Periprocedural Myocardial Damage Research Articles

1024 PROGNOSTIC VALUE OF CI-AKI AND HIS RELATIONSHIP WITH PERIPROCEDURAL MYOCARDIAL DAMAGE IN NSTEMI

Abstract Background Periprocedural myocardial damage and contrast-induced acute kidney injury (CI-AKI) are frequent complications of percutaneous coronary intervention (PCI) and impact prognosis. The possible associations and the prognostic role of these peri-procedural complications are still not well understood. Purpose To evaluate predictors and prognostic role of CI-AKI in patients with NSTEMI and the relationship between CI-AKI and periprocedural myocardial damage. Methods Patients with NSTEMI undergoing coronary angiography within 72 hours were enrolled from January 2016 to September 2021. To detect post-PCI acute myocardial damage in this setting of NSTEMI patients, we included only those with stable (≤ 20% variation) or falling pre-procedure baseline cardiac troponin (cTn) values. Serum cTnI were measured at baseline and at 3-6-12 hours after PCI in all patients. Periprocedural myocardial damage was evaluated according to postprocedural hsTnI criteria provided by most recent consensus documents. Renal injury was documented when absolute serume creatinine increased of ≥ 0.3 mg/dL or ≥ 50% within 72 hours or urine output reduced to ≤ 0.5 mL/Kg/hour for at least 6 hours. Results We enrolled 878 patients with NSTEMI undergoing PCI and with pre procedure stable cTn levels. 53 patients suffered from AKI post contrast and among these 8 patients exhibited myocardial periprocedural injury and 20 patients had periprocedural myocardial infarction according to European Society of Cardiology guidelines. Myocardial periprocedural damage occurred more frequently in the CI- AKI group compared to non-CI-AKI group (52% vs 38%, p = 0.01). Patients who experienced CI-AKI were significantly older (mean age 86 ± 4) and had more frequently cardiovascular risk factors such as diabetes (p < 0.001) and hypertension (p = 0.006), compared to non-CI-AKI group. Moreover NSTEMI patients with CI-AKI were more often on beta-blockers (p= 0.001) and statins (p < 0.001) and exhibited more frequently at admission ST-T segment (p < 0.000) and wall motion alterations at echocardiography evaluation (p = 0.004).Regarding intra-hospital outcomes, CI-AKI population experienced more frequently reinfarction (p = 0.02) and arrhythmias (p < 0.000) compared to others . Surprisingly, the multivariate logistic regression showed that the stronger predictor of CI-AKI was periprocedural myocardial infarction (p < 0.001). Finally, at 3 years of follow-up, in patients with CI-AKI there was more incidence of all-cause mortality (p = 0.001) and the composite of all-cause death, re-acute myocardial infarction and hospitalization for heart failure (p = 0.05) compared to non-CI-AKI group. Conclusion In NSTEMI patients, contrast-induced acute kidney injury was associated with majors adverse events, both intra-hospital and at long-term follow-up. Subjects who experienced acute kidney injury were older, had more comorbidities and had a worse clinical and instrumental profile at admission. CI-AKI was also associated with peri-procedural acute myocardial injury and infarction. More studies are needed to understand the patophysiological relations between these to post-PCI complications to improve their management.

Tobacco smoking protective effect via remote ischemic preconditioning on myocardial damage after elective percutaneous coronary intervention: Subanalysis of a randomized controlled trial

BackgroundRemote ischemic preconditioning (RIPC) is promising for preventing periprocedural myocardial damage (pMD) in patients undergoing percutaneous coronary intervention (PCI). However, the impact of RIPC on pMD on smokers is not well elucidated. The aim of this study was to investigate an association between tobacco smoking and RIPC on pMD in patients planning to undergo PCI. MethodsThis study used data from a multicenter randomized controlled trial involving patients with stable angina who planned to undergo elective PCI. We analyzed data for 262 patients in the control (n = 133) and upper-limb RIPC (n = 129) groups, including 166 current or former smokers. The major outcome was the pMD incidence following PCI, with pMD defined as an elevated level of highly sensitive cardiac troponin T or a creatine kinase myocardial band 12 or 24 h after PCI. ResultsThe incidence of pMD was significantly lower in the upper-limb RIPC group than in the control group (28/83 patients [33.8%] vs. 43/83 patients [51.8%], respectively; p = 0.018). In a multiple logistic regression model, tobacco smoking was an independent predictor of interacting with and enhancing the effect of RIPC on reducing the incidence of pMD after PCI (regression coefficient, −0.4 [95% confidence interval, −0.74 to −0.082]; p = 0.015). ConclusionsTobacco smoking may have a beneficial effect on RIPC against pMD after PCI.

