Serveur d'exploration COVID et hydrochloroquine

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Coronavirus disease 2019 (COVID-19) and QTc prolongation.

Identifieur interne : 000169 ( Main/Corpus ); précédent : 000168; suivant : 000170

Coronavirus disease 2019 (COVID-19) and QTc prolongation.

Auteurs : Khalid Changal ; David Paternite ; Sean Mack ; Spiro Veria ; Rehana Bashir ; Mitra Patel ; Ronak Soni ; Muhammad Ali ; Tanveer Mir ; Mujeeb Sheikh ; P Kasi Ramanathan

Source :

RBID : pubmed:33784966

English descriptors

Abstract

INTRODUCTION

The cause-and-effect relationship of QTc prolongation in Coronavirus disease 2019 (COVID-19) patients has not been studied well.

OBJECTIVE

We attempt to better understand the relationship of QTc prolongation in COVID-19 patients in this study.

METHODS

This is a retrospective, hospital-based, observational study. All patients with normal baseline QTc interval who were hospitalized with the diagnosis of COVID-19 infection at two hospitals in Ohio, USA were included in this study.

RESULTS

Sixty-nine patients had QTc prolongation, and 210 patients continued to have normal QTc during hospitalization. The baseline QTc intervals were comparable in the two groups. Patients with QTc prolongation were older (mean age 67 vs. 60, P 0.003), more likely to have underlying cardiovascular disease (48% versus 26%, P 0.001), ischemic heart disease (29% versus 17%, P 0.026), congestive heart failure with preserved ejection fraction (16% versus 8%, P 0.042), chronic kidney disease (23% versus 10%, P 0.005), and end-stage renal disease (12% versus 1%, P < 0.001). Patients with QTc prolongation were more likely to have received hydroxychloroquine (75% versus 59%, P 0.018), azithromycin (18% vs. 14%, P 0.034), a combination of hydroxychloroquine and azithromycin (29% vs 7%, P < 0.001), more than 1 QT prolonging agents (59% vs. 32%, P < 0.001). Patients who were on angiotensin-converting enzyme inhibitors (ACEi) were less likely to develop QTc prolongation (11% versus 26%, P 0.014). QTc prolongation was not associated with increased ventricular arrhythmias or mortality.

CONCLUSION

Older age, ESRD, underlying cardiovascular disease, potential virus mediated cardiac injury, and drugs like hydroxychloroquine/azithromycin, contribute to QTc prolongation in COVID-19 patients. The role of ACEi in preventing QTc prolongation in COVID-19 patients needs to be studied further.


