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 Table of Contents  
CASE REPORT
Year : 2022  |  Volume : 8  |  Issue : 1  |  Page : 45-47

A rare case of premature and parallel posterior descending artery and posterior left ventricular branch with conus crossing the right ventricular outflow tract causing provocative coronary ischemia


Department of Cardiology, AIIMS, Bhubaneswar, Odisha, India

Date of Submission17-Jul-2021
Date of Decision01-Dec-2021
Date of Acceptance08-Feb-2022
Date of Web Publication26-Apr-2022

Correspondence Address:
Debasish Das
Department of Cardiology, AIIMS, Bhubaneswar - 751 019, Odisha
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jpcs.jpcs_50_21

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  Abstract 


We report a rarely encountered case of premature and parallel posterior descending artery (PDA) and posterior left ventricular branch (PLVB) in a case of 22-year-old male with effort angina Class II for the last 6 months in whom treadmill test (TMT) was strongly positive for provocative coronary ischemia with structurally normal heart and good biventricular function. Interestingly, all the coronaries were normal without any obstructive coronary lesion. Paradoxically, those two prematurely separating branches were small making the distal right coronary artery (RCA) territory relatively ischemic attributing toward a strongly positive TMT. Small anomalous coronary is a well-known cause of demand ischemia, but our case is unique to describe small prematurely originating PDA and PLVB were the culprit behind coronary ischemia in a young male without conventional risk factors. Furthermore, much premature separation of PDA and PLVB is rarely encountered in routine clinical practice, and recognition of this anomaly is important as it should not be mistaken for duplicate RCA, dual RCA, or split RCA. Our case is also unique to illustrate the association of the premature and parallel PDA and PLVB with a conus crossing the right ventricular outflow tract without the presence of structural heart disease.

Keywords: Premature, Parallel, PDA, PLVB


How to cite this article:
Das D, Das T, Singh S, Gupta JD, Pramanik S. A rare case of premature and parallel posterior descending artery and posterior left ventricular branch with conus crossing the right ventricular outflow tract causing provocative coronary ischemia. J Pract Cardiovasc Sci 2022;8:45-7

How to cite this URL:
Das D, Das T, Singh S, Gupta JD, Pramanik S. A rare case of premature and parallel posterior descending artery and posterior left ventricular branch with conus crossing the right ventricular outflow tract causing provocative coronary ischemia. J Pract Cardiovasc Sci [serial online] 2022 [cited 2022 Jul 1];8:45-7. Available from: https://www.j-pcs.org/text.asp?2022/8/1/45/344130




  Introduction Top


Coronary anomaly is prevalent in more than 1% of the general population. Coronary anomalies are roughly categorized into the anomaly of origin, course, or distribution. We describe a rarely encountered anomaly in the course of right coronary artery (RCA) where RCA was prematurely dividing into relatively small posterior descending artery (PDA) and posterior left ventricular branch (PLVB) attributing toward a strongly positive stress test in a young male of 22 years. Although this embryological variation per se is not dangerous or more frequently associated with coronary artery disease, recognition of this anomaly is of utmost importance because when they are smaller than expected, they can be a reason of demand ischemia in the young or provocative coronary ischemia and also, they should not be confused with dual RCA, duplicate RCA, or split RCA.


  Case Report Top


A 22-year-old male nondiabetic, nonhypertensive, nonsmoker without any family history of coronary artery disease presented with effort angina Class II for the last 6 months. During the presentation, his vitals were within the normal limit. All the serum chemistries including hemoglobin, lipid profile, and thyroid panel were normal, an electrocardiogram was within normal limit, and echocardiography revealed a structurally normal heart with normal left ventricular systolic function and was subjected to a treadmill test which was strongly positive [Figure 1] and was subjected for right transradial coronary angiogram which revealed normal left coronaries with RCA anomaly with premature division of RCA to PDA and PLVB [Figure 2] and [Figure 3]. Interestingly, those two branches were relatively small rendering the distal RCA territory relatively ischemic attributing toward a strongly positive stress test. We treated the patient with optimum beta-blocker metoprolol 50 mg twice daily with trimetazidine 35 mg twice daily to improve the blood flow to the myocardial microcirculation. Although premature separation of PDA and PLVB can be seen in a busy intervention laboratory, their parallel nature is not yet described in the literature. Our case is an illustration of a relatively benign coronary anomaly when small in nature can attribute toward demand-driven ischemia or provocative ischemia.
Figure 1: Strongly positive treadmill test

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Figure 2: Small premature and parallel posterior descending artery and posterior left ventricular branch with distal relatively ischemic myocardium (Marked)

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Figure 3: Premature division of right coronary artery to posterior descending artery and posterior left ventricular branch and their parallel orientation

