The chest X-ray was normal.The transthoracic echocardiography (TTE) showed normal valves, normal chamber dimensions, normal left ventricle (LV) systolic function (ejection fraction by Biplane 60%), normal right ventricle (RV) systolic function, no regional wall motion abnormality.

The patient underwent primary percutaneous coronary intervention (PPCI) via the right femoral artery access. During the diagnostic coronary angiogram (DCA), multiple attempts for cannulation of the RCA by the right Judkins catheter were unsuccessful and could not engage in the ostium of the RCA. Aortic root angiography showed no definite origin for RCA on the right sinus of Valsalva (Figure 2A-C). The left coronary ostium was identified, and cannulation was performed and showed LCA originating from the left coronary ostium, having a wide diameter and no stenosis. The LAD had 99% critical stenosis in the proximal LAD with a thrombus (culprit lesion) and normal Diagonal 1 and Diagonal 2 arteries. The proximal LAD gave a branch that provides the territory ordinarily supplied by the RCA (considered "RCA") (Figure 2D). The LCX was dominant and normal without stenosis, Obtus Marginal arteries (OM) were normal, and distal LCX branched into a posterior descending artery (PDA) and posterolateral branch (PLB) without stenosis. Following the administration of 6,000 units of intravenous (IV) heparin, PPCI was conducted, thrombus aspiration was performed in the LAD, and a white thrombus was obtained. The operator then performed a 12-atmosphere 10-second dilatation with a Saphire II Pro 2.5 x 15 mm balloon in the proximal LAD, and a 2.75 x 24 mm Sirolimus stent was implanted in the proximal LAD. The post-stent evaluation showed satisfactory results with TIMI flow III. The patient was diagnosed with anteroseptal STEMI Killip I, with an onset of 7 hours, accompanied by a hypertensive emergency in acute coronary syndrome and SCA with RCA originating from the proximal LAD.

Figure 2: The diagnostic coronary angiogram showed no right coronary ostium was observed (A and B); Only the left coronary ostium was present (yellow arrow) (C); Large and normal-diameter dominant left circumflex (LCx) and normal obtuse marginal (OM) branches; Critical stenosis was observed in the proximal left anterior descending artery (LAD), and the proximal LAD gave a branch providing the territory ordinarily supplied by the right coronary artery (considered "RCA") (D).

Post PPCI, the patient was admitted to ICCU in 24 hours. The patient's complaints improved, allowing the patient to be transferred to the ward. During treatment, the patient received an infusion of normal saline 500 mL/24 hours IV, aspirin 100mg once a day, ticagrelor 90 mg twice a day, candesartan 8mg once a day, bisoprolol 2.5mg once a day, isosorbide dinitrate (ISDN) 5mg three times a day, and atorvastatin 40mg once a day. The next day, the patient's clinical condition improved without complications. The optimal therapeutic dose adjustment the patient can tolerate had been applied, allowing the patient to return home.

After two months of outpatient follow-up, the patient was scheduled to undergo a 128-slice CCTA. It revealed the origin of RCA was from the proximal LAD (benign type), coursed anteriorly to the pulmonary artery (PA) through the right atrioventricular groove (Figure 3 and 4). There was also a soft plaque in the proximal RCA with moderate-severe stenosis (68%-75%). The LAD showed evident stent in proximal LAD with in-stent restenosis (ISR) at the proximal margin with a good distal flow; mixed plaque (remodeling plaque) in proximal LAD (just above the stent) with mild-moderate stenosis (35%-50%). LCA and LCX were normal, with no stenosis, calcification, or soft plaque. Occasionally, patients experience chest pain in association with moderate physical exercise. For the next step, we advise patients to undergo DCA evaluation and continue getting optimal medical therapy (OMT).

Figure 3: The coronary computed tomography angiography showed a single coronary artery as the left coronary artery (LCA) originating from the left coronary cusp, which branched into the left anterior descending (LAD) and left circumflex (LCx) arteries. No right coronary ostium is present from the aorta. The right coronary artery (RCA) anomaly arises from the proximal LAD, coursed anteriorly to the pulmonary artery (PA) to reach the right atrioventricular groove. The stent was located in the proximal LAD.

