LCX culprit lesion in STEMI increased early CV death risk (30-day OR 4.64) due to longer FMC-to-diagnosis time and reduced cardiac rehab, but no impact at 5 years.
Does having the left circumflex artery as the culprit lesion increase mortality in STEMI patients?
LCX culprit lesions in STEMI are associated with increased early mortality, which appears largely driven by prolonged diagnostic delays and lower participation in cardiac rehabilitation.
Absolute Event Rate: 0% vs 0%
Abstract Introduction The left circumflex artery (LCX) has been identified as a potential factor for elevated mortality and diagnostic delays in NSTEMI. However, whether these findings also apply to STEMI for short- and long-term outcomes, remains uncertain. Material and Methods We included all patients from the EVALFAST registry, which enrolls STEMI patients transferred directly to the catheterization laboratory at Fribourg Hospital since June 2008. The primary endpoint was cardiovascular (CV) and non-CV-death at 30 days, 90 days, 1 year, and 5 years using exact logistic regression adjusted for cofounders. Secondary endpoints included time from first medical contact (FMC) to diagnosis, LVEF, and peak CK-MB using generalized linear models. Results We included 1,205 patients, with similar baseline characteristics in LCX (n=137) and non-LCX (n=1,038) groups, except for more dyslipidaemia (p=0.04) and reduced cardiac rehabilitation (23.4% vs. 33.4%, p=0.009) in LCX. Although symptom-to-FMC intervals were similar (p=0.96), LCX patients had longer FMC-to-diagnosis times (50.0 vs. 42.8 minutes, p=0.009), higher peak CK-MB (261.8 vs. 212.9, p=0.005), and paradoxically higher LVEF (52.5% vs. 46.0%, p0.001). LCX was independently associated with early CV death (30-days adjusted odds ratio OR 4.64; p0.001), though this effect partially diminished after adjusting for only for FMC-to-diagnosis (OR 2.51; p=0.021). LCX remained predictive at 90 days (p=0.008) and 1 year (p=0.016) but lost significance after accounting for cardiac rehabilitation (p0.06). By 5 years, LCX had no CV death impact, whereas rehabilitation remained protective (OR 0.53, p=0.009) (Figure 1 & 2). Non-CV deaths were similar in both groups at all time points. Conclusion LCX culprit lesion was associated with prolonged diagnostic delays, elevated peak CK-MB, reduced cardiac rehabilitation, and increased early mortality, despite higher LVEF. Extended FMC-to-diagnosis intervals and lower rehabilitation participation emerged as key drivers of mortality, emphasizing the need for prompt recognition and comprehensive post-infarct care in LCX STEMI.
Garin et al. (Sat,) reported a other. LCX culprit lesion in STEMI increased early CV death risk (30-day OR 4.64) due to longer FMC-to-diagnosis time and reduced cardiac rehab, but no impact at 5 years.