DOI: 10.1186/s12872-021-01963-1
PubMed: 33784966
PubMed Central: PMC8007653

Links to Exploration step

pubmed:33784966

Le document en format XML

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<term>COVID-19 (complications)</term>
<term>COVID-19 (drug therapy)</term>
<term>COVID-19 (epidemiology)</term>
<term>COVID-19 (physiopathology)</term>
<term>COVID-19 (therapy)</term>
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<term>Correlation of Data (MeSH)</term>
<term>Electrocardiography (methods)</term>
<term>Electrocardiography (statistics & numerical data)</term>
<term>Female (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Long QT Syndrome (diagnosis)</term>
<term>Long QT Syndrome (epidemiology)</term>
<term>Long QT Syndrome (etiology)</term>
<term>Male (MeSH)</term>
<term>Middle Aged (MeSH)</term>
<term>Outcome and Process Assessment, Health Care (MeSH)</term>
<term>Renal Insufficiency, Chronic (epidemiology)</term>
<term>Risk Assessment (methods)</term>
<term>SARS-CoV-2 (isolation & purification)</term>
<term>Survival Analysis (MeSH)</term>
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<term>COVID-19</term>
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<term>Long QT Syndrome</term>
<term>Renal Insufficiency, Chronic</term>
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<term>Long QT Syndrome</term>
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<keywords scheme="MESH" qualifier="isolation & purification" xml:lang="en">
<term>SARS-CoV-2</term>
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<keywords scheme="MESH" qualifier="methods" xml:lang="en">
<term>Electrocardiography</term>
<term>Risk Assessment</term>
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<term>Correlation of Data</term>
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<front>
<div type="abstract" xml:lang="en">
<p>
<b>INTRODUCTION</b>
</p>
<p>The cause-and-effect relationship of QTc prolongation in Coronavirus disease 2019 (COVID-19) patients has not been studied well.</p>
</div>
<div type="abstract" xml:lang="en">
<p>
<b>OBJECTIVE</b>
</p>
<p>We attempt to better understand the relationship of QTc prolongation in COVID-19 patients in this study.</p>
</div>
<div type="abstract" xml:lang="en">
<p>
<b>METHODS</b>
</p>
<p>This is a retrospective, hospital-based, observational study. All patients with normal baseline QTc interval who were hospitalized with the diagnosis of COVID-19 infection at two hospitals in Ohio, USA were included in this study.</p>
</div>
<div type="abstract" xml:lang="en">
<p>
<b>RESULTS</b>
</p>
<p>Sixty-nine patients had QTc prolongation, and 210 patients continued to have normal QTc during hospitalization. The baseline QTc intervals were comparable in the two groups. Patients with QTc prolongation were older (mean age 67 vs. 60, P 0.003), more likely to have underlying cardiovascular disease (48% versus 26%, P 0.001), ischemic heart disease (29% versus 17%, P 0.026), congestive heart failure with preserved ejection fraction (16% versus 8%, P 0.042), chronic kidney disease (23% versus 10%, P 0.005), and end-stage renal disease (12% versus 1%, P < 0.001). Patients with QTc prolongation were more likely to have received hydroxychloroquine (75% versus 59%, P 0.018), azithromycin (18% vs. 14%, P 0.034), a combination of hydroxychloroquine and azithromycin (29% vs 7%, P < 0.001), more than 1 QT prolonging agents (59% vs. 32%, P < 0.001). Patients who were on angiotensin-converting enzyme inhibitors (ACEi) were less likely to develop QTc prolongation (11% versus 26%, P 0.014). QTc prolongation was not associated with increased ventricular arrhythmias or mortality.</p>
</div>
<div type="abstract" xml:lang="en">
<p>
<b>CONCLUSION</b>
</p>
<p>Older age, ESRD, underlying cardiovascular disease, potential virus mediated cardiac injury, and drugs like hydroxychloroquine/azithromycin, contribute to QTc prolongation in COVID-19 patients. The role of ACEi in preventing QTc prolongation in COVID-19 patients needs to be studied further.</p>
</div>
</front>
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<AbstractText Label="INTRODUCTION">The cause-and-effect relationship of QTc prolongation in Coronavirus disease 2019 (COVID-19) patients has not been studied well.</AbstractText>
<AbstractText Label="OBJECTIVE">We attempt to better understand the relationship of QTc prolongation in COVID-19 patients in this study.</AbstractText>
<AbstractText Label="METHODS">This is a retrospective, hospital-based, observational study. All patients with normal baseline QTc interval who were hospitalized with the diagnosis of COVID-19 infection at two hospitals in Ohio, USA were included in this study.</AbstractText>
<AbstractText Label="RESULTS">Sixty-nine patients had QTc prolongation, and 210 patients continued to have normal QTc during hospitalization. The baseline QTc intervals were comparable in the two groups. Patients with QTc prolongation were older (mean age 67 vs. 60, P 0.003), more likely to have underlying cardiovascular disease (48% versus 26%, P 0.001), ischemic heart disease (29% versus 17%, P 0.026), congestive heart failure with preserved ejection fraction (16% versus 8%, P 0.042), chronic kidney disease (23% versus 10%, P 0.005), and end-stage renal disease (12% versus 1%, P < 0.001). Patients with QTc prolongation were more likely to have received hydroxychloroquine (75% versus 59%, P 0.018), azithromycin (18% vs. 14%, P 0.034), a combination of hydroxychloroquine and azithromycin (29% vs 7%, P < 0.001), more than 1 QT prolonging agents (59% vs. 32%, P < 0.001). Patients who were on angiotensin-converting enzyme inhibitors (ACEi) were less likely to develop QTc prolongation (11% versus 26%, P 0.014). QTc prolongation was not associated with increased ventricular arrhythmias or mortality.</AbstractText>
<AbstractText Label="CONCLUSION">Older age, ESRD, underlying cardiovascular disease, potential virus mediated cardiac injury, and drugs like hydroxychloroquine/azithromycin, contribute to QTc prolongation in COVID-19 patients. The role of ACEi in preventing QTc prolongation in COVID-19 patients needs to be studied further.</AbstractText>
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