CT imaging of myocardial viability: experimental and clinical evidence

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Summary

Over the last decade, imaging of myocardial viability has become a well-established indication in patients suffering from myocardial infarction. Myocardial viability imaging is routinely performed using ¹⁸F-fluorodeoxyglucose positron emission tomography, single-photon emission computed tomography or magnetic resonance imaging. Only recently have several multi-slice spiral computed tomography (MSCT) techniques been evaluated for visualisation of myocardial infarction. This review describes the different concepts of MSCT viability imaging. MSCT assessment of myocardial morphology, myocardial perfusion imaging and delayed myocardial contrast enhancement are introduced, with the latter evolving as the key concept of MSCT viability imaging. Clinical relevance of the different MSCT techniques is described.

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The stunned myocardium: prolonged, postischemic ventricular dysfunction.

R Kloner, E Braunwald (1982)

Myocardial ischemia has, for many decades, been viewed as an all-or-none process that causes myocardial necrosis when prolonged and severe, but whose effects are transient when it is brief or mild. In view of the evidence that the ischemic process may "hit, run and stun," perhaps our thinking about the consequences of myocardial ischemia should be expanded. According to this formulation, an ischemic insult not of sufficient severity of duration to produce myocardial necrosis may acutely affect myocardial repolarization and cause angina (hit); but these changes wane rapidly (run), when the balance between myocardial oxygen supply and demand has been reestablished. However, the ischemia may interfere with normal myocardial function, biochemical processes and ultrastructure for prolonged periods (stun). The severity and duration of these postischemic changes depend on the length and intensity of the ischemia, as well as on the condition of the myocardium at the onset of the ischemic episode. Furthermore, it is likely that when the myocardium is repeatedly stunned, it may exhibit chronic postischemic left ventricular dysfunction, an ill-defined condition. If prolonged, chronic postischemic left ventricular dysfunction can progress to myocardial scarring and ischemic cardiomyopathy, it may be important to determine how often it can be ameliorated by permanent improvement of myocardial perfusion by surgical treatment.

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Molecular and cellular mechanisms of myocardial stunning.

R Bolli, E Marban (1999)

The past two decades have witnessed an explosive growth of knowledge regarding postischemic myocardial dysfunction or myocardial "stunning." The purpose of this review is to summarize current information regarding the pathophysiology and pathogenesis of this phenomenon. Myocardial stunning should not be regarded as a single entity but rather as a "syndrome" that has been observed in a wide variety of experimental settings, which include the following: 1) stunning after a single, completely reversible episode of regional ischemia in vivo; 2) stunning after multiple, completely reversible episodes of regional ischemia in vivo; 3) stunning after a partly reversible episode of regional ischemia in vivo (subendocardial infarction); 4) stunning after global ischemia in vitro; 5) stunning after global ischemia in vivo; and 6) stunning after exercise-induced ischemia (high-flow ischemia). Whether these settings share a common mechanism is unknown. Although the pathogenesis of myocardial stunning has not been definitively established, the two major hypotheses are that it is caused by the generation of oxygen-derived free radicals (oxyradical hypothesis) and by a transient calcium overload (calcium hypothesis) on reperfusion. The final lesion responsible for the contractile depression appears to be a decreased responsiveness of contractile filaments to calcium. Recent evidence suggests that calcium overload may activate calpains, resulting in selective proteolysis of myofibrils; the time required for resynthesis of damaged proteins would explain in part the delayed recovery of function in stunned myocardium. The oxyradical and calcium hypotheses are not mutually exclusive and are likely to represent different facets of the same pathophysiological cascade. For example, increased free radical formation could cause cellular calcium overload, which would damage the contractile apparatus of the myocytes. Free radical generation could also directly alter contractile filaments in a manner that renders them less responsive to calcium (e.g., oxidation of critical thiol groups). However, it remains unknown whether oxyradicals play a role in all forms of stunning and whether the calcium hypothesis is applicable to stunning in vivo. Nevertheless, it is clear that the lesion responsible for myocardial stunning occurs, at least in part, after reperfusion so that this contractile dysfunction can be viewed, in part, as a form of "reperfusion injury." An important implication of the phenomenon of myocardial stunning is that so-called chronic hibernation may in fact be the result of repetitive episodes of stunning, which have a cumulative effect and cause protracted postischemic dysfunction. A better understanding of myocardial stunning will expand our knowledge of the pathophysiology of myocardial ischemia and provide a rationale for developing new therapeutic strategies designed to prevent postischemic dysfunction in patients.

