Corresponding author’s Full name: Lam Truong Hoai
Affiliation: Tam Anh Hospital
Address: Hanoi Capital, Vietnam
Email:
truonglamcs@gmail.com
Tel : +84036875579
Keywords: Slow flow
& no-Reflow, acute coronary syndrome, acute crisis thrombosis, balloon
angioplasty, autologous blood injection
Abbreviation: percutaneous coronary intervention (PCI), Acute
coronary syndrome (ACS), Intact related artery(IRA), Right coronary
artery (RCA), Posterior left ventricular (PLV), Ventricular tachycardia
(Vtach), Blood pressure (BP), ST-elevation myocardial infarction
(STEMI),Clinical key message:
Management of the slow-flow and no-reflow when the conventional
therapy isn’t already.
That may be a new technique that considers when hemodynamic unstable
and isn’t suitable with the medication especially without IIb/IIIa
inhibitor
Abstract
Slow
flow and no-reflow phenomenon are taken to sudden loss of coronary
artery flow, typically after stenting or angioplasty in primary PCI.
Otherwise conventional therapy, we
report a technique, which autologous
blood into intracoronary to supply oxygen and break process thrombosis
results in successfully management no-reflow in primary PCI in ACS
Introduction
Early
revascularization of an intact related artery ( IRA) plays an important
role in ACS to prevent myocardium injury. With all the recent advances
in equipment and techniques, revascularization has become a faster and
good result. However, the no-reflow phenomenon occurs in a considerable
number of patients undergoing primary PCI ranging between 12% and
32.8%(1). This phenomenon is associated with arrhythmias, poor
in-hospital survival, and poor one-year survival. Intracoronary
vasodilators such as verapamil, nitroprusside, or adenosine are being
administered for the treatment of no-reflow via the microcatheter.
But sometimes distal flow restoration
is not satisfactory especially in patients with TIMI 0 flow because of
hemodynamic unstable and heart shock result in less effective medication
lead to the circuit pathology is that no flow, thrombosis, heart shock,
arrhythmias with consequence death. The use of blood with high O2
saturation pump into the intracoronary to supply oxygen for the
myocardium while the no-reflow phenomenon occurs, and this helps to
maintain flow in the vessel to prevent thrombosis. We report a clinical
case using the self blood pump into the coronary artery to treat no flow
intracoronary in ACS patients with primary PCI successfully.
Presentation
A 61-year-old man with a history of hypertension was admitted to the
hospital because of severe chest pain. In the emergency department, the
patient suddenly cardiac arrest, and chest compressions immediately with
Adrenaline 1mg/1ml x 5 ampoules, after that monitoring showed Vtach and
defibrillation with 200J. ECG showed BAV III, ST elevated in DII, DIII,
aVF, and heart rate was 40 bpm (figure 1). Blood pressure was 90/60 mmHg
with Noreadrenalin 0.1mcg/kg/h, Dobutamine 10mcg/kg/h and mechanical
ventilation. Patient transferred to cath lab immediately with totally
medication which was, Lidocaine 40mg/2ml x 2 ampoules , Magnesisulfat
15%x10ml x 2 ampoules, Lovenox 0,5mg/kg, Aspirin x 300mg, Ticagrelor
180mg, Rosuvastatin 40mg.
A temporary pacemaker was implanted on the right femoral vein with HR 80
bpm, output 3mv, sensing 3mv. The angiography on the right femoral
artery showed proximal RCA occlusion (figure 2A). The thrombus
aspiration device had been used, which wasn’t effective. Balloon
angioplasty which complaint ballon 2.5x20mm was used, angiogram showed
RCA TIMI III flow and lesion were RCA I-II and RCA III with 95% and
90% irrespectively. Stents were implanted with DES 3.5x40mm (20atm) for
RCA I-II, and DES 2.75x40mm (12atm) for RCA III-PLV. The hemodynamic was
stable BP 100/60mmHg (with noradrenaline and dobutamine) and the TIMI
III flow was showed on the angiogram. After 5 minutes the angiogram
showed thrombus in the proximal RCA (Figure 2B) (ACT was 230sec). With
the mud thrombosis which the thrombus aspiration device wasn’t
effective, we decided active balloon angioplasty with a compliant
balloon (3.5x20mm) to maintain the flow but as a result slow-flow on the
angiogram (TIMI I), which may be microvascular constriction result in
hemodynamic unstable and arrhythmia (Vtach or Vfib). The medication was
indicated which wasn’t suitable because of low BP and arrhythmia,
include Adenosine, Nitroglycerin. To
maintain flow in RCA we decided active angioplasty balloon and the use
of blood with high O2 saturation pump into the intracoronary to supply
oxygen for the myocardium while the no-reflow phenomenon occurs
through a contralateral femoral
artery. Using syringe 10ml pumped through thrombus aspiration device,
hand force just enough to reduce erythrocyte rupture, with a frequency
of about 5 pumps/min, active angioplasty balloon every 5 minutes to
maintain open vessel lumen and maintain flow. Thrombus aspiration still
measures coronary perfusion pressure which demonstrates perfusion in the
coronary artery while couldn’t measure pressure through guiding
catheter. The patient became more stable, which arrhythmia and pressure
drop weren’t apparent while we did the procedure.
