Assessment of the Human Coronary Collateral Circulation
2010; Lippincott Williams & Wilkins; Volume: 122; Issue: 12 Linguagem: Inglês
10.1161/circulationaha.109.930651
ISSN1524-4539
AutoresTobias Traupe, Steffen Gloekler, Stefano F. de Marchi, Gerald S. Werner, Christian Seiler,
Tópico(s)Cardiac Ischemia and Reperfusion
ResumoHomeCirculationVol. 122, No. 12Assessment of the Human Coronary Collateral Circulation Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBAssessment of the Human Coronary Collateral Circulation Tobias Traupe, MD, Steffen Gloekler, MD, Stefano F. de Marchi, MD, Gerald S. Werner, MD and Christian Seiler, MD Tobias TraupeTobias Traupe From the Department of Cardiology, University Hospital Bern, Bern, Switzerland (T.T., S.G., S.F.d.M., C.S.); and Department of Cardiology and Intensive Care Medicine, Medizinische Klinik I, Klinikum Darmstadt, Darmstadt, Germany (G.S.W.). , Steffen GloeklerSteffen Gloekler From the Department of Cardiology, University Hospital Bern, Bern, Switzerland (T.T., S.G., S.F.d.M., C.S.); and Department of Cardiology and Intensive Care Medicine, Medizinische Klinik I, Klinikum Darmstadt, Darmstadt, Germany (G.S.W.). , Stefano F. de MarchiStefano F. de Marchi From the Department of Cardiology, University Hospital Bern, Bern, Switzerland (T.T., S.G., S.F.d.M., C.S.); and Department of Cardiology and Intensive Care Medicine, Medizinische Klinik I, Klinikum Darmstadt, Darmstadt, Germany (G.S.W.). , Gerald S. WernerGerald S. Werner From the Department of Cardiology, University Hospital Bern, Bern, Switzerland (T.T., S.G., S.F.d.M., C.S.); and Department of Cardiology and Intensive Care Medicine, Medizinische Klinik I, Klinikum Darmstadt, Darmstadt, Germany (G.S.W.). and Christian SeilerChristian Seiler From the Department of Cardiology, University Hospital Bern, Bern, Switzerland (T.T., S.G., S.F.d.M., C.S.); and Department of Cardiology and Intensive Care Medicine, Medizinische Klinik I, Klinikum Darmstadt, Darmstadt, Germany (G.S.W.). Originally published21 Sep 2010https://doi.org/10.1161/CIRCULATIONAHA.109.930651Circulation. 2010;122:1210–1220Cardiovascular disease is the leading cause of death in industrialized countries and may become the most important reason for mortality worldwide.1 In patients suffering from coronary artery disease (CAD), the size of myocardial infarction mainly determines outcome.2 Accordingly, the primary strategy to reduce cardiovascular mortality is by shrinking infarct size (IS) (Figure 1A).3 In the clinical setting of acute myocardial infarction, Antoniucci et al4,5 documented in 1164 patients undergoing primary percutaneous coronary intervention (PCI) that the presence of angiographic collaterals before PCI purported a survival benefit compared with the situation without them (Figure 2). As a surrogate for IS, studies on the effect of myocardial salvage procedures have employed the magnitude of ECG ST-segment elevation during coronary balloon occlusion (Figure 3).6,7 IS, measured as the degree of ECG ST-segment elevation during a 1-minute coronary occlusion, is influenced by the following factors: duration of occlusion, ischemic area at risk for myocardial infarction (AR), collateral blood supply to the ischemic zone, ischemic preconditioning, and myocardial oxygen consumption.8 In the context of a single brief artificial coronary occlusion of uniform duration without preceding bouts of ischemia (Figure 3),6 ECG signs of ischemia are influenced predominantly by the AR and by collateral supply to this region. Furthermore, Figure 1B3 illustrates that AR and collateral supply are inversely related to each other (ie, AR tends to shrink toward zero in the presence of well-functioning collaterals). They are termed sufficient if they prevent an ECG ST-segment elevation of ≥0.1 mV during a 1-minute coronary balloon occlusion; otherwise, they are termed insufficient collaterals.Download figureDownload PowerPointFigure 1. Schematic drawing of the coronary artery circulation without (A) and with interarterial anastomoses (B) between the right coronary artery and the occluded left anterior descending artery (occluded downstream of the third diagonal branch). A, The gray area indicates the AR (finally corresponding to IS) in the case of left anterior descending artery occlusion and in the absence of collaterals. B, The AR is equal to zero because of the extended collaterals. Reprinted from Gloekler and Seiler with permission of the publisher.3 Copyright © 2007, the American Heart Association.Download figureDownload PowerPointFigure 2. Cumulative survival curves of 264 patients with acute myocardial infarction and angiographic evidence of coronary collaterals supplying the infarct area (collaterals present; solid line) compared with 900 patients without collaterals (collaterals absent; dashed line). Reprinted from Seiler5 with kind permission of Springer Science and Business Media. Copyright © 2009, Springer Science and Business Media.Download figureDownload PowerPointFigure 3. Mean