scholarly journals Transcatheter closure of ventricular septal rupture with prolonged support of intra-aortic balloon pump after primary PCI: a case report

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Chuan Yang ◽  
Yong Sun ◽  
Deling Zou ◽  
Zhaoqing Sun ◽  
Xinzhong Zhang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Transcatheter Closure ◽  
Interventricular Septum ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Drug Eluting Stent ◽  
Ventricular Septal Rupture ◽  
Total Occlusion ◽  
Ventricular Ejection Fraction ◽  
Intra Aortic Balloon Pump

Abstract Background Ventricular septal rupture (VSR) is a rare but severe complication of acute myocardial infarction (AMI). For such cases, surgical repair is recommended by major guidelines, but not always possible for such cases. Case presentation A 72-year-old man presented to the emergency room. ECG showed the ST-segment was elevated by 2–3 mm in lead II, III, and aVF, with Q-waves. Coronary angiography (CAG) showed multi-vessel disease with a total occlusion of the right coronary artery (RCA) and severe stenosis of the left anterior descending artery (LAD). A diagnosis of acute inferior myocardial infarction was made. VSR occurred immediately after percutaneous coronary intervention (a 2.5 × 20 mm drug-eluting stent implanted in RCA), and the patient developed cardiogenic shock. An intra-aortic balloon pump (IABP) was used to stabilize the hemodynamics. Transthoracic echocardiography (TTE) revealed an 11.4-mm left-to-right shunt in the interventricular septum. An attempt was made to reduce the IABP augmentation ratio for weaning on day 12 but failed. Transcatheter closure was conducted using a 24-mm double-umbrella occluder on day 28. The patient was weaned from IABP on day 31 and underwent secondary PCI for LAD lesions on day 35. The patient was discharged on day 41. Upon the last follow-up 6 years later, CAG and TTE revealed no in-stent restenosis, no left-to-right shunt, and 51% left ventricular ejection fraction. Conclusions Prolonged implementation of IABP can be a viable option to allow deferred closure of VSR in AMI patients, and transcatheter closure may be considered as a second choice for the selected senior and vulnerable patients, but the risk is still high.

scholarly journals Post-myocardial infarction ventricular septal rupture in a patient with large secundum atrial septal defect: a case report

2019 ◽  
Vol 3 (2) ◽  
Author(s):  
Shabir Hussain Shah ◽  
Muhammad Azam Shah
Keyword(s):  
Myocardial Infarction ◽  
Atrial Septal Defect ◽  
Septal Defect ◽  
Interventricular Septum ◽  
Left Ventricular ◽  
Post Myocardial Infarction ◽  
Left Ventricular Ejection ◽  
Ventricular Septal Rupture ◽  
Secundum Atrial Septal Defect ◽  
Ventricular Ejection Fraction

Abstract Background Ventricular septal rupture (VSR) is an uncommon but potentially fatal complication of acute myocardial infarction (AMI). The management of VSR is challenging, and its surgical correction is associated with the highest mortality among all cardiac surgery procedures. Case summary A 57-year-old man with a history of smoking presented with AMI with a large apical VSR in addition to a large secundum atrial septal defect (ASD). His left ventricular ejection fraction was 30%, and the right ventricle was moderately dilated with normal systolic function. Cardiac catheterization revealed that the left anterior descending artery was diffusely diseased with total mid occlusion, whereas other coronary arteries had non-obstructive disease. This unique combination resulted in distinctive presentation with paradoxically better outcomes. After stabilization, the patient’s interventricular septum was reconstructed, and the ASD was closed with a pericardial patch. The post-operative period was uneventful, and the patient was discharged 1 week after surgery. A follow-up echocardiography revealed no residual shunt. Discussion Post-myocardial infarction VSR presents differently in patients with pre-existing right ventricular volume overload. In such cases, the absence of significant cardiogenic shock at presentation may result in better surgical outcomes.

scholarly journals Total Occlusion of the Infarct-Related Artery in Non-ST-Elevation Myocardial Infarction (NSTEMI)—How Can We Identify These Patients?

Medicina ◽  
2021 ◽  
Vol 57 (11) ◽  
pp. 1196
Author(s):  
Irmina Morawska ◽  
Rafał Niemiec ◽  
Maria Stec ◽  
Karolina Wrona ◽  
Paweł Bańka ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricular Ejection Fraction ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Total Occlusion ◽  
Ventricular Ejection Fraction ◽  
Infarct Related Artery ◽  
History Of ◽  
St Elevation ◽  
One Year

