Search

Open in new tab Download slide OBJECTIVES The influence of preoperative left ventricular size in outcomes following centrifugal-flow left ventricular assist device (LVAD) implantation has not been well characterized. METHODS A cohort of 313 patients who received a centrifugal-flow LVAD at a single institution was analysed. Using a maximally selected log-rank statistic, we investigated whether a left ventricular end-diastolic dimension (LVEDD) cut-off point was associated with worse outcomes. The cohort was then divided in 2 groups based on the LVEDD cut-off point. RESULTS An LVEDD cut-off point of 59 mm was found to predict worse survival. Smaller LVEDD patients (≤59 mm, N = 52) were older and more likely to have a history of coronary artery disease compared those with a larger LVEDD (>59 mm, N = 261). Smaller LVEDD patients had lower survival compared to larger LVEDD patients (71% vs 85% at 1 year and 58% vs 80% at 2 years, P = 0.003). The need for temporary right ventricular mechanical support was significantly higher in the smaller LVEDD cohort (11.5% vs 1.9%, P = 0.002). Pump flows at time of discharge were lower in the smaller LVEDD group (3.8 vs 4.2 l/min, P = 0.005), who also had a higher incidence of late right ventricular failure (23% vs 12%, P = 0.02), higher rates of gastrointestinal bleeding (0.416 vs 0.256 events per patient-year, P = 0.025) and higher readmissions secondary to low flow alarms (0.429 vs 0.240 events per patient-year, P = 0.007). Multivariable analysis demonstrated that smaller LVEDD, older age, high BUN and high bilirubin levels were independent predictors of worse survival. CONCLUSIONS In patients receiving a centrifugal-flow LVAD, smaller preoperative LVEDD (≤59 mm) was associated with lower survival and higher incidence of adverse outcomes. [ABSTRACT FROM AUTHOR]

Background: Due to anatomic and physiologic concerns, prior generations of the left ventricular assist devices (LVAD) have frequently been denied to patients with small body size. However, outcomes in patients with small body surface area (BSA) following HeartMate 3 (HM3) LVAD implantation remain relatively unknown. Methods: A cohort of 220 patients implanted at a single center was divided into two groups: BSA ≤1.8 m2 (small BSA, n = 37) and BSA >1.8 m2 (large BSA, n = 183). We investigated baseline characteristics and clinical outcomes including survival and incidence of adverse events. Results: Small BSA patients were older (60 vs. 57 years), more likely female (60% vs. 20%), had a lower body mass index (24 vs. 32 kg/m2), lower incidence of diabetes (32% vs. 51%), history of stroke (5% vs. 19%), and left ventricular thrombus (0% vs. 11%). They had smaller left ventricular end diastolic diameter (64.8 vs. 69.3 mm). Pump speed and pump flows at discharge were lower in the small BSA group. Survival at 1 year and 2 years was 86% versus 87% and 86% versus 79% for small versus large BSA groups (p = 0.408), respectively. The rates of adverse events were similar between groups and there were no cases of confirmed pump thrombosis. The incidence of readmissions for low flow alarms was higher in the small BSA group (0.55 vs. 0.24 EPPY). Conclusions: These findings demonstrate comparable outcomes in patients with small body size and suggest that this parameter should not be an exclusion criterion on patients who are otherwise candidates for HM3 LVAD implantation. [ABSTRACT FROM AUTHOR]

