Portal de Periódicos da CAPES

Comparison of Outcomes in Patients With COVID-19 and Thrombosis Versus Those Without Thrombosis

2021; Elsevier BV; Volume: 160; Linguagem: Inglês

10.1016/j.amjcard.2021.08.038

1879-1913

Brian C. Case, Jonathan S. Abramowitz, Corey Shea, Hank Rappaport, Giorgio A. Medranda, Charan Yerasi, Brian J. Forrestal, Chava Chezar‐Azerrad, Cheng Zhang, Lowell F. Satler, Itsik Ben‐Dor, Hayder Hashim, Toby Rogers, William S. Weintraub, Ron Waksman,

COVID-19 and healthcare impacts

The occurrence of venous thromboembolisms in patients with COVID-19 has been established. We sought to evaluate the clinical impact of thrombosis in patients with COVID-19 over the span of the pandemic to date. We analyzed patients with COVID-19 with a diagnosis of thrombosis who presented to the MedStar Health system (11 hospitals in Washington, District of Columbia, and Maryland) during the pandemic (March 1, 2020, to March 31, 2021). We compared the clinical course and outcomes based on the presence or absence of thrombosis and then, specifically, the presence of cardiac thrombosis. The cohort included 11,537 patients who were admitted for COVID-19. Of these patients, 1,248 had noncardiac thrombotic events and 1,009 had cardiac thrombosis (myocardial infarction) during their hospital admission. Of the noncardiac thrombotic events, 562 (45.0%) were pulmonary embolisms, 480 (38.5%) were deep venous thromboembolisms, and 347 (27.8%) were strokes. In the thrombosis arm, the mean age of the cohort was 64.5 ± 15.3 years, 53.3% were men, and the majority were African-American (64.9%). Patients with thrombosis tended to be older with more co-morbidities. The in-hospital mortality rate was significantly higher (16.0%) in patients with COVID-19 with concomitant non-cardiac thrombosis than in those without thrombosis (7.9%, p <0.001) but lower than in patients with COVID-19 with cardiac thrombosis (24.7%, p <0.001). In conclusion, patients with COVID-19 with thrombosis, especially cardiac thrombosis, are at higher risk for in-hospital mortality. However, this prognosis is not as grim as for patients with COVID-19 and cardiac thrombosis. Efforts should be focused on early recognition, evaluation, and intensifying antithrombotic management for these patients. The occurrence of venous thromboembolisms in patients with COVID-19 has been established. We sought to evaluate the clinical impact of thrombosis in patients with COVID-19 over the span of the pandemic to date. We analyzed patients with COVID-19 with a diagnosis of thrombosis who presented to the MedStar Health system (11 hospitals in Washington, District of Columbia, and Maryland) during the pandemic (March 1, 2020, to March 31, 2021). We compared the clinical course and outcomes based on the presence or absence of thrombosis and then, specifically, the presence of cardiac thrombosis. The cohort included 11,537 patients who were admitted for COVID-19. Of these patients, 1,248 had noncardiac thrombotic events and 1,009 had cardiac thrombosis (myocardial infarction) during their hospital admission. Of the noncardiac thrombotic events, 562 (45.0%) were pulmonary embolisms, 480 (38.5%) were deep venous thromboembolisms, and 347 (27.8%) were strokes. In the thrombosis arm, the mean age of the cohort was 64.5 ± 15.3 years, 53.3% were men, and the majority were African-American (64.9%). Patients with thrombosis tended to be older with more co-morbidities. The in-hospital mortality rate was significantly higher (16.0%) in patients with COVID-19 with concomitant non-cardiac thrombosis than in those without thrombosis (7.9%, p <0.001) but lower than in patients with COVID-19 with cardiac thrombosis (24.7%, p 1 ng/ml or high-sensitivity troponin >30 ng/ml. The baseline characteristics and co-morbidities were collected for all patients. In this analysis, co-morbidities were identified using the ICD-10 codes. Laboratory