Coronary anatomy and angiographic views

Coronary anatomy and
Angiographic views
Presenter: Dr Thanigai arasu E
DM Cardiac anaesthesia(1st year PG)

History
• 1650= Vieussens described first.
• 1799=Edward Jenner established the relationship between the
coronary artery and angina pectoris.
• 1809=Allan Burns described the same.
• 1958=Maron Sones performed the first selective coronary
arteriography.
• 1968=Rene Favalan and Dudley Johnson introduced the coronary
artery
• bypass surgery.

• The coronary arteries and their major
branches are sub-epicardially located

- Lt Main coronary Artery (LMCA) - from the left coronary sinus just
below the sinotubular ridge passes behind the pulmoary trunk, -
forwards and to the left between pulmonary trunk and left
auricle-bifurcates into LAD and LCx.
- 1-25mm in length & Diameter of 2-5.5mm(mean of 4mm). Short if
it is <1mm.
- Trifurcates in 1/3rd : Ramus intermedius/ median artery/ left
diagonal artery/straight LV artery
- Rare variations – absent LMCA/ pentafurcation

Contd..
• LAD runs in the anterior IV groove towards the apex and it terminates
-Beyond the ventricular apex along the diaphragmatic aspect in 78%-Type
III
-At the apex-Type II
-Before the apex in 22%-Type I
• 10-13cmin length, 2-5mm in diameter(mean of 3.6)
Branches:
1. septal branches are vary in No and size originates at a right angle-
anterosuperior 2/3rd IVS(Inter ventricular septum)
2. 1-3 diagonal course laterally over the free wall of lt ventricle in the
angle between Lad and LCx-anterolateral portion of LV & AL papillary
muscle
Angiographical classification: Proximal-origin to 1st major septal perforator
Mid-1st perforator -D2
Distal-D2 to end.

Contd..
 Lcx travels in the left AV groove and finally reaches crux of the
heart(Posterior part of AV groove), it anastomoses with branches of
the RCA.
 6-8cm in length, 1.5-5.5mm in diameter(mean of 3mm).
Branches: LA branches: 1-2 supplies Left atrium
OM : 1-3 in no supplies lateral free wall of LV
In case of Left dominant(8%)- PDA, PLV, SA nodal (40-50%), AV nodal
Artery(10-20%).
Angiographical classification: proximal-origin to OM1
Mid: OM1-OM2
Distal: OM2-end.

contd..
RCA arises- Rt CS - lower in position than that of Lt CS,
Course- forwards and to the Rt between the pulmonary trunk and Rt
auricle, - winds round the inferior border of the heart to reach the
diaphragmatic surface of the heart.
Here, it passes upwards and to the left in the right posterior coronary
sulcus and reaches crux of the heart and terminates by anastomosing with
the branches of the Lcx.
Branches:
1. Conus A-1st branch-infundibulum of RV, but in 40-50%-separate ostium in
the Rt CS(3rd coronary A)
2. SA nodal A-50-60% runs along the rt atrium to SVC where it encircles in a
clock wise or anticlockwise before it penetrates the SA node—supplies RA.
3. Right ventricular branch-AM-supplies anterior wall of rt ventricle.
 In Right Dominant circulation(85%) – AV nodal A-AV node,

 PDA- postero inferior 1/3rd of IVS & PM papillary muscle,
communicates with the of the LAD artery around the apex.
 Where there is a major blockade of the LAD, a patent right
dominant system can supply the LAD region in a retrograde way.
 PLV- posterolateral portion of LV.
Angiographic classification of RCA.
Proximal - Ostium to 1st main RV branch
Mid - 1st RV branch to acute marginal branch
Distal - acute margin to the crux

Dominance(Crux cordis):
• Definition 1:
the coronary artery which reaches the crux of the
heart and then gives off the PDA
• Definition 2: (Allows for codominance)
the artery which gives off the PDA as well as a
large posterolateral branch
Super dominant RCA- in type 1 LAD the larger
and longer PDA from RCA supplies the ventricular
apex also.

