Remote Ischaemic Postconditioning
Of the 266 patients recruited, 12 were excluded as their baseline troponin values were higher than 1 ng/mL (exclusion criterion). A further 18 patients could not be included in the analysis as no 24-h troponin sample was available (nine patients in each group), and four were excluded who had extreme troponin release values (above the mean plus three SDs), only one of whom belonged to the postconditioning group. Three of the patients randomised to postconditioning could not tolerate the protocol, as it caused intense pain in the arm and necessitated deflating the cuff, at which time the pain disappeared with no complications.
The mean age was 64.6 years and 68.1% were men (Table 1). No differences were found between the groups in renal function. The indication for PCI was stable angina in 71.5% of the patients.
The variables related with the revascularised coronary disease are shown in Table 2. No differences were found between the two groups concerning the coronary artery revascularised, the use of predilatation or postdilatation, number of inflations, number of stents implanted or whether these were drug-eluting or conventional. The heart rate and the blood pressure during the procedure were also similar between the two groups.
A total of 118 patients were randomised to the ischaemic postconditioning arm and 114 received the placebo. The peak troponin I in the RIP group was very similar to that of the placebo group (0.476 vs 0.478 ng/mL, respectively; p=0.99) (Table 3). Of all the patients, 33.2% experienced a PCI-MI (36% in the RIP group and 30.5% in the control group; OR 1.27; 95% CI 0.74 to 2.21; p=0.378) according to the 2007 definition. The new definition resulted in 28.9% being diagnosed with PCI-MI in the RIP group versus 22% in the placebo group (OR 1.44; 95% CI 0.796 to 2.61; p=0.23).
In the subgroup of diabetic patients randomised to RIP, using the 2007 definition resulted in 40.9% having a PCI-MI versus 25.9% of the diabetic controls (OR 1.97; 95% CI 0.84 to 4.65; p=0.12). Using the 2012 definition resulted in significantly more of the diabetic patients randomised to RIP having a PCI-MI as compared with the diabetic controls (18.5% vs 38.6%; OR 2.7; 95% CI 1.10 to 6.92; p=0.027).
The diabetic patients had a peak troponin release of 0.51 vs 0.45 ng/mL in the non-diabetic patients (p=0.69). The percentage of PCI-MI in the diabetic patients was 32.7% with the classical definition and 29.6% with the new definition versus 33.6% (OR 0.88; p=0.96) and 32.7% (OR 1.23; p=0.48), respectively, for the non-diabetic patients.
The patients who underwent two or more vessel angioplasty had a significantly greater elevation in troponins (0.66 vs 0.36 ng/mL, p=0.03), though this was not changed by the RIP. The peak CKMB in the RIP patients was 1.62 vs 2.01 ng/mL in the controls (p=0.56). The ultrasensitive CRP showed no significant differences between the two groups: 3.26 mg/mL in the RIP group versus 4.16 mg/mL in the control group.
No differences were seen in the primary endpoint between the patients with stable angina and those with unstable angina. In those with stable angina the peak troponin level was 0.56 ng/dL in the RIP group and 0.47 ng/dL in the placebo group (p=0.57). In those with unstable angina the peak troponin level was 0.21 vs 0.48 ng/dL in the placebo group (p=0.27).
The follow-up analysis included all the study patients, including the 18 patients randomised to receive either RIP or placebo but who were excluded from the analysis of the primary endpoint due to lack of a 24-h troponin measurement. The median follow-up was 12 months, during which time an adverse event (death, hospital admission, new revascularisation due to stable angina or acute coronary syndrome) was experienced by 17 RIP patients and 13 control patients (p=0.44) (figure 1). Four RIP patients had an acute coronary syndrome versus just one control patient (p=0.18). Repeat revascularisation due to acute coronary syndrome or stable angina was required by nine RIP patients and five controls (p=0.27). Only two patients required surgical revascularisation, one in each group. Two patients died, both from cardiovascular causes and both in the postconditioning group; one of these had been excluded from the study due to lack of a 24-h troponin measurement.
(Enlarge Image)
Figure 1.
Kaplan–Meier curve of the combined adverse events during the 1-year follow-up (overall and cardiovascular mortality, acute coronary syndrome, revascularisation due to stable angina, hospital admission).
In the subgroup of diabetic patients an adverse event was experienced by eight RIP patients and seven control group patients (p=0.40): two patients had acute coronary syndrome, both in the RIP group (p=0.12), and seven patients required repeat revascularisation (five RIP patients, p=0.14).
