Original Article
Hypercholesterolemia is Accounted for Atherosclerosis at the Proximal Arterial Segments of Myocardial Bridging: A Pilot Study
Clinical and Applied Thrombosis/Hemostasis 1-6 ª The Author(s) 2014 Reprints and permission: sagepub.com/journalsPermissions.nav DOI: 10.1177/1076029614554995 cat.sagepub.com
Mustafa Aparci, MD1, Cengiz Ozturk, MD2, Sevket Balta, MD3, Sercan Okutucu, MD1, and Zafer Isilak, MD4
Abstract Arterial shear stress was generally implicated in the development of atherosclerotic plaque (AP). Atherosclerotic plaque may be associated with myocardial bridging (MB). We evaluated the metabolic abnormalities which could determine the localization of AP at the proximal coronary segment of MB. We analyzed the patients with MB, AP&MB, and AP on left anterior descending (LAD) artery who were diagnosed by multislice computed tomography coronary angiography. Serum levels of metabolic parameters were compared among study groups. Patients with MB&AP and AP were significantly older than those in the MB group. Patients with MB&AP had AP and MB at the proximal and middle segments of LAD artery, respectively. Total cholesterol, low-density lipoprotein (LDL) cholesterol and very LDL, and triglyceride levels were significantly higher in patients with MB&AP and AP compared to only MB. Low-density lipoprotein cholesterol was significantly correlated with the type of coronary artery disease in multiple regression analysis. Myocardial bridging may be an anatomical determinant for the localization of AP proximal to itself in the presence of hypercholesterolemia. Keywords myocardial bridging, atherosclerosis, hypercholesterolemia, hyperlipidemia
Introduction Tropism and development of atherosclerotic plaques (APs) on the middle and large arteries, for example, coronary and carotid arteries have been investigated for several decades. Wall shear stress (WSS) is a significant determinant for the initiation and progression of an AP on the arterial wall. Numerous factors including abnormal flow dynamics (eg, pulsatile, helical, or turbulence flow), osteal, and bifurcated and branching segments of arteries may induce WSS, whereas laminar flow property is less associated with AP.1 Diameter of arterial vessel, wall thickness, heart rate, and blood pressure are additional factors that could contribute the localization and progression of AP.2 Myocardial bridging (MB) is a congenital abnormality in which one or more segments of an epicardial coronary artery course under it.3 It is an anatomic obstacle which constricts the coronary artery from the outside. Although it could be diagnosed by means of systolic compression artery during invasive coronary imaging, it physiologically causes myocardial perfusion abnormality by producing a diastolic flow gradient between the proximal and distal segments of MB.4 So, a raised intracoronary flow pressure and also a turbulent flow inevitably occur at the coronary segment proximal to it. Close relationship between the hypercholesterolemia and
atherosclerotic coronary artery disease (CAD) is precisely documented by numerous studies. It was documented that the content of AP was rich in cholesterol crystals and inflammatory cells.5 Various mechanisms related to morphological features of coronary arteries and hypercholesterolemia had been proposed for the tropism, initiation, and progression of AP in association with hypercholesterolemia.6 In this study, we retrospectively evaluated whether the MB was anatomically associated with the localization of AP on the coronary artery of patients with CAD diagnosed by multislice computed tomography (MSCT) coronary angiography. We also evaluated the coexisting laboratory abnormalities which could be related to the development of AP.
1
Department of Cardiology, Etimesgut Military Hospital, Ankara, Turkey Department of Cardiology, Gulhane Military Medical Faculty, Ankara, Turkey 3 Department of Cardiology, Eskisehir Military Hospital, Ankara, Turkey 4 Department of Cardiology, Haydarpasa Training Medicine, Istanbul, Turkey 2
Corresponding Author: Sevket Balta, MD, Department of Cardiology, Eskisehir Military Hospital, Vis¸ nelik Mah., Atatu¨rk Cd. 26020 Akarbas¸ ı/ Eskis¸ ehir, Turkey. Email: [email protected]
Downloaded from cat.sagepub.com at WASHINGTON UNIV SCHL OF MED on November 14, 2015
2
Clinical and Applied Thrombosis/Hemostasis
Material and Method Study Design
Table 1. Localization of Atherosclerotic Plaques and Myocardial Bridging on LAD Coronary Artery in Patients With MB, MB&AP, and AP.