Black women have been underrepresented in left ventricular assist device (LVAD) clinical trials and published reports. The aim of this study was to examine the outcomes of Black women undergoing LVAD implantation. We retrospectively identified Black women who underwent LVAD implantation at a single center between January 1, 2007 and October 31, 2020. Outcomes of patients who received HeartMate II (HMII), HeartWare (HVAD), and HeartMate 3 (HM3) devices were compared. Adverse events (AEs) for all patients were calculated as events per patient-year (EPPY). Reasons for readmissions, including incidence and rates, were reviewed. A total of 154 Black female patients underwent LVAD implantation during the study period. Sixty-six received HVAD, 36 received HMII, and 52 received HM3 devices (Figure 1). Median age for all patients was 57.7 years (IQR 46.9-64). At baseline, patients supported with HMII and HM3 were more likely to have diabetes compared to those supported with HVAD (HM3 50% vs HMII 50% vs HVAD 22.7%, p=0.003). HM3 recipients had a higher incidence of stroke pre-operatively (17.3% vs HMII 13.9% vs HVAD 3%, p=0.03). Post-operatively, HM3 recipients were on inotropes for longer duration (14 days vs HMII 9 days vs HVAD 8.5 days (IQR 5.3-16), p=0.004) and were placed on Epoprostenol at higher frequency (65.4% vs HMII 27.8% vs HVAD 39.4%, p=0.001). In regards to AEs, the incidence of LVAD-related infections was 25.3%, gastrointestinal bleeding was 33.8%, and cerebrovascular accidents was 14.3%. Twenty-nine pump thrombosis events occurred in 20 (13%) patients. Overall, patients supported with HM3 demonstrated lower rates of pump thrombosis (EPPY: 0.008 vs HMII 0.216 vs HVAD 0.062, p<0.001 and p=0.034, respectively)(Figure 1). HM3 patients experienced fewer readmissions for LVAD infection compared to HMII patients (EPPY: 0.19 vs HMII 0.49, p=0.001) as well as for cardiac arrhythmias (EPPY: 0.07 vs HMII 0.26, p=0.003). Hospitalization for LVAD alarms was significantly higher in the HM3 population (44% vs. HMII 19.4%, p<0.001). Black Women LVAD recipients experienced differential outcomes post-LVAD by device type including rates of pump thrombosis, infection, and hospitalization for LVAD alarms. Additional studies are warranted to further examine racial and sex disparities in pre- and post-LVAD clinical outcomes. [ABSTRACT FROM AUTHOR]

Cardiac sarcoidosis (CS) may present with cardiomyopathy that progresses to end-stage heart failure requiring left ventricular assist device (LVAD) therapy. Advanced cardiac imaging including fluorodeoxyglucose-positron emission tomography (FDG-PET) has emerged as a tool in the management of CS. The utility of FDG-PET in guiding immunosuppressive (IS) therapy after LVAD remains unclear. The present study aimed to examine the use of FDG-PET to monitor CS post-LVAD and to assess its clinical impact on IS treatment practices. A single-center, retrospective cohort study was performed. The Japanese Circulation and Heart Rhythm Society diagnostic criteria was used to characterize CS LVAD recipients between 2013 and 2021. Thirty-nine CS patients underwent LVAD implantation during the study period (Figure 1). Fourteen patients (35.9%) were classified as having possible CS, 11 (28.2%) probable CS, and 14 (35.9%) definite CS. Median age of LVAD implantation was 51.5 years (IQR 44.6-58.8), 25 (64.1%) were men, and 32 (82.1%) were Black individuals. Twenty (51.3%) had prior VT/VF and 29 (74.4%) had an established diagnosis of sarcoidosis prior to LVAD, with a median age of diagnosis of 49.5 years (IQR 41.3-57.1). Pre-LVAD, cardiac FDG-PET uptake was present in 16 (41%) patients and 17 (43.4%) were treated with corticosteroids. Fifteen (38.5%) patients underwent FDG-PET post-LVAD (Figure 1). A total of 23 FDG-PET scans were performed, 8 (34.5%) of which were found to have an LVAD artifact challenging interpretation. Of the 15 patients, 12 were on IS and 3 were not on IS based on FDG-PET findings negative for active inflammation. IS was adjusted on the basis of PET findings in 6 out of 12 (50%) patients. Among these 6 patients, 3 had IS adjustments made based on surveillance only, while 3 had IS adjusted due to surveillance and IS side effects. Six of the 12 (50%) patients had IS changes made due to IS side effects. The management of IS therapy in CS LVAD recipients is driven by FDG-PET findings, changes in clinical status and IS side effects. Surveillance imaging may help direct IS management in CS with advanced heart failure, but additional studies are required to further evaluate and establish how to best manage CS patients post-LVAD. [ABSTRACT FROM AUTHOR]

