Posts in Category: Coronary Artery Disease

Fractional Flow Reserve and Coronary Computed Tomographic Angiography: A Review and Critical Analysis

Fractional Flow Reserve and Coronary Computed Tomographic Angiography: A Review and Critical Analysis

Harvey S. Hecht, Jagat Narula, William F. Fearon

Myocardial perfusion imaging (MPI) by computed tomography (CT). Stress (dipyridamole) perfusion CT (A, mid-diastole 4- and 2-chamber multiplanar reconstruction [MPR] using a smooth filter are shown) was performed in view of the high pretest coronary artery disease likelihood using conventional static CT-MPI protocol with a 256-detector scanner and demonstrated an extensive reversible perfusion defect at the anterior wall (*) and a mild subendocardial reversible perfusion defect at the inferior wall (arrow). Single-photon emission CT confirmed the findings (B). The patient was referred to invasive coronary angiography (C), which showed 3-vessel disease with totally occluded right coronary artery, critical lesion at the left anterior descending artery, and severe lesion at the distal circumflex artery. Reprinted from Gonçalves et al54 with permission of the publisher. Copyright ©2015, Elsevier. [Powerpoint File]

Prognostic Determinants of Coronary Atherosclerosis in Stable Ischemic Heart Disease: Anatomy, Physiology, or Morphology?

Prognostic Determinants of Coronary Atherosclerosis in Stable Ischemic Heart Disease: Anatomy, Physiology, or Morphology?

Amir Ahmadi, Gregg W. Stone, Jonathon Leipsic, Leslee J. Shaw, Todd C. Villines, Morton J. Kern, Harvey Hecht, David Erlinge, Ori Ben-Yehuda, Akiko Maehara, Eloisa Arbustini, Patrick Serruys, Hector M. Garcia-Garcia, Jagat Narula

Modification of the natural history of coronary disease by local implantation of a bioresorbable scaffold. From left to right: Intimal thickening (a), intimal xanthoma (b), pathological intimal thickening (c), fibroatheroma (d), thin-capped fibroatheroma (e) (reprinted from García-García et al92 with permission of the publisher. Copyright © 2009, Europa Digital & Publishing). As coronary disease progresses, does the endothelial function worsen. After the implantation of the scaffold, it can be seen that the 3-dimensional (3D) structure of the device can be delineated by means of optical coherence tomography (OCT) (f). In histology, it can be appreciated the polymeric struts overlying on the vessel wall (black arrow). On the 2D OCT image, the squared-shape struts are translucent and therefore their whole thickness can be appreciated (f′). At 5 o clock, the metallic marker can be seen (*). Invasive imaging by means of angiography and OCT allows the reconstruction of the scaffolded artery (f″). Thereafter, blood flow simulation was performed on the luminal surface and around struts at baseline and the local shear stress conditions were measured. As times goes by, the struts are integrated into the vessel wall and cover by neointima (g and g′). When the shear stress at baseline is portrayed into the follow-up OCT images (g″), it became apparent that the low shear stress areas at baseline (blue) correlate with thicker neointima thickness at follow-up as compared to high shear stress areas (on top of struts in red color), which showed thinner neointima thickness (reprinted from Bourantas et al93 with permission of the publisher. Copyright © 2014, American College of Cardiology Foundation. Published by Elsevier Inc.). Eventually, the polymeric struts will disappear (h) and somewhat vessel wall thinning is observed (i). As the bioresorbable vascular scaffold (BVS) integrates and dissolves, there is some vasomotion restoration (reprinted from Serruys et al94 with permission of the publisher. Copyright © 2014, American College of Cardiology Foundation. Published by Elsevier Inc.). EL indicates extracellular lipid; FC, fibrous cap; NC, necrotic core. BVS is a product of Abbott Vascular, Santa Clara, CA. [Powerpoint File]

MicroRNAs for Restenosis and Thrombosis After Vascular Injury

MicroRNAs for Restenosis and Thrombosis After Vascular Injury

Clarice Gareri, Salvatore De Rosa, Ciro Indolfi

The cartoon represents the hypothetical structure of a vascular scaffold able to elute microRNAs (miRNAs). The scaffold (blue) is coated by poly-lactic-co-glycolic acid (PLGA) (green). At the bottom of the figure, the most promising miRNAs to be modulated for therapeutic use are listed. [Powerpoint File]

MicroRNAs for Restenosis and Thrombosis After Vascular Injury

MicroRNAs for Restenosis and Thrombosis After Vascular Injury

Clarice Gareri, Salvatore De Rosa, Ciro Indolfi

The figure illustrates specific vascular (upper section) or platelet-derived (lower section) microRNAs that can be measured in the flowing bloodstream. [Powerpoint File]

