Dual LAD - Case report of a calcified four vessels disease

Maximilian Bayer (Dresden)1, M. Galandova (Chemnitz)2, A. Youssef (Chemnitz)3, K. Ibrahim (Chemnitz)2

1Herzzentrum Dresden GmbH an der TU Dresden Klinik für Innere Medizin und Kardiologie Dresden, Deutschland; 2Klinikum Chemnitz gGmbH Innere Medizin I - Kardiologie Chemnitz, Deutschland; 3MVZ am Küchwald GmbH Klinik für Innere Medizin I Chemnitz, Deutschland


Background: Duplication of the left anterior descending artery (LAD) is a rare congenital coronary disorder and presents with an incidence variation between 0,68 % and 6 %1. There are many anomalies which can be summarized under the term of dual LAD, currently there are 13 identified and classified variants.2
A profound understanding of morphological characteristics of these different anomalies leads to better treatment strategies and therefore to more successful revascularization. We present a case of a male with a calcified 3-vessels disease which turned out to be a 4-vessels disease.

Case presentation: A 69-year-old Patient presented with acute typical angina pectoris. ECG showings and troponin levels were normal. Transthoracic echocardiography showed a left ventricular systolic function of 70% without wall abnormalities. We proceeded a coronary CT angiography first, which showed a calcified 3-vessels coronary artery disease and raised suspicion of LAD anomaly (Figure 1). Coronary catheterization was performed right away (Figure 2 & 3) and a dual LAD Type 13 (Table 1) was diagnosed. The patient was transferred for heart surgery where he successfully underwent a MIDCAB operation (LIMA ad LAD1, CABG ad PLA1 and RIVP) Figure 1 Figure 2 (blue= LAD1 + diagonal branch, red= LAD2 + diagonal branch)

Discussion and Conclusions: The first data and classification referring to dual LAD goes back until 1983, where three variants were described3. Until today the classification has extended until 13 variants, as seen in Table 12 Theoretically and rationally one could think that morbidity and mortality is lower in patients with two LADs.4 Conceivably this could even be one of the reasons our patient presented neither with suspect ECG findings, high cardiac enzymes nor echocardiographic abnormalities. Nevertheless data to support such hypothesis are currently lacking5. To the best of our knowledge this is only the second time a type 13 DLAD is presented in the literature.2 Due to the many variants and the complex classification, Jariwala et. al. promoted a novel classification, where DLADs are placed on three patterns based on their origins ((I) both LADs arise from LCS, (II) LAD from LCS and RCS each, (III) both originate from RCS) and then can be further characterized into subgroups1. However looking at the LAD as perhaps the most crucial coronary artery, knowing and identifying the possibility of a dual LAD is essential for clinicians and especially interventionalists to avoid misinterpretation and provide optimal treatment. 

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