Follow-up Transthoracic Echocardiogram Research Articles

Ten years follow-up after aortic valve replacement with bioprosthesis trifecta: a single center retrospective cohort

Abstract Introduction St. Jude’s Trifecta (TF) bioprosthesis were adopted at most centers due to their unique design and hemodynamic performance. However, concerns regarding durability have been raised and long-term follow-up studies (≥10 years) are scarce. Purpose To report hemodynamic performance as well as early and long-term results of TF valve. Material and Methods In this longitudinal, single-center study, consecutive patients that underwent surgical aortic valve replacement with TF, from July 2011 to June 2019 were included. Pre-, intra- and post-operative data, including routine and first outpatient ambulatory postoperative transthoracic echocardiogram (TTE) (median 4 months) were collected. Hospital mortality was defined as in-hospital or within the first 30 days after surgery. Survival and need for reoperation were accessed in December 2021. Median follow-up was 4 years and maximum was 10,5 years. Kaplan-Meier method was used for time-to-event outcomes (all-causes mortality and need for reoperation). Results We included 1084 patients, 54% being male, with a mean age of 74±8 years. Surgery priority was elective in 840 (78%) of cases. Most patients received a TF prothesis of size 23 (35%), followed by size 21 (30%). There were 563 (52%) multiple procedures, mostly coronary artery bypass grafting (46% within the multiple procedures). Bypass and clamping times were 86±31 minutes and 62±22 minutes, respectively for isolated procedures, and 143±27 minutes and 100±40 minutes, respectively, for multiple procedures. Hospital mortality was 6%. Excluding these patients, cumulative survival at 1-, 3-, 5- and 10-years, were, respectively, 96%, 89%, 78% and 52%. There were 27 patients who needed reoperation: 16 due to endocarditis, 5 due to structural valve deterioration (SVD) and 6 due to non-structural valve dysfunction. Freedom from reoperation at 1-, 3-, 5- and 10- years were of 99%, 98%, 98% and 95%, respectively. At follow-up TTE (n=995), transvalvular mean gradient was 11±4 mmHg and the effective orifice area mean was 2.1±0.5cm2. Patient-prosthesis mismatch occurred in 79 (9.1%), being severe in 8 (0,9%) cases. Conclusion Our findings confirm the satisfactory hemodynamics and safety profile of TF bioprosthesis. Long-term results are comparable with published TF series and there seems to be no particular sign of adverse valve-related events in our population.

Incidence and types of significant tricuspid regurgitation in atrial fibrillation and sinus rhythm

Abstract Background Atrial fibrillation (AF) is associated with increased risk of incident tricuspid regurgitation (TR), but types of incident TR in AF versus sinus rhythm (SR) are not well-defined. Purpose We aimed to compare the risk of the different types of incident ≥moderate TR in AF and SR. Methods Adults first diagnosed with AF (2010-2021) who had a transthoracic echocardiogram (TTE) within 30 days after AF and adults with no diagnosis of AF who had a TTE in the same period were identified. Patients with previous cardiac surgeries, congenital heart disease, cardiomyopathy, cardiac devices, primary valve disease, previous or current ejection fraction (EF) <50%, severe diastolic dysfunction (SDD), ≥moderate left-sided valve disease (LVD), right ventricular systolic pressure (RVSP) ≥50 mmHg, ≥moderate TR, any tricuspid stenosis, or with no follow-up TTE ≥6 months from baseline were excluded. Patients were followed for the development of ≥moderate TR, the type of which was identified in a hierarchal order: 1) pacemaker-associated TR, 2) LVD-associated TR in the setting of ≥moderate LVD, 3) low EF or SDD-related TR, 4) pulmonary hypertension (PH)-associated TR if RVSP was ≥50 mmHg, 5) other ventricular functional TR (VFTR) if there was >mild RV enlargement or dysfunction, and 6) atrial functional TR (AFTR) when none of the previous was present. Patients were also followed for the occurrence of risk factors for TR (pacemaker insertion, ≥moderate LVD, low EF or SDD, PH, >mild RV enlargement or dysfunction) in a hierarchal order, and both the prevalence and future risk of the corresponding type of ≥moderate TR was determined at the onset of these conditions in AF and SR. Results Overall, 1,360 patients with new-onset AF (median age 67 years, 34% females) and 20,438 patients in SR (median age 60 years; 54% females) were included. Over median 3.8 (IQR 1.8-6.6) years, incident ≥moderate TR occurred in 110 patients with new-onset AF [2.13 per 100-person years] compared to 378 patients in SR [0.41 per 100-person years, p <.001]. All types of incident ≥moderate TR occurred more frequently in AF (p <.001 for all). The distribution and incidence of each type of TR in AF and SR are shown in Figure 1. The incidence of risk factors associated with the development of TR was higher in the AF group, except for pre-capillary PH, Figure 2A. At time of diagnosis or occurrence of these conditions, the prevalence of the corresponding TR types was higher in AF, except for pacemaker-TR, Figure 2B. The incidence of the corresponding TR type after occurrence of TR risk factors was higher in the AF group for LVD-TR and low EF/SDD-associated TR (p ≤0.03); although numerically higher in AF, the association was only borderline for PH-TR (p =0.05), Figure 2C. Conclusion Incident ≥moderate TR of all types occurred more frequently in patients with AF vs. SR and the distribution of TR types differed by rhythm. Patients with AF may benefit from a closer follow-up.Distribution and incidence rates of TRIncidence of TR risk factors & TR after

