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3.
J Am Coll Cardiol ; 76(17): 1965-1977, 2020 10 27.
Artículo en Inglés | MEDLINE | ID: covidwho-872172

RESUMEN

BACKGROUND: Coronavirus disease 2019 (COVID-19) is a growing pandemic that confers augmented risk for right ventricular (RV) dysfunction and dilation; the prognostic utility of adverse RV remodeling in COVID-19 patients is uncertain. OBJECTIVES: The purpose of this study was to test whether adverse RV remodeling (dysfunction/dilation) predicts COVID-19 prognosis independent of clinical and biomarker risk stratification. METHODS: Consecutive COVID-19 inpatients undergoing clinical transthoracic echocardiography at 3 New York City hospitals were studied; images were analyzed by a central core laboratory blinded to clinical and biomarker data. RESULTS: In total, 510 patients (age 64 ± 14 years, 66% men) were studied; RV dilation and dysfunction were present in 35% and 15%, respectively. RV dysfunction increased stepwise in relation to RV chamber size (p = 0.007). During inpatient follow-up (median 20 days), 77% of patients had a study-related endpoint (death 32%, discharge 45%). RV dysfunction (hazard ratio [HR]: 2.57; 95% confidence interval [CI]: 1.49 to 4.43; p = 0.001) and dilation (HR: 1.43; 95% CI: 1.05 to 1.96; p = 0.02) each independently conferred mortality risk. Patients without adverse RV remodeling were more likely to survive to hospital discharge (HR: 1.39; 95% CI: 1.01 to 1.90; p = 0.041). RV indices provided additional risk stratification beyond biomarker strata; risk for death was greatest among patients with adverse RV remodeling and positive biomarkers and was lesser among patients with isolated biomarker elevations (p ≤ 0.001). In multivariate analysis, adverse RV remodeling conferred a >2-fold increase in mortality risk, which remained significant (p < 0.01) when controlling for age and biomarker elevations; the predictive value of adverse RV remodeling was similar irrespective of whether analyses were performed using troponin, D-dimer, or ferritin. CONCLUSIONS: Adverse RV remodeling predicts mortality in COVID-19 independent of standard clinical and biomarker-based assessment.


Asunto(s)
Infecciones por Coronavirus/diagnóstico por imagen , Ecocardiografía , Corazón/diagnóstico por imagen , Neumonía Viral/diagnóstico por imagen , Remodelación Ventricular , Anciano , Anciano de 80 o más Años , Betacoronavirus , Biomarcadores/sangre , COVID-19 , Estudios de Cohortes , Infecciones por Coronavirus/sangre , Infecciones por Coronavirus/mortalidad , Infecciones por Coronavirus/fisiopatología , Femenino , Corazón/fisiopatología , Humanos , Masculino , Persona de Mediana Edad , Ciudad de Nueva York/epidemiología , Pandemias , Neumonía Viral/sangre , Neumonía Viral/mortalidad , Neumonía Viral/fisiopatología , Medición de Riesgo , SARS-CoV-2
4.
Circ Heart Fail ; 13(9): e007516, 2020 09.
Artículo en Inglés | MEDLINE | ID: covidwho-748835

RESUMEN

The coronavirus disease 2019 (COVID-19) pandemic imposed severe restrictions on traditional methods of patient care. During the pandemic, the heart failure program at New York-Presbyterian Hospital in New York, NY rapidly and comprehensively transitioned its care delivery model and administrative organization to conform to a new healthcare environment while still providing high-quality care to a large cohort of patients with heart failure, heart transplantation, and left ventricular assist device. In addition to the widespread adoption of telehealth, our program restructured outpatient care, initiating a shared clinic model and introducing a comprehensive remote monitoring program to manage patients with heart failure and heart transplant. All conferences, including administrative meetings, support groups, and educational seminars were converted to teleconferencing platforms. Following the peak of COVID-19, many of the new changes have been maintained, and the program structure will be permanently altered as a lasting effect of this pandemic. In this article, we review the details of our program's transition in the face of COVID-19 and highlight the programmatic changes that will endure.


