RU2365380C1 - Method of acute myocardial infarction treatment - Google Patents

Abstract

FIELD: medicine.

SUBSTANCE: invention concerns medicine, namely to cardiology. The puncture of a femoral artery under local anaesthesia and medicamnetla sedation, selective catheterisation and coronarography of a coronary artery, installation of a guiding catheter in a mouth of the damaged coronary artery, performance of a balloon angioplasty of a stenosis place or occlusion of a coronary artery under the roentgenoscopy and coronarography control and medical product administration is carried out. Thus the coronary intravascular prosthesis - a stent is implanted into a stenosis or occlusion place after balloon angioplasty under the roentgenoscopy and coronarography control. Then a medical product in the form of a single eptifibatide dose in amount of 20 mg, dissolved in a 0.9% sodium chloride solution to 1 mg/ml concentration with rate of 4 mg/min within 5 minutes with the subsequent intravenous eptifibatide administration in amount of 2 mkg a minute on each kg of body mass of the patient within 12 hours is entered through a guiding catheter immediately into a mouth of the damaged coronary artery.

EFFECT: restoration normal coronary blood flow level in an Infarct-dependent coronary artery.

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Description

The invention relates to medicine, namely to cardiology, and can be used in the treatment of acute myocardial infarction.

The closest technical solution is a method for treating acute myocardial infarction, including puncture of the femoral artery under local anesthesia and drug sedation, selective catheterization and coronary angiography of the coronary artery, placement of a guide catheter at the mouth of the affected coronary artery, balloon angioplasty of the stenosis site or occlusion using the device atherosclerotic plaque, control coronary angiography, immediately after restoration of normal blood flow and turnip infusion of a heart attack - a responsible coronary artery introducing phosphocreatine catheter in physiological saline with a constant bulk velocity of 0.1-4 ml / sec in an amount of 0.5-4 grams for 40-180 seconds, followed by removal of the catheter and device and suturing and dressing on the hip.

(RF patent No. 2267323, M.cl. A61K 31/661, A61P 9/10, A61B 17/00, A61M 25/10, 09.09.2004)

The disadvantages of this method are only balloon angioplasty of the lesion and the introduction of phosphocreatine into the infarct-dependent coronary artery after restoration of normal blood flow and reperfusion, which reduces the reperfusion reaction of the body. However, in acute myocardial infarction, balloon angioplasty does not always ensure the restoration of normal blood flow in the infarction-dependent coronary artery due to several reasons.

One of these reasons lies in the mechanism of angioplasty itself. The mechanism of coronary angioplasty is the dissection of the intima of the coronary artery, which in different types and severity occurs in all cases. Dissection is a mechanical obstacle to normal blood flow through the artery, up to the complete occlusion of the vessel and serves as a provoking factor for the recurrence of thrombosis. Coronary angioplasty is also accompanied by elastic subsidence and residual stenosis of the coronary artery, embolism of the distal coronary artery with plaque and thrombus fragments.

In addition, the myocardium of the affected area of the heart contains vasospasm and impaired microcirculation, insufficiency of capillary autoregulation, vasoconstriction with occlusion of the microvessels by its mediators, platelet and leukocyte aggregates, inflammatory cytokines and endothelial dysfunction, inflammation and edema with macrobrotomy and trombosis the occurrence of the phenomenon of "no-reflow" - the absence or sharp deceleration of blood flow through the coronary artery after the removal of the initial mechanical obstruction and the absence or sharp weakening of myocardial perfusion at the microcirculatory level.

The phenomenon of "no-reflow" develops in 10-20% of cases after transcatheter interventions for acute myocardial infarction. [Piana RN, Paik GY, Moscucci M, et al. Incidence and treatment of “no-reflow" after percutaneous coronary intervention. Circulation 1994; 89: 2514-8].

The objective of the proposed method for the treatment of acute myocardial infarction is to improve the results of angioplasty in restoring normal blood flow through a heart attack coronary artery and a normal level of myocardial perfusion in the affected area of the heart.

