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Published on: May 17, 2024
A review of homocysteine and heart failure
Markus Herrmann1, Omid Taban-Shomal, Ulrich Hübner
1Institut für Klinische Chemie und Laboratoriumsmedizin/Zentrallabor, Universitätsklinikum des Saarlandes, D-66421 Homburg/Saar, Germany.
Insights
Hyperhomocysteinemia (HHCY), or elevated homocysteine (HCY) levels, is linked to increased chronic heart failure (CHF) risk and severity. Lowering HCY may improve outcomes for CHF patients.
Area of Science:
- Cardiology
- Clinical Medicine
- Biochemistry
Background:
- Chronic heart failure (CHF) presents a significant public health challenge.
- Elevated plasma homocysteine (HCY) is increasingly recognized as a potential risk marker in CHF.
- Hyperhomocysteinemia (HHCY) may contribute to CHF incidence and disease severity.
Purpose of the Study:
- To review existing literature on the association between hyperhomocysteinemia (HHCY) and chronic heart failure (CHF).
- To explore potential mechanisms linking HHCY to adverse cardiac remodeling and impaired myocardial function.
Main Methods:
- Literature review of clinical and mechanistic studies on HHCY and CHF.
- Analysis of data associating HCY levels with CHF incidence, severity, and cardiac function.
Main Results:
- Clinical data show HHCY is associated with increased CHF incidence and severity.
- Preliminary findings suggest HHCY induces cardiac fibrosis, myocardial stiffness, and affects cardiac pump function.
- Mechanisms may involve direct HCY effects on myocardium and NO-independent vascular effects.
Conclusions:
- HHCY is a potential etiological factor in CHF.
- Further research is needed to elucidate the mechanistic role of HHCY in CHF.
- HCY-lowering therapy could offer therapeutic benefits for CHF patients.
Abstract:
Chronic heart failure (CHF) is a major public health problem causing considerable morbidity and mortality. Recently, plasma homocysteine (HCY) has been suggested to be increased in CHF patients potentially representing a newly recognized risk marker. This manuscript reviews the existing literature regarding hyperhomocysteinemia (HHCY) and CHF. Clinical data indicate that HHCY is associated with an increased incidence of CHF as well as with the severity of the disease. Mechanistic studies of HHCY and CHF are rare. However, preliminary results suggest that HHCY causes adverse cardiac remodelling characterized by interstitial and perivascular fibrosis resulting in increased myocardial stiffness. In addition, HHCY seems to affect the pump function of the myocardium. The mechanisms leading from an elevated HCY level to reduced pump function and adverse cardiac remodelling are a matter of speculation. Existing data indicate that direct effects of HCY on the myocardium as well as NO independent vascular effects are involved. In conclusion, HHCY might be a potential aetiological factor in CHF. Future studies need to clarify the mechanistic role of HHCY in CHF as a useful paradigm with most interesting therapeutic implications, because HCY lowering therapy could favourably influence the prognosis in CHF patients.
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