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Biopsy-proven autoimmune myocarditis in HIV-associated dilated cardiomyopathy.

Frustaci A, Petrosillo N, Francone M, Verardo R, Ippolito G, Chimenti C - BMC Infect. Dis. (2014)

Bottom Line: Dilated cardiomyopathy occurring in HIV-infected patients raises both diagnostic and therapeutic challenging problems.Steroid treatment was followed by recovery of cardiac dimension and function.Presence of auto-reactive myocarditis should be considered in patients with HIV-associated dilated cardiomyopathy.

View Article: PubMed Central - PubMed

Affiliation: Biocardiology Laboratory, National Institute for Infectious Diseases "Lazzaro Spallanzani", IRCCS, Via Portuense, 292, 00149, Rome, Italy. biocard@inmi.it.

ABSTRACT

Background: Dilated cardiomyopathy occurring in HIV-infected patients raises both diagnostic and therapeutic challenging problems. Indeed myocardial involvement in HIV infection has been variously attributed to several causes, including viral, toxic, nutritional and autoimmune, but no specific treatment capable to substantially improve patients' prognosis has been recognized so far.

Case presentation: Hereby we describe the case of an autoimmune myocarditis manifesting with heart failure in a3 9-year-old man with HIV infection. Left ventricular endomyocardial biopsy showed a lymphocytic myocarditis characterized by over-expression of HLA-DR and negative polymerase chain reaction for cardiotropic viruses. Steroid treatment was followed by recovery of cardiac dimension and function.

Conclusion: Presence of auto-reactive myocarditis should be considered in patients with HIV-associated dilated cardiomyopathy. Its recognition by endomyocardial biopsy followed by steroid administration may result in a complete resolution of cardiac disease.

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Related in: MedlinePlus

Cardiac magnetic resonance and left ventricular endomyocardial biopsy before (upper panels) and after recovery from autoimmune myocarditis (lower panels) in HIV- infected patient. Long axis images (panel A = diastole, panel B = systole) show a severe dilated and dysfunctional left ventricle recovering (ejection fraction from 20 to 45%) after 4 months of steroid treatment (panel G = diastole, panel H = systole). T2 short-tau inversion recovery images (T2-STIR) in mid ventricular short axis show subepicardial edematous imbibition of the infero-lateral segment of the left ventricular myocardium (panel C, arrows), and thickening of pericardial layers with minimal amount of effusion (panel C, arrowheads) corresponding to late gadolinium enhancement (LGE) with the same distribution (panel D, arrows). At 4-month follow up T2w-STIR e LGE images (panel I and L) show complete regression of tissue edema and late enhancement. Severe lymphocytic myocarditis (panel E, H&E, 200x) with overexpression of HLA-DR on cardiomyocyte membrane (arrow in panel F, immunoperoxidase, 400x) and positivity of cardiac serum to antiheart autoantibodies (panel F insert) resulted in healed myocarditis with disappearance of inflammatory infiltrates (panel M, H&E, 200x) and interstitial and focal replacement fibrosis (panel N, Masson’s trichrome, 200x).
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Fig1: Cardiac magnetic resonance and left ventricular endomyocardial biopsy before (upper panels) and after recovery from autoimmune myocarditis (lower panels) in HIV- infected patient. Long axis images (panel A = diastole, panel B = systole) show a severe dilated and dysfunctional left ventricle recovering (ejection fraction from 20 to 45%) after 4 months of steroid treatment (panel G = diastole, panel H = systole). T2 short-tau inversion recovery images (T2-STIR) in mid ventricular short axis show subepicardial edematous imbibition of the infero-lateral segment of the left ventricular myocardium (panel C, arrows), and thickening of pericardial layers with minimal amount of effusion (panel C, arrowheads) corresponding to late gadolinium enhancement (LGE) with the same distribution (panel D, arrows). At 4-month follow up T2w-STIR e LGE images (panel I and L) show complete regression of tissue edema and late enhancement. Severe lymphocytic myocarditis (panel E, H&E, 200x) with overexpression of HLA-DR on cardiomyocyte membrane (arrow in panel F, immunoperoxidase, 400x) and positivity of cardiac serum to antiheart autoantibodies (panel F insert) resulted in healed myocarditis with disappearance of inflammatory infiltrates (panel M, H&E, 200x) and interstitial and focal replacement fibrosis (panel N, Masson’s trichrome, 200x).