Effect of tailored use of tirofiban in patients with Non-ST-elevation acute coronary syndrome undergoing percutaneous coronary intervention: a randomized controlled trial

BackgroundWe conducted a randomized controlled trial to investigate whether an additional platelet inhibition with tirofiban would reduce the extent of myocardial damage and prevent periprocedural myonecrosis in patients with Non-ST-elevation acute coronary syndrome (NSTE-ACS) with a high residual platelet activity (HPR).MethodsPatients with an HPR, defined as P2Y12 reaction unit (PRU) > 230, were randomly assigned to group A (tirofiban treatment, n = 30) or C1 (n = 30) and patients without an HPR to C2 (n = 78). Periprocedural myocardial damage was assessed using the area under the curve (AUC) of serial cardiac enzyme levels from the time of the procedure to post-36 h. Periprocedural myonecrosis incidence was evaluated.ResultsThe troponin I AUC was not different between the groups (197.2 [41.5395.7], 37.9 [8.9313.9], 121.3 [43.7481.8] h∙ng/mL; p = 0.088). The results did not change when the baseline levels were adjusted (365.3 [279.5, 451.1], 293.0 [207.1, 379.0], and 298.0 [244.7, 351.3] h∙ng/mL; p = 0.487). The rate of periprocedural myonecrosis was also not different between the groups (53.0% vs. 50.0% vs. 33.3%, p = 0.092). The CK-MB isoenzyme analysis showed similar results. No difference in complications was noted.ConclusionAdditional tirofiban administration was not beneficial to patients with NSTE-ACS even with an HPR.Trial registrationClinical trial no. NCT03114995, registered 11 April, 2017, retrospectively.

The periprocedural myocardial damage prevention during elective percutaneous coronary intervention as a result of pharmacological preconditioning with an oral form of nicorandil in patients with stable coronary artery disease. Pilot study.

The purpose of the study is to prove the effectiveness of pharmacological preconditioning caused by nicorandil in patients with stable coronary heart disease (CHD) during the elective percutaneous coronary intervention (PCI). We included 88 patients with a stable form of CHD, who were going to pass the elective PCI, in the study. As the method of blind randomization envelope method was used. There were formed two groups or patients: the first group involved 45 patients - were treated with nicorandil (Cordinic, PIQ-FHARMA LLC) (the main group) the other group included 43 patients who were treated by the standard therapy (the comparison group). The basic antianginal therapy was allowed to use in both groups: beta-blockers, calcium antagonists, ATE inhibitors / angiotensin II receptor blockers, statins, acetylsalicylic acid, blockers of P2Y12 receptor platelets. The admission of prolonged form of nitrates before the PCI was allowed in the second group. Patients from the 1st group were to take nicorandil 2 days and 1 day before the PCI at the 30 mg/day dose, then 20 mg orally 2 hours just before PCI, and one more time 6 hours after the PCI - 10 mg nicorandil. Highly sensitive troponin (HS-Tp) as a biomarker of irreversible damage to the myocardium was evaluated before PCI and after PCI in 24 hours. Were used highly sensitive troponin (HF-Tr) and creatine phosphokinase-MB as an irreversible myocardial damage biomarkers. The analysis of which was conducted before PCI and 24 hours after the surgery. The obtained data shows the significant differences of an increase in hs-Tp in 24 hours after PCI in patients with no admission of nicorandil (117 ng/l) as compared with the nicorandil group (73 ng/l), p = 0.04. There were significant differences in the 24 hours increment in hs-Tp in the control group, it was higher (112 ng/l) than in the nicorandil group (67 ng/l), p = 0.03. There was also a significant -decrease in CK-MB after 24 hours in the nicorandil group (2.7 ng/L) compared to the control group (2.0 ng/L), p = 0.008. Also the frequency of the troponin increase above the UNL(upper normal level) in the nicorandal group, was significantly (p = 0.03) lower (in 62% of cases compared to 85% of the control group). The prevention of the complications during the percutaneous myocardial revascularization should be considered with the position of the most suitable pharmacological support. The appointment of the oral form of nicorandil (Cordinic, PIQ-FHARMA LLC) for 2 days and 1 day before PCI 30 mg/day, then 20 mg 2 hours before the PCI and 10 mg after 6 hours after the surgery reduces the risk of intraoperative myocardial damage. The obtained data give an opportunity to extend the indications for nicorandil's appointment in the drug support during PCI in patients with stable coronary artery disease.

