I just wanted to let you know that even though I'm looking quite old, I'm still a millenial.
So I just had a "New Year, New Me" moment and my resolution is to become a new and improved version of myself in a couple of weeks.
Don't worry, my wisdom won't change. You're still going to find the same useful information here. Stay tuned!
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The inferior wall is akinetic. The indications that a wall is infarcted is akinesis or dyskinesis, calcification, and a thinned myocardial segment. The indications of a hibernating myocardial segment is a normal/thick myocardial segment, abscence of calcification, and a biphasic response (akinesis-hypokineis-akinesis) to dobutamine stress test. The gold standard for detection of myocardial hibernation is a MRI with gadolinium. Thallium stress test and PET scans are also quite accurate in determining if a myocardial segment is hibernating. Contrast echocardiography has also been shown to be accurate in the diagnosis of myocardial hibernation. Absence of Q wave on the ECG is also an indication that hibernating myocardium may be present.
Difinitions:(from the EHJ in the link below - a free article - please read it)
The term â‚Ç¨?ìviableâ‚Ç¨¬ù describes myocardial cells that are alive and hence also the myocardium that they constitute. This begs the question of how to define â‚Ç¨?ìaliveâ‚Ç¨¬ù since nuclear function, metabolic function, contractile function, membrane function, etc., may not be equally affected by an ischaemic insult. Fortunately, this nicety does not normally have clinical implications. Although individual myocytes may only be viable or nonviable to a first approximation, the macroscopic myocardium in ischaemic heart disease exhibits a continuum of states from fully viable, through partially viable in areas of partial-thickness infarction, to nonviable, or scarred, in areas of full-thickness infarction with no remaining myocytes. Whether applied to a myocyte or to a segment of myocardium, the term â‚Ç¨?ìviableâ‚Ç¨¬ù implies nothing with regard to contractile state. Thus, viable myocardium may contract normally or it may be dysfunctional, depending on other circumstances.
Stunning is a form of contractile dysfunction of viable myocardium caused by a brief period of ischaemia followed by restoration of perfusion.8 It may be the result of reperfusion injury whereby restoration of normal blood flow leads to generation of free radicals and a transitory overload of calcium within the myocytes and temporary damage to the contractile mechanism.9,10 Regional myocardial stunning has been demonstrated after myocardial infarction that is aborted by thrombolysis, after an episode of unstable angina, and after ischaemia induced by exercise testing.11 The dysfunction may persist from an hour to several days, but function ultimately returns to normal if normal perfusion is maintained.
Hibernation is also a state of contractile dysfunction in viable myocardium, but now in the setting of chronic ischaemic heart disease.12 In contrast to stunned myocardium, in which function recovers spontaneously, hibernating myocardium requires an intervention such as revascularisation for recovery. Hibernating myocardium is therefore normally defined as viable but dysfunctional myocardium that improves in function after revascularisation, but it is possible that medical therapy might also be effective in relieving hibernation by abolishing ischaemia.13 The definition, of course, assumes that revascularisation is successful and that the procedure itself does not lead to damage of the relevant area of myocardium.
It is important to distinguish between retrospective and prospective definitions of hibernation. Myocardium cannot strictly be defined as hibernating until improvement of contraction after intervention has been demonstrated. However, identification of hibernation is needed preoperatively for patient management and so a number of prospective definitions are used in the imaging literature. For instance, in positron emission tomography (PET), reduced ammonia uptake with normal or increased 2-fluorodeoxyglucose (FDG) uptake (PET mismatch) has been used to define hibernation, but this is a surrogate definition. A similar surrogate definition that is commonly used is â‚Ç¨?ìviable and dysfunctional myocardiumâ‚Ç¨¬ù, but this is less reliable because hibernation may be only one cause of viable myocardium that fails to contract. Others may be tethering caused by subendocardial infarction or neighbouring transmural infarction, and remodelling with loss of mechanical advantage. The demonstration of inducible ischaemia in the relevant section of myocardium is therefore a helpful addition to the definition since hibernation is an ischaemic syndrome and it is unlikely to be present in the absence of inducible ischaemia.14 Thus, the most useful surrogate definition of hibernation is viable and dysfunctional myocardium in which impaired perfusion reserve leads to inducible ischaemia.
Because we do not fully understand the pathophysiologic mechanisms underlying stunning and hibernation, it is better to avoid including these mechanisms in their definition. For instance, hibernation was originally defined as â‚Ç¨?ìa state of persistently impaired myocardial and left ventricular function at rest due to reduced coronary blood flow that can be partially or completely restored to normal if the myocardial oxygen supply/demand ratio is favourably altered.â‚Ç¨¬ù12 It is still controversial whether or not perfusion is reduced at rest,15 although we know that it is not always reduced.16 This aspect of the definition is therefore better omitted.
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Lack of pathologic Q waves: a specific marker of viability in myocardial hibernation.
Identification of hibernating myocardium with myocardial contrast echocardiography: comparison with late gadolinium-enhanced magnetic resonance.
Stress echocardiography: basics and noninvasive assessment of myocardial viability.
Imaging techniques for the assessment of myocardial hibernation
Comparison of sestamibi
echocardiography and PET for the detection of hibernating myocardium.