English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Remote ischemic conditioning (RIC) by brief intermittent episodes of ischemia and reperfusion of an organ or tissue remote from the heart protects the myocardium against ischemia-reperfusion injury. Experimental studies have established RIC as a powerful cardioprotective intervention. The ability to produce the protective effect by simply inflating a blood pressure cuff placed on the upper arm or thigh inducing periods of ischemiareperfusion has been important for its translation to the clinical setting. In proof-of-concept clinical studies, RIC reduced myocardial infarct (MI) size assessed by cardiac enzymes, single-photon emission computed tomography (SPECT) perfusion imaging, or cardiac magnetic resonance (CMR) imaging by 20% to 30% when applied as an adjunct to primary percutaneous coronary intervention (PCI) or thrombolysis in patients with acute MI. The effect of RIC on long-term clinical outcomes is currently being evaluated in acuteMI patients in the Effect of Remote Ischemic Conditioning Before Hospital Admission (CONDI) trial. The coronary vasculature has been considered as a target of RIC in addition to direct effect on the myocardium. Mechanisms of RIC can be briefly summarized as activation of nociceptive fibers during brief, local injury that releases an unidentified molecule into the circulation and/or signal through the spinal cord to activate both cardiac vagal and sympathetic efferent neurons to release cardioprotective substances. Many endogenously derived preconditioning agents are vasoactive (e.g., adenosine, nitric oxide, and bradykinin). Thus, it has been hypothesized that RIC can improve vascular function. Studies have shown that RIC prevents peripheral endothelial dysfunction associated with ischemia, but the effects on coronary blood flow have been controversial. In an experimental model, repeated transient limb ischaemia lead to reduced coronary resistance and increased basal flow in the left anterior descending coronary artery in healthy pigs. Similarly, basal blood flow velocity in the left anterior descending coronary artery assessed by transthoracic Doppler echocardiography was increased shortly after RIC in healthy human subjects. However, similar findings were not observed in patients with ischemic heart disease undergoing PCI. Upper limb RIC did not reduce microvascular resistance or improve basal or hyperemic coronary flow velocity in response to ischemia-induced vasodilation when assessed by intravascular probe placed distal to a coronary stenosis. Positron emission tomography (PET) with radiotracer kinetic modeling can be used to quantify myocardial blood flow (MBF) in absolute terms (mL/g/ minute) at rest and during vasodilator stress that allows the computation of coronary flow reserve (CFR). Quantification of regional MBF and CFR by PET may identify microvascular dysfunction associated with early stages of atherosclerosis, better characterize the extent and severity of coronary artery disease (CAD) burden in multivessel disease, and detect balanced decreases of MBF in all major coronary artery vascular territories. Furthermore, several studies have demonstrated that reduced CFR is a powerful predictor of increased risk of future cardiac events. Quantification of MBF is accurate and technically feasible by dynamic PET with the generator-produced flow tracer Rubidium (Rb) that has made the technique available also at sites without an onsite Reprint requests: Antti Saraste, MD, PhD, Heart Center, Turku University hospital, Hämeentie 11, 20520 Turku, Finland; antti.saraste@utu.fi J Nucl Cardiol 2018;25:897–9. 1071-3581/$34.00 Copyright 2016 American Society of Nuclear Cardiology.

Protection of coronary circulation: Evaluation by PET perfusion imaging