Injury In Percutaneous Coronary Intervention Research Articles

Cost to Medicare of acute kidney injury in percutaneous coronary intervention

Acute kidney injury (AKI), including contrast-induced AKI (CI-AKI), is an important complication of percutaneous coronary intervention (PCI), resulting in short- and long-term adverse clinical outcomes. While prior research has reported an increased cost burden to hospitals from CI-AKI, the incremental cost to payers remains unknown. Understanding this incremental cost may inform decisions and even policy in the future. The objective of this study was to estimate the short- and long-term cost to Medicare of AKI overall, and specifically CI-AKI, in PCI. Patients undergoing inpatient PCI between January 2017 and June 2020 were selected from Medicare 100% fee-for-service data. Baseline clinical characteristics, PCI lesion/procedural characteristics, and AKI/CI-AKI during the PCI admission, were identified from diagnosis and procedure codes. Poisson regression, generalized linear modelling, and longitudinal mixed effects modelling, in full and propensity-matched cohorts, were used to compare PCI admission length of stay (LOS) and cost (Medicare paid amount inflated to 2022 US$), as well as total costs during 1-year following PCI, between AKI and non-AKI patients. The study cohort included 509,039 patients, of whom 104,033 (20.4%) were diagnosed with AKI and 9,691 (1.9%) with CI-AKI. In the full cohort, AKI was associated with+4.12 (95% confidence interval=4.10, 4.15) days index PCI admission LOS, +$11,313 ($11,093, $11,534) index admission costs, and +$14,800 ($14,359, $15,241) total 1-year costs. CI-AKI was associated with+3.03 (2.97, 3.08) days LOS, +$6,566 ($6,148, $6,984) index admission costs, and +$13,381 ($12,118, $14,644) cumulative 1-year costs (all results are adjusted for baseline characteristics). Results from the propensity-matched analyses were similar. AKI, and specifically CI-AKI, during PCI is associated with significantly longer PCI admission LOS, PCI admission costs, and long-terms costs.

When Prevention is Truly Better than Cure: Contrast-Associated Acute Kidney Injury in Percutaneous Coronary Intervention.

Contrast-associated acute kidney injury (CA-AKI) is a fairly frequent complication of cardiovascular angiography and percutaneous coronary intervention (PCI). The risk is significantly higher in patients with advanced chronic kidney disease (CKD). Prevention is the only option for avoiding the significant morbidity and mortality associated with CA-AKI. This review provides a concise and clinically directed appraisal of the latest pre-procedural and peri-procedural strategies to minimize the risk of CA-AKI in all patients undergoing PCI. By broadly implementing these evidence-based care bundles, we can dramatically improve outcomes in this vulnerable patient population.

Colchicine to Prevent Periprocedural Myocardial Injury in Percutaneous Coronary Intervention: The COPE-PCI Pilot Trial.

Periprocedural myocardial infarction and injury (PM-injury) are the most common complications of percutaneous coronary intervention (PCI) and are associated with future adverse cardiac events. Inflammation plays a pivotal role in the development of PM-injury. In this randomized pilot trial, we assessed the effect of an anti-inflammatory medication colchicine on periprocedural myocardial injury. Patients undergoing PCI for stable angina or non–ST-segment–elevation myocardial infarction were randomized to oral colchicine (1 mg followed by 0.5 mg 1 hour later) or placebo, 6 to 24 hours preprocedure. Blood samples were taken immediately pre- and 24-hours post-PCI. The primary outcome, periprocedural myocardial infarction, was defined by an increase in post-PCI troponin >5×99th% upper reference limit when the pre-PCI troponin was normal, or >20% increase in post-PCI troponin when the pre-PCI troponin was raised, including supporting evidence of new myocardial ischemia. Major PM-injury was defined as per periprocedural myocardial infarction without supporting evidence of new myocardial ischemia. Minor PM-injury was defined by post-PCI troponin increase >99th% upper reference limit but ≤5×99th% upper reference limit. A total of 196 patients met inclusion criteria and were randomized. One hundred twenty-one patients were excluded (no PCI, unstable troponin before PCI, or poor-quality measurements) leaving a study population of 75 patients. Thirty-six patients were randomized to colchicine and 39 to placebo preprocedure. Forty-four presented with non–ST-segment–elevation myocardial infarction and 31 with stable angina. High-sensitive (hs) troponin-I pre-PCI was similar between treatment groups (colchicine: 79 ng/L [4–1336] versus placebo: 35 [5–448], P=0.42). Absolute change in hs-troponin-I (calculated as 24-hour post-PCI minus pre-PCI measurements) was significantly lower in the colchicine group: 59 (1–221) versus placebo: 166 (53–530), P=0.02. No patients developed periprocedural myocardial infarction in either group. Significantly fewer patients developed major PM-injury: 11 (31%) versus 21 (54%), P=0.04 or minor PM-injury: 21 (58%) versus 33 (85%), P=0.01, if given colchicine pre-PCI. In this randomized pilot trial, colchicine given 6 to 24 hours pre-PCI reduces periprocedural myocardial injury.

