history of coronary scoring

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1 Coronary Scoring Systems A Historical Perspective Merril Knudtson, MD Background The coronary artery reporting system adopted by APPROACH © between 1995 and 2008 was based upon the graphic tool known as Heartview © with modifications from the literature to increase the tool’s precision. 1 A new graphic coronary anatomy and intervention reporting tool called CARAT © (Coronary Artery Reporting and Archiving Tool) has been developed for use by APPRAOCH to achieve, inter alia, the following anatomical reporting goals: 1. To capture greater patient-level detail 2. To develop a clinically relevant expression of lesion severity 3. To present a credible expression of the size and location of the myocardial bed supplied by diseased arteries 4. To abandon the historic three-region (anterolateral, lateral and posterolateral) LV model in favour of the 17-segment model currently adopted by most cardiac imaging systems. 2 This document summarizes observations from literature reports that influenced the design of CARAT © with summary comments concerning how this information was used. Classifying Lesion Severity – What’s in a number? Although attempts have been made to create more complicated and ‘granular’ lesion severity grading systems, none of these have improved upon the early lesion severity categorization of Oberman et al (1972) 3 . These clinically important severity ranges are explained below (see also Figure below): <50% diameter reduction. Lesions in this range are very unlikely to have hemodynamic and clinical significance based upon severity alone and further severity subdivisions within this range have no proven value. >50% and <70% diameter reduction. Lesions in this range are of borderline hemodynamic and clinical significance but 35% were found to have a compromised hyperemic response in one large series 4 . This is an important range to capture from a clinical perspective for interventions on lesions in this range would benefit from confirmation of their

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Page 1: History of Coronary Scoring

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Coronary Scoring Systems A Historical Perspective

Merril Knudtson, MD

Background The coronary artery reporting system adopted by APPROACH © between 1995 and 2008 was based upon the graphic tool known as Heartview © with modifications from the literature to increase the tool’s precision.1 A new graphic coronary anatomy and intervention reporting tool called CARAT © (Coronary Artery Reporting and Archiving Tool) has been developed for use by APPRAOCH to achieve, inter alia, the following anatomical reporting goals:

1. To capture greater patient-level detail 2. To develop a clinically relevant expression of lesion severity 3. To present a credible expression of the size and location of the myocardial

bed supplied by diseased arteries 4. To abandon the historic three-region (anterolateral, lateral and

posterolateral) LV model in favour of the 17-segment model currently adopted by most cardiac imaging systems.2

This document summarizes observations from literature reports that influenced the design of CARAT © with summary comments concerning how this information was used. Classifying Lesion Severity – What’s in a number? Although attempts have been made to create more complicated and ‘granular’ lesion severity grading systems, none of these have improved upon the early lesion severity categorization of Oberman et al (1972)3. These clinically important severity ranges are explained below (see also Figure below):

• <50% diameter reduction. Lesions in this range are very unlikely to have hemodynamic and clinical significance based upon severity alone and further severity subdivisions within this range have no proven value.

• >50% and <70% diameter reduction. Lesions in this range are of borderline hemodynamic and clinical significance but 35% were found to have a compromised hyperemic response in one large series4. This is an important range to capture from a clinical perspective for interventions on lesions in this range would benefit from confirmation of their

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hemodynamic significance by prior non-invasive testing or by FFR assessment at the time of angiography.

• >70% but <100%. Almost all lesions in this range are hemodynamically significant, thus seeking supplementary confirmation of hemodynamic significance is not warranted in most cases. Further there is no established benefit to assigning a more precise stenosis grade within this range. Gould5-7 has shown that the hyperemic response falls off geometrically in the 65-85% diameter reduction range, a range that Gensini refers to as “the resistance elbow”. In this range, angiography simply lacks adequate discriminating power. Lesions >85% may demonstrate reduced flow at rest, the apparent justification for the addition of a “90-99%” category by some investigators8-11, but it is not clear whether this category is clinically useful.

• 100%. A separate category for completely occluded vessels is warranted for multiple clinical and therapeutic reasons.