Management of Cardiovascular Implantable Electronic Device Infections (CIEDI) in patients with Left Ventricular Assist Devices (LVADs) poses a clinical challenge. There is a paucity of data regarding evidence-based treatment approach and outcomes of these patients. The aim of the study was to describe CIEDI occurring in patients with concomitant LVADs, their treatment approach, and clinical outcomes. We identified 390 LVAD patients who had a coexisting CIED between January 1st, 2010, to December 31st, 2019, at a single institution. A retrospective cohort analysis was performed. Follow up period was one year from the time of the first CIEDI. Mean age of the patients was 58 ± 12 years, and 10 (71%) of them were men. The incidence of CIEDI was four percent (n=14, Figure 1). Five (36%) of these patients had prior LVAD infections; 2 had LVAD pump infection, 2 had driveline infection, and 1 had both pump and driveline infection. The most common pathogen identified in CIEDI was Staphylococcus aureus (n=4); other common organisms included Staphylococcus epidermidis (n=3), and Enterococcus faecalis (n=2). Eleven (79%) patients had CIED lead vegetations, 2 (14%) had pocket infection, and 2 (14%) had tricuspid valve endocarditis. Thirteen (93%) patients underwent device extraction and 8 (57%) were placed on lifelong antimicrobial therapy. Five (36%) patients had resolution of the infection, all of them having undergone successful device extraction. Seven (50%) patients had relapse after the initial treatment. Two died prior to completion of therapy to allow for determination of outcome, cause of death being stroke and septic shock respectively. Nine (64%) patients were alive at 1 year follow up. Incidence of CIEDI in LVAD patients is low, however, the burden of morbidity and mortality associated with the infection remains high despite aggressive multimodality treatment approach. [ABSTRACT FROM AUTHOR]

The feasibility of using chronic intravenous inotropic support (CIIS) in patients with advanced heart failure due to cardiac sarcoidosis (CS) has not been evaluated. Given the known clinical manifestations of this disease, CS patients may be at higher risk for complications including ventricular arrhythmias (VAs), infections, and acute decompensated heart failure (ADHF) requiring hospitalizations. We sought to evaluate the utilization of CIIS in CS patients as bridge therapy to surgical treatments such as durable left ventricular assist device (LVAD) or heart transplantation (HT). A single center retrospective review of all CS patients placed on CIIS as bridge therapy from 2011 to 2021 was conducted. Adverse events including hospitalizations due to VAs, infections and ADHF occurring <30days, 30-90days, and >90days of CIIS were observed and analyzed using descriptive statistics. Of 41 patients 63% men (n=26), 82% Black (n=34), with a mean age 52 ± 11 years, 78% (n=32) patients were on CIIS for less than 90 days prior to receiving LVAD/HT, with 53% (17 out of 32) of these patients requiring LVAD/HT within 30 days of CIIS initiation. Worsening shock (42%, 4 out 7 admissions) was the leading cause of all hospitalizations in the <30day cohort (n=17), requiring escalation of inotropic support and/or urgent LVAD implantation. Admissions secondary to ADHF, worsening cardiogenic shock, and elective LVAD implantation or HT were all equally distributed in the 30-90d group (n=15) with 25% (4 out of 16 hospitalizations) each. Four patients were electively admitted to receive an LVAD in this group. Amongst the >90d CS subgroup (n=9), the leading cause was ADHF (32%, 7 out of 22 admissions), followed by infections (23%, 5 out of 22) and non-cardiac events (23%, 5 out 22). Three patients were admitted for worsening cardiogenic shock (14%) and two patients (9%) were electively hospitalized for LVAD or HT surgeries in this cohort. There was no incidence of VAs or hospitalizations for ICD discharges in this group. ICD- lead malfunction, central line access complications, and thromboembolic events were some of the additional events that brought patients into the hospital. Overall, there were no deaths amongst the CS group awaiting LVAD/HF therapies. In a large single center cohort, CIIS successfully bridged all 41 CS patients to LVAD/HT. The incidence of VAs and ICD discharges was low. Future research should be focused on assessing the best strategies to assist advanced HF CS patients to receive LVAD and Heart Transplantation. [ABSTRACT FROM AUTHOR]