Artificial intelligence-enabled electrocardiogram in the detection of patients at risk of atrial functional mitral regurgitation

Abstract Background Atrial functional mitral regurgitation (AFMR) is an increasingly recognized cause of functional MR thought to result from left atrial enlargement and myopathy in the setting of preserved left ventricular geometry and function. AFMR mostly occurs in patients with atrial fibrillation (AF) and/or heart failure with preserved ejection fraction. Purpose We investigated whether the use of an artificial intelligence-based electrocardiogram (AI-ECG) can identify patients with new-onset AF and sinus rhythm (SR) who are at highest risk of developing AFMR. Methods Adults with a new diagnosis of AF between 2010 and 2021 who had a transthoracic echocardiogram (TTE) within 1 month after AF diagnosis were identified. Similarly, adults in SR who never had AF diagnosis and had a TTE during the same period were identified. Exclusion criteria from both groups included >mild MR at baseline, primary mitral valve disease, cardiomyopathy, ≥moderate aortic valve disease, current or previous low ejection fraction, enlarged left ventricle, cardiac devices, previous cardiac surgeries, and the absence of follow-up TTE ≥6 months from baseline. Only patients who had ECG within 10 days of the TTE were included. When multiple ECGs were available, the closest was considered. A previously trained AI-ECG algorithm to detect the probability of AF was utilized. Incident AFMR was defined as >mild functional MR in the absence of >mild left ventricle enlargement or dysfunction. Diastolic dysfunction was defined according to ASE/EACVI guidelines. Results Overall, 1,570 patients with new-onset AF (median age 67 years; 34% females) and 16,802 patients in SR (median age 59 years; 46% females) were included. The median AI ECG probability for AF was 43% (IQR 26%-59%) in the new-onset AF group and 2% (0.5%-7%) in the SR group, Figure 1. Incident AFMR occurred in 152 patients in the AF group over median 3.06 (IQR 1.5-5.2) years of follow-up and in 482 patients in the SR group over median 3.0 (1.5-5.6) years of follow-up. The probability of silent AF by the AI-ECG was associated with incident AFMR in the new-onset AF group [hazard ratio 1.19 (95% CI 1.11-1.28) per 10%, p <.001] and the SR group [hazard ratio 1.19 (95% CI 1.12-1.25) per 10%, p <.001]. The AI ECG-derived AF probability remained as an independent risk factor for AFMR in multivariable analysis in both AF and SR, Table 1. Conclusion The AI ECG for AF might be able to reflect the degree of left atrial myopathy and thus the risk of incident AFMR in patients with AF and SR.Distribution of AI ECG probability of AFMultivariable risk factors for AFMR

PO-02-021 DIRECTION OF REPOLARIZATION IN BASELINE ECG IS PREDICTIVE OF RESPONSE TO CARDIAC RESYNCHRONIZATION THERAPY

Cardiac resynchronization therapy (CRT) is a cornerstone of treatment for advanced heart failure, but not all patients derive equal benefit from this intervention. Current approaches of using electrocardiographic and echocardiographic parameters to identify likely CRT responders demonstrate poor predictive ability. We seek to identify electrocardiographic parameters that can improve prediction of benefit with CRT This was a retrospective analysis of patients who underwent CRT-D placement at University of Pittsburgh Medical Center from 2014-2020. Patients were excluded if pre-implantation EKG or pre- and post-implantation echocardiograms were not available. Each patient’s immediate pre-implantation ECG was processed using the CineECG software (EKG Excellence) to obtain the mean temporospatial isochrone of ventricular activation. 192 features quantifying the activation and recovery pathways were computed for each patient. Response to CRT was defined as an improvement in ejection fraction (EF) of 5% on follow-up transthoracic echocardiogram 3-12 months after CRT implantation. Forward sequential feature selection was used to identify the features of highest importance based on negative logistic loss. 276 patients were included in this analysis (36% female, mean age 69 years, mean pre-procedural EF 27%). The 10 most important CineECG features were identified. When these features were used in a multivariate logistic regression, three features were independently predictive of CRT response: left bundle branch block (LBBB); leftward direction of late repolarization potentials (i.e., Tpeak - Tend rotated toward LV in the horizontal plane); and location of center-of-mass of terminal cardiac activation. Compared to CRT responders (n=169, 62%), non-responders were more likely to have abnormal direction of late repolarization potentials in both LBBB group (-0.34±0.30 vs. -0.45±0.30 vs, p=0.027) and RBBB group (0.25±0.51 vs. 0.61±0.27, p=0.031). In the latter group, direction of later repolarization potentials correlated with magnitude of change in post-procedural EF (r=0.23, p=0.016). Our findings confirm that the presence of LBBB is predictive of response to CRT. In addition, our data suggests that in patients with RBBB, a more leftward direction of late repolarization potentials is independently predictive of CRT response. Further studies into repolarization dynamics as a predictor of CRT response in RBBB are warranted.

