In acute myocardial infarction, culprit stent placement is the first choice for coronary recanalization. However, due to the acute vascular occlusion, the vascular endothelial cells are hypoxic-ischemic and edematous, combined with the presence of vasospasm and other factors, resulting in changes in the area of the coronary lumen, which will have a certain impact on the selection of stents; On the other hand, under special conditions, such as patients who are allergic to metal stents, have a bleeding tendency and cannot take double-antibody drugs for a long time, or who refuse stent placement for any other reason, how to effectively protect the culprit's vascular reperfusion? Preventing restenosis of blood vessels is a problem.
At present, DCB is a Class I recommendation in the interventional treatment of restenosis and small vessel stenosis in metal stents. The mechanism of action of DCB includes [12]: ① Anti-cell proliferation drugs are delivered to the target diseased vessel through balloon dilation, thereby inhibiting the intimal proliferative inflammation;② The blood vessel wall has uniform absorption of the drug, and the tiny drug carrier covers the blood vessel wall to ensure the continuous release of the drug; ③ The pre- dilation of the balloon can form a micro dissection, thereby promoting the transport of the drug through the intima and dissection. With the continuous deepening of the clinical application of DCB, it has been found that DCB treatment of primary coronary lesions in situ in non-STEMI patients also has a good effect [13–14]. However, STEMI lesions secondary to plaque rupture are accompanied by varying degrees of thrombus load [15]. The presence of thrombus may affect the rapid and effective entry of DCB antiproliferative drugs into the subintima of coronary artery lesions. Therefore, for the clinical application of DCB, STEMI is a special kind of in situ disease. Internationally, there are inconsistent conclusions about the effectiveness of DCB in treating STEMI [16].
More and more evidence supports the use of DCB in coronary De Novo lesions [17]. Even if it is used in large vessels with a diameter of > 2.8 mm, it can be as safe and effective as in small vessels, but there are only few reports at present. However, there are only a few reports on the use of DCB alone in patients with acute myocardial infarction. More than 60% of ISR patients present with acute coronary syndrome, and about 10% of them have clinical manifestations of acute myocardial infarction. Small vessel disease causes a relatively small area of myocardial infarction, which is also common clinically. The obstruction of the diagonal branch, obtuse marginal branch, middle branch or right coronary artery branch can be clinically manifested as acute ST-segment elevation myocardial infarction (STEMI), and can also be manifested as non-ST-elevation myocardial infarction (NSTEMI). The value of DCB in acute myocardial infarction caused by these two diseases is still affirmative. In 2018, Professor Wu Jiongren's team published a retrospective study of 117 patients with DES in stent restenosis manifested clinically as myocardial infarction (NSTEMI89%, STEMI11%) [17], 75 cases were treated with DCB, 42 cases were re-implanted with DES. There was no significant difference between the two groups in 1-year clinical cardiovascular and cerebrovascular major adverse events and cardiovascular mortality. Does DCB therapy have its advantages in acute myocardial infarction lesions that are not caused by the above two conditions? In theory, late stent adhesion and delayed endothelial healing after STEMI emergency interventional stent placement are more common phenomena than elective stable disease. DCB can avoid the metal left behind, reduce the late stent thrombosis and the loss of vascular motor function. DCB therapy may be able to avoid the need for long-term dual antiplatelet therapy, and may benefit more patients with high-risk bleeding.
Limited results show that with LLL and TLR as the observation indicators, DCB and bare metal stent (BMS) or DCB + BMS have the same effect, but are inferior to paclitaxel drug-coated stent (PES) [18]. Unlike patients with stable coronary heart disease, patients with acute myocardial infarction often have a large number of thrombi in the occluded blood vessels, which will affect the penetration of drugs in DCB into the blood vessel wall. Therefore, in this study, in order to remove thrombus as much as possible, vascular aspiration and intracoronary injection of tirofiban were actively used. Compared with drug-eluting stent (DES) implantation, vascular pretreatment before DCB application is more important, because dissections above type C can affect coronary blood flow, so if DCB intervention is planned, the occurrence of dissection should be prevented as far as possible or at least controlled. In order to achieve this goal, cutting balloons or spinous process balloons are used more in this study, because the above two kinds of balloons can not only effectively increase the diameter of the lumen while reducing the occurrence of severe dissection, but also can improve the blood vessel wall, thereby promoting the absorption of drugs in the intima and media [10].