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  Discussion Top


Angelini[1] defined normal human coronary should have branches adequate for the dependent myocardium. When branching of the coronary is premature and falls short of the area of intended supply, it may result in demand ischemia or may be a reason behind provocative coronary ischemia. Anomalies of the origin of RCA can be of three types: high, low, or commissural. High origin of RCA with an ascending curve is popularly known as Shepherd crook RCA. RCA arising from the left coronary sinus is the most common anomaly noted in clinical practice. It can have anomalous course in the form of retroaortic, retrocardiac, interarterial, intraseptal, anterior to right ventricular outflow tract (RVOT), or wrap-around course.[2] Premature separation of RCA into PDA and PLVB before the midsegment has not been so frequently described in the literature. When they separate much prematurely, they relatively fall short of the intended area of supply as demonstrated in our case and contributes toward myocardial ischemia. Angelini[1] also described inadequate arteriolar or capillary ramification also constitutes a coronary anomaly as the intended area of supply remains under perfused. The above angiogram illustrates less ramification of the PLVB branch responsive of provocative left ventricular ischemia in the young without the presence of obstructive coronary lesion. This premature separation per se does not predispose the patient to the increased incidence of coronary artery disease or sudden cardiac death as noted in the interarterial course, i.e., between aorta and pulmonary artery due to systolic compression.[3] Another interesting finding in our coronary angiogram was conus crossing the RVOT [Figure 2] which is rare to encounter in structurally normal heart. Conus crossing the RVOT bears a great surgical significance in congenital heart diseases such as Tetralogy of Fallot.[4] Simultaneous presence of premature division of RCA into parallelly running PDA and PLVB with conus crossing the RVOT has not been described in the literature so far. In [Figure 2], the small white arrow indicates conus crossing the RVOT. PDA and PLVB normally intend a right angle at the crux of the heart as PDA descends down in the posterior interventricular groove and PLVB wraps the back of the heart running in the left posterior atrioventricular groove. Our case is a unique illustration of parallelly running PDA and PLVB which were relatively small with less arborization of PLVB contributing toward myocardial ischemia. Without the presence of obstructive coronary artery disease, coronary anomaly may give rise to obligatory ischemia if associated with coronary ostial stenosis, atresia, bridging, or fistula. Tangential origin of ectopic orifice has also been recognized as a cause of coronary ischemia in anomalous coronaries.[5] We put the patient on optimum beta-blockade to prevent demand-driven ischemia or provocative ischemia in the young. Asano et al. described 2%–9% of TOF patients have an ACA crossing the RVOT.[6] Angina with normal coronaries otherwise known as microvascular angina was ruled out as patient did not have any comorbidity in the form of diabetes mellitus, was quite young, and nonobese also. Relatively, nonperfused myocardium gives rise to angina due to deficit in the coronary microcirculation. In the absence of atherosclerotic stenosis, ischemia in anomalous coronary artery can be a result of anatomical malformations, including an acute take-off angle of the anomalous vessel, myocardial squeezing, vasospasm, and a small artery.[7] Duplicate RCA or split RCA also when small can attribute toward the development of demand angina when they are small or terminate prematurely before the intended area of supply. It is not always the obstructive coronary lesion that gives rise to ischemia, across anomalous coronaries abnormal proximal angulation, and variation in course such as subendocardial, myocardial bridge, premature termination, or deficit arborization may also contribute toward the development of coronary ischemia as noted in our case. Each coronary anomaly is itself a distinct entity and behaves strikingly differently; as noted in our case, a premature division of RCA into PDA and PLVB with early termination with less arborization of PLVB was the cause of coronary ischemia in the young.


  Conclusion Top


Our case is a rare illustration of premature division of RCA into PDA and PLVB with early termination with less arborization of PLVB and relatively nonperfused distal myocardium as a cause of provocative ischemia in a young. It is also a unique to illustrate the association of the premature and parallel PDA and PLVB with a conus crossing the RVOT in the index patient without structural heart disease. In-depth analysis of the coronary anatomy is a prerequisite to discover the cause of ischemia in the young.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Angelini P. Coronary artery anomalies: An entity in search of an identity. Circulation 2007;115:1296-305.  Back to cited text no. 1
    
2.
Driscoll DJ. Congenital coronary artery anomalies. In: Garson A, Bricker TJ, McNamara DG, editors. The Science and Practice of Pediatric Cardiology. Philadelphia: Lea & Febiger; 1990. p. 1453-61.  Back to cited text no. 2
    
3.
Taylor AJ, Rogan KM, Virmani R. Sudden cardiac death associated with isolated congenital coronary artery anomalies. J Am Coll Cardiol 1992;20:640-7.  Back to cited text no. 3
    
4.
Hyder SN, Ali Hasan AK, Mehmood N. The anomalous origin and course of coronaries in Tetralogy of Fallot (TOF). Pak J Med Health Sci 2015;9:795-7.  Back to cited text no. 4
    
5.
Angelini P, Villason S, Chan AV, Diez JG. Normal and anomalous coronary arteries in humans. In: Angelini P, editor. Coronary Artery Anomalies: A Comprehensive Approach. Philadelphia: Lippincott Williams & Wilkins; 1999. p. 27-150.  Back to cited text no. 5
    
6.
Asano M, Nomura N, Sasaki S, Mishima A. Surgical repair of tetralogy of Fallot with large conus artery. Pediatr Cardiol 2003;24:601-3.  Back to cited text no. 6
    
7.
Tuncer C, Batyraliev T, Yilmaz R, Gokce M, Eryonucu B, Koroglu S. Origin and distribution anomalies of the left anterior descending artery in 70,850 adult patients: Multicenter data collection. Catheter Cardiovasc Interv 2006;68:574-85.  Back to cited text no. 7
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]



 

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