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Cardiac inflammation and microvascular procoagulant changes are decreased in second wave compared to first wave
Linghe Wu1, Umit Baylan2, Britt van der Leeden3
1Dept. of Pathology and Amsterdam Cardiovascular Sciences (ACS), Amsterdam University Medical Centre (AUMC), location VUmc, De Boelelaan 1017, 1081HV Amsterdam, the Netherlands.
Insights
Cardiac inflammation and injury were significantly lower in second wave COVID-19 patients compared to the first wave. This suggests improved COVID-19 treatments, possibly due to increased steroid use, may reduce cardiac pathology.
Area of Science:
- Cardiovascular Pathology
- Infectious Diseases
- Immunology
Background:
- Cardiac involvement is a known complication of COVID-19.
- Previous studies primarily focused on the first wave of the pandemic.
- Emerging evidence suggests differences in disease course and mortality between COVID-19 waves.
Purpose of the Study:
- To analyze and compare cardiac pathology in COVID-19 patients between the first and second waves.
- To investigate changes in cardiac inflammation, cardiomyocyte injury, and microvascular thrombogenicity.
Main Methods:
- (Immuno)histochemical analysis of autopsied hearts from first-wave (n=15), second-wave (n=10) COVID-19 patients, and controls (n=18).
- Quantification of leukocyte, macrophage, and T lymphocyte infiltration.
- Assessment of cardiomyocyte necrosis, microvascular thrombosis, and specific procoagulant/anticoagulant factors (Tissue Factor, Factor VII, Factor XII, DPP4, CML).
Main Results:
- Significantly decreased cardiac inflammation in second-wave patients, primarily due to reduced lymphocyte infiltration and lymphocytic myocarditis.
- Accompanied by significant reductions in cardiomyocyte injury and microvascular thrombosis in second-wave patients.
- Lower microvascular deposits of Factor VII and CML observed in second-wave COVID-19 hearts.
Conclusions:
- Cardiac inflammation, cardiomyocyte injury, and microvascular thrombogenicity were markedly reduced in second-wave COVID-19 patients compared to the first wave.
- These findings may indicate the positive impact of evolving COVID-19 treatment strategies.
- Increased use of steroids during the second wave could be a contributing factor to the observed decrease in cardiac pathology.
Background:
Compelling evidence has shown cardiac involvement in COVID-19 patients. However, the overall majority of these studies use data obtained during the first wave of the pandemic, while recently differences have been reported in disease course and mortality between first- and second wave COVID-19 patients. The aim of this study was to analyze and compare cardiac pathology between first- and second wave COVID-19 patients.
Methods:
Autopsied hearts from first- (n = 15) and second wave (n = 10) COVID-19 patients and from 18 non-COVID-19 control patients were (immuno)histochemically analyzed. CD45+ leukocyte, CD68+ macrophage and CD3+ T lymphocyte infiltration, cardiomyocyte necrosis and microvascular thrombosis were quantified. In addition, the procoagulant factors Tissue Factor (TF), Factor VII (FVII), Factor XII (FXII), the anticoagulant protein Dipeptidyl Peptidase 4 (DPP4) and the advanced glycation end-product N(ε)-Carboxymethyllysine (CML), as markers of microvascular thrombogenicity and dysfunction, were quantified.
Results:
Cardiac inflammation was significantly decreased in second wave compared to first wave COVID-19 patients, predominantly related to a decrease in infiltrated lymphocytes and the occurrence of lymphocytic myocarditis. This was accompanied by significant decreases in cardiomyocyte injury and microvascular thrombosis. Moreover, microvascular deposits of FVII and CML were significantly lower in second wave compared to first wave COVID-19 patients.
Conclusions:
These results show that in our cohort of fatal COVID-19 cases cardiac inflammation, cardiomyocyte injury and microvascular thrombogenicity were markedly decreased in second wave compared to first wave patients. This may reflect advances in COVID-19 treatment related to an increased use of steroids in the second COVID-19 wave.
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