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Cystatin C and risk of heart failure in the Physicians' Health Study (PHS)
Luc Djoussé1, Tobias Kurth, J Michael Gaziano
1Department of Medicine, Division of Aging, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02120, USA. ldjousse@rics.bwh.harvard.edu
Insights
Higher cystatin C levels indicate increased heart failure (HF) risk, particularly in hypertensive individuals. This study highlights cystatin C as a potential biomarker for HF risk stratification in specific populations.
Area of Science:
- Cardiology
- Nephrology
- Biomarkers
Background:
- Chronic kidney disease is a known risk factor for heart failure (HF).
- Cystatin C is a marker for early kidney dysfunction.
- Limited data exist on the association between cystatin C and HF risk.
Purpose of the Study:
- To investigate the association between plasma cystatin C levels and incident heart failure (HF) risk.
- To determine if this association is stronger in individuals with hypertension.
Main Methods:
- Prospective nested case-control study within the PHS.
- 220 incident HF cases and 220 matched controls.
- Plasma cystatin C measured by immunonephelometry; conditional logistic regression used.
Main Results:
- Higher cystatin C tertiles showed increased multivariable-adjusted HF risk (RR 1.78 for highest tertile).
- Association attenuated after adjusting for blood pressure and hypertension history.
- A 4-fold increased HF risk was observed with higher cystatin C in hypertensive individuals, but not in non-hypertensives.
Conclusions:
- Elevated cystatin C levels are associated with higher HF risk.
- This association appears primarily limited to hypertensive individuals.
- Further research is needed to clarify the interplay between hypertension, cystatin C, and HF risk.
Background:
Chronic kidney disease is a risk factor for heart failure (HF). Although cystatin C can detect early kidney dysfunction, limited data are available on the association between cystatin C and HF.
Methods:
In a prospective nested case-control study design, we examined whether cystatin C is associated with an increased risk of HF in the PHS and whether such an association is stronger in hypertensive subjects. We selected 220 cases of incident HF and 220 controls, matched on age, year of birth, and time of blood collection. Plasma cystatin C was measured using an immunonephelometry method. We used conditional logistic regression to estimate relative risks (RRs).
Results:
Compared with the lowest tertile, the multivariable adjusted RR (95% CI) for HF was 1.15 (0.69-1.89) and 1.78 (1.01-3.13) for the second and third tertiles of cystatin C, respectively. Additional adjustment for systolic blood pressure and history of hypertension attenuated this association (RR = 1.0, 1.23 [0.73-2.09], and 1.61 [0.90-2.88] from the lowest to the highest tertile, respectively). Furthermore, we observed a 4-fold increased risk of HF in the second and third tertiles of cystatin C among hypertensive individuals and no meaningful effects of cystatin C on HF among nonhypertensive subjects.
Conclusions:
Our data demonstrated that higher levels of cystatin C are associated with an increased risk of HF and that such association may be limited to hypertensive individuals. Additional studies are warranted to further examine the relationship between hypertension and cystatin C on the risk of HF.
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