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PP-040 Relationship of Platelet Indices and the Mortality from STEMI and NSTEMI Acute Coronary Syndromes
MARCH 26e29, 2015 Table. Death STEMI (n¼22) WBCx1000
15.95.7 15.6, (5.4-26.0)
Death NSTEMI Survivors of ACS (n¼28) (n¼29) 13.75.6 13.7, (3.6-28.7)
9.22.3 9.2, (5.1-13.2)
Neutrophil 60.017.6 72.514.4 Percentage 55.8, (36.3-86.8) 78.9, (31.0-87.9) Lymphocyte 28.516.3 17.913.5 Percentage 34.4, (6.5-53.4) 12.1, (4.6-57.8)
64.012.7, 65.1, 34.0-88.1 24.910.9 24.1 (6.0-50.2)
Monocyte Percentage Eosinophil percentage
7.11.4 7.1 (4.2-9.4) 1.60.7 1.4, (0.6-3.3)
7.62.1 7.7, (3.2-12.8) 1.20.9 0.9, (0.5-4.0)
7.72.1 7.8, (2.8-11.6) 2.41.5 1.9, (0.7-6.9)
Basophil percentage
0.80.3 0.7, (0.2-1.5)
0.60.2 0.5, (0.1-1.3)
0.60.4 0.6, (0.2-2.4)
NLR
4.34.3, 1.6, (0.68-13.35)
6.74.5, 6.4, (0.54-19.11)
3.63.1, 2.7, (0.7-14.6)
p <0.001* <0.001z <0.001† 0.029* 0.006† 0.015* 0.006† 0.035x 0.474* <0.001* 0.017z <0.001† 0.002x 0.022* 0.011z 0.030x 0.019* 0.006† 0.048x
Comparison of WBC, neutrophil%, and lymphocyte%, eosinophil% and basophil% among the patients suffered death from NSTEMI and STEMI ACS and ones survived from ACS and subgroup analysis of the data (z p DeathSTEMI vs SurvivorsACS; †p DeathNSTEMI vs SurvivorsACS; xp DeathSTEMI vs DeathNSTEMI)
- PP-040 Relationship of Platelet Indices and the Mortality from STEMI and NSTEMI Acute Coronary Syndromes. Mustafa Aparci1, Cengiz Ozturk2, Sevket Balta3, Atilla Iyisoy2, Turgay Celik2, Ali Osman Yildirim2, Mustafa Demir2, Murat Unlu2. 1Dept. of Cardiology Kasimpasa Military Hospital, Istanbul, Turkey; 2Dept. of Cardiology, Gulhane Military Medical Academy, Ankara, Turkey; 3Eskis¸ehir Military Hospital, Dept. of Cardiology and Aviation Medicine. Aim: Mortality of patients from STEMI or NSTEMI mainly depends on the burden of thrombotic process and myocardial injury and consequently the irreversible loss of myocardial function. Platelet indices could present variation since they could be influenced by the highly active thrombotic process resulting high turnover and large myocardial tissue injury resulting with increased inflammatory activity. From this point of view we evaluated whether platelet indices variation in patients suffered death from STEMI and NSTEMI acute coronary syndrome (ACS) and in patients who survived from ACS. Material-Method: We evaluated the platelet indices; platelet count, Mean platelet volume, and Platelet distribution width; from the CBC parameters among those patient suffered death from STEMI (n¼22) and NSTEMI (n¼28) acute coronary syndrome (ACS) and survived from ACS (n¼29). Comparisons and subgroup analysis were performed by Kruskal Wallis test and Mann Whitney U test. Results: We observed that platelet count were significantly reduced in death from NSTEMI ACS group compared to other groups while MPV significantly elevated in NSTEMI ACS group compared to only survivor group (p¼0.032) and PDW were significantly elevated both in NSTEMI (p¼0.011) and STEMI (0.039) group compared to survivors from ACS (Table 1, Figure 1). Conclusion: NSTEMI generally develops on a fissure of an atherosclerotic plaque which results with a ongoing thrombotic process
Figure. Comparison of MPV, PDW, and platelet count among the patients suffered death from STEMI, NSTEMI ACS and survived from AC. Table: DeathSTEMI DeathNSTEMI ACSSurvivors (n¼22) (n¼28) (n¼29) Mean Platelet 8.60.8 8.91.2 7.42.7 Volume 8.6, (7.1-10.8) 9.0, (6.7-11.3) 8.1, (0.7-10.0) 15.72.0 16.53.2 14.32.3 Platelet Distribution 15.8, (12.5-20.5) 16.2, (10.0-22.5) 14.0, (9.2-18.5) Width Platelet Count 283.585.1 196.168.4 279.298.2 259 (143-487) 188 (59-354) 258, (143-475)
p 0.076* 0.032† 0.020* 0.039z 0.011† 0.001* 0.003† <0.001x
Comparison and subgroup analysis of MPV, PDW, and platelet count among the patients suffered death from STEMI, NSTEMI ACS and survived from ACS (z p DeathSTEMI vs SurvivorsACS; †p DeathNSTEMI vs SurvivorsACS; xp DeathSTEMI vs DeathNSTEMI) while STEMI is caused by an acute occlusion of coronary artery due to thrombosis of an atherosclerotic plaque. An activated thrombotic process continuing several days and ongoing platelet production due to increased turnover between thrombotic process and thrombolysis will certainly influence the platelets physical features beside their aggregability. Grading the underlying thrombotic process by using those physical properties of platelets may allow determining the severity of myocardial injury or ongoing thrombosis and also necessity to the level of antiaggregant and anticoagulant therapy. This parameter should be evaluated in large populated ACS studies in order to determine the cut off values that could inform about the underlying thrombosis.
