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Native Coronary Disease Progression Exceeds Failed Revascularization As Cause of Angina After Five Years in the Bypass Angioplasty Revascularization Investigation (BARI)

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Date 2004 Aug 18
PMID 15312856
Citations 23
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Abstract

Objectives: Coronary angiograms obtained five years following revascularization were examined to assess the extent of compromise in myocardial perfusion due to failure of revascularization versus progression of native disease.

Background: The Bypass Angioplasty Revascularization Investigation (BARI) randomized revascularization candidates between bypass surgery and angioplasty. Entry and five-year angiograms from 407 of 519 (78%) patients at four centers were analyzed.

Methods: Analysis of the distribution of coronary vessels and stenoses provided a measure of myocardial jeopardy that correlates with presence of angina. The extent to which initial benefits of revascularization were undone by failed revascularization versus native disease progression was assessed.

Results: Myocardial jeopardy fell following initial revascularization, from 60% to 17% for percutaneous coronary intervention (PCI)-treated patients compared with 60% to 7% for coronary artery bypass graft (CABG) surgery patients (p < 0.001), rebounding at five years to 25% for PCI and 20% for surgery patients (p = 0.01). Correspondingly, angina prevalence was higher at five years in PCI-treated patients than in surgery-treated patients (28% vs. 18%; p = 0.03). However, myocardial jeopardy at five years, and not initial treatment (PCI vs. surgery), was independently associated with late angina. Increased myocardial jeopardy from entry to five-year angiogram occurred in 42% of PCI-treated patients and 51% of CABG-treated patients (p = 0.06). Among the increases in myocardial jeopardy, two-thirds occurred in previously untreated arteries.

Conclusions: Native coronary disease progression occurred more often than failed revascularization in both PCI- and CABG-treated patients as a cause of jeopardized myocardium and angina recurrence. These results support intensive postrevascularization risk-factor modification.

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