 RA-RCA. LA-Left circumflex
 RV=Anterior portion adjacent to the interventricular septum-branches of LAD;
rest-RCA
 LV= 50% from the LAD. 25% from the left circumflex, 25%-posterior
descending a.(from rt. Coronary or the left circumflex).
 . The anterolateral papillary muscle-blood supply - diagonal branches of LAD.
 The posterior papillary muscle-dual blood flow from circumflex and terminal
branches of RCA.
 Sinus node-In majority by RCA, in a small proportion by the circumflex.
 AV node-The first posterior perforator of the PDA.
 Bundle of His-dual blood supply from both the PDA and LAD, more resistant to
ischemia than the AV node.
 Rt. Bundle-LAD and RCA. Left bundle-mainly from the diagonals.
REGIONAL MYOCARDIAL BLOOD SUPPLY

• ? Coronary artery Variation vs Anomalies
• A broad spectrum of variations of which some
may cause adverse effects
• Most of the coronary variations may have no
clinical implications as can be proven by
myocardial perfusion studies.
• The regional distribution of a coronary artery,
rather than its absolute origin and
characteristics.

Coronary artery variations
• Definition of a coronary artery is not based on its origin
and proximal course, but by focusing on its intermediate
and distal segments/ its dependent microvascular bed.
Angelini P – Coronary artery anomalies – current clinical issues. Definition, classifications, incidence, clinical relevance and treatment guidelines. Tex Heart Inst
J 2002;29:271-278

• Level of variables
1) Ostium 2) Size 3) Proximal course
4) Mid-course 5) Intramyocardial ramifications 6) Termination
A. Anomalies without a shunt:
1. Abnormal number : 1/ 3/ 4 ostia
2. Anomalous origin: a) Outside SOV
b) Independent origin from same sinus
c) Opposite sinus
d) Other artery
3. Myocardial bridge
4. Segmental stenosis/hypoplasia
B. Anomalies with shunt:
1) Fistula 2) APOCA
C. Aneurysms

Abnormal position of ostia
• Coronary orifice below the cuspal margin:
- 10% RCS
- 15% LCS
• Coronaries above the sinotubular jn ~ 6% - leads to difficult
cannulation, esp RCA with a high anterior ostium.

Absent LMCA
• ~0.4%
- 1 ostia at the LCS/ 2 ostia in LCS/ 1 ostia in LCS & other RCS
- Increased incidence of Left dominance
- 6% incidence of bridging
- Not usually associated with CHDs
- Similar incidence of atherosclerosis
- Difficulty in selective cannulation
Topaz et al. Absent left main coronary artery: angiographic findings in 83 patients with separate ostia of the
left anterior descending and circumflex arteries at the left aortic sinus.
Am Heart J.1991 Aug;122(2):447-52.

Shepherd’s-crook RCA
• ~5%
• Acute superiorly angled take-off of the RCA
from the aorta.
• Difficult RCA lesion angioplasty
Ethan Halpern. Cardiac CT . Functional anatomy.

Dual LAD (Duplication)
• ~0.13 - 1% of normal hearts
• Proximal LAD (LAD proper) bifurcates early into a
short and long LAD
-Type I : Short LAD in AIVS, Long LAD on prox AIVS, LV side, distal AIVS
-Type II : Short LAD in AIVS, Long LAD on prox AIVS, RV side, distal AIVS
-Type III: Short LAD in AIVS, Long LAD intra-myocardially in septum
-Type IV: Very short LAD proper and short LAD, Long LAD from RCA
Spindola-Franco H et al. Dual left anterior descending coronary artery: angiographic description of Important variants
and surgical implications. Am Heart J 1983:105;445–55.

• Level of variables
1) Ostium 2) Size 3) Proximal course
4) Mid-course 5) Intra-myocardial ramifications
6) Termination
• MSCT with retrospective ECG gating is now
considered the gold standard for characterization of
coronary anomalies.
• Prompt a search for underlying CHDs

LCA from PA
Large
RCA
Collaterals
to LAD
LAD arising
from PA

Normal and Anomalous
Origins of the Coronary
Arteries

Coronary artery Ectasia
• 1 - 5% in angiographic series, more in males
• 20- 30 % are congenital
• Dilatation of a segment to at least 1.5times of the
adjacent normal coronary artery.

Collateral Circulation-Development
• Preexisting arterial anastomosis seen in
intracoronary/intercoronary levels in abundance. Significant in
forming collaterals in CAD.
• Intracoronary : 1-2cm X 20- 250 micm
• Inter-coronary: 2-3 cm X 20-350 micm
• First 24 hours-passive widening
• One day-3 weeks
cellular proliferation, luminal diameter increases 10 fold.
• 3 weeks-6 months
more cellular proliferation and development of extracellular matrix;
channels may reach 1mm in caliber.
• Ischemia and occlusion are the only triggers.
• Usually need very high grade coronary artery occlusion for
collaterals to be angiographically apparent.