This object is achieved in that in a method for the treatment of acute myocardial infarction, including puncture of the femoral artery under local anesthesia and drug sedation, selective catheterization and coronary angiography of the coronary artery, placement of a guiding catheter at the mouth of the affected coronary artery, balloon angioplasty of the site of stenosis or occult the control of fluoroscopy and coronary angiography and the administration of a drug new in the method is that after balloon angioplasty a coronary intravascular prosthesis is implanted into the site of stenosis or occlusion - a stent is under the control of fluoroscopy and coronarography, then, through a conduction catheter, a drug is administered directly in the mouth of the affected coronary artery as a single dose of an inhibitor of platelet receptor IIb / IIIa glycoprotein in the amount of 20 mg of diluted 0 mg eptifibatide in the amount of 20 , 9% sodium chloride solution to a concentration of 1 mg / ml at a rate of 4 mg / min for 5 minutes, followed by intravenous administration of eptifibatide in an amount of 2 μg per minute for every kilogram of patient’s body weight for 12 hours.

The relevance of the problem of the development of the "no-reflow" phenomenon in patients with acute myocardial infarction is shown in studies by Abbo et al., Who identified an increased risk of recurrence of heart attack and death when this phenomenon occurs [Abbo K, Dooris M, Glazier S, et al. Features and outcome of no-reflow after percutaneous coronary intervention, Am J Cardiol 1995; 75: 778-82.] And De Luca et al., Who showed the effect of the degree of restoration of blood flow in a heart attack-dependent coronary artery after transcatheter intervention as an independent factor influencing prognosis [De Luca G., Suryapranata H., van't HofA. et at. Prognostic Assessment of Patients With Acute Myocardial Infarction Treated With Primary Angioplasty // Circulation. - 2004 .-- Vol.109. - P.2737-2743].

As a means of removing a mechanical obstruction to the blood flow in the coronary artery, stents have been shown to be highly effective. There are studies showing the advantage of stenting over angioplasty in acute myocardial infarction, which is manifested by better angiographic results than angioplasty and better survival without adverse events [Grines C., Cox D., Stone G., et al. Coronary angioplasty with or without stent implantation for acute myocardial infarction. Stent Primary Angioplasty in Myocardial Infarction Study Group. // N. Engl. J. Med. - 1999. - Vol. 341. - P. 1949-1956.

Maillard L., Hamon M., Khalife K., et al. A comparison of systematic stenting and conventional ball angioplasty during primary percutaneous transluminal coronary angioplasty for acute myocardial infarction. STENTIM-2 Investigators. // J. Am. Coll. Cardiol. - 2000. - Vol. 35. - P.1729-1736].

Despite the high urgency of the problem of treating the “no reflow” phenomenon, there are no methods in the world for effective assistance in its occurrence.

Intravenous administration of eptifibatide, initiated before transcatheter interventions on the coronary arteries, reduces the number of thrombotic complications during and in the near future after manipulation by reducing blood coagulation. The drug binds fibrinogen and other adhesive proteins that activate adjacent platelets through glycoprotein IIb / IIIa receptors into a single whole as the final process of the formation of a platelet thrombus. However, the drug is rapidly limited in distribution due to its high affinity for IIb / IIa receptors on the surface of circulating platelets. The number of antibodies that directly enter the target coronary artery, thus, when administered intravenously, is limited. Moreover, the antiplatelet effect of eptifibatide is dose-dependent, expressed all the time of administration and lasts a short time after the termination of administration.

The dependence of the effectiveness of eptifibatide as a means of accompanying transcatheter interventions on the dose when administered intravenously has been shown in several studies with stable and unstable angina pectoris. In the IMPACT II study [The IMPACT II Investigators. Randomized placebo - controlled trial of effect of eptinbatide on complications of percutaneous coronary intervention. // N. Eng. J. Med. - 1997 .-- Vol.349. - P.1422-1428] in patients with unstable angina, eptifibatide was administered intravenously at a dose of 135 μg / kg, followed by intravenous infusion of 0.5 μg / kg / min for 24 hours. The use of eptifibatide did not show a significant decrease in the primary endpoint (death, acute myocardial infarction or repeated rsvascularization) within 30 days, compared with placebo. At the same time, the PURSUIT study [PURSUITE Trial Investigators. Inhibition of platelet glycoprotein IIb / IIIa with eptifibatide in patients with acute coronary syndromes. The PURSUITE Trial Investigators Platelet Glycoprotein IIb / IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy. // N. Eng. J. Med. - 1998 .-- Vol.339. - P.436-443] in the group of patients with unstable angina, in which 4KB was performed on the background of intravenous administration of eptifibatide at a higher dosage, there was a significant decrease in the number of deaths or acute myocardial infarction compared with the placebo group.