Asunto(s)
Cardiología/organización & administración , Infecciones por Coronavirus/epidemiología , Atención a la Salud/organización & administración , Insuficiencia Cardíaca/terapia , Neumonía Viral/epidemiología , Telemedicina/organización & administración , Planificación Anticipada de Atención , Atención Ambulatoria/organización & administración , Betacoronavirus , COVID-19 , Trasplante de Corazón , Corazón Auxiliar , Humanos , Ciudad de Nueva York/epidemiología , Enfermeras Practicantes , Pandemias , Médicos , Rol Profesional , SARS-CoV-2 , Grupos de Autoayuda , Telecomunicaciones , Centros de Atención Terciaria/organización & administración , Comunicación por Videoconferencia
5.
Clin Immunol ; 219: 108555, 2020 10.
Artículo en Inglés | MEDLINE | ID: covidwho-696063

RESUMEN

Respiratory failure and acute kidney injury (AKI) are associated with high mortality in SARS-CoV-2-associated Coronavirus disease 2019 (COVID-19). These manifestations are linked to a hypercoaguable, pro-inflammatory state with persistent, systemic complement activation. Three critical COVID-19 patients recalcitrant to multiple interventions had skin biopsies documenting deposition of the terminal complement component C5b-9, the lectin complement pathway enzyme MASP2, and C4d in microvascular endothelium. Administration of anti-C5 monoclonal antibody eculizumab led to a marked decline in D-dimers and neutrophil counts in all three cases, and normalization of liver functions and creatinine in two. One patient with severe heart failure and AKI had a complete remission. The other two individuals had partial remissions, one with resolution of his AKI but ultimately succumbing to respiratory failure, and another with a significant decline in FiO2 requirements, but persistent renal failure. In conclusion, anti-complement therapy may be beneficial in at least some patients with critical COVID-19.


Asunto(s)
Lesión Renal Aguda/inmunología , Anticuerpos Monoclonales Humanizados/uso terapéutico , Betacoronavirus/patogenicidad , Inactivadores del Complemento/uso terapéutico , Infecciones por Coronavirus/inmunología , Síndrome de Liberación de Citoquinas/inmunología , Neumonía Viral/inmunología , Síndrome Respiratorio Agudo Grave/inmunología , Lesión Renal Aguda/complicaciones , Lesión Renal Aguda/tratamiento farmacológico , Lesión Renal Aguda/virología , Adulto , Betacoronavirus/inmunología , Biomarcadores/metabolismo , COVID-19 , Activación de Complemento/efectos de los fármacos , Complemento C4b/antagonistas & inhibidores , Complemento C5/antagonistas & inhibidores , Complejo de Ataque a Membrana del Sistema Complemento/antagonistas & inhibidores , Infecciones por Coronavirus/complicaciones , Infecciones por Coronavirus/tratamiento farmacológico , Infecciones por Coronavirus/virología , Síndrome de Liberación de Citoquinas/complicaciones , Síndrome de Liberación de Citoquinas/tratamiento farmacológico , Síndrome de Liberación de Citoquinas/virología , Femenino , Productos de Degradación de Fibrina-Fibrinógeno/metabolismo , Humanos , Inmunidad Humoral/efectos de los fármacos , Masculino , Serina Proteasas Asociadas a la Proteína de Unión a la Manosa/genética , Serina Proteasas Asociadas a la Proteína de Unión a la Manosa/inmunología , Persona de Mediana Edad , Neutrófilos/inmunología , Neutrófilos/patología , Pandemias , Fragmentos de Péptidos/antagonistas & inhibidores , Neumonía Viral/complicaciones , Neumonía Viral/tratamiento farmacológico , Neumonía Viral/virología , SARS-CoV-2 , Síndrome Respiratorio Agudo Grave/complicaciones , Síndrome Respiratorio Agudo Grave/tratamiento farmacológico , Síndrome Respiratorio Agudo Grave/virología
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