Percutaneous coronary angioplasty is a minimally invasive procedure aimed at unclogging a coronary artery with a low complication rate (with a serious complication rate of 3% to 7% and a mortality rate of 1.2%). Device entrapment during PCI is a rare but life-threatening complication that occurs in < 1% of PCIs and balloon entrapment comes second after coronary guidewires. We present the case of 68-years-old man, smoker, hypertensive and type2 diabetic that presents angina with evidence of ischemia on myocardial tomoscintigraphy and in whom the radial coronary angiography reveals a tight calcified mid LAD stenosis. During his PCI and after dilatation with an NC balloon 2.5 × 12 the latter refuses to deflate and remains trapped in the lesion with the appearance of pain and ST-elevation despite several attempts to dilute the product in the inflator and to burst it by overexpansion. Traction on the balloon resulted in the deep intubation of the guiding-catheter, which comes in contact with the trapped balloon, and the rupture of the latter’s hypotube, which remains inflated at the site of the lesion and mounted on the 0.014 guidewire. We put a second 0.014 guidewire distally in the LAD and twisted with the distal part of the first guidewire, then we introduced a second balloon 2.0 × 20 over the second guidewire until the distal part of the guiding-catheter and inflated to trap the stucked balloon. We gradually removed this emergency assembly that allowed us to retrieve the trapped balloon. The control injection revealed a thrombotic occlusion of the LAD treated by thrombectomy and anti-GPIIbIIIa followed by a DES 2.75 × 28 placement. The patient was discharged 48 hours later with a good LVEF. The possible balloon entrapment mechanisms are an acute recoil of a highly calcified lesion with compression of the incompletely deflated balloon, which seems to be the case in our patient, strangulation of the proximal balloon end by the guiding-catheter if the balloon is removed before complete deflation and break or bend of the hypotube. The solutions in case of undeflatable balloon entrapment are to dilute the product in the inflator, to burst it by overexpansion, to pierce it through a stiff guidewire (or through its other end on a Microcatheter or OTW balloon), to cut its outer part and let it empty passively, to introduce a second guide-wire and perform a Buddy-Balloon or to transfer the patient to Surgery. Material entrapment remains a rare but life-threatening complication, its eviction requires the choice of material size and gentle manipulations (small balloons in the event of a calcified lesion) and its management uses different techniques, the choice of which depends on the clinical and anatomical situation.
Introduction: Atrial Septal Defect (ASD) is the most common congenital heart disease, accessible to percutaneous closure in 90% of cases. The closure procedure is performed usually under local anesthesia and TTE by femoral access. The association of OS-ASD with an azygos continuation of the inferior vena cava is very rare (< 0.1/1000 births) making femoral access impossible. Only a few cases are mentioned in the literature, here we describe the procedure as faithfully as possible. Important clinical finding: We present a case of a 32-years-old female candidate for percutaneous closure of OS-ASD with right cavity dilatation who present during her procedure an unusual guidewire path suspecting an azygos continuation of the inferior vena cava, confirmed by CT angiography, making impossible the closure via the femoral approach. Therapeutic intervention: After being confronted with the categorical patient refusal of the surgery, we performed successfully the procedure; one month later; under general sedation by internal jugular approach. We finished with manual compression before extubating the patient. Outcomes: The follow-up was favorable at the cost of a hematoma at the puncture site and brachial plexus compression, which regressed after 3 days. Conclusion: We opted for general anesthesia and intubation to guide the procedure by TEE. We placed it in the aorta, which gave us good stability to continue successfully the procedure. We underestimated the risk of complication at the puncture site, which could have been avoided by using a vascular suture device or more prolonged compression. Main takeaway lesson: Percutaneous closure is the reference treatment for OS-ASD. In case of is associated with an azygos continuation of the inferior vena cava, the right internal jugular vein remains a reasonable approach; it requires discussion and rigorous preparation by the whole team. The management of the puncture site in this situation remains delicate and requires great concentration.
