Peak Troponin Research Articles

Rescue transventricular off-pump mitral valve repair with artificial neochords for acute mitral regurgitation due to postinfarction papillary muscle rupture.

BackgroundWe report 3 cases of rescue transventricular off-pump mitral valve (MV) repair in high-risk patients with acute mitral regurgitation (MR) due to post–myocardial infarction (MI) papillary muscle rupture (PMR).MethodsThe 3 patients presented with acute inferior ST elevation myocardial infarction, cardiogenic shock, and pulmonary edema. Their preoperative peak troponin I levels were 1909 ng/L, 16,963 ng/L, and 8299 ng/L. All 3 patients underwent successful percutaneous intervention to the culprit coronary artery, and antiplatelet therapy was initiated. All patients required inotropic support and had an intra-aortic balloon pump inserted preoperatively. Transesophageal echocardiography (TEE) demonstrated severe eccentric MR due to the leaflet prolapse secondary to PMR. The patients’ estimated EuroSCORE II scores were 16.03%, 16.68%, and 7.81%, and their Society of Thoracic Surgeons scores were 14.77%, 18.24%, and 9.8%, respectively. All 3 patients underwent urgent transventricular off-pump MV repair using artificial chords, with 2 or 3 three neochords implanted. The duration of operation was <2 hours, and intraoperative and postoperative drainage was minimal in all cases. MV function was assessed by qualitative and semiquantitative TEE.ResultsIntraoperative MR reduction to a mild level was achieved in all 3 patients. All patients had moderate MR at discharge, likely due to left ventricular remodeling. Severe MR recurred in all patients, at 5, 4, and 2 months of follow-up, respectively. All 3 patients underwent an elective MV reoperation via conventional approach.ConclusionsOff-pump transventricular MV repair may offer a safe and feasible alternative to stabilize high-risk patients with acute MR due to post-MI PMR. Although early MR recurrence is concerning, urgent transventricular MV repair may serve as a bridge to conventional surgery in such unstable patients.

IMPACT OF ADMISSION TROPONIN AND TROPONIN RISE DURING HOSPITALIZATION ON MORTALITY IN COVID-19 PNEUMONIA WITH ACUTE RESPIRATORY FAILURE

TOPIC: Chest Infections TYPE: Original Investigations PURPOSE: COVID-19 can cause multi-organ failure and death. Troponin levels may be elevated in such patients from demand ischemia due to hypoxia versus direct myocardial injury. The information regarding association between troponin levels and mortality is limited in COVID 19 patients. In our study, we specifically determined the correlation of admission troponin as well as troponin rise during hospitalization in COVID-19 patients with acute respiratory failure with mortality. METHODS: Medical records of seventy one (71) patients with COVID-19 pneumonia and acute respiratory failure were reviewed to determine demographic features, admission troponin, rise in troponin (peak troponin - admission troponin) and survival. Pearson’s correlation analysis was performed to evaluate the correlation between admission troponin, rise in troponin and mortality. Independent t-test was used to determine the impact of admission troponin on hospital mortality. P < 0.05 was deemed statistically significant. RESULTS: Seventy-three percent (73%) of studied patients were male. Average age was 47.7 ± 16.7 years. Twenty-two percent (22%) of patients expired. Mean admission troponin was: 0.18 ± 1.1 ng/mL. Mean troponin rise (peak troponin - admission troponin) during hospital stay was: 0.7 ± 3.18 ng/mL. Admission troponin in survivors was 0.03 ± 0.04 ng/mL and in non-survivors was: 0.9 ±2.6 ng/mL (p = 0.02, independent t-test). Troponin rise in survivors was 0.7 ± 3.5 ng/mL and in non-survivors was: 0.55 ± 1.6 ng/mL (p=0.8, independent t-test). Pearson’s correlation analysis showed significant correlation between admission troponin and mortality (r = -0.292, p= 0.028) but no correlation between troponin rise and mortality (r = 0.02;p= 0.83). CONCLUSIONS: A higher troponin at admission has a significant correlation with mortality in COVID19 patients with acute respiratory failure. However, there was no significant correlation between rise in troponin levels and mortality which may have been due to a small sample size in our study. CLINICAL IMPLICATIONS: Troponin levels on admission can be utilized to predict outcomes in patients with COVID-19 pneumonia and acute respiratory failure. Further studies need to be done to determine whether a rise in troponin levels can also be predictor of mortality. Future studies can also determine if increased mortality is seen at specific troponin levels in patients with COVID 19 pneumonia DISCLOSURES: No relevant relationships by Debapriya Datta, source=Web Response No relevant relationships by Manasvi Gupta, source=Web Response No relevant relationships by Gaurav Manek, source=Web Response No relevant relationships by Suong Nguyen, source=Web Response

