Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 15 de 15
Filter
3.
Clin Cardiol ; 44(10): 1360-1370, 2021 Oct.
Article in English | MEDLINE | ID: covidwho-1490731

ABSTRACT

There is limited evidence about the prognostic utility of right ventricular dysfunction (RVD) in patients with coronavirus disease 2019 (COVID-19). We assessed the association between RVD and mortality in COVID-19 patients. We searched electronic databases from inception to February 15, 2021. RVD was defined based on the following echocardiographic variables: tricuspid annular plane systolic excursion (TAPSE), tricuspid S' peak systolic velocity, fractional area change (FAC), and right ventricular free wall longitudinal strain (RVFWLS). All meta-analyses were performed using a random-effects model. Nineteen cohort studies involving 2307 patients were included. The mean age ranged from 59 to 72 years and 65% of patients were male. TAPSE (mean difference [MD], -3.13 mm; 95% confidence interval [CI], -4.08--2.19), tricuspid S' peak systolic velocity (MD, -0.88 cm/s; 95% CI, -1.68 to -0.08), FAC (MD, -3.47%; 95% CI, -6.21 to -0.72), and RVFWLS (MD, -5.83%; 95% CI, -7.47--4.20) were significantly lower in nonsurvivors compared to survivors. Each 1 mm decrease in TAPSE (adjusted hazard ratio [aHR], 1.22; 95% CI, 1.08-1.37), 1% decrease in FAC (aHR, 1.09; 95% CI, 1.04-1.14), and 1% increase in RVFWLS (aHR, 1.33; 95% CI, 1.19-1.48) were independently associated with higher mortality. RVD was significantly associated with higher mortality using unadjusted risk ratio (2.05; 95% CI, 1.27-3.31), unadjusted hazard ratio (3.37; 95% CI, 1.72-6.62), and adjusted hazard ratio (aHR, 2.75; 95% CI, 1.52-4.96). Our study shows that echocardiographic parameters of RVD were associated with an increased risk of mortality in COVID-19 patients.


Subject(s)
COVID-19 , Ventricular Dysfunction, Right , Aged , Humans , Male , Middle Aged , SARS-CoV-2 , Systole , Ventricular Dysfunction, Right/diagnostic imaging , Ventricular Dysfunction, Right/etiology , Ventricular Function, Right
4.
J Virol ; 96(2): e0106321, 2022 01 26.
Article in English | MEDLINE | ID: covidwho-1476388

ABSTRACT

COVID-19 affects multiple organs. Clinical data from the Mount Sinai Health System show that substantial numbers of COVID-19 patients without prior heart disease develop cardiac dysfunction. How COVID-19 patients develop cardiac disease is not known. We integrated cell biological and physiological analyses of human cardiomyocytes differentiated from human induced pluripotent stem cells (hiPSCs) infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in the presence of interleukins (ILs) with clinical findings related to laboratory values in COVID-19 patients to identify plausible mechanisms of cardiac disease in COVID-19 patients. We infected hiPSC-derived cardiomyocytes from healthy human subjects with SARS-CoV-2 in the absence and presence of IL-6 and IL-1ß. Infection resulted in increased numbers of multinucleated cells. Interleukin treatment and infection resulted in disorganization of myofibrils, extracellular release of troponin I, and reduced and erratic beating. Infection resulted in decreased expression of mRNA encoding key proteins of the cardiomyocyte contractile apparatus. Although interleukins did not increase the extent of infection, they increased the contractile dysfunction associated with viral infection of cardiomyocytes, resulting in cessation of beating. Clinical data from hospitalized patients from the Mount Sinai Health System show that a significant portion of COVID-19 patients without history of heart disease have elevated troponin and interleukin levels. A substantial subset of these patients showed reduced left ventricular function by echocardiography. Our laboratory observations, combined with the clinical data, indicate that direct effects on cardiomyocytes by interleukins and SARS-CoV-2 infection might underlie heart disease in COVID-19 patients. IMPORTANCE SARS-CoV-2 infects multiple organs, including the heart. Analyses of hospitalized patients show that a substantial number without prior indication of heart disease or comorbidities show significant injury to heart tissue, assessed by increased levels of troponin in blood. We studied the cell biological and physiological effects of virus infection of healthy human iPSC-derived cardiomyocytes in culture. Virus infection with interleukins disorganizes myofibrils, increases cell size and the numbers of multinucleated cells, and suppresses the expression of proteins of the contractile apparatus. Viral infection of cardiomyocytes in culture triggers release of troponin similar to elevation in levels of COVID-19 patients with heart disease. Viral infection in the presence of interleukins slows down and desynchronizes the beating of cardiomyocytes in culture. The cell-level physiological changes are similar to decreases in left ventricular ejection seen in imaging of patients' hearts. These observations suggest that direct injury to heart tissue by virus can be one underlying cause of heart disease in COVID-19.


