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Aim: was to evaluate the safety and efficacy of delayed endovascular treatment without stent implantation in ST-elevation myocardial infarction (STEMI) caused by massive thrombotic load and ectasia of infarct-related coronary artery.

Material and methods: out of 4263 primary percutaneous coronary interventions (PCI) performed for STEMI for the period from January 2016 to September 2021, retrospective analysis included data of 21 patients with ectasia of infarct-related coronary artery and massive thrombotic load (TTG ? 3).

Results: method of delayed endovascular treatment, without stent implantation, in STEMI caused by massive thrombotic load and ectasia of infarct-related coronary artery, allowed to significantly improve parameters of epicardial coronary blood flow according to  TIMI and CFTC scales in 71% and 67% of examined patients (p <0,001, p=0,001); increase myocardial perfusion according to MBG in 62% of patients (p=0,001); reduce the severity of thrombotic load according to TTG scale in 71% of the subjects (p=0,001).

Conclusion: in patients with ST-elevation myocardial infarction caused by massive thrombotic load and ectasia of infarct-related coronary artery, the strategy of delayed endovascular treatment with-out stent implantation is safe and effective at the hospital stage.




Introduction: the main methods for diagnosing cardiac neoplasms, allowing to determine the localization, size, involvement of heart structures, to suggest the nature of the pathological process and to plan treatment tactics, are: echocardiography (EchoCG), contrast multispiral computed coronary angiography (MSCT CAG), magnetic resonance imaging (MRI) and positron emission computed tomography (PET CT). At the same time, any additional information about the pathological process can improve the quality of diagnosis and treatment. So, for example, selective coronary angiography (CAG), which in this case can be performed to clarify the coronary anatomy and exclude concomitant coronary atherosclerosis, in hands of attentive and experienced specialist of endovascular diagnostic and treatment methods can make a significant contribution to understanding the nature of blood supply of heart neoplasm, thereby bringing closer the formulation of the correct diagnosis and, ultimately, improving results of surgical treatment.

Aim: was to study the nature of blood supply of heart myxoma based on results of a detailed analysis of data of selective coronary angiography in patients with this pathology.

Material and methods: since 2005, 20 patients underwent surgery to remove heart myxoma. The average age of patients was 56,6 + 8,0 (43-74) years. According to data of ultrasound examination, sizes of myxomas ranged from 10 to 46 mm in width and from 15 to 71 mm in length (average size ? 25,6 ? 39,1 mm). In 2/3 of all cases (15 out of 20,75%), the fibrous part of the inter-atrial septum (fossa oval region) was the base of myxomas. In 8 of 20 (40%) cases, tumor prolapse into the left ventricle through structures of the mitral valve was noted in varying degrees. In order to exclude coronary pathology, CAG was performed in 14 cases, in the rest - MSCT CAG.

Results: of 14 patients with myxoma who underwent selective coronary angiography, 12 (85,7%) patients had distinct angiographic signs of vascularization. In all 12 cases, the sinus branch participated in the blood supply of myxoma, begins from the right coronary artery (RCA) in 10 cases: in 7 case it begins from proximal segment of the RCA and, in 3 cases, from the posterior-lateral branch (PLB) of the RCA. In one case, the source of blood supply of neoplasm was the sinus branch extending from PLB of dominant (left type) circumflex artery of the left coronary artery (PLB CxA LCA). In one case, the blood supply to the neoplasm involved branches both from the RCA and CxA, mainly from the left atrial branch of CxA. Moreover, in all 12 cases, sinus branch formed two branches: branch of sinus node itself and left atrial branch. It was the left atrial branch that was the source of blood supply of myxoma. Analysis of angiograms in patients with myxoma of LA showed that left atrial branch in terminal section formed a pathological vascularization in the LA projection, accumulating contrast-agent in the capillary phase (MBG 3-4). In addition to newly formed vascularization, lacunae of irregular shape were distinguished, the size of which varied from 2 to 8 mm along the long axis. In 8 cases, hypervascular areas with areas of lacunar accumulation of contrast-agent showed signs of paradoxical mobility and accelerated onset of venous phase. In two cases, there were distinct angiographic signs of arteriovenous shunt. In 2 cases (when the size of the myxoma did not exceed 15-20 mm according to EchoCG and CT), angiographic signs allowing to determine the presence of LA myxoma were not so convincing: there was no lacunar accumulation of contrast-agent; small (up to 10 mm) hypervascular areas were noticed, the capillary network of which stood out against the general background of uniform contrasting impregnation and corresponded to MBG grade 1-2.

Conclusion: according to our data, angiographic signs of vascularization of myxomas are detected in most cases with this pathology (85,7%). The source of blood supply, in the overwhelming majority of cases, is branch of coronary artery, which normally supplies the structure of the heart, on which the basement of the pathological neoplasm is located. The aforementioned angiographic signs characteristic of myxomas deserve the attention of specialists in the field of endovascular diagnosis and treatment and should be described in details in protocols of invasive coronary angiography.