CASE OF MULTISYSTEM INFLAMMATORY SYNDROME IN CHILDREN (MIS-C) PRESENTING WITH RASH AND SHOCK

TOPIC: Critical Care TYPE: Fellow Case Reports INTRODUCTION: Multisystem inflammatory syndrome in children (MIS-C) is a multisystem inflammatory disorder sharing the clinical features of Kawasaki disease (KD) and toxic shock syndrome. CASE PRESENTATION: A 19-year-old male with no known past medical history presented to the emergency room with myalgia, headache, fever, photophobia, and rash on bilateral upper and lower extremities for more than one week. He tested positive for SARS-CoV-2 by RT-PCR 6 weeks prior to the presentation. Symptoms worsened with the development of a maculopapular skin rash, high-grade fevers, diarrhea, and vomiting. On admission he was afebrile (97.6 °F), had tachycardia (133/min) and tachypnea (48/min) along with hypotension (78/33 mmHg), and saturating 85% on 4L/min. Lab abnormalities included WBC of 28.2 k/uL with 55% bands, procalcitonin 42.91 ng/mL, lactic acid 4 mmol/L, BUN 65 mg/dl, serum creatinine 7 mg/dl and elevated D-dimer of 3.1 mg/L. Cardiac labs were remarkable for proBNP 76,275 pg/mL, and peak troponin 31.10ng/mL in 12 hours. EKG consistent with myopericarditis. CT scan of the abdomen/pelvis found edema of the cecum and ascending colon with pericolonic fat stranding of ascending colon possible mesenteric adenitis. He initially required 3 vasopressors to maintain his MAP>65mmHg. Echocardiography revealed a left ventricle ejection fraction (LVEF) of 20% with moderate global hypokinesis of the left ventricle. Cardiac catheterization revealed elevated wedge pressure and had clean coronaries with no aneurysms. MIS-C was suspected and was started on 1g/kg IVIG, high dose aspirin, methylprednisolone, and anakinra. Rash dissipated in days after starting steroids. His LVEF recovered to 55-60% prior to discharge from the hospital. He was kept on Anakinra, continued for 4 weeks till normalization of ferritin. DISCUSSION: MIS-C is a rare sequela of COVID-19 manifesting 2-8 weeks after the initial SARS-CoV-2 infection. In severe cases, cardiac involvement leads to cardiogenic shock. The echocardiographic findings of myocarditis and pericarditis have been frequently reported[1]. Inflammatory markers including ESR, C-reactive protein, ferritin, and IL-6 are reported to be elevated in all the cases [2]. Though its pathogenesis is not well defined, proposed hypotheses include hyper-immune response, macrophage activation, and T cell stimulation with a delayed cytokine storm. Various case have reported clinical outcomes with the use of intravenous immunoglobulin, corticosteroids, IL-1 inhibitor (anakinra), or IL-6 receptor inhibitor (tocilizumab) [3]. However, further research is needed to define clinical predictors and treatment modalities to manage MIS-C. CONCLUSIONS: Our case emphasizes the complexity of MIS-C with multisystem involvement, and it highlights a timely use of IVIG, high dose aspirin, anakinra, and methylprednisolone as potential therapeutics for this hyperinflammatory condition. REFERENCE #1: Alsaied T, Tremoulet AH, Burns JC, et al. Review of Cardiac Involvement in Multisystem Inflammatory Syndrome in Children. Circulation. 2021;143(1):78-88. doi:10.1161/CIRCULATIONAHA.120.049836 REFERENCE #2: Abrams JY, Godfred-Cato SE, Oster ME, et al. Multisystem Inflammatory Syndrome in Children Associated with Severe Acute Respiratory Syndrome Coronavirus 2: A Systematic Review [published online ahead of print, 2020 Aug 5]. J Pediatr. 2020;226:45-54.e1. doi:10.1016/j.jpeds.2020.08.003 REFERENCE #3: Tanner T, Wahezi DM. Hyperinflammation and the utility of immunomodulatory medications in children with COVID-19. Paediatr Respir Rev. 2020;35:81-87. doi:10.1016/j.prrv.2020.07.003 DISCLOSURES: No relevant relationships by Faran Ahmad, source=Web Response No relevant relationships by Sunil Nair, source=Web Response No relevant relationships by Sanu Rajendraprasad, source=Web Response

Assessment of Coronary Inflammation by Pericoronary Fat Attenuation Index in Clinically Suspected Myocarditis with Infarct-Like Presentation

Background: The pathophysiology of angina-like symptoms in myocarditis is still unclear. Perivascular fat attenuation index (pFAI) by coronary computed tomography angiography (CCTA) is a non-invasive marker of coronary inflammation (CI) in atherosclerosis. We explored the presence of CI in clinically suspected myocarditis with infarct-like presentation. Methods: We retrospectively included 15 consecutive patients (67% male, age 30 ± 10 years) with clinically suspected infarct-like myocarditis who underwent CCTA to rule out coronary artery disease. Right coronary artery (RCA) pFAI mean value was compared with that of healthy volunteers. Results: Mean RCA pFAI value was −92.8 ± 8.4 HU, similar to that of healthy volunteers (−95.2 ± 6.0, p = 0.8). We found no correlation between RCA pFAI mean values and peak Troponin I (r = −0.43, p = 0.11) and C-reactive protein at diagnosis (r = −0.25, p = 0.42). Patients with higher pFAI values showed higher biventricular end-systolic volumes (ESV) (p = 0.038 for left and p = 0.024 for right ventricle) and lower right ventricular ejection fraction (RVEF) (p = 0.038) on cardiovascular magnetic resonance. Conclusions: In clinically suspected myocarditis with infarct-like presentation, RCA pFAI values are lower than those validated in atherosclerosis. The correlation between higher pFAI values, higher biventricular ESV and lower RVEF, may suggest a role of pFAI in predicting non-atherosclerotic CI (i.e., infective/immune-mediated “endothelialitis”).

