scholarly journals Coronary Perforation- A Nightmare in Cath Lab

Author(s):  
Ashok Kumar Thakur ◽  
Puneet Aggarwal ◽  
Rajeev Bharadwaj ◽  
Bhagya Narayan Pandit ◽  
Ranjit Kumar Nath

Percutaneous Coronary Intervention (PCI) is now the standard of care in patients with coronary artery disease. With advances in modern technology, the success of PCI has relatively increased, and so is its complication, specifically in complex coronary intervention. Coronary perforation is one of the most dreadful and life-threatening complications of PCI. The most vital step in the management of coronary perforation is its identification and quick action. Multiple methods for management are now recommended in the literature, but the mainstay of treatment is still prevention. This review discusses the incidence, risk factors, prevention, identification, and management of Coronary Artery Perforation (CAP).

2019 ◽  
Vol 04 (02) ◽  
pp. 110-120
Author(s):  
Tripti Deb ◽  
Jyotsna Maddury ◽  
Prasant Kr. Sahoo

AbstractPercutaneous coronary intervention (PCI) is considered as the standard treatment of obstructive coronary artery disease in indicated patients. Even though PCI gives symptomatic angina improvement, but associated with serious complications like coronary artery perforation (CAP), the incidence is quite low. With the more complex lesions for successful angioplasty, different devices are required, which in turn increase the incidence of CAP in these patients. Here we review the classification, incidence, pathogenesis, clinical sequela, risk factors, predictors, and management of CAP in the current era due to PCI.


1970 ◽  
Vol 3 (2) ◽  
pp. 239-247 ◽  
Author(s):  
Z Rahman ◽  
M Ullah ◽  
AK Choudhury

After its introduction by Andrew R. Gruentzig in 1977 percutaneous coronary intervention (PCI) is widely utilized in the treatment of symptomatic coronary artery disease. Though it has numerous benefits, serious and potentially life-threatening complications of PCI can occur, including iatrogenic coronary artery dissection and perforation. The incidence of these complications has been augmented by the development of coronary interventional devices intended to remove or ablate tissue. Here we review the classification, incidence, pathogenesis, clinical sequelae and management of coronary artery dissection and perforation in the current era due to PCI. Specifically, the current angiographic classifications of coronary artery dissections and perforations are reviewed. The findings of several recent, registries of PCI-related coronary artery perforations and dissection are summarized. The management of coronary artery dissection and perforation is discussed in details, including the application of newer modalities such as covered stents. Keywords: Percutaneous coronary intervention (PCI); Coronary artery dissection DOI: http://dx.doi.org/10.3329/cardio.v3i2.9198   Cardiovasc. J. 2011; 3(2): 239-247


2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Xiangfei Wang ◽  
Junbo Ge

Coronary artery perforation is an uncommon complication in patients with coronary heart disease undergoing percutaneous coronary intervention. However, pericardial tamponade following coronary artery perforation may be lethal, and prompt treatment is crucial in managing such patients. Balloon occlusion and the reversal of anticoagulant activity are the common methods used to prevent cardiac tamponade by reducing the amount of bleeding. Herein, we discuss the pros and cons of currently used occlusion types for coronary perforation. Optimal balloon occlusion methods should reduce the amount of bleeding and ameliorate subsequent myocardial ischemia injury, even during cardiac surgery.


2021 ◽  
Vol 5 (11) ◽  
Author(s):  
Atit A Gawalkar ◽  
Navreet Singh ◽  
Ankush Gupta ◽  
Parag Barwad

Abstract Background Coronary artery perforation (CAP), although rare, can often be a life-threatening complication of percutaneous coronary intervention. Looped wire tip or buckling of wire is conventionally considered safer due to reduced risk of migration into smaller branches and false lumen. Occasionally, buckling can indicate the entry of tip into dissection plane, or the advancement of looped wire can cause small vessel injury leading to perforation. Distal coronary perforation can be life threatening and coil, foam, and thrombin injection are some of the material widely used for sealing it. Case summary We hereby report three different cases illustrating the vessel injury that the looped wire can cause in the distal vasculature related to various mechanisms like high elastic recoil tension, dissection by the non-leading wire tip, or hard wire lacerating the fragile small branches. All these mechanisms lead to distal coronary perforation leading to cardiac tamponade. Each case also illustrate the novel technique of autologous fat globule embolization for the management of distal CAP. Discussion Distal coronary perforation is often due to guidewire-related vessel injury and is more common with hydrophilic wires. Looped wire tip can sometime indicate vessel injury and its advancement further down the coronary artery may result in serious vessel injury and perforation. Management of distal coronary perforation is challenging, and here we demonstrate the steps of using the readily available autologous fat globules by selectively injecting them into the small coronary artery to control the leak.