Figure 4: The right coronary artery(RCA) (white arrow) began its path from the proximal left anterior descending(LAD) (red arrow) through the anterior of pulmonary artery (PA). There was no right coronary ostium or bud observed.The left circumflex (LCx) (yellow arrow) originated at the left coronary artery (LCA) and coursed down the left atrioventricular groove. The distal LCx branched into the posterior descending artery (PDA) (blue arrow) and PLB (orange arrow).

Figure 5: The curved multiplanar reconstruction showed the left anterior descending artery (LAD) had a stent in the proximal segment (red asterisk) and mixed plaque (remodeling plaque) with mild-to-moderate stenosis (35-50%) above the stent (yellow arrow) (A). The anomalous right coronary artery (RCA) originated from the proximal LAD and coursed anteriorly to the pulmonary artery (PA), anda soft plaque (red arrow) was observed at proximal RCA with moderate-to-severe stenosis (68-75%) (B). In-stent restenosis (white arrow) was observed at the proximal margin of the stent in LAD (C).

DISCUSSION:

The anatomical characteristics of a normal coronary artery are: (1) it has 2-4 ostium, (2) arises from just above the free margin of the aortic valve from the ascending aorta and is located in the right and left anterior sinuses, (3) its proximal orientation is 45^o-90^o off the aortic wall, (4) proximal common stem or trunk only from left (LAD and LCx), (5) proximal course: directly from ostium to final destination, (6) mid-course: extramural (subepicardial), (7) essential territories: RCA (RV free wall), LAD (anteroseptal), OM (LV free wall), and (8) termination to capillary bed⁸. The name and nature of a coronary artery or its branches are determined by the pattern of distal vascularization of the vessel or vessel's territory (not by origin). A condition is called an anomaly if there is abnormal variation in <1% of the general population^7–11.

The two coronary ostia should arise about 10mm from the sinotubular junction, and variations in this distance are considered normal. An ostium >10mm above or below the sinotubular junction is classified as having a high or low take-off. The coronary arteries arise from the aortic sinus closest to the pulmonary artery. The left coronary ostium or left coronary aortic sinus is usually single, then a short common LCA trunk appears called the left main coronary artery (LMCA/LCA). The LCA arises from the center of the left coronary sinus, just above the level of the free margin of the aortic valve leaflet and generally below the sinotubular junction. The LCA runs between the left atrial appendage (LAA) and RVOT (right ventricular outflow tract) for 1-2cm. It branches into the LAD artery, which runs in the anterior interventricular groove to descend the apex, and the LCx, which runs posteriorly in the left interventricular groove. In 70% of patients, the LCA has three branches, between the diagonal branch of the LAD and the branch of the LCx, namely the ramus intermedius (or medianus/intermediate) supplying the anterolateral area. Generally, the LAD reaches the apex of the heart and consists of proximal, mid, and distal segments. The proximal LAD consists of the end of the LCA to the first major septal branch or the first diagonal (D1), which is more proximal. The mid LAD consists of the proximal end of the LAD to half the distance to the apex. The distal LAD consists of the end of the mid-LAD to the end of the LAD¹². The LAD divides into the anterior perforating septal artery, which extends to the apex of the heart and the anterior and basal two-thirds of the interventricular septum, a smaller branch that lies on the anterior wall of the RV, and a diagonal branch (D1 and D2) that runs at a downward angle to the anterior free wall and anterolateral LV^9–13.

A portion of the inferior wall area and the lateral wall of the LV are supplied by the LCx. The LCx is located along the left atrioventricular groove, near the obtuse marginal, and posterior to the cardiac crux. The LCx has branches of the obtuse marginal arteries (OM1 and OM2) that serve the inferolateral and lateral sides of the LV, and in 40% of cases, atrial branches supply the sinus node¹².