Protective Effect of Remote Ischemic Preconditioning on Myocardial Damage After Percutaneous Coronary Intervention in Stable Angina Patients With Complex Coronary Lesions - Subanalysis of a Randomized Controlled Trial.

The effect of remote ischemic preconditioning (RIPC) on periprocedural myocardial damage (pMD) in patients undergoing percutaneous coronary intervention (PCI) is controversial. The aim of this study was to investigate the effect of RIPC or intravenous nicorandil on pMD following elective PCI in a subgroup of patients with complex coronary lesions from a multicenter randomized controlled trial.Methods and Results:Patients with stable angina who underwent elective PCI were assigned to 3 groups: control, upper-limb RIPC or intravenous nicorandil. The major outcome was pMD incidence following PCI, with pMD defined as an elevated level of high-sensitivity cardiac troponin T or creatine kinase myocardial band at 12 or 24 h after PCI. A total of 171 patients with complex coronary lesions (ACC-AHA coronary classification type B2 or C) were analyzed. The incidence of pMD following PCI was significantly lower in the RIPC group than in the control group (44.4% vs. 66.1%; P=0.023). The adjusted odds ratio (95% confidence interval) for pMD in the RIPC vs. the controls was 0.41 (0.18-0.94). The incidence of pMD in the nicorandil group was not significantly reduced compared with the control groups. This substudy suggested that RIPC prior to PCI prevented pMD in patients with complex coronary lesions. Further investigation in a multicenter prospective study is needed to confirm these results.

Vitamin D deficiency and periprocedural myocardial infarction in patients undergoing percutaneous coronary interventions.

Vitamin D deficiency has been implicated in the progression of atherosclerosis and acute thrombotic events. We aimed at evaluating the impact of vitamin D deficiency on periprocedural myocardial infarction (PMI) in patients undergoing percutaneous coronary interventions (PCI). We included 934 patients undergoing non-urgent PCI. Assessment of myocardial biomarkers was performed from 6 to 48 h after PCI. PMI was defined as Creatine Kinase-MB increase by 3 times the Upper Limit Normal or by 50% of an elevated baseline value, periprocedural myocardial damage as Troponin I increase by 3 × ULN or 50% of baseline. Patients were divided according to vitamin D tertiles values (<10.2 ng/ml; 10.2-18.7 ng/ml; ≥18.8 ng/ml). Lower tertiles values of vitamin D were associated with age (p = 0.04), female gender, (p = 0.001), and a higher cardiovascular risk profile. Lower vitamin D levels related with PCI of descending anterior coronary artery or bypass vein grafts (p = 0.03), treatment of bifurcations (p = 0.05) and side branch loss (p = 0.05) and inversely with direct stenting (p = 0.002). However, lower vitamin D levels did not influence the risk of PMI (adjusted OR [95% CI] = 0.81[0.65,1.18], p = 0.09) or periprocedural myocardial damage (adjusted OR [95% CI] = 0.93[0.77,1.13], p = 0.48). Similar results were achieved when considering the severity of vitamin D deficiency. Therefore, in patients undergoing PCI, no association was observed between vitamin D deficiency and the risk of periprocedural MI and myocardial damage.

Effects of the P-Selectin Antagonist Inclacumab on Myocardial Damage After Percutaneous Coronary Intervention According to Timing of Infusion: Insights From the SELECT-ACS Trial.

