Clinical profile of patients with congestive heart failure due to coronary artery disease

The non‐invasive assessment of hibernating myocardium in ischaemic cardiomyopathy—a myriad of techniques

“…Intracellular structural changes include myofibrillar and sarcoplasmic reticulum loss without cell volume reduction and glycogen accumulation. These changes differ markedly from those seen in permanently damaged atrophied or infarcted tissue where extensive cell volume loss occurs in association with cell membrane damage, cytoplasmic vacuolisation, mitochondrial swelling and lipid droplet accumulation [34]. Intracellular metabolic changes include a reduction in fatty acid beta‐oxidation and an increase in anaerobic glycolysis, with glucose now becoming the major substrate for metabolism [42].…”

“…This dysfunction may persist for some time following the ischaemic event and restoration of normal coronary blood flow. Cellular mechanisms underlying stunning are thought to involve a number of factors including: altered energy utilisation by contractile proteins following a rapid decline in myocardial creatine phosphate stores and adenosine triphosphate (ATP); impaired sarcoplasmic reticulum function and calcium regulation; reduced myofilament responsiveness to calcium ion influx; production of cytotoxic oxygen‐free radicals, and neutrophilic infiltration of previously ischaemic tissue with damage to the extracellular connective tissue matrix and further production of oxygen free radicals [34,35]. It has been hypothesised that myocardial stunning consists of two components: (1) a component that develops during ischaemia (ischaemic injury) which is not responsive to anti‐oxidant therapy and (2) a component that develops after reperfusion (reperfusion injury) which can be mitigated by early antioxidant therapy [35].…”

“…Whilst stunning is typically a short‐term process, myocardial hibernation is a chronic process with persistently impaired myocardial contractile function until blood‐flow is re‐established. Although there is currently some controversy as to whether underlying resting blood flow is reduced in hibernating myocardium as initially postulated [21,36–38], or whether resting blood flow is maintained with this phenomenon simply reflecting repeated stunning [39,40] and reduced coronary flow‐reserve [41], repeated or continuous reduction in myocardial perfusion leads to a reversible down regulation of myocardial function as a result of intracellular structural and metabolic changes [34]. This leads to matching between the reduced perfusion and reduced energy demand preserving cellular viability.…”

“…As a result of this observation, several protocols have now been established to further improve the ability of thallium imaging to differentiate myocardial hibernation from myocardial scar by allowing either: increased plasma thallium concentration, increased rest perfusion, or prolonged time for redistribution, thus allowing greater thallium uptake into viable tissues [66]. Such techniques include: late (24–72 h) redistribution imaging; stress‐redistribution‐reinjection thallium imaging, where imaging is repeated after an additional dose of thallium is given at rest 3–4 h after a stress image, and nitrate‐enhanced rest‐redistribution protocols, where thallium is injected at rest following the prior administration of sublingual nitrate medication [27,34,67,68]. Although both reversible and mild‐to‐moderate irreversible (fixed defects with greater than 50% of normal thallium uptake) thallium defects remain metabolically active as assessed by PET, Kitsiou et al have shown that functional recovery is more likely in regions with reversible defects and at least moderate rest perfusion, as compared to regions with mild‐to‐moderate fixed thallium defects [69].…”

Section 13: Evaluation and Therapy for Heart Failure in the Setting of Ischemic Heart Disease

“…48 In addition to ischemia, hibernating myocardium should be considered in all patients with CAD and chronic LV systolic dysfunction of any degree. 54 Hibernating myocardium can be identified using low-dose dobutamine stress echocardiography to assess contractile reserve, single photon emission tomography with thallium-201 or technetium-99m perfusion tracers to assess membrane integrity, and positron emission tomography to assess residual metabolic activity. 55,56 More recently, magnetic resonance imaging (MRI) has been used to identify potentially viable but dysfunctional myocardium.…”