Fractional flow reserve

\u3cp\u3eFractional flow reserve has become an essential tool in the modern catheterization laboratories. FFR has shown to be more accurate for the detection of ischemia than available non-invasive methods. Unlike these modalities, FFR is able to pinpoint the lesions causing ischemia, thereby achieving unequaled spatial resolution. Its use has been validated in numerous studies and different populations. It is easy to use, gives virtually dichotomous information, and is readily available worldwide. In this chapter, the principle concepts of FFR measurements to assess the hemodynamic severity of coronary artery lesions are reviewed.\u3c/p\u3

Fractional flow reserve in unstable angina and non-ST-segment elevation myocardial infarction experience from the FAME (Fractional flow reserve versus Angiography for Multivessel Evaluation) study

The use of fractional flow reserve (FFR) to guide percutaneous coronary intervention (PCI) is well established in stable angina (SA) but has not been prospectively researched in unstable angina (UA) or non–ST-segment elevation myocardial infarction (NSTEMI). The FAME (Fractional flow reserve versus Angiography for Multivessel Evaluation) study compared angiography-guided PCI with FFR-guided PCI in patients with multivessel disease and included patients with SA and UA or NSTEMI. At 2 years, the benefit of using FFR to guide PCI does not differ between patients with UA or NSTEMI, compared with patients with SA

Fractional flow reserve for the assessment of nonculprit coronary artery stenoses in patients with acute myocardial infarction

\u3cp\u3eObjectives: We investigated the reliability of fractional flow reserve (FFR) of nonculprit coronary stenoses during percutaneous coronary intervention (PCI) in acute myocardial infarction. Background Assessing the hemodynamic severity of the nonculprit coronary artery stenoses at the acute phase of a myocardial infarction could improve risk stratification and shorten the diagnostic work-up. Methods One hundred one patients undergoing PCI for an acute myocardial infarction (n = 75 with ST-segment elevation myocardial infarction [STEMI], and n = 26 with nonST-segment elevation myocardial infarction) were prospectively recruited. The FFR measurements in 112 nonculprit stenoses were obtained immediately after PCI of the culprit stenosis and were repeated 35 ± 4 days later. In addition, left ventricular ejection fraction, quantitative coronary angiographic measurements of the nonculprit stenoses, Thrombolysis In Myocardial Infarction (TIMI) flow, corrected TIMI frame count (cTFC), and the index of microcirculatory resistance (n = 14) of the nonculprit vessels were assessed in the acute phase and at control angiogram. Results The FFR value of the nonculprit stenoses did not change between the acute and follow-up (0.77 ± 0.13 vs. 0.77 ± 0.13, respectively, p = NS). In only 2 patients, the FFR value was higher than 0.8 at the acute phase and lower than 0.75 at follow-up. The TIMI flow, cTFC, percentage diameter stenosis, minimum lumen diameter, and index of microcirculatory resistance did not change. Left ventricular ejection fraction increased significantly in patients with STEMI (from 54 ± 13% to 57 ± 13%, p = 0.03). Conclusions During the acute phase of acute coronary syndromes, the severity of nonculprit coronary artery stenoses can reliably be assessed by FFR. This allows a decision about the need for additional revascularization and might contribute to a better risk stratification.\u3c/p\u3

Increased cytokine response after toll-like receptor stimulation in patients with stable coronary artery disease

\u3cp\u3eObjective: Atherosclerosis is associated with increased levels of plasma cytokines and expression of Toll-like receptors (TLRs). Yet, little is known about the potential use of TLR ligand induced cytokine release as a biomarker of coronary artery disease (CAD). In this study, we investigated whether TLR ligand induced cytokine release is associated with atherosclerotic disease severity and its predictive value for future cardiovascular events. Methods: Blood samples were obtained from 260 patients with stable angina and 15 healthy controls. Cytokine levels of TNFα, IL-8 and IL-6 were measured after 2h of whole blood stimulation with 10ng/ml lipopolysaccharide (LPS, TLR4 ligand) and P3C 500ng/ml (TLR2 ligand). In a subgroup, dose-response curves were created using additional LPS concentrations. Results: LPS induced whole blood release of TNFα and IL-6, but not IL-8, was significantly higher in patients compared to healthy controls. Among CAD patients, TLR responses did hardly differ when associated with the presence of traditional risk factors and atherosclerotic disease severity (number of diseased vessels and coronary stenosis degree). Patients with secondary events during follow-up showed a trend towards an increased TLR response. Furthermore, positive associations were found between CRP levels and TLR-induced TNFα (CRP<2: 2055pg/ml; CRP>2: 2364pg/ml) and IL-6 production (CRP<2: 1742pg/ml; CRP>2: 2250pg/ml). Conclusion: In conclusion, TLR-induced whole blood cytokine release in patients with stable angina indicates the presence of coronary atherosclerosis but does not reflect its severity.\u3c/p\u3