Collateral “Connections”
• Occur where coronary arteries are in proximity
– Distal LADDistal PDA
– Cx AV grooveR AV groove
– SeptalSeptal
– MarginalMarginal
– DiagonalMarginal
• Also
– Bridging collaterals-associated with chronicity
– Kugel’s artery-prox RCA to distal RCA via AV groove
– Always look for conus to LAD collaterals when LAD is
occluded and appears uncollateralized.

Collateral
Development
After RCA
Occlusion

Collateral
Pathways
After LAD
Occlusion

Collateral Pathways After Circumflex Occlusion

Classification of Collaterals
• 0 No epicardial filling at baseline or during balloon
inflation
• 1 No epicardial filling at baseline with partial epicardial filling
during balloon inflation
• 2 Partial baseline filling with partial or complete filling during
balloon inflation
• 3 Complete epicardial filling at baseline
Rentrop Grade
“Recruitable collaterals”—collaterals which can become
angiographically apparent only during occlusion, such as those
observed during PTCA.
Collaterals can be dilated by nitrates, B-adrenergic agents,
NO and prostacyclin

Recruitable Collaterals
RCA Injection during LAD PTCA
RCA angiogram demonstrates complete filling of LAD.
No collaterals were apparent prior to balloon inflation.

An extensive intercommunicating network by
a. the coronary sinus
b. the anterior right ventricular veins.
c. the thebesian veins.
Coronary sinus= in the left posterior AV groove-drains predominantly the
left ventricle and the left atrium.
Tributaries:a)The anterior inter-ventricular vein-ends as great cardiac v
b) The middle cardiac vein-from the posterior
interventricular region.
c) the oblique vein of Marshell-from the posterior aspect of
left atrium.
- opens into the rt.atrium between the orifice of IVC and septal tricuspid
leaflet.
VENOUS DRAINAGE

Contd…
• The anterior cardiac v.-2-4 in no. They drain the anterior right
ventricular wall and end at the base of the right atrium.
• The small cardiac v.-receives from rt.atrium and opens into RA.
• The thebesian veins-tiny venous outlets draining the myocardium
directly into the cardiac chambers(rt. Atrium and rt.ventricle).
 INNERVATION
Sympathetic: from superior, middle and inferior cervical ganglia+
upper 5 ganglia of the symp.chain.
Para-symathetic: nodose ganglion.
At the heart, both mingle to form cardiac plexus-superficial and deep
portion.

• 5% of the blood flow of the total cardiac output(250-275ml/min).
• AV oxygen content difference=10 ml/100 ml(5 ml/100 ml in other
vascular beds).
• Oxygen consumption-25 ml/min.(beating heart at rest).
-6 ml/min(non-beating heart).
-0.12 ml/min(for electrical activation)]
Distribution of blood volume and O2 consumption

• Anatomical factor: arranged as
a) epicardial conductance vessels (constrict to alpha stimulation and dilate
to NTG.)
b) intramyocardial resistance vessels(at right angles to the above).
c)subendocardial plexus of vessels-dense capillary network of about 4000
capillaries/sq.mm, not uniformly patent-pre-capillary sphincters serve a
regulatory role-opens out when myocardial demand increases.
• Under basal conditions, blood flow to the subendocardium/subepicardial
layer=125:1 (maximal preferential dilatation of the subendocardial plexus of
vessels.
• Significance: In the presence of a significant coronary artery
obstruction, subendocardial vessels can’t dilate further and suffer the
most by way of ischemia.
REGULATION OF THE CORONARY BLOOD FLOW

• CPP = AoDP-LVEDP
All organs are perfused during systole except the LV(since the
resistance vessels are compressed during systole).
RV-thinner ventricle. Receives its major blood flow during
systole.