Mentions: A 39-year-old HIV infected caucasian man was admitted because of progressive heart failure beginning 9 months earlier after an episode of upper respiratory tract infection. His clinical history was marked by a serious compromise of lymphocyte count (CD4+ lymphocytes 95/cmm) and high blood viral load (1.3 × 106 copies/ml) at the time of HIV infection recognition at the age of 29 years. He experienced several infectious events including gastroenteritis, pneumonia and toxoplasma encephalitis before the introduction of anti- retroviral therapy seven years before. Since then he was under antiretroviral treatment (ritonavir, darunavir and emtricitabine/tenofovir) registering a recovery of lymphocyte count (CD4+ up to 500/cmm) and an undetectable viral load in the peripheral blood. The time course of heart failure symptoms and laboratory/instrumental changes from antiretroviral therapy was about seven years. His heart failure was characterized by progressive dyspnea, absence of fever and chest pain but mild and constant increase of troponin T (between 0.1 and 0.8 μg/L, normal values < 0.014). The electrocardiogram documented a sinus tachycardia (125 bts/min) with low QRS voltages while 2D-echocardiogram showed normal valvular pattern but a progressive bi-ventricular dilatation (right and left ventricular end diastolic diameter was 36 and 68 mm respectively) and dysfunction (RV and LV ejection fraction 35 and 25%) despite an optimized dose of carvedilol (50 mg bid), digoxin (0.125 mg/daily), enalapril (20 mg bid) and furosemide (up to 250 mg/daily). Cardiac magnetic resonance showed a left ventricular (LV) end-diastolic volume of 231.6 ml (Figure 1A), a LV end-systolic volume of 184.2 ml (Figure 1B) and an ejection fraction of 20% with remarkable edema (Figure 1C) and delayed gadolinium enhancement of the lateral LV free wall (Figure 1D), with minimal pericardial effusion.Figure 1


Biopsy-proven autoimmune myocarditis in HIV-associated dilated cardiomyopathy.

Frustaci A, Petrosillo N, Francone M, Verardo R, Ippolito G, Chimenti C - BMC Infect. Dis. (2014)

