Frequency of myocarditis, left ventricular dysfunction and ventricular tachycardia in the acquired immune deficiency syndrome

Reilly, Joseph; Cunnion, Robert E.; Anderson, David; O'Leary, Timothy J.; Simmons, J T; Lane, H. Clifford; Fauci, Anthony S.; Roberts, William C.; Virmani, Renu; Parrillo, Joseph E.

doi:10.1016/0002-9149(88)91223-4

Cited by 99 publications

(41 citation statements)

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“…Potential etiologies include direct HIV-1 infection of the heart (Barbaro et al, 1998;Calabrese et al, 1987;Grody et al, 1990;Lipshultz et al, 1990;Wu et al, 1990), myocarditis caused by HIV-1 or by concomitant (or opportunistic) myocardial infection Barbaro et al, 1998;Reilly et al, 1988), cardiotoxicity of prolonged administration of antiviral therapeutics including zidovudine (AZT; 3Ј-azido-2Ј,3Ј-deoxythymidine; Dalakas et al, 1991;Herskowitz et al, 1992;Lewis et al, 1991) or other agents, cardiodepressant effects from localized or systemic cytokine expression, cardiotoxicity of illicit or selfprescribed drugs (particularly alcohol, cocaine, or heroin) or pharmaceuticals, and toxicity of home remedies (reviewed in Lewis, 1998;Lewis and Dalakas, 1995).…”

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confidence: 99%

Cardiac Dysfunction Occurs in the HIV-1 Transgenic Mouse Treated with Zidovudine

Lewis

Grupp

et al. 2000

Laboratory Investigation

129

107

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SUMMARY:Cardiomyopathy in AIDS is an increasingly important clinical problem. Mechanisms of AIDS cardiomyopathy were explored using AIDS transgenic mice that express replication-incompetent HIV-1 (NL4 -3⌬ gag/pol). Transgenic and FVB/n mice (n ϭ 3 to 6 per cohort) received water ad libitum with and without zidovudine (3Ј-azido-2Ј,3Ј-deoxythymidine; AZT; 0.7 mg/ml) for 21 or 35 days. After 21 days, echocardiographic studies were performed and abundance of mRNA for cardiac sarcoplasmic reticulum calcium ATPase (SERCA2), sodium calcium exchanger (NCX1), and atrial natriuretic factor were determined individually using Northern analysis of extracts of left ventricles. After 35 days, contractile function and relaxation were analyzed in isolated work-performing hearts. Histopathological and ultrastructural (transmission electron microscopy) changes were identified. After 21 days, molecular indicators of cardiac dysfunction were found. Depressed SERCA2 and increased atrial natriuretic factor mRNA abundance occurred in left ventricles from AZT-treated transgenic mice. NCX1 abundance was unchanged. Eccentric left ventricle hypertrophy was determined echocardiographically. After 35 days, cardiac dysfunction was worst in AZT-treated and AZT-untreated transgenic mice. Decreases in the first derivative of the maximal change in left ventricle systolic pressure with respect to time (ϩdP/dt) occurred in transgenic mice with and without AZT. Increased half-time of relaxation and ventricular relaxation (ϪdP/dt) occurred in AZT-treated and -untreated transgenic mice. Increased time to peak pressure was found only in AZT-treated transgenic mice. In AZT-treated FVB/n mice, ϪdP/dt was decreased. Ultrastructurally, mitochondrial destruction was most pronounced in AZT-treated transgenic mice, but also was found in AZT-treated FVB/n mice. Transgenic mice that express HIV-1 demonstrate cardiac dysfunction. AZT treatment of FVB/n mice causes mitochondrial ultrastructural alterations that are similar to those in other species. In transgenic mice, AZT treatment worsens molecular and ultrastructural features of cardiomyopathy. HIV-1 constructs and AZT each contribute to cardiac dysfunction in this murine model of AIDS cardiomyopathy.

