Micro Flows in the Cardiopulmonary System: A Surgical Perspective - Bioanalysis Advanced Materials Methods and Devices - page 71

associated with a worse prognosis at follow-up. The phenomenon has a multifacto-
rial pathogenesis including: distal embolization, ischemia-reperfusion injury, and
individual predisposition of coronary microcirculation to injury. Several therapeu-
tic strategies have been tested for the prevention and treatment of no-reflow. In
particular, thrombus aspiration before stent implantation prevents distal emboliza-
tion during stent deployment and has been recently shown to improve myocardial
perfusion and clinical outcome as compared with the standard procedure. However,
it is conceivable that the relevance of each pathogenetic component of no-reflow is
different in different patients, thus explaining the occurrence of no-reflow despite
the use of mechanical thrombus aspiration [ 14 ].
Another term used to indicate reduced microvessel flow, commonly occurring
following percutaneous coronary interventions (PCI), is Microvascular obstruction
(MVO) which may lead to myocardial injury, and is an independent predictor of
adverse outcome. Severe MVO may manifest angiographically as reduced flow in
the patent upstream epicardial arteries, a situation that is termed, as mentioned
above, “no-reflow.” Microvascular obstruction can be broadly categorized
according to the duration of myocardial ischemia preceding PCI. In “interventional
MVO” (e.g., elective PCI), obstruction typically involves myocardium that was
not exposed to acute ischemia before PCI. Conversely “reperfusion MVO”
(e.g., primary PCI for acute myocardial infarction) occurs within a myocardial
territory that was ischemic before the coronary intervention. Interventional and
reperfusion MVO have distinct pathophysiological mechanisms and may require
individualized therapeutic approaches. Interventional MVO is triggered predomi-
nantly by downstream embolization of atherosclerotic material from the epicardial
vessel wall into the distal microvasculature. Reperfusion MVO results from both
distal embolization and ischemia-reperfusion injury within the subtended ischemic
tissue. Management of MVO and no-reflow may be targeted at different levels: the
epicardial artery, microvasculature, and tissue [ 8 ]
The no-reflow phenomenon, being inadequate myocardial perfusion of a given
coronary segment, without angiographic evidence of mechanical vessel obstruc-
tion, after PCI, is difficult to understand and treat due to the large variability
between patients and the experimental difficulties in assessing the different
interacting processes at tissue level, such as ischemic injury, reperfusion injury,
distal embolization, susceptibility of microcirculation to injury, which contribute to
no reflow [ 15 , 18 ]. Increasingly, however, techniques to analyze microvascular
function in experiments and in patients are developed [ 17 ]. For the clinical routine,
approaches based on catheterization, including the index of microvascular resis-
tance (IMR, a measure of microvascular function), and the fractional flow reserve
(FFR, a measure of the epicardial component) have been introduced and used under
different conditions [ 13 ].
The no-reflow phenomenon is a type of coronary microvascular dysfunction
(CMD) occurring with an acute myocardial infarction [ 5 ]. The pathogenetic
mechanisms of CMD include structural : luminal obstruction, vascular wall infiltra-
tion, perivascular fibrosis, functional : endothelial dysfunction, dysfunction of smooth-
muscle cell, autonomic dysfunction extravascular : extramural compression. Research