AIMS:We sought to characterize circulating protein biomarkers associated with cardiogenic shock (CS) using highly multiplex proteomic profiling. METHODS AND RESULTS:This analysis employed a cross-sectional case-control study design using a biorepository of patients admitted to a cardiac intensive care unit between 2017 and 2020. Cases were patients adjudicated to have CS, and controls were those presenting for cardiac critical care without shock, including subsets of patients with isolated hypotension or heart failure (HF). The Olink platform was used to analyse 359 biomarkers with Bonferroni correction. The analysis included 239 patients presenting for cardiac critical care (69 cases with CS, 170 non-shock controls). A total of 63 biomarkers (17.7%) were significantly associated with CS after Bonferroni correction compared with all controls. Of these, nine biomarkers remained significantly associated with CS when separately cross-validated in subsets of controls presenting with isolated hypotension and HF: cathepsin D, fibroblast growth factor (FGF)-21 and -23, growth differentiation factor (GDF)-15, insulin-like growth factor-binding protein-1, N-terminal pro-B-type natriuretic peptide, osteopontin, oncostatin-M-specific receptor subunit beta (OSMR), and soluble ST2 protein (sST2). Four biomarkers were identified as providing complementary information for CS diagnosis with development of a multi-marker model: sST2, FGF-23, CTSD, and GDF-15. CONCLUSION:In this pilot study of targeted proteomic profiling in CS, we identified nine biomarkers significantly associated with CS when cross-validated against non-shock controls including those with HF or isolated hypotension, illustrating the potential application of a targeted proteomic approach to identify novel candidates that may support the diagnosis of CS.

HomeCirculation: Heart FailureVol. 14, No. 12Epidemiology of Cardiogenic Shock in Hospitalized Adults With COVID-19: A Report From the American Heart Association COVID-19 Cardiovascular Disease Registry Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBEpidemiology of Cardiogenic Shock in Hospitalized Adults With COVID-19: A Report From the American Heart Association COVID-19 Cardiovascular Disease Registry Anubodh S. Varshney, Wally A. Omar, Erica L. Goodrich, Ankeet S. Bhatt, Ann E. Wolley, Jingyi Gong, Balimkiz C. Senman, Danuzia Silva, Michael W. Levangie, David D. Berg, Robert W. Yeh, James A. de Lemos, David A. Morrow, Dhruv S. Kazi and Erin A. Bohula Anubodh S. VarshneyAnubodh S. Varshney https://orcid.org/0000-0002-9697-8948 Levine Cardiac Intensive Care Unit, Thrombolysis in Myocardial Infarction Study Group, Cardiovascular Division, Department of Medicine (A.S.V., E.L.G., A.S.B., M.W.L., D.D.B., D.A.M., E.A.B.), Brigham and Women's Hospital and Harvard Medical School, Boston, MA. , Wally A. OmarWally A. Omar Richard A. and Susan F. Smith Center for Outcomes Research in Cardiology, Division of Cardiovascular Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA (W.A.O., R.W.Y., D.S.K.). , Erica L. GoodrichErica L. Goodrich https://orcid.org/0000-0002-8541-264X Levine Cardiac Intensive Care Unit, Thrombolysis in Myocardial Infarction Study Group, Cardiovascular Division, Department of Medicine (A.S.V., E.L.G., A.S.B., M.W.L., D.D.B., D.A.M., E.A.B.), Brigham and Women's Hospital and Harvard Medical School, Boston, MA. , Ankeet S. BhattAnkeet S. Bhatt Levine Cardiac Intensive Care Unit, Thrombolysis in Myocardial Infarction Study Group, Cardiovascular Division, Department of Medicine (A.S.V., E.L.G., A.S.B., M.W.L., D.D.B., D.A.M., E.A.B.), Brigham and Women's Hospital and Harvard Medical School, Boston, MA. , Ann E. WolleyAnn E. Wolley Division of Infectious Disease, Department of Medicine (A.E.W.), Brigham and Women's Hospital and Harvard Medical School, Boston, MA. , Jingyi GongJingyi Gong Department of Medicine (J.G., B.C.S.), Brigham and Women's Hospital and Harvard Medical School, Boston, MA. , Balimkiz C. SenmanBalimkiz C. Senman Department