Comparison of Perioperative High-Sensitive Troponin T and Troponin I Assays in Cardiac Surgery

Troponin measurements are among the standard parameters for monitoring perioperative myocardial ischaemia after cardiosurgical procedures. As high-sensitive assays continue to replace older analytic parameters with lower sensitivity, this study aimed to compare perioperative profiles of a high-sensitive troponin T assay (hsTnT, Roche Diagnostics, Mannheim, Germany) with a troponin I assay (sTnI, Siemens Healthcare Diagnostics, Eschborn, Germany). A total of 287 consecutive patients undergoing a typical spectrum of cardiac procedures from August 2017 to March 2018 monitored with the hsTnT assay were compared with a propensity-matched collective analysed with the sTnI assay. For side-by side comparison, the peak troponin (Tmax) values were scaled to a z-score distribution before comparison. Despite absolute postoperative hsTnT and sTnI values differing by an order of magnitude, parameters could be scaled to a common distribution with kernel density curves overlapping 92%. Both parameters showed equal behaviour in subgroup analyses regarding relevant perioperative factors, such as type of procedure, cross-clamping time, and type of cardioplegic solution. However, there were some differences regarding pre-existing renal impairment between both parameters. In both groups, renal failure patients with chronic kidney disease stages IV or V as well as patients on haemodialysis exhibited a marked Tmax increase of >100% compared with normal kidney function (hsTnT,+121%; 2,383.5 vs 1,078.8 ng/L; p=0.0006; and sTnI,+149%; 27.3 ng/mL vs 11.0 ng/mL; p=0.009). However, in patients with moderately impaired renal function, those in the hsTnT group, but not in the sTnI cohort, showed significantly increased Tmax values (CKD stages II or III, 1,233.5 ng/L [+14%] and 1,314.1 ng/L [+22%] vs 1,078.8 ng/L; p=0.01 and p=0.03). In these patients, the postoperative interval until Tmax was reached was also significantly increased (14.4 and 19.0 hrs vs 12.4 hrs for chronic kidney disease stages II and III; p=0.0038 and p<0.001), indicating a higher rate of accumulation in the hsTnT parameter. In the context of cardiac surgery, this study found that both parameters behaved in a similar manner under most relevant circumstances. Despite significant difference in the absolute serum concentration, hsTnT and sTnI can be scaled to virtually identical distributions. However, renal impairment did affect both parameters differently with troponin T but not troponin I, showing evidence of accumulation in moderately impaired renal disease.

Cardiac Complications in Patients Hospitalised With COVID-19 in Australia

ObjectivesDescribe the incidence of cardiac complications in patients admitted to hospital with COVID-19 in Australia.DesignObservational cohort study.SettingTwenty-one (21) Australian hospitals.ParticipantsConsecutive patients aged ≥18 years admitted to hospital with laboratory confirmed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.Main outcome measuresIncidence of cardiac complications.ResultsSix-hundred-and-forty-four (644) hospitalised patients (62.5±20.1 yo, 51.1% male) with COVID-19 were enrolled in the study. Overall in-hospital mortality was 14.3%. Twenty (20) (3.6%) patients developed new atrial fibrillation or flutter during admission and 9 (1.6%) patients were diagnosed with new heart failure or cardiomyopathy. Three (3) (0.5%) patients developed high grade atrioventricular (AV) block. Two (2) (0.3%) patients were clinically diagnosed with pericarditis or myopericarditis. Among the 295 (45.8%) patients with at least one troponin measurement, 99 (33.6%) had a peak troponin above the upper limit of normal (ULN). In-hospital mortality was higher in patients with raised troponin (32.3% vs 6.1%, p<0.001). New onset atrial fibrillation or flutter (6.4% vs 1.0%, p=0.001) and troponin elevation above the ULN (50.3% vs 16.4%, p<0.001) were more common in patients 65 years and older. There was no significant difference in the rate of cardiac complications between males and females.ConclusionsAmong patients with COVID-19 requiring hospitalisation in Australia, troponin elevation was common but clinical cardiac sequelae were uncommon. The incidence of atrial arrhythmias and troponin elevation was greatest in patients 65 years and older.

