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326AJR:185, August 2005
2005; 185:326–3290361–803X/05/1852–326© American Roentgen Ray Society
Khanna et al.AnomalousOrigin of LeftCoronaryArtery
Cardiovascular ImagingCase Report
Anomalous Origin of theLeftCoronary Artery from thePulmonary Artery inAdulthoodonCT and MRI
Arati Khanna
Drew A. Torigian
Victor A. Ferrari
Robert J. Bross
Mark A. Rosen
Khanna A, Torigian DA, Ferrari VA, Bross RJ,Rosen MA
Received July 15, 2004; accepted after revisionSeptember27, 2004.
Department of Radiology, Drexel University College ofMedicine, Philadelphia, PA 19102.
Department of Radiology, Hospital of the University ofPennsylvania, 3400 Spruce St., Philadelphia, PA19104-4283. Address correspondence to D. A. Torigian(Drew.Torigian@uphs.upenn.edu).
Department of Medicine, Hospital of the University ofPennsylvania, Philadelphia, PA 19102.
Department of Family Practice, Virtua Memorial Hospitalof Burlington County, Mt. Holly, NJ 08060.
e report the clinical, CT, andMRI findings of an intermit-tently symptomatic elderlywoman with the rare congeni-tal syndrome of anomalous origin of the leftcoronary artery from the pulmonary artery(ALCAPA) with marked intercoronary col-lateral arteries and retrograde filling of theleft coronary arterial system. To our knowl-edge, this finding as seen on MRI has notbeen reported in the literature.
Case Report
A 74-year-old woman with a history of hy-pertension, borderline hypercholesterolemia,hypothyroidism, asthma, and a remote historyof near syncopal episodes presented withcough and chronic intermittent nonexertionalchest discomfort that was atypical for angina.No shortness of breath or diaphoresis was re-ported. Physical examination was significantfor mild hypertension but was otherwise un-remarkable.Chest radiography showed mild bibasilaratelectasis or scarring. Stress echocardio-graphy/ECG showed mild left atrial enlarge-ment, normal left and right ventricular size,borderline left ventricular hypertrophy, nor-mal biventricular systolic function, mild leftventricular diastolic dysfunction, mild mitralvalve regurgitation, and trace to mild tricus-pid regurgitation. In addition, a right bundlebranch block, nonsustained supraventriculartachycardia during exercise, a hypertensiveblood pressure response to exercise, transient1-mm horizontal downsloping ST depression just meeting borderline criteria in the V4–V6,II, III, and aVF leads during exercise recov-ery, and moderate–severe hypokinesis of thedistal septum during exercise recovery werenoted, although the patient did not experiencechest pain during the study.Subsequent cardiac catheterization revealedan ejection fraction of 55%, normal left ven-triculography, a patent, large-caliber right cor-onary artery (RCA); anomalous origin of theleft main coronary artery (LMCA) from theright coronary sinus, a large-caliber left ante-rior descending artery (LAD) with functionalocclusion in its proximal portion and reconsti-tution by left-left collaterals, and a large-cali-ber patent left circumflex artery (LCx).Subsequent contrast-enhanced CT of thechest was performed, showing an enlargedLMCA that originated from the posterior as-pect of the main pulmonary artery (PA) alongwith a markedly dilated and tortuous LAD(Fig.1A) and an enlarged tortuous RCA thatoriginated orthotopically from the right coro-nary sinus of the aortic root (Fig.1B), in keep-ing with ALCAPA. The remainder of the coro-nary arterial system appeared markedly dilatedand tortuous (Fig.1B). Confirmatory cardiacMRI revealed similar anatomic findings(Figs.1C–1H). In addition, dynamic gadolin-ium-enhanced images showed late enhance-ment of ALCAPA relative to the PA (Figs.1Eand 1F). Myocardial contractility and thicknessof the ventricles appeared normal.Conservative management rather than sur-gical intervention was implemented, and atclinical follow-up 3years after initial diagno-sis at imaging, the patient did not have newcardiac-related symptomatology.
In 1885, Brooks [1] was the first to show thatcoronary arteries may anomalously originatefrom the PA. ALCAPA, otherwise known asBland-White-Garland syndrome, is a rare con-genital defect that accounts for 0.25–0.5% of allcongenital heart defects [2]. It most often pre-sents as an isolated defect, but in 5% of cases itmay be associated with other cardiac anoma-lies, including atrial septal defect, ventricularseptal defect, and aortic coarctation [3].Symptoms usually occur in infants afterthey are 1–2 months old because of left-to-
Anomalous Origin of Left Coronary Artery
AJR:185, August 2005327
right shunting from the higher pressure leftcoronary arterial system to the lower pressurepulmonary arterial system.This most often re-sults in death due to circulatory insufficiencyfrom left ventricular dysfunction or mitralvalve incompetence, myocardial infarction,or life-threatening cardiac dysrhythmias. Be-fore they are 1month old, however, physio-logic pulmonary arterial hypertension tendsto preserve antegrade blood flow within theleft coronary artery (LCA), accounting for theusual lack of symptomatology in this agegroup [4]. Without treatment, approximately90% of infants die within the first year of life[5]. Rarely, however, they survive into adult-hood with clinical presentations varying fromsymptomatic chronic mitral insufficiency orglobal ischemic cardiomyopathy to little or
74-year-old woman with cough and chronic intermittent nonexertional chest discomfort atypical for angina.
Axial enhanced CT shows dilated left main coronary artery (LMCA) (
black arrow 
) originating from posterior main pulmonary artery (P) leading to dilated and tortuous leftanterior descending (LAD) artery (
white arrow 
Axial enhanced CT at level of aortic root shows enlarged tortuous right coronary artery (RCA) and intercoronary collateral arteries (
) along epicardial surface ofheart.
Confirmatory cardiac MRI shows anomalous origin of left coronary artery from pulmonary artery (ALCAPA). Axial thin-section and oblique coronal maximal-inten-sity-projection (MIP) postgadolinium fat-suppressed T1-weighted gradient-echo images (TR/TE, 150/1.6/flip angle [FA] 90° and TR/TE, 3.8/0.9/FA 20°, respectively) show dilatedLMCA (
black arrow 
) originating anomalously from posterior main P, leading to dilated and tortuous LAD (
(Fig.1 continues on next page)
Khanna et al.
328AJR:185, August 2005
no symptomatology. Furthermore, the risk forsudden cardiac death due to ischemic malig-nant ventricular dysrhythmias exists even inasymptomatic adult patients [5, 6]. Factorsthat may lead to survival beyond infancy in-clude the development of abundant intercoro-nary collateral arteries, an alteration in hemo-dynamics that encourages antegrade bloodflow into the left coronary arterial tree, and a
74-year-old woman with cough and chronic intermittent nonexertional chest discomfort atypical for angina.
Oblique sagittal postgadolinium fat-suppressed T1-weighted gradient-echo MIP images (TR/TE, 3.8/0.9/FA 20°) during early and late phases of enhancement revealearly lack of enhancement of ALCAPA (
) during enhancement of P with subsequent late enhancement of ALCAPA, implying retrograde flow of blood within ALCAPAfrom RCA.
Oblique coronal postgadolinium fat-suppressed T1-weighted gradient-echo MIP image (TR/TE, 3.8/0.9/FA 20°) shows orthotopic dilated and tortuous RCA (
Axial T1-weighted cine gradient-echo image (TR/TE, 36/3.3/FA 30°) through ventricles shows high-signal-intensity flow in enlarged intercoronary collateral arteries (

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