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Martes 25 de Agosto, 2026
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Movimentors: Masters en movimiento inteligente

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Lección 1: Placa vulnerable: por qué el control del LDL ya no es suficiente

Video cápsula | 15:00 min

Dr. Xavier Escudero Cañedo
Especialista en Cardiología

Descripción del módulo:

En este módulo se revisará una actualización sobre el riesgo cardiovascular residual, la fisiopatología de la placa vulnerable y el papel de estrategias terapéuticas dirigidas, incluyendo el uso de omega-3 en pacientes que potencialmente se puedan beneficiar de dicho tratamiento.

Objetivos de aprendizaje:

  • Comprender los mecanismos del riesgo residual más allá del LDL-C.
  • Identificar factores relacionados con la vulnerabilidad de la placa aterosclerótica.
  • Reconocer los perfiles de pacientes que pueden beneficiarse de terapias basadas en omega-3.

Referencias

  1. Libby P. Inflammation in atherosclerosis. Nature. 2002 Dec;420(6917):868-74.
  2. Abtan J, et al. Residual Ischemic Risk and Its Determinants in Patients With Previous Myocardial Infarction and Without Prior Stroke or TIA: Insights From the REACH Registry. Clin Cardiol. 2016 Nov;39(11):670-677.
  3. Jernberg T, et al. Cardiovascular risk in post-myocardial infarction patients: nationwide real world data demonstrate the importance of a long-term perspective. Eur Heart J. 2015 May 14;36(19):1163-70.
  4. Mach F, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. Eur Heart J. 2020 Jan 1;41(1):111-188.
  5. Stone GW, et al. A prospective natural-history study of coronary atherosclerosis. N Engl J Med. 2011 Jan 20;364(3):226-35.
  6. Narula J, et al. Histopathologic characteristics of atherosclerotic coronary disease and implications of the findings for the invasive and noninvasive detection of vulnerable plaques. J Am Coll Cardiol. 2013 Mar 12;61(10):1041-51.
  7. Shapiro MD, Fazio S. Biologic bases of residual risk of cardiovascular events: A flawed concept. Eur J Prev Cardiol. 2018 Nov;25(17):1831-1835.
  8. ISIS-2 (Second International Study of Infarct Survival). Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. Lancet. 1988 Aug 13;2(8607):349-60.
  9. Yusuf S, et al. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N Engl J Med. 2001 Aug 16;345(7):494-502.
  10. Chen ZM, et al. Addition of clopidogrel to aspirin in 45,852 patients with acute myocardial infarction: randomised placebo-controlled trial. Lancet. 2005 Nov 5;366(9497):1607-21.
  11. Sabatine MS, et al. Addition of clopidogrel to fibrinolytic therapy for myocardial infarction with ST-segment elevation. N Engl J Med. 2005 Mar 24;352(12):1179-89.
  12. Mehta SR, et al. Double-dose versus standard-dose clopidogrel and high-dose versus low-dose aspirin in individuals undergoing percutaneous coronary intervention for acute coronary syndromes (CURRENT-OASIS 7): a randomised factorial trial. Lancet. 2010;376(9748):1233-43.
  13. Wiviott S, et al. Prasugrel versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2007 Nov 15;357(20):2001-15.
  14. Wallentin L, et al. Ticagrelor versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2009 Sep 10;361(11):1045-57.
  15. Byrne RA, et al. 2023 ESC Guidelines for the management of acute coronary syndromes. Eur Heart J. 2023 Oct 12;44(38):3720-3826.
  16. Rao SV, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2025 Apr;151(13):e771-e862.
  17. Ference BA, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J. 2017 Aug 21;38(32):2459-2472.
  18. Rodriguez F, et al. Association Between Intensity of Statin Therapy and Mortality in Patients With Atherosclerotic Cardiovascular Disease. JAMA Cardiol. 2017 Jan 1;2(1):47-54.
  19. Nicholls SJ, et al. Effect of Evolocumab on Progression of Coronary Disease in Statin-Treated Patients: The GLAGOV Randomized Clinical Trial. JAMA. 2016 Dec 13;316(22):2373-2384.
  20. Nicholls SJ, et al. Effect of Evolocumab on Coronary Plaque Phenotype and Burden in Statin-Treated Patients Following Myocardial Infarction. JACC Cardiovasc Imaging. 2022 Jul;15(7):1308-1321.
  21. Kini AS, et al. Intracoronary Imaging and Transcriptomic Characteristics Before and After Maximum Lipid-Lowering Therapy: YELLOW-III Study of Evolocumab and Maximum Statin Therapy in Chronic Coronary Disease. JACC Cardiovasc Imaging. 2026 Apr;19(4):516-534.
  22. Webb NR. Getting to the core of aterosclerosis. Nat Med. 2008 Oct;14(10):1015-6.
  23. Mach F, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. Eur Heart J. 2020 Jan 1;41(1):111-188.
  24. Zinman B, et al. Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2 Diabetes. N Engl J Med. 2015 Nov 26;373(22):2117-28.
  25. Patel SM, et al. Sodium-Glucose Cotransporter-2 Inhibitors and Major Adverse Cardiovascular Outcomes: A SMART-C Collaborative Meta-Analysis. Circulation. 2024 Jun 4;149(23):1789-1801.
  26. Sardu C, et al. SGLT2-inhibitors effects on the coronary fibrous cap thickness and MACEs in diabetic patients with inducible myocardial ischemia and multi vessels non-obstructive coronary artery stenosis. Cardiovasc Diabetol. 2023 Apr 1;22(1):80.
  27. Neuen BL, et al. Estimated Lifetime Cardiovascular, Kidney, and Mortality Benefits of Combination Treatment With SGLT2 Inhibitors, GLP-1 Receptor Agonists, and Nonsteroidal MRA Compared With Conventional Care in Patients With Type 2 Diabetes and Albuminuria. Circulation. 2024 Feb 6;149(6):450-462.
  28. Gitto M, et al. GLP-1 receptor agonists and coronary plaques regression in diabetic patients after acute coronary síndromes. Acta Diabetol. 2026 Feb;63(2):179-191.
  29. Fei Y, et al. Cardiovascular outcomes in trials of new antidiabetic drug classes: a network meta‑analysis. Cardiovasc Diabetol. 2019 Aug 28;18(1):112.
  30. Ridker PM, et al. C-reactive protein levels and outcomes after statin therapy. N Engl J Med. 2005 Jan 6;352(1):20-8.
  31. Ridker PM, et al. Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease. N Engl J Med. 2017 Sep 21;377(12):1119-1131.
  32. Nidorf SM, et al. Colchicine in Patients with Chronic Coronary Disease. N Engl J Med. 2020 Nov 5;383(19):1838-1847.
  33. Jolly SS, et al. Colchicine in Acute Myocardial Infarction. N Engl J Med. 2025 Feb 13;392(7):633-642.
  34. Ndumele CE, et al. Cardiovascular-Kidney-Metabolic Health: A Presidential Advisory From the American Heart Association. Circulation. 2023 Nov 14;148(20):1606-1635.
  35. Freitas LLC, et al. Adipokines, diabetes and atherosclerosis: an inflammatory association. Front Physiol. 2015 Nov 3:6:304.
  36. Iacobellis G. Epicardial adipose tissue in contemporary cardiology. Nat Rev Cardiol. 2022 Sep;19(9):593-606.
  37. Hendricks S, et al. Epicardial adipose tissue is a robust measure of increased risk of myocardial infarction – a meta-analysis on over 6600 patients and rationale for the EPIC-ACS study. Medicine (Baltimore). 2021 Dec 30;100(52):e28060.
  38. Fuchs FD, et al. High Blood Pressure and Cardiovascular Disease. Hypertension. 2020 Feb;75(2):285-292.
  39. Blood Pressure Lowering Treatment Trialists’ Collaboration. Pharmacological blood pressure lowering for primary and secondary prevention of cardiovascular disease across different levels of blood pressure: an individual participant-level data meta-analysis. Lancet. 2021 May 1;397(10285):1625-1636.
  40. Covani M, et al. Plaque Vulnerability and Cardiovascular Risk Factor Burden in Acute Coronary Syndrome: An Optical Coherence Tomography Analysis. J Am Coll Cardiol. 2025 Jul 15;86(2):77-89.
Evaluación