Abstract P121: Combining Extracellular Matrix Biomarkers Using Cluster Analysis More Accurately Predicts The Development Of Systolic Dysfunction In Acute Myocardial Infarction Compared To Single Biomarker Analysis

Introduction: The extracellular matrix (ECM) is central to cardiac repair following acute myocardial infarction (AMI), and pathological ECM activity may result in adverse ventricular remodeling. Systolic dysfunction is a manifestation of adverse remodeling, and the utility of combined biomarker analysis for prognosis remains undetermined. Cluster analysis is a statistical methodology that can combine biomarkers, while also accounting for collinearity. Hypothesis: In this study, we assessed the hypothesis that combining biomarkers using cluster analysis may more accurately predict the development of systolic dysfunction in AMI patients when compared to single biomarker analysis. Methods: In a cohort of 120 AMI patients, plasma levels of matrix metalloproteinase (MMP) -3, -8, -9 and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) were measured using ELISA and multiplexing assays during hospital admission. All patients had an echocardiogram within 1 year of AMI (median [IQR], 145 [89 - 252] days). Patients were divided into impaired (n=37, LVEF &lt;50%) and preserved (n=83, LVEF ≥50%) systolic function. Hierarchical clustering was performed using Ward’s method of minimum variance. Mann-Whitney U and Chi-Squared testing was performed for univariate analysis, and binary logistic regression was performed for multivariate analysis. Results: Upon univariate analysis, current smoking, prescription of ACE inhibitor at discharge, peak Troponin T &gt; 610 ng/L (median), and MMP-8 levels were predictive of impaired systolic function. Cluster analysis partitioned patients into two clusters (Cluster One, n=31; Cluster Two, n=89). Cluster One comprised a higher proportion of patients with impaired systolic function when compared to Cluster Two (15 out of 31 [48.4%] versus 22 out of 89 [24.7%]). Upon multivariate analysis, Cluster One assignment (odds ratio [95% CI], 2.74 [1.04-7.23], p=0.04) remained an independent predictor of systolic dysfunction in combination with clinical variables, while MMP-8 levels did not (3.43 [0.32-36.68], p=0.308). Conclusion: Findings from our study demonstrate a combined biomarker approach outperforms single biomarker analysis for predicting the development of systolic dysfunction following AMI.

Association between tissue oxygenation and myocardial injury in patients undergoing major spine surgery: a prospective cohort study

ObjectiveTo describe the association between intraoperative tissue oxygenation and postoperative troponin elevation in patients undergoing major spine surgery. We hypothesised that a decrease in intraoperative skeletal muscle tissue oxygenation (SmO2)...

Takotsubo Syndrome Associated with Benzodiazepine Withdrawal: A Case Report

Since the 1960s, benzodiazepines have been a clinical mainstay, utilized for sedation, anxiety, and withdrawal states. Between 1996 and 2013 alone, benzodiazepine prescriptions increased annually by 2.5%. Rather than risk symptoms of withdrawal such as muscle pain and severe cardiomyopathy, patients must be properly informed about how to taper their medications. A 75-year-old female with a history of anxiety, hypertension, lupus, and degenerative disc disease presented with palpitations, mid-sternal chest pain, diaphoresis, and progressive shortness of breath. The patient was found to have elevated troponins (peak troponin of 1.45) and EKG showed sinus rhythm and ST segment abnormalities. The patient stated that her chest pain started 24 hours ago, 48 hours after she had stopped taking lorazepam which she had been taking for the past 50 years for anxiety. Her PCP gave her a plan to taper down the dose of lorazepam safely, but the patient opted to stop “cold turkey.” Due to the patient’s typical chest pain and elevating troponin level, ACS protocol was initiated. Initial echocardiogram showed an ejection fraction of 35-40% with hypokinesis of the anterioseptal wall with impaired left ventricular diastolic filling. The cardiology team performed a catheterization which showed minimal coronary artery disease and no significant stenosis in the left anterior descending artery. Within the next few days, the patient’s chest pain resolved and her troponins were negative. The medical team concluded that the physical stress from withdrawing from benzodiazepine caused the patient to go into Takotsubo Cardiomyopathy. This case illustrates the risks involved with benzodiazepine in an era of polypharmacy. More importantly, this case illustrates the strong need to taper benzodiazepines properly. Because this patient had taken a benzodiazepine for 50 years, the tapering should have been as slow as possible. The result was Takotsubo cardiomyopathy.

Establishment and validation of a new predictive equation with multiple risk factors for the development of cardiorenal syndrome type 1 in patients with acute myocardial infarction