0 10 20 30 40 50 60 70 80 90 100

0 10 20 30 40 50 60 70 80 90 100 Luminal Diameter Reduction (%)

If a single threshold for clinical significance were adopted, the literature is divided on whether this threshold should be 50% 3, 8, 12-14 or 75%1, 9, 15, 16. Clearly the 70% cutoff has the greatest physiologic support 7, 15 and has been labeled the “gold standard” threshold for clinical significance7. Rather than accepting a fixed threshold for significance, several investigators have assigned a lesion score that is graded by lesion severity 13, 16-19. This graded value is then used alone, or used as a multiplier along with some expression of myocardial territory at risk, with the belief that a graded valuation and/or a

>70%

50-70%

<50%

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combined score is a more sensitive and reliable outcome predictor than a binary designation of significance. The 7 published lesion-weighting systems are listed below with the score shown in bold print beside the severity ranges used:

• 1 = <50%; 2= 50-90% single lesion; 3=50-90% multiple lesions; 4=90%; 5=100% 20

• 1=Trivial; 2=<50%; 3=50-75%; 4=75-90%; 5=100% 3 • 1=<50%; 2=50-75%; 3=75-99%; 4=100% 17, 19, 21, 22 • 0.2=<50%; 0.4=50-75%; 0.6=75-90%; 0.8=90-99%; 1.0=100% 16 • 1=70-90%; 3=90-99%; 5=100% 18 • 1=25-50%; 2=50-75%; 4=75-90%; 8=90-99%; 16=100% 10 • 0=<50%; 2=50-99%; 5=100% 13

The lesion range weighting scores above lack appropriate validation and face validity. For example, it is not clear why a 100% occlusion, usually associated with collateral support and frequently associated with an area of prior infarction, should be given a consistently higher weighting than more vulnerable lesions in the 70-90% range. APPROACH has not adopted a weighting system based upon diameter severity and will employ the single threshold stenosis value of 75% (50% for LM). As 50%, 70% and 100% luminal diameter obstruction thresholds have clinical utility and a strong evidence base, is there clinical value in including other intermediate severity levels in a clinical scoring system? It has been shown that simple visual estimates of severity, particularly in more severe lesions, have a stronger correlation with baseline exercise test performance than automated quantitative techniques 23. One may conclude from this that there be value in providing 60, 80 and 90% options to angiographers in order to allow expression of their clinically integrated impressions of lesion severity. A “60%” designation, for example, may be selected as a cautionary statement of borderline severity. There is no value in attempting to sub-classify lesion severity in the <50% range; a simple statement of the existence of angiographically identifiable disease should suffice19. Also, a strategy of intervening on lesions <50% has been discredited24. Myocardial Jeopardy – A critical dimension From the earliest days of angiography, estimations of the amount of myocardium supplied by diseased coronary vessels and the impact of these estimates on treatment and outcome have received close study20, 25 Initially these estimates were based upon a simple statement of the number of diseased major epicardial vessels8, but the lack of precision of this approach soon became evident and

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adjustments were made for the dominant influence of proximal LAD and LM disease8, 26. In the later part of the 1970’s standardized myocardial templates were developed and used in natural history studies, but the wide anatomic variability seen between individual patients in clinical practice pointed to the obvious deficiencies in these over simplified models. Unfortunately precise measurement of the relative amounts of LV myocardium supplied by each major epicardial artery is available from a single pathologic study, that of Kalbfleisch and Hort (1977)27. The following table indicates the percentage of the LV volume assigned to each major epicardial artery in five classic clinical studies as well as the landmark pathology measurements of Kalbfleisch and Hort. The variable size of LCx and RCA distributions in these studies is not surprising due to the wide variability in the source of blood supply the posterolateral LV free wall.

LAD LCx RCA Alderman et al (1992)12 48 28 24 Gensini (1975)17 42 42 16 Brandt (1977)16 47 40 13 Jenkins (1978)21 43 29 28 Dash (1977)14 50 33 17 Kalbfleisch & Hort (1977)27 49-53 18-27 18-33 The table below indicates the percentage of the LV volume attributed to the septum as well as the anterior, lateral and posterolateral free wall territories in three clinical models along with the pathological work of Kalbfleisch and Hort.

Anterior Lateral Inferolateral Septum Brandt (1977)16 13 20 20 47 Dash (1977)14 17 17 17 49 Graham (2006)1 20 19 19 42 Fulton (1952)28 - - - 31 Lorenz (1999)29 - - - 34 Kalbfleisch & Hort (1977)27

27-32 18-27 9-22 34 (2/3 LAD) Assumed

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Challenges in quantifying septal coronary flow Recent imaging studies are consistent with pathologic studies over the last 80 years that the septum accounts for 31-34% of the LV mass28, 30, 31. Unfortunately, it is equally clear that the relative contribution of LAD and PDA septal perforators to septal blood flow is highly variable and remains difficult to measure or estimate due to their large number and variable size and location. Based upon an autopsy series of 31 patients, James et al (1958) reported that the LAD provided 60-70% of septum in 23% of patients, 70-80% of patients in 29% and 80-90% of patients in 48%.32 (Although this report did not give individual anatomic detail, one would suspect that the third group included patients with a Type 3 LAD or a ‘septal arcade’ variant.) A Canadian autopsy series of 12 human hearts reported that the LAD supplied 50% of the septum in half of the specimens and 2/3 of the septum in the remaining half.33 The review of Smith (1962) stated that the LAD contribution to septal blood flow was two-thirds30, and this estimate continues to receive wide support. Assigning relative contributions of LAD and PDA perforator flow to this substantial and functionally important part of the LV myocardium remains a challenge. Alderman et al (1992) in the angiographic methods used by the BARI study assigned 3 of the 5 septal points (60%) to the LAD, 2 of these points to the largest perforator.12 Toward an optimal myocardium-focused coronary reporting tool The reporting strategies summarized in this document have had modest value in evaluating group behavior in clinical trails and epidemiologic investigations, but they all lack precision and have significant shortcomings in capturing individual patient variability. The following features are desirable in a reporting tool:

1. Variability in the number, size and location of LV free wall branches should be provided for with dynamic adjustment of the amount and regional location of myocardium assigned to each1, 12, 16.

2. Allow for variation in length of distal LAD (Types 1-3)1. 3. Characterize the geometry and size of LV segments in the 17-segment

model. Currently jeopardy calculations in CARAT assume a size of 6% for each segment. This value could be easily substituted for by actual CMR measurements in normal hearts, when they are available.

4. Capture the variations in RCA and LCx supply of posterolateral LV. 5. Allow for anomalous coronary origins and pathways.

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6. Capture the variable contribution of anterior septals from LAD (variation from 50 – 90%) and inferior septals from PDA (variation from 10 to 33%) to the interventricular septum. There is no literature that would help in making this decision.

Diffuseness of Coronary Disease – Is it measurable? Although pathologic studies have consistently shown a strong correlation between the endothelial extent of atherosclerosis and the severity of lipid disorders and other risk factors19, 34, attempts to develop clinically useful measures of diffuseness of atherosclerosis continue to be disappointing10.

Literature Summary

• Parker et al (1966) – Kingston, Ontario 25 o Purpose – Correlate angiographic severity with prior MI, symptoms

and resting ECG changes o Coronary Score

• Lesion Grade (Variable) • Grade 1 - <50% area stenosis; • Grade 2 - >50% area stenosis but <100%; • Grade 3 – 100%

• LV Extent • Number of major vessels with > Grade 2 lesions

o Conclusions • 100% occlusion correlated with prior MI • Presence of symptoms and resting ECG changes correlated

with severe multi-vessel disease • No correlation of variable lesion grade with outcome • Historical importance – this Canadian centre was the first to

report association of CAD extent and clinical status

• Friesinger et al (1970) – Vanderbilt 20 o Purpose – Establish a coronary scoring system that will permit

anatomy correlation with outcome o Coronary Score

• Lesion Grade (Variable) • 0 – no disease; • 1 – lesions <50% area stenosis; • 2 – single lesion >50% but <90%; • 3 – multiple lesions >50% but <90%; • 4 – 90%; • 5 – 100%.

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• LV Extent • Three regions: LAD, LCx and RCA

• Score calculation • Friesinger Score - Sum of most severe lesion grade

1 to 5) for each of 3 regions o Maximum score total is 15.

o Conclusions • The coronary score was a stronger predictor of mortality

than all measured clinical factors •

• Manuscript does not validate lesion grading system used

• Oberman et al (1972) – Birmingham 3 o Purpose – Establish correlation between lesion severity and

subsequent mortality o Coronary Score

• Lesion Grade (Variable) • 1 – trivial disease; • 2 – lesions < 50% diameter reduction; • 3 – 50 – 75%; • 4 – 75 – 90%; • 5 – 100%

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• LV Extent • LAD, RCA and LCX divided into proximal and distal

segments and graded separately. LM treated as 1 segment. Total segments possible – 7.

• Number of diseased vessels • Score calculation

• Oberman Score - Sum of lesion grade for each of the 7 individual segments. (A LM lesion is given the sum of scores for LAD plus LCx.)

o Maximum score is 35 • Number of diseased major vessels with diameter

stenosis >50% (0-3) o Conclusions

• Confirms correlation of 2 and 3-vessel disease with mortality, but minor effect with 1 vessel disease.

• There was a mortality multiplying effect if CHF present. • Of note, the Oberman Score described above was not used

in the analysis, only the number of diseased vessels.

• Bruschke et al (1973) – Cleveland 8 o Purpose – Correlate mortality over 4 years with number of diseased

vessels in patients not treated with CABG o Coronary Score

• Lesion Grade (Fixed) • Diameter reduction >50% defines significant disease • Grading system: normal, <30%, 30-50%, 50-90%,

>90% and 100% • LV Extent

• Number of major vessels (0-3) o Conclusions

• Mortality increases with number of diseased vessels. • Single vessel disease mortality not significantly influenced by

lesions <50% in other vessels.