Keep in mind that with the introduction of eptifibatide there is a risk of bleeding shown in the PURSUITE study. Bleeding in this study was observed in 3.0% of patients undergoing transcatheter interventions and receiving eptifibatide and in 1.3% of patients receiving placebo (p <0.001). Although bleeding occurs at the site of vascular arterial access without increasing the number of intracranial hemorrhages, the results of the PURSUITE study indicate that increasing the effectiveness of the drug due to a simple further increase in dose is unacceptable.

Myocardium is in second place after the brain in terms of sensitivity to ischemia, and the loss of time waiting for intervention after administration of the drug in a specialized hospital is unacceptable.

Thus, it is necessary to search for new methods of treatment, on the one hand, to avoid wasting time, and on the other hand, to maximize the use of the entire administered dose of the drug for treatment directly at the lesion site.

There are no reports of the use of eptifibatide in the treatment of the "no-reflow" phenomenon, including in acute myocardial infarction. Given the data from a study by Cutlip et al. [Cutlip D.E., Cove C.J., Irons D., et al. Emergency room administration of eptifibatide before primary angioplasty for ST elevation acute myocardial infarction and its effect on baseline coronary flow and procedure outcomes // Am. J. Cardiol. - 2001 .-- Vol.88. - P.62-64, A6], on increasing the frequency of patency of the coronary artery after administration of eptifibatide, we can assume the possibility of its use in the development of the phenomenon of "no-reflow" after angioplasty.

Given the existing dependence of the degree of platelet disaggregation on time and dose in the treatment with eptifibatide, intracoronary administration of the drug at a concentration of 1 mg / ml at a rate of 4 ml per minute for 5 minutes with a total dose of intracoronary administration of 20 mg provides a high concentration of the drug directly in the infarct-dependent coronary artery potentially facilitates the dissolution of a blood clot in a vessel, thrombotic microemboli in the myocardium and prevents further platelet aggregation. This leads to the restoration of coronary artery patency, an increase in the degree of myocardial perfusion and an improvement in prognosis in patients with acute myocardial infarction in cases of the development of the "no-reflow" phenomenon.

The proposed method for the treatment of acute myocardial infarction is as follows.

Under local anesthesia and drug sedation, the femoral artery is punctured according to Seldinger. Selective catheterization of the left coronary artery, the introduction of an X-ray contrast medium into the coronary artery, and X-ray filming — coronarography — are performed in several projections to evaluate the anatomy of all its sections and branches. Coronary angiography of the right coronary artery is then selectively performed.

If a significant lesion is detected - coronary artery occlusion, or hemodynamically significant stenosis (narrowing), they proceed to the treatment phase of the intervention.

Before performing medical manipulations on the coronary arteries, an unfractionated heparin is administered at the rate of 100 units for each kg of the patient’s body weight through the intraducer in the femoral artery. Given the individual sensitivity to heparin, the achievement of the required level of heparinization is assessed by the level of blood ACT, in accordance with existing recommendations, and proceed with the intervention.

Transcatheter coronary intervention is performed as follows: a conductor catheter is installed in the mouth of the affected coronary artery and a coaxial system — a coronary conductor with a coronary dilated balloon catheter — is passed through it. A mechanical recanalization of the artery is performed by the coronary conductor with the installation of the tip of the conductor in the peripheral section of the artery distal to the lesion site. Then, a coronary dilatation balloon of a diameter corresponding to the diameter of the adjacent unchanged part of the artery and a length equal to the length of the lesion is installed along the conductor to the lesion site and dilation is performed. If the extent of the lesion is higher than the length of the working part of the balloon catheters available on the market (40 mm), successive dilations of the entire affected segment of the artery are performed. After dilatation, the balloon is withdrawn into the guide catheter, and the guide is left in the same position.