Cardiac magnetic resonance and left ventricular endomyocardial biopsy before (upper panels) and after recovery from autoimmune myocarditis (lower panels) in HIV- infected patient. Long axis images (panel A = diastole, panel B = systole) show a severe dilated and dysfunctional left ventricle recovering (ejection fraction from 20 to 45%) after 4 months of steroid treatment (panel G = diastole, panel H = systole). T2 short-tau inversion recovery images (T2-STIR) in mid ventricular short axis show subepicardial edematous imbibition of the infero-lateral segment of the left ventricular myocardium (panel C, arrows), and thickening of pericardial layers with minimal amount of effusion (panel C, arrowheads) corresponding to late gadolinium enhancement (LGE) with the same distribution (panel D, arrows). At 4-month follow up T2w-STIR e LGE images (panel I and L) show complete regression of tissue edema and late enhancement. Severe lymphocytic myocarditis (panel E, H&E, 200x) with overexpression of HLA-DR on cardiomyocyte membrane (arrow in panel F, immunoperoxidase, 400x) and positivity of cardiac serum to antiheart autoantibodies (panel F insert) resulted in healed myocarditis with disappearance of inflammatory infiltrates (panel M, H&E, 200x) and interstitial and focal replacement fibrosis (panel N, Masson’s trichrome, 200x).
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
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Fig1: Cardiac magnetic resonance and left ventricular endomyocardial biopsy before (upper panels) and after recovery from autoimmune myocarditis (lower panels) in HIV- infected patient. Long axis images (panel A = diastole, panel B = systole) show a severe dilated and dysfunctional left ventricle recovering (ejection fraction from 20 to 45%) after 4 months of steroid treatment (panel G = diastole, panel H = systole). T2 short-tau inversion recovery images (T2-STIR) in mid ventricular short axis show subepicardial edematous imbibition of the infero-lateral segment of the left ventricular myocardium (panel C, arrows), and thickening of pericardial layers with minimal amount of effusion (panel C, arrowheads) corresponding to late gadolinium enhancement (LGE) with the same distribution (panel D, arrows). At 4-month follow up T2w-STIR e LGE images (panel I and L) show complete regression of tissue edema and late enhancement. Severe lymphocytic myocarditis (panel E, H&E, 200x) with overexpression of HLA-DR on cardiomyocyte membrane (arrow in panel F, immunoperoxidase, 400x) and positivity of cardiac serum to antiheart autoantibodies (panel F insert) resulted in healed myocarditis with disappearance of inflammatory infiltrates (panel M, H&E, 200x) and interstitial and focal replacement fibrosis (panel N, Masson’s trichrome, 200x).
Mentions: A 39-year-old HIV infected caucasian man was admitted because of progressive heart failure beginning 9 months earlier after an episode of upper respiratory tract infection. His clinical history was marked by a serious compromise of lymphocyte count (CD4+ lymphocytes 95/cmm) and high blood viral load (1.3 × 106 copies/ml) at the time of HIV infection recognition at the age of 29 years. He experienced several infectious events including gastroenteritis, pneumonia and toxoplasma encephalitis before the introduction of anti- retroviral therapy seven years before. Since then he was under antiretroviral treatment (ritonavir, darunavir and emtricitabine/tenofovir) registering a recovery of lymphocyte count (CD4+ up to 500/cmm) and an undetectable viral load in the peripheral blood. The time course of heart failure symptoms and laboratory/instrumental changes from antiretroviral therapy was about seven years. His heart failure was characterized by progressive dyspnea, absence of fever and chest pain but mild and constant increase of troponin T (between 0.1 and 0.8 μg/L, normal values < 0.014). The electrocardiogram documented a sinus tachycardia (125 bts/min) with low QRS voltages while 2D-echocardiogram showed normal valvular pattern but a progressive bi-ventricular dilatation (right and left ventricular end diastolic diameter was 36 and 68 mm respectively) and dysfunction (RV and LV ejection fraction 35 and 25%) despite an optimized dose of carvedilol (50 mg bid), digoxin (0.125 mg/daily), enalapril (20 mg bid) and furosemide (up to 250 mg/daily). Cardiac magnetic resonance showed a left ventricular (LV) end-diastolic volume of 231.6 ml (Figure 1A), a LV end-systolic volume of 184.2 ml (Figure 1B) and an ejection fraction of 20% with remarkable edema (Figure 1C) and delayed gadolinium enhancement of the lateral LV free wall (Figure 1D), with minimal pericardial effusion.Figure 1

Bottom Line: Dilated cardiomyopathy occurring in HIV-infected patients raises both diagnostic and therapeutic challenging problems.Steroid treatment was followed by recovery of cardiac dimension and function.Presence of auto-reactive myocarditis should be considered in patients with HIV-associated dilated cardiomyopathy.

View Article: PubMed Central - PubMed

Affiliation: Biocardiology Laboratory, National Institute for Infectious Diseases "Lazzaro Spallanzani", IRCCS, Via Portuense, 292, 00149, Rome, Italy. biocard@inmi.it.

ABSTRACT

Background: Dilated cardiomyopathy occurring in HIV-infected patients raises both diagnostic and therapeutic challenging problems. Indeed myocardial involvement in HIV infection has been variously attributed to several causes, including viral, toxic, nutritional and autoimmune, but no specific treatment capable to substantially improve patients' prognosis has been recognized so far.

Case presentation: Hereby we describe the case of an autoimmune myocarditis manifesting with heart failure in a3 9-year-old man with HIV infection. Left ventricular endomyocardial biopsy showed a lymphocytic myocarditis characterized by over-expression of HLA-DR and negative polymerase chain reaction for cardiotropic viruses. Steroid treatment was followed by recovery of cardiac dimension and function.

Conclusion: Presence of auto-reactive myocarditis should be considered in patients with HIV-associated dilated cardiomyopathy. Its recognition by endomyocardial biopsy followed by steroid administration may result in a complete resolution of cardiac disease.

Show MeSH
Related in: MedlinePlus