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o

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• Brymer et al (1974) – Ann Arbor, Michigan 26 o Purpose – Correlate coronary anatomy with outcome o Coronary Score

• See Friesinger Score • Also - number of diseased vessels (>50% area reduction)

with and without LAD involvement o Conclusions

• Significant influence of proximal LAD disease on mortality when added to number of diseased vessels or to Friesinger score.

• Gould et al (1974, 1974 and 2009) - Houston 5-7

o Purpose – Animal work correlating diameter stenosis to reduction in flow

o Conclusions o 50-85% diameter stenosis defines threshold for clinical

significance (Hyperemic response starts to diminish >50% ldr with resting flow reduced when ldr is >85%)

o Propose >70% as the “gold standard” for defining a single significant clinical endpoint

o 65-95% diameter stenosis needed to see impaired flow, but angiographic measurement limitations do not allow finer discrimination within this range

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• Gensini G.G. (1975) – Syracuse 17 o Purpose – Description of a Coronary Artery Disease Scoring and

Retrieval System (Cardscores). The system was intended to take into account: (1) Geometrically increasing severity of lesions – 25, 50, 75, 90, 99 and 100% diameter reduction; (2) cumulative effect of multiple lesions; (3) lesion location; (4) influence of collaterals; (b) vessel graftability.

o Coronary Score – • Severity score – With each step in the 25 – 50 – 75 – 90 –

99 – 100% diameter reduction progression, the impact on flow doubles in accordance with Poiseuille’s law. As a result severity scores for lesions in this progression were assigned the values 1 – 2 – 4 – 8 – 16 – 32.

• Region multiplying factors for coronary segments were designated to express the relative amount of myocardium supplied by a diseased segment (see diagram)

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• Collateral factor – The severity score adjustment for

collaterals is indicated on the right side of the table below. The adjustment is reduced by the extent of disease in the vessel that is the source of collaterals (left column).

• Gensini Score Calculation: severity score X the segment

location multiplying factor X Collateral adjustment factor

• Brandt et al (1977) – Auckland, NZ16 o Purpose – Propose a flexible myocardial reporting and scoring

model o Scoring System

• Grade of Stenosis severity (x-sectional area) • 100 % - Correction value = 1.0 • 90-99% - Correction value = 0.8 • 75-90% - Correction value = 0.6 • 50-75% - Correction value = 0.4 • <50% - Correction value = 0.2

• Myocardial Value • The Green Lane Model was loosely based upon the

definitions of WG Austen et al 35 and the 15 point scoring system of GC Friesinger et al 20, modified by a 5-region diagram used by Auckland radiologists to diagram coronary anatomy. The regions are LAD septum, PDA septum, diagonal region, marginal region and posterolateral region and the percentage of LV myocardium assigned to each region is listed below:

o LAD septum -30% (Value – 5) o PDA septum -17% (Value – 2) o Diagonals -13% (Value – 2) o Marginals -20% (Value – 3) o Posterolaterals -20% (Value – 3)

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• The angiographer draws the location of LV free wall branches on a template of the above 5 regions and the percentage area of each region supplied by each diseased vessel is estimate visually (see diagram below).

• Myocardial Score - The myocardial value of each diseased artery is multiplied by the Stenosis Severity Correction value and is then summed to obtain the Myocardial Score. This is an expression of the combined influence of jeopardized myocadial area and stenosis severity.

• The LV myocardium percentages specified above are similar to Kalbfleish and Hort (1977) and Dash (1977), but perhaps undervalue the PDA and overvalue the circumflex contributions.

o Conclusions • Rationale for specified stenosis grading not given in paper • An elegant but operator dependent scoring system

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• Kalbfleisch and Hort – 1977 - Marburg an der Lahn, Germany 27 This is an elegant and landmark pathologic study of the amount of myocardium supplied by the left anterior descending, circumflex and right coronary arteries in 171 human hearts. The hearts were categorized by “vascular type”: “left coronary type” with LCA supplying all of LV (left dominant system); “RCA type” with RCA supplying only the posterior-septal wall (co-dominant system); and three “normal” types in which the RCA and LCx both supply variable portions of the posterior wall (right dominant systems). Based upon this data, the following regional LV mass calculations can be reasoned for the five Green Lane regions. The LAD-PDA septum division was calculated using the Green Lane 64:36 split of LAD and PDA blood supply to the septum.

o LAD (Anterior septum and adjacent Ant. Wall) -32% o PDA (Inferior septum and adjacent PL wall) -18% o Diagonals -15% o Marginals -18% o Posterolaterals -17%

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• Dash et al (1977) – Harvard 14 o Purpose

Coronary anatomy - LV function correlation Does the development and extent of ischemic

cardiomyopathy correlate with coronary anatomy? o Coronary Score

Lesion Grade (Fixed) • Primary threshold level - “Significant” defined as

Area reduction >70% LV Extent

• Two points are assigned to each of 6 specified segments with a significant proximal stenosis (see diagram below). The territory assignments are clear except dLAD (1) is unspecified but is likely a combination of anterior wall and septum.

o Conclusions An angiographic scoring system grade based upon

myocardial volume at risk is a better predictor of ischemic cardiomyopathy development than a 1, 2 or 3 vessel disease classification.