 Local metabolism: primary controller. Local arterial vasodilatation in
response to muscle need for nutrition. Chemical agents responsible are:
a) adenosine
b) potassium ions
c) hydrogen ions
d) bradykinin
e) prostaglandins.PGI2 and PGE2.
 Oxygen lack: opening of ATP dependent K+ channels-hyper-polarization-
Ca2+ channel opening prevented-vasodilatation.
 Auto-regulation: At perfusion pressures from 60-130 mm of Hg, CBF is the
same(myogenic, metabolic factor and release of endothelial vaso-active
factors are implicated).
 Neural factor: α-vaso-constriction ß-vaso-dilatation. Para symp-dilates
 Endothelial control: EDRF(released by several stimuli), prostacyclin,
endothelin.
CONTROL OF CVR

Indications
Known or suspected CAD (Class I and III only)
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
 CCS class III and IV angina on medical treatment
 High-risk criteria on noninvasive testing regardless of anginal severity
 Patients who have been successfully resuscitated from sudden cardiac
death or have sustained (>30 seconds) monomorphic ventricular
tachycardia or non-sustained (<30 seconds) polymorphic ventricular
tachycardia
 Angina in patients who are not candidates for coronary revascularization
or in whom revascularization is not likely to improve quality or duration
of life
 As a screening test for CAD in asymptomatic patients
 After CABG or angioplasty when there is no evidence of ischemia on
noninvasive testing
 Coronary calcification on fluoroscopy, electron beam computed
tomography, or other screening tests without criteria listed above
Source: Scanlon PJ et al. ACC/AHA Guidelines for Coronary Angiography: Executive Summary and Recommendations. A Report of the American College of Cardiology/American Heart Association Task Force on
Practice Guidelines (Committee on Coronary Angiography). Circulation 1999;99;2345-2357

Indications
Patients With Nonspecific Chest Pain
 High-risk findings on noninvasive testing
 Patients with recurrent hospitalizations for chest pain who have
abnormal (but not high-risk) or equivocal findings on noninvasive
testing
 All other patients with nonspecific chest pain

Indications
Patients With Unstable Acute Coronary Syndromes (Class I and III only)
 An early invasive strategy (i.e., diagnostic angiography with intent to
perform revascularization) is indicated in UA/NSTEMI patients who have
refractory angina or hemodynamic or electrical instability (without serious
comorbidities or contraindications to such procedures)
 An early invasive strategy is indicated in initially stabilized UA/NSTEMI
patients (without serious comorbidities or contraindications to such
procedures) who have an elevated risk for clinical events
 An early invasive strategy is not recommended in patients with extensive
comorbidities (e.g., liver or pulmonary failure, cancer), in whom the risks of
revascularization and comorbid conditions are likely to outweigh the
benefits of revascularization
 An early invasive strategy is not recommended in patients with acute chest
pain and a low likelihood of ACS
 An early invasive strategy should not be performed in patients who will not
consent to revascularization regardless of the findings
Source: Anderson JL et al. ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction. J Am Coll Cardiol 2007;50:e1–157

Indications
Patients With STEMI (Class I and III only)
 Diagnostic coronary angiography should be performed:
a. In candidates for primary or rescue PCI
b. In patients with cardiogenic shock who are candidates for
revascularization
c. In candidates for surgical repair of ventricular septal rupture
(VSR) or severe MR
d. In patients with persistent hemodynamic and/or electrical
instability
 Coronary angiography should not be performed in patients with
extensive comorbidities in whom the risks of revascularization are
likely to outweigh the benefits
Source: Antman EM et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task
Force on Practice Guidelines. 2004. Available at www.acc.org/clinical/guidelines/stemi/index.pdf.

Indications
Patients With Post-revascularization Ischemia (Class I and III only)
 Suspected abrupt closure or subacute stent thrombosis after percutaneous
revascularization.
 Recurrent angina or high-risk criteria on noninvasive evaluation within 9
months of percutaneous revascularization
 Symptoms in a post bypass patient who is not a candidate for repeat
revascularization
 Routine angiography in asymptomatic patients after percutaneous
transluminal coronary angioplasty (PTCA) or other surgery, unless as part of
an approved research protocol

