Elias B. Hanna

Practical Cardiovascular Medicine


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the GRAVITAS randomized trial. JAMA 2011; 305: 1097–105.

      14 164. Pereira NL, Farkouh ME, So D, et al. Effect of Genotype-Guided Oral P2Y12 Inhibitor Selection vs Conventional Clopidogrel Therapy on Ischemic Outcomes After Percutaneous Coronary Intervention: The TAILOR-PCI Randomized Clinical Trial. JAMA 2020 Aug 25; 324(8):761–771.

      15 165. Oler A, Whooley MA, Oler J, Grady D. Adding heparin to aspirin reduces the incidence of myocardial infarction and death in patients with unstable angina. A meta-analysis. JAMA 1996; 276: 811–15.

      16 166. Antman EM, McCabe CH, Gurfinkel EP, et al. Enoxaparin prevents death and cardiac ischemic events in unstable angina/non-Q wave myocardial infarction: results of the Thrombolysis In Myocardial Infarction (TIMI) 11B trial. Circulation 1999; 100: 1593–601.

      17 167. Cohen M, Demers C, Gurfinkel EP, et al. A comparison of low molecular-weight heparin with unfractionated heparin for unstable coronary artery disease. Efficacy and safety of subcutaneous enoxaparin in non-Q-wave coronary events study group. N Engl J Med 1997; 337: 447–52.

      18 168. SYNERGY Trial Investigators. Enoxaparin vs unfractionated heparin in high-risk patients with non-ST-segment elevation acute coronary syndromes managed with an intended early invasive strategy: primary results of the SYNERGY randomized trial. JAMA 2004; 292: 45–54.

      19 169. Blazing MA, de Lemos JA, White HD, et al. Safety and efficacy of enoxaparin vs unfractionated heparin in patients with non-ST-segment elevation acute coronary syndromes who receive tirofiban and aspirin: a randomized controlled trial. JAMA 2004; 292: 55–64. A-to-Z trial.

      20 170 Levine GN, Ferrando T. Degree of anticoagulation after one subcutaneous and one subsequent intravenous booster dose of enoxaparin: implications for patients with acute coronary syndromes undergoing early percutaneous coronary intervention. J Thromb Thrombolysis 2004; 17: 167–71.

      21 171. Yusuf S, Mehta SR, Chrolavicius S, et al. Comparison of fondaparinux and enoxaparin in acute coronary syndromes. N Engl J Med 2006; 354: 1464–76. OASIS 5 trial.

      22 172. Mehta SR, Boden WE, Eikelboom JW, et al. Antithrombotic therapy with fondaparinux in relation to interventional management strategy in patients with ST- and non-ST-segment elevation acute coronary syndromes: an individual patient-level combined analysis of the fifth and sixth organization to assess strategies in ischemic syndromes (OASIS 5 and 6) randomized trials. Circulation 2008; 118: 2038–46.

      23 173 Erlinge D, Omerovic E, Fröbert O, et al. Bivalirudin versus Heparin Monotherapy in Myocardial Infarction. N Engl J Med. 2017;377(12):1132-1142. (VALIDATE-SWEDEHEART). +Another trial, MATRIX: Valgimigli M, Frigoli E, Leonardi S, et al. Bivalirudin or Unfractionated Heparin in Acute Coronary Syndromes. N Engl J Med. 2015; 373(11):997-1009.

      24 174. White HD, Chew DP, Hoekstra JW, et al. Safety and efficacy of switching from either unfractionated heparin or enoxaparin to bivalirudin in patients with non-ST-segment elevation acute coronary syndromes managed with an invasive strategy: results from the ACUITY trial. J Am Coll Cardiol 2008; 51: 1734–41.

      Plaque erosion

      1 175. Arbustini E, Dal Bello B, Morbini P, et al. Plaque erosion is a major substrate for coronary thrombosis in acute myocardial infarction. Heart 1999; 82: 269–72.

      2 176. Virmani R, Burke AP, Farb A. Plaque rupture and plaque erosion. Thromb Haemost 1999; 82 Suppl 1: 1–3.

      3 177. Braunwald E. Coronary plaque erosion: recognition and management. JACC Cardiovasc Imaging 2013; 6: 288–9.

      Spontaneous coronary artery dissection

      1 178. Saw J, Aymong E, Sedlak T, et al. Spontaneous coronary artery dissection. Association with predisposing arteriopathies and precipitating stressors and cardiovascular outcomes. Circ Cardiovasc Interv 2014; 7: 645–55.

