealed Left bundle branch block and transthoracic echocardiogram (TTE) showed a normal ejection fraction (EF) and Left Ventricular (LV) internal Dimension-Diastole of 5.4cm. Stress test, nuclear imaging and Left Heart Catheterization were normal. An event monitor documented exercise induced bradycardia leading to the placement of a dual chamber pacemaker. Repeat ECHO done at the time showed normal EF and a mild circumferential pericardial effusion. In the following two months the patient developed worsening exertional dyspnea (NYHA III). A CT angiogram revealed a large pericardial effusion with tamponade physiology. The aspirate showed 304 cells with 94% monocytes, protein of 4.4g/dl, and cytology revealed reactive mesothelial and chronic inflammatory cells. CRP was elevated. Repeat ECHO showed LV EF of 30% with akinesis of inferior and inferolateral wall as well as diffuse hypokinesis and severely increased RV size and RV thrombus. He was begun on anticoagulation. Subsequently, right heart catherization showed elevated RA pressures and cardiac MRI showed Biventricular dilation and nondiagnostic delayed gadolinium enhancement imaging. Endomyocardial biopsy from RV was not suggestive of GCM. Patient subsequently developed progressive cardiogenic shock requiring dual Ventricular Assist Device placement. On analysing excised core of LV apex for cannula placement, it revealed granulomatous myocarditis with Giant cell formation and pericarditis. He was started on milrinone, high dose steroids and anticoagulation for suspected GCM. An RVAD was placed. Eventually patient returned with fulminant septic shock and died. DISCUSSION: This case reveals the rapidly progressive nature of GCM,which from presentation, has a median survival of 3 months to death or transplant without appropriate therapy. Biopsy is diagnostic in >70% cases if done early, however false negatives are frequent due to the patchy nature of the disease CONCLUSIONS: With immunotherapy, the 5-year survival rate free of transplant is between 52-72%. Transplant is an effective strategy however GCM can recur in around 25% of transplanted hearts. Reference #1: Giant Cell Myocarditis: A Brief Review ; Arch Pathol Lab Med. 2016 Dec;140(12):1429-1434 : Xu J, Brooks EG Reference #2: Diagnosis, Treatment, and Outcome of Giant-Cell Myocarditis in the Era of Combined Immunosuppression;Riina Kandolin, Jukka Lehtonen, Kaisa Salmenkivi: DOI:10.1161/CIRCHEARTFAILURE.112.969261 Reference #3: Idiopathic Giant-Cell Myocarditis — Natural History and Treatment; Leslie T. Cooper, Jr., Gerald J. Berry : N Engl J Med 1997; 336:1860-1866 DISCLOSURES: No relevant relationships by Tanya Chandra, source=Web Response No relevant relationships by Abhas Khurana, source=Web Response No relevant relationships by Osama Mukarram, source=Web Response No relevant relationships by Anand Muthu Krishnan, source=Web Response No relevant relationships by Rudra Ramanathan, source=Web Response No relevant relationships by Nitya Sthalekar, source=Web Response

“Mini- Stroke” with Troponin Leak in a Child with Left Ventricular Cardiac Myxoma

“Mini- Stroke” with Troponin Leak in a Child with Left Ventricular Cardiac Myxoma

742. “Troponin Leaks” in Patients with Acute Respiratory Viral Infections Enrolled in SUPERNOVA: A Marker of Worse Clinical Outcomes