Paper does not specify the basis for the jeopardy scoring system but is very similar to Kalbfleisch and Hort (1977)

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• Proudfit et al (1978) – Cleveland 11 o Purpose - Explore association of clinical and angiographic variables

with 5-9 year survival in a cohort of 600 non-surgical patients. o Coronary Score

Lesion grade - diameter reduction • < 30% • 30-50% • 50-90% - Primary threshold level • Subtotal • 100%

o Conclusions Mortality increases with the number of vessels with diameter

lesions > 50% In patients with 2 and 3 vessel disease who are referred for

surgery, complete revascularization is associated with a better survival than patients incompletely revascularized

• Jenkins et al (1978) – Victoria, Australia 21

Purpose - Correlate serum cholesterol with angiographic extent of disease

o Coronary Score Lesion Grade

• 1 - <50% luminal diameter reduction • 2 – 50-75% • 3 – 75-99% • 4 – 100%

LV Extent – 8 proximal coronary segments analyzed Gensini score – sum of lesion grade for each of 8

segments

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o Conclusions Serum lipids correlate with extent of coronary disease

• Harris et al (1980) – Duke 9

o Purpose - To determine the incremental influence of 50% lesions on survival in 1183 medically treated patients with 1, 2 or 3 vessels (lesions greater than 75% luminal diameter reduction)

o Coronary Score Lesion grade - diameter reduction

• <25% • 25% • 50% - Secondary threshold level • 75% - Primary threshold level • 90% • 100%

o Conclusions The presence of one or more lesions of 50% severity was

not associated with an increased mortality in patients with 1, 2 or 3 vessels with 75% lesions.

• Lee et al – 1981 - Duke 36

o Purpose –Study of 18 autopsy human hearts confirming the correlation of relative infarction size and vessel distribution area.

o Results The ischemic bed sizes by major coronary region were:

• Circumflex -30% (varied from 21% to 43%) • RCA -32% (varied from 24% to 37%) • LAD -44% (varied from 29% to 66%)

o Conclusions Although this is a small study that does not provide enough

detail to arrive at a 5-region breakdown of myocardial mass, the study presents an important confirmation that infarct size correlates closely with the regional LV mass.

• Leaman et al (1981) – Rotterdam 18

o Purpose To fashion a coronary scoring system that takes into account

lesion severity and distribution area. To evaluate the score as a means to predict symptoms and

LV function

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o Coronary Score Lesion grade – diameter reduction

• 70-90% • 90-99% • 100%

LV Weighing Factor – see diagram – after Gensini (1975) Leaman Score Calculation - Multiply lesion score by

weighting factor for each segment

o Conclusions\ Symptoms and LV function do not correlate with this score. No supporting comments on the validity of magnifying the

LV weighting factor by the lesion severity.

• White et al (1984) – Iowa City37 o Purpose – Does lesion angiographic severity predict maximum

hyperemic response o Methodology

Correlate caliper-assistant diameter measurements with hyperemic flow Doppler measurements

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o Conclusions Poor correlation between angiographic lesion severity and

physiologic maximal hyperemic response as measured by flow Doppler

• Reardon et al (1985) – Victoria, Australia 19

o Purpose - Correlate lipid concentrations with coronary severity o Coronary Score – Gensini score (See Jenkins et al (1978)

Lesion grade • 1 - <50% luminal diameter reduction • 2 – 50-75% • 3 – 75-99% • 4 – 100%

LV Extent – 8 Segment method o Conclusion

22% of the variation in coronary severity can be accounted for by lipid concentrations

• Califf et al (1985) – Duke 38

o Purpose Prognostic value of Jeopardy score Incremental value of score over coding number of diseased

arteries o Coronary Score

Lesion grade • Diameter stenosis >75% considered significant

(rather than >50% used in work of Harris et al (1978) LV Extent

• Uses the Dash et al (1977) 6-segment grading system Score Calculation

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o Conclusions Jeopardy score is an improvement over classifying CAD

severity on basis of number of diseased arteries Further refinement needed, in particular paying more

attention to pLAD disease and other anatomic factors

• Hamsten et al (1986) – Stockholm, Sweden 10 o Purpose

Correlate lipoprotein risk factors with angiographic score Score designed to capture disease diffuseness/extent

o Coronary Score Segments – 15 proximal segments (AHA) Diffuseness score – Hamsten Score