Background and Objectives: Regardless of the improvement in key recommendations in non-ST-elevation myocardial infarction (NSTEMI), the prevalence of total occlusion (TO) of infarct-related artery (IRA), and the impact of TO of IRA on outcomes in patients with NSTEMI, remain unclear. Aim: The study aimed to assess the incidence and predictors of TO of IRA in patients with NSTEMI, and its clinical significance. Material and Methods: The study was a single-center retrospective cohort analysis of 399 consecutive patients with NSTEMI (293 male, mean age: 71 ± 10.1 years) undergoing percutaneous coronary intervention. The study population was categorized into patients with TO and non-TO of IRA on coronary angiography. In-hospital and one-year mortality were analyzed. Results: TO of IRA in the NSTEMI population occurred in 138 (34.6%) patients. Multivariate analysis identified the following independent predictors of TO of IRA: left ventricular ejection fraction (odds ratio (OR) 0.949, p < 0.001); family history of coronary artery disease (CAD) (OR 2.652, p < 0.001); and high-density lipoprotein (HDL) level (OR 0.972, p = 0.002). In-hospital and one-year mortality were significantly higher in the TO group than the non-TO group (2.8% vs. 1.1%, p = 0.007 and 18.1% vs. 6.5%, p < 0.001, respectively). The independent predictors of in-hospital mortality were: left ventricular ejection fraction (LVEF) at admission (OR 0.768, p = 0.004); and TO of IRA (OR 1.863, p = 0.005). Conclusions: In the population of patients with NSTEMI, TO of IRA represents a considerably frequent phenomenon, and corresponds with impaired outcomes. Therefore, the utmost caution should be paid to prevent delay of coronary angiography in NSTEMI patients with impaired left ventricular systolic function, metabolic disturbances, and a family history of CAD, who are at increased risk of TO of IRA.

scholarly journals Plasma Heat Shock Protein 70 Is Associated With the Onset of Acute Myocardial Infarction and Total Occlusion in Target Vessels

2021 ◽  
Vol 8 ◽  
Author(s):  
Runda Wu ◽  
Wei Gao ◽  
Zheng Dong ◽  
Ya Su ◽  
Yuyao Ji ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Heat Shock ◽  
Left Ventricular Ejection Fraction ◽  
Heat Shock Protein 70 ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Hsp70 Level ◽  
Total Occlusion ◽  
Ventricular Ejection Fraction

Background: Whether the role of plasma heat shock protein 70 (HSP70) in acute myocardial infarction (AMI) is protective or detrimental remains debated, and the relationship between HSP70 and total occlusion remains elusive.Methods: A total of 112 patients with primary diagnosis of AMI and 52 patients with chronic coronary syndrome (CCS) were enrolled into the study. Plasma HSP70 level was determined by ELISA on day 1 and day 7 after the onset of AMI and was examined before angiography in patients with CCS. Peak NT-proBNP, high-sensitivity C-reactive protein (CRP), troponin T (cTnT), and left ventricular ejection fraction were measured.Results: Plasma HSP70 was significantly higher in CCS than AMI (P &lt; 0.0001), and it showed a significant decrease from day 1 to day 7 after AMI (P &lt; 0.01). Elevated HSP70 was associated with decreased levels of LDL-C (P &lt; 0.05), peak cTnT (R = −0.3578, P &lt; 0.0001), peak NT-proBNP (R = −0.3583, P &lt; 0.0001), and peak CRP (R = −0.3539, P &lt; 0.0001) and a lower diagnosis of AMI (R = −0.4016, P &lt; 0.0001) and STEMI (R = −0.3675, P &lt; 0.0001), but a higher diagnosis of total occlusion in target vessels (R = 0.1702, P &lt; 0.05). HSP70 may provide certain predictive value for the diagnosis of AMI, STEMI, and total occlusion in target vessels, and the area under the receiver operating characteristic curves were 0.7660, 0.7152, and 0.5984, respectively. HSP70 was also negatively associated with in-hospital stay (P &lt; 0.001) and positively correlated with left ventricular ejection fraction (LVEF) at 1-year follow-up (P &lt; 0.05), despite no association with in-hospital major adverse cardiovascular events (MACE).Conclusion: Plasma HSP70 level was found to decrease from day 1 to day 7 post-AMI, but the overall level of patients with AMI was lower than that of patients with CCS. However, the ability of HSP70 to identify clinically significant AMI and STEMI was moderate, and the predictive value to total occlusion was slight.

scholarly journals A case of de Winter syndrome presenting with chest tightness

2021 ◽  
Vol 49 (7) ◽  
pp. 030006052110121
Author(s):  
Dongmei Jiang ◽  
Guosheng Fu
Keyword(s):  
Myocardial Infarction ◽  
Coronary Intervention ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Chest Tightness ◽  
Total Occlusion ◽  
Ventricular Ejection Fraction ◽  
St Segment Elevation ◽  
St Segment ◽  
Percutaneous Coronary

de Winter syndrome, also termed anterior ST-segment elevation myocardial infarction (STEMI) equivalent, is estimated to be present in approximately 2% of patients with acute myocardial infarction, but is often under-recognized by clinicians. Therefore, de Winter syndrome is associated with increased morbidity and mortality. We report a 51-year-old man with typical chest tightness and a characteristic electrocardiographic pattern without classic ST-segment elevation, but with acute nearly total occlusion of the left anterior descending coronary artery. Although the patient presented as a non-STEMI case, the definite diagnosis of de Winter syndrome was made on the basis of clinical and electrocardiographic findings. The patient’s symptom of chest tightness was relieved immediately after acute percutaneous coronary intervention and the left ventricular ejection fraction had not deteriorated at 1 month of follow-up.

