Ninety-three patients constituted the final study population. The prevalence rates of coronary artery disease, heart failure history, cerebrovascular disease history, and hypertension were 24.7%, 52.7%, 20.4%, and 68.8%, respectively. Twenty-three (24.7%) patients died during the follow-up.
Patients who died during the follow-up had a longer duration of diabetes (Table 1). The prevalence of preexisting heart failure was higher among patients in the mortality group than among those who survived (78. 3% vs. 44.3%, P = 0.005). The percentage of patients with a preexisting coronary artery disease history and stroke history showed no significant difference between the 2 groups. The revised cardiac risk index of the mortality group was higher than that of the survivor group (3 vs. 2, P = 0.001). In addition, 17 (73.9%) patients in the mortality group had cardiac valve calcification, which was significantly higher than the proportion of cardiac valvular calcification in the survivor group (47.1%, P = 0.025). The prevalence of calcified aortic valve was significantly higher in the mortality group (70.0% vs. 42.8% P = 0.026). Although the mortality group had a higher proportion of mitral valve calcification (21.7% vs. 10%), there was no significant difference between the two groups (P = 0.145). In comparison to the patients who died during the follow-up, the ejection fraction was significantly higher in patients who survived (P = 0.047). Patients in the mortality group had lower HDL-c, higher procalcitonin (PCT), higher urea nitrogen, and higher NT-proBNP at admission than those who survived.
Table 1
Baseline clinical, biochemical and echocardiographic characteristics of the survivor group and the mortality group
Variable | Survivor (n = 70) | Mortality (n = 23) | P |
Gender, n (%) Male Female | 41 (58.6) 29 (41.4) | 16 (69.6) 7 (30.4) | 0.461 |
Age (year) | 68.09 ± 10.69 | 66.39 ± 9.60 | 0.501 |
BMI (kg/m2) | 21.62 (18.82–23.75) | 22.86 (21.19–23.44) | 0.160 |
History of smoking, n (%) | 26 (37.1) | 10 (43.5) | 0.588 |
Hypertension, n (%) | 48 (68.6) | 16 (69.6) | 0.929 |
History of coronary artery disease, n (%) | 15 (21.4) | 7 (30.4) | 0.378 |
History of cerebrovascular disease, n (%) | 12 (17.1) | 7 (30.4) | 0.138 |
History of chronic heart failure, n (%) | 31 | 18 | 0.005 |
Revised Cardiac Risk Index | 2 (1–2) | 3 (2–4) | 0.001 |
Duration of diabetic history (year) | 10 (5–15) | 20 (7–20) | 0.013 |
eGFR (ml/min∙1.73m2) | 59.75 ± 29.73 | 48.87 ± 26.65 | 0.133 |
HbA1c (%) | 9.24 ± 3.95 | 9.28 ± 2.55 | 0.968 |
Serum Creatinine (µmol/L) | 95 (68–132) | 103 (77–283) | 0.262 |
BUN (mmol/L) | 9.23 ± 8.29 | 13.53 ± 9.55 | 0.041 |
LDL-c (mmol/L) | 2.32 ± 0.89 | 2.13 ± 0.63 | 0.364 |
HDL-c (mmol/L) | 0.81 ± 0.28 | 0.58 ± 0.15 | 0.001 |
TG (mmol/L) | 1.32 ± 0.89 | 1.22 ± 0.45 | 0.622 |
Cholesterol (mmol/L) | 3.49 (2.67–4.27) | 3.07 (2.37–3.60) | 0.072 |
Serum Uric Acid (µmol/L) | 330.26 ± 138.40 | 381.12 ± 150.73 | 0.231 |
PCT (ng/ml) | 0.13 (0.60–0.77) | 0.39 (0.21–1.23) | 0.022 |
WBC (×109/L) | 14.23 ± 7.29 | 18.29 ± 9.65 | 0.074 |
NT-proBNP (pg/ml) | 2118 (483–4702) | 9917 (3254–25621) | 0.000 |
Cardiac valvular calcification, n (%) | 33 (47.1) | 17(73.9) | 0.025 |
Eject fraction (%) | 64 (59–71) | 61.50 (50.50–66) | 0.047 |
Aortic valve calcification, n (%) | 30 (42.9) | 16 (26.1) | 0.026 |
Mitral annular calcification, n (%) | 7 (10%) | 5 (21.7) | 0.145 |
A 2-tailed p value < 0.05 was considered statistically significant. BMI, body mass index; eGFR, estimated glomerular filtration rate; HbA1c, glycosylated hemoglobin, type A1C; BUN, blood urea nitrogen; LDL-c, low-density lipoprotein cholesterol; HDL-c, high-density lipoprotein cholesterol; TG, triglyceride; PCT, procalcitonin; WBC, white blood cell; NT-proBNP, N-terminal pro-B-type natriuretic peptide. |
To identify independent predictors of mortality, variables that had p < 0.1 in univariate analysis (heart failure history, RCRI, duration of diabetes, BUN, serum creatinine, HDL-c, cholesterol, WBC, NT-proBNP, eject fraction, cardiac valvular calcification) were analyzed using backward multivariate analysis (Table 2). The duration of diabetes (HR = 1.067, 95% CI = 1.008–1.128), HDL-c (HR = 0.020, 95% CI = 0.001–0.338), NT-pro BNP (HR = 1.000, 95% CI = 1.0–1.0), and cardiac valvular calcification (HR = 3.427, 95% CI = 1.125–10.443) were independent predictors for all-cause mortality during the 1-year follow-up. Moreover, after adjusting for the same variables (Hdl-c, NT-pro BNP, duration of diabetes), aortic valve calcification was found to be an independent predictor for mortality (HR = 2.882 95% CI = 1.012–8.209), while the prediction value of mitral valve calcification showed no statistical significance (Table 3).
