International journal of cardiology. Heart & vasculature · 2026
Cellular communication network factor 1 (CCN1) associates with all-cause mortality in patients with dilated cardiomyopathy.
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Klingenberg Roland, Gross Stefan, Lehnert Kristin, Grote Karsten, Benkner Alexander, Wegner Danilo, Hamm Christian W, Felix Stephan B, Keller Till, Pankuweit Sabine, Dörr Marcus
Аннотация
BACKGROUND: Circulating cellular communication network factor 1 (CCN1) improves risk stratification in patients with acute coronary syndrome. We here investigated the association of CCN1 with all-cause mortality in patients with dilated cardiomyopathy (DCM).
METHODS: Patients with a primary diagnosis of DCM, defined as LVEF <45% and increased LVEDD (LVEDD >117%), were included in a derivation (SFB/TR19 Greifswald) and a validation (IKARUS Marburg) cohort. Exclusion criteria comprised primary valvular diseases, acute myocarditis, active infectious diseases, pulmonary diseases, cancer, chronic alcoholism, and heart failure of other origins. CCN1 levels were determined in serum from study inclusion using an enzyme-linked immunosorbent assay. An adjusted multivariable Cox regression model was used to assess the association (hazard ratios) between tertiles of CCN1 concentration and all-cause mortality.
RESULTS: In the SFB/TR19 cohort and [IKARUS cohort], respectively a total of 283 [236] predominantly male (78% [75%]) DCM patients with a median age of 56 [51] years with a severely reduced LVEF (31% [30%]), increased LVEDD (67.0 [67.0]), and normal eGFR (90.9 [83.6] ml/min) were analyzed. During a median follow-up of 10.6 [14.9] years, a total of 107 (37%) [100 (42%)] patients died. Patients in the highest CCN1 tertile had a significantly higher mortality risk than those in the lower tertile (p = 0.007 [p = 0.004]). In both cohorts, CCN1 remained associated (1.92; 95% CI: 1.14-3.24; p = 0.014 [1.69; 1.00-2.85; p = 0.049]) in adjusted multivariable Cox regression models.
CONCLUSION: CCN1 is associated with all-cause mortality in DCM patients, warranting further research into the underlying pathophysiology.
METHODS: Patients with a primary diagnosis of DCM, defined as LVEF <45% and increased LVEDD (LVEDD >117%), were included in a derivation (SFB/TR19 Greifswald) and a validation (IKARUS Marburg) cohort. Exclusion criteria comprised primary valvular diseases, acute myocarditis, active infectious diseases, pulmonary diseases, cancer, chronic alcoholism, and heart failure of other origins. CCN1 levels were determined in serum from study inclusion using an enzyme-linked immunosorbent assay. An adjusted multivariable Cox regression model was used to assess the association (hazard ratios) between tertiles of CCN1 concentration and all-cause mortality.
RESULTS: In the SFB/TR19 cohort and [IKARUS cohort], respectively a total of 283 [236] predominantly male (78% [75%]) DCM patients with a median age of 56 [51] years with a severely reduced LVEF (31% [30%]), increased LVEDD (67.0 [67.0]), and normal eGFR (90.9 [83.6] ml/min) were analyzed. During a median follow-up of 10.6 [14.9] years, a total of 107 (37%) [100 (42%)] patients died. Patients in the highest CCN1 tertile had a significantly higher mortality risk than those in the lower tertile (p = 0.007 [p = 0.004]). In both cohorts, CCN1 remained associated (1.92; 95% CI: 1.14-3.24; p = 0.014 [1.69; 1.00-2.85; p = 0.049]) in adjusted multivariable Cox regression models.
CONCLUSION: CCN1 is associated with all-cause mortality in DCM patients, warranting further research into the underlying pathophysiology.