BackgroundCardiac troponin I (cTnI) is a specific marker of cardiac muscular injury. Many patients hospitalized with acute respiratory illness (ARI) have elevated cTnI levels but do not meet EKG criteria for an acute ischemic cardiac event. Troponin leaks could be due to demand ischemia or acute inflammation of the myocardium. We hypothesized that patients with viral ARI and elevated cTnI have worse cardiopulmonary outcomes than those with viral ARI and normal cTnI.MethodsFrom November 11, 2016–September 30, 2017 nasopharyngeal swabs from patients enrolled in SUPERNOVA ARI Study, a CDC/2-VA site, active surveillance platform to evaluate the incidence of viral infection in patients hospitalized with symptoms and/or signs of ARI, were tested using a FilmArray Respiratory Panel. Based on detection of any virus, patients were categorized as positive (vPCR+) or negative (vPCR−). Patient enrolled at the Houston site with cTnI obtained <48 hours of admission were included in the analysis. cTnI above upper limit of normal (>0.03 ng/dL) was defined as elevated. Demographic and clinical data were abstracted from chart review. Outcomes were myocardial infarction (MI) on admission, 30- and 90-day re-admissions due to cardio-respiratory illness and 30- and 90-day all-cause mortality. For the univariable analysis of baseline factors and outcomes we used unpaired t-tests for continuous variables and χ2 or Fisher exact test for categorical variables as appropriate.ResultsNinety-four of 332 cases were vPCR positive and cTnI levels on admission were available in 86. Demographics and comorbidities were all similar for the high (N = 42) and normal (N = 44) cTnI groups. Compared with normal cTnI group, those with high cTnI had similar 30- and 90-day readmission rates (14% vs. 9%, P = 0.4 and 26% vs. 16%, respectively, P = 0.2). However, 30- and 90-day mortality rates were higher for high cTnI patients (10% vs. 0% and 19% vs. 5%, P < 0.03).ConclusionTroponin elevation on patients with a documented viral respiratory infection is associated with higher 30- and 90-day mortality rates. Troponin leaks should not be dismissed as a trivial finding in this group of patients. Further work on its pathogenesis is warranted.Disclosures All authors: No reported disclosures.

Survival Outcome of Patients in Acute Variceal Bleeding With Acute Coronary Syndrome Discharged on Anti-Platelet Agents

Introduction: Acute variceal bleeding is one of major and killing complication of advanced liver disease, and these patients are not immune from developing acute coronary syndrome. Data regarding outcome of patients with acute variceal bleeding with acute coronary syndrome is scarce. The aim of this study was to look for survival outcome of those patient who were discharged on anti-platelet agents. Methods: All the patients diagnosed with acute variceal bleeding based on gastroscopy along with acute coronary syndrome based on troponin leak with or without EKG changes, presented at The Aga Khan University Hospital, from February 2002 to February 2017 were included in the study. The medical records were reviewed to evaluate the survival outcome for 1 year. Results: Out of 39 files that were coded (ICD-9) with acute variceal bleeding and acute coronary syndrome, only data of 27 patients could be retrieved, out of them, 3 patients had no active bleeding at the time of acute coronary syndrome and 1 patient had ulcer bleed so excluded from study. So only 23 patients were included in the study. The mean age of patient 59.22 ± 11 years, 17 (74 %) of the patients were males. 10 (44 %) patients had child pugh C liver disease, followed by 8 (35 %) with child pugh B liver disease. Overall 7 (30%) had also underlying hepatocellular carcinoma. 12(52 %) patient had underlying ischemic heart disease. Out of 23, 7 (30 %) patients died during same admission, and out of 7 patients only one patient was on dual antiplatelet agents. Out of remaining 16 (70 %) patients, 4 (18 %) patients lost to follow up after discharge. Only 12 patients followed for 1 year survival and out of them only 3 patients were started on single antiplatelet agents (2 patients discharged on asprin and one patient on clopidogrel). 9/12 patients survived over 1 year and those patients with antiplatelet agent didn't developed re-bleeding. Still results are pre-liminary, final result may have little change. Conclusion: Survival outcome in patients with variceal bleeding with acute coronary syndrome is not good, and fear of re-bleed stops to offer antiplatelet agents in this setting, which is other wise, standard treatment for acute coronary syndrome. Comparing risks versus benefit, single antiplatelet agent looks relatively safer option, which can be offered cautiously in such dilemmas, after achieving hemostasis. For validation, large scale prospective studies should be considered.