aortic (Pao) and distal coronary pressure tracings during 3 consecutive 2-minute angioplasty balloon occlusions (Poccl) with corresponding intracoronary (i.c.) ECG recordings (top) showing diminishing ST-segment elevation with increasing Poccl during subsequent occlusions (ie, coronary collateral recruitment). Reprinted from Billinger et al6 with permission of the publisher. Copyright © 1999, Elsevier.The functional relevance of coronary collaterals in humans was a matter of debate for decades,9,10 most likely because of inadequate means for gauging collaterals and study populations that were too small and thus not representative of all patients with CAD.5 In the individual patient, the functional relevance of collaterals with myocardial salvage is evident in the presence of preserved left ventricular (LV) systolic function without regional wall motion abnormalities despite total proximal occlusion of a coronary artery (Figure 4).5 In regard to the collective prognostic impact of collaterals, the cumulative 10-year survival rates of patients with chronic stable CAD are significantly higher in patients with versus those without sufficient collaterals or high collateral relative to normal flow (collateral flow index [CFI]; Figure 5).11 On the basis of these prognostic benefits and the given therapeutic options of collateral growth promotion (termed arteriogenesis)12,13 and in the context of frequently unfeasible conventional revascularization options, an individual quantitative assessment of collateral function is important. The purpose of this article is to review the theoretical background and the different methods for assessment of collateral function, with a specific focus on quantitative methods (for a summary, see the Table).Download figureDownload PowerPointFigure 4. Normal LV angiogram (top middle and right panels) in a patient with proximal left anterior descending coronary artery occlusion (LAD; black arrow; top left panel). Angiography of the right coronary artery (RCA; bottom panel; anteroposterior cranial view) shows extensive collateral supply to the left anterior descending coronary artery via apical branch collaterals (white arrow) and via septal collaterals. Reprinted from Seiler5 with kind permission of Springer Science and Business Media. Copyright © 2009, Springer Science and Business Media.Download figureDownload PowerPointFigure 5. Cumulative survival rates related to all-cause (left) and cardiac (right) mortality in patients with low and with high CFI. Reprinted from Meier et al11 with permission of the publisher. Copyright © 2007, the American Heart Association.Table. Methods for Assessment of Coronary Collateral CirculationMethodPrecisionAdvantageDisadvantageConclusions/RemarksWarm-up anginaQualitativeObtainable during history takingLow prevalence not reflecting prevalence of sufficient collateralsSpecific for sufficient collateralsAngina during occlusionQualitativeEasy and cost-free; no technical equipment neededLarge interindividual and likely intraindividual variabilityHelpful for crude risk stratificationECG during occlusionQualitativeEasy and cost-free; more accurate than angina pectorisLarge interindividual variability; variable with artery examinedHelpful for crude risk stratificationRegional LV functionQualitativeWith CTO and normal LV function, no further assessment necessaryNot applicable in stenotic arteries without second catheter or simultaneous echocardiographyApplicable in CTOs, otherwise too elaborate for limited informationAngiographyQualitativeWith CTO, easy and cost-free to performOtherwise too elaborate for limited information (second catheter)Appropriate only for CTOs and crude risk stratificationWashout angiographySemiquantitativeEasy and cost-free to perform; assesses ipsilateral and contralateral collaterals; no second catheter neededOnly semiquantitativeApplicable in all coronary arteries; more accurate risk stratificationCoronary pressure (CFIp) and Doppler sensor (CFIv) measurementsQuantitativeFeasible in most arteries; robust pressure measurementsExpensive; challenging in complex anatomy (sensor wire); potential dissection or thrombotic occlusionCurrent gold standard; appropriate for risk stratification and clinical studiesCollateral perfusion measurement (collateral perfusion index)QuantitativeNoninvasive assessment with CTOComplex procedure; variable image quality; extensive postprocessing; operator dependentAppropriate for risk stratification and clinical studiesTheoretical Aspects Relevant to Assessment of Coronary CollateralsThe basic theoretical characteristics operative in the coronary circulation in general also apply to its anastomoses (ie, the collateral vessels). Oxygen is the principal nutrient for the myocardium, whose demand is determined by ventricular wall stress, heart rate, and myocardial contractility.14 Under normal metabolic conditions, oxygen extraction is close to maximal in myocardial tissue, and therefore changes in oxygen demand are regulated by altering rates