Protecting the myocardial cell during coronary revascularization. The William W. L. Glenn Lecture.
BACKGROUND
Using the ischemic myocardial cell as a paradigm, competitive coronary revascularization technologies will be analyzed for their potential in causing additional myocardial cell damage during the course of therapeutic procedures.


RESULTS
Percutaneous coronary intervention (PCI) using balloon and/or stent (bare metal or coated) approaches may be associated with myonecrosis related to atherosclerotic debris plugging the downstream coronary microcirculation as well as ischemia/reperfusion injury associated with revascularization of occluded coronary vessels. The placement of distal mechanical devices and filters during the course of PCI has not been successful in ameliorating this problem. Coronary revascularization using coronary artery bypass grafting (CABG) similarly may be associated with myocardial stunning and cell necrosis associated with ischemia/reperfusion injury. Surgically induced myocardial ischemia secondary to aortic cross clamping, results from the attenuation or cessation of coronary blood flow such that oxygen delivery to the myocardium is insufficient to meet basal myocardial requirements to preserve cellular membrane stability and viability. Recovery involves: (1) resumption of normal oxidative metabolism and the restoration of myocardial energy reserves; (2) reversal of ischemia induced cell swelling and loss of membrane ion gradients and the adenine nucleotide pool; (3) repair of damaged cell organelles such as the mitochondria and the sarcoplasmic reticulum. Despite meticulous adherence to presently known principles of surgical myocardial protection using advanced cardioplegic technologies, some patients require inotropic support and/or mechanical assist devices postoperatively, when none was required preoperatively.


CONCLUSIONS
Which method of coronary revascularization causes the least amount of myocardial cell injury and is associated with superior long-term outcomes remains an area of increasing controversy.
Levitsky
Sidney
S
Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center and Harvard Medical School, LMOB 2A, 110 Francis St, Boston, Massachusetts 02215, USA. slevitsk@caregroup.harvard.edu
D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects; D001769:Blood; D002118:Calcium / Q000378:metabolism; D002314:Cardioplegic Solutions / Q000494:pharmacology; D002316:Cardiotonic Agents / Q000494:pharmacology / Q000627:therapeutic use; D001026:Coronary Artery Bypass / Q000009:adverse effects; D004734:Energy Metabolism; D005609:Free Radicals; D006324:Heart Arrest, Induced / Q000009:adverse effects / Q000379:methods; D006801:Humans; D017136:Ion Transport; D008955:Models, Cardiovascular; D017202:Myocardial Ischemia / Q000473:pathology / Q000601:surgery / Q000628:therapy; D015428:Myocardial Reperfusion Injury / Q000473:pathology / Q000517:prevention & control*; D009204:Myocardial Revascularization / Q000009:adverse effects* / Q000379:methods; D017682:Myocardial Stunning / Q000473:pathology / Q000517:prevention & control; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000473:pathology*; D009336:Necrosis; D018384:Oxidative Stress; D015607:Stents / Q000009:adverse effects; D016896:Treatment Outcome; D052096:Warm Ischemia / Q000009:adverse effects
D002314:Cardioplegic Solutions; D002316:Cardiotonic Agents; D005609:Free Radicals; D002118:Calcium