After 1 hour of active balloon angioplasty and pump blood with high O2
saturation, the angiogram showed TIMI III flow and thrombus apparent,
hemodynamically stable, the patient was transferred to CCU for
monitoring and treatment. After 3 days of wearing off ventilators and
vasoconstriction. After a total of 10 days, the patient was discharged
with a stable condition.
Discussion
Originally, it was thought prolonged ischemia and extensive myocardial
damage led to microvascular (capillary bed) damage, or microvascular
vasoconstriction resulting in incomplete reperfusion, other factors have
been thought to play an important role in the development of
no-reflow, Platelets may be implicated in slow flow and no-reflow
through several mechanisms, including micro-vascular vasoconstriction or
obstruction by platelet aggregates. Although the exact mechanism of
no-reflow remains unknown, it is most likely complex and
multi-factorial. The selective use of Glycoprotein IIb/IIIa inhibitors
and thrombectomy devices during the intervention may be also appropriate
in the selected case, but the mud
thrombus almost failed with the thrombectomy device, and Glycoprotein
IIb/IIIa lack of randomized controlled clinical trials remains a
limitation. Unfortunately, In Vietnam, the Glycoprotein IIb/IIIa hasn’t
already. However, no-reflow can still occur even under the best-provided
care, which emphasizes the need for more specific mechanical and/or
medical treatments. This is particularly true in the setting of an acute
STEMI. Various vasodilators have been shown to affect some cases of
success including nicardipine, nitroprusside, and verapamil, but the
longer-acting drugs are somewhat limited by significant hemodynamic
unstable and arrhythmia, negative inotropy, which are of particular
importance in the acutely ischemic heart. Two drugs in particular
(nitroprusside and adenosine) have been studied as possible adjuncts to
reperfusion therapy in some trials(2, 3) but the effect isn’t strong
enough to succeed in all cases especially in an unstable hemodynamic and
significantly arrhythmias situation while
continuously autologous blood
injection into the intracoronary artery through aspiration thrombus
device is an important role to good choice to keep flowing compensate
flow disturbance.
Autologous blood injection which is high O2 saturation into the coronary
artery with the pressure and velocity stable to demand myocardium to
reduce the myocardium injury when slow flow and no-reflow occurred,
which is promised technique. In addition, active balloon angioplasty to
break thrombus formation and fibrin results in decrease crisis
thrombosis and maintain flow. As a result, the coronary flow is
preserved. Keep do it until the crisis thrombosis pass away and the flow
is improved. The time to pass to crisis thrombosis is important due to
such thrombin activity and fibrin polymerization fronts typically travel
slowly at a rate of 3mm in 60 min, consistent with simulation(4). Slow
traveling wave propagation to the physics in stagnant blood clotting,
while blood injection can warrant the pressure and velocity of flow with
high oxygen while the patient suffers from cardiac shock, is that the
medication show less effect.
Moreover, in a critical setting, continuous autologous blood injection
intracoronary artery can play an important role until all disturbance
disappeared. Similar to ECMO and
IABP are ensure hemodynamic and oxygen for myocardium by systemic
support, and autologous blood injection to supply for local ischemic
myocardium.
Virchow’s triad shows the 3rd factor is that vessel injury, stasis of
blood, and hypercoagulability of blood, which is correlative with the
mechanism of crisis thrombosis after stenting due to STEMI, while blood
artery can cover include stasis of blood by injecting blood into
intracoronary with stable pressure and active balloon angioplasty to
maintain flow, to supply oxygen for myocardium to reduce endothelium
damages, necrosis, supplying more fibrinogen form another site where the
crisis thrombosis doesn’t occur. Moreover slow flow and no re-flow could
preserve. This is the reason why we should keep do procedures while
waiting for the flow preserve to become normal.
Conclusion
Autologous blood which high oxygen inject to the intracoronary artery
and active balloon angioplasty is a role of treating slow flow & no
re-flow when the other conventional therapy isn’t suitable especially in
hemodynamic unstable and arrhythmias situation. Keep flowing and demand
high blood oxygen to reduce endothelial damage and myocardium necrosis
result in increase survival when
crisis thrombosis and disturbance
flow appearance.Funding: NoneDisclosures: None