BackgroundThe Effects of the P‐Selectin Antagonist Inclacumab on Myocardial Damage After Percutaneous Coronary Intervention for Non‐ST‐Segment Elevation Myocardial Infarction (SELECT‐ACS) trial suggested beneficial effects of inclacumab, a monoclonal antibody directed against P‐selectin, on periprocedural myocardial damage. This study evaluated the effect of inclacumab on myocardial damage according to varying time intervals between study drug infusion and percutaneous coronary intervention (PCI).Methods and ResultsPatients (n=544) enrolled in the SELECT‐ACS trial and randomized to receive 1 infusion of placebo or inclacumab (5 or 20 mg/kg, administered between 1 and 24 hours before PCI) were divided according to the time interval between study drug infusion and PCI. The primary end point was the change in troponin I from baseline at 16 and 24 hours after PCI. In patients receiving inclacumab 20 mg/kg with a short (less than median) time interval between infusion and PCI, placebo‐adjusted geometric mean percent changes in troponin I, creatine kinase–myocardial band, and peak troponin I at 24 hours were −45.6% (P=0.005), −30.7% (P=0.01), and −37.3% (P=0.02), respectively. No significant changes were observed in patients with a long (greater than median) time interval between infusion and PCI. Placebo‐adjusted geometric mean percent changes in troponin I and creatine kinase–myocardial band were −43.5% (P=0.02) and −26.0% (P=0.07), respectively, when inclacumab 20 mg/kg was administered between 1 and 3 hours before PCI, whereas the drug had no effect with longer intervals.ConclusionsInclacumab 20 mg/kg significantly reduces myocardial damage after PCI in patients with non–ST‐segment elevation myocardial infarction, and benefits are larger when the infusion is administered <3 hours before PCI.Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT01327183.

Relation of Neutrophil to Lymphocyte Ratio With Periprocedural Myocardial Damage in Patients Undergoing Elective Percutaneous Coronary Intervention

Neutrophil to lymphocyte ratio (NLR) has been proposed as a marker of cardiovascular risk. The potential relation between NLR and periprocedural myocardial damage after percutaneous coronary intervention (PCI) is unclear. We enrolled 502 consecutive patients with stable coronary artery disease undergoing elective PCI. Blood samples were drawn in all patients at baseline, 6 hours, and 24 hours after PCI for complete blood cell count and cardiac biomarkers (creatine kinase-MB and troponin T [Tn-T]) assessment. NLR was calculated as the ratio between the absolute number of neutrophil over the absolute number of lymphocyte. Periprocedural myocardial infarction (PMI) was defined according to the 2012 universal definition of myocardial infarction. In the overall population, a significant postprocedural increase in NLR was observed (3.255 [2.763 to 3.995] at baseline, 4.430 [3.390 to 6.020] at 6hours, 4.720 [3.940 to 5.750] at 24 hours, p <0.0001). PMI occurred in 33 patients (6.6%). Baseline NLR was similar in patients with and without PMI (3.250 [2.820 to 3.885] vs 3.260 [2.750 to 4.000], p= 0.898); however, patients who developed PMI showed significantly higher NLR both at 6 hours (5.750 [4.360 to 9.095] vs 4.370 [3.370 to 5.950], p <0.001) and 24hours (5.180 [4.440 to 8.065] vs 4.670 [3.920 to 5.710], p= 0.003). Among patients who developed PMI, periprocedural NLR increase showed a moderate positive correlation with both creatine kinase-MB (rho= 0.377, p= 0.031) and troponin T increase (rho= 0.506, p= 0.003). In conclusion, preprocedural NLR values do not impact on the occurrence of PMI during elective PCI; however, PCI procedures induce a significant increase in NLR that seems to be proportional to the magnitude of periprocedural myocardial damage.

Effect of Danlou Tablet (丹蒌片) on peri-procedural myocardial injury among patients undergoing percutaneous coronary intervention for non-ST elevation acute coronary syndrome: A study protocol of a multicenter, randomized, controlled trial

