Impact of calcification on percutaneous coronary intervention: MACE‐Trial 1‐year results

Abstract

Objectives The Multi‐center Prospective Study to Evaluate Outcomes of Moderate to Severely Calcified Coronary Lesions (MACE—Trial) was designed to provide further insight on the impact of calcification on procedural and long‐term percutaneous coronary intervention outcomes. Background Prior studies evaluating the impact of lesion calcification on percutaneous coronary intervention outcomes are limited by: retrospective nature, pooled data from multiple studies, or lack of specificity around calcification with only operator assessment and without core lab evaluation. Methods The MACE‐Trial was a prospective, multicenter, observational clinical study that enrolled 350 subjects at 33 sites from September 2013 to September 2015. Core lab assessed subject stratification by lesion calcification (none/mild [N = 133], moderate [N = 99], and severe [N = 114]). Endpoints were lesion success, procedural success, and 1‐year major adverse cardiac events (MACEs). Results Presence of severe calcification had significant impact on lesion success ([83.3%] versus none/mild calcification [94.7%, P = 0.006]) and procedural success ([86.8%] versus moderate [95.0%, P = 0.028], and none/mild [97.7%, P = 0.001]). 1‐year MACE rates were associated with presence of calcification in subjects with none/mild (4.7%), moderate (8.7%), and severe (24.4%) (P < 0.001) calcification; however, no difference was noted between none/mild and moderate (P = 0.237). The risk adjusted multivariable model identified severe calcification and decreasing eGFR as predictors of 30‐day and 1‐year MACE. Conclusions In this prospective study, patients with severe calcification had significantly worse outcomes compared to those without; however, unlike previous retrospective studies, moderate calcium resulted in similar outcomes as none/mild calcium. Clinical Trial Registration URL: https://clinicaltrials.gov/ct2/show/NCT01930214. Unique Identifier: NCT01930214.

Coronary lesion complexity in patients with heterozygous familial hypercholesterolemia hospitalized for acute myocardial infarction: data from the RICO survey

“…In asymptomatic FH patients, Pang et al [16] also found more calcified plaques, especially on the left main artery, and a higher calcium score using coronary computed tomography (CT). PCI are high-risk procedures when done in calcified and bifurcated lesions, and recent studies, including a metaanalysis, have shown that these complex features have a major impact on the recurrence of ischemic events and long-term mortality [30,31]. Moreover, in randomized clinical trials, the lesion complexity score was an independent predictor of short-and medium-term ischemic risk.…”

Impact of successful recanalisation of chronically occluded coronary arteries on clinical outcomes in patients with coronary artery disease

“…В другом крупном проспективном исследовании выраженная кальцификация коронарных артерий статистически значимо снижала показатели успеха процедуры и ассоциировалась с более высокой частотой серьезных неблагоприятных сердечно-сосудистых и церебральных событий через 1 год по сравнению с пациентами с отсутствием или минимальным количеством кальция (24,4 против 4,7 %, р < 0,001). При этом данное различие было обусловлено повышенным риском инфаркта миокарда (1,5 против 13,2 %, р < 0,001) и повторной реваскуляризации целевого поражения (0,0 против 6,6 %, р < 0,001) [16].…”

Breaking the deadlock of calcified coronary artery lesions: A contemporary review

“…Coronary calcification itself is an independent risk factor for stent thrombosis, ISR, and major adverse cardiovascular events (MACE) 2,3,5,28 . The MACE‐Trial evaluated the impact of lesion calcification on PCI outcomes and showed that severe calcification had significant impact on lesion success (83.3 vs 94.7% for none/mild calcification) as well as higher 1‐year MACE rates (24.4 vs 4.7% none/mild calcification) 29 . In addition, extensive calcium can also damage the polymer coating on drug eluting stents (DES) and impair delivery of drug into the vessel wall, hence contributing to long‐term risk of restenosis and target vessel failure (TVF) 4,30,31 …”