data and the use of ventilation were compared between the 2 groups. The primary end point was in-hospital mortality. The study was conducted in accordance with the Declaration of Helsinki and was approved by our institutional review board. Descriptive statistics such as frequencies, means, and SDs were used to describe the study population. Student t test or analysis of variance was used to compare the mean values of normally distributed data. Cox-regression method was used to evaluate risk factors for the primary outcome. Two-tailed Fisher's exact test or chi-square test was used to compare categorical variables. The odds ratio for in-hospital mortality and ventilation requirement was estimated from a multivariate logistic regression. Statistical significance was considered to be p <0.05. All analyses were done in SAS version 9.4 (SAS Institute, Cary, North Carolina). One author (B.C.C.) has full access to all the data in the study and takes full responsibility for its integrity and the data analysis. This study included 11,537 patients with COVID-19 who were admitted during the pandemic. Of these patients, 1,248 (10.8%) had noncardiac thrombotic events (stroke or VTE) during their hospital admission and 1,009 (8.7%) had cardiac thrombosis (myocardial infarction). Of the noncardiac thrombotic events, 562 (45.0%) were pulmonary embolisms, 480 (38.5%) were deep VTEs, and 347 (27.8%) were strokes. The baseline characteristics are displayed in Table 1. In the non-cardiac thrombosis cohort, the majority of patients were men (53.3%) with a mean age of 64.5 ± 15.3 years. Patients with COVID-19 with non-cardiac thrombosis tended to have a higher rate of co-morbidities than patients with COVID-19 without thrombosis. However, the rate of co-morbidities in the non-cardiac thrombosis cohort was lower than in patients with COVID-19 with cardiac thrombosis, except for those with a history of stroke.Table 1Baseline characteristics of patients with COVID-19 overall, thrombosis present, cardiac thrombosis only, and those without thrombosisOverall (N = 11,537)Non-Cardiac Thrombosis*Venothromboembolism and Pulmonary Embolism. (N = 1,248)Cardiac Thrombosis**ST-Elevation Myocardial Infarction and Non-ST Elevation Myocardial Infarction. (N = 1,009)No Thrombosis (N = 9,280)p ValueDemographics Age ± SD (years)61.21 +/- 17.6864.48 +/- 15.3470.2 +/- 14.0859.79 +/- 17.98<0.001 Male48.7%53.3%53.4%47.65<0.001Ethnicity White26.3%24.5%26.9%26.5%0.294 Black58.0%64.9%64.5%56.4%<0.001 Asian1.3%0.9%1.5%1.4%0.350 Native American0.2%0.0%0.1%0.2%0.157 Other14.1%9.7%6.9%15.5%<0.001Co-Morbidities Active malignancy8.0%9.5%9.7%7.6%0.008 Heart disease27.3%33.3%64.3%22.4%<0.001 Diabetes mellitus33.8%45.5%35.0%32.4%<0.001 Kidney disease8.9%9.4%20.2%7.7%<0.001 Liver disease4.1%5.3%5.9%3.7%<0.001 Lung disease36.7%34.2%47.1%35.9%<0.001 Venothromboembolism and Pulmonary Embolism. ST-Elevation Myocardial Infarction and Non-ST Elevation Myocardial Infarction. Open table in a new tab During their hospital admissions, the white blood cell count and concentration of creatinine, C-reactive protein, lactate dehydrogenase, and ferritin were significantly higher in patients with thrombosis than in patients without thrombosis. However, these laboratory values and those of troponin and N-terminal prohormone B-type natriuretic peptide were significantly higher in the cardiac thrombosis arm than in the non-cardiac thrombosis and no-thrombosis cohorts. Laboratory data are displayed in Table 2.Table 2Laboratory data of patients with COVID-19 overall, thrombosis present, cardiac thrombosis only, and those without thrombosisVariableOverall (N = 11,537)Non-Cardiac Thrombosis*Venothromboembolism and Pulmonary Embolism. (N = 1,248)Cardiac Thrombosis**ST-Elevation Myocardial Infarction and Non-ST Elevation Myocardial Infarction. (N = 1,009)No Thrombosis (N = 9,280)p ValueMaximum troponin-I (ng/mL)0.59 +/- 6.320.64 +/- 