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Oxidative myocardial damage in human cocaine-related cardiomyopathy
Andrea Frustaci1, Matteo A Russo, Emanuela Morgante
1Department of Cardiovascular, Respiratory, Nephrologic, Anesthesiologic and Geriatric Sciences, University 'La Sapienza', Viale del Policlinico 155, I-00161, Rome, Italy; Cellular and Molecular Cardiology Lab, IRCCS L. Spallanzani, Rome, Italy.
Aims:
The pathogenesis of cocaine-related cardiomyopathy (CCM) is still unclear. Oxidative damage from cocaine-generated reactive oxygen species (ROS) overcoming myocardial antioxidant reserve has been hypothesized by experimental studies.
Methods And Results:
Ten (2.3%) of 430 consecutive cases with dilated cardiomyopathy (DCM) were attributed to CCM. Endomyocardial biopsies from CCM were retrospectively investigated with histology, electron microscopy, immunohistochemistry (graded 0-3), and Western blot analysis for inducible nitric oxide synthase (iNOS) and nitrotyrosine. Oxidative damage to DNA was investigated by immunostaining for 8-hydroxydeoxyguanosine (8-OHdG), while apoptosis and necrosis were evaluated by in situ ligation with hairpin probes. Myocardial anti-oxidant reserve was evaluated through assessment of superoxide dismutase (SOD1-2) and catalase (CT) activity in two frozen samples from each patient. Results were compared with idiopathic DCM and normal controls. Cardiomyocytes were bigger and myocardial fibrosis was more pronounced in CCM than in the DCM cohort. Contraction band necrosis was always detectable only in CCM with sparse lymphocytic infiltrates in three cases. Both iNOS and nitrotyrosine were significantly more expressed in CCM than in DCM. Immunostaining for 8-OHdG, cardiomyocyte apoptosis, and necrosis were significantly increased in CCM compared with controls and DCM. Myocardial SOD1 and CT activity was significantly decreased compared with DCM and controls, and correlated with cell death and severity of left ventricular dysfunction.
Conclusion:
Oxidative stress is a major mechanism of myocardial damage in human CCM. It concurs with calcium overload to myocyte dysfunction and death.
Insights
Cocaine-related cardiomyopathy (CCM) involves significant oxidative stress, leading to myocardial damage. This study found reduced antioxidant activity and increased markers of cell death in CCM patients, highlighting oxidative damage as a key mechanism.
Area of Science:
- Cardiology
- Toxicology
- Pathology
Background:
- The exact cause of cocaine-related cardiomyopathy (CCM) remains unknown.
- Experimental studies suggest that oxidative damage from cocaine-induced reactive oxygen species (ROS) may overwhelm the heart's antioxidant defenses.
Purpose of the Study:
- To investigate the role of oxidative stress in the pathogenesis of human cocaine-related cardiomyopathy (CCM).
- To compare markers of oxidative damage and antioxidant capacity in CCM patients versus those with idiopathic dilated cardiomyopathy (DCM) and healthy controls.
Main Methods:
- Retrospective analysis of endomyocardial biopsies from 10 CCM patients and comparison with DCM and control groups.
- Histology, electron microscopy, immunohistochemistry for iNOS and nitrotyrosine, and Western blot analysis were performed.
- Assessment of DNA oxidative damage (8-OHdG), apoptosis, necrosis, and myocardial antioxidant enzymes (SOD1-2, CT).
Main Results:
- CCM hearts showed larger cardiomyocytes and more pronounced fibrosis than DCM.
- Contraction band necrosis was specific to CCM.
- Increased expression of iNOS and nitrotyrosine was observed in CCM.
- Elevated markers of DNA oxidative damage, cardiomyocyte apoptosis, and necrosis were found in CCM.
- Significantly decreased myocardial SOD1 and CT activity correlated with cell death and cardiac dysfunction in CCM.
Conclusions:
- Oxidative stress is a primary mechanism contributing to myocardial injury in human CCM.
- This oxidative damage, alongside calcium overload, leads to myocyte dysfunction and death in CCM.
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