of coronary blood flow (Q). According to Ohm's law, the drop in perfusion pressure (P) along increasingly smaller tubes can be described as the product of the vascular resistance (R) to flow and the flow rate Q: ΔP=R · Q. In the systemic circulation, ΔP is the difference between aortic perfusion pressure (Pao; mm Hg) and central venous pressure (CVP; mm Hg). R is mainly due to viscous friction between the blood and the vascular wall of small vessels, which can be appreciated by the fact that the pressure drop in a normal epicardial coronary tree is equal to only ≈5 mm Hg. On the basis of Ohm's law, pressure drop along the vascular path is further described by Hagen-Poiseuille's law, which specifies the components of vascular geometry contributing to its resistance against flow (R=8ηl/πr4, with l being vascular segment length, r being the vessel radius, and η being the blood viscosity). The balance between 2 energy-consuming factors related to the transport of blood (ie, the "cost" of pumping the blood through the circulation as opposed to the "cost" of building and maintaining the circulation) defines the term minimum energy dissipation, the principle of which governs the structural design of the entire coronary artery tree, including its anastomoses.15–17 With the use of various measurement techniques, normal myocardial perfusion under resting conditions has been documented to be close to 1 mL/min per gram of tissue.18 Thus, numerically (unity between the flow rate and the regional mass in grams), Q in Ohm's or Hagen-Poiseuille's law can be replaced by regional myocardial mass (M, supplied by blood at any point of interest in the coronary tree), which is equal to AR for myocardial infarction (Figure 1A). AR and M can also be defined angiographically in terms of summed coronary artery branch lengths distal to any point in the coronary tree relative to the entire coronary artery tree length.19 This definition of AR illustrates the relation between collaterals and AR (see immediately below).With regard to the absence or presence of epicardial anastomoses within the coronary tree, the traditionally held view of the normal human coronary circulation as an end-arterial system20 would have no adjacent myocardial regions with overlapping supply (Figure 1A). Thus, AR (M) would correspond to the summed coronary artery branch lengths distal to any point within the coronary tree.19 In contrast, an anastomotic system21 would be built with overlapping areas at risk by collateral arteries or arterioles extending beyond the vascular territorial borders (Figure 1B). Acutely increased oxygen requirements must be met by instantaneous augmentation of coronary blood flow, whose regulation occurs via coronary microvascular resistance changes. In the absence of collateral flow, a brief coronary artery occlusion of 1 minute normally induces a 4- to 5-fold increase in flow or flow velocity above resting level immediately after release of the occlusion. Analogous to possible collaterals crossing the boundaries of vascular territories, there also might be a functional or vasomotor response of collateral vessels to hyperemic stimuli such as brief vascular occlusion. The clinical equivalent of such functional collateral response or recruitment would be the development of tolerance to repetitive bouts of myocardial ischemia (eg, a relief of angina pectoris usually termed warm-up or walking-through angina pectoris, first described by Heberden in 180222). Aside from collateral recruitment in response to multiple episodes of ischemia (Figure 3),6 a biochemical mechanism responsible for myocardial tolerance to ischemia (ischemic preconditioning), exercise-induced permanent structural growth of coronary anastomoses (arteriogenesis), and a combination of all 3 could explain the phenomenon described by Heberden.Noninvasive Characterization of CollateralsThe aforementioned "warm-up" or "walking-through" angina pectoris is information obtained easily during the patient's history taking, which is quite specific for the presence of well-developed coronary collaterals (Table). However, its prevalence is low, and, accordingly, the sensitivity to detect well-grown collaterals is limited.5Well-established determinants of collateralization are the duration of angina pectoris and the severity of coronary artery stenoses.23,24 In chronic stable CAD, indicators for severely narrowed coronary arteries are the degree of angina pectoris, the level of physical effort at which ECG signs of ischemia or chest pain occur, and the incidence of specific ECG signs during exercise. All of the ECG signs are markers for myocardial electric stability (bradycardia) or instability during ischemia. Resting bradycardia, which is unrelated to β-blockade, may indicate collateral-promoting (ie, arteriogenic) effects due to augmented (ie, prolonged) coronary blood flow, leading to extended tangential vascular shear stress.5,25 Because of prolongation of diastole, bradycardia prolongs the period of longitudinal