Typically, the RCA begins anterior to the right coronary aortic sinus (just below the sinotubular junction of the right anterior Valsalva sinus). The RCA reaches the heart's posterior surface via the right atrioventricular groove. Three segments comprise the RCA: proximal, intermediate, and distal^11,12. In 85%-90% of cases, the RCA branches into the posterior descending artery (PDA) in the posterior interventricular groove, supplying the AV node and the posterior section of the interventricular septum. Fifty percent of patients with a dominant RCA will have a substantial posterolateral artery (PLB) branch that supplies the inferior and inferolateral walls of the LV⁹. It is essential to identify this branch because it supplies the inferoseptal papillary muscle of the mitral valve¹⁴. The PDA and/or PLB are supplied by branches of RCA and LCx in co-dominant coronary circulation situations (5%)¹⁰.

Certain people have typical variants, such as the 3% of patients with a branch of the right superior perforator septal artery that emerges from the right Valsalva sinus or the proximal RCA and supplies the anterior septum. It is a collateral source in illness proximal to the LAD, similar to the conus artery. Small branches may develop straight from the ascending aorta rather than through the RCA or LCA. There are also variations in the vasculature of the inferior wall¹². The RCA artery, the LCx artery, or both arteries may give rise to the PDA and PLB branches that supply the inferior wall. In most patients, the PDA originates from the distal coronary artery; however, some patients have an early take-off of the PDA from the RCA (split RCA), which proceeds along the diaphragmatic surface of the RV to the apex. Another patient had the LAD artery partially feed the inferior apical wall by wrapping around the apex. It is essential to understand that the supply of the SA node varies from individual to individual, as this condition is sometimes confused with a coronary fistula. Some people also have smaller branches that originate straight from the aorta, as opposed to the coronary arteries (in addition to having LCA and RCA originating from the aorta). The natural origin of the conus branch or SA node from the aorta is a common variation of this kind¹⁵.

The classification of coronary artery (CA) anomalies according to hemodynamic significance is divided into four categories: (1) Benign (associated with myocardial ischemia): coronary fistula; (2) Relevant (associated with single coronary artery R-L, I-II-III, A-P; LCA, ectopic origin from the pulmonary artery; CA atresia; and CA hypoplasia; and (3) Severe (potentially fatal). Another classification scheme splits coronary artery anomalies into two main groups: those that develop abnormally from the pulmonary artery (left coronary artery from the pulmonary artery/ALCAPA or right coronary artery originating from the pulmonary/ARCAPA) and those that develop abnormally from the coronary aorta (AAOCA). The AAOCA is categorized as a right coronary artery anomaly from the left sinus, a left coronary artery abnormality from the right sinus, and a single coronary artery. The LCx artery's independent origin from the LAD accounts for 0.41% of cases, while the LCx artery's origin from the RCA accounts for 0.37% of cases^16,17.

Single coronary artery (SCA) is a rare anomalous condition. In SCA, only one coronary artery arises from the aortic stem without discontinuing the vessel branch. This single coronary artery becomes RCA or LCA soon after the origin, divided into two or three main vessels. SCA is associated with other congenital heart defects such as transposition of the great vessels, persistent truncus arteries, coronary arterio-venous fistula, Tetralogy of Fallot, interventricular septal defect, patent ductus arteriosus, bicuspid aortic valve, patent foramen ovale, and double outlet right ventricle (DORV) in 40% of cases. Patients with persistent truncus arteriosus had significant coronary artery abnormalities. This coronary artery abnormality leads to a high operative mortality rate and sudden death later in life. SCA can have multiple courses, such as retro-aortic (posterior to the aortic root), trans-septal/interseptal/sub-pulmonic (via the proximal interventricular septum), pre-pulmonic (via the RVOT or PA), or intraarterial (between the aorta and the PA)^12,18.