4.974.1 +/- 17.420.09 +/- 1.63<0.001Maximum high-sensitivity troponin (ng/mL)310.7 +/- 2824.62784.65 +/- 5604.181,590.25 +/- 6145.0377.93 +/- 539.01<0.001N-terminal-pro-hormone BNP (ng/L)5,321.95 +/- 20,010.594,754.7 +/- 14,685.1515,151.82 +/- 34,976.653,630.63 +/- 16,015.69<0.001Maximum creatinine (mg/dL)2.08 +/- 2.52.5 +/- 2.713.51 +/- 3.621.88 +/- 2.27<0.001Maximum white blood cell (K/µL)8.94 +/- 8.8810.2 +/- 6.6210.17 +/- 8.838.68 +/- 9.09<0.001C-reactive protein (mg/dL)69.89 +/- 54.4278.68 +/- 54.2285.4 +/- 61.5 (394)67.04 +/- 53.18 (<0.001Lactate dehydrogenase (U/L)420.73 +/- 299.6420.73 +/- 299.6553.76 +/- 538.32397.74 +/- 247.57<0.001Ferritin (ng/mL)1,071.99 +/- 2,409.211,337.77 +/- 2,456.671,967.09 +/- 4,165.481,967.09 +/- 4,165.48<0.001BNP = B-type natriuretic peptide. Venothromboembolism and Pulmonary Embolism. ST-Elevation Myocardial Infarction and Non-ST Elevation Myocardial Infarction. Open table in a new tab BNP = B-type natriuretic peptide. Our primary end point, in-hospital mortality (Figure 1), was significantly higher (16.0%) in patients with COVID-19 with non-cardiac thrombosis than in those without a thrombotic event (7.9%, p <0.001) but was lower than in patients with COVID-19 with cardiac thrombosis (24.7%, p <0.001). With regard to our secondary end points, patients with COVID-19 with non-cardiac thrombosis required ventilation (28.2%) at a higher rate than patients with COVID-19 with cardiac thrombosis (26.8%) or those without thrombosis (9.7%). Primary and secondary end point data are displayed in Table 3.Table 3Primary and secondary outcomes. In-hospital mortality and ventilator requirement of patients with COVID-19 during the pandemic era overall, with thrombosis present, cardiac thrombosis only, and those without thrombosisVariableOverall (N = 11,537)Non-Cardiac Thrombosis*Venothromboembolism and Pulmonary Embolism. (N = 1,248)Cardiac Thrombosis**ST-Elevation Myocardial Infarction and Non-ST Elevation Myocardial Infarction. (N = 1,009)No Thrombosis (N = 9,280)p ValueOverall In-Hospital Mortality10.2%16.0%24.7%7.9%<0.001Ventilator Requirement13.2%28.2%26.8%9.7%<0.001 Venothromboembolism and Pulmonary Embolism. ST-Elevation Myocardial Infarction and Non-ST Elevation Myocardial Infarction. Open table in a new tab Finally, the odds ratio for in-hospital mortality (area under the receiver operator characteristic curve of 0.85) and ventilation requirement (area under the receiver operator characteristic curve of 0.84) was estimated from a multivariate logistic regression and the results are presented in Table 4. Thrombosis versus no thrombosis appeared to be significant for in-hospital mortality, whereas thrombosis versus no thrombosis and then cardiac thrombosis versus noncardiac thrombosis appeared to be significant for ventilation requirement.Table 4Adjusted in-hospital mortality in patients with COVID-19. Adjusted odds ratios of thrombosis versus no thrombosis and cardiac thrombosis versus non-cardiac thrombosis, adjusting for inflammatory markersIn-hospital mortalityOdds Ratio95% confidence intervalThrombosis versus no thrombosis0.680.50 – 0.93Cardiac thrombosis versus non-cardiac thrombosis1.190.80 – 1.77Creatinine1.081.04 – 1.11C-reactive protein1.011.01 – 1.01Lactate dDehydrogenase1.001.00 – 1.00Ferritin1.001.00 – 1.00Ventilation requirementOdds Ratio95% Confidence IntervalThrombosis versus no thrombosis0.320.25 – 0.42Cardiac thrombosis versus non-cardiac thrombosis0.630.44 – 0.89Creatinine1.101.07 – 1.14C-reactive protein1.011.04 – 1.08Lactate dehydrogenase1.001.00 -1.00Ferritin1.001.00 – 1.00 Open table in a new tab The primary findings of our analysis suggest that patients with COVID-19 with concomitant non-cardiac thrombosis have a significantly increased risk of mortality when compared with patients with COVID-19 without thrombosis but not as high of a risk as patients with COVID-19 with cardiac thrombosis. Patients