- PP-041 Spontaneous Right Coronary Artery Dissection Causing Isolated Right Ventricular Myocardial Infarction Misinterpreted as Anterior Wall Myocardial Infarction. Funda Bas¸yigit, Özgül Uçar Elalmıs¸, Ümit Güray, Havva Tugba Gürsoy, Bekir Demirtas¸, Deniz S¸ahin, Pınar Bayır, Mehmet Ileri. Department of Cardiology, Ankara Numune Education and Research Hospital, Ankara, Turkey. Objective: Spontaneous coronary artery dissection (SCAD) is a rare entity, with an incidence of 0.2% among patients who undergo coronary angiography. Here, we describe a case of SCAD, which caused isolated acute right ventricular myocardial infarction (MI), in a 51-year-old man. Methods: A 51-year-old male presented with sudden onset of chest pain that started two hours prior to admission. He described the pain as sharp, tearing and radiating to his back. His past medical history was remarkable for ascending aortic aneurysm diagnosed ten years ago. There was family history of coronary artery disease. He declined any drug abuse, herbal medications or other over-the-counter medicines. His blood pressure was 140/80 mm Hg; equal in both arms, and pulse rate was 90 per minute. Physical examination was unremarkable with regular heart sounds without murmurs, rubs or gallops. The electrocardiogram (ECG) revealed ST elevation in leads V1-V3 and reciprocal ST depression in leads II, III, aVF. On transthoracic echocardiogram, the ascending aorta was 4.8 cm at sinus Valsalva level and neither
The American Journal of Cardiologyâ MARCH 26e29, 2015 11th INTERNATIONAL CONGRESS OF UPDATE IN CARDIOLOGY AND CARDIOVASCULAR SURGERY ABSTRACTS / Poster S115
P O S T E R A B S T R A C T S
15.95.7 15.6, (5.4-26.0)
Death NSTEMI Survivors of ACS (n¼28) (n¼29) 13.75.6 13.7, (3.6-28.7)
9.22.3 9.2, (5.1-13.2)
Neutrophil 60.017.6 72.514.4 Percentage 55.8, (36.3-86.8) 78.9, (31.0-87.9) Lymphocyte 28.516.3 17.913.5 Percentage 34.4, (6.5-53.4) 12.1, (4.6-57.8)
64.012.7, 65.1, 34.0-88.1 24.910.9 24.1 (6.0-50.2)
Monocyte Percentage Eosinophil percentage
7.11.4 7.1 (4.2-9.4) 1.60.7 1.4, (0.6-3.3)
7.62.1 7.7, (3.2-12.8) 1.20.9 0.9, (0.5-4.0)
7.72.1 7.8, (2.8-11.6) 2.41.5 1.9, (0.7-6.9)
Basophil percentage
0.80.3 0.7, (0.2-1.5)
0.60.2 0.5, (0.1-1.3)
0.60.4 0.6, (0.2-2.4)
NLR
4.34.3, 1.6, (0.68-13.35)
6.74.5, 6.4, (0.54-19.11)
3.63.1, 2.7, (0.7-14.6)
p <0.001* <0.001z <0.001† 0.029* 0.006† 0.015* 0.006† 0.035x 0.474* <0.001* 0.017z <0.001† 0.002x 0.022* 0.011z 0.030x 0.019* 0.006† 0.048x
Comparison of WBC, neutrophil%, and lymphocyte%, eosinophil% and basophil% among the patients suffered death from NSTEMI and STEMI ACS and ones survived from ACS and subgroup analysis of the data (z p DeathSTEMI vs SurvivorsACS; †p DeathNSTEMI vs SurvivorsACS; xp DeathSTEMI vs DeathNSTEMI)
- PP-040 Relationship of Platelet Indices and the Mortality from STEMI and NSTEMI Acute Coronary Syndromes. Mustafa Aparci1, Cengiz Ozturk2, Sevket Balta3, Atilla Iyisoy2, Turgay Celik2, Ali Osman Yildirim2, Mustafa Demir2, Murat Unlu2. 1Dept. of Cardiology Kasimpasa Military Hospital, Istanbul, Turkey; 2Dept. of Cardiology, Gulhane Military Medical Academy, Ankara, Turkey; 3Eskis¸ehir Military Hospital, Dept. of Cardiology and Aviation Medicine. Aim: Mortality of patients from STEMI or NSTEMI mainly depends on the burden of thrombotic process and myocardial injury and consequently the irreversible loss of myocardial function. Platelet indices could present variation since they could be influenced by the highly active thrombotic process resulting high turnover and large myocardial tissue injury resulting with increased inflammatory activity. From this point of view we evaluated whether platelet indices variation in patients suffered death from STEMI and NSTEMI acute coronary syndrome (ACS) and in patients who survived from ACS. Material-Method: We evaluated the platelet indices; platelet count, Mean platelet volume, and Platelet distribution width; from