Indications
Perioperative Evaluation Before (or After) Noncardiac Surgery (Class I and III only)
 Evidence for high risk of adverse outcome based on noninvasive test results
 Angina unresponsive to adequate medical therapy
 Unstable angina, particularly when facing intermediate or high-risk noncardiac
surgery
 Equivocal noninvasive test result in a high-clinical- risk in patients
 Low-risk noncardiac surgery, with known CAD and no high-risk results on
noninvasive testing
 Asymptomatic after coronary revascularization with excellent exercise capacity
(>7 METs)
 Mild stable angina with good left ventricular function and no high-risk
noninvasive test results
 Noncandidate for coronary revascularization owing to concomitant medical
illness, severe left ventricular dysfunction (eg, LVEF <0.20), or refusal to consider
revascularization.
 Candidate for liver, lung, or renal transplant >40 years old as part of evaluation
for transplantation, unless noninvasive testing reveals high risk for adverse
outcome

Indications
Patients With Valvular Heart Disease (Class I and III only)
 Before valve surgery or balloon valvotomy in an adult with chest
discomfort, ischemia by noninvasive imaging, or both
 Before valve surgery in an adult free of chest pain but of substantial age
and/or with multiple risk factors for coronary disease
 Infective endocarditis with evidence of coronary embolization
 Before cardiac surgery for infective endocarditis when there are no risk
factors for coronary disease and no evidence of coronary embolization
 In asymptomatic patients when cardiac surgery is not being considered
 Before cardiac surgery when preoperative hemodynamic assessment by
catheterization is unnecessary, and there is neither preexisting evidence
of coronary disease nor risk factors for CAD

Indications
Patients With Congenital Heart Disease (Class I and III only)
II IIa IIb IIIII IIa IIb IIIII IIa IIb IIIIIa IIb III
 Before surgical correction of congenital heart disease when chest
discomfort or noninvasive evidence is suggestive of associated CAD
 Before surgical correction of suspected congenital coronary anomalies
such as congenital coronary artery stenosis, coronary arteriovenous
fistula, and anomalous origin of left coronary artery
 Forms of congenital heart disease frequently associated with coronary
artery anomalies that may complicate surgical management
 Unexplained cardiac arrest in a young patient
 In the routine evaluation of congenital heart disease in asymptomatic
patients for whom heart surgery is not planned

Indications
Patients With CHF (Class I and III only)
II IIa IIb IIIII IIa IIb IIIII IIa IIb IIIIIa IIb III
 CHF due to systolic dysfunction with angina or with regional wall motion
abnormalities and/or scintigraphic evidence of reversible myocardial
ischemia when revascularization is being considered
 Before cardiac transplantation
 CHF secondary to postinfarction ventricular aneurysm or other
mechanical complications of MI.
 CHF with previous coronary angiograms showing normal coronary
arteries, with no new evidence to suggest ischemic heart disease

 There are no absolute contraindications to cardiac catheterization
 Relative contraindications include:
 Coagulopathy (Radial approach can be attempted based on urgency)
 Decompensated congestive heart failure
 Uncontrolled hypertension
 Pregnancy
 Inability for patient cooperation
 Active infection
 Renal failure
 Contrast medium allergy
Contraindications

 Conscious sedation using a narcotic and a benzodiazepine
 Vascular access: Either femoral (described in the section on vascular access
and closure devices), radial, or brachial
 Flush the selected diagnostic catheter with saline to ensure an air-free
system
 Once arterial access is obtained (as described in the section on vascular
access and closure devices) a catheter of appropriate size and
configuration is advanced over a 0.035 or 0.038 inch guidewire
 Once in the ascending aorta, the guidewire is removed, the catheter
allowed to bleed back to remove any thrombus or atherosclerotic debris
 The catheter is then connected to a manifold assembly connected to a
pressure transducer for continuous central pressure monitoring
 The catheter is flushed to ensure an air-free system
Equipment & Technique

 Zeroing and referencing: The transducer should be opened to air to zero
the system. Care must be taken to ensure that the pressure transducer is
at the level of phlebostatic axis, which is roughly the midportion
between the anterior and posterior chest wall along the left 4th
intercostal space
 The central aortic pressure should be recorded and compared with the
cuff measured brachial pressure. If there is considerable difference
between the two, subclavian artery stenosis should be in the differential
 The catheter should then be filled with 3-4 cc of contrast and advanced
to engage the coronary ostium, in the LAO projection
 After ensuring that there is no ventricularization or damping of the
pressure, a 2 to 3 cc of contrast should be injected to confirm the
position of the catheter in the coronary ostium
 The overall risk of major complications with coronary angiography is 1-
2%. This includes death, myocardial infarction, stroke, bleeding, vascular
complications and contrast reaction.
Technique