with COVID-19 with non-cardiac thrombosis tended to require ventilation at a higher rate than patients with COVID-19 with cardiac thrombosis and those without any thrombosis. There are multiple factors that contribute to the development of thrombosis in patients with COVID-19. First, patient risk factors include acute critical illness, being bedridden, active infection or sepsis, underlying liver or kidney disease, or the presence of a malignancy.9Chong PY Chui P Ling AE Franks TJ Tai DY Leo YS Kaw GJ Wansaicheong G Chan KP Ean Oon LL Teo ES Tan KB Nakajima N Sata T Travis WD Analysis of deaths during the severe acute respiratory syndrome (SARS) epidemic in Singapore: challenges in determining a SARS diagnosis.Arch Pathol Lab Med. 2004; 128: 195-204Crossref PubMed Google Scholar, 10Peiris JS Chu CM Cheng VC Chan KS Hung IF Poon LL Law KI Tang BS Hon TY Chan CS Chan KH Ng JS Zheng BJ Ng WL Lai RW Guan Y Yuen KY HKU/UCH SARS Study GroupClinical progression and viral load in a community outbreak of coronavirus-associated SARS pneumonia: a prospective study.Lancet. 2003; 361: 1767-1772Abstract Full Text Full Text PDF PubMed Scopus (1980) Google Scholar, 11Tsui KL Leung TC Yam LY So LK Poon E Lung KC Li SK Coronary plaque instability in severe acute respiratory syndrome.Int J Cardiol. 2005; 99: 471-472Abstract Full Text Full Text PDF PubMed Scopus (15) Google Scholar, 12Umapathi T Kor AC Venketasubramanian N Lim CC Pang BC Yeo TT Lee CC Lim PL Ponnudurai K Chuah KL Tan PH Tai DY Ang SP. Large artery ischaemic stroke in severe acute respiratory syndrome (SARS).J Neurol. 2004; 251: 1227-1231Crossref PubMed Scopus (214) Google Scholar In our analysis, co-morbidities were significantly higher in patients with thrombosis than in patients without thrombosis. Second, the infection itself causes an inflammatory response with lymphopenia, elevated fibrinogen, and increased inflammatory markers and cytokines. Furthermore, SARS-CoV-2 infection leads to further superimposed infections.9Chong PY Chui P Ling AE Franks TJ Tai DY Leo YS Kaw GJ Wansaicheong G Chan KP Ean Oon LL Teo ES Tan KB Nakajima N Sata T Travis WD Analysis of deaths during the severe acute respiratory syndrome (SARS) epidemic in Singapore: challenges in determining a SARS diagnosis.Arch Pathol Lab Med. 2004; 128: 195-204Crossref PubMed Google Scholar,13Lew TW Kwek TK Tai D Earnest A Loo S Singh K Kwan KM Chan Y Yim CF Bek SL Kor AC Yap WS Chelliah YR Lai YC Goh SK Acute respiratory distress syndrome in critically ill patients with severe acute respiratory syndrome.JAMA. 2003; 290: 374-380Crossref PubMed Scopus (364) Google Scholar Again, these findings were demonstrated to be higher in our analysis with increased white blood cell count and concentration of creatinine, C-reactive protein, lactate dehydrogenase, and ferritin in the thrombosis arm. This reiterates the importance of checking for these markers because they may help in predicting outcomes and guiding the treatment. The combination of patient risk factors and the SARS-CoV-2 infection leads to intravascular coagulopathy, which causes myocardial injury and pulmonary microthrombi. These abnormalities ultimately lead to VTE, myocardial infarction, hyperinflammation, and, in some cases, disseminated intravascular coagulation.14Lippi G Plebani M Laboratory abnormalities in patients with COVID-2019 infection.Clin Chem Lab Med. 2020; 58: 1131-1134Crossref PubMed Scopus (641) Google Scholar,15Cui S Chen S Li X Liu S Wang F Prevalence of venous thromboembolism in patients with severe novel coronavirus pneumonia.J Thromb Haemost. 