1.     Петровский Б.В., Константинов Б.А., Нечаенко М.А. Первичные опухоли сердца. М.: Медицина, 1997; 152.

Petrovskiy BV, Konstantinov BA, Nechaenko MA. Primary heart tumors. M.: Medicina, 1997 [In Russ].

2.     Balci AY, Sargin M, Akansel S, et al. The importance of mass diameter in decision-making for preoperative coronary angiography in myxoma patients. Interact Cardiovasc Thorac Surg. 2019; 28(1): 52-57.

3.     Omar HR. The value of coronary angiography in the work-up of atrial myxomas. Herz. 2015; 40(3): 442-446.

4.     Gupta PN, Sagar N, Ramachandran R, Rajeshekharan VR. How does knowledge of the blood supply to an intracardiac tumour help? BMJ Case Rep. 2019; 12(2): 225900.

5.     Marshall WHJr., Steiner RM, Wexler L. Tumor vascularity in left atrial myxoma demonstrated by selective coronary arteriography. Radiology. 1969; 93(4): 815-816.

6.     Lee SY, Lee SH, Jung SM, et al. Value of Coronary Angiography in the Cardiac Myxoma. Clin Anat. 2020; 33(6): 833-838.



Background: atrial septal defect (ASD) is characterized by a progressive increase in pulmonary vascular resistance and, accordingly, pressure in small circulation circle. It is noteworthy that these hemodynamic changes go in parallel with morphofunctional changes in small vessels of pulmonary artery system. At the same time, changes in hemodynamics of small circulatory circulation after endovascular closure in this category of patients and reversibility of pulmonary hypertension are not fully studied.

Aim: was to assess clinical course, indicators of cardiac chamber geometry and hemodynamics of small circulation circle after transcatheter closure of secondary ASD in adult patients with moderate and significant pulmonary hypertension in immediate and long-term periods.

Material and methods: from 2009 to 2020, 103 patients (mean age 48,3 ± 15,3 years) with secondary ASD underwent endovascular transcatheter closure of the defect. 60 (58,3%) patients had pulmonary hypertension. Depending on systolic pulmonary arterial pressure (SPAP), patients were divided into 3 groups: the first group consisted of 41 (68,3%) patients with mild PH (from 40 to 49 mm Hg); the second group included 10 (16,6%) patients with moderate PH (50 to 59 Hg); and the third group consisted of 9 (15%) patients with high SPAP (? 60 mm Hg). Average pulmonary artery systolic pressure in groups was: 43,6 ± 2,9 mm Hg; 52,1 ± 2,5 mm Hg; 64,4 ± 5,2 mm Hg, respectively. Average sizes of ASD (according to Pre-TEE data) were 18,7 + 6,1 mm; 22,1 ± 7,5 mm and 21,3 ± 5,3 mm, respectively. In all cases, echocardiographic signs of the right heart volume overload were detected. Follow-up was performed on an outpatient basis with an assessment of the clinical status and TTE in the long-term period.

Results: technical success of endovascular defect closure was 100%. Average size of the occluder was 26,3 + 6,96 (from 12 to 40) mm. Immediately after implantation of device, complete closure of ASD was observed in 55 (91,7%) cases. Residual flow (<3 mm) was observed in 5 cases (2 cases in the first group, 1 case in second group, and 2 cases in third group, (p >0,05)). In the vast majority of cases - 54 (90%) hospital period proceeded smoothly. All patients were examined in the long-term period (on average 12,5 + 6,5 months). The survival rate in groups was 100%. In the long- term follow-up remodeling of the right heart was observed in all patients. In the first group the size of RA decreased from 6,0 ± 0,5 cm to 3,3 ± 0,4 cm, RV size decreased from 4,7 ± 0,5 to 3,1 ± 0,4 cm; in the second group RA from 5,7 ± 0,7 cm to 3,8 ± 0,5 cm, RV - from 4,7 ± 0,9 to 3,8 ± 0,6 cm; in the third group RA - from 5,5 ± 0,6 cm and 4,2 ± 0,5 cm, the size of RV decreased from 4,5 ± 0,6 4,0 ± 0,5 cm, respectively. In all patients, significant decrease in SPAP was observed, in some cases up to normalization. In the first group, SPAP decreased from 43,7 ± 2,9 to 32,1 ± 2,6 mmHg, in the second group - from 52,1 ± 2,5 to 34,3 ± 2,6 mmHg; in the third group - from 64,4 ± 5,2 to 50,3 ± 4,8 mmHg. The most expressed decrease of pressure occurred in the second group of patients. At the same time, in the third group, dynamics of pressure reduction was significantly less expressed in comparison with the other two groups. At the same time in two patients of third group high PH remained in the long-term period, despite the successful closure of the defect.