Objective: To investigate the independent risk factors of cardiorenal syndrome type 1 (CRS1) in patients with acute myocardial infarction (AMI) and to build a predictive equation for the development of CRS1 in these patients. Method: Consecutive inpatients with AMI, who hospitalized from January 2017 to December 2018 in the Hunan Provincial People's Hospital, were enrolled in this case-control study. Patients were divided into CRS1 group and non-CRS1 group according to the presence or absence of CRS1.The clinical data were collected through the electronic medical record system of Hunan Provincial People's Hospital. The matching process was conducted with a minimum-distance scoring method and a 1∶1 match between the CRS1 group and the no-CRS1 group, the propensity score was calculated through the logistic regression model. Factors with statistically significant differences in univariate analysis were included in the multivariate logistic regression model to analyze the risk factors of AMI patients with CRS1, then the independent risk factors were used to establish a predicting equation for CRS1 by logistic regression function for model building. Area under the curve (AUC) value and the best cut-off value of the combined predictors was determined according to the ROC curve. Python 3.8 software was used to perform 10-fold cross-validation on modeling samples. Results: A total of 942 patients were included, there were 113 cases in CRS1 group and 829 cases in non-CRS1 group. Ultimately, 99 CRS1 patients were successfully matched to 99 non-CRS1 patient using 1∶1 matching. After propensity score matching, the baseline age and sex along with heart rate, mean arterial pressure, percentage of people with a history of diabetes, hypertension, ST-segment elevation myocardial infarction, myocardial ischemia time, angiotensin converting enzyme inhibitors or angiotensin Ⅱ receptor blockers use, and β receptor blocker use were similar between the two groups(all P>0.05). The contrast agent dosage was also similar between the two groups (P=0.266). The peak cardiac troponin I (cTnI), N-terminal pro-brain natriuretic peptide(NT-proBNP), white blood cell count, base estimated glomerular filtration rate (eGFR), albumin and hemoglobin levels were statistically significant between the two groups (all P<0.05). Multivariate logistic regression analysis showed that decreased baseline eGFR, increased NT-proBNP, peak cTnI concentrations and white blood cell count were independent risk factors of CRS1 in AMI patients (all P<0.01).The predicting equation of the combined predictor was established by transforming the logistic model equation, L=0.031×cTnI+0.000 2×NT-proBNP-0.024×eGFR+0.254×white blood cell count, where L represented the combined predictor. ROC curve analysis indicated that the AUC of the peak cTnI, NT-proBNP, baseline eGFR, white blood cell count, and combined predictor were 0.76, 0.85, 0.79, 0.81, and 0.92 respectively (all P<0.05), and the cutoff value of combined predictor was 2.6. The AUC of ROC curve after the model's ten-fold cross validation was 0.89. Conclusions: Decreased baseline eGFR, increased NT-proBNP, peak cTnI concentrations and white blood cell count are the independent risk factors for CRS1 in AMI patients. The combined predictor equation based on the above 4 biomarkers presents a good predictive value for CRS1 in AMI patients.

Prognostic Value of Electrocardiographic QRS Diminution in Patients Hospitalized With COVID-19 or Influenza

During the clinical care of hospitalized patients with COVID-19, diminished QRS amplitude on the surface electrocardiogram (ECG) was observed to precede clinical decompensation, culminating in death. This prompted investigation into the prognostic utility and specificity of low QRS complex amplitude (LoQRS) in COVID-19. We retrospectively analyzed consecutive adults admitted to a telemetry service with SARS-CoV-2 (n = 140) or influenza (n = 281) infection with a final disposition—death or discharge. LoQRS was defined as a composite of QRS amplitude <5 mm or <10 mm in the limb or precordial leads, respectively, or a ≥50% decrease in QRS amplitude on follow-up ECG during hospitalization. LoQRS was more prevalent in patients with COVID-19 than influenza (24.3% vs 11.7%, p = 0.001), and in patients who died than survived with either COVID-19 (48.1% vs 10.2%, p <0.001) or influenza (38.9% vs 9.9%, p <0.001). LoQRS was independently associated with mortality in patients with COVID-19 when adjusted for baseline clinical variables (odds ratio [OR] 11.5, 95% confidence interval [CI] 3.9 to 33.8, p <0.001), presenting and peak troponin, D-dimer, C-reactive protein, albumin, intubation, and vasopressor requirement (OR 13.8, 95% CI 1.3 to 145.5, p = 0.029). The median time to death in COVID-19 from the first ECG with LoQRS was 52 hours (interquartile range 18 to 130). Dynamic QRS amplitude diminution is a strong independent predictor of death over not only the course of COVID-19 infection, but also influenza infection. In conclusion, this finding may serve as a pragmatic prognostication tool reflecting evolving clinical changes during hospitalization, over a potentially actionable time interval for clinical reassessment.

The prognostic value of myocardial perfusion imaging in patients with type 2 myocardial infarction

ObjectivesThe aim of this retrospective study is to evaluate the prognostic role of myocardial perfusion imaging (MPI) in patients with type 2 myocardial infarction (T2MI). BackgroundT2MI is an increasingly common diagnosis in clinical practice. The management of this condition is controversial and the prognostic value of MPI has not been established in this setting. MethodsWe retrospectively studied T2MI patients who underwent vasodilator gated MPI within 90 days of T2MI at a single tertiary care institution in 2013. Abnormal myocardial perfusion was defined as the perfusion defect involving ≥ 5% of left ventricular (LV) myocardium. Abnormal LV ejection fraction (EF) was defined as < 50% by gated images. The primary outcome was a composite of death, myocardial infarction (other than index event) or coronary revascularization (CR). ResultsThere were 234 patients (62 ± 14 years, 57% men) with T2MI (peak troponin 0.2 ng/ml, interquartile 0.1-1.4), of whom 136 (58%) had an abnormal MPI. During a median follow-up of 20 months, 155 patients (66%) had the primary outcome (39% death, 42% MI, 5% CR). An abnormal MPI was associated with an increased risk of the primary outcome with a hazard ratio of 1.56, 95%CI (1.12-2.18, P = .008) that remained statistically significant after multivariate adjustment (1.45, 95%CI (1.02-2.06, P = .04))). ConclusionsPatients with T2MI are at high risk for death or cardiac events in the intermediate term. More than one-half of patients with T2MI have an abnormal MPI and this is associated with the increased risk of cardiac events during follow-up. Risk stratification with MPI after T2MI may identify patients who would benefit from aggressive risk reduction.

