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Curso de Atualização em Medicina Cardiovascular 2019
Reunião Anual Conjunta dos Grupos de Estudo de Cirurgia Cardíaca, Doenças Valvulares e Ecocardiografia da SPC
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A. Basics
B. Imaging
C. Arrhythmias and Device Therapy
D. Heart Failure
E. Coronary Artery Disease, Acute Coronary Syndromes, Acute Cardiac Care
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01. History of Cardiology
02. Clinical Skills
03. Imaging
04. Arrhythmias, General
05. Atrial Fibrillation
06. Supraventricular Tachycardia (non-AF)
07. Syncope and Bradycardia
08. Ventricular Arrhythmias and Sudden Cardiac Death (SCD)
09. Device Therapy
10. Chronic Heart Failure
11. Acute Heart Failure
12. Coronary Artery Disease (Chronic)
13. Acute Coronary Syndromes
14. Acute Cardiac Care
15. Valvular Heart Disease
16. Infective Endocarditis
17. Myocardial Disease
18. Pericardial Disease
19. Tumors of the Heart
20. Congenital Heart Disease and Pediatric Cardiology
21. Pulmonary Circulation, Pulmonary Embolism, Right Heart Failure
22. Aortic Disease
23. Peripheral Vascular and Cerebrovascular Disease
24. Stroke
25. Interventional Cardiology
26. Cardiovascular Surgery
27. Hypertension
28. Risk Factors and Prevention
29. Rehabilitation and Sports Cardiology
30. Cardiovascular Disease in Special Populations
31. Pharmacology and Pharmacotherapy
32. Cardiovascular Nursing
33. e-Cardiology / Digital Health
34. Public Health and Health Economics
35. Research Methodology
36. Basic Science
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Lipoprotein a and cardiovascular risk: gender analysis
Session:
Posters 4 - Écran 7 - Prevenção
Speaker:
M. Raquel Santos
Congress:
CPC 2019
Topic:
J. Preventive Cardiology
Theme:
28. Risk Factors and Prevention
Subtheme:
28.2 Risk Factors and Prevention – Cardiovascular Risk Assessment
Session Type:
Posters
FP Number:
---
Authors:
M. Raquel Santos; Andreia Pereira; Flávio Mendonça; Joao Adriano Sousa; Joel Monteiro; Micaela Rodrigues Neto; Ana Célia Sousa; Mariana Rodrigues; Eva Henriques; Ilídio Ornelas; A. Drumond de Freitas; Roberto Palma dos Reis; Isabel Mendonça
Abstract
<p><strong><u>Introduction:</u></strong> Despite consideration of modifiable and non-modifiable risk factors, 40% of the deaths are still attributed to coronary artery disease (CAD). This residual risk appears to be partially attributed to others risk markers, like elevation of lipoprotein a (Lpa). More knowledge about Lpa can guide us in therapeutic decisions. Elevation of lipoprotein has been controversially associated with a increased risk, namely in women.</p> <p><strong><u>Objective</u></strong>: To evaluate if the elevation of Lpa is associated with MACE in females, males or both.</p> <p><strong><u>Materials and methods:</u></strong> Case control study of 3050 subjects from the GENEMACOR study population. In female population (n=676): cases were 341 patients with at least one >75% coronary stenosis (median age 55.7±7.2) and 335 normal controls (median age 55.8±6) adjusted by age with cases. In male population (n= 2374): 1278 patients with at least one >75% coronary stenosis (median age 52.7±8) and 1096 controls (median age 51.9±8) also adjusted by age. X<sup>2</sup> and T student tests were used to analyze the demographic, laboratorial, angiographic and anthropometric characteristics of the population. Lipoprotein a was determined by immunoturbidimetry. High Lpa level was considered if superior to 30 mg/dl. Logistic regression was used to evaluate Lpa as a risk factor for CAD in total, female and male populations.</p> <p><strong><u>Results:</u></strong> In female population 44.0% patients vs 21.2% controls (p<0.000) had Lpa> 30mg/dl. In male population 39.4% patients vs 23.8% controls (p<0.000) had Lpa> 30mg/dl. In total population Lpa >30mg/dl was a predictor for CAD (OR 2.24, 95% CI: 1.91-2.62, p <0.0001). analyzing by gender, Lpa >30mg/dl was also a predictor for CAD either in male (OR 2.08, 95% CI: 1.74-2.5, p <0.0001) or female population (OR 2.92, 95% CI: 2.08-4.09, p <0.0001).</p> <p><strong><u>Conclusions</u>: </strong>In our population elevated Lpa levels (>30mg/dl) were associated with CAD disease, regardless of gender. We conclude that Lpa can be considered an independent risk factor for CAD disease in both sexes, and further strategies for Lpa reduction may indeed translate in improved outcomes in CAD disease.</p>
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