313 BRUGADA SYNDROME MIMICRY: THE IMPORTANCE OF AN EXTENDED FOLLOW-UP

Abstract Introduction Brugada Syndrome (BrS) is a genetically inherited condition associated with the risk of fatal arrhythmias and sudden cardiac death (SCD) occurring in a structurally normal heart. This disorder was historically related to mutations in the SCN5A gene, but recent observations suggest a more complex genetic inter-play, highlighting the possible overlap with structural cardiomyopathies, including hypertrophic cardiomyopathy (HCM). Case Presentation In May 2005, an asymptomatic 56-year-old man with a family history of unexplained SCD was referred to our outpatient clinic. A 12-lead ECG showed a type 2 Brugada pattern whilst transthoracic echocardiogram (TTE) was normal. Ventricular fibrillation (VF) was induced during an elective electrophysiological study and a transvenous implantable cardioverter-defibrillator (ICD) was implanted for primary prevention. More than 10 years later, in March 2022, our patient was admitted to the hospital because of palpitations. The ECG revealed a typical atrial flutter with a high ventricular rate, successfully treated with catheter ablation. Post-procedural ECG showed the persistence of type 2 Brugada pattern in association with new-onset T wave inversion in inferolateral leads and signs of ventricular hypertrophy. TTE revealed asymmetric left ventricular hypertrophy, with left ventricular outflow tract (LVOT) obstruction determined by mitral systolic anterior motion and preserved LV systolic function. The patient was treated with optimal medical therapy with symptom improvement and reduction of LVOT obstruction at a 3-month follow-up TTE. Discussion The distinction between Brugada phenocopy and BrS electrocardiogram patterns is not obvious, and according to our experience a Brugada type 2 pattern could be an early ECG marker of a concealed HCM which became manifest over an extended follow-up. Brugada ECG phenocopies are clinical entities characterized by type 1 or type 2 Brugada patterns elicited by an underlying condition, the disappearance of the pattern with the resolution of the condition and the absence of classical symptoms. Several pathogenic variants involving other and different genes have been recently reported suggesting a possible overlap with structural cardiomyopathies. Recently, two other cases of incidental findings of a Brugada ECG pattern in the context of HCM were described. Both patients had a common pathogenetic splicing mutation in the MYBPC3 sarcomeric gene (encoding for the cardiac myosin-binding protein C) responsible for HCM with no genetic mutations associated with Brugada syndrome. This fact suggests that patients are not simultaneously affected by BrS and HCM but a clinically manifest HCM with a specific genetic background can lead to an early BrS electrical manifestation. Conclusion Our experience confirms that a Brugada type 2 ECG pattern could be a very early sign of a concealed HCM manifested over 10 years later. The importance of proper risk stratification and regular follow-up has thus crucial implications in patient clinical management. However, whether Brugada pattern associated with structural heart disease is linked to an increased risk of sudden cardiac death is still unknown and needs further investigations.

Abstract 159: Time-course Of Left Ventricular Systolic Dysfunction Recovery After Cardiac Arrest

Introduction: Myocardial dysfunction is a well-documented feature of post-cardiac arrest syndrome. The natural history of left ventricular systolic dysfunction (LVSD) remains largely unknown. We sought to characterize the change in left ventricular systolic function after return of spontaneous circulation (ROSC). Methods: This is a retrospective review of cardiac arrest patients at a single tertiary center between 2015 and 2020. We included patients with a transthoracic echocardiogram (TTE) documenting left ventricular ejection fraction (EF) within 1 day of ROSC and at least one follow-up TTE within 6 months after cardiac arrest. LVSD was defined as EF <40% on TTE. Patients with known LVSD preceding cardiac arrest were excluded. Using paired t-test, we compared initial (within 1 day of ROSC) and follow up TTEs, stratified by shockable rhythm status. Recovery of LVSD was defined as improvement in EF to >50%. Results: Of 477 cardiac arrest patients, 89 (18.7%) patients met the inclusion criterion. 28 (31.5%) had a baseline TTE on file; 5 patients had LVSD prior to arrest and were excluded, leaving a cohort of 84 patients. Thirty-one (36.9%) patients had LVSD on TTE after ROSC, of which 16 (51.6%) had recovery of EF on follow up TTE. The figure shows the timeline of EF recovery for the whole cohort. In-hospital follow up TTE (n=84) was done at a median (IQR) of 7 (4,16) days and post-discharge follow up (n=26) at 63 (29, 115) days. In patients with shockable rhythm arrest, EF improved from ROSC to inpatient follow up TTE [mean (SD) 36% (2.6) to 50% (2.5), P <0.001]. Patients with non-shockable rhythm arrest had a higher baseline EF with a non-significant change at follow up [50% (2.6) to 56% (2.5), p=0.072]. Conclusion: Among survivors of cardiac arrest, significant recovery of LVSD was common. Further work is necessary to elucidate predictors of myocardial recovery and to determine optimal timing for repeat echocardiography.

Abstract 15146: A Flying Saucer- Asymptomatic Migration of an Atrial Septal Defect Occluder Device to the Aortic Arch - No Good Deed Goes Unpunished!

Introduction: Though safe, the transcatheter closure with an atrial septal defect for secundum atrial septal defect (ASD) is associated with complications, such as device dislodgement. Case report: A 51-year-old female with a complex fenestrated secundum ASD (16mm superior defect and 14mm inferior defect with insufficient aortic rim) with hemodynamically significant shunt causing right heart dysfunction underwent placement of two atrial septal defect occluder devices (Amplatzer). While there was no shunting noted on immediate post-procedure transthoracic echocardiogram (TTE), a follow-up TTE after a year showed residual left to right shunting across the ASD. Transesophageal echocardiogram (TEE) showed a single occluder device (inferior) in place and a second device (superior) lodged in the distal aortic arch at the level of the left common carotid and left subclavian artery with mild local flow acceleration (aortic velocity 2.6 ms/s) and no superimposed device thrombus. Her only complaint was recurrent headaches, which pre-dated the procedure and were attributed to ocular migraine by her neurologist. The patient underwent a transcatheter procedure to attempt the retrieval of the dislodged device. The proximal end of the device was found adherent to the aortic wall. Aortogram revealed excellent flow around the device. The procedure was aborted due to the risk of dissection. Since the device did not cause any adverse effects and would likely continue to endothelialization. Conclusion: Atrial septal occluder device dislodgement can occur several months after implantation. Careful monitoring is required particularly when the ASD rim is insufficient. In cases of migration and adherence to the aortic wall without hemodynamic consequences, the device can likely be safely left in place to endothelialize. Despite a faster recovery with percutaneous procedures, a surgical approach should be considered in younger patients to avoid such complications.