In this study, there was no statistically significant difference in the CCS classification of angina between the two groups of patients in the routine follow-up at 1 month, 6 months and 1 year after operation. Cardiac color Doppler ultrasound showed that the cardiac function of the two groups improved in the 6th month and 1 year after the operation compared with the hospitalization period. The difference was statistically significant, but there was no statistical difference between the two groups, which proves the effectiveness of DCB in the treatment of STEMI. The coronary angiography was followed up 1 year after the operation. The target lesion LLL in the balloon group was (-0.12 ± 0.46) mm, while the target lesion in the stent group was (0.14 ± 0.37) mm. The difference was statistically significant. It is suggested that positive remodeling occurred in the balloon group, which may be related to more and more uniform anti-proliferative drugs delivered by the drug balloon to the tube wall [19], avoiding the "blind zone" of drug release. In addition, the absence of metal beams reduces the impact on the original vascular anatomy, maintains the vasoconstrictor response and vascular geometry, thereby reducing abnormal blood flow. In addition, during the 1-year follow-up in this study, the incidence of MACEs in the balloon group was 11%, and the total number of MACEs in the stent group within 1 year was 5 cases and the incidence of events was 12%. There was no statistical difference between the two groups. This illustrated the safety and effectiveness of DCB in the treatment of STEMI, and showed good clinical results during the 1-year follow-up period. Coronary angiography supported the above results. In summary, the application of DCB alone in STEMI patients is safe and effective.
Compared with DES treatment strategy, DCB treatment has obvious advantages. First of all, according to the current consensus of experts, it only takes 1 to 3 months to perform dual antiplatelet therapy after DCB treatment, which greatly shortens the application time of dual antiplatelet drugs, thereby reducing bleeding complications. Therefore, it is more suitable for patients with high risk of bleeding. It is likely to be a more optimized interventional treatment option for STEMI patients, and it can reduce the treatment time of dual antiplatelet drugs. Secondly, the paclitaxel of DCB has an anti-proliferation effect of smooth muscle cells and can also promote cell apoptosis. Studies have found that after the use of DCB, the vascular lumen will be enlarged during follow-up, and even coronary aneurysm-like dilation will occur [20]. The more abundant the smooth muscle of the vessel wall, the stronger the elastic retraction effect, which is one of the reasons to exclude the use of DCB in left main artery disease and proximal anterior descending artery disease. The positive remodeling of blood vessels after DCB expansion is also related to the repair of endothelial injury and the inhibition of inflammation. In animal experiments, the blood vessels treated by DCB showed that inflammatory reaction and focal fibrin deposition were obviously inhibited, while apoptosis was increased for 6 months [9]. In addition, the regression of acute endothelial cell edema during follow-up and the reduction of atherosclerotic plaques also play a role in the positive remodeling of blood vessels. Finally, the DCB strategy has another obvious benefit, that is, delayed thrombosis after DCB use is extremely rare. It is speculated that this may be related to the shorter time for DCB to reach the target lesion through the guiding catheter, because the shorter the immersion time in the blood, the less the drug eluted, as a result, the drug reaching the target lesion vessel wall increased [21].
This study suggests that in clinical practice, if patients with acute myocardial infarction cannot accept metal stent implantation, the use of DCB for expansion is an alternative, safe and effective. The premise is to remove the thrombus as much as possible and control the dissection below the AB type.
First of all, as a single-center clinical study, the number of patients enrolled is relatively small; second, although the screening of lesions in this trial is strict, the selection is singular, basically simple lesions and non-bifurcated lesions. Therefore, the scope of application of the conclusions of this study is limited. It is only applicable to patients who meet the conditions for DCB use after lesion pretreatment. In the future, multi-center clinical trials are needed to expand the number of patients in order to further evaluate the efficacy of DCB in more suitable lesions.