of Medicine (J.G., B.C.S.), Brigham and Women's Hospital and Harvard Medical School, Boston, MA. , Danuzia SilvaDanuzia Silva University of Minnesota Medical School, Minneapolis (D.S.). , Michael W. LevangieMichael W. Levangie Levine Cardiac Intensive Care Unit, Thrombolysis in Myocardial Infarction Study Group, Cardiovascular Division, Department of Medicine (A.S.V., E.L.G., A.S.B., M.W.L., D.D.B., D.A.M., E.A.B.), Brigham and Women's Hospital and Harvard Medical School, Boston, MA. , David D. BergDavid D. Berg https://orcid.org/0000-0002-0366-5492 Levine Cardiac Intensive Care Unit, Thrombolysis in Myocardial Infarction Study Group, Cardiovascular Division, Department of Medicine (A.S.V., E.L.G., A.S.B., M.W.L., D.D.B., D.A.M., E.A.B.), Brigham and Women's Hospital and Harvard Medical School, Boston, MA. , Robert W. YehRobert W. Yeh https://orcid.org/0000-0002-0564-4468 Richard A. and Susan F. Smith Center for Outcomes Research in Cardiology, Division of Cardiovascular Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA (W.A.O., R.W.Y., D.S.K.). , James A. de LemosJames A. de Lemos https://orcid.org/0000-0003-2211-7261 Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center and Parkland Health and Hospital System, Dallas (J.A.d.L.). , David A. MorrowDavid A. Morrow https://orcid.org/0000-0002-9589-5382 Levine Cardiac Intensive Care Unit, Thrombolysis in Myocardial Infarction Study Group, Cardiovascular Division, Department of Medicine (A.S.V., E.L.G., A.S.B., M.W.L., D.D.B., D.A.M., E.A.B.), Brigham and Women's Hospital and Harvard Medical School, Boston, MA. , Dhruv S. KaziDhruv S. Kazi https://orcid.org/0000-0002-9510-2979 Richard A. and Susan F. Smith Center for Outcomes Research in Cardiology, Division of Cardiovascular Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA (W.A.O., R.W.Y., D.S.K.). and Erin A. BohulaErin A. Bohula Correspondence to: Erin A. Bohula, MD, DPhil, TIMI Study Group, 60 Fenwood Rd, Ste 7022, Boston, MA 02115. Email E-mail Address: [email protected] https://orcid.org/0000-0002-5559-8172 Levine Cardiac Intensive Care Unit, Thrombolysis in Myocardial Infarction Study Group, Cardiovascular Division, Department of Medicine (A.S.V., E.L.G., A.S.B., M.W.L., D.D.B., D.A.M., E.A.B.), Brigham and Women's Hospital and Harvard Medical School, Boston, MA. Originally published18 Nov 2021https://doi.org/10.1161/CIRCHEARTFAILURE.121.008477Circulation: Heart Failure. 2021;14:e008477Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: November 18, 2021: Ahead of Print Patients with coronavirus disease 2019 (COVID-19) may develop cardiac injury, ranging from low-level cardiac biomarker elevation to myocardial infarction to cardiogenic shock (CS).1 However, the incidence and outcomes of CS in adults hospitalized with COVID-19 are poorly defined.2 We investigated the epidemiology, clinical management, and outcomes of CS in the American Heart Association COVID-19 Cardiovascular Disease Registry.The design of the American Heart Association COVID-19 Cardiovascular Disease Registry has been described.3 This registry is available to US hospitals treating adults with acute COVID-19. All data and materials were accessed through the American Heart Association Precision Medicine Platform (https://precision.heart.org) and are available to qualified researchers through a formal research proposal. Standardized definitions were used to collect demographics, medical history, presentation details, laboratories, resource utilization, and in-hospital outcomes for consecutive COVID-19 admissions. As deidentified data are retrospectively abstracted, individual patient consent is not required. The protocol was approved by the Mass General Brigham Institutional Review Board. This analysis included COVID-19 admissions between January 14, 2020, to September 20, 2020, from 104 hospitals (58% with <500 beds, 96% urban, and 85% teaching). Shock was identified and categorized by the investigator according to the first in-hospital event as CS, distributive shock (DS), mixed shock (MS; ie, vasodilatory CS, defined as having components of cardiogenic and DS), and other/unknown using the best available clinical data. Admissions complicated by CS or MS were compared with those with DS or without shock.Among 15 208 COVID-19 admissions, 1882 (12%) developed shock, including 105 (0.7%) CS, 159 (1%) MS, 1409 (9%) DS, and 209 (1%) as other shock. In a sensitivity analysis excluding patients with preexisting heart failure(n=13 540), the prevalence of shock and shock subtypes was similar to the overall cohort. Patients with CS were predominantly male and non-White (Table). Compared with patients with DS or without shock, patients with CS had a higher prevalence of prior myocardial infarction, coronary revascularization, and heart failure (Table). Patients with CS had higher rates of abnormal chest imaging and troponin, d-dimer, C-reactive protein, and natriuretic peptide elevations at admission compared with patients without shock (Table). Compared with MS and DS, CS admissions had lower prevalence of pulmonary infectious signs and symptoms. Among admissions where echocardiography was obtained, 28% of CS admissions had left ventricular ejection fraction <30%, compared with 6% of admissions without shock.Table. Baseline Characteristics, Presenting Variables, Resource Utilization, and Outcomes of COVID-19 Patients According to Shock StatusCS (n=105)MS (n=159)DS (n=1409)No shock (n=13 326)Baseline characteristics Age, y; median (IQR)64 (54–73)67 (59–75)66 (56–74)62 (48–75) BMI, kg/m2; median (IQR)28.1 (23.1–31.6)30.0 (25.1–36.6)30.0 (25.7–35.7)29.0 (25.0–34.6) Female sex38 (36%)61 (38%)528 (37%)6185 (46%) Race White40 (38%)50 (31%)445 (32%)4645 (35%) Black/African American28 (27%)54 (34%)442 (31%)3381 (25%) Asian5 (5%)13 (8%)68 (5%)567 (4%) Diabetes48 (46%)72 (45%)641 (45%)4498 (34%) Established ASCVD32 (30%)49 (31%)294 (21%)2931 (22%) Prior MI11 (10%)19 (12%)75 (5%)658 (5%) Prior coronary revascularization16 (15%)21 (13%)103 (7%)844 (6%) Prior heart failure34 (32%)37 (23%)193 (14%)1380 (10%) Chronic kidney disease17 (16%)39 (25%)237 (17%)1605 (12%)Presenting variables Selected COVID-19 symptoms Fever or chills42 (40%)95 (60%)904 (64%)7433 (56%) Cough59 (56%)82 (52%)876 (62%)7542 (57%) Shortness of breath57 (54%)107 (67%)1022 (73%)7371 (56%) Symptom onset to admission, d; median (IQR)4 (1–7)5 (3–9)5 (3–9)5 (2–9) Infiltrates on chest imaging81/105 (77%)136/158 (86%)1242/1405 (88%)8514/13 024 (65%) Elevated NT-proBNP or BNP*42/58 (72%)65/105 (62%)364/723 (50%)1902/5286 (36%) Troponin >2× ULN7/66 (11%)6/115 (5%)64/749 (9%)255/6497 (4%) CRP ≥10 mg/L57/62 (92%)102/111 (92%)828/915 (90%)6021/7456 (81%) D-dimer ≥500 ng/mL34/45 (76%)45/59 (76%)424/625 (68%)3218/5571 (58%) LVEF during admission LVEF <30%18/65 (28%)17/86 (20%)15/491 (3%)68/1114 (6%) LVEF 30%–50%22/65 (34%)26/86 (30%)76/491 (15%)217/1114 (19%) LVEF >50%25/65 (38%)43/86 (50%)400/491 (81%)829/1114 (74%)Management and resource utilization Empirical COVID-19 therapies Glucocorticoids45/104 (43%)101/158 (64%)763/1404 (54%)3336/13 274 (25%) Hydroxychloroquine41/105 (39%)73/158 (46%)739/1404 (53%)4958/13 257 (37%) Remdesivir17/105 (16%)20/158 (13%)206/1404 (15%)1243/13 273 (9%) Tocilizumab14/104 (13%)36/158 (23%)281/1404 (20%)747/13 274 (6%) COVID-19 convalescent plasma9/105 (9%)29/158 (18%)186/1403 (13%)545/12 970 (4%) Inotropes or vasopressors95/101 (94%)155/155 (100%)1345/1356 (99%)0 (0%) Mechanical ventilation94/105 (90%)14/1586 (92%)1257/1406 (89%)1354/13 326 (10%) V-V ECMO8/105 (8%)5/158 (3%)46/1402 (3%)21/13 307 (0.2%) Acute renal replacement therapy20/105 (19%)50/158 (32%)345/1406 (25%)171/13 307 (1.3%) Mechanical circulatory support11/101 (11%)6/155 (4%)6/1356 (0.4%)0/13 326 (0%) IABP7/101 (7%)2/155 (1.3%)0 (0%)0 (0%) PVAD6/101 (6%)2/155 (1.3%)3/1356 (0.2%)0 (0%) V-A ECMO0 (0%)2/155 (1.3%)3/1356 (0.2%)0 (0%) Coronary angiography10/105 (10%)3/158 (2%)4/1406 (0.3%)48/13 309 (0.4%) ≥1 obstructive coronary lesion5/9 (56%)2/2 (100%)1/3 (33%)25/37 (68%) PCI8/105 (8%)1/158 (0.6%)1/1406 (0.1%)27/13 310 (0.2%)In-hospital events Composite of death, cardiac arrest, AMI, or stroke81 (77%)124 (78%)898/1408 (64%)1667 (13%) Death Overall66 (63%)110 (69%)802 (57%)1379 (10%) In patients with IHCA39/47 (83%)40/41 (98%)292/318 (92%)323/346 (93%) In patients without IHCA27/28 (47%)69/117 (59%)506/1087 (47%)1040/12 960 (8%) Cause of death Respiratory31 (48%)74 (68%)616 (78%)967 (73%) Cardiovascular†21 (32%)13 (12%)50 (6%)152 (11%) Other13 (20%)22 (20%)128 (16%)205 (16%)Values reflect count (n) and proportion (%) unless otherwise specified. Differences in categorical variables were assessed across the study groups using the χ2 test or Fisher exact test as appropriate. Differences in continuous variables were assessed using the Kruskal-Wallis test. P value <0.05 for all comparisons between CS and no shock with the exception of age, race, chronic kidney disease, cough, shortness of breath, hydroxychloroquine, remdesivir, and convalescent serum. P value <0.05 for all comparisons between MS and no shock with the exception of race, fever or chills, cough, remdesivir, PCI, and cause of death. ASCVD includes established cerebrovascular disease, peripheral artery disease, prior MI, or prior coronary revascularization. AMI indicates acute myocardial infarction; ASCVD, atherosclerotic cardiovascular disease; BMI, body mass index; BNP, brain natriuretic peptide; COVID-19, coronavirus disease 2019; CRP, C-reactive protein; CS, cardiogenic shock; DS, distributive shock; IABP, intra-aortic balloon pump; IHCA, in-hospital cardiac arrest; IQR, interquartile range; LVEF, left ventricular ejection fraction; MI, myocardial infarction; MS, mixed shock; NT-proBNP, N-terminal pro-B-type natriuretic peptide; PCI, percutaneous coronary intervention; PVAD, percutaneous ventricular assist device; ULN, upper limit of normal; V-A ECMO, veno-arterial extracorporeal membrane oxygenation; and V-V ECMO, veno-venous extracorporeal membrane oxygenation.* Defined as NT-proBNP ≥450 pg/mL or BNP ≥100 pg/mL.† Includes death due to acute MI, arrhythmia, heart failure, or stroke.Inotropes and vasopressors, mechanical ventilation, renal replacement therapy, and empirical COVID-19 therapies were frequently utilized in patients with CS. Temporary mechanical circulatory support was used in 11% of patients, and 10% underwent invasive or noninvasive coronary angiography.The mortality rate for the overall cohort was 16%; 63% of patients with CS died during hospitalization, compared with 57% with DS and 10.3% without shock (P<0.001). While respiratory failure remained the most common cause of death in all patients, cardiovascular causes of death were more common in patients with CS compared with those with DS or no shock. The composite of in-hospital mortality, cardiac arrest, myocardial infarction, or stroke occurred in 77% of admissions with CS, compared with 64% with DS and 13% without shock. In a secondary analysis, patients with MS had generally similar baseline characteristics, clinical presentation, and event rates as patients with classic CS but were less likely to undergo coronary angiography or receive mechanical circulatory support (Table).In this analysis of a large and diverse population of patients hospitalized for COVID-19 predominantly in US urban teaching hospitals, ≈1 in 10 patients developed any shock. While CS or MS was rare (<2%), these disease states were associated with exceedingly high morbidity and mortality. Despite a high prevalence of cardiovascular risk factors and cardiovascular disease in patients with CS or MS, only ≈20% had acute myocardial infarction during hospitalization (inclusive of demand-related events). This is consistent with growing evidence implicating mechanisms of cardiac involvement in COVID-19 beyond acute coronary syndromes, including stress-induced cardiomyopathy, inflammatory myocarditis, microvascular dysfunction and thrombosis, and decompensation of underlying heart failure.1 Notably, coronary angiography, percutaneous coronary