stretch of endothelial cells, increasing the expression of various proarteriogenic signaling pathway components.26 Indicators of repolarization heterogeneity have been documented to be valuable for assessing the collateral circulation: ECG U-wave appearance at rest or during exercise is known to point to CAD with critical arterial narrowing.27 In stable effort angina pectoris, patients with exercise-induced U-wave changes exhibit fewer ischemic ECG ST changes and less chest pain during coronary occlusion than those without.28 Additionally, the QT-interval dispersion (maximal minus minimal QT interval on a 12-lead ECG) has become a noninvasive measure for assessing the degree of myocardial repolarization heterogeneity29 and may also identify patients with sufficient coronary collaterals.30In comparison to chronic CAD and except for chronic total coronary occlusion (CTO), the setting of acute ECG ST-segment elevation myocardial infarction is much more distinctive for the purpose of noninvasive collateral assessment because the acute total coronary occlusion allows interpretation of the extent and the degree of ST-segment elevation on the basis of its contributing factors, AR and collateral supply. The initial standard 12-lead ECG provides insight into AR and collateral flow and can estimate subsequent IS,31 as follows. For anterior myocardial infarction, AR (in percentage)=4.5(number of leads with ST elevation ≥1 mm)−1.2; for inferior myocardial infarction, IS/AR=1.8(mm of ST elevation in leads II, III, aVF)+6.0. However, infarct location may no longer identify the coronary artery responsible for the event when abundant collaterals are present.The Coronary Occlusion Model: Natural Versus ArtificialAt present, invasive cardiac examination is a prerequisite for reliable quantitative assessment of the human coronary collateral circulation (Figure 6)5 because without a natural or artificial occlusion of the collateral receiving artery, the obtained blood flow reaching the downstream vascular bed or regional myocardium cannot be distinguished by its origin from the native or anastomotic path (Figure 6). In patients with CAD, approximately one third of all coronary angiograms show a CTO of a coronary artery, and only approximately half of these patients have viable myocardium in the collateralized area.32 Once an invasive examination has established the diagnosis of a CTO, the viable collateralized myocardial region can be examined noninvasively in this natural occlusion model by an array of different imaging techniques, which potentially can even measure the reference parameter for coronary blood supply, absolute tissue perfusion in milliliters per minute per gram. Because the invasive examination is needed to confirm CTO in the natural occlusion model (Figure 4), it is, on the other hand, essential for an artificial occlusion model to briefly block the vessel with an adequately sized angioplasty balloon catheter (Figure 7). The model of permanent or temporary occlusion of the epicardial collateral receiving or ipsilateral artery yields the so-called recruitable, as opposed to spontaneously visible, collateral flow (Figures 4, 6, and 7). It is most reasonable to perform the angioplasty balloon occlusion at the site of the stenosis to be treated. However, and on purely theoretical grounds, it would be most advantageous to assess the collateral circulation in an AR as large as possible (ie, at a most proximal occlusion site) because then one would account for the sum of all supplying collateral vessels.Download figureDownload PowerPointFigure 6. Schematic drawing illustrating the hemodynamic parameters needed for quantitative collateral assessment. Pressure-derived collateral quantification requires coronary occlusion and measurement of mean aortic pressure (Pao), mean distal coronary pressure (Pocc; coronary wedge pressure), and central venous or right atrial pressure (CVP). In addition, coronary volume flow rate Q for the calculation of coronary conductance can be obtained by Doppler-derived coronary flow velocity and the respective vascular caliber at the same site (combined coronary pressure/velocity measurement) or, alternatively, by myocardial contrast echocardiography–derived perfusion measurement. Curved arrows between the left anterior descending artery (LAD) and the left circumflex coronary artery (LCX) symbolize collateral arteries. Reprinted from Seiler5 with kind permission of Springer Science and Business Media. Copyright © 2009, Springer Science and Business Media.Download figureDownload PowerPointFigure 7. Right coronary angiogram with double-intubation technique (anteroposterior cranial view) in a patient with normal systolic LV function and chronic total occlusion of the proximal left anterior descending coronary artery (same patient as in Figure 4). The purpose of the left coronary intubation is to perform a balloon occlusion at the site of the recanalized chronic occlusion with positioning of a pressure sensor wire distal to