Clinical Trial Details
— Status: Completed
Administrative data
| NCT number |
NCT02732080 |
| Other study ID # |
373 |
| Secondary ID |
|
| Status |
Completed |
| Phase |
N/A
|
| First received |
|
| Last updated |
|
| Start date |
April 2016 |
| Est. completion date |
December 30, 2018 |
Study information
| Verified date |
February 2023 |
| Source |
Istanbul University |
| Contact |
n/a |
| Is FDA regulated |
No |
| Health authority |
|
| Study type |
Interventional
|
Clinical Trial Summary
After reopening of the infarct related artery by primary percutaneous coronary interventions
(PPCI), microvascular damage at the related myocardial territory is not terminated
immediately. This ongoing nature of microvascular damage leading to myocardial malperfusion
is related to final infarct size. However, time course of the microvascular impairment
/obstruction after PPCI in patients presented with ST-elevating acute myocardial infarction
(STEMI) is not known. Routine primary percutaneous coronary interventions (PPCI) for
ST-elevation acute myocardial infarction (STEMI) includes balloon angioplasty (or
thrombectomy) followed immediately by stent implantation. However, stent implantation
performed in this thrombotic setting may lead to a further microvascular damage by causing
more distal embolisation and by inducing distal microvascular spasm by stretching the
coronary vessel wall. Furthermore, sudden exposure of distal microcirculation to a high
distal intracoronary pressure achieved by immediate stent implantation may exaggerate
myocardial oedema which contributes microvascular damage substantially by external
compression. However, results of studies investigating the efficacy of delayed stenting
(24-48 hours later) in patients in whom TIMI -3 flow was achieved after balloon angioplasty
were inconsistent.
In this study, STEMI patients undergoing PPCI, in whom epicardial reperfusion was achieved
(TIMI-3 flow) by wire crossing or by balloon angioplasty or aspiration thrombectomy, will be
randomised to immediate and delayed stenting groups. Delayed stenting will be performed at
the time when coronary auto regulation was recovered which is going to be determined based on
the continuous intracoronary hemodynamic monitoring after reperfusion.
Description:
It was shown in ischemia/reperfusion models that after reopening of the occluded epicardial
coronary artery, following initial hyperemic flow, myocardial blood flow in the area at risk
rapidly and progressively declines and get stabilised approximately within 30 minutes.This
finding implies that, in spite of the initial ischemic insult, coronary auto-regulation in
the reperfused myocardial territory recovers. Nevertheless, this recovery requires some time
after reperfusion was achieved. During total occlusion of an epicardial coronary artery,
pre-arteriolar sphincters can be expected to be paralysed in widely open position in response
to severely increased distal myocardial demand. Ischemic myocyte damage also contributes to
malfunctioned pre-arteriolar sphincters. Therefore, full restoration of perfusion pressure
distal to the infarct related artery by immediate stenting (direct or after angioplasty) may
then fail to induce an immediate adaptive autoregulatory response (compensatory
vasoconstriction) in the related microvascular territory, resulting in an inappropriately
increased pressure in the damaged microcirculation. During total epicardial occlusion,
ischemia/hypoxia induced damage and increased permeability at the capillary level lead to
loss of structural integrity in the related microvascular territory. After immediate
stenting, this severely damaged microcirculation is exposed to a suddenly increased
uncontrolled intracoronary pressure which may consequently substantially contribute to
intramyocardial haemorrhage and oedema.
Therefore, it was hypothesised that gradual reperfusion with delayed stenting performed when
coronary auto regulatory function was recovered may lessen the myocardial oedema and/or
haemorrhage by preventing/limiting uncontrolled increase in pressure in the distal
microcirculation.
The recovery of coronary autoregulatory function in reperfused STEMI patients can be assessed
by continuous monitoring of coronary (microvascular) blood flow and resistance values after
restoration of epicardial blood flow by balloon angioplasty in individual basis.
In this study, following establishment of TIMI-3 flow by balloon angioplasty, patients will
be randomized to immediate or delayed stenting groups. Continuous intracoronary hemodynamic
monitorization will be performed in re-opened infarct related artery using a coronary guide
wire equipped with pressure and flow sensors for a total of 1hour in both groups.
In delayed stent group, stent implantation will be performed in individual basis when
coronary hemodynamic data indicates that coronary autoregulation was recovered (when initial
hyperaemic flow response was subsided and baseline microvascular resistance was increased).
Recovery of autoregulatory function will be determined by identification of stabilisation of
baseline coronary flow velocity and baseline microvascular resistance in infarct related
artery after balloon angioplasty. Stabilization will be decided by comparing basal coronary
flow velocity and microvascular resistance values measured in non-infarct related coronary
artery immediately before PPCI with the values that was being measured in re-opened infarct
related artery. When baseline flow velocity and resistance values being recorded in IRA got
close to the values measured in non-IRA, IRA will be stented. Intracoronary pressure and flow
data will continuously be monitored until the end of 1 hour follow-up period.
In immediate stenting group, stent implantation will be performed immediately following
angioplasty. Intracoronary pressure and flow data will continuously be monitored using dual
sensor coronary guide wire until the end of 1 hour follow up period.