Coronary artery compression from epicardial leads: More common than we think

A child with an epicardial pacemaker presented with sudden death at our institution, secondary to coronary artery compression. This case prompted enhanced surveillance of all patients with epicardial pacing or defibrillation systems. The purpose of this study was to determine the incidence of coronary artery compression and the diagnostic yield of catheter angiography (CA) and computed tomography (CT). All patients with epicardial leads who underwent CA or cine CT were retrospectively reviewed. A patient with postmortem diagnosis of coronary compression was also included. Coronary compression was noted in 8 of 145 patients (5.5%) with epicardial leads. Median age at diagnosis was 11.4 years (range 3.0-29.6 years). Six patients had compression noted by CA, 6 by CT, and 1 by postmortem analysis. Chest radiography had sensitivity and specificity of 57% and 96%, respectively; CT 100% and 93%, respectively; and CA 86% and 100%, respectively. There was no difference in age or weight at the time of lead implant between those who did and those who did not have compression (age: median 1.3 vs 2.4 years; P = .36; weight: 9.5 vs 11.8 kg; P = .46). Among those with coronary compression, 6 of 8 (75%) had symptoms (1 sudden death, 3 chest pain [2 with associated troponin leak]), 2 unexplained fatigue). Seven patients had surgical repositioning of their lead. We found a higher incidence of coronary artery compression by epicardial leads (5.5%) than previously reported in the literature. Chest radiography can serve as a good surveillance tool, with cine CT scans considered in those with concerning radiographs or with symptoms. Confirmatory CA can be performed before surgical intervention.

What is hot …

It is not unusual for high sensitivity cardiac troponin (cTnT) to be measured when a patient presents to hospital with chest symptoms. Often the result can be slightly raised despite the primary problem not being cardiac. It seems logical that a severe pneumonia may cause a troponin leak by causing strain on the heart. This study by Vestjens et al (http://dx.doi.org/10.1111/resp.12996) sought to see if elevated troponin is a prognostic marker in patients admitted with community-acquired pneumonia (CAP).The study looked at cTnT levels on admission in 295 patients admitted with CAP. Levels were elevated (>14 ng/L) in 45%. Short-term (30 days) and long-term (up to 4.1 years) mortality were significantly higher in those with elevated cTnT. Elevated cTNT >28 ng/L was found to be a strong independent risk factor for mortality both short-term (OR 21.9, 95% CI 4.7 to 101.4) and long-term (OR 10.7, 95% CI 5.0 to 22.8). The study also combined troponin levels with the Pneumonia Severity Index (PSI) and found this was a stronger predictor of short-term mortality than PSI score alone. …

Cardiac Vignette: Ruptured Coronary Sinus of Valsalva

A 35-year-old male with no significant past cardiac history presented to our institution with chest pain, dyspnoea and palpitations. On presentation, he was hypotensive and tachycardic. Examination revealed a Grade IV pansystolic murmur, loudest over the left parasternal region. Electrocardiogram revealed sinus tachycardia, right-axis deviation and right bundle branch block morphology. Blood tests showed a high sensitivity troponin leak of 900. Computed tomographic pulmonary angiography revealed right lower lobe segmental pulmonary embolus. Bedside transthoracic echocardiogram revealed a severely dilated right ventricle (RV) with severe impairment of systolic function. Left ventricular (LV) function was normal. Colour Doppler showed presence of a shunt between the LV and right atrium (RA) in the superior aspect of the septal leaflet. Transoesophageal echocardiography demonstrated a dilated RA and RV with a small peri-membranous ventricular septal defect located high in the interventricular septum with turbulent flow from the LV to the RV. An additional shunt was observed from the LV into the RA. Overall findings were consistent with a ruptured coronary sinus of Valsalva. The patient had a complicated clinical course with cardiogenic shock, acute liver injury and renal impairment. Decision was made for cardiothoracic intervention. Repair of sinus of Valsalva from the aortic non-coronary sinus to the right atrium with repair of the aortic valve and closure of secundum atrial septal defect. The patient had an uneventful intra-operative and postoperative course. Aneurysm of the coronary sinus of Valsalva is a rare congenital cardiac anomaly. Multimodality imaging is essential for accurate diagnosis and management.

Clozapine in a patient with treatment-resistant schizophrenia and hypertrophic cardiomyopathy: a case report.