Control coronary angiography is performed to evaluate dilatation results. If dissection, residual stenosis, elastic collapse of the artery or other mechanical obstruction that impedes blood flow along the peripheral part of the artery is detected, the intervention is supplemented by implantation of a coronary stent in the affected segment. For coronary stenting, special stents mounted on a balloon dilated catheter are used. The stent implantation is carried out by inflating the balloon and is carried out according to the method described for dilatation. If the extent of the lesion is greater than the length of the coronary stent available on the market, several stents are successively placed.

Follow-up coronary angiography is performed to assess vascular anatomy, blood flow and absence of complications. Blood flow levels are evaluated using the TIMI system, which is an international standard. If blood flow is detected at the TIMI-III level, the intervention is completed. If the blood flow slows below the level of TIMI - II or its absence (TIMI - 0) and there is no obvious mechanical obstacle, the situation is regarded as a "no-reflow" phenomenon. In this case, the treatment of this phenomenon is performed in order to restore the normal blood flow through the coronary artery and full blood supply to the heart muscle.

To do this, after preliminary heating, take 20 mg of eptifibatide at an initial concentration of 2 mg / ml, dilute in 10 ml of a 0.9% sodium chloride solution to a concentration of 1 mg / ml and slowly enter through a catheter directly into the mouth of the coronary artery at a speed 4 mg / min. A dose of 20 mg is injected into the coronary artery completely without titration by weight of the patient for 5 minutes. After the introduction of the drug, control coronarography is performed. On the control coronarograms, an improvement in blood flow through the artery is observed. Immediately after the selective administration of 20 mg of the drug into the coronary artery, intravenous administration of eptifibatide at a dose of 2.0 μg / kg / min begins for 12 hours.

With the restoration of blood flow and the absence of a mechanical obstacle, the intervention is completed. The catheter is removed, the patient is transferred to the cardiac intensive care unit. Intraducer from arterial access is removed 4-8 hours after the end of the intravenous infusion of eptifibatide, since the aggregation ability of platelets is normalized 4-8 hours after the cessation of the administration of eptifibatide.

In cases of acute myocardial infarction, the time "onset of pain - x-ray" is a decisive factor in the prognosis of future life and human health. Thus, preliminary drug preparation for the intervention is not performed. In an X-ray patient, a loading dose of 375 mg of clopidogrel is administered orally with a further maintenance dose of clopidogrel of 75 mg per day. The patient is prescribed orally aspirin at a dose of 125 mg per day.

4 hours after the intervention, subcutaneous administration of low molecular weight heparin - enoxiparin at a dose of 0.4 ml every 12 hours is started.

The claimed method of treatment of acute myocardial infarction is confirmed by examples.

Example 1

Patient Z., a man aged 64 years old, weighing 74 kilograms, was admitted to the Regional Clinical Hospital with complaints of prolonged intense pain behind the sternum of a burning character with radiation to the left arm, shortness of breath at rest.

Anamnesis: For 4 years he suffered from hypertension with a maximum increase in blood pressure to 180/100 mm Hg. Within 1 year, angina attacks began to be disturbed during heavy loads. On the eve of shortness of breath appeared during exercise and at rest. Today, a typical pronounced long-term anginal syndrome has developed with a time from the onset of pain of 4-5 hours.

Diagnosis: ischemic heart disease. Acute myocardial infarction with ST segment elevation with localization on the anterior, lateral wall of the left ventricle, interventricular septum. Ventricular extrasystole. CH II A Art. (II f.cl. according to NYHA), hypertension - III tbsp. The risk is 4.

The ECG determined the elevations of the ST segment in I, II, and from VI to V5 to 1 centimeter. Ventricular extrasystoles.