Tricuspid Regurgitation (TR) is a common risk factor for acute decompensated heart failure (ADHF). However, less is known about the impact of TR on the response of non-invasive indices of decongestion such as weight loss/fluid loss, and right atrial pressure (RAP) to diuretic therapy. We examined these associations in patients hospitalized with ADHF. We studied 54 consecutive advanced HF patients admitted for ADHF, who underwent two right heart catheterizations during their hospitalization. These patients also had two-dimensional echocardiographic (TTE) assessments performed during the same hospitalization. Most patients were African American (65%), men (77%) with a mean age of 58 years. Twenty-one (39%) patients had at least moderate and severe TR (mod-sev TR) vs 33 (61%) had no to mild TR (no-mild TR). Compared to patients with mod-sev TR, those with no-mild TR had similar mean weight loss (3.7 ± 7.7 vs. 3.7 ± 7.6 kg, p =0.35) and similar mean fluid loss of (7.8 ± 8.7 vs. 8 ± 9 liters, p =0.62). The 2 groups had similar mean RAP at baseline (no-mild TR 15 ± 7.8 mm Hg; mod-sev TR 16 ± 5.9 mm Hg; p= 0.59). They also had similar changes in mean RAP after diuresis (-5.8 ± 8.9 mm Hg vs. -6.6 ± 6.9 mm Hg, p =0.72). There was modest correlation noted between net fluid loss and weight loss in no-mild TR group (r= 0.44; p= 0.01) whereas no correlation was noted between net fluid loss and weight loss in mod-sev group (r= 0.86; p =0.99). There was also no correlation between change in weight and change in RAP (no-mild TR r= 0.12; p= 0.51; mod-sev TR r= 0.11; p= 0.68) or change in fluid balance and change in RAP (no-mild TR r= 0.01; p =0.95; mod-sev TR r= 0.35; p =0.94) in either group. In patients with advanced heart failure admitted with acute decompensation, there is no effect of TR on decongestion or changes in RAP as conventional noninvasive methods to assess decongestion such as change in weight and in fluid balance, poorly reflect changes in RAP in patients with no-mild TR and those with mod-sev TR. This warrants a need to identify novel non-invasive markers of decongestion in patients admitted with acute decompensated heart failure. [ABSTRACT FROM AUTHOR]

Iatrogenic chordal rupture with severe mitral regurgitation is a rare but serious complication associated with the use of Impella device. We present a case of a 47-year-old man with ischemic cardiomyopathy who required insertion of an Impella 5.0 device. During Impella support, he developed acute pulmonary edema secondary to newly diagnosed posterior mitral valve chordal rupture and subsequent severe mitral regurgitation. He underwent implantation of a durable left ventricular assist device with concomitant edge-to-edge mitral valve repair through the apex. [ABSTRACT FROM AUTHOR]

A 73-year-old white female with history of bilateral carpal tunnel syndrome, lumbar spinal stenosis, and family history of cardiomyopathy presented with worsening dyspnea on exertion. Exam showed right-sided crackles. There was no jugular venous distention, edema, macroglossia, or peri-orbital ecchymosis. ECG demonstrated low voltage in all leads and no significant ST segment changes (Figure 1A). Labs showed undetectable troponin-I and normal NT-proBNP (119pg/mL). TTE revealed LVEF 55-65%, grade II diastolic dysfunction, thick and bright ventricular walls and global longitudinal strain of -17.9% with relative apical sparing (Figure 1B, Figure 1C). TTE findings raised concern for an infiltrative cardiomyopathy, specifically amyloidosis. Additional labs found polyclonal gammopathy on serum immunofixation with increased IgA (590mg/dL), kappa (20.4mg/L) and lambda (14.0mg/L). However, free kappa-to-lambda ratio (1.46) was normal. There was no monoclonal spike on urine immunofixation. Anti-neutrophil antibody screen was negative, and cobalt was undetectable. Ferritin (17ng/mL), C-reactive protein (0.8mg/L), and erythrocyte sedimentation rate (27mm/hr) were normal. Cardiac MRI found mild concentric left ventricular wall thickening up to 11 mm and late gadolinium enhancement throughout the myocardium (Figure 1D). Endomyocardial biopsy showed patchy fibrosis but no evidence of amyloidosis on Congo red staining. No granulomatous disease or inflammatory infiltrate was seen. Cutaneous nerve biopsy was also negative for amyloidosis. Technetium-99m pyrophosphate scan was negative for transthyretin amyloidosis with normal heart-to-lung ratio (1.3). Genetic testing for infiltrative cardiomyopathy genotypes revealed phenotypically silent heterozygosity for HFE hereditary hemochromatosis. Hereditary amyloidosis testing was negative. Twelve-day ambulatory cardiac monitoring showed 11% PVC burden with multiple morphologies and three episodes of non-sustained VT. Amiodarone 200mg daily was initiated as opposed to therapeutic ablation due to multifocal nature of PVCs. The patient continued to have dyspnea on exertion but remained functionally independent. PET imaging was attempted, however the patient did not tolerate the dietary preparation. A total evaluation is essential for infiltrative cardiomyopathy. History, exam, and preliminary testing in this case suggested cardiac amyloidosis; however, comprehensive evaluation could not support this diagnosis or an alternate mechanism. Despite diagnostic innovations including advanced cardiac imaging and genetic testing, the cause of infiltrative cardiomyopathy can remain obscure. [ABSTRACT FROM AUTHOR]