It has been shown that administration of statins reduced the risk of peri-procedural myocardial damage. However, it remains unclear whether Chinese medicine Danlou Tablet (), similar to statins, may protect patients undergoing percutaneous coronary intervention (PCI) from peri-procedural myocardial damage. To demonstrate the hypothesis whether treatment with Danlou Tablet would improve clinical outcome in patients undergoing selective PCI with non-ST elevation acute coronary syndrome (NSTE-ACS) in China. Approximately 220 patients with unstable angina or non-ST-segment elevation myocardial infarction undergoing PCI will be enrolled and randomized to Danlou Tablet treatment (4.5 g/day for 2 days before intervention, with a further 4.5 g/day for 90 days thereafter) or placebo. All patients will not receive Danlou Tablet before procedure. The primary end point is to evaluate the incidence of cardiac death, myocardial infarction or unplanned re-hospitalization and revascularization after 30 days in patients undergoing selective PCI treated with Danlou Tablet compared with placebo. Secondary endpoints include the incidence of peri-procedural myocardial injury, 3-month clinical outcomes, the quality of life and Chinese medicine syndromes assessment. This study protocol will provide important evidence of Danlou Tablet treatment on the peri-procedural myocardial injury in patients with NSTE-ACS undergoing selective PCI, which may support a strategy of routine Danlou Tablet therapy to improve the clinical outcomes.

HDL-C and Plaque Calcification are Associated with Microcirculatory Damage after Percutaneous Coronary Intervention

Aims : Microvascular disturbance followed by percutaneous coronary intervention (PCI) was sometimes occurred. There were no report of the quantitative evaluation about microvascular disturbance after PCI. The aim of this study was to quantitate microcirculatory injury caused by elective PCI using index of microcirculatory resistance (IMR), and to clarify preprocedural predictors of microvascular damage. Methods : Fifty patients with stable angina and planned PCI for single vessel disease were enrolled in this study. IMR was measured after PCI. Plaque components were analyzed by integrated backscatter intravascular ultrasound. Results : Post-PCI IMR tended to correlate with high-density lipoprotein cholesterol levels (r = –0.298, p = 0.078) and plaque calcification (r = -0.22, p = 0.058) in the univariate analysis. Multivariate logistic analysis adjusted for these covariates revealed that the high-density lipoprotein cholesterol levels and plaque calcification were inversely associated with higher post-PCI IMR (odds ratio = 0.919, p = 0.049; and odds ratio = 0.546, p = 0.049, respectively). Conclusion : Low levels of high-density lipoprotein cholesterol and plaque calcification independently predict higher post-PCI IMR. Based on these results, Serum lipid and plaque calcification profiles might be important for predicting and preventing periprocedural myocardial damage during elective PCI.

The rise of cardiac biomarkers due to planned PCI and 1-year prognosis in patients with stable coronary artery disease and arterial hypertension

Aim. The aim of our study was to assess the prevalence of myocardial infarction (MI) type 4a and myocardial damage due to planned percutaneous interventions (PCI) in patients with stable coronary artery disease (CAD) and arterial hypertension (AH).Material and methods. 281 patients were screened before the enrollment in our study. 183 patients with stable CAD were included in our study whose levels of cardiac troponin I and CK-MB (creatine kinase-MB fraction) were studied after PCI. We divided patients into the groups according to their levels of cardiac troponin I after PCI and CK-MB (group 1 - no elevation; 2 - elevation 1-3 upper limits of normal - ULN; III - more than 3 ULN).167 patients had AH. In case of detected rise of CK-MB and/or troponin echocardiography and cardiac magnetic resonance imaging (MRI) were performed. Results. The prevalence of MI type 4a was 10,8% and periprocedural myocardial damage - 16,2% respectively. After performing the discriminant analysis we sought to build a prognostic model and calculate the formula of periprocedural myocardial damage probability: 0,871 × gender (male = 0; female = 1)+0,516 × angina pectoris functional class + 0,022 × age (years) - 0,011 × (estimated glomerular filtration rate (eGFR) using the Modification of Diet in Renal Disease - MDRD formula) + 0,27 × number of diseased coronary arteries ≥2,731.Conclusion. Women with low EGFR (MDRD), mutivessel disease and angina pectoris class 3-4 (NYHA) have the highest risk of MI type 4a. The most difficult localization for PCI is circumflex artery.