The study was designed retrospectively. Approval of local ethics committee was obtained. The entire laboratory data were gathered from the digital recordings of medical archives of the patients diagnosed with CAD by MSCT coronary angiography. The study populations are the subgroups of a cohort of 34 patients who were diagnosed as having CAD by MSCT coronary angiography. The criteria for the subgroups were presence of MB and/or AP.
Localization AP on LAD Artery Groups of Patients Patients with MB&AP Patients with AP
0 4
Total 7 9
Proximal
Middle
Distal
3 0
14 7
1 0
18 7
Luminal narrowing due to MB
We retrospectively reviewed the medical recordings of patients with CAD. They were grouped according to the findings on the MSCT coronary angiography. Images were reconstructed with 0.5-mm slices and analyzed with postprocess study. The study groups were defined as patients with MB (n ¼ 18), MB&AP (n ¼ 7), and AP (n ¼ 9) on left anterior descending (LAD) coronary artery. The patients underwent MSCT angiography due to equivocal or positive results on treadmill test.
Patients with MB Patients with MB&AP
Laboratory Data
Patients with MB&AP Patients with AP
Blood samples were obtained from all patients by a venous route at a 12-hour fasting state at 08 00 AM. Serum levels of total cholesterol; low-density lipoprotein cholesterol (LDLC), high-density lipoprotein cholesterol (HDL-C), and very low-density lipoprotein cholesterol (VLDL-C); and triglyceride (TG) were measured from serums derived from the venous blood sample by centrifuging at 4000 rpm for a 4-minute period. Additionally, fasting blood glucose (FBG), liver enzymes (aspartate aminotransferase [AST] and alanine aminotransferase [ALT]), blood urea, and creatinine were studied. Serum levels of all laboratory parameters were measured through auto-analysis and auto-calculation using Olympus AU640 (Beckman Coulter Inc., Japan) device. Complete blood count was studied from the blood sample obtained at a 12-hour fasting state in the morning and performed using Mindray Auto Hematology Analyzer-BC-6800 (A. Menarini Diagnostics, China) device.
7 5
Mid LAD
Localization MB on LAD Artery
Patients with MB Patients with MB&AP
Coronary Artery Imaging
Proximal LAD
None
Mild
Moderate
2 0
11 4
5 3
18 7
Arterial stenoses due to AP
Hypercholesterolemia is Accounted for Atherosclerosis at the Proximal Arterial Segments of Myocardial Bridging: A Pilot Study
Clinical and Applied Thrombosis/Hemostasis 1-6 ª The Author(s) 2014 Reprints and permission: sagepub.com/journalsPermissions.nav DOI: 10.1177/1076029614554995 cat.sagepub.com
Mustafa Aparci, MD1, Cengiz Ozturk, MD2, Sevket Balta, MD3, Sercan Okutucu, MD1, and Zafer Isilak, MD4
Abstract Arterial shear stress was generally implicated in the development of atherosclerotic plaque (AP). Atherosclerotic plaque may be associated with myocardial bridging (MB). We evaluated the metabolic abnormalities which could determine the localization of AP at the proximal coronary segment of MB. We analyzed the patients with MB, AP&MB, and AP on left anterior descending (LAD) artery who were diagnosed by multislice computed tomography coronary angiography. Serum levels of metabolic parameters were compared among study groups. Patients with MB&AP and AP were significantly older than those in the MB group. Patients with MB&AP had AP and MB at the proximal and middle segments of LAD artery, respectively. Total cholesterol, low-density lipoprotein (LDL) cholesterol and very LDL, and triglyceride levels were significantly higher in patients with MB&AP and AP compared to only MB. Low-density lipoprotein cholesterol was significantly correlated with the type of coronary artery disease in multiple regression analysis. Myocardial bridging may be an anatomical determinant for the localization of AP proximal to itself in the presence of hypercholesterolemia. Keywords myocardial bridging, atherosclerosis, hypercholesterolemia, hyperlipidemia
Introduction Tropism and development of atherosclerotic plaques (APs) on the middle and large arteries, for example, coronary and carotid arteries have been investigated for several decades. Wall shear stress (WSS) is a significant determinant for the initiation and progression of an AP on the arterial wall. Numerous factors including abnormal flow dynamics (eg, pulsatile, helical, or turbulence flow), osteal, and bifurcated and branching segments of arteries may induce WSS, whereas laminar flow property is less associated with AP.1 Diameter of arterial vessel, wall thickness, heart rate, and blood pressure are additional factors that could contribute the localization and progression of AP.2 Myocardial bridging (MB) is a congenital abnormality in which one or more segments of an epicardial coronary artery course under it.3 It is an anatomic obstacle which constricts the coronary artery from the outside. Although it could be diagnosed by means of systolic compression artery during invasive coronary imaging, it physiologically causes myocardial perfusion abnormality by producing a diastolic flow gradient between the proximal and distal segments of MB.4 So, a raised intracoronary flow pressure and also a turbulent flow inevitably occur at the coronary segment proximal to it. Close relationship between the hypercholesterolemia and
atherosclerotic coronary artery disease (CAD) is precisely documented by numerous studies. It was documented that the content of AP was rich in cholesterol crystals and inflammatory cells.5 Various mechanisms related to morphological features of coronary arteries and hypercholesterolemia had been proposed for the tropism, initiation, and progression of AP in association with hypercholesterolemia.6 In this study, we retrospectively evaluated whether the MB was anatomically associated with the localization of AP on the coronary artery of patients with CAD diagnosed by multislice computed tomography (MSCT) coronary angiography. We also evaluated the coexisting laboratory abnormalities which could be related to the development of AP.
