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Multivessel myocardial infarction: a window to future treatments of myocardial infarction
  1. Philip D Houck1,
  2. Walter J Linz2
  1. 1Division of Cardiology, Department of Medicine, Scott & White Healthcare, Temple, Texas, Texas A&M Health Science Center College of Medicine, College Station, Texas, USA
  2. 2Department of Pathology, Scott & White Healthcare, Temple, Texas, Texas A&M Health Science Center College of Medicine, College Station, Texas, USA
  1. Correspondence to Dr Philip D Houck, Division of Cardiology, 2401 S 31st Street, Temple, TX 76508, USA; phouck{at}swmail.sw.org

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Introduction

During the last 50 years, the treatment of myocardial infarction has evolved. Monitoring of arrhythmias,1 defibrillation of the detected arrhythmias and the eventual implantation of defibrillators have decreased the risk of sudden death.2 Anticoagulation, antiplatelets and thrombolytics attacked the initiating event of thrombosis within the artery.3–8 This event, easily accepted today, required visualisation of the thrombus in live patients, since the clot was often absent in pathological examination.9–12 A great deal of effort has been spent in refining antithrombotic drugs and the development of protocols that would reduce thrombosis with the least risk of bleeding. The observation of clot in a vessel enabled cardiology to decrease the mortality of myocardial infarction from 50% to less than 5%. Although many agents have been added to the patient to reduce thrombosis, there has never been a consideration to remove offending agents from the patient.

A new paradigm in the aetiology of myocardial infarction has been growing in our clinical trials. This new concept is the role of inflammation.13–15 Inflammation of blood vessels is one explanation for the onset of the clinical syndrome. Coronary atherosclerosis is present in 75% of individuals over the age of 21. This fact has been known since the Korean War.16 17 Inflammation weakens the lipid-filled plaque wall. The thinned plaque ruptures, exposing the blood vessel to thrombogenic factors, and attracts clumping platelets to initiate clots. Inflammation occurs in a smaller percentage of individuals explaining why acute events are less frequent than the prevalence of disease.18 Inflammation can be helpful by signalling for repair progenitors, but may also impede the healing of the myocardium by destroying the progenitor cells or disrupting differentiation that would replace the damaged myocardium. Inflammation of the vessel wall is more difficult to visualise than clots, but appears to …

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