The pain syndrome was partially copied by the administration of narcotic analgesics. The patient was urgently taken to an X-ray to perform coronary angiography and transcatheter revascularization. Under local anesthesia with a 0.5% solution of novocaine according to the Seldinger method, coronary angiography of the left and right coronary arteries was performed through access to the right femoral artery. According to the results of coronarography, the patient revealed a left type of myocardial blood supply and diffuse lesion of all coronary arteries. In particular, stenosis of the right coronary artery was revealed in the middle third of 60%, stenosis of the distal part of the envelope branch of the left coronary artery up to 90%. The main lesion was proximal stenosis of the anterior interventricular branch (LAD) of the left coronary artery up to 99%, including the area of bifurcation of the LAD with 1 diagonal branch with signs of intravascular thrombosis. The blood flow through the LAD was slowed down to the level of TIMI II. The blood flow along the 1st diagonal branch was sharply weakened to the level of TIMI I. A decision was made to perform transcatheter intervention - balloon angioplasty and stenting of the infarct-dependent artery - LAD. To do this, 10,000 units of unfractionated heparin were introduced into the femoral artery through the intradermus artery, and on the table the patient was given a loading dose of 375 mg of clopidogrel. The diagnostic catheter was replaced with a Jadkins left guide catheter, the distal tip of which was installed at the mouth of the trunk of the left coronary artery. Coronary angiography was performed to evaluate the position of the catheter and select the best projection for the instrument. Under fluoroscopic control, the coronary conductor was conducted in the permanent lesion through the affected area. The tip of the conductor was installed in the peripheral department of permanent residence. A balloon with a diameter of 3.5 mm was passed through the conductor into the artery, and it was installed in the stenosis zone of the permanent prostate. Repeated dilations of the entire affected area of the permanent residence were performed with a pressure of 8-12-16 atmospheres until the balloon was completely expanded. At the end of the dilatation, the balloon was withdrawn into a guide catheter. Coronary angiography performed. The coronary angiogram revealed elastic collapse of the artery up to 40-50% in the area of stenosis of the upper third of the LAD and a contrast defect at the site of bifurcation of the LAD and 1 diagonal branch. However, the level of blood flow through the LAD was restored as a result of dilatation at the level of TIMI III, the blood flow in 1 diagonal branch slightly improved to the level of TIMI I-II. The patient showed clinically positive dynamics - the pain syndrome was stopped, the ST segment elevations on the monitor decreased to the isoline. The balloon catheter was removed. A catheter with a mounted Multi-Link Zeta 4.0 × 38 mm stent (Abbot vascular, United States) was inserted into the lesion site along the guidewire. The stent was positioned in the artery, its implantation was performed with a pressure of 14 atmospheres. After deflation of the balloon and its removal into the guide catheter, control coronary angiography was performed. On coronary angiograms, the stent was straightened, however, the phenomenon of "no-reflow" was revealed - no contrast between the permanent lesion and the middle third of the stent was detected. The TIMI blood flow level is 0. Clinically, the patient resumed pain, the ST segment rises again on the ECG monitor. Decided to intracoronary administration of eptifibatide. To do this, they took 20 mg of eptifibatide at an initial concentration of 2 mg / ml and diluted in 10 ml of a 0.9% sodium chloride solution to obtain a concentration of 1 mg / ml. Through a guide catheter, the drug was slowly injected into the left coronary artery at a rate of 4 mg per minute. At the end of selective intracoronary administration, a maintenance intravenous infusion of eptifibatide was started at a dose of 148 micrograms per minute. After the introduction of a selective dose of eptifibatide, the patient underwent control coronary angiography. Coronary angiograms were used to determine the restoration of patency of the LAD and its lateral branches to peripheral regions with a TIMI III blood flow level. The pain syndrome in the patient was stopped, according to the monitor, there was a decrease in the elevations of the ST segment to the isoline. The coronary conductor and catheter guide were removed. The total duration of intravenous infusion of eptifibatide was 12 hours. Intraducer in the femoral artery was left until blood coagulation normalized and removed 6 hours after the end of the intravenous infusion of eptifibatide. The patient was prescribed double disaggregated therapy with aspirin at a dose of 100 mg per day continuously and clopidogrel at a dose of 75 mg per day for 1 month. 4 hours after the intervention, the administration of enoxiparin at a dose of 0.4 ml was started subcutaneously with an interval of 12 hours with a treatment duration of 72 hours. The patient’s pain did not recur further.