BackgroundThere is currently limited experience in the initiation and maintenance of clozapine for treatment-resistant psychosis in adults with established structural heart disease. These complex patients require close supervision and liaison between colleagues. Here we present the successful experience of treating one such patient within our service and describe a monitoring plan to ensure that these treatments can be provided both safely and effectively.Case presentationA 36-year-old man with treatment-resistant schizophrenia and known hypertrophic cardiomyopathy (HCM) was admitted to a specialist unit for a trial of clozapine. His psychiatric illness was characterised by multimodal hallucinations and delusions combined with low mood and poor motivation. The diagnosis of HCM was made 3 years previously following a routine electrocardiogram (ECG), and he had remained asymptomatic throughout this time; there were concerns about the risk of initiating clozapine given his pre-existing cardiac condition.Baseline investigations were performed as per local guidelines prior to commencing clozapine; these were within normal limits other than a mildly raised troponin level of 54 ng/L (normal <16 ng/L), which was attributed to the HCM. In addition, baseline transthoracic echocardiography (TTE) was performed which showed no change in the structural heart disease in comparison with previous TTEs.Clozapine was started at 12.5 mg daily and up-titrated to 150 mg twice daily over 14 days as per our institute’s guidelines. The patient was monitored with regular testing of troponins, inflammatory markers and ECG. On day 18, the troponin level increased to 1371 ng/L. Creatine kinase and inflammatory markers remained stable. No changes in ECG or TTE were noted and the patient remained clinically asymptomatic.Cardiology opinion was sought and reported that the finding of an isolated elevated troponin was likely to reflect a ‘troponin leak’ in the context of increased cardiac muscle mass associated with HCM. In the absence of any clinical compromise, it was not felt to be of concern. Clozapine was continued with good effect on mental state. Troponin levels gradually reduced and the patient remained well.ConclusionsWhile multiple cases of clozapine-induced cardiotoxicity have been reported in the literature, its implications for pre-existing structural disease are unclear. This case report suggests that clozapine can be safely introduced in pre-existing HCM, explores strategies for monitoring and highlights the importance of liaising with experienced cardiologists.Declaration of interestNone.Copyright and usage© The Royal College of Psychiatrists 2016. This is an open access article distributed under the terms of the Creative Commons Non-Commercial, No Derivatives (CC BY-NC-ND) license.

Surgical Apgar score is associated with myocardial injury after noncardiac surgery

Study ObjectiveTo assess the impact of intraoperative hemodynamics in the development of perioperative myocardial infarction (MI) and myocardial ischemia after noncardiac surgery. DesignSingle-center retrospective cohort study of surgical patients from 2007 to 2012. SettingPostanesthesia care unit, intensive care unit, and medical-surgical ward at an academic tertiary medical center. PatientsA total of 46,799 adult noncardiac, nonthoracic surgery patients, for which 2290 peak cardiac troponin (cTn) levels were available. MeasurementsThe 10-point Surgical Apgar Score (SAS) was calculated from intraoperative heart rate, blood pressure, and blood loss. Peak troponin (cTn) levels, hospital length of stay, 7- and 30-day postoperative mortality, patient demographics, and prior medical conditions were gathered. Troponin leak was defined as cTn-I 0.6 to 1.5 ng/mL or cTn-T 0.1 to 0.3 ng/mL; perioperative MI criteria were cTn-I greater than 1.5 ng/mL or cTn-T greater than 0.30 ng/mL. Main resultsOf 46,799 noncardiac surgical cases, 209 (0.4%) and 192 (0.4%) suffered cTn leak and MI, respectively. Low SAS (0-4) was associated with increased risk of cTn leak and perioperative MI (univariate odds ratio, 2.76 and 2.06; 95% confidence interval, 2.20-3.45 and 1.57-2.70, respectively). In multivariable analysis, Surgical Apgar Score, age 65 years or older, American Society of Anesthesiologists physical status greater than or equal to III, emergency surgery, history of MI or hypertension, prolonged intraoperative tachycardia (heart rate >100 beats/min for >59 minutes), and prolonged hypotension (mean arterial pressure <40 mm Hg for >2 minutes) were independently associated with cTn leak and perioperative MI. ConclusionsLow SAS scores (0-4) may be associated with cTn elevation after noncardiac surgery. SAS-based risk stratification may guide perioperative cTn surveillance in lieu of routine postoperative screening.

Electrocardiography changes in acute aortic dissection—association with troponin leak, coronary anatomy, and prognosis