Background: The PDA defines the pathological persistence after the birth of a fetal physiological communication between the aorta and the pulmonary artery frequently encountered in preterm infants and whose clinical and hemodynamic consequences depend on the importance of the shunt directly bound to the diameter of the canal. Percutaneous closure is the most frequent management modality with excellent immediate and long-term results (two modes of closure: using coil or Occluder). The surgery remains reserved for complex anatomies or associated with other surgical congenital anomalies. Case presentation: We detail in this document the two methods of percutaneous closure step by step illustrated by pediatric cases. The first case concerns a 7 years old girl of 17 kg weight with a history of heart murmur that presented in the TTE a PDA estimated at 1mm with LV dilation. The second case concerns a 12 years old girl of 30 kg weight with also a history of heart murmur that presented on TTE a PDA of 4.5mm with LV dilation. Therapeutic intervention: In the first case, we perform a closure with coil 5/5 by a unique femoral arterial approach as a standardized attitude in our center avoiding additional venous access. For the second case, we opted for closure with prosthesis N° 6/8 by a double femoral approach (arterial and venous access). Outcomes: The follow-up was favorable for both patients, with total sealing of the defect immediately after the procedures that persist during the 6 months of control. Conclusion: The closure of PDA in children is a challenging procedure whose safety requires a good pre-and per-procedural evaluation allowing the right choice of the method and size of the closing device. The respect of the different closure stages and the critical per procedural ultrasound and angiographic control reduce the rate of complications making this technique accessible and safe. In our series of 108 PDA closures by Coil in children, the unique femoral arterial approach is the standardized attitude in the first line in all patients avoiding additional venous access, which allows the Coil release in the basic technique while the arterial access allows opacification and measurement of the channel. The unique arterial approach has reduced the risk of local complications at the puncture site and the duration of the procedure without difference in closure efficiency and embolization risk. In our series of 92 PDA closures by Occluder in children the double femoral approach is the standardized attitude for all patients, the venous access allows the device release while the arterial access allows opacification/ measurement of the channel and control device deployment.
Introduction: Cardiovascular diseases are the leading cause of death in the world, headed by coronary artery disease, which is secondary to atherosclerosis. The latter recognizes classic risk factors such as diabetes, high blood pressure, tobacco, and dyslipidemia and other less classic factors such as chronic inflammation of rheumatoid arthritis. Many studies have highlighted the correlation between this chronic inflammation and clinical coronary disease but very few have focused on the anatomical correlation. Objective: To describe the correlation between the chronic biological inflammation of rheumatoid arthritis and anatomical coronary lesions on angiography. Method: This observational, retrospective, single-center study, including over 10 years, of patients with rheumatoid arthritis, confirmed the EULAR 2010 criteria and presented with coronary artery disease requiring coronary angiography. Patients with missing data or in whom coronary angiography was not done were excluded (n = 14). We divided then the patients according to the existence or not of chronic inflammation to study the impact of the latter on the existence (Stenosis < 50% vs. stenosis ≥ 50%), the extent (single vs. multivessel disease), and the severity of the coronary lesions (syntax score < 32 vs. ≥ 32). Results: 202 patients (49♂/153♀) aged between 30-75 years with a history of rheumatoid arthritis have had a coronary event requiring coronary angiography, were included; The mean ejection fraction at baseline was 57.3% +/- 5.8 (37 vs.-65%). 75% of them were ≥ 65 years old. 55% were diabetics, 61% with hypertension, 38% with dyslipidemia, and 19% were smokers. Chronic inflammation was diagnosed in 70% of them on non-specific parameters (ESR, CRP, fibrinogen, anemia, and rheumatoid factor). All patients had coronary angiography, which made it possible to identify the coronary lesions according to their existence (Stenosis < 50%: 51 patients vs. stenosis ≥ 50%: 151 patients), the extent (single: 86 patients vs. multivessel disease: 116 patients) and the severity of the coronary lesions (syntax score < 32: 142 patients vs. ≥ 32: 60 patients). Chronic inflammation of rheumatoid arthritis was correlated in bivariate and multivariate analysis (after excluding the impact of other risk factors) with the existence and extent of coronary lesions (p < 0.05) but not with their severity (p > 0.05). Discussion: The two limitations of this work are the monocentric nature of the study and the absence of specific inflammatory parameters such as anti-CCP antibodies. Strengths are anatomical correlations and multivariate analysis. Chronic inflammation apart from any influence of the various risk factors predisposes to the existence and extent of coronary lesions (p < 0.05). The severity of coronary lesions assessed by Syntax Score was not correlated with chronic inflammation, although other studies suggest that this inflammation is the cause of complex lesions. Interpretation: Rheumatoid arthritis is associated with an increase in cardiac morbidity and mortality. Atheromatous lesions are more frequent in those patients than the existence of classic cardiovascular risk factors would suggest. Several explanations could account for this risk: the inflammatory syndrome and its impact on the cardiovascular risk factors and the vessel and the deleterious effect of the treatments. This requires stricter screening and management of risk factors in rheumatoid arthritis.
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