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The “no-reflow” phenomenon: basic science and clinical correlates
  1. Thorsten Reffelmann,
  2. Robert A Kloner
  1. Correspondence to:
    Robert A Kloner, MD, PhD, The Heart Institute, Good Samaritan Hospital, University of Southern California, 1225 Wilshire Boulevard, Los Angeles, CA 90017-2395, USA;

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To achieve early and complete reperfusion of the myocardium in acute coronary syndromes is the daily challenge for every physician in clinical cardiology. However, restoration of epicardial blood flow by thrombolysis, primary angioplasty or bypass surgery does not necessarily imply complete reperfusion, even if the target stenosis is adequately removed or bypassed. The amount of microvascular integrity may limit reperfusion to the previously ischaemic tissue despite complete restoration of epicardial vessel diameters.

A 74 year old man with acute distress is admitted to the emergency room because of acute onset of severe, substernal, crushing chest pain two hours ago. He has never suffered from similar symptoms before. The ECG shows ST segment elevation in leads I, aVL, V2–V4. After aspirin and heparin, the patient is immediately transferred to the catheterisation laboratory. Coronary angiography confirms a thrombotic occlusion of the proximal left anterior descending artery. The guide wire easily crosses the occlusion. After coronary artery balloon dilatation and stent implantation the epicardial artery appears to have gained sufficient luminal diameter. However, the contrast medium is only slowly conveyed to the distal artery and not adequately washed out. Even the final angiogram after glyceryl trinitrate in different projections shows no satisfactory flow albeit no visible flow limiting obstacles, such as coronary artery dissection or recurrent thrombus formation. The battle, undertaken to restore myocardial blood supply, seems to be lost and won, finally leading to compromised tissue perfusion despite a successful restoration of patency to the epicardial blood vessel.

A bolus of abciximab, followed by a continuous infusion, is initiated. ST segment elevations resolve only slightly during the next hours; the patient requires prolonged intensive medical care because of recurrent pulmonary oedema. Finally, the patient is stabilised on cardiovascular medication including an angiotensin converting enzyme (ACE) inhibitor, oxygen, and aspirin. The echocardiography shows …

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    BMJ Publishing Group Ltd and British Cardiovascular Society
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    BMJ Publishing Group Ltd and British Cardiovascular Society