In 1979, Lipton et al. classified isolated SCA according to the site of origin, branch pattern, and coronary artery course on angiography⁵. Yamanaka and Hobbs modified this classification in 1990 to include a septal course¹. Based on the course from one side of the heart to the other, the Lipton II and III groups classify the SCA into the abbreviations A, B, P, S, or C. Lipton-Yamanaka divides SCA according to anatomical origin into two main groups, namely: R (Right; vessels originating from the right sinus) and L (Left; vessels originating from the left sinus), then according to the branching pattern into three classes (I-III), and according to the course of coronary arteries into A (anterior to pulmonary or pre-pulmonic arteries), B (between the aorta and pulmonary trunk-intraarterial course), P (posterior of the aorta-retroaortic course), S (trans-septal course through the interventricular septum), and C (different combination pathways)^12,18.Our patient had SCA with type LII-A variation. In cases where the RCA arises from the LAD, it usually arises after the first septal perforator branch. Less commonly, it may arise from the proximal segment¹⁹. In our patient, the RCA originates from the proximal LAD, an extremely rare presentation with less than 50 cases reported in the medical literature²⁰. This anomaly falls under the spectrum of a single coronary artery anomaly, indicating that the coronary arteries originate from a single coronary ostium within the aorta. This anomaly is commonly associated with no other structural abnormalities or congenital heart disease¹⁹. The mechanism of the anomalous coronary artery was divided into cellular and molecular mechanisms.

An anomalous coronary artery's cellular mechanism comes from embryonic development disruptions. First, the connection of the coronary anomaly (CA) stems to the cardiac arterial pole; any disruption of this process causes anomalous CA connections to the aorta. Second, differentiation of coronary progenitor cells (including possibly abnormal epithelial-to-mesenchymal transition/EMT), disruption of this process can reduce the number of embryonic coronary progenitor cells, and their maturation is delayed or premature. Third, the interaction between coronary vessels and myocardium. Disruption of the coronary-myocardial interaction will impact the CA mapping over the ventricular space¹⁸.

Moreover, the molecular mechanism of an anomalous coronary artery can arise from disturbances in a large number of molecular and cellular mechanisms, such as evidence from phenotype analysis of animal models for cardiovascular developmental studies. Wilms tumor suppressor gene (Wt1) is a zinc-finger transcription factor that regulates epicardial secreted retinoate signaling. Impaired retinoic acid synthesis due to Wt1 in the epicardium can directly or indirectly downregulate the expression of PDGF receptor a,bon EPDCs (epicardial-derived cells), impairing the differentiation of coronary smooth muscle progenitor cells. Another essential factor for coronary vessel development is the Notch/Delta cell-to-cell signaling pathway, which is vital in triggering arterial endothelial destiny during coronary vessel development. Down-regulation of nuclear transcription factor Coup-tfII, a Notch repressor, and up-regulation of Ephrinb2 expression in CA progenitor cells are also associated with endothelial CA specification.However, the underlying genetic mechanism is unknown. Myocardium-secreted FGF and VEGF also play a role in regulating coronary endothelial cell fate and vascular assembly. These two growth factors are closely related¹⁸.

Imaging methods like invasive angiography, CCTA, and cardiac magnetic resonance imaging (MRI) can assist in diagnosing SCA. Coronary angiography is the gold standard imaging method for visualizing coronary arteries. However, its disadvantages are that it is invasive, associated with problems, and is inferior in portraying coronary artery anatomy in complex instances. Consequently, CCTA is becoming an additional imaging modality of the highest caliber. One of the clinical justifications for cardiac computed tomography (CT) is to exclude or exclude coronary artery abnormalities from imaging. The benefits of cardiac CT in evaluating coronary artery anomalies are non-invasive with high temporal/spatial resolution and suitable for assessing the origin and course of coronary anomalies (malignant vs. benign). It can depict relationships with surrounding structures, and volume-rendered 3D images can show a special relationship between the aortic root and anomaly coroner. Unlike MRI, cardiac CT allows reliable visualization of the entire vessel to illustrate the anatomical relationships between prominent veins and heart chambers^10,21,22.

