Coronary Calcification in Obstructive CAD Treated by PCI
Coronary Calcification in Obstructive CAD Treated by PCI
The Syntax score, and the clinical and the follow-up data were available for 6296 patients out of the 7639 patients that were enrolled in the seven clinical trials. Most of the studied patients were male with a history of hypertension and hypercholesterolaemia and were admitted because of an acute coronary event. Four out of 10 patients were treated with a first-generation DES (ie, a sirolimus or paclitaxel-eluting stent), and six out of 10 patients with a second-generation device (ie, an everolimus, zotarolimus, or a biolimus-eluting platform).
Twenty per cent of the studied patients had severely calcified lesions on coronary angiography ( Table 1 ). These patients were older and were more likely to suffer from hypertension and hypercholesterolaemia compared to the group of patients without severe lesion calcium who were more often diabetic. Patients with severe calcification had a higher Syntax score (12.1 units higher than those without severe calcification, 95% CI 11.5 to 12.7; p<0.001), and were less likely to have undergone complete revascularisation (data with regards complete revascularisation was available only for the ARTS II the STRATEGY, MULTISTRATEGY and the SYNTAX study). No differences were noted between the two groups with regards to the cause of admission, the incidence of LV systolic dysfunction, and the prevalence of peripheral vascular disease (PVD).
All studied patients were followed-up for 3 years. During follow-up, 359 (5.7%) patients died, of whom 139 had severely calcified lesions ( Table 2 ). The Kaplan–Meier analysis showed that patients with severely calcified lesions had significantly higher all-cause mortality (10.8% vs 4.4%, log-rank test=79.35; p<0.001) compared to those without. Landmark analysis showed an increased mortality in the group of patients with severely calcified lesions at 1 year post-procedure, and also for the period between 1 and 3 years follow-up (Figure 1A).
(Enlarge Image)
Figure 1.
Kaplan–Meier and landmark analysis for the all-cause mortality (A, B), death—myocardial infarction (C, D) and for the combined end-point death—myocardial infarction-any revascularisation (E, F) in patients with and without severe lesion calcification. The landmark analysis was performed for the first year and for the period 1–3 years follow-up.
Severe calcification appeared as a predictor of increased mortality in the univariate Cox regression analysis (HR: 2.41, 95%CI 1.92 to 3.00; p<0.001). Table 3 shows all the predictors of all-cause mortality identified by univariate Cox regression analysis. In the multivariate model, that included all the independent predictors of worse outcomes, apart from the history of cerebrovascular disease and PVD because of missing data, the presence of calcified lesions was independently associated with an increased all-cause mortality ( Table 3 ).
The combined end-point death—MI was reported in 840 patients. Patients with severe lesion calcification were at a higher risk of experiencing an event compared to those without calcified lesions (23.2% vs 11.0%; log-rank=130.29; p<0.001). Landmark analysis showed a worse prognosis in the group of patients with severely calcified lesions at the first year post-procedure, but also for the period between 1 and 3 years follow-up (figure 1B).
In univariate Cox regression analysis, severe calcification was a predictor of death—MI (HR: 1.86, 95% CI 1.60 to 2.16; p<0.001). In the multivariate model built, excluding the history of cerebrovascular and PVD, severe calcification was a predictor of death—MI ( Table 4 ).
Outcome data with regards the combined end-point death—MI—any revascularisation was available in 5018 patients. At 3-year follow-up, 1213 events were reported, of which 860 (22.4%) occurred in patients without severely calcified lesions, and 373 (31.8%) in patients with severe lesion calcification (log-rank=14.55; p<0.001, figure 1C). Similarly to what has been reported for the other end-points, landmark analysis showed a worse outcome in the group of patients with severely calcified lesions at 1 year post-procedure, and also for the period between 1 and 3 years follow-up (figure 1C). Severe lesion calcification was a predictor of worse outcome in univariate and multivariate Cox regression analysis ( Table 5 ).
During follow-up, 269 ST events occurred, of which 129 were definite, 43 probable and 97 possible ST ( Table 3 ). Patients with calcified coronaries had an increased incidence of ST compared to those without coronary calcification (definite ST: 3% vs 1.8%, log-rank=6.97; p=0.008; definite/probable ST: 4.3% vs 2.1%, log-rank=17.06, p<0.001). Severe lesion calcification was a predictor of ST in univariate analysis (definite ST: HR: 1.66, 95% CI 1.13 to 2. 42; p<0.001; definite/probable ST: HR: 1.95, 95% CI 1.37 to 2.76; p<0.001), but it was not an independent predictor in the multivariate models (definite ST: HR: 1.41, 95% CI 0.87 to 2.28; p=0.167; definite/probable ST: HR: 1.40, 95% CI 0.91 to 2.15; p=0.124).