Подъем маркеров некроза миокарда у больных с хронической ишемической болезнью сердца и артериальной гипертензией и однолетний прогноз

Aim. The aim of our study was to assess the prevalence of myocardial infarction (MI) type 4a and myocardial damage due to planned percutaneous interventions (PCI) in patients with stable coronary artery disease (CAD) and arterial hypertension (AH).Material and methods. 281 patients were screened before the enrollment in our study. 183 patients with stable CAD were included in our study whose levels of cardiac troponin I and CK-MB (creatine kinase-MB fraction) were studied after PCI. We divided patients into the groups according to their levels of cardiac troponin I after PCI and CK-MB (group 1 - no elevation; 2 - elevation 1-3 upper limits of normal - ULN; III - more than 3 ULN).167 patients had AH. In case of detected rise of CK-MB and/or troponin echocardiography and cardiac magnetic resonance imaging (MRI) were performed. Results. The prevalence of MI type 4a was 10,8% and periprocedural myocardial damage - 16,2% respectively. After performing the discriminant analysis we sought to build a prognostic model and calculate the formula of periprocedural myocardial damage probability: 0,871 × gender (male = 0; female = 1)+0,516 × angina pectoris functional class + 0,022 × age (years) - 0,011 × (estimated glomerular filtration rate (eGFR) using the Modification of Diet in Renal Disease - MDRD formula) + 0,27 × number of diseased coronary arteries ≥2,731.Conclusion. Women with low EGFR (MDRD), mutivessel disease and angina pectoris class 3-4 (NYHA) have the highest risk of MI type 4a. The most difficult localization for PCI is circumflex artery.

Lack of association between peri-procedural myocardial damage and CYP2C19 gene variant in elective percutaneous coronary intervention.

Peri-procedural myocardial damage (MD) is associated with increased risk of major in-hospital complications and adverse clinical events. The aim of this study was to evaluate the effects of on-clopidogrel platelet aggregation and CYP2C19-reduced-function gene variants on elective percutaneous coronary intervention (PCI)-related MD. We measured changes in serum high-sensitive troponin T (hs-TnT) levels, CYP2C19 genotype, and on-clopidogrel platelet aggregation (PA) using VerifyNow(®) P2Y12 system in 91 patients who received stent implantation (stent group). The control group comprised 30 patients who did not receive PCI. Blood samples were obtained before and 24h after PCI or coronary angiography (CAG). Patients of the stent group were divided into high and low MD groups based on the median value of hs-TnT level at 24h after PCI. Serum hs-TnT levels were significantly higher 24h after PCI (86.8±121.5pg/ml) compared with before PCI (9.4±5.3, p<0.001), whereas the levels were identical before and 24h after CAG in the control group. Simple logistic regression analysis demonstrated that MD correlated with age (p=0.014), estimated GFR (p=0.003), hemoglobin A1c (p=0.015), baseline serum hs-TnT (p=0.049), and stent length (p<0.001). Multiple logistic regression analysis identified old age, high hemoglobin A1c level, and long stent, but not CYP2C19 reduced-function allele or high on-clopidogrel PA, as independent predictors of elective PCI-related MD. The present study demonstrated no significant relation between peri-procedural MD and high on-clopidgrel PA associated with CYP2C19 reduced-function allele in patients undergoing elective PCI.

Efficacy of chronic high-dose statin therapy in procedural myocardial injury and long-term outcomes in patients undergoing rotablational atherectomy

Background: Periprocedural myocardial injury remains the most common complication associated with rotational atherectomy (ROTA). Furthermore, previous studies have demonstrated that even a small elevation of cardiac enzymes is associated with higher risk of mortality during follow-up. Otherwise, pre-treatment with high-dose statins reduced the risk of procedural myocardial injury after coronary intervention. This study was to verify whether chronic high-dose statin before PCI might protect periprocedural myocardial damage and improve long-term outcomes after ROTA. Methods: We prospectively studied 476 patients (age 67.4±9.2 years, 398 men) with chronic stable angina who underwent ROTA. The patients were divided into three groups according to use of statin; 1) no statin treatment before procedure (195 patients), 2) standard dose statin (189 patients), and 3) high-dose statin (92 patients). The primary end point was periprocedual CPK and hs-CRP and long-term outcomes (death and ACS). Results: There were no significant differences among 3 groups in clinical and angiographic background. Markers of myocardial injury of the all groups were elevated after ROTA; however, the high-dose statin arm had significantly lower periprocedural levels of CPK and hs-CRP than standard-statin group and no-statin group. In the no statin group, 8% of patients had CK increases >3 times the upper limit of normal compared with 2% in the high-dose statin group (p = 0.02). By logistic regression analysis, the independent predictors of CPK elevation >3 times after ROTA were statin pre-treatment (OR=0.53; 95% CI=0.13-0.86; p=0.02). The patients with high statin group had lower events rate than other groups. Multivariable analysis identified high dose statin as a predictor of decreased adverse events (HR: 0.46, 95% CI: 0.28 to 0.74; p= 0.001). Conclusions: Pretreatment with high-dose statin significantly reduces procedural myocardial injury and improves the long-term prognosis in patients with stable angina undergoing ROTA.