MicroRNAs for Restenosis and Thrombosis After Vascular Injury

MicroRNAs for Restenosis and Thrombosis After Vascular Injury

Clarice Gareri, Salvatore De Rosa, Ciro Indolfi

Schematic representation of the most relevant microRNAs (miRNAs) that modulate vascular smooth muscle cell (VSMCs) proliferation, with their direct molecular targets. The red area includes miRNAs that inhibit VSMCs proliferation (thus preventing ISR), whereas the green area indicates miRNAs that promote the synthetic phenotype of VSMCs. BMPR2 indicates bone morphogenetic protein receptor type II; Cdc-42, cell division control protein 42; FOXO4, Forkhead box protein O4; KLF-4, Kruppel-like factor 4; KLF-5, Kruppel-like factor 5; PTEN, phosphatase and tensin homolog; SMAD3, small mother against decapentaplegic; uPA, urokinase-type plasminogen activator; and WWP1, NEDD4-like E3 ubiquitin-protein ligase. [Powerpoint File]

MicroRNAs for Restenosis and Thrombosis After Vascular Injury

MicroRNAs for Restenosis and Thrombosis After Vascular Injury

Clarice Gareri, Salvatore De Rosa, Ciro Indolfi

Representative case of arterial restenosis, observed by means of intravascular optical coherence tomography (OCT). The picture shows a human artery with intimal hyperplasia 2 years after PCI with implantation of a coronary scaffold (struts-remnants indicated by yellow arrows). A thick neointimal layer is evident at the adluminal side of the struts-remnants (neointimal area included between the yellow dotted line and the green line). [Powerpoint File]

The Human Microcirculation: Regulation of Flow and Beyond

The Human Microcirculation: Regulation of Flow and Beyond

David D. Gutterman, Dawid S. Chabowski, Andrew O. Kadlec, Matthew J. Durand, Julie K. Freed, Karima Ait-Aissa, Andreas M. Beyer

Proposed mechanism for the stress-induced switch in the mediator of flow-induced dilation. In arterioles from healthy subjects, shear activates production of NO to stimulate dilation and vascular homeostasis (left side of diagram). Vascular stress or presence of coronary disease stimulates pathological basal levels of oxidants and initiates a switch in the mediator of flow-induced dilation from NO to hydrogen peroxide. This switch requires ceramide and a reduction in telomerase. Dilation is maintained but at the expense of vascular inflammation and its consequences. Ang II indicates angiotensin II; CAD, coronary artery disease, HTN, hypertension; NO, nitric oxide; and TERT, catalytic subunit of telomerase. [Powerpoint File]

The Human Microcirculation: Regulation of Flow and Beyond

The Human Microcirculation: Regulation of Flow and Beyond

David D. Gutterman, Dawid S. Chabowski, Andrew O. Kadlec, Matthew J. Durand, Julie K. Freed, Karima Ait-Aissa, Andreas M. Beyer

In a healthy heart (left), arteriolar endothelium produces NO, prostacyclin (PGI2), and epoxyeicosatrienoic acids (EETs) as well as low levels of hydrogen peroxide, which support a quiescent nonproliferative state. With onset of disease, flow through the microvasculature releases hydrogen peroxide, creating a proinflammatory environment throughout the organ, potentially leading to hypertrophy, fibrosis, and atherosclerosis. NO indicates nitric oxide. [Powerpoint File]

Cellular Origin and Developmental Program of Coronary Angiogenesis

Cellular Origin and Developmental Program of Coronary Angiogenesis

Xueying Tian, William T. Pu, Bin Zhou

Formation of the nascent coronary vessel plexus in the developing heart. A and B, The 3 major sources of coronary vessels: the proepicardium (PE), sinus venosus (SV), and endocardium (Endo) are intimately associated with each other during heart development. The PE is a transient structure (gray color) that wedged into the atrioventricular groove between liver sinusoids and SV, and eventually gives rise to the epicardium covering the heart. The SV (blue) is the venous inflow tract. Venous cells from SV sprout onto the heart and produce subepicardial coronary vessels. The endocardium (green) lines the heart lumen. Black-dashed arrows denote movement from one compartment to another, potentially complicating lineage-tracing experiments. Numbers in B correspond to those in A showing location of migration events. C, Three putative sources for intramyocardial coronary arteries (CAs) in the developing heart. Arrows indicate corresponding migration path. EC indicates endothelial cell; VEC, vascular endothelial cell. [Powerpoint File]

Cellular Origin and Developmental Program of Coronary Angiogenesis

Cellular Origin and Developmental Program of Coronary Angiogenesis

Xueying Tian, William T. Pu, Bin Zhou

Epicardial contribution to developing and adult heart. In early embryonic stage, epicardial cells form an epithelial sheet that covers the heart. At later embryonic stages, epicardial cells (Ep cells) form mesenchymal epicardium-derived cells (EPDCs) by epithelial to mesenchymal transition. EPDCs seem in the subepicardial layer (Sub Ep) and migrate into compact myocardium (Comp myo), where they differentiated into fibroblasts (Fb, 1), smooth muscle cells (SMC, 2), cardiomyocytes (CM, 3), and endothelial cells (ECs, 4). In adult heart under normal homeostatic conditions, most epicardial cells remain quiescent (gray color). Myocardial infarction (MI) activates the embryonic program (red) and these epicardial cells differentiate into SMC (5) and Fb (6), but rarely if at all to CMs or ECs. Paracrine factors, such as modRNA encoding Vegfa or thymosin β4 stimulates a subset of EPDCs to differentiate into EC (7) or CM (8) lineages, respectively in the post-MI hearts. Endo indicates endocardium. [Powerpoint File]

