Abstract:Background The purpose of this review is to critically analyse data regarding the prevalence and risk factors for developing a prolonged QTc interval and subsequent sudden cardiac death (SCD) in persons living with HIV (PLWH). Methods A systematic literature search using PubMed and Google Scholar databases was performed using the following search terms: ‘HIV and prolonged QTc’ and ‘managing HIV-patients with prolonged QTc’. References within articles of interest were also evaluated. Results/Discussion PLWH are… Show more
“…Baseline QT interval abnormalities in the setting of SARS-Cov-2 infection can be secondary to the viral infection per se, the inflammatory state associated with SARS-Cov-2 infection, and ischemia or hypoxia [ 1 ]. Indeed, several viral infections like human immunodeficiency virus (HIV) and dengue have been independently associated with a prolonged QT interval [ 7 , 8 , 9 ]. Interestingly, acute coronavirus infection has been associated with a prolonged QT interval in rabbits [ 10 ], which suggests that the virus might have a direct effect on the heart.…”
Background: The prognostic value of a prolonged QT interval in SARS-Cov2 infection is not well known. Objective: To determine whether the presence of a prolonged QT on admission is an independent factor for mortality in SARS-Cov2 hospitalized patients. Methods: Single-center cohort of 623 consecutive patients with positive polymerase-chain-reaction test (PCR) to SARS Cov2, recruited from 27 February to 7 April 2020. An electrocardiogram was taken on these patients within the first 48 h after diagnosis and before the administration of any medication with a known effect on QT interval. A prolonged QT interval was defined as a corrected QT (QTc) interval >480 milliseconds. Patients were followed up with until 10 May 2020. Results: Sixty-one patients (9.8%) had prolonged QTc and only 3.2% had a baseline QTc > 500 milliseconds. Patients with prolonged QTc were older, had more comorbidities, and higher levels of immune-inflammatory markers. There were no episodes of ventricular tachycardia or ventricular fibrillation during hospitalization. All-cause death was higher in patients with prolonged QTc (41.0% vs. 8.7%, p < 0.001, multivariable HR 2.68 (1.58–4.55), p < 0.001). Conclusions: Almost 10% of patients with COVID-19 infection have a prolonged QTc interval on admission. A prolonged QTc was independently associated with a higher mortality even after adjustment for age, comorbidities, and treatment with hydroxychloroquine and azithromycin. An electrocardiogram should be included on admission to identify high-risk SARS-CoV-2 patients.
“…Baseline QT interval abnormalities in the setting of SARS-Cov-2 infection can be secondary to the viral infection per se, the inflammatory state associated with SARS-Cov-2 infection, and ischemia or hypoxia [ 1 ]. Indeed, several viral infections like human immunodeficiency virus (HIV) and dengue have been independently associated with a prolonged QT interval [ 7 , 8 , 9 ]. Interestingly, acute coronavirus infection has been associated with a prolonged QT interval in rabbits [ 10 ], which suggests that the virus might have a direct effect on the heart.…”
Background: The prognostic value of a prolonged QT interval in SARS-Cov2 infection is not well known. Objective: To determine whether the presence of a prolonged QT on admission is an independent factor for mortality in SARS-Cov2 hospitalized patients. Methods: Single-center cohort of 623 consecutive patients with positive polymerase-chain-reaction test (PCR) to SARS Cov2, recruited from 27 February to 7 April 2020. An electrocardiogram was taken on these patients within the first 48 h after diagnosis and before the administration of any medication with a known effect on QT interval. A prolonged QT interval was defined as a corrected QT (QTc) interval >480 milliseconds. Patients were followed up with until 10 May 2020. Results: Sixty-one patients (9.8%) had prolonged QTc and only 3.2% had a baseline QTc > 500 milliseconds. Patients with prolonged QTc were older, had more comorbidities, and higher levels of immune-inflammatory markers. There were no episodes of ventricular tachycardia or ventricular fibrillation during hospitalization. All-cause death was higher in patients with prolonged QTc (41.0% vs. 8.7%, p < 0.001, multivariable HR 2.68 (1.58–4.55), p < 0.001). Conclusions: Almost 10% of patients with COVID-19 infection have a prolonged QTc interval on admission. A prolonged QTc was independently associated with a higher mortality even after adjustment for age, comorbidities, and treatment with hydroxychloroquine and azithromycin. An electrocardiogram should be included on admission to identify high-risk SARS-CoV-2 patients.