intervention, and temporary mechanical circulatory support placement were utilized in <10% of cases of CS or MS, reflecting rates that are substantially lower than in contemporary non–COVID-19 CS populations.4 Additionally, veno-arterial extracorporeal membrane oxygenation was used in only 5 admissions in the entire cohort, none of which had CS. Less than half of CS patients received glucocorticoids during this period. While evidence of benefit of glucocorticoids in COVID-19 exists,5 their role in patients with CS, who may benefit from suppression of cytokine storm yet may be harmed by resultant fluid retention, is uncertain.This analysis relied on site-level characterization of events by the local investigator using the best available clinical data and lacked centralized adjudication. Event rates may have been affected by center-level variation in cardiac testing. Absence of hemodynamic data precluded classification of CS severity. Nevertheless, this large multicenter registry of COVID-19 hospitalizations during 2020 provides generalizable insights into classic or vasodilatory CS resulting from COVID-19. Although rare, development of either form of CS was a marker for high rates of cardiovascular complications, including cardiac arrest, and worse hospital outcomes than observed in non–COVID-19 CS populations.4Article InformationAcknowledgmentsThe Get With The Guidelines programs are provided by the American Heart Association (AHA). The AHA Precision Medicine Platform (https://precision.heart.org/) was used for data analysis. IQVIA (Parsippany, NJ) serves as the data collection and coordination center.Sources of FundingThe American Heart Association (AHA) suite of registries is funded by multiple industry sponsors. AHA's COVID-19 Cardiovascular Disease Registry is partially supported by the Gordon and Betty Moore Foundation.DisclosuresDr Varshney is on the Advisory Board for Broadview Ventures and is supported by the National Heart, Lung, and Blood Institute T32 postdoctoral training grant T32HL007604 and the Daniel Pierce Family Fellowship in Advanced Heart Disease. Dr Bhatt reports speaking fees from Sanofi Pasteur and is supported by the National Heart, Lung, and Blood Institute T32 postdoctoral training grant T32HL007604. Dr Berg is supported by Harvard Catalyst KL2/Catalyst Medical Research Investigator Training (National Institutes of Health/National Center for Advancing Translational Sciences UL 1TR002541) and has received consulting fees from AstraZeneca. Dr Yeh is a consultant for Abbott Vascular, AstraZeneca, Boston Scientific, Edwards Life Sciences, Medtronic, Shockwave Medical, and Zoll Medical and receives research funding from AstraZeneca, BD Bard, Boston Scientific, Cook Medical, Medtronic, and Philips. Dr de Lemos reports grant support from Roche Diagnostics and Abbott Diagnostics and consulting fees from Ortho Clinical Diagnostics, Siemen's Health Care Diagnostics, Quidel, Eli Lilly, and Novo Nordisk. Dr Morrow has received consulting fees from Bayer Pharma, InCarda, Merck, Novartis, and Roche Diagnostics. Dr Bohula has received consulting fees from Novo Nordisk, Amgen, Medscape, Servier, and Kowa. Drs Morrow, Bohula, and Berg, M.W. Levangie, and E.L. Goodrich are members of the TIMI study group, which has received institutional research grant support through the Brigham and Women's Hospital from Abbott Laboratories, Amgen, Anthos Therapeutics, Arca Biopharma, AstraZeneca, Bayer HealthCare Pharmaceuticals Inc, BRAHMS, Daiichi-Sankyo, Eisai, GlaxoSmithKline, Intarcia, Janssen, Merck, Novartis, Pfizer, Poxel, Quark Pharmaceuticals, Regeneron, Roche, Siemens, Takeda, The Medicines Company, and Zora Biosciences. The other authors report no conflicts.Footnotes*A.S. Varshney and W.A. Omar contributed equally.