Abstract 10206: Misleading Transvalvular Hemodynamics for Patients With Moderate Aortic Stenosis

Introduction: Aortic stenosis (AS) is a progressive disease that leads to cardiac remodeling. Appropriate management depends on accurate assessment of AS severity. Transvalvular gradients are central to echocardiographic assessment of AS though can be impacted by any conditions that decrease transvalvular flow. Hypothesis: 1) Decline in peak transvalvular gradient over time is associated with more significant cardiac remodeling and 2) Cardiac damage is associated with lower transvalvular flow and masks progression of AS. Methods: Retrospective single center study of patients with moderate AS (defined as peak gradient 25-40mmHg) from 2013-2020 with > 1 transthoracic echocardiogram (TTE). Each TTE was classified into established stages of cardiac damage: no damage (Stage 0), left ventricular damage (Stage 1), left atrial or mitral valve damage (Stage 2), pulmonary vasculature or tricuspid valve damage (Stage 3), or right ventricular damage or subclinical heart failure (Stage 4). Results: Sixty patients with at least 1 follow-up TTE were included. The mean age was 73.5 +/- 11 years with 47% women (28/60) and median time of 381 days (IQR 12.7 months) between echocardiograms. On initial assessment, mean AVA and peak AV gradient were 1.2cm 2 +/- 0.33 and 37mmHg +/- 11.3 respectively. At follow-up, the mean AVA and peak AV gradient were 1.1cm 2 +/- 0.20 and 38mmHg +/- 12.6. Forty-three of 60 patients (72%) had evidence of cardiac damage on initial assessment compared to 55 of 60 patients (92%) on follow-up. Thirty-five (58%) patients displayed a decrease in peak AV gradient over time (average decrease -16% +/- 0.12). Twenty-one of the patients with declining peak gradients (60%) demonstrated progressive cardiac damage compared to 9 of 25 patients (36%) with increasing peak gradients (p= 0.06). Conclusions: Over half of patients with moderate AS demonstrated a decrease in peak AV gradient over time. Reliance on transvalvular gradients as a reflector of AS severity can be misleading as there was a trend toward more significant cardiac damage in this subset of patients. The presence of underlying cardiac damage can obscure traditional echocardiographic assessment and progression of AS and should be incorporated into assessments of disease severity and progression.

Abstract 11476: The Clot Thickens: Massive Left Ventricular Thrombus After Sub-Acute Myocardial Infarction

Introduction: Left ventricular thrombus (LVT) following myocardial infarction (MI) can affect up to 19.2% of patients with anterior wall MI. The mechanism is thought to be due to stasis from LV regional wall akinesia, endothelial injury from prolonged ischemia, and hypercoagulability from acute coronary syndrome. In patients with LVT after MI, anticoagulation choice and duration is still a matter of debate. Case Report: A 51-year-old woman with diabetes and prior anterior wall MI with LVT presented with non-healing diabetic leg wounds. One year ago at the time of the MI, transthoracic echocardiogram (TTE) showed a 4.0 x 1.3 cm mural thrombus. She was discharged on prasugrel and apixaban. Apixaban was discontinued after five months, with follow-up TTE showing resolution of LVT, with 30% LV ejection fraction and evidence of LV remodeling. This hospitalization, while awaiting discharge, the patient developed sudden undifferentiated shock requiring norepinephrine and dobutamine. Repeat TTE revealed a 6.0 x 5.5 cm apical LVT filling more than 50% of the LV cavity, with unchanged LV ejection fraction. Heparin drip was started. Prior to evaluation by cardiothoracic surgery, patient became acutely unresponsive, had a cardiac arrest, and expired. Cause of death suspected to be due to cardioembolic events, worsened with mixed shock and low-output heart failure from LVT. Discussion: Management of LVT after MI remains unclear. Current guidelines indicate treatment with vitamin K antagonist (VKA) for at least 3 - 6 months, and consideration of prophylactic anticoagulation with VKA for patients with apical dyskinesis after MI. Retrospectively, this patient may have benefitted from a prolonged course of anticoagulation given the extent of LV remodeling five months after initial event despite resolution of LVT. Anticoagulation must be evaluated on a case-by-case basis weighing propensity of thrombotic events with risk of bleeding.

Coronavirus disease 2019 and cardiovascular disease: what we have learnt during the last 2 years.

Coronavirus disease 2019 and cardiovascular disease: what we have learnt during the last 2 years.

