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      Improvement in coronary haemodynamics after percutaneous coronary intervention: assessment using instantaneous wave-free ratio

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          Abstract

          Objective

          To determine whether the instantaneous wave-free ratio (iFR) can detect improvement in stenosis significance after percutaneous coronary intervention (PCI) and compare this with fractional flow reserve (FFR) and whole cycle Pd/Pa.

          Design

          A prospective observational study was undertaken in elective patients scheduled for PCI with FFR ≤0.80. Intracoronary pressures were measured at rest and during adenosine-mediated vasodilatation, before and after PCI. iFR, Pd/Pa and FFR values were calculated using the validated fully automated algorithms.

          Setting

          Coronary catheter laboratories in two UK centres and one in the USA.

          Patients

          120 coronary stenoses in 112 patients were assessed. The mean age was 63±10 years, while 84% were male; 39% smokers; 33% with diabetes. Mean diameter stenosis was 68±16% by quantitative coronary angiography.

          Results

          Pre-PCI, mean FFR was 0.66±0.14, mean iFR was 0.75±0.21 and mean Pd/Pa 0.83±0.16. PCI increased all indices significantly (FFR 0.89±0.07, p<0.001; iFR 0.94±0.05, p<0.001; Pd/Pa 0.96±0.04, p<0.001). The change in iFR after intervention (0.20±0.21) was similar to ΔFFR 0.22±0.15 (p=0.25). ΔFFR and ΔiFR were significantly larger than resting ΔPd/Pa (0.13±0.16, both p<0.001). Similar incremental changes occurred in patients with a higher prevalence of risk factors for microcirculatory disease such as diabetes and hypertension.

          Conclusions

          iFR and FFR detect the changes in coronary haemodynamics elicited by PCI. FFR and iFR have a significantly larger dynamic range than resting Pd/Pa. iFR might be used to objectively document improvement in coronary haemodynamics following PCI in a similar manner to FFR.

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          Most cited references41

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          Nonoperative dilatation of coronary-artery stenosis: percutaneous transluminal coronary angioplasty.

          In percutaneous transluminal coronary angioplasty, a catheter system is introduced through a systemic artery under local anesthesia to dilate a stenotic artery by controlled inflation of a distensible balloon. Over the past 18 months, we have used this technic in 50 patients. The technic was successful in 32 patients, reducing the stenosis from a mean of 84 to 34 per cent (P less than 0.001) and the coronary-pressure gradient from a mean of 58 to 19 mm Hg (P less than 0.001). Twenty-nine patients showed improvement in cardiac function during follow-up examination. Because of acute deterioration in clinical status, emergency bypass was later necessary in five patients; three showed electrocardiographic evidence of infarcts. Patients with single-vessel disease appear to be most suitable for the procedure, and a short history of pain indicates the presence of a soft (distensible) atheroma likely to respond to dilatation. We estimate that only about 10 to 15 per cent of candidates for bypass surgery have lesions suitable for this procedure. A prospective randomized trial will be necessary to evaluate its usefulness in comparison with surgical and medical management.
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            Effects of adenosine on human coronary arterial circulation.

            Adenosine is a potent vasodilator used extensively to study the coronary circulation of animals. Its use in humans, however, has been hampered by lack of knowledge about its effects on the human coronary circulation and by concern about its safety. We investigated in humans the effects of adenosine, administered by intracoronary bolus (2-16 micrograms), intracoronary infusion (10-240 micrograms/min), or intravenous infusion (35-140 micrograms/kg/min) on coronary and systemic hemodynamics and the electrocardiogram. Coronary blood flow velocity (CBFV) was measured with a 3F coronary Doppler catheter. The maximal CBFV was determined with intracoronary papaverine (4.5 +/- 0.2.resting CBFV). In normal left coronary arteries (n = 20), 16-micrograms boluses of adenosine caused coronary hyperemia similar to that caused by papaverine (4.6 +/- 0.7.resting CBFV). In the right coronary artery (n = 5), 12-micrograms boluses caused maximal hyperemia (4.4 +/- 1.0.resting CBFV). Intracoronary boluses caused a small, brief decrease in arterial pressure (similar to that caused by papaverine) and no changes in heart rate or in the electrocardiogram. The duration of hyperemia was much shorter after adenosine than after papaverine administration. Intracoronary infusions of 80 micrograms/min or more into the left coronary artery (n = 6) also caused maximal hyperemia (4.4 +/- 0.1.resting CBFV), and doses up to 240 micrograms/min caused a minimal decrease in arterial pressure (-6 +/- 2 mm Hg) and no significant change in heart rate or in electrocardiographic variables. Intravenous infusions in normal patients (n = 25) at 140 micrograms/kg/min caused coronary vasodilation similar to that caused by papaverine in 84% of patients (4.4 +/- 0.9.resting CBFV). At submaximal infusion rates, however, CBFV often fluctuated widely. During the 140-micrograms/kg/min infusion, arterial pressure decreased 6 +/- 7 mm Hg, and heart rate increased 24 +/- 14 beats/min. One patient developed 1 cycle of 2:1 atrioventricular block, but otherwise, the electrocardiogram did not change. In eight patients with microvascular vasodilator dysfunction (delta CBFV, less than 3.5 peak/resting velocity after a maximally vasodilating dose of intracoronary papaverine), the dose-response characteristics to intracoronary boluses and intravenous infusions of adenosine were similar to those found in normal patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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              Fractional flow reserve for the assessment of nonculprit coronary artery stenoses in patients with acute myocardial infarction.

              We investigated the reliability of fractional flow reserve (FFR) of nonculprit coronary stenoses during percutaneous coronary intervention (PCI) in acute myocardial infarction. 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. One hundred one patients undergoing PCI for an acute myocardial infarction (n = 75 with ST-segment elevation myocardial infarction [STEMI], and n = 26 with non-ST-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. 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). 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. Copyright © 2010 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Heart
                Heart
                heartjnl
                heart
                Heart
                BMJ Publishing Group (BMA House, Tavistock Square, London, WC1H 9JR )
                1355-6037
                1468-201X
                1 December 2013
                18 September 2013
                : 99
                : 23
                : 1740-1748
                Affiliations
                [1 ]Imperial College London , London, UK
                [2 ]Wellstar Cardiology, North Fulton Hospital , Roswell, Georgia, USA
                [3 ]VAMC , Little Rock, Arkansas, USA
                [4 ]John Radcliffe Hospital , Oxford, UK
                [5 ]Cardiovascular Institute, Hospital Clínico San Carlos , Madrid, Spain
                [6 ]NIHR Cardiovascular Biomedical Research Unit, Royal Brompton Hospital, Imperial College , London, UK
                Author notes
                [Correspondence to ] Dr Justin E Davies, International Centre for Circulatory Health, National Heart and Lung Institute, Imperial College London, 59-61 North Wharf Road, London W2 1LA, UK; justin.davies@ 123456imperial.ac.uk
                Article
                heartjnl-2013-304387
                10.1136/heartjnl-2013-304387
                3841762
                24047640
                5f8f48ef-6c2a-4d51-b174-098d804a71c2
                Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions

                This is an Open Access article distributed in accordance withunder the terms of the Creative Commons Attribution (CC BY 3.0) license, which permits others to distribute, remix, adapt and build upon this work, for commercial use, provided the original work is properly cited. See: http://creativecommons.org/licenses/by/3.0/

                History
                : 31 May 2013
                : 7 August 2013
                : 10 August 2013
                Categories
                1506
                Coronary Revascularisation
                Original article
                Custom metadata
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                Cardiovascular Medicine
                coronary physiology
                Cardiovascular Medicine
                coronary physiology

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