†D.S. Kazi and E.A. Bohula contributed equally.For Sources of Funding and Disclosures, see page 1356.Correspondence to: Erin A. Bohula, MD, DPhil, TIMI Study Group, 60 Fenwood Rd, Ste 7022, Boston, MA 02115. Email ebohula@bwh.harvard.eduReferences1. Atri D, Siddiqi HK, Lang JP, Nauffal V, Morrow DA, Bohula EA. COVID-19 for the cardiologist: basic virology, epidemiology, cardiac manifestations, and potential therapeutic strategies.JACC Basic Transl Sci. 2020; 5:518–536. doi: 10.1016/j.jacbts.2020.04.002CrossrefMedlineGoogle Scholar2. Alhazzani W, Møller MH, Arabi YM, Loeb M, Gong MN, Fan E, Oczkowski S, Levy MM, Derde L, Dzierba A, et al. Surviving sepsis campaign: guidelines on the management of critically ill adults with coronavirus disease 2019 (COVID-19).Crit Care Med. 2020; 48:e440–e469. doi: 10.1097/CCM.0000000000004363CrossrefMedlineGoogle Scholar3. Alger HM, Rutan C, Williams JH, Walchok JG, Bolles M, Hall JL, Bradley SM, Elkind MSV, Rodriguez F, Wang TY, et al. American Heart Association COVID-19 CVD registry powered by get with the guidelines.Circ Cardiovasc Qual Outcomes. 2020; 13:e006967. doi: 10.1161/CIRCOUTCOMES.120.006967LinkGoogle Scholar4. Berg DD, Bohula EA, van Diepen S, Katz JN, Alviar CL, Baird-Zars VM, Barnett CF, Barsness GW, Burke JA, Cremer PC, et al. Epidemiology of shock in contemporary cardiac intensive care units.Circ Cardiovasc Qual Outcomes. 2019; 12:e005618. doi: 10.1161/CIRCOUTCOMES.119.005618LinkGoogle Scholar5. Horby P, Lim WS, Emberson JR, Mafham M, Bell JL, Linsell L, Staplin N, Brightling C, Ustianowski A, Elmahi E, et al; RECOVERY Collaborative Group. Dexamethasone in hospitalized patients with COVID-19.N Engl J Med. 2021; 384:693–704. doi: 10.1056/NEJMoa2021436CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Meyerowitz E, Scott J, Richterman A, Male V and Cevik M (2023) Clinical course and management of COVID-19 in the era of widespread population immunity, Nature Reviews Microbiology, 10.1038/s41579-023-01001-1, 22:2, (75-88), Online publication date: 1-Feb-2024. Sunnaa M, Kerolos M, Ruge M, Gill A, Du-Fay-de-Lavallaz J, Rabin P, Gomez J, Williams K, Rao A, Volgman A, Marinescu K and Suboc T (2023) Association between number of vasopressors and mortality in COVID-19 patients, American Heart Journal Plus: Cardiology Research and Practice, 10.1016/j.ahjo.2023.100324, 34, (100324), Online publication date: 1-Oct-2023. Agarwal S, Bansal A, Debnath C, Akhtar K and Krishan S (2023) The impact of COVID-19 infection on outcomes of patients hospitalized for non-acute myocardial infarction cardiogenic shock, The American Journal of Emergency Medicine, 10.1016/j.ajem.2023.03.051, 68, (207-209), Online publication date: 1-Jun-2023. Boulos P, Freeman S, Henry T, Mahmud E and Messenger J (2023) Interaction of COVID-19 With Common Cardiovascular Disorders, Circulation Research, 132:10, (1259-1271), Online publication date: 12-May-2023. Bashir H, Yildiz M, Cafardi J, Bhatia A, Garcia S, Henry T and Chung E (2023) A Review of Heart Failure in Patients with COVID-19, Heart Failure Clinics, 10.1016/j.hfc.2023.03.002, 19:2, (e1-e8), Online publication date: 1-Apr-2023. Gorder K, Young W, Kapur N, Henry T, Garcia S, Guddeti R and Smith T (2023) Mechanical Circulatory Support in COVID-19, Heart Failure Clinics, 10.1016/j.hfc.2022.08.003, 19:2, (205-211), Online publication date: 1-Apr-2023. 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Girerd N, Chapet N, Roubille C, Roncalli J, Salvat M, Mouquet F, Lamblin N, Gueffet J, Damy T, Galinier M, Tartiere J, Janssen C, Berthelot E, Aguilhon S, Escamilla R and Roubille F (2022) Quels schémas vaccinaux contre les infections respiratoires chez l'insuffisant cardiaque ?, Archives des Maladies du Coeur et des Vaisseaux - Pratique, 10.1016/j.amcp.2022.07.004, 2022:311, (19-26), Online publication date: 1-Oct-2022. Gorder K, Young W, Kapur N, Henry T, Garcia S, Guddeti R and Smith T (2022) Mechanical Circulatory Support in COVID-19, Cardiology Clinics, 10.1016/j.ccl.2022.03.003, 40:3, (329-335), Online publication date: 1-Aug-2022. December 2021Vol 14, Issue 12 Advertisement Article InformationMetrics © 2021 American Heart Association, Inc.https://doi.org/10.1161/CIRCHEARTFAILURE.121.008477PMID: 34789004 Originally publishedNovember 18, 2021 KeywordsCOVID-19data collectionintensive care unitsregistriesshock, cardiogenicPDF download Advertisement SubjectsEpidemiologyQuality and Outcomes