Periprocedural myocardial damage during percutaneous coronary intervention: a point-of-care platelet testing and intravascular ultrasound/virtual histology study

Recent studies have implied that platelet reactivity as well as certain lesion morphology may be linked to myocardial injury during percutaneous coronary intervention (PCI). However, to date the abovementioned features have not been investigated simultaneously in one population. To determine if and how high on-treatment platelet reactivity, different lesion morphology, and plaque components are associated with increased risk of periprocedural myocardial injury in patients referred for elective coronary stenting. Sixty patients pretreated with aspirin and clopidogrel and undergoing elective PCI with stent(s) implantation were included. On-treatment platelet reactivity was measured with VerifyNow Aspirin and P₂Y₁₂ assays (Accumetrics, USA) before PCI. Grey-scale intravascular ultrasound (IVUS) and virtual histology were performed before stent(s) implantation (Volcano, USA). Two levels of myocardial injury were considered: any elevation of troponin I (periprocedural myocardial damage, PMD) and/or > 3 times the upper normal limit (periprocedural myocardial infarction, PMI). By receiver-operating characteristics analysis, the following factors, ranked from strongest to weakest, were able to distinguish between patients with and without PMD: remodelling index (RI), fibrous tissue, fibro-fatty tissue volume (FFT), plaque and media cross-sectional area, and external elastic membrane cross-sectional area (EEM CSA). Only platelet count and RI could differentiate patients with and without PMI. PMD as well as PMI could not be predicted either by VerifyNow Aspirin or P₂Y₁₂ assay. Likewise, there was no association between necrotic core volume and PMD or PMI. In logistic regression analysis, after adjusting for possible clinical and procedural confounding factors, only EEM CSA > 14.6 mm² (OR 23.7, 95% CI 1.9-302, p = 0.015), RI > 1.044 (OR 12.3, 95% CI 1.2-121.9, p = 0.032) and FFT > 11.2 mm³ (OR 13.6, 95% CI 1.1-160.9, p = 0.038) were independent predictors of PMD. Only RI > 1.044 was identified as an independent predictor of PMI (OR 7.5, 95% CI 1.92-29.6, p = 0.004). Greater total vessel area, positive remodelling at the lesion site, and high volume of FFT in the coronary plaque are independently associated with increased risk of myocardial injury. Only positive RI was an independent predictor of PMI. Simple lesion morphology, rather than more complex VH-IVUS analysis or platelet reactivity, seems to predict myocardial injury after elective PCI.

Usefulness of Preprocedural Levels of Advanced Glycation End Products to Predict Restenosis in Patients With Controlled Diabetes Mellitus Undergoing Drug-Eluting Stent Implantation for Stable Angina Pectoris (From the Prospective ARMYDA-AGEs Study)

Diabetes mellitus (DM) remains the main predictor of restenosis rates and cardiovascular events following successful percutaneous coronary intervention (PCI) despite the use of drug-eluting stents (DES). HbA1c <6.0% is considered an index of optimized metabolic control in patients with DM, but several studies are downsizing its role in the clinical management of these patients. Increasing evidence points at the role of advanced glycation end products (AGEs) in restenosis pathogenesis independently on Hb1AC levels. Thus, we investigated the predictive value of preprocedural AGE levels for in-stent restenosis in a population of euglycaemic diabetic patients undergoing PCI with DES implantation. One hundred twenty-five consecutive patients with DM in optimized glycemic control admitted for stable angina pectoris and treated with elective DES implantation at a tertiary hospital were prospectively included. The primary end point of the ARMYDA-AGEs study was to compare rates of angiographic ISR at 6 months after the intervention according to pre-PCI levels of AGEs. Secondary end points were the correlations of AGE levels with occurrence of periprocedural myocardial damage, major adverse cardiac events, and in-stent late loss at 6-month control coronary angiography. AGE levels >17 μM was found to be an independent predictor of ISR at 6 months and stent lumen loss. AGEs failed to predict occurrence of secondary endpoints. In conclusion, elevated AGE levels predict occurrence of in-stent restenosis after DES implantation in patients with DM on optimized glycemic control and might represent a dosable marker of adverse outcome after PCI.