Also, CCTA can detect or rule out coronary artery stenosis. Consequently, there is a discrepancy between coronary angiography and CCTA results in our patient's case, as the proximal LAD and proximal RCA appeared normal (without stenosis) on coronary angiography. In this present case, CCTA demonstrated proximal LAD remodeling plaque (mixed plaque) above the stent with mild to moderate stenosis (35-50%). A Soft plaque was observed at proximal RCA with moderate to severe stenosis (68-75%). Nevertheless, RCA stenosis is likely when adjusted for the ECG results of the patient exhibiting ischemia in the inferior lead and the patient who occasionally complains of shortness of breath. Patients with SCA have an elevated risk of ischemia and sudden cardiac arrest (SCA), particularly in athletes and young people; however, this only happens in SCA with an intraarterial (aortopulmonary) course or SCA type RIIB. Although the anomalous connection of the RCA and LCA to the defective aortic sinus involves hazards, it is believed that the anomalous connection of the LCA to the right coronary sinus is more malignant due to the increased risk of myocardial ischemia¹⁸. Due to its inability to produce collateral channels, stenosis in the proximal region of the SCA might cause widespread myocardial infarction (as in our instance).

If the patient is asymptomatic, no additional treatment is required; if the SCA has an intraarterial course without an intramural segment, pulmonary artery translocation can be performed to move the pulmonary artery away from the coronary arteries (laterally or anteriorly). In individuals with angina, the treatment for SCA with a transseptal course is CABG. In contrast, retroaortic SCA does not necessitate particular treatment because it is not hemodynamically significant¹². Our patient with SCA had a pre-pulmonary course. A pre-pulmonic course is an abnormal coronary artery path that travels anteriorly to the pulmonary artery orRVOT. The LMCA is the artery with the most common pre-pulmonary course. RCAs originating atypically from the LMCA or LAD may also have a pre-pulmonary course.

In most cases, these people have no symptoms. Nevertheless, some patients have reported experiencing angina. Coronary arteries may complicate the correction of RVOT stenosis in individuals with Tetralogy of Fallot¹².Current guidelines propose evaluating coronary artery anatomy prior to RVOT intervention to prevent potential issues during the intervention²³. Our patient had an SCA with a pre-pulmonic course, no family history of SCD, and a normal LVEF (even after a STEMI); hence the risk of SCD was low. Invasive coronary angiography is the gold standard for diagnosing and treating coronary disorders²⁴, although it reveals just the artery lumen and provides no information about the vessel wall or surrounding tissues.

Unless the RCA runs between the aorta and pulmonary artery, the RCA arising from the LAD is typically asymptomatic, incidentally detected, and has a favorable prognosis. There is no consensus regarding the atherosclerosis risk in SCA patients. SCA is not related to an elevated risk for the development of atherosclerotic coronary artery disease, according to earlier research^25,26. Contrary to popular belief, coronary segments with an anomalous course are not more susceptible to obstructive disease than normal segments in the same individual. The most likely cause of atherosclerotic lesions in our patient was the patient's risk factors, which included smoking for more than ten years and uncontrolled hypertension. Since the patient arrived with STEMI, we performed PPCI with OMT to treat acute coronary syndrome and hypertensive emergency. ISDN, aspirin and ticagrelor, candesartan, bisoprolol, and atorvastatin are among the treatments we administered. The Eropean Society of Cardiology Guideline for STEMI suggests double anti-platelet in the form of a combination of aspirin and a P2Y12 inhibitor (prasugrel, ticagrelor, or clopidogrel) for up to 12 months in STEMI patients undergoing PPCI, oral beta-blockers in hemodynamically stable STEMI patients undergoing PPCI, nitrates, and angiotensin-converting enzyme inhibitor or angiotensin receptor blocker in patients with LV dysfunction, heart failure, or hypertension. Current guidelines propose evaluating coronary artery anatomy prior to RVOT intervention to prevent potential issues during the intervention²³.

