RESUMO
AIMS: Fractional flow reserve measurement is based upon achieving maximum hyperemia. A 40 microg intracoronary (IC) adenosine bolus sometimes seems insufficient, and we therefore sought to assess the possible role of 100-150 microg boli in routine. METHODS AND RESULTS: 108 intermediate (49+/-16%) stenoses were consecutively studied with 6F catheters. A history of myocardial infarction in the territory of the explored artery or myocardial hypertrophy were the exclusion criteria. Mean FFR was 0.82+/-0.12 with a 40 microg adenosine bolus and decreased to 0.80+/-0.12 and 0.80+/-13 respectively with 100microg and 150 microg boli (P<0.001 vs 40microg in both cases; 100 vs 150 microg, NS). The 40 microg bolus failed to diagnose 8 out of 30 (27%) significant stenoses (i.e., final FFR <0.75). The large boli led to 12 (11%) transient asymptomatic and spontaneously resolving AV blocks without other side-effects. CONCLUSION: FFR underestimated a quarter of intermediate stenoses with the currently used 40microg IC adenosine bolus. A large bolus up to 150 microg appears to be accurate and safe for routine FFR measurement.
RESUMO
The impact of blood flow reductions on the intramyocardial inotropic reserve has not yet been established in coronary artery disease (CAD). We therefore evaluated in severe CAD the relationship between positron emission tomography (PET) patterns of perfusion and glucose uptake and the corresponding tagged magnetic resonance imaging (tagged MRI) values of midmyocardial strains under low-dose dobutamine. Eighteen patients underwent tagged MRI (at rest, with dobutamine) and H2(15)O/18F-fluorodeoxyglucose PET. Regional midmyocardial circumferential shortening (Ecc) and PET patterns (normal, match viable, mismatch viable, and infarcted) were assessed in three tagged MRI/PET short-axis slices. Regional Ecc at rest correlated with both perfusion (r = 0.49) and glucose uptake (r = 0.58). The presence of the inotropic reserve was similar in normal, match viable, and infarcted (approximately 40% of regions vs. 52% in mismatch viable, P < 0.05), but the extent of the increase after dobutamine was lower in infarcted regions (P = 0.06). Within each PET pattern, regions were grouped according to their Ecc values at rest into three categories (high, intermediate, and low contractile performance). In mismatch viable (hibernation), the inotropic reserve was similar among the three categories, but in the other PET patterns the presence and extent of the inotropic reserve was higher in those regions with lowest Ecc (without significant differences in perfusion). In severe CAD, the presence of the inotropic reserve assessed by midmyocardial changes under dobutamine does not relate to resting perfusion. At a similar level of perfusion, the presence of the inotropic reserve is inversely related to contractile performance at rest, but our results suggest that it may not be true for hibernating myocardium.