1966
DOI: 10.1136/jcp.19.1.60
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Occurrence of lymphopenia in heart failure

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Cited by 9 publications
(8 citation statements)
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“…Endothelial cells are then incited on releasing even more chemokines and stimulating factors, in a positive feedback of proinflammatory response.³⁰ This role of proinflammatory protein release, triggered by SARS-CoV-2, may be exacerbated, which would be classically called "the cytokine storm".⁵¹ This typical immunological pattern, found among patients with COVID-19, is currently correlated with the evolution of the disease to more severe stages.⁵¹ The "cytokine storm" is associated to the pathophysiology of the pneumonia and the Acute Respiratory Distress Syndrome (ARDS), on SARS-CoV-2 positive patients.⁵¹ In the heart, inflammation plays a critical role on CVDs, like acute coronary events, left ventricular remodeling and heart failure.⁵² Thus, the cytokine storm must raise attention to the cardiovascular consequences in COVID-19, since its cardiac deployments are already described.⁵³ In this line, autopsies performed on COVID-19 deceased individuals have shown infiltration of interstitial mononuclear inflammatory cells on the myocardium,⁵³ corroborating that the cytokine storm may lead to cardiac outcomes, in which myocarditis could be one of these possible consequences.³ Furthermore, lymphopenia was also documented on COVID-19 patients, specially associated to low levels of CD4+ and CD8+ T cells, despite the late high levels of antiviral factors interferons (IFN-γ), which are secreted, mainly, by CD4+ T cells.²⁸ Lymphopenia is reversed by Tocilizumab, the anti-IL-6 antibody.⁵⁴ This kind of immune pattern is usually correlated with the evolution of the disease and associated with more severe cases when compared to moderate ones.⁵⁵ Studies already demonstrated that white blood cells count can be excellent predictor of coronary heart disease, as well as heart failure worst prognosis.⁵² One of the first works to demonstrate the association of lymphopenia and heart failure was the work of Hurdle, Gyde, & Willoughby in 1966. 56 The authors reported an association between the heart failure patients and the 'cold' controls in respect of lymphopenia, eosinopenia, and cortisol levels.⁵⁶ In agreement with this data, a previous study have associate lymphopenia with worse outcomes in patients with heart failure, chronic ischemic heart disease and acute coronary syndromes.⁵⁷ Also, the lymphopenia was proposed a key prognostic marker in heart failure. In this line it was demonstrated that lymphocyte count was inversely associated with survival at 1, 2 and 3 years after adjusting for clinical, laboratory, and pharmacological variables.⁵⁸ As described above, within the cytokines, IL-1B plays an important role in the SARS-CoV-2 physiopathology.…”
Section: Lymphopenia and Heart Functionsupporting
confidence: 66%
“…Endothelial cells are then incited on releasing even more chemokines and stimulating factors, in a positive feedback of proinflammatory response.³⁰ This role of proinflammatory protein release, triggered by SARS-CoV-2, may be exacerbated, which would be classically called "the cytokine storm".⁵¹ This typical immunological pattern, found among patients with COVID-19, is currently correlated with the evolution of the disease to more severe stages.⁵¹ The "cytokine storm" is associated to the pathophysiology of the pneumonia and the Acute Respiratory Distress Syndrome (ARDS), on SARS-CoV-2 positive patients.⁵¹ In the heart, inflammation plays a critical role on CVDs, like acute coronary events, left ventricular remodeling and heart failure.⁵² Thus, the cytokine storm must raise attention to the cardiovascular consequences in COVID-19, since its cardiac deployments are already described.⁵³ In this line, autopsies performed on COVID-19 deceased individuals have shown infiltration of interstitial mononuclear inflammatory cells on the myocardium,⁵³ corroborating that the cytokine storm may lead to cardiac outcomes, in which myocarditis could be one of these possible consequences.³ Furthermore, lymphopenia was also documented on COVID-19 patients, specially associated to low levels of CD4+ and CD8+ T cells, despite the late high levels of antiviral factors interferons (IFN-γ), which are secreted, mainly, by CD4+ T cells.²⁸ Lymphopenia is reversed by Tocilizumab, the anti-IL-6 antibody.⁵⁴ This kind of immune pattern is usually correlated with the evolution of the disease and associated with more severe cases when compared to moderate ones.⁵⁵ Studies already demonstrated that white blood cells count can be excellent predictor of coronary heart disease, as well as heart failure worst prognosis.⁵² One of the first works to demonstrate the association of lymphopenia and heart failure was the work of Hurdle, Gyde, & Willoughby in 1966. 56 The authors reported an association between the heart failure patients and the 'cold' controls in respect of lymphopenia, eosinopenia, and cortisol levels.⁵⁶ In agreement with this data, a previous study have associate lymphopenia with worse outcomes in patients with heart failure, chronic ischemic heart disease and acute coronary syndromes.⁵⁷ Also, the lymphopenia was proposed a key prognostic marker in heart failure. In this line it was demonstrated that lymphocyte count was inversely associated with survival at 1, 2 and 3 years after adjusting for clinical, laboratory, and pharmacological variables.⁵⁸ As described above, within the cytokines, IL-1B plays an important role in the SARS-CoV-2 physiopathology.…”
Section: Lymphopenia and Heart Functionsupporting
confidence: 66%
“…Lymphocytopenia in obese rats is a common finding during the systemic inflammatory response due to reduction of T-cells in peripheral blood, spleen, and thymus ( Nunez et al, 2011 , Tanaka et al, 1998 ). Moreover, stress of obesity that may lead to increase of corticosteroids production ( Baudrand and Vaidya, 2015 ) that has been shown to produce lymphocytopenia ( Claman, 1975 , Hurdle et al, 1966 ). Amelioration of HFD induced neutrophilia and lymphopenia could be attributed for their anti-obesity and antioxidant potentials that reduced oxidative stress promotion by corticosteroids ( Paliwal et al, 2011 ) and cytokines as IL-6 ( Fard et al, 2015 , Göncü et al, 2016 ) that were observed in the present results.…”
Section: Discussionmentioning
confidence: 99%
“…Catecholamine levels were directly correlated with HF severity and inversely proportional to lymphocyte counts, proving the interdependence of these conditions [19]. The incidence of lymphopenia was also linked to cortisol levels in the acute phases of HF, and recovering lymphocyte counts were recorded proportionally to cortisol decrease after the initiation of specific treatment [21].…”
Section: Introductionmentioning
confidence: 81%