CONCLUSION:

An extremely unusual coronary abnormality is the genesis of the RCA from the LAD. Once diagnosed, the physician must undertake a CT scan of the cardiac anatomy to comprehend better the complete course of the anomalous coronary artery and its anatomical relationship to the major vessels. CT cardiac is the gold standard investigational method for diagnosing coronary anomalies, and new guidelines urge using it for a thorough study of coronary anomalies.

ACKNOWLEDGMENTS:

We would like to thank the General Hospital Soetomo Surabaya where this case was carried out.

CONFLICT OF INTEREST:

No conflicts of interest were disclosed

REFERENCES:

1. Prayogo ARS, Yunita E, Yolanda R, Fahri I, Lestari N, Asteria M, Nasution AA, Jusup E, Sipriyadi, Djatmiko EM. Carotid intima-media thickness in the first descendant of coronary artery disease patients with Apolipoprotein-E4 genotype. Bali Med J. 2022; 11(3): 1774–1779. DOI: 10.15562/bmj.v11i3.3798

2. Nur Yahya T, Sembiring YE, Soelistijo SA. The The outcome of sternum healing among diabetic patients undergoing open heart surgery: a literature review. Bali Med J. 2022; 11(2): 818–826. DOI: 10.15562/bmj.v11i2.3513

3. Limantoro C, Santoso F, Suharti C, Nugroho T. The relationship between inflammatory markers and vitamin D levels with the severity of coronary artery disease in elderly patients. Bali Med J. 2022; 11(3): 1865–1869. DOI: 10.15562/bmj.v11i3.3631

4. Yosaputra C, Lefrandt RL, Panda AL, Pangemanan J. Correlation between Left Ventricular Ejection Fraction (LVEF) and six-month mortality risks after hospital discharge following myocardial infarction in patients with Non-ST-Elevation Myocardial Infarction (NSTEMI) at Prof. Dr. R. D. Kandou General Hospita. Bali Med J. 2021; 10(3): 975–978. DOI: 10.15562/bmj.v10i3.2749

5. Vianney T, Ida BRW, Ida SI, Ketut BN. Evaluating Low Values of Early Diastolic Velocity (e’) as a Predictor of Major Cardiovascular Events in Patients with Acute Myocardial Infarction. Bali Med J. 2022; 11(1), 418–424. DOI: 10.15562/bmj.v11i1.3360

6. Rampengan SH, Untu VBFP. Acute myocardial infarction (AMI) in a patient with Human Immunodeficiency Virus infection. Bali Med J. 2022; 11(2): 619–627. DOI: 10.15562/bmj.v11i2.3569

7. Gentile F, Castiglione V, De Caterina R. Coronary Artery Anomalies. Circulation. 2021;144:983–96. DOI: 10.1161/CIRCULATIONAHA.121.055347

8. Angelini P. Coronary Artery Anomalies: An Entity in Search of an Identity. Circulation. 2007;115:1296–305. DOI: 10.1161/CIRCULATIONAHA.106.618082

9. Carrascosa PM, Capuñay CM, Deviggiano A, Rodriguez-Granillo GA. Clinical Atlas of Cardiac and Aortic CT and MRI. Capuñay C, Carrascosa P, Deviggiano A, Rodríguez-Granillo G, editors. Switzerland: Springer Nature; 2019. 1–373 p.

10. Kadoch M, Becker H. CT of the Heart. 2nd Editio. Schoepf U, editor. USA: Humana Press; 2019. 1–903 p.

11. Bezold L, Windle M, Stewart J, Berger S, Alejos J. Coronary Artery Anomalies. Medscape. 2019. p. 1.

12. Rajeshkannan R, Viswamitra S, Raj V. CT and MRI in Congenital Heart Diseases. Rajeshkannan R, Viswamitra S, Raj V, editors. Singapore: Springer Nature; 2021. 1–584 p.

13. Ahmadi A, Ferencik M, Bhatia M, Budoff M, Foldyna B, Bull R. Oxford Specialist Handbooks in Cardiology: Cardiovascular Computed Tomography. 2nd Editio. Stirrup J, Bull R, Williams M, Nicol E, editors. United Kingdom: Oxford University Press; 2020. 1–573 p.