2020; 18: 1421-1424Crossref PubMed Scopus (1283) Google Scholar Furthermore, there is the concept of "thromboinflammation," which is thrombosis leading to more inflammatory activation. This phenomenon can be challenging to treat and has been seen in patients with COVID-19.16Mitchell WB Thromboinflammation in COVID-19 acute lung injury.Paediatr Respir Rev. 2020; 35: 20-24PubMed Google Scholar As outlined by our analysis, patients with thrombosis carry a worse prognosis than patients without thrombosis. However, myocardial infarction in patients with COVID-19 carry the worst prognosis. One way to ensure a favorable outcome is rapid disease awareness and early admission of the patient to the hospital for treatment therapy, especially for anticoagulation and antithrombotic therapy. Throughout the course of the COVID-19 pandemic, treatment strategies evolved significantly as the guidelines changed and clinical knowledge improved. In the early stages of the pandemic, the standard of care was initially supportive, including the use of supplemental oxygen, prone positioning,17Bouadma L Lescure FX Lucet JC Yazdanpanah Y Timsit JF Severe SC Severe SARS-CoV-2 infections: practical considerations and management strategy for intensivists.Intensive Care Med. 2020; 46: 579-582Crossref PubMed Scopus (193) Google Scholar,18Coppo A Bellani G Winterton D Di Pierro M Soria A Faverio P Cairo M Mori S Messinesi G Contro E Bonfanti P Benini A Valsecchi MG Antolini L Foti G Feasibility and physiological effects of prone positioning in non-intubated patients with acute respiratory failure due to COVID-19 (PRON-COVID): a prospective cohort study.Lancet Respir Med. 2020; 8: 765-774Abstract Full Text Full Text PDF PubMed Scopus (342) Google Scholar conservative fluid management,19Kazory A Ronco C McCullough PA SARS-CoV-2 (COVID-19) and intravascular volume management strategies in the critically ill.Proc (Bayl Univ Med Cent). 2020; 33: 1-6PubMed Google Scholar prophylactic antibiotics, management of co-morbidities, avoiding mechanical ventilation whenever possible, and a variety of antithrombotic management protocols. More recently, the use of corticosteroids, in particular dexamethasone, is recommended for patients with COVID-19 who require supplemental oxygen or mechanical ventilation to decrease all-cause mortality.20Sterne JAC Murthy S Diaz JV Slutsky AS Villar J Angus DC Annane D Azevedo LCP Berwanger O Cavalcanti AB Dequin PF Du B Emberson J Fisher D Giraudeau B Gordon AC Granholm A Green C Haynes R Heming N Higgins JPT Horby P Jüni P Landray MJ Le Gouge A Leclerc M Lim WS Machado FR McArthur C Meziani F Møller MH Perner A Petersen MW Savovic J Tomazini B Veiga VC Webb S Marshall JC WHO Rapid Evidence Appraisal for COVID-19 Therapies (REACT) Working GroupAssociation between administration of systemic corticosteroids and mortality among critically ill patients with COVID-19: a meta-analysis.JAMA. 2020; 324: 1330-1341Crossref PubMed Scopus (1621) Google Scholar,21Müterthies K Colorants de maquillage pour céramique concus [Surface coloring for built ceramic].Rev Fr Prothes Dent. 1988; (37–8, 51–32)PubMed Google Scholar Other treatment strategies include convalescent plasma infusions.22Simonovich VA Burgos Pratx LD Scibona P Beruto MV Vallone MG Vázquez C Savoy N Giunta DH Pérez LG Sánchez MDL Gamarnik AV Ojeda DS Santoro DM Camino PJ Antelo S Rainero K Vidiella GP Miyazaki EA Cornistein W Trabadelo OA Ross FM Spotti M Funtowicz G Scordo WE Losso MH Ferniot I Pardo PE Rodriguez E Rucci P Pasquali J Fuentes NA Esperatti M Speroni GA Nannini EC Matteaccio A Michelangelo HG Follmann D Lane HC Belloso WH PlasmAr Study GroupA randomized trial of convalescent plasma in COVID-19 severe pneumonia.N Engl J Med. 2021; 384: 619-629Crossref PubMed Scopus (618) Google Scholar Finally, in October 2020, the antiviral medication remdesivir received Emergency Use Authorization from the US Food and Drug Administration because it was shown to be superior to a placebo at reducing the time to recovery in those hospitalized patients with COVID-19;23Beigel JH Tomashek KM Dodd LE Mehta AK Zingman BS Kalil AC Hohmann E Chu HY Luetkemeyer A Kline S Lopez de Castilla D Finberg RW Dierberg K Tapson V Hsieh L Patterson TF Paredes