Ascertainment of any and all neurologic and myocardial damage in carotid revascularization: the key to optimization?

The majority of carotid revascularization procedures performed at present are in asymptomatic patients. Since such procedures convey no immediate benefit, but rather protect from future hazard, optimization of procedural safety is mandatory. The authors focus their discussion on the methodologies that assess periprocedural myocardial damage and brain injury, as used in past clinical trials, from the fields of perioperative medicine and neurovascular imaging, and discuss methodologies to reduce both events in carotid revascularization.

PERIPROCEDURAL MYOCARDIAL DAMAGE

Percutaneous coronary intervention (PCI), as a method of myocardial revascularisation, is widely and effectively used for the treatment of coronary heart disease (CHD), with immediate success rates of &gt;90%. Depending on the diagnostic criteria, 5–30% of these patients could develop the signs of periprocedural myocardial damage (PMD) or periprocedural myocardial infarction (PMI). PMD predictors, mechanisms of PMD development, and its specific clinical features play an important role in the PMI prevention. At present, there is no universal agreement on the definition and diagnostics of periprocedural myocardial necrosis and PMI, or on their impact on the clinical outcomes. According to the results of the recent studies, which are presented in this review, the current criteria of PMI might need to be modified, due to the increasingly high sensitivity of the modern threshold levels of troponin.

The prognosis of periprocedural myocardial infarction after percutaneous coronary interventions

An increase of biomarkers of myocardial necrosis is observed frequently after percutaneous coronary interventions (PCI) even when the procedure seems angiographically successful and otherwise uncomplicated. The recently updated Universal Definition of Myocardial infarction (MI) arbitrarily defined periprocedural MI (type 4a) by elevation of cardiac troponin (cTn) values >5 × the upper reference limit (URL) in patients with normal baseline values or a rise of cTn values >20% if the baseline values are elevated, together with either angina or new ECG changes or angiographic loss of patency of a coronary artery or a side branch or persistent slow or no-flow or embolization, or imaging demonstration of new loss of viable myocardium. Most frequent causes of such event are side-branch closure and/or plaque microembolization. The present review is focused on the prognostic implication of periprocedural necrosis. The risk related to a PCI-induced MI is significantly lower as compared to a spontaneous event where a similar increase of biomarkers is detected. Moreover, although an association between CK-MB elevations and adverse prognosis after PCI has been documented, existing data do not support the statement that an isolated elevation of troponins after PCI is associated with an adverse prognosis after PCI; increased troponin levels before PCI seem far more predictive of future events than a peri-procedural itself. Caution should be paid in the interpretation of clinical trials using type 4a MI as a primary endpoint. Nevertheless, patients with periprocedural myocardial damage should be treated as a higher-risk cohort, carefully monitored and receive an intensified secondary prevention program.

Troponins in the definition of myocardial infarction after percutaneous coronary interventions

The recently updated Universal Definition of Myocardial infarction (MI) arbitrarily defined periprocedural MI (type 4a) by elevation of cardiac troponin (cTn) values >5× the upper reference limit (URL) in patients with normal baseline values or a rise of cTn values >20% if the baseline values are elevated, together with either angina or new ECG changes or angiographic loss of patency of a coronary artery or a side branch or persistent slow or no-flow or embolization, or imaging demonstration of new loss of viable myocardium.Although an association between CK-MB elevations and adverse prognosis after PCI has been documented, existing data do not however support the statement that an isolated elevation of cTn after PCI is associated with an adverse prognosis after PCI; increased cTn levels before PCI seem far more predictive of future events than a periprocedural increase itself.Caution should be paid in the interpretation of clinical trials using type 4a MI as a primary endpoint. Nevertheless, patients with periprocedural myocardial damage should be treated as a higher-risk cohort, carefully monitored and receive an intensified secondary prevention program.