B-PO05-033 PACEMAKER IMPLANTATION AFTER SELECTIVE ALCOHOL SEPTAL ABLATION

Complete heart block (CHB) with permanent pacemaker (PPM) placement is a known risk of alcohol septal ablation (ASA) for hypertrophic cardiomyopathy. Historically, the incidence has been around 10% in all-comer populations. However, rates of 25% are reported in centers that selectively target older, higher risk patients (pts). Understanding predictors of CHB in this evolving cohort is important. Report baseline characteristics, associated factors (AF) of PPM placement, longer-term pacing need following ASA in a high-volume HCM center. 94 consecutive pts underwent ASA from 2/2017 to 12/2020. 25 were excluded due to prior septal reduction or device. Criteria for PPM included persistent post-ASA CHB >24 hours, recurrent pacing due to 2nd degree HB/ transient CHB >24 hours. 69 pts (mean age 65.7 ± 11 years, females 53.6%) were included. 19 (27.5%) required PPM prior to discharge, 6 (31.5%) of whom were prohibitive surgical risk for myectomy (20.3% PPM rate in pts not at prohibitive surgical risk). All had reduction in peak provoked gradient (pre-procedure mean 149.8 mm Hg vs. post-procedure mean 10.5 mmHg, p<0.01) and improved NYHA class. Comparison of baseline clinical, ECG, and procedural characteristics (e.g., peak troponin and gradient reduction) yielded no AF of PPM implantation, with exception of intraprocedural CHB (OR 12.4, 95% CI 3.4 - 45.3, p<0.0001). Post procedure PR prolongation >50 ms (OR 6.1, 95% CI 1.5 - 24.5, p = 0.01), first-degree AV block with RBBB and LAFB (OR 6.1, 95% CI 1.5 - 24.5, p = 0.01) and change in QRS axis >700 (OR 5.3, 95% CI 1.4 - 18.9, p= 0.01) was also associated with PPM. At 1 month, 16 pts (84.2%) required >1% RV pacing (mean 59.2%) suggesting appropriateness of PPM implantation. At 3 months 10 pts (52.6%) required pacing (mean 52.4%) indicating some late recovery. No procedural factors were associated with PPM following ASA with exception of intraprocedural CHB. Daily ECGs identified dynamic abnormalities associated with PPM. Short term follow up suggests PPM criteria are appropriate, with longer term follow up showing some recovery. As higher risk cohorts are targeted for ASA, PPM risk factors of long term pacing will be vital.

Saving critically ill COVID-19 patients with mechanical circulatory support.

BackgroundCoronavirus disease 2019 (COVID-19) is an ongoing public health crisis that has led to many deaths due to multiple organ dysfunction syndromes (MODS). This article describes the clinical characteristics, management, and outcomes of critically ill COVID-19 patients who survived the disease through mechanical circulatory support (MCS).MethodsWe studied 25 critically ill COVID-19 patients who underwent MCS from January 20, 2020, to April 10, 2020, at the Tongji Hospital of Huazhong University of Science and Technology.ResultsThirteen (52%) of the 25 patients survived with MCS support, while 12 (48%) died. At the time of their hospital admission, we identified significant differences in their peak cardiac troponin I (cTnI) and interleukin 6 (IL-6) levels, as well as in their lymphocyte count and C-reactive protein (CRP) levels. Cox proportional hazards regression model revealed that receipt of renal replacement therapy (RRT) was associated with an approximately 20-fold improvement in survival [hazard ratio (HR) =0.049, 95% confidence interval (CI) =0.008 to 0.305]. The number of days spent on extracorporeal membrane oxygenation (ECMO) support and the use of hydrogen (pH) at the time of MCS was also associated with an increase in survival. This contrasted with high-sensitivity C-reactive proteins (hs-CRP) and lactate, associated with a decrease in survival during MCS. Further analysis of the determinants relating to a COVID-19 patient’s chance of survival on/after MCS was also indicated by levels of IL-6 (β=0.009, P=0.006), IL-8 (β=0.031, P=0.020), and TNF-α (β=0.107, P=0.014), which saw a significant increase in the 12 patients who died. This contrasts with the non-significant decrease in IL-6, IL-8, and TNF-α levels in the 13 patients who survived.ConclusionsThese results indicate that pH, lactate, hs-CRP, ECMO duration, and RRT are important clinical determinants for assessing how MCS can increase the chances of critically ill COVID-19 patients surviving the disease.

Prognostic assessment following acute myocarditis requires convalescent scanning: neither peak troponin nor index scan T2 signal predicts convalescent late gadolinium enhancement