Echocardiographic outcomes of left bundle branch versus deep septal pacing

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Left bundle branch area pacing (LBBAP) is a rising technique that aims to preserve physiologic activation of the left ventricle. However, left bundle branch capture (LBBC) is not always achieved despite good progression of the lead into the interventricular septum, leading to what has been called deep septal pacing (DSP). In the latter, the conduction system is not captured, whose consequences on systolic function are not well known. The goal of the present work is to evaluate the repercussion on transthoracic echocardiogram (TTE) of capturing or not the left bundle branch. Methods Unicentric prospective study where patients in whom LBBAP was performed were consecutively included if: Previous TTE was available with a left ventricular ejection fraction (LVEF) > 40% A follow-up TTE performed >30 days after the implant was available Ventricular pacing was >40% of the time at the device follow-up LBBC was accepted if any of the following were present: Sudden change of QRS morphology during ventricular threshold test Left bundle potential was registered with an interval to left ventricular activation time (LVAT) equal to stimulus-LVAT time. T-test was used to compare means between continuous variables and chi-squared to test differences between groups in the categorical ones. Two-tailed p value <0.05 was considered statistically significant. Results 20 patients were included, 12 (60%) males, with a mean age of 74.4±10.6 years. Half of the patients (n=10) fulfilled LBBC criteria whereas the rest received DSP. Image 1 summarizes baseline characteristics and differences observed in the control TTE. After a median follow-up of 322 (interquartile range 114-325) days, LVEF increased in LBBC group whereas it decreased in DSP patients. Image 2 shows a slopegraph of the evolution of LVEF by type of stimulation. Indexed LVEDV increased in DSP group, but it was diminished in LBBC patients (p=0.03). Control TTE showed no significant differences in other parameters. Conclusions In non-selected patients with comparable pre-implant baseline characteristics, deep septal pacing was associated with a decrease in LVEF and an increase in LVEDV, while LBB capture showed better outcomes in these two parameters.

Anomalía de Ebstein en la edad pediátrica: algoritmos de manejo y cirugía de reconstrucción del cono de Da Silva

ObjectivesThe objective of this study is to report our casuistry in the Ebstein's anomaly surgery in the last 10 years, to analyze the considerations for surgical decision making in the neonate and present our results in da Silva's “cone” tricuspid reconstruction. MethodsRetrospective observational study that includes 11 patients diagnosed with Ebstein's anomaly operated on at our center from January 2011 to August 2021. Two neonates underwent Starnes procedure and 9 (beyond the neonatal period) Da Silva's “cone” surgery. ResultsThe 2 neonates in follow-up are in Fontan's situation and in functional class i (New York Heart Association). The mean age of patients operated beyond the neonatal period was 9.1±6.0 years. There was no hospital mortality or at follow-up. As postoperative complications, one patient was placed on ECMO for severe right ventricular dysfunction. There was no AV block. The mean follow-up was 5.3 years. Follow-up transthoracic echocardiogram demonstrated a significant reduction in tricuspid regurgitation from 3.7±0.6 to 1.1±0.9 (P<.0001), and the New York Heart Association class improved from 2.3±0.7 to 1.2±0.4 (P<.001). There has been no immediate or follow-up tricuspid valve replacement. ConclusionsThe “Cone” procedure can be performed safely with low morbidity and mortality. In the medium-term follow-up, the echocardiogram shows a significant reduction in the degree of tricuspid regurgitation, the patients have improved their functional class and none have required tricuspid valve replacement.

Ventricular Changes in Patients with Acute COVID-19 Infection: Follow-up of the World Alliance Societies of Echocardiography (WASE-COVID) Study

BackgroundCOVID-19 infection is known to cause a wide array of clinical chronic sequelae, but little is known regarding the long-term cardiac complications. We aim to report echocardiographic follow-up findings and describe the changes in left (LV) and right ventricular (RV) function that occur following acute infection.MethodsPatients enrolled in the World Alliance Societies of Echocardiography-COVID study with acute COVID-19 infection were asked to return for a follow-up transthoracic echocardiogram. Overall, 198 returned at a mean of 129 days of follow-up, of which 153 had paired baseline and follow-up images that were analyzable, including LV volumes, ejection fraction (LVEF), and longitudinal strain (LVLS). Right-sided echocardiographic parameters included RV global longitudinal strain, RV free wall strain, and RV basal diameter. Paired echocardiographic parameters at baseline and follow-up were compared for the entire cohort and for subgroups based on the baseline LV and RV function.ResultsFor the entire cohort, echocardiographic markers of LV and RV function at follow-up were not significantly different from baseline (all P > .05). Patients with hyperdynamic LVEF at baseline (>70%), had a significant reduction of LVEF at follow-up (74.3% ± 3.1% vs 64.4% ± 8.1%, P < .001), while patients with reduced LVEF at baseline (<50%) had a significant increase (42.5% ± 5.9% vs 49.3% ± 13.4%, P = .02), and those with normal LVEF had no change. Patients with normal LVLS (<−18%) at baseline had a significant reduction of LVLS at follow-up (−21.6% ± 2.6% vs −20.3% ± 4.0%, P = .006), while patients with impaired LVLS at baseline had a significant improvement at follow-up (−14.5% ± 2.9% vs −16.7% ± 5.2%, P < .001). Patients with abnormal RV global longitudinal strain (>−20%) at baseline had significant improvement at follow-up (−15.2% ± 3.4% vs −17.4% ± 4.9%, P = .004). Patients with abnormal RV basal diameter (>4.5 cm) at baseline had significant improvement at follow-up (4.9 ± 0.7 cm vs 4.6 ± 0.6 cm, P = .019).ConclusionsOverall, there were no significant changes over time in the LV and RV function of patients recovering from COVID-19 infection. However, differences were observed according to baseline LV and RV function, which may reflect recovery from the acute myocardial injury occurring in the acutely ill. Left ventricular and RV function tends to improve in those with impaired baseline function, while it tends to decrease in those with hyperdynamic LV or normal RV function.