Standard Angiographic Views
 An easy way to identify the tomographic views is to use the anatomic
landmarks - catheter in the descending aorta, spine and the diaphragm.
The rough rules are:
 RAO vs. LAO- If the spine and the catheter are to the right of the
image, it is LAO and vice versa. If central, it is likely a PA view
 Cranial vs. caudal - If diaphragm shadow can be seen on the image, it
is likely cranial view, if not, it is caudal
Catheter
and spine to
the LEFT
RAO view
No diaphragm
shadow
Caudal view
Catheter at
the CENTER PA view
No diaphragm
shadow
Caudal
view
Spine to
the
RIGHTLAO view
Diaphragm
shadow
Cranial view

 LAO-Caudal view: 400 to 600 LAO and 100 to 300 caudal
 Best for visualizing left main, proximal LAD and proximal LCx
 RAO-Caudal view: 100 to 200 RAO and 150 to 200 caudal
 Best for visualizing left main bifurcation, proximal LAD and the proximal
to mid LCx
 Shallow RAO-Cranial view: 00 to 100 RAO and 250 to 400 cranial
 Best for visualizing mid and distal LAD and the distal LCx (LPDA and LPL)
 Separates out the septals from the diagonals
 LAO-Cranial view: 300 to 600 LAO and 150 to 300 cranial
 Best for visualizing mid and distal LAD, and the distal LCx in a left
dominant system
 Separates out the septals from the diagonals
Left Coronary Artery

 PA projection: 00 lateral and 00 cranio-caudal
 Best for visualizing ostium of the left main
 PA-Caudal view: 00 lateral and 200 to 300 caudal
 Best for visualizing distal left main bifurcation as well as the proximal
LAD and the proximal to mid LCx
 PA-Cranial view: 00 lateral and 300 cranial
 Best for visualizing proximal and mid LAD
 Left lateral view:
 Best for visualizing proximal LCx, proximal and distal LAD
 Also good for visualizing LIMA to LAD anastomotic site
Left Coronary Artery (other views)

RAO 20 Caudal 20
LM
LAD
Diagonal
Septals
Distal
LAD
LCx
RAO 20 Caudal 20
Knowledge of the orientation of the artery
for a given view can help identify the
probable path of the artery in the setting of
complete occlusion
Distal LAD
fills by
collaterals
LAD
Best for visualization of LM
bifurcation and proximal
LAD and LCx

LAO 50 Cranial 30
LM
LAD
Diagonal
Septals
Distal
LAD
LCx
PA 0 Cranial 30
LM
LAD
Diagonal
Septals
Distal
LAD
LCx
proximal and mid LAD
Best for visualization of proximal and
mid LAD and splaying of the septals
from the diagonals. Also ideal for
visualization of distal LCx

PA0 Caudal 30
LM
LAD
Diagonal
Septals
Distal
LAD
LCx
LAO 50 Caudal 30
OM
LM
LAD
Diagonal
Distal
LAD
LCx
OM
‘Spider’ view
bifurcation and proximal LAD
and LCx
bifurcation, proximal LAD and LCx and
OM

 LAO 30: 300 LAO
 Best for visualizing ostial and proximal RCA
 RAO 30: 300 RAO
 Best for visualizing mid RCA and PDA
 PA Cranial: PA and 300 cranial
 Best for visualizing distal RCA bifurcation and the PDA
Right Coronary Artery

Right Coronary Artery
LAO 30
Proximal
RCA
PDA
Distal
RCA
Mid
RCA
RAO 30
Mid
RCA
PDA/
PLV
PA 0 Cranial 30
Proximal
RCA
PDADistal
RCA
Mid
RCA
Best for visualization of ostial
and proximal RCA
Best for visualization of mid
RCA and PDA
Best for visualization of distal
RCA and its bifurcation

Optimal angiographic views for coronary segments
Carlo Di Mario, Nilesh Sutaria. CORONARY ANGIOGRAPHY IN THE ANGIOPLASTY ERA: PROJECTIONS WITH A MEANING
Heart 2005;91:968–976.
There is no single magical projection that can be
applied uniformly to all patients for visualizing
a particular coronary atery

Panoramic coronary angiography
GIORGIO TOMMASINI et al. Panoramic Coronary Angiography. JACC 31(4),March 15, 1998:871–7

Pitfalls of CAG –
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