Conclusion: results show that in case of left-right shunt in the absence of hypoxemia, transcatheter closure of ASD in adult patients with moderate and significant pulmonary hypertension is a pathophysiologically and clinically justified, is a highly effective treatment method that allows achieving significant improvement of both clinical manifestations and intracardiac and systemic hemodynamics. In patients with a significant degree of pulmonary hypertension and a high probability of the latter, the following tactical approaches may be considered:

1. primary closure of defect with further drug therapy;

2. primary drug therapy aimed on regulating of the anatomic-functional state of the arterial bed of the small circulation and hence reducing pulmonary vascular resistance followed by endovascular ASD-closure;

3. closure of the defect with a fenestrated occluder (in case of a negative test for temporary balloon occlusion), followed by drug therapy. This assumption can be considered in future research.



1.     Jain S, Dalvi B. Atrial septal defect with pulmonary hypertension: when/how can we consider closure? J Thorac Dis. 2018; 10(24): 2890-2898.

2.     Fraisse, et al. Atrial Septal Defect Closure: Indications and Contra-Indications. J Thorac Dis. 2018; 10(24): 2874-2881.

3.     Akagi T. Current concept of transcatheter closure of atrial septal defect in adults. J Cardiol. 2015; 65(1): 17-25.

4.     Kefer J. Percutaneous Transcatheter Closure of Interatrial Septal Defect in Adults: Procedural Outcome and Long-Term Results. Catheter Cardiovasc Interv. 2012; 79(2): 322-30.

5.     Gruner C, Akkaya E, Kretschmar O, et al. Pharmacologic preconditioning therapy prior to atrial septal defect closure in patients at high risk for acute pulmonary edema. J Interv Cardiol. 2012; 25: 505-12.

6.     Abaci A, Unlu S, Alsancak Y, et al. Short- and long-term complications of device closure of atrial septal defect and patent foramen ovale: metaanalysis of 28,142 patients from 203 studies. Catheter Cardiovasc Interv. 2013; 82(7): 1123-1138.

7.     Humenberger M, Rosenhek R, Gabriel H, et al. Benefit of atrial septal defect closure in adults: impact of age. Eur Heart J. 2011; 32: 553-560.

8.     Ioseliani DG, Kovalchuk IA, Rafaeli TR, et al. Simultaneous Percutaneous Coronary Intervention and Endovascular Closure of Atrial Septal Defect in Adults. Kardiologia. 2019; 59(2): 56-60 [In Russ].

9.     Correction to: 2018 AHA/ACC Guideline for the Management of Adults with Congenital Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019; 139(14): 833-834.

10.   Gali? N, Humbert M, Vachiery JL, et al. 2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension: The Joint Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS): Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC), International Society for Heart and Lung Transplantation (ISHLT). Eur Heart J. 2016; 37(1): 67-119.

11.   Haas NA, Soetemann DB, Ates I, et al. Closure of secundum atrial septal defects by using the occlutech occluder devices in more than 1300 patients: the IRFACODE project: a retrospective case series. Catheter Cardiovasc Interv. 2016; 88: 71-81.

12.   Nakahawa K, Akagi T, Taniguchi M, et al. Transcatheter closure of atrial septal defect in a geriatric population. Catheter Cardiovasc Interv. 2012.

13.   Marwick TH, Gillebert TC, Aurigemma G, et al. Recommendations on the Use of Echocardiography in Adult Hypertension: A Report from the European Association of Cardiovascular Imaging (EACVI) and the American Society of Echocardiography (ASE). J Am Soc Echocardiogr. 2015; 28(7): 727-754.

14.   Galderisi M, Cosyns B, Edvardsen T, et al. Standardization of adult transthoracic echocardiography reporting in agreement with recent chamber quantification, diastolic function, and heart valve disease recommendations: an expert consensus document of the European Association of Cardiovascular Imaging. Eur Heart J Cardiovasc Imaging. 2017; 18(12): 1301-1310.

15.   Bossone E, D'Andrea A, D'Alto M, et al. Echocardiography in pulmonary arterial hypertension: from diagnosis to prognosis. J Am Soc Echocardiogr. 2013; 26(1): 1-14.

16.   Miranda WR, Hagler DJ, Reeder GS, et al. Temporary balloon occlusion of atrial septal defects in suspected or documented left ventricular diastolic dysfunction: Hemodynamic and clinical findings. Catheter Cardiovasc Interv. 2019; 93(6): 1069-1075.

17.   Shin C, Kim J, Kim J-Y, et al. Determinants of serial left ventricular diastolic functional change after device closure of atrial septal defect. JACC. 2020; 75(11).

18.   Martin-Garcia AC, Dimopoulos K, Boutsikou M, et al. Tricuspid regurgitation severity after atrial septal defect closure or pulmonic valve replacement. Heart. 2020; 106(6): 455-461.

19.   Zwijnenburg RD, Baggen VJM, Witsenburg M, et al. Risk Factors for Pulmonary Hypertension in Adults After Atrial Septal Defect Closure. Am J Cardiol. 2019; 123(8): 1336-1342. (АНГИОЛОГИЯ.ру) - портал о диагностике и лечении заболеваний сосудистой системы