IN THE HEART OF IT: A RARE PRESENTATION OF DISSEMINATED CRYPTOCOCCUS

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Since the emergence of highly active antiretroviral therapy (HAART), incidence cryptococcosis has fallen. We discuss a rare presentation of disseminated cryptococcosis. CASE PRESENTATION: A previously well 31 year old woman presented with 3 weeks of nausea, vomiting & headache. She was sent to hospital when she developed dizziness & palpitations after a positive HIV test was found on an outpatient visit. Examination revealed diffuse adenopathy. Urine was positive for opiates, cannabinoids & barbiturates. Non-contrast computed tomography head revealed no acute abnormalities, but abdomen/pelvis found abdominal & retroperitoneal lymphadenopathy. On day 2, she developed diaphoresis, cold extremities with HR160bpm, BP89/53mmhg, RR44bpm, SpO289% & T100F. She was intubated & put on vasopressors. She subsequently had 3 PEA cardiac arrests with return of spontaneous circulation after several minutes. Bedside transthoracic echocardiogram (TTE) revealed a severely hypokinetic dilated right ventricle (RV) & underfilled left ventricle (LV). Bedside transesophageal echocardiogram noted hyperdynamic apex, akinetic base & echogenic material within the right pulmonary artery, concerning for a pulmonary embolism. Hemodynamic instability was refractory to thrombolytics & she was placed on veno-arterial ECMO. She was empirically given vancomycin, piperacillin-tazobactam & clindamycin/primaquine. Blood cultures were later positive for yeast, so caspofungin & fluconazole added. Follow-up TTE showed minimal improvement in RV or LV function. On day 3, after 24 hours off sedation, pupils were dilated & brainstem reflexes absent. Apnea test confirmed brain death. After expiration, HIV viral load was found to be 528,000 copies/ml (reference range: not detected), CD4 was <20 cells/mcl (490-1740cells/mcl), & Cryptococcus neoformans was isolated, with titer ≥1:2560 (normal: negative). DISCUSSION: Cryptococcosis is the most common fungal disease in HIV, but its incidence has decreased in the US. Earlier HIV diagnosis & HAART explain this. It most commonly affects the nervous system. Occasionally, blood cultures are positive indicating disseminated disease. We postulate that pulmonary vascular occlusion can occur due to disseminated cryptococcal infection. Cryptococcomas are extremely rare solid tumor-like masses which have been reported to invade the central nervous system & the skin. Our suspicion for this is high given her poor response to TPA & significant fungemia which likely led to right heart failure & cardiovascular collapse. Literature review identified one other such case. More common sequelae include meningitis or pulmonary involvement. Amphotericin B & Flucytosine represent the most potent therapy for severe disease. CONCLUSIONS: Cardiopulmonary collapse from right heart failure with disseminated cryptococcus is extremely rare. Early diagnosis & treatment of HIV remains the most important tool. REFERENCE #1: Bramantono, B., Danial, A., & Hadi, U. (2020). A case of an AIDS patient with Cryptococcus neoformans infection. The Pan African medical journal, 36, 88. https://doi.org/10.11604/pamj.2020.36.88.20406 REFERENCE #2: Gültaşli NZ, Ercan K, Orhun S, Albayrak S. MRI findings of intramedullary spinal cryptococcoma. Diagn Interv Radiol. 2007 Jun;13(2):64-7. PMID: 17562509. REFERENCE #3: Sperry BW, Howard EW, Gitterman S, Panza JA. A case of cryptogenic dyspnea: disseminated cryptococcosis. Am J Med. 2014 Aug;127(8):707-10. doi: 10.1016/j.amjmed.2014.04.007. Epub 2014 Apr 21. PMID: 24769024. DISCLOSURES: No relevant relationships by Janeen Grant-Sittol, source=Web Response No relevant relationships by Lena Makartian, source=Web Response No relevant relationships by Priya Patidar, source=Web Response No relevant relationships by Rani Sittol, source=Web Response