Background: Percutaneous ventricular assist devices (VAD) are used in ~1/3 of patients (pts) with cardiogenic shock (CS). A percutaneous microaxial intracardiac VAD can offer hemodynamic support weighed against a risk of vascular complications. However, few studies have addressed the incidence of thrombotic complications, particularly in pts who require extended mechanical circulatory support (MCS). Methods: We conducted an observational cohort study to quantify the risk of thrombotic events during MCS in pts managed with a microaxial VAD for CS or mixed shock from 2015-2020 in a quaternary referral center. All consecutive pts were captured in a prospective registry of MCS and retrospectively reviewed for potentially device-related thrombotic events by 2 physician adjudicators. All pts received systemic anticoagulation with unfractionated heparin and/or bivalirudin. Results: The study included 106 pts (72% male, mean age 59.8). Peripheral artery disease, and a significant smoking history were present in 12% and 44% of cases respectively. The duration of microaxial VAD use was 5.3 days on average and >7 days in 25%. A concurrent microaxial VAD and other MCS were used in 28% of cases. Thrombotic/ischemic events were observed in 24.5% and were subcategorized into limb ischemia with visualized thrombus (n=6), limb ischemia without visualized thrombus (n=6), systemic embolism (n=6), intraventricular thrombus (n=2), device thrombus (n=6), and device dysfunction (n=3). Three pts had more than one complication. Moderate to severe thrombocytopenia (<100mcg/dL) was observed in 78% of pts. In-hospital mortality was 51% and was not higher in pts with thrombotic events (p=0.14). Conclusion: Thrombotic events are common with a microaxial intracardiac VAD with an observed rate that was higher than previously reported. Larger studies of all-comers with MCS for CS are needed to better define the rate of MCS-associated complications.

Introduction: Thrombocytopenia is associated with poor outcomes in general medical intensive care unit (ICU) populations; however, the burden and prognostic significance of thrombocytopenia in cardiac ICU (CICU) populations have not been rigorously studied. Methods: The Critical Care Cardiology Trials Network (CCCTN) is an investigator-initiated multicenter network of CICUs (n=25) in North America. Consecutive admissions to the CICU during annual snapshots (mostly 2 months) were submitted to the coordinating center (TIMI Study Group, Boston, MA) between September 2017 and September 2019. Patients were stratified by platelet counts on admission to the CICU and nadir platelet counts. Thrombocytopenia was classified as mild (100-149 K/uL), moderate (50-99 K/uL), or severe (<50 K/uL). Results: Of 8206 CICU admissions with complete laboratory data, 21.7% had thrombocytopenia (platelets <150 K/uL) on admission and 38.4% had thrombocytopenia at any point during their CICU course ( Fig-left ). Among those with normal platelet counts on admission (n=6423), 21.3% developed thrombocytopenia during their CICU course. Patients with thrombocytopenia on admission were more likely to have active cancer, underlying liver disease, and CKD as compared to those who did not (each p<0.001). Among patients with cardiogenic shock (n=1478), 56.8% had thrombocytopenia (mild: 28.6%; moderate: 19.4%; severe: 8.9%). Among patients managed with mechanical circulatory support (MCS) (n=926), 65.0% had thrombocytopenia (mild: 27.0%; moderate: 24.3%; severe: 13.7%). There were stepwise gradients of increasing CICU and in-hospital mortality associated with lower nadir platelet counts (p-trend <0.001) ( Fig-right ). Conclusions: Thrombocytopenia is common in CICU patients, including more than half of patients with cardiogenic shock and those managed with MCS. Thrombocytopenia is an adverse prognostic marker in CICU patients.