Abstract
Because randomized coronary revascularization trials in stable coronary artery disease (CAD) have shown no reduced myocardial infarction (MI) or mortality, the threshold of quantitative myocardial perfusion severity was analyzed for association with reduced death, MI, or stroke after revascularization within 90 d after PET. Methods: In a prospective long-term cohort of stable CAD, regional, artery-specific, quantitative myocardial perfusion by PET, coronary revascularization within 90 d after PET, and all-cause death, MI, and stroke (DMS) at 9-y follow-up (mean ± SD, 3.0 ± 2.3 y) were analyzed by multivariate Cox regression models and propensity analysis. Results: For 3,774 sequential rest–stress PET scans, regional, artery-specific, severely reduced coronary flow capacity (CFC) (coronary flow reserve ≤ 1.27 and stress perfusion ≤ 0.83 cc/min/g) associated with 60% increased hazard ratio for major adverse cardiovascular events and 30% increased hazard of DMS that was significantly reduced by 54% associated with revascularization within 90 d after PET (P = 0.0369), compared with moderate or mild CFC, coronary flow reserve, other PET metrics or medical treatment alone. Depending on severity threshold for statistical certainty, up to 19% of this clinical cohort had CFC severity associated with reduced DMS after revascularization. Conclusion: CFC by PET provides objective, regional, artery-specific, size–severity physiologic quantification of CAD severity associated with high risk of DMS that is significantly reduced after revascularization within 90 d after PET, an association not seen for moderate to mild perfusion abnormalities or medical treatment alone.
Highlights
Cardiac PET remains underutilized despite being the gold standard for quantitative myocardial perfusion to define physiologically severity of coronary artery disease (CAD)
Clinical Follow-up As approved by our Committee For Protection of Human Subjects, prospective programmed follow-up is obtained after every PET scan systematically and continuously by a trained masked research assistant for allcause death, myocardial infarction (MI), stroke, first or repeat percutaneous intervention (PCI), or coronary artery bypass grafting (CABG) from clinic or hospital records, mailed questionnaires, phone calls, email, or web searches of newspaper obituaries as an ongoing monthly routine, repeated 3 times for initial nonresponders
Since regional precision of quantitative PET may not be widely familiar, Figure 1 illustrates a 59-y-old marathon runner with hyperlipidemia, hypertension, and family history of CAD who had early morning ventricular fibrillation, CPR by his wife, defibrillation by a 911 team, and ST elevation MI with thrombus in the patent left anterior descending coronary artery (LAD) that was stented as the culprit artery
Summary
The Weatherhead PET Center for Preventing and Reversing Atherosclerosis, McGovern Medical School, University of Texas Health Science Center at Houston, obtained 5,373 routine diagnostic rest–stress, quantitative, myocardial perfusion PET scans on sequential patients of the authors, referrals by other physicians, and self-referred patients with or at risk of CAD. Clinical Follow-up As approved by our Committee For Protection of Human Subjects, prospective programmed follow-up is obtained after every PET scan systematically and continuously by a trained masked research assistant for allcause death, MI, stroke, first or repeat percutaneous intervention (PCI), or coronary artery bypass grafting (CABG) from clinic or hospital records, mailed questionnaires, phone calls, email, or web searches of newspaper obituaries as an ongoing monthly routine, repeated 3 times for initial nonresponders. Statistical Analysis We used SAS 9.4 (SAS Institute, Inc.) for multiple Cox regression modeling of covariates of PET metrics plus other clinical characteristics for association with time to first composite MACE (PCI/CABG, DMS) or DMS or all-cause death. The rest perfusion defect was larger and more severe, comprising 36% of LV, indicating a large first diagonal branch as the source of angina, whereas LAD distribution showed excellent CFC throughout the septum and apex with no scar. On the basis of PET-quantified extent, severity, and arteryspecific location of the original MI and source of recurrent angina, a repeated angiogram showed the culprit subtotal occlusion of the diagonal branch (inset Fig. 1) that was opened with a double balloon procedure (inset) through the mesh of the LAD stent (inset) with
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