Abstract Funding Acknowledgements Type of funding sources: None. Background Cardiovascular magnetic resonance (CMR) is a key diagnostic investigation in acute myocarditis (1) and permits quantification of late gadolinium enhancement (LGE) and myocardial oedema. Follow-up CMR imaging is recommended to check for persistence of scar and oedema (2). Persistent late gadolinium enhancement is associated with a worse prognosis (3). It is not known whether all patients require follow-up scanning or whether the initial scan can provide useful information to identify which patients need convalescent assessment. Purpose In this study we considered whether extent of troponin elevation, extent of T2 elevation and initial late gadolinium enhancement burden predicted long-term late gadolinium enhancement at follow-up. Methods Index and follow-up CMR scans of consecutive patients presenting with a diagnosis of acute myocarditis between 2019 and 2020 across three hospitals were included. Inclusion criteria were: follow-up scan within 9 months of the index scan, CMR with LGE imaging and T2 mapping, and acute myocarditis being the primary diagnosis of the index scan. Myocardial T2 values in the area affected by myocarditis and percentage of LV myocardium showing late enhancement (using a threshold-based full height half width or manual region of interest strategy) were extracted. Results 20 patients were included in the study (80% male; mean age 37 years). Mean interval between the index and follow-up scan was 4.1 months. Peak troponin level during the acute illness was not associated with the proportion of LV myocardium affected by LGE in the index scan (R^2 &amp;lt;0.01) (Figure 1A). Myocardial T2 values in the first scan were not associated with the proportional resolution in LGE between the index and follow-up scans (R^2 0.02) (Figure 1B). The mean change in LGE was -61.7% (+/-22.8%) but the initial LGE burden did not predict the proportional degree of improvement in LGE between scans (R^2 &amp;lt;0.01)(Figure 1C). Conclusions The extent of troponin elevation and initial CMR phenotype was not a good predictor of the burden of long-term late gadolinium enhancement. Although most cases showed improvement in LGE scar burden between index and follow-up imaging, neither peak troponin level during the acute episode, nor T2 values at the first CMR scan were predictive of initial or change in scar burden. Serial CMR assessment is required to identify those patients who have residual long-term scarring.

The role of peak troponin in patients with a working diagnosis of myocardial infarction with non-obstructive coronary arteries (MINOCA)

Abstract Funding Acknowledgements Type of funding sources: Private grant(s) and/or Sponsorship. Main funding source(s): Rosetrees Trust James Tudor Foundation Background 6-10% of patients who present with an acute coronary syndrome have a myocardial infarction with non-obstructive coronary arteries (MINOCA). Troponin T predicts infarct size and outcomes in patients with ST-elevation myocardial infarction. The value of peak troponin T in patients with a working diagnosis of MINOCA is not well understood. Purpose The aim of this study is to investigate the diagnostic and prognostic role of troponin in patients with MINOCA. Methods Consecutive patients with a working diagnosis of MINOCA (n = 719) from a single tertiary centre who underwent comprehensive cardiovascular magnetic resonance (CMR) imaging with late gadolinium enhancement (LGE) were followed prospectively. The primary endpoint was all-cause mortality. Results Peak troponin T ≥211 ng/L and time to CMR of ≤17 days have a positive predictive value of 94% for being able to make a diagnosis on CMR. If the scan was performed in ≤17 days the diagnostic yield was still 75% even in the lowest troponin decile, but this was 59% if performed after 17 days. Each increase in troponin decile increases the mean diagnostic yield of the CMR by 3.7% (p &amp;lt; 0.001, 95% CI 3.4 – 3.9; R2 0.84; Figure 1). There is no overall difference in median troponin in patients who died and those who survived (229 ng/l v. 424 ng/l; p = 0.157), however mortality is significantly lower in the highest two troponin quartiles (11.9% versus 6.9%; p = 0.009, figure 2). Conclusions Peak troponin T and time to CMR can be used by cardiologists to determine the likelihood of making a diagnosis using CMR. A higher troponin quartile is associated with lower mortality.

Evaluation of Myocardial Damage in Relation to HbA1c in Patients with Previously Unrecognized Diabetes Presenting with STEMI

Objective: The mechanisms underlying worse clinical outcomes in previously unrecognized diabetic (DM) patients in ST-elevation myocardial infarction (STEMI) are unclear. It was hypothesized that poor chronic glucose control might be related to greater myocardial damage.&#x0D; Material and Method: 51 newly diagnosed DM patients with glycated hemoglobin A1c (HbA1c) &gt; 6.5 comprised the DM group, 54 sex- and age-matched individuals with normal glucose metabolism served as the non-DM group. Each patient underwent primary angioplasty for STEMI. The levels of cardiac specific markers before angioplasty, during angioplasty, at 6, 12, and 18 h after angioplasty were recorded. SPSS 10 package program was used to analyse data.&#x0D; Results: In both DM and non-DM groups troponin peaked at 6 h. Peak troponin levels were similar in both groups (diabetics, 22.89 ± 18.19 vs. non-diabetics, 32.67 ± 17.68 ng/ml, p=0.168).&#x0D; Conclusions: HbA1c &gt; 6.5 is not related to extent of infarction in previously unrecognized DM patients presenting with STEMI. Future studies assessing the effects of other factors unrelated to chronic glucose control on myocardial damage and cardiovascular event rates in these patients would be of great interest.

Elevated myocardial wall stress after percutaneous coronary intervention in acute ST elevation myocardial infraction is associated with increased mortality.

