Taxonomy of segmental myocardial systolic dysfunction

McDiarmid, Adam K; Pellicori, Pierpaolo; Cleland, John G.F.; Plein, Sven

doi:10.1093/eurheartj/ehw140

Cited by 11 publications

(12 citation statements)

References 150 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…2012; McDiarmid et al. 2017), which validates the proposed rabbit model and supports its application to investigation of ischemic HF in future studies.…”

Section: Discussionsupporting

confidence: 75%

The Structure-function remodeling in rabbit hearts of myocardial infarction

Niu

et al. 2017

Physiol Rep

View full text Add to dashboard Cite

Animal models are of importance to investigate basic mechanisms for ischemic heart failure (HF). The objective of the study was to create a rabbit model through multiple coronary artery ligations to investigate the postoperative structure‐function remodeling of the left ventricle (LV) and coronary arterial trees. Here, we hypothesize that the interplay of the degenerated coronary vasculature and increased ventricle wall stress relevant to cardiac fibrosis in vicinity of myocardial infarction (MI) precipitates the incidence and progression of ischemic HF. Echocardiographic measurements showed an approximately monotonic drop of fractional shortening and ejection fraction from 40% and 73% down to 28% and 58% as well as persistent enlargement of LV cavity and slight mitral regurgitation at postoperative 12 weeks. Micro‐CT and histological measurements showed that coronary vascular rarefaction and cardiac fibrosis relevant to inflammation occurred concurrently in vicinity of MI at postoperative 12 weeks albeit there was compensatory vascular growth at postoperative 6 weeks. These findings validate the proposed rabbit model and prove the hypothesis. The post‐MI rabbit model can serve as a reference to test various drugs for treatment of ischemic HF.

show abstract

“…2012; McDiarmid et al. 2017), which validates the proposed rabbit model and supports its application to investigation of ischemic HF in future studies.…”

Section: Discussionsupporting

confidence: 75%

The Structure-function remodeling in rabbit hearts of myocardial infarction

Niu

et al. 2017

Physiol Rep

View full text Add to dashboard Cite

show abstract

“…Early nuclear cardiology studies established that the degree of myocardial dysfunction in hibernation correlates with the extent of inducible perfusion defects [ 9 ]. Hibernation is therefore presumed to be an adaptation to chronic hypoperfusion, such that contractile function is chronically but reversibly downregulated [ 10 •]. Despite ongoing research, the extent and chronicity of hypoperfusion needed to induce hibernation has been a contentious subject.…”

Section: Introductionmentioning

confidence: 99%

“…Following brief periods of hypoperfusion and ischaemia contractile function is reduced. This process, termed “stunning”, has been observed experimentally [ 10 •]. It may persist for some time, but a single episode of ischaemia normally results in a return to normal myocardial function over some hours once normal perfusion is restored.…”

Section: Introductionmentioning

confidence: 99%

“…Dobutamine stress echocardiography (DSE), myocardial perfusion imaging (SPECT), late gadolinium enhanced cardiac MRI (LGE-CMR) and invasive coronary angiography are all in routine clinical use. A recent review article provides a succinct but highly relevant summary of the role of each modality in identifying myocardial pathology [ 10 •].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Identifying and Managing Hibernating Myocardium: What’s New and What Remains Unknown?

Ryan

Perera

2018

Curr Heart Fail Rep

View full text Add to dashboard Cite

Purpose of ReviewHibernation is an important and reversible cause of myocardial dysfunction in ischaemic heart failure.Recent FindingsHibernation is an adaptive process that promotes myocyte survival over maintaining contractile function. It is innate to mammalian physiology, sharing features with physiological hibernation in other species. Advanced imaging methods have reasonable accuracy in identifying hibernating myocardium. Novel superior hybrid methods may provide diagnostic potential. New evidence supports the role of surgical revascularisation in ischaemic heart failure, but the role of viability tests in planning such procedures remains unclear. Research to date has exclusively involved patients with ambulatory heart failure: Investigating the role of hibernation in ADHF is a key avenue for the future.SummaryWhilst our understanding of hibernation pathophysiology has improved dramatically, the clinical utility of identifying and targeting hibernation remains unclear.

show abstract

“…The myocardial blood flow is maintained in true mammalian hibernation likely due to a nitric oxide (NO) mechanism ( Kudej and Vatner, 2003 ). Downregulation of myocyte mitochondria ( McDiarmid et al, 2017 ) and altered expression of plasma membrane Cx43 ( Kaprielian et al, 1998 ) are present in hibernating myocardium. However, the intrinsic mechanisms of ischemia-induced myocardial hibernation remain to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

Connexins and Nitric Oxide Inside and Outside Mitochondria: Significance for Cardiac Protection and Adaptation

et al. 2018

View full text Add to dashboard Cite

Irreversible myocardial damage happens in the presence of prolonged and severe ischemia. Several phenomena protect the heart against myocardial infarction and other adverse outcomes of ischemia and reperfusion (IR), namely: hibernation related to stunned myocardium, ischemic preconditioning (IPC), ischemic post-conditioning, and their pharmacological surrogates. Ischemic preconditioning consists in the induction of a brief IR to reduce damage of the tissue caused by prolonged and severe ischemia. Nitric oxide (NO) signaling plays an essential role in IPC. Nitric oxide-sensitive guanylate cyclase/cyclic guanosine-3′,5′-monophosphate (cGMP)-dependent protein kinase type I-signaling pathway protects against the IR injury during myocardial infarction. Mitochondrial ATP-sensitive and Ca2+-activated K+ channels are involved in NO-mediated signaling in IPC. Independently of the cGMP-mediated induction of NO production, S-nitrosation represents a regulatory molecular mechanism similar to phosphorylation and is essential for IPC. Unlike conditioning phenomena, the mechanistic basis of myocardial stunning and hibernation remains poorly understood. In this review article, we hypothesize that the disruption of electrical syncytium of the myocardium may underly myocardial stunning and hibernation. Considering that the connexins are the building blocks of gap junctions which represent primary structural basis of electrical syncytium, we discuss data on the involvement of connexins into myocardial conditioning, stunning, and hibernation. We also show how NO-mediated signaling is involved in myocardial stunning and hibernation. Connexins represent an essential element of adaptation phenomena of the heart at the level of both the cardio- myocytes and the mitochondria. Nitric oxide targets mitochondrial connexins which may affect electrical syncytium continuum in the heart. Mitochondrial connexins may play an essential role in NO-dependent mechanisms of myocardial adaptation to ischemia.

show abstract

Taxonomy of segmental myocardial systolic dysfunction

Cited by 11 publications

References 150 publications

The Structure-function remodeling in rabbit hearts of myocardial infarction

The Structure-function remodeling in rabbit hearts of myocardial infarction

Identifying and Managing Hibernating Myocardium: What’s New and What Remains Unknown?

Connexins and Nitric Oxide Inside and Outside Mitochondria: Significance for Cardiac Protection and Adaptation

Contact Info

Product

Resources

About