Physiological assessment of coronary artery disease in the cardiac catheterization laboratory: a scientific statement from the American Heart Association Committee on Diagnostic and Interventional Cardiac Catheterization, Council on Clinical Cardiology.

With advances in technology, the physiological assessment of coronary artery disease in patients in the catheterization laboratory has become increasingly important in both clinical and research applications, but this assessment has evolved without standard nomenclature or techniques of data acquisition and measurement. Some questions regarding the interpretation, application, and outcome related to the results also remain unanswered. Accordingly, this consensus statement was designed to provide the background and evidence about physiological measurements and to describe standard methods for data acquisition and interpretation. The most common uses and support data from numerous clinical studies for the physiological assessment of coronary artery disease in the cardiac catheterization laboratory are reviewed. The goal of this statement is to provide a logical approach to the use of coronary physiological measurements in the catheterization lab to assist both clinicians and investigators in improving patient care.

Noninvasive identification of patients with early coronary atherosclerosis by assessment of digital reactive hyperemia.

OBJECTIVES: We investigated the value of reactive hyperemia peripheral arterial tonometry (RH-PAT) as a noninvasive tool to identify individuals with coronary microvascular endothelial dysfunction. BACKGROUND: Coronary endothelial dysfunction, a systemic disorder, represents an early stage of atherosclerosis; RH-PAT is a technique to assess peripheral microvascular endothelial function. METHODS: Using RH-PAT, digital pulse volume changes during reactive hyperemia were assessed in 94 patients without obstructive coronary artery disease and either normal (n = 39) or abnormal (n = 55) coronary microvascular endothelial function; RH-PAT index, a measure of reactive hyperemia, was calculated as the ratio of the digital pulse volume during reactive hyperemia divided by that at baseline. RESULTS: Average RH-PAT index was lower in patients with coronary endothelial dysfunction compared with those with normal coronary endothelial function (1.27 +/- 0.05 vs. 1.78 +/- 0.08: p < 0.001). An RH-PAT index <1.35 was found to have a sensitivity of 80% and a specificity of 85% to identify patients with coronary endothelial dysfunction. CONCLUSIONS: Digital hyperemic response, as measured by RH-PAT, is attenuated in patients with coronary microvascular endothelial dysfunction, suggesting a role for RH-PAT as a noninvasive test to identify patients with this disorder.

Pulse transmission coefficient: a nonhyperemic index for physiologic assessment of procedural success following percutaneous coronary interventions.

Intracoronary pressure measurements and the determination of fractional flow reserve (FFR) after percutaneous coronary intervention (PCI) predict adverse events. Coronary lesions may impair the transmission of pressure waves across a stenosis, potentially acting as a high-frequency filter. The pulse transmission coefficient (PTC) is a nonhyperemic parameter that calculates the transmission of high-frequency components of the pressure signal through a stenosis. It was shown recently that PTC is highly correlated with FFR. This study was designed to examine the change of PTC as compared to FFR following PCI. Pressure signals were obtained by pressure guidewire in 27 lesions pre- and post-PCI and were analyzed with an algorithm that identifies the high-frequency component in the pressure signal. The PTC was calculated at baseline as the ratio between distal and proximal high-frequency components of the pressure waveform across the lesion. FFR measurements were assessed with intracoronary adenosine. There was a significant increase in PTC following PCI (0.15 +/- 0.17 at baseline vs. 0.84 +/- 0.11 post-PCI; P < 0.001). Comparable changes were observed for FFR (0.58 +/- 0.12 at baseline vs. 0.91 +/- 0.05 post-PCI; P < 0.001). PTC is a nonhyperemic parameter for physiologic assessment of coronary artery stenoses. Similar to FFR, PTC is significantly increased following PCI. Thus, it may serve as an adjunct index for the functional assessment of procedural success following PCI.

Role of incremental doses of intracoronary adenosine for fractional flow reserve assessment.

BACKGROUND: The achievement of maximal vasodilatation of the coronary microvessels is mandatory for the accurate determination of fractional flow reserve (FFR); the optimal dosing to achieve maximal vasodilation is unclear. This study was designed to address the hypothesis that incremental doses of intracoronary adenosine are necessary to ensure complete vasodilatation of the coronary microcirculation and accurate assessment of FFR. We also examined the relationship between FFR and coronary artery disease risk factors. METHODS: A total of 191 patients (215 vessels) with intermediate coronary lesions were examined. FFR was measured during cardiac catheterization with a pressure monitoring wire. Incremental doses of intracoronary adenosine (12-42 microg, left coronary artery; 12-48 microg, right coronary artery) were administered. RESULTS: Diabetes mellitus was present in 23% of patients, hypertension was present in 65% of patients, and prior myocardial infarction had occurred in 25% of patients. The average percent stenosis in vessels was 57% +/- 15%. Vessels were subdivided on the basis of initial FFR (group 1, <0.75; group II, 0.75-0.79; group III, 0.80-0.89; group IV, >or=0.9). Five of the 24 (21%) vessels with an initial FFR in the 0.75 to 0.80 range had a subsequent FFR of <0.75. There was no difference in FFR or doses of adenosine in the patients with coronary artery disease risk factors. The average adenosine dose given at the achievement of minimal FFR was 26 microg in the right coronary artery (RCA) and 34 microg in the left coronary artery (LCA). The average maximum dose of intracoronary adenosine administered was 29 microg for the RCA and 37 microg for the LCA. The maximum dose of adenosine ever required to achieve minimum FFR was 42 microg in both the LCA and RCA. CONCLUSION: This study suggests that a single high dose of 42 microg of intracoronary adenosine for both the RCA and LCA is sufficient to achieve maximum hyperemia and accurate FFR in most patients, independent of risk factors. Alternatively, when a lower initial dose is administered and FFR is in the 0.75 to 0.90 range, incremental doses of adenosine should be administered to ensure maximal hyperemia.