• Multiply “Extension” by “Mean plaque size” score (maximum – 9) for each of 15 segments

Stenosis score (Modified Gensini score) • 0 - <25% luminal diameter reduction • 1 – 25-50% • 2 – 50-75% • 4 – 75-90% • 8 – 90-99% • 16 – 100%

Jenkins et al (1978) Score o Conclusion

Poor correlation between extent of lipid disorder and coronary severity and diffuseness measures

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• Sulllivan et al (1990) – Sydney, Australia 22 o Purpose

Correlate lipoprotein risk factors with angiographic score Score designed to reflect the amount of endothelial surface

area involved with atheroma o Coronary Score

Vessel score – number of vessels with stenosis >70% luminal diameter reduction

Stenosis score • 1 - <50% luminal diameter reduction • 2 – 50-75% • 3 – 75-99% • 4 – 100%

Gensini Score - Sum the severity score above for each of the 8 segments (maximum score – 32)

“Extent score” – Novel score in this study. The following is a list of hypothesized percent distribution of coronary artery endothelial surface area:

• LM – 5% • LAD – 20% • Main diagonal – 10% • Septal perforator – 5% • Left circumflex – 20% • OM and PL vessels – 10% • RCA – 20% • PDA – 10%

o Conclusions Age and lipid profile correlates with the “Extent Score

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• Alderman et al (1992) – Stanford 12 o Purpose

Describe definitions used by the BARI Trial o LV free wall branch sizes

o Coronary Score

Lesion grade • Significant if diameter reduction is >50%

BARI coronary map

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BARI “Myocardial Territory Units”

• Score Calculation

• “Lesion jeopardy unit score” divided by the “Global left ventricular territory unit score”

o Conclusions Advantages: flexibility in branch sizing and numbers and

adjusting for coronary dominance Jeopardy expressed as % of total LV Problems:

• No value assignment to inferoseptal area • PDA relative size appears to be too small at 8% • Excessive points given to branched side branches

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• Seller et al (1993) - Houston39 o Purpose - Establish mathematical relationship between epicardial

vessel length and amount of myocardium supplied o Method

Radiolabelled microsphere injection into in vivo and PM hearts with measurement of LV mass and summed epicardial 1st, 2nd and 3rd generation coronary branch length

o Conclusions Summed length of epicardial vessel length is closely and

linearly related to the size of the myocardial bed

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• Sianos et al (2005) – Rotterdam 13 o Purpose - Create a single numerical score that captures CAD

complexity (including the number and location of lesions) o Coronary Score

Lesion grade – Segment modifiers

• <50% - 0 • 50-99% - score 2 • 100% - score 5

LV Extent –16 segments as per ARTS modification of AHA • Segment Weighting Factors (Leamon et al (1981)

o PDA – 1 o PL – 0.5 o LM – 5 o Proximal, Mid and apical LAD – 3.5 / 2.5 / 1 o D1 and D2 – 1 / 0.5 o RI – 1 o OM and Distal LCx – 1 / 0.5

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Adverse Features Score

Score Calculation – Summation of lesion and adverse feature scores for each of 16 segments

• Graham et al (2006) – Alberta 1

o Purpose Correlate APPROACH Jeopardy score with mortality in

patients subsequently treated with CABG, PCI or no intervention in first year

Compare APPROACH Jeopardy score with those of Dash et al (1977) and Alderman et al (1992)

o Coronary Score Lesion grade – significance threshold

• >70% diameter reduction, but >50% for LM lesions

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LV Extent • Named free-wall branches: small = 1; medium=2;

large = 3. • Myocardial territories (and relative sizes) specified as

per the diagram below. Small-unnamed diagonal branches supply the “LAD Anterolateral Region” and similar small branches of the PDA supply the “PDA Posterolateral Region”.

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Score Calculation (APPROACH Jeopardy Score) • For free-wall LV branches: 44 X Diseased Branch

size/summed score of all branches • For LAD: 33 for proximal LAD lesion; 22 for mid LAD

and 11 for distal LAD, plus a portion of the apical value of 5 depending upon the LAD type.