Subject(s)
COVID-19/immunology , Induced Pluripotent Stem Cells , Interleukin-10/immunology , Interleukin-1beta/immunology , Interleukin-6/immunology , Myocytes, Cardiac , Cells, Cultured , Humans , Induced Pluripotent Stem Cells/immunology , Induced Pluripotent Stem Cells/pathology , Induced Pluripotent Stem Cells/virology , Myocytes, Cardiac/immunology , Myocytes, Cardiac/pathology , Myocytes, Cardiac/virology
5.
JACC Cardiovasc Imaging ; 13(8): 1857-1858, 2020 08.
Article in English | MEDLINE | ID: covidwho-1382507
7.
J Med Internet Res ; 22(11): e24018, 2020 11 06.
Article in English | MEDLINE | ID: covidwho-979821

ABSTRACT

BACKGROUND: COVID-19 has infected millions of people worldwide and is responsible for several hundred thousand fatalities. The COVID-19 pandemic has necessitated thoughtful resource allocation and early identification of high-risk patients. However, effective methods to meet these needs are lacking. OBJECTIVE: The aims of this study were to analyze the electronic health records (EHRs) of patients who tested positive for COVID-19 and were admitted to hospitals in the Mount Sinai Health System in New York City; to develop machine learning models for making predictions about the hospital course of the patients over clinically meaningful time horizons based on patient characteristics at admission; and to assess the performance of these models at multiple hospitals and time points. METHODS: We used Extreme Gradient Boosting (XGBoost) and baseline comparator models to predict in-hospital mortality and critical events at time windows of 3, 5, 7, and 10 days from admission. Our study population included harmonized EHR data from five hospitals in New York City for 4098 COVID-19-positive patients admitted from March 15 to May 22, 2020. The models were first trained on patients from a single hospital (n=1514) before or on May 1, externally validated on patients from four other hospitals (n=2201) before or on May 1, and prospectively validated on all patients after May 1 (n=383). Finally, we established model interpretability to identify and rank variables that drive model predictions. RESULTS: Upon cross-validation, the XGBoost classifier outperformed baseline models, with an area under the receiver operating characteristic curve (AUC-ROC) for mortality of 0.89 at 3 days, 0.85 at 5 and 7 days, and 0.84 at 10 days. XGBoost also performed well for critical event prediction, with an AUC-ROC of 0.80 at 3 days, 0.79 at 5 days, 0.80 at 7 days, and 0.81 at 10 days. In external validation, XGBoost achieved an AUC-ROC of 0.88 at 3 days, 0.86 at 5 days, 0.86 at 7 days, and 0.84 at 10 days for mortality prediction. Similarly, the unimputed XGBoost model achieved an AUC-ROC of 0.78 at 3 days, 0.79 at 5 days, 0.80 at 7 days, and 0.81 at 10 days. Trends in performance on prospective validation sets were similar. At 7 days, acute kidney injury on admission, elevated LDH, tachypnea, and hyperglycemia were the strongest drivers of critical event prediction, while higher age, anion gap, and C-reactive protein were the strongest drivers of mortality prediction. CONCLUSIONS: We externally and prospectively trained and validated machine learning models for mortality and critical events for patients with COVID-19 at different time horizons. These models identified at-risk patients and uncovered underlying relationships that predicted outcomes.


Subject(s)
Coronavirus Infections/diagnosis , Coronavirus Infections/mortality , Machine Learning/standards , Pneumonia, Viral/diagnosis , Pneumonia, Viral/mortality , Acute Kidney Injury/epidemiology , Adolescent , Adult , Aged , Aged, 80 and over , Betacoronavirus , COVID-19 , Cohort Studies , Electronic Health Records , Female , Hospital Mortality , Hospitalization/statistics & numerical data , Hospitals , Humans , Male , Middle Aged , New York City/epidemiology , Pandemics , Prognosis , ROC Curve , Risk Assessment/methods , Risk Assessment/standards , SARS-CoV-2 , Young Adult
8.
Future Cardiol ; 17(4): 655-661, 2021 07.
Article in English | MEDLINE | ID: covidwho-841164

ABSTRACT

COVID-19 infection can affect the cardiovascular system. We sought to determine if left ventricular global longitudinal strain (LVGLS) is affected by COVID-19 and if this has prognostic implications. Materials & methods: Retrospective study, with LVGLS was measured in 58 COVID-19 patients. Patients discharged were compared with those who died. Results: The mean LV ejection fraction (LVEF) and LVGLS for the cohort was 52.1 and -12.9 ± 4.0%, respectively. Among 30 patients with preserved LVEF (>50%), LVGLS was -15.7 ± 2.8%, which is lower than the reference mean LVGLS for a normal, healthy population. There was no significant difference in LVGLS or LVEF when comparing patients who survived to discharge or died. Conclusion: LVGLS was reduced in COVID-19 patients, although not significantly lower in those who died compared with survivors.


Subject(s)
COVID-19/complications , Echocardiography/methods , Ventricular Dysfunction, Left/diagnostic imaging , Ventricular Dysfunction, Left/virology , Female , Humans , Male , Middle Aged , Prognosis , Retrospective Studies , Risk Factors , SARS-CoV-2 , Stroke Volume
10.
Future Cardiol ; 17(4): 663-667, 2021 07.
Article in English | MEDLINE | ID: covidwho-694246

ABSTRACT

The COVID-19 infection adversely affects the cardiovascular system. Transthoracic echocardiography has demonstrated diagnostic, prognostic and therapeutic utility. We report biventricular myocardial strain in COVID-19. Methods: Biventricular strain measurements were performed for 12 patients. Patients who were discharged were compared with those who needed intubation and/or died. Results: Seven patients were discharged and five died or needed intubation. Right ventricular strain parameters were decreased in patients with poor outcomes compared with those discharged. Left ventricular strain was decreased in both groups but was not statistically significant. Conclusion: Right ventricular strain was decreased in patients with poor outcomes and left ventricular strain was decreased regardless of outcome. Right ventricular strain measurements may be important for risk stratification and prognosis. Further studies are needed to confirm these findings.


Subject(s)
COVID-19/complications , Echocardiography/methods , Ventricular Dysfunction/diagnostic imaging , Ventricular Dysfunction/virology , Adult , Female , Humans , Male , Middle Aged , Prognosis , SARS-CoV-2
14.
JACC Case Rep ; 2(5): 845-846, 2020 May.
Article in English | MEDLINE | ID: covidwho-306605
SELECTION OF CITATIONS
SEARCH DETAIL