Bioprosthetic Valve Thrombosis Associated With COVID-19 Infection

HomeCirculation: Cardiovascular ImagingVol. 14, No. 5Bioprosthetic Valve Thrombosis Associated With COVID-19 Infection Free AccessCase ReportPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplementary MaterialsFree AccessCase ReportPDF/EPUBBioprosthetic Valve Thrombosis Associated With COVID-19 Infection Steven A. Alexander, MD, Icilma V. Fergus, MD and Stamatios Lerakis, MD, PhD Steven A. AlexanderSteven A. Alexander Steven A. Alexander, MD, Icahn School of Medicine at Mt Sinai, 1 Gustave L. Levy Pl, Box 1030, New York, NY 10029. Email E-mail Address: [email protected] https://orcid.org/0000-0002-0719-9177 The Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, NY. Search for more papers by this author , Icilma V. FergusIcilma V. Fergus The Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, NY. Search for more papers by this author and Stamatios LerakisStamatios Lerakis https://orcid.org/0000-0001-7487-1990 The Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, NY. Search for more papers by this author Originally published5 Feb 2021https://doi.org/10.1161/CIRCIMAGING.120.012118Circulation: Cardiovascular Imaging. 2021;14:e012118Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: February 5, 2021: Ahead of Print Obstructive bioprosthetic valve thrombosis is a rare but potentially devastating complication.1 Coronavirus disease 2019 (COVID-19) predisposes patients to both venous and arterial thrombosis.2–4 The impact this may have on patients with endovascular prosthetic material is unknown. We report a case of obstructive bioprosthetic aortic valve thrombosis in a patient hospitalized with COVID-19.A 79-year-old woman presented to clinic with a 2-month history of dyspnea and cough. Four months prior, she was treated for a type A aortic dissection with hemiaortic arch and bioprosthetic aortic valve replacement. She initially recovered but was hospitalized 2 months later with COVID-19 pneumonia. Laboratory evaluation at that time showed elevated C-reactive protein (79.8 mg/dL), activated partial thromboplastin time (44.2 s), fibrinogen (489 mg/dL), and D-dimer (2.14 μg/mL). She was treated with convalescent plasma and received prophylactic low molecular weight heparin. Her hospital course was uncomplicated, and she was discharged on apixaban 5 mg twice daily.A transthoracic echocardiogram showed prosthetic aortic valve stenosis with a peak aortic velocity of 3.8 m/s, increased from 2.2 m/s postoperatively. A transesophageal echocardiogram revealed markedly thickened bioprosthetic valve leaflets (Figure 1, Movie I in the Data Supplement). A computed tomography scan showed hypoattenuated leaflet thickening involving all 3 valve leaflets consistent with leaflet thrombosis (Figure 2).Download figureDownload PowerPointFigure 1. Prosthetic aortic valve thrombosis. Biplane transesophageal echocardiogram (TEE) at the level of the aortic valve showing marked thickening of the bioprosthetic aortic valve leaflets, consistent with leaflet thrombosis.Download figureDownload PowerPointFigure 2. Hypoattenuated leaflet thickening of the prosthetic aortic valve.A, Short axis and (B) long-axis views of the aortic valve on computed tomography showing hypoattenuated leaflet thickening (HALT; white arrows). Ao indicates aorta; LA, left atrium; PA, pulmonary artery; and RA, right atrium.The patient was admitted to the hospital, started on an unfractionated heparin infusion, and bridged to warfarin with a goal internationalized normalized ratio of 2.5 to 3.5. Follow-up transthoracic echocardiogram performed 3 months later showed improvement of her aortic valve gradient back to baseline (Figure 3).Download figureDownload PowerPointFigure 3. Prosthetic aortic valve gradient before and after 3 mo of warfarin.A, The peak aortic valve velocity was 3.8 m/s before treatment and (B) decreased to 2.2 m/s after treatment.To our knowledge, this is the first report of prosthetic aortic valve thrombosis associated with COVID-19 infection. This case reminds us that patients with prosthetic heart valves and endovascular devices may be at particular risk of thrombotic complications from COVID-19. Health care providers should have a high index of suspicion for such complications and consider diagnostic imaging when appropriate. Further research is needed to determine the optimal anticoagulation strategy for both the prevention and treatment of bioprosthetic valve thrombosis in the setting of COVID-19 infection.Sources of FundingNone.Supplemental MaterialData Supplement Movie IDisclosures None.FootnotesThe Data Supplement is available at https://www.ahajournals.org/doi/suppl/10.1161/CIRCIMAGING.120.012118.Steven A. Alexander, MD, Icahn School of Medicine at Mt Sinai, 1 Gustave L. Levy Pl, Box 1030, New York, NY 10029. Email steven.[email protected]org

The Impact of Aortic Valvular Calcium on Transcatheter Heart Valve Distortion.

Objectives To investigate the relationship between the eccentric calcification of aortic valve and transcatheter heart valve (THV) distortion and the impact of THV distortion on echo parameters and clinical outcomes. Background The effects of eccentric calcification of the aortic valve on the THV distortion and the relationship between THV distortion and clinical impact were not fully understood. Methods Patients with symptomatic severe aortic stenosis who were undergoing THV implantation were enrolled. Patients underwent preprocedural, postprocedural multislice computed tomography (MSCT), and follow-up transthoracic echocardiogram (TTE). Delta calcium score (ΔCS) is defined as the difference between the maximum and minimal calcium scores of the three cusps, while valve distortion score (VDS) is defined as the difference between the longest and shortest stent frame, as obtained using MSCT. Patients were divided into two groups according to ΔCS: “noneccentric calcification group” and “eccentric calcification group.” Results A total of 118 patients were enrolled (59 patients in noneccentric and 59 in eccentric calcification groups). VDS was significantly lower in the noneccentric calcification group than in the eccentric calcification group (1.31 ± 0.82 mm vs. 1.73 ± 0.76 mm, p=0.004). VDS was not associated with the degree of paravalvular leak (PVL) and aortic valvular mean pressure gradient (AVPG) at 30-day and 1-year follow-up TTE and the cumulative rates of all-cause death and rehospitalization at 2-year clinical follow-up. Conclusions Eccentric valvular calcification was associated with longitudinal THV distortion. However, THV distortion was not associated with PVL, AVPG, and adverse clinical events during midterm follow-up.

Echocardiographic diagnosis of permanent pacemaker lead malposition in the left ventricle: A case study.

Inadvertent endocardial lead malposition is recognized as a rare incident which is usually underreported and if recognized during implantation can be easily corrected. This phenomenon is caused by the ventricular lead unintentionally crossing a pre-existing patent foremen ovale, septal defects (atrial or ventricular) or directly from the aorta via an accidental subclavian puncture resulting in the lead implanting into the left ventricle. While this is a rare occurrence we report, the incidental finding of pacemaker lead malposition during a routine follow-up transthoracic echocardiogram and the benefits of three-dimensional transesophageal echocardiography in this patient prior to lead extraction.