      2 179. Mahmoud AN, Taduru SS, Mentias A. Trends of incidence, clinical presentation, and in-hospital mortality among women with acute myocardial infarction with or without spontaneous coronary artery dissection: a population-based analysis. J Am Coll Cardiol Intv 2018; 11:80–90

      3 180. Tweet MS, Eleid MF, Best PJM, et al. Spontaneous coronary artery dissection. Revascularization versus conservative therapy. Circ Cardiovasc Interv 2014; 7: 777–86.

      4 181. Jneid H. Spontaneous coronary artery dissection. J Am Coll Cardiol Intv 2018; 11 /(1): 91-94

      5 182 Saw J, Mancini GB, Humphries KH. Contemporary review on spontaneous coronary artery dissection. J Am Coll Cardiol 2016; 68:297–312.

      6 183. Spontaneous coronary artery dissection: current state of the science. A scientific statement from the American Heart Association. Circulation 2018; 137:e523–e557.

      Physiology of hs-troponin

      1 184. Turer AT, Addo TA, Martin JL, et al. Myocardial ischemia induced by rapid atrial pacing causes troponin T release detectable by a highly sensitive assay: insights from a coronary sinus sampling study. J Am Coll Cardiol 2011; 57(24):2398–2405.

      2 185 Sabatine M.S., Morrow D.A., de Lemos J.A., et al. Detection of acute changes in circulating troponin in the setting of transient stress test-induced myocardial ischaemia using an ultrasensitive assay: results from TIMI 35. Eur Heart J 30:162–169.

      3 186 de Lemos JA, Drazner MH, Omland T, et al. Association of troponin T detected with a highly sensitive assay and cardiac structure and mortality risk in the general population. JAMA 2010; 304 (22):25032512.

      4 187. Januzzi JL Jr, Suchindran S, Coles A, et al. High-sensitivity troponin I and coronary computed tomography in symptomatic outpatients with suspected coronary artery disease: insights from the PROMISE trial. J Am Coll Cardiol Img 2018;Epub ahead of prin. In this study of healthy individuals with no known CAD or typical symptoms (mean age 57), highest hs/troponin quartile was only >2.5 ng/L, and the highest quartile had 16% risk of significant CAD (low, but higher than lower quartiles (<5%, and 10%)). Risk of MI/death was low in all at 1 yr (0.4-1.2%),

      5 188. Januzzi JL, Jr, Suchindran S, Hoffmann U, et al. Single-molecule hsTnI and short-term risk in stable patients with chest pain. J Am Coll Cardiol 2019; 73:251–260 (from PROMISE trial).

      6 189. Sandoval Y, Bielinski SJ, Daniels LB, et al. Atherosclerotic Cardiovascular Disease Risk Stratification Based on Measurements of Troponin and Coronary Artery Calcium. J Am Coll Cardiol. 2020;76(4):357-370. Either calcium score of 0 or undetectable hs-troponin predicts a very low cardiac risk at 10 years. 38% of patients had discordant result and the 2 tests are complementary: the lowest risk is in patients with a calcium score of 0+undetectable hs-troponin.

      7 190. Neilan TG,Januzzi JL, Lee-Lewandrowski E, et al. myocardial injury and ventricular dysfunction related to training levels among nonelite participants in the Boston marathon. Circulation 2006; 114:2325–2333.

      8 191. Mousavi N, Czarnecki A, Kumar K, et al. Relation of biomarkers and cardiac magnetic resonance imaging after marathon running. Am J Cardiol. 2009; 103(10):1467–1472.

      Notes

      1 * A very small group of individuals have heterophile antibodies that agglutinate with the murine antibodies used in the troponin assay, causing the very rare “falsely positive troponin elevation”. These patients have chronic troponin elevation, sometimes severe, discrepant with the stable clinical setting. An alternative troponin assay or a special heterophilic blocking reagent is used for confirmation.

      2 ** Late gadolinium enhancement and/or edema on T2 may be seen with myocarditis or infarction. Only edema may be seen in takotsubo, not late gadolinium enhancement. The distribution of the anomaly distinguishes myocarditis from an ischemic pattern:26Distribution not consistent with an arterial territory + subepicardial or mid-wall predominance → myocarditisDistribution consistent with an arterial territory + subendocardial or transmural