1
Department of Cardiology, Etimesgut Military Hospital, Ankara, Turkey Department of Cardiology, Gulhane Military Medical Faculty, Ankara, Turkey 3 Department of Cardiology, Eskisehir Military Hospital, Ankara, Turkey 4 Department of Cardiology, Haydarpasa Training Medicine, Istanbul, Turkey 2
Corresponding Author: Sevket Balta, MD, Department of Cardiology, Eskisehir Military Hospital, Vis¸ nelik Mah., Atatu¨rk Cd. 26020 Akarbas¸ ı/ Eskis¸ ehir, Turkey. Email: [email protected]
Downloaded from cat.sagepub.com at WASHINGTON UNIV SCHL OF MED on November 14, 2015
2
Clinical and Applied Thrombosis/Hemostasis
Material and Method Study Design
Table 1. Localization of Atherosclerotic Plaques and Myocardial Bridging on LAD Coronary Artery in Patients With MB, MB&AP, and AP.
The study was designed retrospectively. Approval of local ethics committee was obtained. The entire laboratory data were gathered from the digital recordings of medical archives of the patients diagnosed with CAD by MSCT coronary angiography. The study populations are the subgroups of a cohort of 34 patients who were diagnosed as having CAD by MSCT coronary angiography. The criteria for the subgroups were presence of MB and/or AP.
Localization AP on LAD Artery Groups of Patients Patients with MB&AP Patients with AP
0 4
Total 7 9
Proximal
Middle
Distal
3 0
14 7
1 0
18 7
Luminal narrowing due to MB
We retrospectively reviewed the medical recordings of patients with CAD. They were grouped according to the findings on the MSCT coronary angiography. Images were reconstructed with 0.5-mm slices and analyzed with postprocess study. The study groups were defined as patients with MB (n ¼ 18), MB&AP (n ¼ 7), and AP (n ¼ 9) on left anterior descending (LAD) coronary artery. The patients underwent MSCT angiography due to equivocal or positive results on treadmill test.
Patients with MB Patients with MB&AP
Laboratory Data
Patients with MB&AP Patients with AP
Blood samples were obtained from all patients by a venous route at a 12-hour fasting state at 08 00 AM. Serum levels of total cholesterol; low-density lipoprotein cholesterol (LDLC), high-density lipoprotein cholesterol (HDL-C), and very low-density lipoprotein cholesterol (VLDL-C); and triglyceride (TG) were measured from serums derived from the venous blood sample by centrifuging at 4000 rpm for a 4-minute period. Additionally, fasting blood glucose (FBG), liver enzymes (aspartate aminotransferase [AST] and alanine aminotransferase [ALT]), blood urea, and creatinine were studied. Serum levels of all laboratory parameters were measured through auto-analysis and auto-calculation using Olympus AU640 (Beckman Coulter Inc., Japan) device. Complete blood count was studied from the blood sample obtained at a 12-hour fasting state in the morning and performed using Mindray Auto Hematology Analyzer-BC-6800 (A. Menarini Diagnostics, China) device.
7 5
Mid LAD
Localization MB on LAD Artery
Patients with MB Patients with MB&AP
Coronary Artery Imaging
Proximal LAD
None
Mild
Moderate
2 0
11 4
5 3
18 7
Arterial stenoses due to AP