Example 2

Patient M., a man aged 53 years old, weighing 86 kilograms, was taken to the Regional Hospital by an ambulance with complaints of severe burning pain behind the sternum, without irradiation, a feeling of lack of air.

Anamnesis: Over the years, he noted an increase in blood pressure to 160/100 mm Hg. I did not receive continuous antihypertensive therapy. Previously, there was no anginal pain. Within 3 days, the patient performed intense physical exertion, in which for the first time in his life he began to worry about burning behind the sternum, passing on his own. Today, without provoking factors, there were severe burning pains behind the sternum, lasting more than two hours. I called an ambulance.

ECG upon admission: sinus rhythm with a heart rate of 82 beats / min. ↑ ST II, III, AVF (-) T, pathological Q; ST depression with V2-V5 (+) high T. Non-specific disorders of intraventricular conduction.

Diagnosis: ischemic heart disease. Acute myocardial infarction with ST segment elevation with localization on the lower wall. CH II A Art. (II f.c. by NYHA). Hypertension III risk IV.

The patient underwent emergency coronarography of the right and left coronary arteries by access through the right femoral artery. Coronary angiograms revealed stenosis 1/3 of the LAD of 70% and acute thrombotic occlusion of the right coronary artery (PKA) in the proximal segment. The distal portion of the PKA was not contrasted. We decided to perform an emergency transcatheter intervention - recanalization and balloon angioplasty of PKA. For this, after introducing into the femoral artery through the lateral port of the intraducer 10,000 units. unfractionated heparin under the control of ACT blood and receiving a loading dose of 375 mg of clopidogrel, the diagnostic catheter was replaced by a guide catheter, which was installed at the mouth of the PCA. Under the control of fluoroscopy and radiography, a coronary conductor was inserted into the PCA through the conduction catheter through the occlusion zone. The tip of the conductor was installed in the distal segment of the artery. A dilatation balloon with a diameter of 3.0 mm was installed along the coronary conductor into the area of the PKA occlusion. Dilatation of the affected PKA segment was performed under the control of fluoroscopy successively with a pressure of 6-8-10 atmospheres until the balloon was completely inflated. After removal of the balloon into the guide catheter, a coronary angiography was performed. On the coronarogram, the elastic collapse of the artery was determined with a residual stenosis of 90%, which limits blood flow along the distal bed of the PCA. Decided to stent the PCA. According to the coronary conductor according to the technique identical to balloon dilatation, the coronary stent R-Stent Evolution ² 3.0 * 18 mm (Orbusneich medical, USA) was positioned at the site of PCA stenosis under the control of fluoroscopy and coronarography. The stent was implanted in a PCA with a pressure of 12 atmospheres until the stent was completely inflated. After removal of the balloon, a coronary angiography was performed into the guide catheter. On the coronarograms, the stent in the PCA was straightened, there were no signs of intimal dissection, no extravasation of the contrast medium, however, the PCA was not contrasted distally to the stent, the blood flow level was TIMI 0. This situation was regarded as a “no-reflow” phenomenon. A decision was made on the intracoronary selective administration of eptifibatide.

To do this, they took 20 mg of eptifibatide at an initial concentration of 2 mg / ml and diluted in 10 ml of a 0.9% sodium chloride solution to obtain a concentration of 1 mg / ml. Through a guide catheter, 20 mg of the drug was slowly injected into the right coronary artery at a rate of 4 mg per minute. At the end of selective intracoronary administration, a supportive intravenous infusion of eptifibatide was started immediately at a rate of 172 micrograms per minute for 12 hours.

After the introduction of a selective dose of eptifibatide, the patient underwent control coronary angiography. Coronary angiography determined the restoration of patency of PKA to the peripheral regions with a blood flow level of TIMI III.

Positive dynamics of the patient's condition, relief of pain and positive ECG dynamics with the return of the ST segment to the isoline were noted. Intervention completed. Intraducer in the femoral artery was left until blood coagulation returned to normal and removed 6 hours after the end of the intravenous infusion of eptifibatide. The patient was prescribed clopidogrel at a dose of 75 mg per day for a month and aspirin at a dose of 100 mg per day for a long period of time. In the future, the patient's pain did not recur. On the 19th day after the intervention, the patient underwent Holter monitoring, in which no ischemic changes were recorded. According to ECHO KG, the contractility of the LV myocardium was preserved. LV ejection fraction 56%.