Results
Of the 266 patients recruited, 12 were excluded as their baseline troponin values were higher than 1 ng/mL (exclusion criterion). A further 18 patients could not be included in the analysis as no 24-h troponin sample was available (nine patients in each group), and four were excluded who had extreme troponin release values (above the mean plus three SDs), only one of whom belonged to the postconditioning group. Three of the patients randomised to postconditioning could not tolerate the protocol, as it caused intense pain in the arm and necessitated deflating the cuff, at which time the pain disappeared with no complications.
Clinical Profile of the Patients Included
The mean age was 64.6 years and 68.1% were men (Table 1). No differences were found between the groups in renal function. The indication for PCI was stable angina in 71.5% of the patients.
Percutaneous Revascularisation
The variables related with the revascularised coronary disease are shown in Table 2. No differences were found between the two groups concerning the coronary artery revascularised, the use of predilatation or postdilatation, number of inflations, number of stents implanted or whether these were drug-eluting or conventional. The heart rate and the blood pressure during the procedure were also similar between the two groups.
Primary Endpoint
A total of 118 patients were randomised to the ischaemic postconditioning arm and 114 received the placebo. The peak troponin I in the RIP group was very similar to that of the placebo group (0.476 vs 0.478 ng/mL, respectively; p=0.99) (Table 3). Of all the patients, 33.2% experienced a PCI-MI (36% in the RIP group and 30.5% in the control group; OR 1.27; 95% CI 0.74 to 2.21; p=0.378) according to the 2007 definition. The new definition resulted in 28.9% being diagnosed with PCI-MI in the RIP group versus 22% in the placebo group (OR 1.44; 95% CI 0.796 to 2.61; p=0.23).
In the subgroup of diabetic patients randomised to RIP, using the 2007 definition resulted in 40.9% having a PCI-MI versus 25.9% of the diabetic controls (OR 1.97; 95% CI 0.84 to 4.65; p=0.12). Using the 2012 definition resulted in significantly more of the diabetic patients randomised to RIP having a PCI-MI as compared with the diabetic controls (18.5% vs 38.6%; OR 2.7; 95% CI 1.10 to 6.92; p=0.027).
The diabetic patients had a peak troponin release of 0.51 vs 0.45 ng/mL in the non-diabetic patients (p=0.69). The percentage of PCI-MI in the diabetic patients was 32.7% with the classical definition and 29.6% with the new definition versus 33.6% (OR 0.88; p=0.96) and 32.7% (OR 1.23; p=0.48), respectively, for the non-diabetic patients.
The patients who underwent two or more vessel angioplasty had a significantly greater elevation in troponins (0.66 vs 0.36 ng/mL, p=0.03), though this was not changed by the RIP. The peak CKMB in the RIP patients was 1.62 vs 2.01 ng/mL in the controls (p=0.56). The ultrasensitive CRP showed no significant differences between the two groups: 3.26 mg/mL in the RIP group versus 4.16 mg/mL in the control group.
No differences were seen in the primary endpoint between the patients with stable angina and those with unstable angina. In those with stable angina the peak troponin level was 0.56 ng/dL in the RIP group and 0.47 ng/dL in the placebo group (p=0.57). In those with unstable angina the peak troponin level was 0.21 vs 0.48 ng/dL in the placebo group (p=0.27).
Secondary Endpoint
The follow-up analysis included all the study patients, including the 18 patients randomised to receive either RIP or placebo but who were excluded from the analysis of the primary endpoint due to lack of a 24-h troponin measurement. The median follow-up was 12 months, during which time an adverse event (death, hospital admission, new revascularisation due to stable angina or acute coronary syndrome) was experienced by 17 RIP patients and 13 control patients (p=0.44) (figure 1). Four RIP patients had an acute coronary syndrome versus just one control patient (p=0.18). Repeat revascularisation due to acute coronary syndrome or stable angina was required by nine RIP patients and five controls (p=0.27). Only two patients required surgical revascularisation, one in each group. Two patients died, both from cardiovascular causes and both in the postconditioning group; one of these had been excluded from the study due to lack of a 24-h troponin measurement.
(Enlarge Image)
Figure 1.
Kaplan–Meier curve of the combined adverse events during the 1-year follow-up (overall and cardiovascular mortality, acute coronary syndrome, revascularisation due to stable angina, hospital admission).
In the subgroup of diabetic patients an adverse event was experienced by eight RIP patients and seven control group patients (p=0.40): two patients had acute coronary syndrome, both in the RIP group (p=0.12), and seven patients required repeat revascularisation (five RIP patients, p=0.14).
SHARE