Evaluación: Movimentors Evaluación Módulo 3 Lección 1

Cardiovascular – Placa vulnerable: por qué el control del LDL ya no es suficiente

Pregunta 1

¿Cuál de las siguientes afirmaciones describe mejor el concepto de riesgo residual en la enfermedad cardiovascular aterosclerosa?​

El riesgo residual se define como los eventos que continúan ocurriendo pese al tratamiento óptimo e involucra componentes trombóticos, inflamatorios, lipídicos, metabólicos y cardiometabólicos.​ El riesgo residual se evalúa después del tratamiento. El LDL es sólo uno de varios componentes del riesgo residual. Además de factores no modificables, existen múltiples factores modificables que contribuyen al riesgo residual.​

Pregunta 2

¿Cuál es la estrategia más adecuada para disminuir el riesgo cardiovascular residual?​

La reducción del riesgo residual requiere actuar sobre múltiples mecanismos fisiopatológicos, incluyendo antitrombóticos, control intensivo de LDL, terapias cardiometabólicas, control de la inflamación y de factores como obesidad e hipertensión.​ El control del LDL por sí solo, aunque fundamental, no elimina todo el riesgo residual. La evidencia antiinflamatoria aún es limitada y constituye sólo uno de los componentes del manejo. La duración e intensidad del tratamiento antitrombótico deben individualizarse según el riesgo isquémico y hemorrágico.​
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