Treatment Dilemma in Systemic Lupus Erythematous Related Cardiomiopathy

Background Systemic Lupus Erythematous (SLE) is an autoimmune disease that is known to cause many cardiac complications including lesions of the valves, myocardium, pericardium, and the coronary vessel. However, the management of SLE induced cardiomyopathy remains controversial. Case presentation A 59-year-old African American woman with a medical history of hypertension presented with dyspnea on exertion for a few days. Physical exam revealed distended neck vein, lung crackles, and leg swelling. EKG showed normal sinus rhythm. Transthoracic echocardiogram (TTE) showed a left ventricular ejection fraction of 10% (LVEF). Decision-making The patient was treated with intravenous diuretic and improved symptomatically. She underwent a coronary angiogram, which showed normal coronary arteries and cardiac MRI didn't reveal any signs of myocarditis or infiltrative cardiomyopathy. We started guideline-directed medical therapy (GDMT) including losartan, carvedilol, and spironolactone, and titrated up accordingly. In a follow-up echocardiogram after 3 months, LVEF remained unchanged while on optimal GDMT. She developed a skin rash with fatigue and further investigations showed evidence of SLE. With the presence of heart failure and newly diagnosed SLE, the underlying cause of cardiomyopathy was most likely due to SLE. At this point, we were perplexed on how to approach SLE related cardiomyopathy and decided to treat underlying autoimmune disease with rituximab, hydroxychloroquine, and methylprednisolone. A follow-up TTE in a month disclosed LVEF of 40-45%. Conclusion The role of GDMT is unclear in SLE induced cardiomyopathy and has never been tested in randomized trials. However, treatment of SLE with immunomodulating therapies could ameliorate and even reverse the cardiomyopathy, which was demonstrated in our case. Early recognition of SLE and aggressive intervention is paramount for recovery in SLE related cardiomyopathy.

Gout and Progression of Aortic Stenosis

BackgroundPatients with aortic stenosis are nearly twice as likely to have a diagnosis of gout compared with individuals without aortic valve disease. MethodsThis retrospective study evaluated consecutive adults age ≥65 years with aortic stenosis between December 2012 and November 2016 who underwent at least 2 transthoracic echocardiograms (TTEs) separated by at least 1 year. Severe aortic stenosis was defined as any combination of an aortic valve peak velocity ≥4.0 m/sec, mean gradient ≥40 mm Hg, aortic valve area ≤1 cm2, or decrease in left ventricular ejection fraction as a result of aortic stenosis. ResultsOf the 699 study patients, gout was present in 73 patients (10%) and not found in 626 patients (90%). Median follow-up was 903 days [552-1302] for patients with gout and 915 days [601-1303] for patients without gout (P = 0.60). The presence of severe aortic stenosis on follow-up transthoracic echocardiogram was more frequent in patients with gout compared to those without gout (74% vs 54%, P = 0.001; hazard ratio [HR] 1.45 [1.09-1.93]), even among the 502 patients without severe aortic stenosis at baseline (63% vs 39%, P = 0.003; hazard ratio 1.43 [1.07-1.91]). Gout remained associated with the development of severe aortic stenosis after multivariable adjustment (adjusted hazard ratio [aHR] 1.46 [1.03-2.08], P = 0.03). The annualized reduction in aortic valve area was numerically greater in the group with gout compared with the group without gout (−0.10 cm2/y [−0.18, −0.03] vs −0.08 cm2/y [−0.16, −0.01], P = 0.09); annualized change in peak velocity and mean gradient did not differ between groups. ConclusionsProgression to severe aortic stenosis was more frequent in patients with gout compared with those without gout, supporting the hypothesis that gout is a risk factor for aortic stenosis.

Cardiac Transplantation Using Hearts With Transient Dysfunction: Role of Takotsubo-Like Phenotype

The impact of different types of regional wall motion abnormalities (RWMAs), including the Takotsubo syndrome-like (TTS-like) phenotype, on posttransplant outcomes when using donor hearts with transient left ventricular systolic dysfunction (LVSD) is unknown. We evaluated the prevalence, clinical characteristics, and prognostic association of different RWMAs including TTS-like hypokinesis and posttransplant outcomes when using donor hearts with transient LVSD. From all adult (≥18 years) heart transplants in United Network of Organ Sharing between January 2007 and September 2015, we identified 472 donor hearts with improving or transient LVSD, defined as left ventricular ejection fraction ≤ 40% on initial transthoracic echocardiogram (TTE) that improved to ≥50% on follow-up TTE during donor evaluation. These improved LVSD donors were then subdivided into 3 groups based on RWMAs on the initial TTE, TTS-like (49, 10.38%), non-TTS RWMAs (74, 15.68%), and diffuse global hypokinesis (349, 73.94%), and compared for baseline characteristics and posttransplant outcomes with follow up until June2018. Donors with TTS-like LVSD were older and more likely to be female. The type of RWMA on initial TTE (including TTS-like) of transient LVSD donor hearts was not associated with 1-year or 5-year posttransplant mortality. Posttransplant functional status scores of recipients (at 1 year) and donor left ventricular ejection fraction (at median follow-up of 3.6 years) improved in all 3 subgroups. Rates of stroke or pacemaker predischarge were also similar. In the largest analysis of transplanted donor hearts with transient LVSD, 1 in 4 had RWMAs on the initial TTE, but this was not associated with adverse posttransplant outcomes. Donor hearts with initial LVSD should be pursued irrespective of TTS-like hypokinesis or other RWMAs.