the inflated balloon (see also the pressure tracings of Figure 9). The left panel is an image taken early after contrast injection; if this would be an image taken late after injection, the angiographic collateral degree would be equal to 2 (ie, part of the main artery [left anterior descending coronary artery] is filled via collaterals). The right panel is an image taken late after contrast injection; it shows complete filling of the main artery (left anterior descending coronary artery) up to the occlusion site (ie, an angiographic collateral degree of 3). The filling of only side branches of the left anterior descending coronary artery without the main artery via collaterals would be equal to an angiographic degree of 1 (not shown in this figure).In studies focusing on a single value of collateral degree or flow, there is just 1 occlusion lasting exactly 1 minute, and the measurement is obtained at the end of the occlusion. However, if the focus is on ischemic preconditioning and collateral recruitment (Figure 3),6 the duration of 1 minute for each of the repetitive occlusions is very likely insufficient to initiate protection from ischemia.33 One of the simplest but rather imprecise ways to qualify collateral function is to ask the patient about the presence of angina pectoris shortly before the end of occlusion. However, the predictive value of absent or present chest pain for the distinction between high and low quantitative collateral function is low (sensitivity and specificity to detect sufficient collaterals=60%; Table).5 It should be remembered that the severity of chest pain developed during myocardial ischemia depends on several factors, such as the duration of ischemia, the degree of recruitment of collaterals, prior transmural myocardial infarction, autonomic nerve dysfunction, psychological and neurobiological characteristics of the patient, and even the degree of stretching of the coronary arterial wall by the occluding angioplasty balloon. Irrespective of simultaneous quantitative collateral measurement, the intracoronary ECG at a threshold of ST-segment elevation ≥0.1 mV is widely accepted as a sensitive tool for the detection of ischemia.34 Accordingly, an independent dichotomous definition of coronary collateral vessels sufficient or insufficient to prevent myocardial ischemia of a briefly occluded vascular area is given by the presence or absence of intracoronary ECG ST-segment elevation ≥0.1 mV (Figure 8).5 Despite the limitation of a 1-minute compared with a 2-minute balloon occlusion,33 the intracoronary ECG ST-segment qualification of coronary collaterals is helpful in predicting long-term survival in patients with chronic CAD (Figure 9).11Download figureDownload PowerPointFigure 8. Left of pressure scale, Example of pressure/intracoronary ECG tracings from a patient with high collateral relative to normal antegrade flow (CFI) and without ECG signs of ischemia during coronary occlusion (tracings from the same patient as in Figures 4 and 8). Right of pressure scale, Example of pressure/ECG tracings from a patient with low CFI and marked ECG signs of ischemia during coronary occlusion. Pressure values are taken at 2 different scales: 160 mm Hg for the phasic and mean aortic (black thick curves) and phasic and mean coronary (red curves) pressure and 40 mm Hg for phasic and mean central venous pressure (black thin curves). On the left side of each tracing, pressure values and ECG are recorded before coronary occlusion; on the right side, pressure values and ECG are recorded during occlusion. The distal coronary pressure (red curve) declines much less in response to the occlusion in the patient with high CFI compared with that in the patient with low CFI. CFI=(Poccl−CVP)/(Pao−CVP). Reprinted from Seiler5 with kind permission of Springer Science and Business Media. Copyright © 2009, Springer Science and Business Media.Download figureDownload PowerPointFigure 9. Cumulative survival rates related to cardiac mortality in patients with or without ECG signs of myocardial ischemia on intracoronary ECG during a 1-minute coronary balloon occlusion. Myocardial ischemia is defined as ECG ST-segment elevation >0.1 mV (ST↑). Reprinted from Meier et al11 with permission of the publisher. Copyright © 2007, the American Heart Association.Even with several CTOs present, there may be an entirely normal systolic LV function because of a well-developed collateral circulation (Figure 4 and Table). However, a substantial number of CTO patients reveal various degrees of systolic LV dysfunction. The possibility of LV functional recovery with its beneficial effect on survival provides the rationale for the technically demanding attempt to recanalize a CTO.35 The recovery of impaired systolic LV function after revascularization of a CTO appears not to depend on the quality of collateral function,36 suggesting that collateral development does not depend on the presence of viable myocardium. Simultaneous assessment of regional LV function with