BackgroundElectrocardiography (ECG) offers some information that may be used to prognosticate acute type A aortic dissection (AAOD) for short- and long-term mortality. MethodsWe retrospectively analyzed the electrocardiograms of patients with AAOD admitted from March 2004 to March 2015. The frequency of ECG findings and their prognostic value on hospital and follow-up mortality were investigated. Findings pertaining to coronary involvement and troponin level were also examined. ResultsA total of 120 men and 64 women were admitted. Acute ischemic changes were reported in 38.0%, whereas T inversion was the most common recorded abnormality, which occurred in 38.6%. Acute ST-elevation myocardial infarction was detected in 16.3%. Troponin increased in 36.6%; 21.9% of the patients underwent coronary angiography among which 70% were normal. Coronary involvement or troponin increase was not different in patients with acute ECG changes. During hospitalization, 45.7% of the patients died. In multivariate analyses, ST elevation in lead aVR was associated with higher hospital death (odds ratio, 5.30; 95% confidence interval, 1.09-25.73; P = .038), whereas QRS greater than 120 milliseconds was associated with long-term mortality (hazard ratio, 2.45; 95% confidence interval, 1.25-3.76; P = .006). ConclusionAcute ischemic ECG changes are common in AAOD, and a completely normal ECG is infrequently encountered. Acute ECG changes were not associated with the increased troponin or the presence of coronary lesions in angiography.

Feature Tracking-Derived Peak Systolic Strain Compared to Late Gadolinium Enhancement in Troponin-Positive Myocarditis: A Case-Control Study.

Cardiac magnetic resonance (CMR) assesses myocardial involvement in myocarditis (MYO). Current techniques are qualitative, subjective, and prone to interpretation error. Feature tracking (FT) analyzes myocardial strain using CMR and has not been examined in MYO. We hypothesize that regional left ventricular (LV) strain is abnormal in MYO. Regional strain by FT was compared to late gadolinium enhancement (LGE) and troponin leak as measures of myocardial involvement. This single-center, retrospective CMR study reviewed patients with clinical MYO and structurally normal hearts who underwent CMR at our institution. Young adults with normal cardiac anatomy, function, and absent LGE served as controls. MYO patients with documented troponin leak and normal global ejection fraction (EF > 50 %) were included in comparison. FT determined regional myocardial peak systolic strain (pkS) in longitudinal and circumferential distributions. T tests compared strain values between cases and controls. Receiver operating characteristic curves determined pkS values with highest sensitivity and specificity for concurrent troponin leak and LGE. FT was performed on 57 patients: 37 MYO and 20 controls. Twenty-eight cases with normal EF, and 20 control patients were included in final analysis. Nearly all cases with normal function demonstrated abnormal regional pkS (27/28, 96 %). Cases had significantly diminished pkS when compared to controls in all regions except the longitudinal 2C distribution. FT-derived longitudinal and circumferential pkS is sensitive and specific in identifying myocardial involvement, namely the presence of troponin leak and LGE. FT may be a useful adjunctive, objective measure of myocardial involvement in patients with MYO and normal LV function.

Catecholamine Surge during Image-Guided Ablation of Adrenal Gland Metastases: Predictors, Consequences, and Recommendations for Management

PurposeTo identify retrospectively predictors of catecholamine surge during image-guided ablation of metastases to the adrenal gland. Materials and MethodsBetween 2001 and 2014, 57 patients (39 men, 18 women; mean age, 65 y ± 10; age range, 41–81 y) at two academic medical centers underwent ablation of 64 metastatic adrenal tumors from renal cell carcinoma (n = 27), lung cancer (n = 23), melanoma (n = 4), colorectal cancer (n = 3), and other tumors (n = 7). Tumors measured 0.7–11.3 cm (mean, 4 cm ± 2.5). Modalities included cryoablation (n = 38), radiofrequency (RF) ablation (n = 20), RF ablation with injection of dehydrated ethanol (n = 10), and microwave ablation (n = 4). Fisher exact test, univariate, and multivariate logistical regression analysis was used to evaluate factors predicting hypertensive crisis (HC). ResultsHC occurred in 31 sessions (43%). Ventricular tachycardia (n = 1), atrial fibrillation (n = 2), and troponin leak (n = 4) developed during HC episodes. HC was significantly associated with maximum tumor diameter ≤ 4.5 cm (odds ratio [OR], 26.36; 95% confidence interval [CI], 5.26–131.99; P < .0001) and visualization of normal adrenal tissue on CT or MR imaging before the procedure (OR, 8.38; 95% CI, 2.67–25.33; P < .0001). No HC occurred during ablation of metastases in previously irradiated or ablated adrenal glands. ConclusionsPatients at high risk of catecholamine surge during ablation of non–hormonally active adrenal metastases can be identified by the presence of normal adrenal tissue and tumor diameter ≤ 4.5 cm on pre-procedure CT or MR imaging.