R Sweeney DA Short WR Touloumi G Lye DC Ohmagari N Oh MD Ruiz-Palacios GM Benfield T Fätkenheuer G Kortepeter MG Atmar RL Creech CB Lundgren J Babiker AG Pett S Neaton JD Burgess TH Bonnett T Green M Makowski M Osinusi A Nayak S Lane HC ACTT-1 Study Group MembersRemdesivir for the treatment of COVID-19 - final report.N Engl J Med. 2020; 383: 1813-1826Crossref PubMed Scopus (4879) Google Scholar however, more recent data on remdesivir may not support this finding as strongly.24Pan H Peto R Henao-Restrepo AM Preziosi MP Sathiyamoorthy V Abdool Karim Q Alejandria MM Hernández García C Kieny MP Malekzadeh R Murthy S Reddy KS Roses Periago M Abi Hanna P Ader F Al-Bader AM Alhasawi A Allum E Alotaibi A Alvarez-Moreno CA Appadoo S Asiri A Aukrust P Barratt-Due A Bellani S Branca M Cappel-Porter HBC Cerrato N Chow TS Como N Eustace J García PJ Godbole S Gotuzzo E Griskevicius L Hamra R Hassan M Hassany M Hutton D Irmansyah I Jancoriene L Kirwan J Kumar S Lennon P Lopardo G Lydon P Magrini N Maguire T Manevska S Manuel O McGinty S Medina MT Mesa Rubio ML Miranda-Montoya MC Nel J Nunes EP Perola M Portolés A Rasmin MR Raza A Rees H Reges PPS Rogers CA Salami K Salvadori MI Sinani N Sterne JAC Stevanovikj M Tacconelli E Tikkinen KAO Trelle S Zaid H Røttingen JA Swaminathan S WHO Solidarity Trial ConsortiumRepurposed antiviral drugs for COVID-19 - interim WHO solidarity trial results.N Engl J Med. 2021; 384: 497-511Crossref PubMed Scopus (1641) Google Scholar Furthermore, the prevention and treatment of thrombosis in patients with COVID-19 has evolved. For patients hospitalized with COVD-19, pharmacologic VTE prophylaxis should be initiated unless contraindicated. In addition, the results from 3 large international clinical trials conducted by the National Institutes of Health suggest that full-dose anticoagulation therapy improved outcomes for patients hospitalized with moderate COVID-19 (in terms of ventilation need and reduced mortality rate).25LaVange L Adam SJ Currier JS Higgs ES Reineck LA Hughes EA Read SW ACTIV Therapeutics-Clinical Working Group. Accelerating COVID-19 Therapeutic Interventions and Vaccines (ACTIV): Designing Master Protocols for Evaluation of Candidate COVID-19 Therapeutics.Ann Intern Med. 2021; 174: 1293-1300Crossref PubMed Scopus (23) Google Scholar This may be a treatment strategy for critically ill patients. Parenteral anticoagulation is recommended in most cases in which anticoagulant therapy is needed for known thrombotic disease. Unfractionated heparin can be used in the setting of anticipated procedures or in patients with deteriorating renal function. If no urgent procedures are anticipated, low-molecular-weight heparin is a reasonable alternative.26Kahn SR Lim W Dunn AS Cushman M Dentali F Akl EA Cook DJ Balekian AA Klein RC Le H Schulman S Murad MH Prevention of VTE in nonsurgical patients: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines.Chest. 2012; 141: e195S-e226SAbstract Full Text Full Text PDF PubMed Scopus (1338) Google Scholar Finally, our analysis demonstrates that myocardial infarction in patients with COVID-19 is a concern. Early in the pandemic, providers may have been more likely to regard elevated troponins as a marker of obstructive coronary artery disease and recommend an angiography. Later in the pandemic, providers may have been aware of the increasing evidence that troponin elevations are seen in patients with COVID-19 without obstructive coronary artery disease and, thus, chose to forgo invasive testing. Particular attention has been directed toward the management of acute coronary syndrome during the COVID-19 pandemic. In patients with STEMI or NSTEMI with high-risk features in which the etiology of their acute myocardial infarction is suspected to be true plaque rupture and not myocarditis or stress-induced cardiomyopathy in the setting of SARS-CoV-2 infection, our cardiac catheterization laboratory