A translational model of chronic heart failure in rats

2018 ◽  
pp. 136-148
Author(s):  
С.А. Крыжановский ◽  
И.Б. Цорин ◽  
Е.О. Ионова ◽  
В.Н. Столярук ◽  
М.Б. Вититнова ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Chronic Heart Failure ◽  
Left Ventricular ◽  
Compensatory Hypertrophy ◽  
Experimental Myocardial Infarction ◽  
Left Ventricular Ejection ◽  
Translational Model ◽  
Innovative Drug ◽  
Ventricular Ejection Fraction

Цель исследования - разработка трансляционной модели хронической сердечной недостаточности (ХСН) у крыс, позволяющей, с одной стороны, изучить тонкие механизмы, лежащие в основе данной патологии, а с другой стороны, выявить новые биомишени для поиска и изучения механизма действия инновационных лекарственных средств. Методика. Использован комплекс эхокардиографических, морфологических, биохимических и молекулярно-биологических исследований, позволяющий оценивать и дифференцировать этапы формирования ХСН. Результаты. Динамические эхокардиографические исследования показали, что ХСН формируется через 90 дней после воспроизведения переднего трансмурального инфаркта миокарда. К этому времени у животных основной группы отмечается статистически значимое по сравнению со 2-ми сут. после воспроизведения экспериментального инфаркта миокарда снижение ФВ левого желудочка сердца (соответственно 55,9 ± 1,4 и 63,9 ± 1,6%, р = 0,0008). Снижение насосной функции сердца (на 13% по сравнению со 2-ми сут. после операции и на ~40% по сравнению с интактными животными) сопровождается увеличением КСР и КДР (соответственно с 2,49 ± 0,08 до 3,91 ± 0,17 мм, р = 0,0002, и с 3,56 ± 0,11 до 5,20 ± 0,19 мм, р = 0,0001), то есть к этому сроку развивается сердечная недостаточность. Результаты эхокардиографических исследований подтверждены данными морфометрии миокарда, продемонстрировавшими дилатацию правого и левого желудочков сердца. Параллельно проведенные гистологические исследования свидетельствуют о наличии патогномоничных для данной патологии изменений миокарда (постинфарктный кардиосклероз, компенсаторная гипертрофия кардиомиоцитов, очаги исчезновения поперечной исчерченности мышечных волокон и т.д.) и признаков венозного застоя в легких и печени. Биохимические исследования выявили значимое увеличение концентрации в плазме крови биохимического маркера ХСН - мозгового натрийуретического пептида. Данные молекулярно-биологических исследований позволяют говорить о наличии гиперактивности ренин-ангиотензин-альдостероновой и симпатоадреналовой систем, играющих ключевую роль в патогенезе ХСН. Заключение. Разработана трансляционная модель ХСН у крыс, воспроизводящая основные клинико-диагностические критерии этого заболевания. Показано наличие корреляции между морфометрическими, гистологическими, биохимическими и молекулярными маркерами прогрессирующей ХСН и эхокардиографическими диагностическими признаками, что позволяет использовать неинвазивный метод эхокардиографии, характеризующий состояние внутрисердечной гемодинамики, в качестве основного критерия оценки наличия/отсутствия данной патологии. Aim. Development of a translational model for chronic heart failure (CHF) in rats to identify new biotargets for finding and studying mechanisms of innovative drug effect in this disease. Methods. A set of echocardiographic, morphological, biochemical, and molecular methods was used to evaluate and differentiate stages of CHF development. Results. Dynamic echocardiographic studies showed that CHF developed in 90 days after anterior transmural myocardial infarction. By that time, left ventricular ejection fraction was significantly decreased in animals of the main group compared with rats studied on day 2 after experimental myocardial infarction (55.9 ± 1.4% vs . 63.9 ± 1.6%, respectively, p<0.0008). The decrease in heart’s pumping function (by 13% compared with day 2 after infarction and by approximately 40% compared to intact animals) was associated with increased ESD and EDD (from 2.49 ± 0.08 to 3.91 ± 0.17 mm, p = 0.0002, and from 3.56 ± 0.11 to 5.20 ± 0.19 mm, respectively, p = 0.0001); therefore, heart failure developed by that time. The results of echocardiographic studies were confirmed by myocardial morphometry, which demonstrated dilatation of both right and left ventricles. Paralleled histological studies indicated presence of the changes pathognomonic for this myocardial pathology (postinfarction cardiosclerosis, compensatory hypertrophy of cardiomyocytes, foci of disappeared transverse striation of muscle fibers, etc.) and signs of venous congestion in lungs and liver. Biochemical studies demonstrated a significant increase in plasma concentration of brain natriuretic peptide, a biochemical marker of CHF. Results of molecular studies suggested hyperactivity of the renin-angiotensin-aldosterone and sympathoadrenal systems, which play a key role in the pathogenesis of CHF. Conclusions. A translational model of CHF in rats was developed, which reproduced major clinical and diagnostic criteria for this disease. Morphometric, histological, biochemical, and molecular markers for progressive CHF were correlated with echocardiographic diagnostic signs, which allows using this echocardiographic, noninvasive method characterizing the intracardiac hemodynamics as a major criterion for the presence / absence of this pathology.

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