Cardiotoxicity of Interferon*

Sonnenblick, M; Rosin, Arnold J.

doi:10.1378/chest.99.3.557

Cited by 208 publications

(102 citation statements)

References 28 publications

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“…However, in a study of infants born to HIV-infected mothers followed from birth to age 5, perinatal exposure to zidovudine was not found to be associated with acute or chronic abnormalities in left ventricular structure or function 32 .Other nucleoside reverse transcriptase inhibitors, such as didanosine, zalcitabine or lamivudine, do not seem to promote or prevent dilated cardiomyopathy. In AIDS patients with Kaposi's sarcoma, reversible cardiac dysfunction was associated with prolonged, high-dose therapy with interferon alpha 33 . High-dose interferon alpha treatment is not associated with myo cardial dysfunction in other patient populations, so it has been proposed that it may have a synergistic effect with HIV-1 infection 33 .…”

Section: Left Ventricular Dysfunction Caused By Drug Cardiotoxicitymentioning

confidence: 99%

“…In AIDS patients with Kaposi's sarcoma, reversible cardiac dysfunction was associated with prolonged, high-dose therapy with interferon alpha 33 . High-dose interferon alpha treatment is not associated with myo cardial dysfunction in other patient populations, so it has been proposed that it may have a synergistic effect with HIV-1 infection 33 . Doxorubicin (adria mycin), which is used to treat AIDS-associated Kaposi's sarcoma and non-Hodgkin's lymphoma, has a dose-related effect on dilated cardiomyopathy 34 , as does foscarnet sodium when used to treat cyto megalovirus esophagitis 35 .…”

Section: Left Ventricular Dysfunction Caused By Drug Cardiotoxicitymentioning

confidence: 99%

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Cardiovascular complications in the acquired immunodeficiency syndrome

Bárbaro

Silva

2009

Rev. Assoc. Med. Bras.

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Section: Left Ventricular Dysfunction Caused By Drug Cardiotoxicitymentioning

confidence: 99%

Section: Left Ventricular Dysfunction Caused By Drug Cardiotoxicitymentioning

confidence: 99%

Cardiovascular complications in the acquired immunodeficiency syndrome

Bárbaro

Silva

2009

Rev. Assoc. Med. Bras.

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“…Although no patient in our series received interferon therapy for HCV, antiviral therapy may be considered to improve cardiac function in DCM with HCV, as already suggested. 1) However, the cardiotoxicity of interferon has been reported in patients with cancer 30) and HCV. 31) Moreover, Sartori, et al 32) showed that in 11 patients with chronic HCV infection who had no cardiac disease, LV ejection fraction in all patients but one decreased 1 month after low dose interferon therapy.…”

Section: Responsiveness To Neurohormonal Antagonism and Long-term Promentioning

confidence: 99%

Pathophysiological Characteristics and Responsiveness to Neurohormonal Antagonism in Idiopathic Dilated Cardiomyopathy Patients With Antihepatitis C Virus Antibody

et al. 2005

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SUMMARYA high prevalence of hepatitis C virus (HCV) infection has been reported among idiopathic dilated cardiomyopathy (DCM) patients. We examined the prevalence of DCM patients with HCV antibody, and the pathophysiological characteristics and responsiveness to neurohormonal antagonism in DCM with HCV. HCV antibodies were determined in 540 patients with cardiac diseases. In 117 DCM patients, clinicopathologic data were evaluated before and 1 year after angiotensin converting enzyme inhibitor and/or betablocker (ACE-inhibitor/BB) administration and their prognosis was followed-up for a mean of 72 ± 41 months. HCV antibodies were found in 12 of 135 DCM patients (8.9%) and in 37 of 405 patients without DCM (9.1%) (P = NS). At baseline, contrary to DCM without HCV, DCM with HCV was associated (P < 0.05) with greater left ventricular (LV) end-diastolic and end-systolic dimension, LV mass, and myocardial diameter in endomyocardial biopsy, and lower % fractional shortening. By multivariate analysis, HCV infection was independently associated with larger LV end-systolic dimension among DCM patients (P = 0.005). The advanced LV dilatation and hypertrophy in DCM with HCV decreased more in response to the ACE-inhibitor/BB therapy compared to DCM without HCV. There were no differences between DCM patients with and without HCV in survival and cardiac event-free rates. In summary, although HCV infection appears not to be the specific cause of DCM, HCV may enhance ventricular remodeling leading to heart failure among DCM patients. Nevertheless, the advanced ventricular remodeling with HCV was adequately reversed by neurohormonal antagonism, and did not lead to an unfavorable outcome. (Int Heart J 2005; 46: 407-417)

