Prospective Identification of Myocardial Stunning Using Technetium-99m Sestamibi–Based Measurements of Infarct Size

Christian, Timothy F.; Gitter, Michael J.; Miller, Todd D.; Gibbons, Raymond J.

doi:10.1016/s0735-1097(97)00409-9

Cited by 29 publications

(11 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Because the uptake and retention of 99m Tc-sestamibi do not appear to be affected by stunning (15,16), reperfused but stunned myocardium areas may explain perfusioncontraction mismatch observed in patients with acute MI. As previously reported by Christian et al (17), 25% of patients with acute MI had a "mismatch stunned" pattern, meaning that these patients had an LVEF lower than expected by their infarct size at hospital discharge owing to myocardial stunning, and these patients showed a late increase in the LVEF. The apparent paradox with respect to univariate analysis is caused by the concomitant presence of myocardial salvage in the multivariable analysis.…”

Section: Discussionsupporting

confidence: 64%

Evolution of Left Ventricular Ejection Fraction and its Relationship to Infarct Size After Acute Myocardial Infarction

Ndrepepa

Mehilli

Martinoff

et al. 2007

Journal of the American College of Cardiology

111

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 64%

Evolution of Left Ventricular Ejection Fraction and its Relationship to Infarct Size After Acute Myocardial Infarction

Ndrepepa

Mehilli

Martinoff

et al. 2007

Journal of the American College of Cardiology

111

View full text Add to dashboard Cite

show abstract

“…28 However, the advantages afforded by increasing the extent of myocardial salvage take time to become clinically apparent, because of the persistence of myocardial stunning with reperfusion therapy. 36 On the basis of our findings, a new reperfusion strategy such as combining stenting with abciximab yields a significantly greater degree of myocardial salvage and a better clinical outcome at six months than does a conventional strategy of fibrinolytic therapy in patients with acute myocardial infarction.…”

Section: Discussionmentioning

confidence: 70%

Coronary Stenting plus Platelet Glycoprotein IIb/IIIa Blockade Compared with Tissue Plasminogen Activator in Acute Myocardial Infarction

et al. 2000

View full text Add to dashboard Cite

show abstract

“…80,81 Ito et al 80 measured ischemic risk zone in patients by performing myocardial contrast echocardiography before reperfusion and simultaneously measuring serial endocardial length of the zone of abnormal contraction assessed by echocardiography. They measured a ratio of endocardial length of abnormal contraction to that of the contrast defect.…”

Section: Clinical Evidence For Stunned Myocardiummentioning

confidence: 99%

Consequences of Brief Ischemia: Stunning, Preconditioning, and Their Clinical Implications

2001

View full text Add to dashboard Cite

Abstract-In experimental studies in the dog, total proximal coronary artery occlusions of up to 15 minutes result in reversible injury, meaning that the myocytes survive this insult. The 15 minutes of ischemia, however, induce numerous changes in the myocardium, including certain monuments to the brief episode of ischemia that may persist for days. One of these monuments is stunned myocardium, which represents "prolonged postischemic contractile dysfunction of myocardium salvaged by reperfusion." The mechanism of stunning involves generation of oxygen radicals as well as alteration in calcium homeostasis and possibly alteration in contractile protein structure. Stunning has been observed in several clinical scenarios, including after percutaneous transluminal coronary angioplasty, unstable angina, stressinduced ischemia, after thrombolysis, and after cardiopulmonary bypass. Oxygen radical scavengers and calcium channel blockers have been shown to enhance function of stunned myocardium in experimental studies, and in a few clinical studies, calcium channel blockers have been shown to ameliorate stunning. Although brief periods of ischemia can contribute to prolonged left ventricular dysfunction and even heart failure, they paradoxically play a cardioprotective role. Episodes of ischemia as short as 5 minutes, followed by reperfusion, protect the heart from a subsequent longer coronary artery occlusion by markedly reducing the amount of necrosis that results from the test episode of ischemia. This phenomenon, called ischemic preconditioning, has been observed in virtually every species in which it has been studied and is a powerful cardioprotective effect. The mechanism of ischemic preconditioning involves both triggers and mediators and involves complex second messenger pathways that appear to involve such components as adenosine, adenosine receptors, the epsilon isoform of protein kinase C, the ATP-dependent potassium channels, as well as others, including a paradoxical protective role of oxygen radicals. Both an early and a late phase of preconditioning have been described, and the mechanisms underlying their induction are under investigation. That preconditioning may occur in humans is suggested by the observations that repetitive balloon inflations in the coronary artery are associated with progressively less chest pain, ST-segment elevation, lactate production, the protective effects of preinfarction angina, the anginal "warm-up phenomenon," and studies performed on human cardiac biopsies that show metabolic properties suggesting preconditioning. Development of pharmacological agents that stimulate second messenger pathways thought to be involved in preconditioning, but without causing ischemia, could result in novel approaches to treating ischemia. Hence, on one hand, brief episodes of ischemia can have a negative effect on the heart: stunning; and on the other hand, they have a protective effect: preconditioning. The future challenge is how to minimize the stunning phenomenon and maximize the preconditioni...

show abstract

Prospective Identification of Myocardial Stunning Using Technetium-99m Sestamibi–Based Measurements of Infarct Size

Cited by 29 publications

References 35 publications

Evolution of Left Ventricular Ejection Fraction and its Relationship to Infarct Size After Acute Myocardial Infarction

Evolution of Left Ventricular Ejection Fraction and its Relationship to Infarct Size After Acute Myocardial Infarction

Coronary Stenting plus Platelet Glycoprotein IIb/IIIa Blockade Compared with Tissue Plasminogen Activator in Acute Myocardial Infarction

Consequences of Brief Ischemia: Stunning, Preconditioning, and Their Clinical Implications

Contact Info

Product

Resources

About