myocardial stunning

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Related to myocardial stunning: Stunned myocardium

myocardial stunning

A term of art for prolonged, nonpermanent, post-ischaemic, systolic and/or diastolic ventricular dysfunction without myocardial necrosis. In myocardial stunning (MS), the myocardium is viable and has contractile reserve. MS may follow successful thrombolytic therapy in evolving acute MI, percutaneous transluminal angioplasty, during exercise, and after relief of ischaemia caused by vasospasm.
Uncertain; MS has been attributed to oxidative stress, or to a transient increase in intracellular calcium.

myocardial stunning

Stunning Cardiology Prolonged nonpermanent postischemic systolic and/or diastolic ventricular dysfunction without myocardial necrosis; MS may follow successful thrombolytic therapy in evolving MI, PCTA, during exercise, and after relief of ischemia caused by vasospasm. Cf Myocardial hibernation.

my·o·car·di·al stun·ning

(mīō-kahrdē-ăl stŭning)
Decreased myocardial contractility occuring in noninfarcted areas due to excess production of free radicals in infarcted areas.

Myocardial stunning

A reversible state of left ventricular dysfunction featuring chest pain, dyspnoea, ECG changes, and sometimes hypotension or heart failure requiring supportive measures. The condition may be precipitated by sudden severe emotional stress and in these cases the levels of catecholamines may be up to 30 times normal.
References in periodicals archive ?
Myocardial stunning is now suspected to be a major contributor to the increased CV mortality rate in the HD population.
Repetitive and at times prolonged myocardial stunning can lead to a proliferation of fibrous connective tissue, called myocardial fibrosis.
The myocardial stunning that contributes to this process may be a potentially modifiable risk factor in the development of chronic heart failure, arrhythmias, and sudden cardiac death.
It is felt that these changes may also occur during HD when myocardial stunning occurs.
A small study by Selby and McIntyre (2011) assessed 10 patients on peritoneal dialysis (PD) for regional wall motion abnormalities and myocardial stunning.
These findings underscored the contribution of the HD treatment itself to myocardial stunning because children do not have the classical atheromatous coronary artery disease.
A number of both patient and treatment factors have been postulated to contribute to HD-induced myocardial stunning.
Myocardial stunning would be a plausible, if only presumed, contributing etiology.
In a follow-up study to evaluate in more detail the factors involved in HD-induced myocardial stunning, Assa et al.
Avoiding UFRs in excess of 13/mL/kg/hour might help minimize non-physiologic fluid shifts, hemodynamic instability, and hypotension, perhaps decreasing the risk of HD-induced myocardial stunning and CV and all cause mortality.
To our knowledge, no study of myocardial stunning has been undertaken while using UF profiling, but might be an area for future research.
This has been shown to virtually eliminate intradialytic hypotension and greatly reduce episodes of myocardial stunning (Jefferies, Virk, Moran, & McIntyre, 2011).