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Erschienen in:
01.01.2021 | EDITORIAL
LVEF reserve: State of the heart is a matter of time, jeopardy and ischemic memory
Erschienen in: Journal of Nuclear Cardiology | Ausgabe 6/2022
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Myocardial stunning was first reported in 1982 by Braunwald and Kloner as prolonged, post-ischemic ventricular dysfunction that occurs after brief periods of nonlethal ischemia. 1 Myocardial stunning was conceptualized as a “hit” of a transient episode of severe ischemia, “run” with restoration of flow before irreversible injury occurs, and “stun” of a relatively long period of post-ischemic contractile dysfunction associated with prolonged biochemical abnormalities that may take days to resolve following initial resolution of ischemia.1,2 Stunned myocardium has been identified in several clinical scenarios including following revascularization of acute coronary occlusion with thrombolysis or angioplasty, in patients with unstable angina pectoris, following exercise and pharmacologically induced ischemia with stress testing, following cardiac surgery, following angioplasty in patients without infarction, in dialysis-related metabolic dysfunction, and in Takotsubo cardiomyopathy.2 Leading hypotheses of proposed mechanisms include oxygen radical damage that occurs in the first few minutes of reperfusion and altered calcium flux with calcium overload that then desensitizes the myofilaments.3,4 Myocardial stunning is by definition transient, resolves spontaneously over time, and is clinically distinguished from irreversible myocardial necrosis with severe unresolved ischemia, and from hibernating, viable myocardium associated with repetitive stunning or chronic reduced flow state associated with persistent dysfunction. Figure 1 schematizes the pathophysiologic states, and Figure 2 illustrates the distinctions of myocardial stunning and hibernating, viable myocardium.
Figure 1
The schematic documents 3 possible outcomes of myocardial ischemia. On the left is the situation of severe and prolonged myocardial ischemia. The myocardial cells die resulting in a myocardial infarction, are replaced by scar tissue, and do not recover contractile function. In the middle is the scenario in which the duration and severity of myocardial ischemia are not long enough or severe enough to kill cells. When the ischemia is relieved by reperfusion, the myocardium is viable but stunned, exhibiting transient post-ischemic contractile and biochemical dysfunction. Recovery of the stunned myocardium eventually occurs but may take days to weeks. The third scenario of ischemia is shown on the right. Chronic low blood flow results in metabolic adaptations allowing the cardiomyocytes to survive, but these cells do not contract at rest and exhibit typical morphology of dedifferentiation. Once revascularized, these hibernating myocardial cells eventually recover function, but this may require weeks to months as the contractile apparatus replenishes. In addition, another theory of hibernating myocardium is shown in which repetitive episodes of ischemic, stunned myocardium occur when coronary artery reserve cannot meet an increase in myocardial oxygen demand. These repetitive episodes of stunning lead to a chronic reduction in contractile function and metabolic adaptation to allow for cell survival (From Ref. 2)
Figure 2
Schematic representation of imaging findings in stunned and hibernating myocardium. Top panel: The heart is shown as a conical structure with the base at the top and the apex at the bottom with the ventricular cavity in the middle. Stunned myocardium occurs after relief of a discreet episode of ischemia. During ischemia, imaging studies (such as nuclear studies using thallium or other tracers, echocardiographic contrast agents, magnetic resonance contrast imaging) will show reduced perfusion. During active ischemia, reduced perfusion of the apex is associated with reduced cardiac function (contractility) in the same apical region. Cardiac function can be measured by a variety of techniques, including real-time nuclear imaging, echocardiography, and magnetic resonance imaging. After restoration of flow (angioplasty, stenting, thrombolysis, relief of coronary vasospasm), perfusion is restored but there is a persistent region of reduced cardiac function. The functional abnormality may last hours to days to weeks but eventually does recover. The myocardium shows positive viability (usually performed with positron emission tomography such as fluorodeoxyglucose uptake showing active metabolism and therefore viable metabolizing cells). Bottom panel: Hibernating myocardium is shown. At the apex there is eventually an area of reduced perfusion. In the early phase, this area may be characterized by normal resting flow with reduced coronary reactivity. Repetitive stunned myocardium may contribute as described in the text. The chronically (months to years) reduced perfusion is matched by a chronic reduction in cardiac function at the apex. The myocardium is viable as shown by studies such as positron emission tomography (From Ref. 2)
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