14. Nicol E, Stirrup J, Kelion AD, Padley SPG, editors. Cardiovascular Computed Tomography. Oxford University Press; 2011.

15. Siripornpitak S, Goo HW. CT and MRI for Repaired Complex Adult Congenital Heart Diseases. Korean J Radiol. 2021 Mar;22(3):308–23. DOI: 10.3348/kjr.2020.0895.

16. Graidis C, Dimitriadis D, Karasavvidis V, Dimitriadis G, Argyropoulou E, Economou F, et al. Prevalence and Characteristics of Coronary Artery Anomalies in an Adult Population Undergoing Multidetector-row Computed Tomography for the Evaluation of Coronary Artery Disease. BMC Cardiovasc Disord. 2015;15(1):112. DOI: 10.1186/s12872-015-0098-x

17. Villa AD, Sammut E, Nair A, Rajani R, Bonamini R, Chiribiri A. Coronary Artery Anomalies Overview: The Normal and the Abnormal. World J Radiol. 2016 Jun;8(6):537–55. DOI: 10.4329/wjr.v8.i6.537

18. Perez-Pomares J, de la Pompa J, Franco D, Henderson D, Ho S, Houyel L. Congenital Coronary Artery Anomalies: A Bridge from Embryology to Anatomy and Pathophysiology—A Position Statement of the Development, Anatomy, and Pathology ESC Working Group. Cardiovasc Res. 2016;109:204–16. DOI: 10.1093/cvr/cvv251

19. Salih M, Abdel-Hafez O, Ibrahim R, Halabi A, Aloka F. A Single Coronary Artery Anomaly: Right Coronary Artery as a Branch From the Left Anterior Descending Artery. Cureus. 2020;12(8). DOI: 10.7759/cureus.9801

20. Balghith M. Anomalous Origin of the Right Coronary Artery from the Proximal Left Anterior Descending Artery and a Single Coronary Artery Anomaly: Three Case Reports. J Saudi Hear Assoc. 2013;25:43–6. DOI: 10.1016/j.jsha.2012.05.002

21. Begemann P, Grigoryev M, Lund G, Adam G, Dewey M. Cardiac CT. 2nd Editio. Dewey M, editor. London: Springer-Verlag Berlin Heidelberg; 2014. 1–491 p.

22. Bhattarai V, Mahat S, Sitaula A, Neupane N, Rajlawot K, Jha S. A Rare Case of Isolated Single Coronary Artery, Lipton’s Type LIIB Diagnosed by Computed Tomography Coronary Angiography. Radiol Case Reports. 2022;17:4704–9. DOI: 10.1016/j.radcr.2022.08.089

23. Babu-Narayan S, Beinart R, Bradlow W, Buchner S, Burkhart H. Cardiac CT and MR for Adult Congenital Heart Disease. Saremi F, editor. London: Springer; 2014. 1–735 p.

24. Forte E, Inglese M, Infante T. Anomalous Left Main Coronary Artery Detected by CT Angiography. Surg Radiol Anat. 2016;38:987–90. DOI: 10.1007/s00276-016-1634-9

25. Juhanna IV, Adiputra IN, Adiatmika IPG, Muliarta IM, Linawati NM, Griadhi IPA. Exercise and cardiomyocyte regeneration. Bali Med J. 2020; 9(3): 947–951. DOI: 10.15562/bmj.v9i3.2029

26. Taylor A, Rogan K, Virmani R. Sudden Cardiac Death Associated with Isolated Congenital Coronary Artery Anomalies. J Am Coll Cardiol. 1992;20:640–7. DOI: 10.1016/0735-1097(92)90019-j

Received on 27.11.2022 Modified on 24.01.2023

Research J. Pharm. and Tech 2023; 16(11):5309-5315.

DOI: 10.52711/0974-360X.2023.00860