J Electrocardiol. 2026 Oct 26;99:154485. doi: 10.1016/j.jelectrocard.2026.154485. Online ahead of print.
ABSTRACT
BACKGROUND: Poor R-wave progression (PRWP) has been interpreted as a marker of anterior myocardial injury since the 1970s, but its temporal stability, substrate, and independent prognostic value in a CAD-free cohort remain uncertain.
METHODS: We studied 6323 MESA participants free of clinical cardiovascular disease with standardized 12‑lead ECGs at baseline (Exam 1, 2000-02) and after a median of 10 years (Exam 5, 2010-12). PRWP was defined as R-wave amplitude ≤3 mm in V3 with RV3 > RV2. We assessed 10-year test-retest stability (Cohen's κ), pulmonary/thoracic correlates, mechanistic substrate via cardiac magnetic resonance, high-sensitivity troponin T, NT-proBNP, and polysomnography, and long-term outcomes (all-cause death, cardiovascular death, MACE) over median 14 years using Cox and Fine-Gray models.
RESULTS: PRWP prevalence was 3.2% at Exam 1 and 6.2% at Exam 5. Binary test-retest agreement was limited (κ = 0.344; 95% CI 0.283-0.406) despite good continuous R-V3 reliability (ICC = 0.73); only 52% of baseline PRWP persisted at 10 years. Self-reported emphysema (OR 4.48; 2.30-8.22) and current smoking (OR 1.77; 1.14-2.73) were the strongest PRWP predictors. PRWP was not associated with RV volumes, RV ejection fraction, NT-proBNP, or sleep apnea. After adjustment for smoking and emphysema, PRWP was not independently associated with all-cause mortality (HR 1.19; 0.90-1.58), cardiovascular death (HR 1.02; 0.67-1.57), or MACE (HR 0.89; 0.54-1.47). Time-updated and Fine-Gray models confirmed null associations.
CONCLUSIONS: In a CAD-free multi-ethnic cohort, isolated PRWP is an ECG pattern with limited binary reproducibility, linked to pulmonary exposure and thoracic habitus rather than myocardial substrate, and carries no independent cardiovascular prognostic value.
PMID:42966028 | DOI:10.1016/j.jelectrocard.2026.154485