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mentioning

confidence: 99%

Cardiac Dysfunction Occurs in the HIV-1 Transgenic Mouse Treated with Zidovudine

Lewis

Grupp

et al. 2000

Laboratory Investigation

129

107

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“…El ingreso del virus a células CD4 negativas es desconocido, propugnándose la participación de células de reservorio, como las dendríticas, o la activación de citoquinas multifuncionales, como TNF, IL-1, IL-6 e IL-10. Se sabe bien que el TNF-alfa produce un efecto inotrópico negativo, alterando la homeostasis de calcio e induciendo la síntesis de óxido nítrico, con efecto similar sobre la contractibilidad del miocito ( 3,14,28 ). Por otro lado, algunos virus cardiotropos (Coksackie virus del grupo B, citomegalovirus) han sido relacionados con el desarrollo de una miocardiopatía de posible origen viral en pacientes con recuentos de CD4s menores de 200 ( [29][30][31][32][33][34][35] ).…”

Section: Discussionunclassified

Compromiso cardíaco en el síndrome de inmunodeficiencia adquirida. Primer reporte nacional

et al. 2013

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ResumenObjetivo: Conocer los patrones de compromiso cardíaco en pacientes infectados por el virus de inmunodeficiencia humana en estadio SIDA. Material y Métodos: Estudio prospectivo de pacientes ambulatorios del Hospital Nacional Guillermo Almenara Irigoyen (HNGAI), que incluyó una evaluación de los parámetros clínico-epidemiológicos, así como una evaluación ecocardiográfica realizada entre marzo de 2002 y marzo de 2003. Resultados: Ciento treinta y dos pacientes fueron evaluados. Tuvieron 40,4 años en promedio (DE 8,7). La mediana del tiempo de diagnóstico fue 48 meses (RIQ 50) y recibieron terapia antiretroviral 63,6%. Los patrones de compromiso cardíaco fueron agrupados en disfunción diastólica (DD) en 28,8%, disfunción sistólica en 3,0%, y derrame pericárdico en 9,1%. La DD se asoció a una historia de internamientos anteriores así como a una mayor edad. Conclusiones: Encontramos un alto porcentaje de anormalidades cardíacas en pacientes ambulatorios con SIDA. La DD fue el hallazgo más frecuente. Palabras clave: Síndrome de inmunodeficiencia adquirida; enfermedades cardiovasculares; ecocardiografía. Cardiac compromise in AIDS. First peruvian report AbstractObjective: To determine the patterns of cardiac compromise in patients infected by human immunodeficiency virus in AIDS-stage. Material and Methods: Prospective study of ambulatory patients at Guillermo Almenara Irigoyen National Hospital between March 2002 and March 200, included assessment of clinical and epidemiological parameters and echocardiographic study. Results: One hundred and thirty-two patients were studied. They had a mean age of 40,4 years (SD 8,7). The median time for AIDS diagnosis was 48 months (IQR 50) and received antiretroviral therapy 63,6%. Cardiac compromise patterns were diastolic dysfunction (DD) in 28,8%, systolic dysfunction in 3,0%, pericardial effusion in 9,1%. DD was associated with a history of previous hospitalization and older age. Conclusions: We found a high percentage of cardiac abnormalities in patients with HIV infection in AIDS stage. DD was the most frequent finding.

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“…Subsequent reports suggested an association between focal nonspecific myocarditis at autopsy and clinical cardiomyopathy [Barbaro et al, 1998a, Reilly et al, 1988. Numerous hypotheses have been suggested to account for the etiology of nonspecific myocarditis and cardiomyopathy observed in HIV-infected patients, including direct HIV-1 infection of myocardial cells or coinfection with other cardiotropic viruses, [Olson 2003] cytokine cardiotoxicity [Suffredini et al, 1989, Lahdevirta et al, 1988, Levine et al, 1990, postviral cardiac autoimmunity [Herskowitz et al, 1989[Herskowitz et al, , 1993, nutritional deficiencies [Olson 2003], and cardiotoxicity due to illicit drugs [Olson 2003] or pharmacologic agents [Herskowitz et al, 1992a, Olson 2003].…”

Section: Pathogenesismentioning

confidence: 99%

Myocarditis in HIV Positive Patients

Cambrea¹

2011

Myocarditis

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Frequency of myocarditis, left ventricular dysfunction and ventricular tachycardia in the acquired immune deficiency syndrome

Cited by 99 publications

References 12 publications

Cardiac Dysfunction Occurs in the HIV-1 Transgenic Mouse Treated with Zidovudine

Cardiac Dysfunction Occurs in the HIV-1 Transgenic Mouse Treated with Zidovudine

Compromiso cardíaco en el síndrome de inmunodeficiencia adquirida. Primer reporte nacional

Myocarditis in HIV Positive Patients

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