“…This systemic inflammation via 3 Case Reports in Cardiology elevated IL-6 is itself an independent risk factor for QTc prolongation, by modulating cardiomyocyte ion channel expression [18]. Other viral illnesses have been reported to exhibit this effect-HIV seropositivity is associated with a prolonged QT [19]. Physiological changes in acute illness can also lead to a temporary ventricular repolarization abnormality-core body temperature can impact QT duration with moderate hypothermia causing temporary prolongation of the QTc as well as fever [20,21].…”
Background. Several cardiovascular manifestations of coronavirus disease 2019 (COVID-19) have been previously described. QT prolongation has been reported in COVID-19 infection in association with medications such as azithromycin, hydroxychloroquine, and chloroquine but has not previously been reported as a direct result of COVID-19 infection. Case summary. We report the case of a 65-year-old female who developed a prolonged corrected QT interval (QTc) during a hospital admission with COVID-19. This patient was not on any QT prolonging treatment, serum electrolytes were normal, and there was no identifiable reversible cause for the QTc lengthening. Daily serial ECGs during admission showed resolution of the ventricular repolarization abnormality in synchronization with resolution of her COVID-19 viral illness. Discussions. Although there have been reports of QTc prolongation in COVID-19 patients, previous reports of this are for patients receiving medication that causes QT prolongation. This case uniquely demonstrates the development and resolution of this temporary ventricular repolarization abnormality in a patient with a structurally normal heart with no evidence of myocardial fibrosis or edema on cardiac MRI, that is unexplained by other confounding factors, such as medication. This suggests there may be a direct association between COVID-19 and temporary QTc prolongation.
“…The inhibition of CYP3A4 by PIs and integrase inhibitors increases the plasma concentration of methadone, leading to an increased therapeutic effect and methadone-induced toxicity [ 59 , 60 ]. Additionally, methadone can contribute to QTc prolongation and sudden cardiac death, through inadvertent inhibition of the human ether-a-go-go-related gene (hERG) potassium ion channels [ 7 ]. On the other hand, induction of CYP3A4 by NNRTIs, would lead to suboptimal plasma concentrations of methadone and might eventually cause therapeutic failure [ 8 , 60 ].…”
Section: Drug–drug Interactionsmentioning
confidence: 99%
“…Numerous studies also described attrition along the HIV care continuum among HIV-infected drug users, including suboptimal HIV testing, delayed entry into HIV care, and initiation of antiretroviral therapy (ART) [ 1 , 2 ]. Additionally, PLWHA and OUD are also more likely to develop more severe viral progression, including neurological complications of HIV/AIDS [ 6 ], and are at risk for serious drug–drug interactions (DDI), through antiretroviral-opioid metabolic pathway-related interactions [ 7 , 8 ]. Barriers to OUD-treatment, such as medication-assisted therapy (MAT), are also apparent for PLWHA with OUD.…”
The opioid epidemic has had a significant, negative impact in the United States, and people living with HIV/AIDS (PLWHA) represent a vulnerable sub-population that is at risk for negative sequela from prolonged opioid use or opioid use disorder (OUD). PLWHA are known to suffer from HIV-related pain and are commonly treated with opioids, leading to subsequent addictive disorders. PLWHA and OUD are at an increased risk for attrition in the HIV care continuum, including suboptimal HIV laboratory testing, delayed entry into HIV care, and initiation or adherence to antiretroviral therapy. Barriers to OUD treatment, such as medication-assisted therapy, are also apparent for PLWHA with OUD, particularly those living in rural areas. Additionally, PLWHA and OUD are at a high risk for serious drug–drug interactions through antiretroviral-opioid metabolic pathway-related inhibition/induction, or via the human ether-a-go-go-related gene potassium ion channel pathways. HIV-associated neurocognitive disorders can also be potentiated by the off-target inflammatory effects of opioid use. PLWHA and OUD might require more intensive, individualized protocols to sustain treatment for the underlying opioid addiction, as well as to provide proactive social support to aid in improving patient outcomes. Advancements in the understanding and management of PLWHA and OUD are needed to improve patient care. This review describes the effects of prescription and non-prescription opioid use in PLWHA.
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