Профилактика перипроцедурного повреждения почек нагрузочными дозами статинов при плановых чрескожных коронарных вмешательствах

To compare the effect of loading doses of atorvastatin and rosuvastatin on the value of the acute kidney injury and acute inflammatory response to elective percutaneous coronary interventions. An open prospective comparative study included 68 patients referred for elective percutaneous coronary intervention (PCI). At baseline, all patients had been taking statins for a long time as a standard lipid-lowering therapy. The first group included 33 patients who received a loading dose of 80 mg of atorvastatin (As) 12 hours before the intervention with saving this dose for 2-6 days. The second group included 35 patients treated with rosuvastatin (Rs) 40 mg / day in the same manner. The levels of creatinine and cystatin C in the blood were determined at baseline and 12, 24, 48 and 72 hours after the intervention. HsCRP level was determined at baseline and 72 hours after PCI. AKI was diagnosed in 5 patients (7.94 %): 4 patients (12.1 %) in group As and 1 patient (3.3 %) in group Rs (p = 0.36). The increase of serum creatinine level in the group As patients was 43.4 % higher than one in the Rs group patients (p = 0.024). The decrease of glomerular filtration rate (GFR) in group As was 15.5 % higher than one in group Rs (p = 0.09). Initially, the level of cystatin C in the groups did not differ (698.9 (560.2-869.6) ng / ml in group As vs 759.5 (673.8-899.9) ng/ml in group Rs, p = 0.75). Significant intergroup differences were found in the level of serum cystatin C 12 hours after PCI (718.3 (555.6-839.6) ng/ml in group As vs 470.6 (378.2-689.4) ng/ml in the Rs group, p = 0.007) that persisted 24 hours after the intervention (732.1 (632.3-887) ng/ml vs 526.4 (357.4-802.7) ng/ml, respectively, p = 0.02). From the second day after PCI, intergroup differences in serum cystatin C disappeared. The level of hsCRP significantly increased 72 hours after the intervention in group As (1.65 (0.9-4) mg/l at baseline vs 4.55 (1.6-8.7) mg/l 72 hours after PCI, p = 0.01). The level of hsCRP did not change significantly at the same time in the Rs group (2.8 (0.8-6.8) mg/l at baseline vs 2.75 (1.5-6.5) mg/l 72 hours after PCI, p = 0.16). The loading dose of rosuvastatin better prevents periprocedural kidney injury in PCI and more significantly reduces the overall inflammatory response to intervention compared to the loading dose of atorvastatin.

Pharmacological Prevention of Peri-, and Post-Procedural Myocardial Injury in Percutaneous Coronary Intervention

In recent years, percutaneous coronary intervention (PCI) has become a well-established technique for the treatment of coronary artery disease. PCI improves symptoms in patients with coronary artery disease and it has been increasing safety of procedures. However, peri- and post-procedural myocardial injury, including angiographical slow coronary flow, microvascular embolization, and elevated levels of cardiac enzyme, such as creatine kinase and troponin-T and -I, has also been reported even in elective cases. Furthermore, myocardial reperfusion injury at the beginning of myocardial reperfusion, which causes tissue damage and cardiac dysfunction, may occur in cases of acute coronary syndrome. Because patients with myocardial injury is related to larger myocardial infarction and have a worse long-term prognosis than those without myocardial injury, it is important to prevent myocardial injury during and/or after PCI in patients with coronary artery disease. To date, many studies have demonstrated that adjunctive pharmacological treatment suppresses myocardial injury and increases coronary blood flow during PCI procedures. In this review, we highlight the usefulness of pharmacological treatment in combination with PCI in attenuating myocardial injury in patients with coronary artery disease.