Author(s):  
Marcos Oliveira ◽  
Valter Trigueiro ◽  
Igor Batista ◽  
Adriano Caixeta

Coronary artery perforation is a rare but potentially lethal complication of percutaneous coronary intervention, mainly due to hemodynamic compromise secondary to cardiac tamponade development. All interventional cardiologists must thus be able to promptly recognize and solve coronary artery perforation. We describe a successfully and conservatively managed type III coronary artery perforation with prolonged balloon inflations, in the absence of covered stents and without compromising the percutaneous coronary intervention result by anticoagulation reversal.


Author(s):  
Г.А. Березовская ◽  
Е.С. Клокова ◽  
Н.Н. Петрищев

Гены тромбообразования и фолатного обмена играют важную роль в развитии и прогрессии ишемической болезни сердца (ИБС). Однако о возможной роли полиморфных маркеров в рецидиве ИБС после чрескожного коронарного вмешательства (ЧКВ) известно недостаточно. Цель исследования: Оценить роль генетических факторов системы тромбообразования и фолатного обмена (полиморфных маркеров генов F5, F2, F13A1, PAI1, HPA1, MTHFR, FGB ), в возобновление клиники ИБС после ЧКВ. Методика: Исследование проводили с использованием выборки из 90 больных ИБС в возрасте от 40 до 75 лет: 75 пациентов после планового ЧКВ (60 мужчин и 15 женщин) и 15 лиц после экстренного ЧКВ (12 мужчин и 3 женщины). Молекулярно-генетическое исследование было выполнено с помощью комплекта реагентов «Сердечно-сосудистые заболевания СтрипМетод»® (ViennaLab Diagnostics GmbH, Австрия), выявляющие следующие варианты: F5, F2, F13A1, PAI1, HPA1, MTHFR, FGB . Результаты: В результате исследования была показана ассоциация полиморфного маркера G103T ( Val34Leu ) гена F13A1 (фактор свертываемости крови 13, субъединица A1) с развитием рецидивирующего состояния ИБС после ЧКВ. Выявлены статистически значимые различия в распределении частот генотипов полиморфного маркера Val34Leu гена F13A1 . Показано, что частота генотипа Val/Val у пациентов с осложнениями была выше, чем у пациентов без таковых: 0,700 и 0,400 соответственно (c = 7,78; p = 0,020), при этом генотип Val/Val проявил себя как фактор риска развития осложнений: ОШ = 3,50 (95%ДИ 1,37-8,93). При сравнении аллелей выявили, что частота аллеля L у больных с осложнениями была ниже, чем у лиц без таковых: 0,167 и 0,375 соответственно (p = 0,004), и носительство аллеля L уменьшало вероятность развития осложнений: ОШ = 0,33 (95%ДИ 0,15-0,72). Заключение: Носительство варианта 34V гена F13A1 , кодирующего A-субъединицу фактора свёртывания 13, предрасполагает к возобновлению клинических проявлений ИБС после ЧКВ. Genes of thrombosis and folate metabolism play an important role in development and progression of coronary artery disease (CAD). However, a possible role of polymorphic markers in CAD relapse following percutaneous coronary intervention (PCI) is not sufficiently understood. Background. Reports have indicated an association of genetic factors generally related with thrombophilia and recurrence of symptoms for coronary artery disease (CAD) following a percutaneous coronary intervention (PCI) due to restenosis and in-stent thrombosis. However, the relapse can also be caused by progression of atherosclerosis and endothelial dysfunction in unoperated blood vessels. Aim: To assess the role of genetic risk factors involved in thrombosis and folate metabolism (polymorphic markers of F5, F2, F13A1, PAI1, HPA1, MTHFR, and FGB genes) in recurrence of CAD symptoms after PCI. Methods: The study included 90 patients with CAD aged 40-75; 75 of these patients had undergone elective PCI (60 men and 15 women) and 15 patients - emergency PCI (12 men and 3 women). Molecular genetic tests were performed using a CVD StripAssays® reagent kit (ViennaLab Diagnostics GmbH, Austria) to identify the following genetic variations: F5, F2, F13A1, PAI1, HPA1, MTHFR, and FGB . Results: The study results showed a significant association of the G103T ( Val34Leu ) polymorphism in the F13A1 gene with relapses of IHD after PCI. Significant differences were found in genotype distribution frequencies of the Val34Leu polymorphism in the F13A1 gene. The frequency of Val / Val genotype was higher in patients with complications than without complications, 0.700 and 0.400, respectively (c = 7.78, p = 0.020). Furthermore, the Val/Val genotype can be classified as a risk factor for complications (OR = 3.50; 95% CI, 1.37-8.93). The L allele frequency was lower in patients with complications than in those without complications (0.167 and 0.375, respectively, p = 0.004), and carriage of the L allele reduced the likelihood of complications (OR = 0.33; 95% CI 0.15-0.72). Conclusion: Carriage of the 34V variant in the F13A1 gene that encodes the coagulation factor XIII A subunit predisposes to a relapse of CAD symptoms after PCI.


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