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High-resolution spiral computed tomography coronary angiography in patients referred for diagnostic conventional coronary angiography.

Giuseppe Runza, Deborah McFadden, Jan De Maeseneer … (2005)

The diagnostic performance of the latest 64-slice CT scanner, with increased temporal (165 ms) and spatial (0.4 mm3) resolution, to detect significant stenoses in the clinically relevant coronary tree is unknown. We studied 52 patients (34 men; mean age, 59.6+/-12.1 years) with atypical chest pain, stable or unstable angina pectoris, or non-ST-segment elevation myocardial infarction scheduled for diagnostic conventional coronary angiography. All patients had stable sinus rhythm. Patients with initial heart rates > or =70 bpm received beta-blockers. Mean scan time was 13.3+/-0.9 seconds. The CT scans were analyzed by 2 observers unaware of the results of invasive coronary angiography, which was used as the standard of reference. All available coronary segments, regardless of size, were included in the evaluation. Lesions with > or =50 luminal narrowing were considered significant stenoses. Invasive coronary angiography demonstrated the absence of significant disease in 25% (13 of 52), single-vessel disease in 31% (16 of 52), and multivessel disease in 45% (23 of 52) of patients. One unsuccessful CT scan was classified as inconclusive. Ninety-four significant stenoses were present in the remaining 51 patients. Sensitivity, specificity, and positive and negative predictive values of CT for detecting significant stenoses on a segment-by-segment analysis were 99% (93 of 94; 95% CI, 94 to 99), 95% (601 of 631; 95% CI, 93 to 96), 76% (93 of 123; 95% CI, 67 to 89), and 99% (601 of 602; 95% CI, 99 to 100), respectively. Noninvasive 64-slice CT coronary angiography accurately detects coronary stenoses in patients in sinus rhythm and presenting with atypical chest pain, stable or unstable angina, or non-ST-segment elevation myocardial infarction.

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Author and article information

Contributors

Andreas H Mahnken

Georg Mühlenbruch

Rolf W. Günther

Joachim E. Wildberger

Journal

Journal ID (nlm-ta): Cardiovasc J Afr

Journal ID (iso-abbrev): Cardiovasc J Afr

Journal ID (publisher-id): TBC

Title: Cardiovascular Journal of Africa

Publisher: Clinics Cardive Publishing

ISSN (Print): 1995-1892

ISSN (Electronic): 1680-0745

Publication date (Print): July 2007

Volume: 18

Issue: 3

Pages: 169-174

Affiliations

Department of Diagnostic Radiology University Hospital, RWTH Aachen University, Germany

Applied Medical Engineering, Helmholtz Institute, RWTH Aachen University, Germany

Department of Diagnostic Radiology University Hospital, RWTH Aachen University, Germany

Article

PMC ID: 4213756

PubMed ID: 17612749

SO-VID: 66d9d78e-4f70-4074-a13d-17be3bee60d4

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This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Non-invasive Imaging in Patients With Chronic Total Occlusions of the Coronary Arteries—What Does the Interventionalist Need for Success?
Authors: Johannes Kersten, Nina Eberhardt, Vikas Prasad …

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CT imaging of myocardial viability: experimental and clinical evidence

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Electron Channelling Contrast Imaging (ECCI)

Most cited references 47

The stunned myocardium: prolonged, postischemic ventricular dysfunction.

Molecular and cellular mechanisms of myocardial stunning.

High-resolution spiral computed tomography coronary angiography in patients referred for diagnostic conventional coronary angiography.

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Cited by 1

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