the CBC parameters among those patient suffered death from STEMI (n¼22) and NSTEMI (n¼28) acute coronary syndrome (ACS) and survived from ACS (n¼29). Comparisons and subgroup analysis were performed by Kruskal Wallis test and Mann Whitney U test. Results: We observed that platelet count were significantly reduced in death from NSTEMI ACS group compared to other groups while MPV significantly elevated in NSTEMI ACS group compared to only survivor group (p¼0.032) and PDW were significantly elevated both in NSTEMI (p¼0.011) and STEMI (0.039) group compared to survivors from ACS (Table 1, Figure 1). Conclusion: NSTEMI generally develops on a fissure of an atherosclerotic plaque which results with a ongoing thrombotic process
Figure. Comparison of MPV, PDW, and platelet count among the patients suffered death from STEMI, NSTEMI ACS and survived from AC. Table: DeathSTEMI DeathNSTEMI ACSSurvivors (n¼22) (n¼28) (n¼29) Mean Platelet 8.60.8 8.91.2 7.42.7 Volume 8.6, (7.1-10.8) 9.0, (6.7-11.3) 8.1, (0.7-10.0) 15.72.0 16.53.2 14.32.3 Platelet Distribution 15.8, (12.5-20.5) 16.2, (10.0-22.5) 14.0, (9.2-18.5) Width Platelet Count 283.585.1 196.168.4 279.298.2 259 (143-487) 188 (59-354) 258, (143-475)
p 0.076* 0.032† 0.020* 0.039z 0.011† 0.001* 0.003† <0.001x
Comparison and subgroup analysis of MPV, PDW, and platelet count among the patients suffered death from STEMI, NSTEMI ACS and survived from ACS (z p DeathSTEMI vs SurvivorsACS; †p DeathNSTEMI vs SurvivorsACS; xp DeathSTEMI vs DeathNSTEMI) while STEMI is caused by an acute occlusion of coronary artery due to thrombosis of an atherosclerotic plaque. An activated thrombotic process continuing several days and ongoing platelet production due to increased turnover between thrombotic process and thrombolysis will certainly influence the platelets physical features beside their aggregability. Grading the underlying thrombotic process by using those physical properties of platelets may allow determining the severity of myocardial injury or ongoing thrombosis and also necessity to the level of antiaggregant and anticoagulant therapy. This parameter should be evaluated in large populated ACS studies in order to determine the cut off values that could inform about the underlying thrombosis.
- PP-041 Spontaneous Right Coronary Artery Dissection Causing Isolated Right Ventricular Myocardial Infarction Misinterpreted as Anterior Wall Myocardial Infarction. Funda Bas¸yigit, Özgül Uçar Elalmıs¸, Ümit Güray, Havva Tugba Gürsoy, Bekir Demirtas¸, Deniz S¸ahin, Pınar Bayır, Mehmet Ileri. Department of Cardiology, Ankara Numune Education and Research Hospital, Ankara, Turkey. Objective: Spontaneous coronary artery dissection (SCAD) is a rare entity, with an incidence of 0.2% among patients who undergo coronary angiography. Here, we describe a case of SCAD, which caused isolated acute right ventricular myocardial infarction (MI), in a 51-year-old man. Methods: A 51-year-old male presented with sudden onset of chest pain that started two hours prior to admission. He described the pain as sharp, tearing and radiating to his back. His past medical history was remarkable for ascending aortic aneurysm diagnosed ten years ago. There was family history of coronary artery disease. He declined any drug abuse, herbal medications or other over-the-counter medicines. His blood pressure was 140/80 mm Hg; equal in both arms, and pulse rate was 90 per minute. Physical examination was unremarkable with regular heart sounds without murmurs, rubs or gallops. The electrocardiogram (ECG) revealed ST elevation in leads V1-V3 and reciprocal ST depression in leads II, III, aVF. On transthoracic echocardiogram, the ascending aorta was 4.8 cm at sinus Valsalva level and neither
The American Journal of Cardiologyâ MARCH 26e29, 2015 11th INTERNATIONAL CONGRESS OF UPDATE IN CARDIOLOGY AND CARDIOVASCULAR SURGERY ABSTRACTS / Poster S115
P O S T E R A B S T R A C T S