46 patients aged 34 to 78 years (59.2 ± 2.8 years) with acute myocardial infarction and the "no-reflow" phenomenon performed transcatheter interventions using stenting and selective intracoronary administration of eptifibatide. In 31 patients (67.4%), the anterior one was determined, in 11 patients (23.9%) the lower one, in 3 patients (6.5%) of the lateral and posterior-basal departments, in one case (2.2%), circular myocardial infarction. According to the results of coronary angiography of the infarct-dependent artery, UCI was present in 30 cases (65.2%), the trunk of the left coronary artery in one patient (2.2%), the combination of UCI and PKA in one (2.2%), the envelope of the branch of the left coronary artery in 5 cases (10.8%), PKA in 9 patients (19.6%). Indications for the administration of eptifibatide were the continued absence of coronary arterial blood flow after angioplasty and stenting, which occurred in 4 cases after interventions for critical stenosis with signs of intravascular thrombosis and in 42 patients after recanalization of total occlusion of a heart attack coronary artery. After administration of eptifibatide in 39 cases (84.8%), normal blood flow in the infarct-dependent coronary artery with a TIMI III level was restored. 13 4 cases (8.7%), despite the administration of the drug, there was no restoration of blood flow through the infarct-dependent artery (TIMI 0-I), 3 patients (6.5%) showed restoration of blood flow to the level of TIMI II. Among patients with acute myocardial infarction and restored blood flow through the coronary artery, there were no fatal outcomes. Among 7 patients in whom the restoration of normal blood flow through the infarct-dependent coronary artery did not occur after the administration of eptifibatide, 2 deaths were noted.

One patient (2.2%) after removal of the intraducer developed bleeding from the site of puncture of the femoral artery, stopped conservatively. In this case, the patient required the introduction of 420 ml of plasma.

The Regional Clinical Hospital in 2004-2007 provided assistance to 447 ± 54 patients with acute myocardial infarction per year. In the Regional Clinical Hospital, in all patients with acute myocardial infarction with successful transcatheter revascularization, the hospital mortality rate was 3.8%. In patients whose transcatheter revascularization was unsuccessful or not performed, hospital mortality was 16.1% with a significant difference (p <0.05). Hospital mortality in 46 patients with acute myocardial infarction and the no-reflow phenomenon treated with stenting and selective intracoronary administration of eptifibatide was 2 patients (4.3%).

The technical result consists in the fact that the use of a combination of stenting of a heart attack-dependent coronary artery and intracoronary administration of eptifibatide at a dose of 20 mg followed by intravenous infusion of eptifibatide at a dose of 2 μg per kilogram per minute for 12 hours is a highly effective way to treat acute myocardial infarction with the development of the phenomenon no-reflow "after transcatheter recanalization of the artery and allows you to restore normal levels of coronary blood flow and myocardial perfusion in 84.8% of cases. The proposed method for the treatment of acute myocardial infarction allows to neutralize the negative impact of this phenomenon on the course of the disease and provides a favorable outcome in most patients.

Claims (1)

A method for treating acute myocardial infarction, including puncture of the femoral artery under local anesthesia and drug sedation, selective catheterization and coronary artery angiography, placement of a guide catheter at the mouth of the affected coronary artery, balloon angioplasty of the site of stenosis or coronary artery occlusion, and radiotherapy under control means, characterized in that after balloon angioplasty coronary implants are inserted into the site of stenosis or occlusion an intravascular prosthesis stent under the control of fluoroscopy and coronarography, then, through a guide catheter, directly in the mouth of the affected coronary artery, a drug is administered in the form of a single dose of an inhibitor of platelet glycoprotein receptors IIb / IIIa in the amount of 20 mg diluted in 0.9% chloride solution sodium to a concentration of 1 mg / ml at a rate of 4 mg / min for 5 minutes, followed by intravenous administration of eptifibatide in an amount of 2 μg per minute for every kilogram of patient body weight for 12 hours .