Infarct size--can it be measured or modified in humans?
Despite more than 15 years of intensive experimental and clinical research in the general area of limiting infarct size, no treatment has been shown to be so efficacious and relatively free of side effects that its routine use can be recommended. In addition, there is no ideal means of measuring infarct size as yet. However, considerable progress has been made in understanding mechanisms responsible for irreversible cellular injury and in identifying factors and anatomic alterations responsible for or contributing to the development of transmural (Q wave) and non-transmural (non-Q wave) myocardial infarcts. Interventions are available that are capable of causing rapid coronary thrombolysis, and techniques are becoming available tht have increasing power to size myocardial infarcts and estimate both segmental and ventricular function. Experimental studies have also suggested a potential benefit from a combination of reperfusion therapy with selected pharmacologic intervention in reducing infarct size and preserving ventricular function. It seems likely that this general area will remain an intensive area of clinical research in the immediate future.
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D002317:Cardiovascular Agents / Q000627:therapeutic use; D004796:Clinical Enzyme Tests; D003326:Coronary Circulation; D004562:Electrocardiography; D006801:Humans; D006821:Hyaluronoglucosaminidase / Q000627:therapeutic use; D009203:Myocardial Infarction / Q000175:diagnosis* / Q000378:metabolism / Q000473:pathology / Q000628:therapy
D000319:Adrenergic beta-Antagonists; D000893:Anti-Inflammatory Agents; D002317:Cardiovascular Agents; D006821:Hyaluronoglucosaminidase