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Homocysteine and heart failure: an overview
Enrico Vizzardi1, Ivano Bonadei, Gregoriana Zanini
1Department of Cardiology, University of Brescia, Brescia, Italy. enrico.vizzardi@tin.it
Insights
Elevated homocysteine (HCY) is linked to vascular disease and may cause congestive heart failure (CHF). Lowering HCY with B-vitamins might improve CHF outcomes, warranting further research.
Area of Science:
- Cardiovascular Medicine
- Biochemistry
- Vascular Biology
Background:
- Elevated plasma homocysteine (HCY) is a known risk factor for thrombotic and atherosclerotic vascular disease.
- Hyperhomocysteinemia (HHCY) is independently associated with increased vascular disease risk.
- HCY elevation is also a risk factor for congestive heart failure (CHF) in individuals without prior myocardial infarction.
Purpose of the Study:
- To investigate the role of hyperhomocysteinemia (HHCY) as a potential etiological factor in congestive heart failure (CHF).
- To explore the mechanisms by which elevated HCY may lead to cardiac dysfunction and remodeling.
- To assess the potential of HCY-lowering therapy for improving CHF markers and outcomes.
Main Methods:
- Review of existing studies and patents linking HCY to vascular disease and CHF.
- Analysis of animal studies demonstrating HHCY-induced cardiac dysfunction and remodeling.
- Consideration of preliminary intervention trial data on HCY-lowering therapy.
Main Results:
- Experimental HHCY in animals induces systolic and diastolic dysfunction and increases BNP expression.
- Hyperhomocysteinemic animals show adverse cardiac remodeling with increased collagen.
- Preliminary data suggest HCY-lowering therapy may improve clinical and laboratory markers of CHF.
Conclusions:
- Hyperhomocysteinemia (HHCY) may be a potential etiological factor in congestive heart failure (CHF).
- Further research is needed to elucidate the precise pathomechanisms of HHCY in CHF.
- Larger intervention trials are required to determine if B-vitamin supplementation improves clinical outcomes in CHF patients.
Abstract:
An elevated plasma level of homocysteine (HCY) is associated with increased risk of thrombotic and atherosclerotic vascular disease. Several studies and recent patents have demonstrated that hyper-homocysteinemia (HHCY) is an independent risk factor for vascular disease. An elevated homocysteine level has been also reported to be a risk factor for the development of congestive heart failure (CHF) in individuals free of myocardial infarction. Animal studies showed that experimental HHCY induces systolic and diastolic dysfunction, as well as an increased BNP expression. Moreover, hyperhomocysteinemic animals exhibit an adverse cardiac remodeling characterized by accumulation of interstitial and perivascular collagen. The mechanisms leading from an elevated HCY level to reduced pump function and adverse cardiac remodeling are a matter of speculation. Existing data indicate that direct effects of HCY on the myocardium, as well as nitric oxide independent vascular effects, are involved. Preliminary data from small intervention trials have initiated the speculation that HCY lowering therapy by micronutrients may improve clinical as well as laboratory markers of CHF. In conclusion, HHCY might be a potential etiological factor in CHF. Future studies need to explore the exact pathomechanisms of HHCY in CHF. Moreover, larger intervention trials are needed to clarify whether modification of plasma HCY by B-vitamin supplementation improves the clinical outcome in CHF patients.
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