implemented procedures to ensure the safety of medical personnel during primary percutaneous coronary intervention. Per the guidelines recommended by the American College of Cardiology's Intervention Council and the Society for Cardiovascular Angiography and Interventions,6Welt FGP Shah PB Aronow HD Bortnick AE Henry TD Sherwood MW Young MN Davidson LJ Kadavath S Mahmud E Kirtane AJ American College of Cardiology's Interventional Council, Society for Cardiovascular Angiography InterventionsCatheterization laboratory considerations during the coronavirus (COVID-19) pandemic: from the ACC's interventional council and SCAI.J Am Coll Cardiol. 2020; 75: 2372-2375Crossref PubMed Scopus (329) Google Scholar we trained everyone in the catheterization laboratory on proper personal protective equipment use, designated 1 laboratory for patients with COVID-19 or those who were under investigation, and performed extensive cleaning after each procedure. We also implemented new treatment and risk stratification algorithms, utilizing noninvasive diagnostic testing such as echocardiography and cardiac magnetic resonance imaging in patients with low-risk features, to ensure that only high-risk patients with COVID-19 with suspected plaque rupture were brought to the catheterization laboratory.27Yerasi C Case BC Forrestal BJ Chezar-Azerrad C Hashim H Ben-Dor I Satler LF Mintz GS Waksman R Treatment of ST-segment elevation myocardial infarction During COVID-19 pandemic.Cardiovasc Revasc Med. 2020; 21: 1024-1029Crossref PubMed Scopus (18) Google Scholar There are limitations to our study. First, the analysis is retrospective and relies on the ICD-10 codes to identify the patient population. Inclusion in our analysis depended only on a positive COVID-19 test and a diagnosis of a thrombotic event as reported by the provider. In addition, STEMI or NSTEMI patients' coronary angiographic findings were not fully captured in our analysis. Analysis of these data would have allowed us to completely separate those with obstructive coronary artery disease from those with other etiologies of myocardial injury (e.g., myocarditis or stress-induced cardiomyopathy).28Khalid N Chen Y Case BC Shlofmitz E Wermers JP Rogers T Ben-Dor I Waksman R COVID-19 (SARS-CoV-2) and the heart - an ominous association.Cardiovasc Revasc Med. 2020; 21: 946-949Crossref PubMed Scopus (32) Google Scholar Furthermore, although we captured whether patients were diagnosed, we did not capture the treatment strategy (pharmacologic, mechanical, and so on). Finally, our data captured patients in the Mid-Atlantic region of the United States where the pandemic had the greatest impact in March 2020 and April 2020. Our findings may not represent the broader United States outcome data. In conclusion, our analysis suggests that patients with COVID-19 with non-cardiac thrombosis are at higher risk for in-hospital mortality. However, this prognosis is not as grim as for patients with cardiac thrombosis. Efforts should focus on early recognition, evaluation, and intensifying care of these patients. Dr. Rogers reports serving as a proctor and consultant for Medtronic and Edwards Lifesciences, serving on the advisory board for Medtronic, and holding equity interest in Transmural Systems. Dr. Waksman reports serving as an advisory board member for Amgen, Boston Scientific, Cardioset, Cardiovascular Systems Inc., Medtronic, Philips, and Pi-Cardia Ltd.; serving as a consultant for Amgen, Biotronik, Boston Scientific, Cardioset, Cardiovascular Systems Inc., Medtronic, Philips, and Pi-Cardia Ltd.; receiving grant support from AstraZeneca, Biotronik, Boson Scientific, and Chieisi; serving on the speakers bureau for AstraZeneca and Chiesi; and being an investor in MedAlliance. The remaining authors have no conflicts of interest to disclose. A special acknowledgment to Jason Wermers, MS, for assistance in preparing this manuscript.