PC140. Routine Postoperative Troponin Testing Following Major Vascular Surgical Procedures Carries Short-Term and Long-Term Prognostic Significance

This study determined the utility of routine postoperative troponin T (PO TnT) measurements in patients undergoing major vascular surgical reconstructions (VSRs). Data from consecutive patients undergoing VSRs and routine PO TnT measurement from 2010 to 2012 were retrospectively analyzed. An elevated Tn was >0.01 ng/mL within the current admission, further characterized as low (0.02-0.2 ng/mL) and high (>0.2 ng/mL). Patients without complete Tn panels or research authorization were excluded. Cox proportional hazards model was used to evaluate the effect of preoperative risk factors, type of procedure and PO TnT levels on early-term and long-term mortality. Of 1814 patients undergoing VSRs over the 3-year period, 1632 (1136 males, 496 females; mean age 70 years) met inclusion criteria. There were 1088 open, 529 endovascular, and 15 hybrid procedures. TnT levels were >0.01 ng/mL in 394 patients (24%). Of these, 56 were attributed to non-ST segment elevation myocardial infarction, 6 ST segment elevation myocardial infarction, 46 demand ischemia, 22 miscellaneous cardiac abnormalities, 96 renal insufficiency, and 168 had asymptomatic troponin leaks. Medical management was optimized in all patients. Coronary catheterizations were performed in 13 patients and intervention in seven. Thirty-day mortality was significantly higher in Tn+ vs Tn– patients (2.9% vs 0.7%, P < .001). On multivariate analysis, elevated Tn (hazard ratio [HR], 2.7; P < .001), Society for Vascular Surgery/American Association for Vascular Surgery Score (HR, 1.08 per 1 point; P < .01) and age (HR, 1.20 per 10 years; P < .05) were associated with mortality. Cumulative probability of death in Tn+ patients remained significantly higher at 1 (13% vs 3%), 2 (17% vs 4%), and 4 years (31% vs 10%; P < .001) and was directly proportional to the maximum Tn level (P < .001, Fig). Comparison of the 168 patients with asymptomatic Tn leaks to Tn– patients yielded similar results, with significantly higher mortality at 30 days (2.5% vs 0.7%), 1 (7% vs 3%), 2 (12% vs 4%), and 4 years (25% vs 10%; P < .001). Elevated TnT levels, including mild asymptomatic elevations, following major VSRs are independently associated with higher early-term and long-term mortality. Routine Tn testing is worthwhile and serves to risk-stratify patients for future medical and surgical care.

High sensitivity troponin T in adult congenital heart disease

BackgroundHigh sensitivity troponin T (hsTnT) assays enable us to detect chronic heart failure (CHF). Adult congenital heart disease (ACHD) patients are classified as being in at least stage B of CHF. The purpose of the study was to assess hsTnT levels in ACHD patients and determine its clinical significance. MethodsThis is a prospective cross-sectional study. We assessed hsTnT in 131 ACHD patients and in 30 healthy controls. All ACHD patients underwent routine clinical and echocardiographic evaluation and had hsTnT and N-terminal brain natriuretic peptide (NT-pro-BNP) level measurements. ResultsThe cut-off value defining an abnormal hsTnT level was established as >0.005ng/mL. 35.1% (n=46) of ACHD patients had abnormal hsTnT compared to 6.7% (n=2) of healthy controls (p=0.002). The prevalence of elevated hsTnT did not differ between simple and complex and between non-cyanotic and cyanotic congenital heart disease (CHD). The sensitivity and specificity of hsTnT for the detection of moderate or severe (significant) systemic ventricular dysfunction was 78.6% and 69.8%, respectively (OR 8.49; CI 95% 2.23–32.30; p<0,0001) whereas for significant pulmonary ventricular dysfunction it was 66.7% and 68.2%, respectively (OR 4.29; CI 95% 1.56–11.79; p=0.003). In multivariate logistic regression models elevated hsTnT, but not NT-pro-BNP, was independently associated with both significant systemic ventricular dysfunction (p=0.004) and significant pulmonary ventricular dysfunction (p=0.011). ConclusionsA troponin leak is observed in a substantial number of ACHD patients and is associated with significant systemic and pulmonary ventricular impairment. Compared to NT-pro-BNP, hsTnT is a more specific independent predictor of ventricular dysfunction in ACHD.