Cellular Origin and Developmental Program of Coronary Angiogenesis

Cellular Origin and Developmental Program of Coronary Angiogenesis

Xueying Tian, William T. Pu, Bin Zhou

Coronary vessel formation in the ventricle wall and ventricular septum. A, C, and E, Sagittal view of developing heart; (B, D, and F), cross-sectional view of the developing heart. Venous cells sprout from sinus venosus (SV) and dedifferentiate into undifferentiated subepicardial endothelial cells (ECs; black) in the dorsal side of heart. Because the heart continues to develop, these subepicardial ECs penetrate the myocardial wall and differentiate into arterial ECs (red), whereas the remaining subepicardial ECs redifferentiate into coronary veins (blue). On the ventral side of heart and in the ventricular septum, coronary ECs arise from endocardium during trabecular compaction (black) and sprout to form a coronary plexus that connects to the coronary vessels in the ventricle wall. a indicates atrium; and VS, ventricular septum. [Powerpoint File]

Cellular Origin and Developmental Program of Coronary Angiogenesis

Cellular Origin and Developmental Program of Coronary Angiogenesis

Xueying Tian, William T. Pu, Bin Zhou

First and second coronary vascular population in neonatal heart. Apln-CreER, induced at E10.5, labeled fetal coronary vascular endothelial cells (VECs) with Cre-activated RFP expression. In the P7 postnatal heart, VECs were present throughout the myocardial wall, as demonstrated by immunostaining for the VEC-selective marker FABP4 (middle), but the RFP lineage tracer of fetal VECs was only observed in the outer myocardial wall (left). The FABP4+RFP+ VECs, descended from fetal VECs, are designated the first coronary vascular population (CVP; red pseudocolor, right), whereas the remaining FABP4+RFP− VECs, formed de novo in the postnatal heart, are designated the second CVP (green pseudocolor, right). Bar, 1 mm. DAPI indicates 4′,6-diamidino-2-phenylindole; and RFP, red fluorenscent protein. [Powerpoint File]

Acute Coronary Syndromes Compendium: Genetics of Coronary Artery Disease

Acute Coronary Syndromes Compendium: Genetics of Coronary Artery Disease

Robert Roberts

Low-density lipoproteinn (LDL) and its cholesterol (LDL-C) are synthesized in the liver, and by binding to the LDL receptor (LDL-R), LDL-C is removed from the circulation. Statin X indicates that the class of drugs known as statins inhibits the synthesis of LDL-C. PCSK9 normally delays removal of LDL-C from the circulation. Inhibition of PCSK9 leads to faster removal of LDL-C and lower levels of circulating LDL-C. Reprinted from Roberts99 with permission of the publisher. Copyright ©2008, Elsevier. Authorization for this adaptation has been obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or adaptation. [Powerpoint FIle]

Acute Coronary Syndromes Compendium: Mechanisms of Plaque Formation and Rupture


Acute Coronary Syndromes Compendium: Mechanisms of Plaque Formation and Rupture

Jacob Fog Bentzon, Fumiyuki Otsuka, Renu Virmani, Erling Falk

Plaque rupture and healing. Rupture of a thin-cap fibroatheroma with nonfatal thrombus and subsequent healing with fibrous tissue formation and constrictive remodeling. [Powerpoint File]

Acute Coronary Syndromes Compendium: Mechanisms of Plaque Formation and Rupture


Acute Coronary Syndromes Compendium: Mechanisms of Plaque Formation and Rupture

Jacob Fog Bentzon, Fumiyuki Otsuka, Renu Virmani, Erling Falk

Lesion types of atherosclerosis and a proposed sequence of their development. A, Adaptive intimal thickening characterized by smooth muscle cell accumulation within the intima. B, Intimal xanthoma corresponding to the accumulation of foam cell macrophages within the intima. Pathological intimal thickening in C denotes the accumulation of extracellular lipid pools in the absence of apparent necrosis. D, Fibroatheroma indicating the presence of a necrotic core. The necrotic core and surrounding tissue may eventually be calcified, which forms fibrocalcific plaque shown in E. Because some of the advanced lesion types (fibroatheromas and fibrocalcific plaques) evolve simultaneously in life, their interrelationships are difficult to resolve in autopsy studies. Movat pentachrome stain. [Powerpoint File]