the use of transthoracic tissue Doppler imaging and invasive collateral function has shown a statistically relevant association between systolic as well as diastolic LV function and collateral function in patients with CAD (Table).37Angiographic Collateral Assessment: Often Used but Overrated?The most widely used invasive method for assessing the coronary collateral circulation is contrast angiography because of its availability and the superior imaging quality in regard to the often small collateral vessels (Table). As opposed to the coronary patency method employed during single-vessel intubation with assessment of spontaneously visible collateral vessels, the coronary occlusion model images recruitable collaterals. With the exception of the one quarter of CAD patients with CTO encountered during coronary angiography and patients undergoing primary PCI in acute myocardial infarction, collaterals are not assessed with the occlusion model in the majority of coronary angiographies. In the presence of a CTO, predominant angiographic collateral pathways run via septal collaterals in more than two fifths of patients, in close to one fifth via distal branch collaterals, and in approximately one third via atrial collaterals with proximal take-off.38 The normal human heart and the heart affected by CAD contain numerous anastomotic vessels ranging between 40 and 200 μm.39,40 Hence, the size of the majority of these vessels is below the spatial resolution of even analog angiographic imaging chains. With modern-day digital storage media and a resolution of >0.2 mm, quantitative coronary angiography of collaterals, which would be ideal, is not applicable.41The most widely used angiographic grading system is that originally described by Rentrop et al,42 who distinguished 4 degrees of collateral recipient artery filling by radiographic contrast medium: grade 0=no collaterals; grade 1=side branch filling of the recipient artery without filling of the main epicardial artery; grade 2=partial filling of the main epicardial recipient artery; and grade 3=complete filling of the main epicardial recipient artery (Figure 7). Current qualitative methods consider further aspects of coronary collateral angiographic appearance, such as collateral flow grade, frame count, bifurcation count, collateral length grade, the relation between AR and collaterals, and collateral recipient vessel filling.43 Of note, occlusion of the collateral receiving artery clearly augments the sensitivity of detecting collateral vessels with the use of angiography (Figure 7) but renders the method of artificial occlusion technically much more demanding because of the necessity of double coronary ostial intubation (Table).A recently reported quantitative angiographic analysis of collateral diameters on high-resolution cine films has underscored the relevance of the collateral diameter for its capacity to supply blood flow in relevant volume rates.41 Moreover, a semiquantitative assessment of collaterals in patients undergoing CTO recanalization has been introduced38 with the use of the recipient filling grade according to Rentrop et al,42 their predominant anatomic location, and a new grading method of collateral connections (collateral connection grade 0=no continuous connection between collateral supplying and receiving vessel, in 14%; collateral connection grade 1=threadlike continuous connection, in 51%; collateral connection grade 2=side-branch–like connection, in 35%). A close association between collateral connection grade and invasively determined parameters of collateral hemodynamics and function has been demonstrated in the same study.38 Similarly, but without the difficulty of identifying collateral versus recipient vessels, the time (or heartbeat count or frame count) to clearance of radiographic contrast medium ("washout") trapped distal to a balloon-occluded collateral receiving artery can be determined. Washout at a threshold of 11 heartbeats accurately distinguishes between sufficient and insufficient collateral supply (sensitivity of 88%, specificity of 81%44; Table).Quantitative Coronary Pressure and Doppler Sensor Measurements: Current Gold StandardsIn addition to their principal angiographic results, Rentrop and coworkers42 first described an angioplasty balloon occlusion model using the ratio between distal coronary occlusive or wedge pressure (Poccl) and aortic pressure (Pao), which correlates with angiographic collateral score groups in patients with 1-vessel CAD.45 In 1987, Meier and coworkers46 published their work in CAD patients undergoing coronary wedge pressure measurements during PCI: A Poccl ≥30 mm Hg was found to accurately predict the presence of spontaneously visible or recruitable collaterals. However, Poccl is not only dependent on the amount of collateral flow to the temporarily or permanently occluded vascular region. Potential determinants of Poccl are the driving pressure across collateral pathway
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