Despite early attempts to salvage myocardium-at-risk with percutaneous coronary intervention (PCI), changes in myocardial wall stress (MWS) leads to ventricular dilatation and dysfunction after acute ST-elevation myocardial infraction (STEMI). Whether this is transient or leads to long-term adverse outcomes major adverse cardiovascular events (MACE) is not known. We studied the association between MWS and MACE in patients after a successful PCI for acute STEMI. To study the MWS in percutaneously revascularized STEMI patients in relation to all-cause mortality and MACE. We prospectively enrolled142 patients who presented to our tertiary care hospital with acute STEMI requiring emergent PCI. In addition to the standard clinical biomarkers, both end-systolic and end-diastolic MWS was calculated using our recently validated Echocardiographic indices. Patients were then prospectively followed up to an average of 16.5(±12.0) months to assess all-cause mortality and MACE. During the follow-up period, 9% of the patients died and 17% developed MACE. Patients who died had significantly elevated end-systolic WS compared to those who survived (mean ESWS, 80.01±36.86vs 59.28±27.68). There was no significant difference in end-diastolic WS, left ventricular systolic function and peak troponin levels among survivors versus non-survivors. Elevated ESWS (>62.5 Kpa) and age remained the significant predictors of mortality on multivariate logistic analysis (OR 7.75, CI 1.33-73.86, P=.03; OR 1.16, CI 1.06-1.31, P=.002). Elevated ESWS measured by echocardiogram is associated with increased odds of long-term mortality in STEMI patients who have undergone emergent PCI. This finding can help clinicians to risk stratify high-risk patients.

Low serum albumin levels and in-hospital outcomes in patients with ST segment elevation myocardial infarction

Background and aimsLow serum albumin (SA) is associated with an increased risk of long-term adverse events (AEs) among patients with chronic coronary syndromes. Its prognostic role in patients with ST-elevation myocardial infarction (STEMI) is less clear. To investigate the association between low SA and in-hospital AEs in STEMI patients. Methods and resultsMulticenter retrospective cohort study of 220 STEMI patients undergoing primary percutaneous coronary intervention within 12 h from the onset of symptoms. Hypoalbuminemia was defined by serum SA <35 g/L. SA. In-hospital AEs were defined as cardiogenic shock, resuscitated cardiac arrest and death. Median SA was 38 (IQR 35.4–41.0) g/L and 37 (16.8%) patients showed hypoalbuminemia (<35 g/L) on admission. Patients with hypoalbuminemia were older, more frequently women and diabetics, prior CAD and HF. Furthermore, they showed lower hemoglobin levels and impaired renal function. At multivariable logistic regression analysis, diabetes (odds ratio [OR]:4.59, 95% confidence interval [CI] 1.71–12.28, p = 0.002) and haemoglobin (OR:0.52, 95%CI 0.37–0.72, p < 0.001) were associated with low SA. In a subgroup of 132 patients, SA inversely correlated with D-Dimer (rS −0.308, p < 0.001). Globally, twenty-eight (14.6%) AEs were recorded. Hypoalbuminemia (OR:3.43, 95%CI 1.30–9.07, p = 0.013), high-sensitive (HS)-Troponin peak above median (OR:5.41, 95%CI 1.99–14.7, p = 0.001), C-reactive protein (CRP) peak above median (OR:6.03, 95%CI 2.02–18.00, p = 0.001), and in-hospital infection (OR:3.61, 95%CI 1.21–10.80, p = 0.022) were associated with AEs. ConclusionLow SA levels are associated with worse in-hospital AEs in STEMI patients, irrespective of HS-troponin and CRP plasma levels. Our findings suggest that low SA may contribute to the pro-thrombotic phenotype of these patients.

Prognostic Value of Multilayer Left Ventricular Global Longitudinal Strain in Patients with ST-segment Elevation Myocardial Infarction with Mildly Reduced Left Ventricular Ejection Fractions

Multilayer (epi-, mid- and endocardium) left ventricular (LV) global longitudinal strain (GLS) reflects the extent of myocardial damage after ST-segment myocardial infarction (STEMI). However, the prognostic implications of multilayer LV GLS remain unclear. We studied the association between multilayer LV GLS and prognosis in patients with mildly reduced or preserved LV ejection fraction (EF) after STEMI. Patients with first STEMI and LVEF>45% were evaluated retrospectively. Baseline multilayer (endocardial, mid-myocardial and epicardial) LV GLS were measured on 2-dimensional speckle tracking echocardiography. Patients were followed up for of all-cause mortality. A total of 569 patients (77% male, 60 ± 11 years) were included. After a median follow-up of 117 (interquartile range 106-132) months, 95 (17%) patients died. We observed no differences in baseline LVEF and peak troponin levels between survivors and non-survivors. However, non-survivors showed more impaired GLS at all layers (epicardium: -11.9 ± 2.8% vs. -13.4 ± 2.8%; mid-myocardium: -14.2 ± 3.2% vs. -15.6 ± 3.2%; endocardium: -16.5 ± 3.7% vs. -17.7 ± 3.6%, p <0.05, for all). On multivariable analysis, increasing age (hazard ratio 1.095; p<0.001) and impaired LV GLS of the epicardial layer (hazard ratio 1.085; p=0.047) were independently associated with higher risk of all-cause mortality. In addition, LV GLS at the epicardium had incremental prognostic value for all-cause mortality (χ2=114, p=0.044). In conclusion, in contemporary STEMI patients with mildly reduced or preserved LVEF, ageing and reduced LV GLS of the epicardium (reflecting transmural scar formation) were independently associated with all-cause mortality after adjusting for clinical and echocardiographic variables.