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Mechanism of myocardial ischemia with an anomalous left coronary artery from the right sinus of Valsalva  Carlo R. Bartoli, PhD, William B. Wead, PhD,

Published bySuryadi Sukarno Sasmita Modified over 6 years ago

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Presentation on theme: "Mechanism of myocardial ischemia with an anomalous left coronary artery from the right sinus of Valsalva  Carlo R. Bartoli, PhD, William B. Wead, PhD,"— Presentation transcript:

1 Mechanism of myocardial ischemia with an anomalous left coronary artery from the right sinus of Valsalva  Carlo R. Bartoli, PhD, William B. Wead, PhD, Guruprasad A. Giridharan, PhD, Sumanth D. Prabhu, MD, Steven C. Koenig, PhD, Robert D. Dowling, MD  The Journal of Thoracic and Cardiovascular Surgery  Volume 144, Issue 2, Pages (August 2012) DOI: /j.jtcvs Copyright © 2012 The American Association for Thoracic Surgery Terms and Conditions

2 Figure 1 Regional myocardial blood flow was measured in a bovine heart with an LCA that emerged from the right sinus of Valsalva and coursed between the great vessels. A, Lead II electrocardiographic tracings demonstrated ST-segment depression that worsened with increasing heart rate. Regional myocardial blood-flow mapping of the ventricles demonstrated a large area of myocardial ischemia. B, At rest, LV myocardial blood flow was greater than RV myocardial blood flow (P = .06). At elevated heart rates this trend reversed, and blood flow to myocardium supplied by the anomalous LCA was significantly lower than to myocardium supplied by the normal RCA (∗P < .01). C, During the transition from normal blood pressure to hypertension, volumetric LCA blood flow tracings showed abnormal decreases in peak and mean systolic and peak diastolic coronary blood flows versus during baseline blood pressure. Similarly, myocardial blood-flow maps showed that, during the hypertension condition, blood flow to LCA myocardium did not increase appropriately and decreased in some regions. Myocardium supplied by the normal RCA showed a normal increase in blood flow during hypertension. D, In control calves (n = 9), hypertension increased coronary blood flow during all phases of the cardiac cycle. However, in the present animal, hypertension decreased systolic and beginning diastolic coronary blood flows. E, The abnormal coronary blood-flow profiles shown in C and D were caused by a large, inappropriate increase in coronary resistance during systole. This abnormal pattern of cardiac cycle-dependent coronary resistance and blood flow demonstrated a pattern consistent with systolic aortic root compression of the LCA. HR, Heart rate; LCA, left coronary artery; RCA, right coronary artery; CAF, coronary artery flow; MAP, mean arterial pressure; S, systole; D, diastole; bpm, beats per minute. ∗P < .01 LCA vs RCA myocardial sections. The Journal of Thoracic and Cardiovascular Surgery  , DOI: ( /j.jtcvs ) Copyright © 2012 The American Association for Thoracic Surgery Terms and Conditions

3 Figure 2 A, In the catheterization laboratory, an aortogram revealed an ectopic LCA that emerged from the right sinus of Valsalva. B, Gross examination from within the aortic root demonstrated that the ostium of the LCA originated at an acute angle from the right aortic sinus (arrow). A normal RCA ostium is visible in the right sinus of Valsalva. C and D, Masson’s trichrome staining exhibited normal levels of fibrosis in RV myocardium (C) and elevated fibrosis and myocyte hypertrophy in LV myocardium. 40×, black bar = 100 μm. E and F, FITC-conjugated wheat-germ agglutinin staining confirmed normal sized myocytes in RV myocardium (E) and grossly hypertrophic myocytes in LV myocardium (F). 40×, white bar = 100 μm. G and H, TUNEL staining revealed an elevated apoptotic rate throughout the heart. G, Two TUNEL+ nuclei are seen in close proximity in a small sample of LV myocardium. DAPI nuclear stain and FITC TUNEL+ nuclear stain overlay. 40×, white bar = 100 μm. H, Numerous TUNEL+ cells are noted in close proximity to a large-caliber intramural coronary artery and vein: Bright field and DAPI nuclear stain and FITC TUNEL+ nuclear stain overlay. 2×, white bar = 1000 μm. I and J, Endothelial staining of transverse and longitudinal myocardial sections with FITC-conjugated isolectin-B4 demonstrated higher capillary density and more collateral channels (longitudinal vessels in the transverse plane) in LV myocardium (J) than in RV myocardium (I), which suggested ischemia-induced neovascularization. 10×, white bar = 400 μm. The Journal of Thoracic and Cardiovascular Surgery  , DOI: ( /j.jtcvs ) Copyright © 2012 The American Association for Thoracic Surgery Terms and Conditions

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