Table 2
Independent predictors of 1-year mortality after surgery
Variable | Univariate | Multivariate |
HR | 95% CI | P-value | HR | 95% CI | P-value |
Age | 0.989 | 0.952–1.027 | 0.563 | | | |
BMI | 1.065 | 0.953–1.190 | 0.269 | | | |
Gender | 1.250 | 0.530–2.948 | 0.610 | | | |
Hypertension | 1.023 | 0.421–2.488 | 0.960 | | | |
History of smoking | 1.248 | 0.547–2.845 | 0.599 | | | |
History of CAD | 1.483 | 0.610–3.605 | 0.385 | | | |
History of cerebrovascular disease | 1.974 | 0.804–4.845 | 0.138 | | | |
History of heart failure | 3.845 | 1.426–10.368 | 0.008 | | | |
Revised Cardiac Risk Index | 1.861 | 1.312–2.639 | 0.000 | | | |
Duration of diabetes | 1.076 | 1.022–1.132 | 0.005 | 1.067 | 1.008–1.128 | 0.024 |
eGFR | 0.989 | 0.974–1.004 | 0.146 | | | |
HbA1c | 0.998 | 0.879–1.133 | 0.973 | | | |
BUN | 1.032 | 1.000-1.064 | 0.047 | | | |
Serum creatinine | 1.002 | 1.000-1.003 | 0.017 | | | |
LDL-c | 0.775 | 0.438–1.371 | 0.382 | | | |
HDL-c | 0.019 | 0.002–0.176 | 0.001 | 0.020 | 0.001–0.338 | 0.007 |
TG | 0.844 | 0.441–1.617 | 0.610 | | | |
WBC | 1.049 | 1.004–1.096 | 0.034 | | | |
PCT | 0.917 | 0.731–1.150 | 0.451 | | | |
NT-proBNP | 1.000 | 1.000–1.000 | 0.000 | 1.000 | 1.000–1.000 | 0.001 |
Eject fraction | 0.942 | 0.898–0.988 | 0.014 | | | |
Cardiac valve calcification | 2.725 | 1.074–6.913 | 0.035 | 3.427 | 1.125–10.443 | 0.030 |
A 2-tailed p value < 0.05 was considered statistically significant. |
BMI, body mass index; CAD, coronary artery disease; eGFR, estimated glomerular filtration rate; HbA1c, glycosylated hemoglobin, type A1C; BUN, blood urea nitrogen; LDL-c, low-density lipoprotein cholesterol; HDL-c, high-density lipoprotein cholesterol; TG, triglyceride; WBC, white blood cell; PCT, procalcitonin; NT-proBNP, N-terminal pro-B-type natriuretic peptide. |
Table 3
Cox regression analysis of 1-year mortality in the adjusted model
| Univariate | Adjusted |
| HR | 95% CI | P-value | HR | 95% CI | P-value |
Mitral Annular Calcification | 2.066 | 0.767–5.566 | 0.151 | 3.053 | 0.939–9.927 | 0.064 |
Aortic Valve Calcification | 2.596 | 1.068–6.312 | 0.035 | 2.882 | 1.012–8.209 | 0.048 |
The adjusted model factors including NT-proBNP, HDL-c, and duration of diabetes. |
Kaplan–Meier graphs showed that mortality differed from the first day following the index event for patients with cardiac valvular calcification and without calcification (Fig. 1, P = 0.025).
To further evaluate the influence of cardiac valvular calcification on 1-year mortality, patients were divided into three groups on the basis of calcified valve number (Fig. 2). The patients with both calcified aortic valve and calcified mitral valve had a higher all-cause death rate (50%). The mortality rate of patients who had calcified aortic valves or calcified mitral valves was higher than that of patients without valve calcification (31.0% vs. 14.0%).
Receiver operator characteristic curve analysis showed a strong predictive ability of calcified valve number for mortality after 1-year follow-up (Fig. 3, AUC = 0.654, 95% CI = 0.524–0.783 P = 0.028). The area under the ROC curve for RCRI to predict 1-year mortality was 0.724 (95% CI = 0.604–0.843, P = 0.001). A stronger performance of the combination with calcified valve number and RCRI was noted when ROC analysis was conducted (AUC = 0.786, 95% CI = 0.676–0.896 P = 0.000).