• For the PDA: 18 for a proximal PDA lesion, 12 for mid lesion and 6 for distal lesion PLUS 5 for the apex with a Type 1 small LAD.

o Conclusions Log mortality odds by treatment group for each Scoring

system. PCI risk lower than Medical group. Surgery mortality, higher than PCI for lower Jeopardy Scores and lower than PCI and Medical for higher Scores

• APPROACH C-statistic highest, but not by much

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• Torino et al (2009)15 and (2010)4 – FAME Study o Purpose

Assess physiologic importance as a function of diameter stenosis

Randomized trial of FFR-guided versus angiographic-guided PCI (FAME)

o Coronary Score Lesion grade

• Lesions < 50% diameter excluded • 50 – 70% diameter reduction • >70% diameter reduction

o Conclusions FFR < 0.8 in 35% of 50-70% lesions and 82% of >70%

lesions FFR-guided intervention – better event-free survival

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References 1. Graham MM, Faris PD, Ghali WA, Galbraith PD, Norris CM, Badry JT, Mitchell

LB, Curtis MJ, Knudtson ML, Investigators A. Validation of three myocardial jeopardy scores in a population-based cardiac catheterization cohort. Am Heart J. 2006;142:254-261

2. Cerqueira MD, Weissman NJ, Dilsizian V, Jacobs AK, Kaul S, Laskey WK, Pennell DJ, Rumberger JA, Ryan T, Verani MS. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart: A statement for healthcare professionals from the cardiac imaging committee of the council on clinical cardiology of the american heart association. Circulation. 2002;105:539-542

3. Oberman A, Jones WB, Riley CP, Reeves TJ, Sheffield LT, Turner ME. Natural history of coronary artery disease. BullNY Acad Med. 1972;48:1109-1125

4. Tonino PAL, Fearon WF, De Bruyne B, Oldroyd KG, Leesar MA, Ver Lee PN, MacCarthy PA, van't Veer M, Pijls NHJ. Angiographic versus functional severity of coronary artery stenoses in the fame study: Fractional flow reserve versus angiography in multivessel evaluation. J Am Coll Cardiol. 2010;55:2816-2821

5. Gould KL, Lipscomb K, Hamilton GW. Physiologic basis for assessing critical coronary stenosis: Instantaneous flow response and regional distribution during coronary hyperemia as measures of coronary flow reserve. The American Journal of Cardiology. 1974;33:87-94

6. Gould KL, Lipscomb K. Effects of coronary stenoses on coronary flow reserve and resistance. The American Journal of Cardiology. 1974;34:48-55

7. Gould KL. Does coronary flow trump coronary anatomy? J Am Coll Cardiol Img. 2009;2:1009-1023

8. Bruschke AVgMD, Proudfit WLMD, Sones FMJMD. Progress study of 590 consecutive nonsurgical cases of coronary disease followed 5-9 years: I. Arterographic correlations. Circulation. 1973;47:1147-1153

9. Harris PJMDP, Behar VSMD, Conley MJMD, Harrell FEJPD, Lee KLPD, Peter RHMD, Kong YMD, Rosati RAMD. The prognostic significance of 50% coronary stenosis in medically treated patients with coronary artery disease. Circulation. 1980;62:240-248

10. Hamsten A, Waldius G, Szamosi A, Dahlen A, De Faire U. Relationship of angiographically defined coronary artery disease to serum lipoproteins and apolipoproteins in young survivors of myocardial infarction. Circulation. 1986;73:1097-1109

11. Proudfit WL, Bruschke AVG, Sones Jr FM. Natural history of obstructive coronary artery disease: Ten-year study of 601 nonsurgical cases. Progress in Cardiovascular Diseases. 1978;21:53-78

12. Alderman EL, Stadius M. The angiographic definitions of the bypass angioplasty revascujlarization investigation. Coronary Artery Disease. 1992;3:1189-1207

13. Sianos G, Morel M-A, Kappetein AP, Morice M-C, Colombo A, Dawkins KD, van den Brand M, Van Dyck N, Russell ME, Mohr FW, Serruys P. The syntax score: An angiographic tool grading the complexity of coronary artery disease. EuroInterv. 2005;1:219-227

Page 31: History of Coronary Scoring

31

14. Dash H, Johnson RA, Dinsmore RE, Harthorne JW. Cardiomyopathic syndrome due to coronary artery disease. I: Relation to angiographic extent of coronary disease and to remote myocardial infarction. British Heart Journal. 1977;39:733-739

15. Tonino PAL, De Bruyne B, Pijls NHJ, Siebert U, Ikeno F, van `t Veer M, Klauss V, Manoharan G, Engstrøm T, Oldroyd KG, Ver Lee PN, MacCarthy PA, Fearon WF. Fractional flow reserve versus angiography for guiding percutaneous coronary intervention. New England Journal of Medicine. 2009;360:213-224

16. Brandt PWT, Partridge JB, Wattie WJ. Coronary arteriography: Method of presentation of the arteriogram report and a scoring system. Clin Radiol. 1977;28:361-365

17. Gensini GGMD. The coronary artery disease scoring and retrrieval system. In: Gensini GGMD, ed. Coronary arteriography. Mount Kisco, New York: Futura Publishing Co.; 1975:271-274.