Results
Baseline Demographics
The Syntax score, and the clinical and the follow-up data were available for 6296 patients out of the 7639 patients that were enrolled in the seven clinical trials. Most of the studied patients were male with a history of hypertension and hypercholesterolaemia and were admitted because of an acute coronary event. Four out of 10 patients were treated with a first-generation DES (ie, a sirolimus or paclitaxel-eluting stent), and six out of 10 patients with a second-generation device (ie, an everolimus, zotarolimus, or a biolimus-eluting platform).
Twenty per cent of the studied patients had severely calcified lesions on coronary angiography ( Table 1 ). These patients were older and were more likely to suffer from hypertension and hypercholesterolaemia compared to the group of patients without severe lesion calcium who were more often diabetic. Patients with severe calcification had a higher Syntax score (12.1 units higher than those without severe calcification, 95% CI 11.5 to 12.7; p<0.001), and were less likely to have undergone complete revascularisation (data with regards complete revascularisation was available only for the ARTS II the STRATEGY, MULTISTRATEGY and the SYNTAX study). No differences were noted between the two groups with regards to the cause of admission, the incidence of LV systolic dysfunction, and the prevalence of peripheral vascular disease (PVD).
Severe Lesion Calcification and Clinical End-points
All studied patients were followed-up for 3 years. During follow-up, 359 (5.7%) patients died, of whom 139 had severely calcified lesions ( Table 2 ). The Kaplan–Meier analysis showed that patients with severely calcified lesions had significantly higher all-cause mortality (10.8% vs 4.4%, log-rank test=79.35; p<0.001) compared to those without. Landmark analysis showed an increased mortality in the group of patients with severely calcified lesions at 1 year post-procedure, and also for the period between 1 and 3 years follow-up (Figure 1A).
(Enlarge Image)
Figure 1.
Kaplan–Meier and landmark analysis for the all-cause mortality (A, B), death—myocardial infarction (C, D) and for the combined end-point death—myocardial infarction-any revascularisation (E, F) in patients with and without severe lesion calcification. The landmark analysis was performed for the first year and for the period 1–3 years follow-up.
Severe calcification appeared as a predictor of increased mortality in the univariate Cox regression analysis (HR: 2.41, 95%CI 1.92 to 3.00; p<0.001). Table 3 shows all the predictors of all-cause mortality identified by univariate Cox regression analysis. In the multivariate model, that included all the independent predictors of worse outcomes, apart from the history of cerebrovascular disease and PVD because of missing data, the presence of calcified lesions was independently associated with an increased all-cause mortality ( Table 3 ).
The combined end-point death—MI was reported in 840 patients. Patients with severe lesion calcification were at a higher risk of experiencing an event compared to those without calcified lesions (23.2% vs 11.0%; log-rank=130.29; p<0.001). Landmark analysis showed a worse prognosis in the group of patients with severely calcified lesions at the first year post-procedure, but also for the period between 1 and 3 years follow-up (figure 1B).
In univariate Cox regression analysis, severe calcification was a predictor of death—MI (HR: 1.86, 95% CI 1.60 to 2.16; p<0.001). In the multivariate model built, excluding the history of cerebrovascular and PVD, severe calcification was a predictor of death—MI ( Table 4 ).
Outcome data with regards the combined end-point death—MI—any revascularisation was available in 5018 patients. At 3-year follow-up, 1213 events were reported, of which 860 (22.4%) occurred in patients without severely calcified lesions, and 373 (31.8%) in patients with severe lesion calcification (log-rank=14.55; p<0.001, figure 1C). Similarly to what has been reported for the other end-points, landmark analysis showed a worse outcome in the group of patients with severely calcified lesions at 1 year post-procedure, and also for the period between 1 and 3 years follow-up (figure 1C). Severe lesion calcification was a predictor of worse outcome in univariate and multivariate Cox regression analysis ( Table 5 ).
During follow-up, 269 ST events occurred, of which 129 were definite, 43 probable and 97 possible ST ( Table 3 ). Patients with calcified coronaries had an increased incidence of ST compared to those without coronary calcification (definite ST: 3% vs 1.8%, log-rank=6.97; p=0.008; definite/probable ST: 4.3% vs 2.1%, log-rank=17.06, p<0.001). Severe lesion calcification was a predictor of ST in univariate analysis (definite ST: HR: 1.66, 95% CI 1.13 to 2. 42; p<0.001; definite/probable ST: HR: 1.95, 95% CI 1.37 to 2.76; p<0.001), but it was not an independent predictor in the multivariate models (definite ST: HR: 1.41, 95% CI 0.87 to 2.28; p=0.167; definite/probable ST: HR: 1.40, 95% CI 0.91 to 2.15; p=0.124).
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