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“…The efficacy of alfa-interferon Correspondence: S Sacchi, Dipartimento di Scienze Mediche, Oncologiche e Radiologiche, Policlinico di Modena, 41100 Modena, Italy; Fax: 39 59 444549 Received 10 February 1997; accepted 8 November 1997 (alfa-IFN) in ET patients has been reported by several authors (Refs 1-10 and others, reviewed in Refs 1, 2 and 9); generally considered non-leukemogenic and non-gonadotoxic, reduces the platelet count rapidly, controls symptoms related to thrombocytosis and can reduce megakaryocytic mass and spleen size. Since chronic alfa-IFN treatment is very expensive and may produce severe side-effects, [11][12][13][14][15][16][17][18][19] this treatment is not generally accepted. The aim of this study is to assess the magnitude of the effect of alfa-IFN on the neoplastic clone; in other words, our goal is to verify whether alfa-IFN can exert not only a 'cosmetic' effect, but also a fundamental influence on this disease.…”

Section: Introductionmentioning

confidence: 99%

Alfa-interferon in the treatment of essential thrombocythemia: clinical results and evaluation of its biological effects on the hematopoietic neoplastic clone

Sacchi¹,

Gugliotta

Papineschi

et al. 1998

Leukemia

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The efficacy of alfa-interferon (alfa-IFN) in essential thrombocythemia (ET) patients has been reported by several authors. The aim of this study is to assess the magnitude of the effect of alfa-IFN on the neoplastic clone. As of December 1993, 11 ET patients received alfa-IFN at a dose of 3-6 MU/s.c./day for 6 months. Ten of 11 obtained complete hematological remission (CHR) and one achieved partial hematological remission. Megakaryocyte concentration was reduced in six cases. The spleen,which was enlarged in four patients, decreased in size in two patients. Seven of eight patients who were symptomatic at diagnosis obtained resolution of symptoms. In order to obtain indications about the structural modifications induced by alfa-IFN in ET megakaryocytes (Mks), Fourier-transform infra-red microspectroscopy analysis performed on 10 single Mks of each patient, was done in seven of 11 patients; the analysis showed a reduction of A 1 /A 2 ratios (A 1 integrated area of the band at 1080 cm −1 due to the nucleic acids absorption; A 2 integrated area of the band at 1540 cm −1 due to proteic components absorption) in five cases, and in three of these five patients A 1 /A 2 ratios achieved normal values. After alfa-IFN treatment we did not observe any change in the methylation pattern of DNA from the granulocyte fraction. Our results confirm the efficacy of alfa-IFN in ET patients, and the decrease of A 1 /A 2 ratios in several patients is a demonstration of the depth of the effect of alfa-IFN on the neoplastic clone. The results of clonality studies showed the persistence of clonal hematopoiesis. Whether higher alfa-IFN dose and/or more prolonged alfa-IFN therapy may allow a restoration of polyclonal hematopoiesis remains to be determined and should be explored in future clinical trials.

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Cardiotoxicity of Interferon*

Cited by 208 publications

References 28 publications

Cardiovascular complications in the acquired immunodeficiency syndrome

Cardiovascular complications in the acquired immunodeficiency syndrome

Pathophysiological Characteristics and Responsiveness to Neurohormonal Antagonism in Idiopathic Dilated Cardiomyopathy Patients With Antihepatitis C Virus Antibody

Alfa-interferon in the treatment of essential thrombocythemia: clinical results and evaluation of its biological effects on the hematopoietic neoplastic clone

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