Cobalt toxicity is a rare cause of infiltrative cardiomyopathy. We describe a case of cobalt-induced cardiomyopathy that progressed to end stage heart failure requiring orthotopic heart transplantation. A 67 year old woman with history of bilateral cobalt-chromium hip replacements presented with dyspnea of 3 weeks duration. She was tachycardic and hypotensive, with elevated NT- proBNP. Electrocardiogram demonstrated sinus tachycardia, low voltage and right bundle branch block. Transthoracic echocardiogram revealed left ventricular ejection fraction of 20-25% with global hypokinesis and a moderate circumferential pericardial effusion. Left and right heart catheterization showed normal coronaries, elevated filling pressures and low cardiac index. Dobutamine infusion was initiated for management of cardiogenic shock. Cardiac magnetic resonance imaging (MRI) illustrated diffuse late gadolinium enhancement concerning for infiltrative cardiomyopathy. Extensive non-ischemic and rheumatologic workup was negative. Cobalt and chromium levels were significantly elevated at 121 mcg/L (Nl <=1mcg/L) and 46 mcg/L (Nl <=5 mcg/L) respectively, concerning for cobalt-induced cardiomyopathy. MRI of the hips showed pseudotumor formation surrounding the left prosthesis. She underwent left hip arthroplasty with removal of the source, and was placed on oral chelation therapy. She was discharged home on inotropic support. Despite decline in serum cobalt and chromium levels, the patient was readmitted with cardiogenic shock requiring a second inotropic agent. She was stabilized and evaluated for heart transplant. She underwent successful cardiac transplantation and was discharged to a rehab facility. Pathology of the native heart with electron microscopy revealed cardiomyocytes with enlarged distorted mitochondria, large lipid droplets and elevated tissue cobalt level of 0.95 mcg/g (reporting limit <0.018 mcg/g) consistent with cobalt-induced cardiomyopathy. Cobalt-induced cardiomyopathy is a potentially reversible cause of infiltrative cardiomyopathy, with the diagnosis hinging on obtaining a thorough medical history. Treatment includes routine heart failure management and removal of the cobalt source with the role of chelation therapy remaining unclear. Once progressed to end stage heart failure, preferred treatment is cardiac transplantation. [ABSTRACT FROM AUTHOR]

Background/purpose: The aim of this study is to characterize the pattern and the severity of coronary artery lesions in cardiac amyloidosis.Methods: We retrospectively compared patients with heart failure who tested positive (i.e., biopsy or gene tests - HF/CA+) against those who tested negative (HF/CA-) for cardiac amyloidosis. Groups were compared demographically and angiographically for qualitative and quantitative variables to determine patterns of involvement in the major epicardial coronary vessels.Results: The study included 110 heart failure patients, of whom 55 patients (88 lesions) were in the HF/CA+ group, and 55 patients (66 lesions) were HF/CA-. Despite the advanced age of HF/CA+ patients (74.5 ± 11.0 years vs. 54.1 ± 15.0 years; p = 0.05), no severe calcification was found in the HF/CA+ group (0.0% vs. 4.5%; p = 0.018). The HF/CA+ group also had fewer ostial lesions (3.4% vs. 15.1%; p = 0.0095) and a higher, albeit not significant, Thrombolysis in Myocardial Infarction frame count (30.4 ± 12.6 vs. 26.6 ± 11 frames; p = 0.06). In the HF/CA+ group, men had a significant number of tandem lesions compared to women (14.5% vs 0.0%, p = 0.02).Conclusions: Overall, heart failure patients with cardiac amyloidosis were older but were found to have less calcified lesions, less ostial involvement, and a reduced anterograde coronary blood flow. This is the first report examining coronary lesions in heart failure patients with cardiac amyloidosis. [ABSTRACT FROM AUTHOR]