18. Leaman D, Brower R, Meester G, Serruys P, van den Brand M. Coronary artery atherosclerosis: Severity of the disease, severity of angina pectoris and compromised left ventricular function. Circulation. 1981;63:285-299

19. Reardon MFPD, Nestel PJMD, Craig IHMD, Harper RWMD. Lipoprotein predictors of the severity of coronary artery disease in men and women. Circulation. 1985;71:881-888

20. Friesinger GC, Page EE, Ross RS. Prognostic significance of coronary arteriography. Transactions of the Association of American Physicians. 1970;83:78-92

21. Jenkins PJ, Harper RW, Nestel PJ. Severity of coronary atherosclerosis related to lipoprotein concentration. BMJ. 1978;2:388-391

22. Sullivan DR, Marwick TH, Freedman SB. A new method of scoring coronary angiograms to reflect extent of coronary atherosclerosis and improve correlation with major risk factors. American Heart Journal. 1990;119:1262-1267

23. Folland ED, Vogel RA, Hartigan P, Bates ER, Beauman GJ, Fortin T, Boucher C, Parisi AF. Relation between coronary artery stenosis assessed by visual, caliper, and computer methods and exercise capacity in patients with single- vessel coronary artery disease. The veterans affairs acme investigators. Circulation. 1994;89:2005-2014

24. Pijls NHJ, van Schaardenburgh P, Manoharan G, Boersma E, Bech J-W, van’t Veer M, Bär F, Hoorntje J, Koolen J, Wijns W, de Bruyne B. Percutaneous coronary intervention of functionally nonsignificant stenosis: 5-year follow-up of the defer study. Journal of the American College of Cardiology. 2007;49:2105-2111

25. Parker JO, DiGiorgi S, West RO. Selective coronary arteriography. Arteriographic patterns in coronary heart disease. Can Med Assoc J. 1966;95:291-294

26. Brymer JF, Buter TH, Walton Jr JA, Willis Iii PW. A natural history study of the prognostic role of coronary arteriography. American Heart Journal. 1974;88:139-143

27. Kalbfleisch H, Hort W. Quantitative study on the size of coronary artery supplying areas postmortem. Am Heart J. 1977;94:183-188

Page 32: History of Coronary Scoring

32

28. Fulton RM, Hutchinson EC, Jones AM. Ventricular weight in cardiac hypertrophy. Br Heart J. 1952;14:413-420

29. Lorenz CH, Walker ES, Morgan VL, Klein SS, Graham TP. Normal human right and left ventricular mass, systolic function, and gender differences by cine magnetic resonance imaging. Journal of Cardiovascular Magnetic Resonance. 1999;1:7-21

30. Smith GT. The anatomy of the coronary circulation. Am J Cardiol. 1962;9:327-342

31. Erich W, de la Chapelle C, Cohn AE. Anatomical ontogeny. B. Man. 1. A study of the coronary arteries. Am J Anat. 1931;49:241-282

32. James TN, Burch GE. Blood supply of the human interventricular septum. Circulation. 1958;17:391-396

33. Bertho E, Gagnon G. A comparative study in three dimension of the blood supply of the normal interventricular septum in human, canine, bovine, porcine, ovine and equine heart. Chest. 1964;46:251-262

34. Solberg L, Strong J. Risk factors and atherosclerotic lesions. A review of autopsy studies. Arteriosclerosis, Thrombosis, and Vascular Biology. 1983;3:187-198

35. Austen WGMD, Edwards JEMD, Frye RLMD, Gensini GGMD, Gott VLMD, Griffith LSCMD, McGoon DCMD, Murphy MLMD, Roe BBMD. A reporting system on patients evaluated for coronary artery disease. Circulation. 1975;51:Page5-Page40

36. Lee JT, Ideker RE, Reimer KA. Myocardial infarct size and location in relation to the coronary vascular bed at risk in man. Circulation. 1981;64:526-534

37. White CW, Wright CB, Doty DB, Hiratza LF, Eastham CL, Harrison DG, Marcus ML. Does visual interpretation of the coronary arteriogram predict the physiologic importance of a coronary stenosis? New England Journal of Medicine. 1984;310:819-824

38. Califf RM, Phillips HR, Hindman MC, Mark DB, Lee KL, Behar VS, Johnson RA, Pryor DB, Rosati RA, Wagner GS, Harrel FE. Prognostic value of a coronary artery jeopardy score. Journal of the American College of Cardiology. 1985;5:1055-1063

39. Seiler C, Kirkeeide RL, Gould KL. Measurement from arteriograms of regional myocardial bed size distal to any point in the coronary vascular tree for assessing anatomic area at risk. Journal of the American College of Cardiology. 1993;21:783-797