scholarly journals Stenting in Coarctation of the Aorta

1970 ◽  
Vol 6 (2) ◽  
pp. 103-106
Author(s):  
Syed Ali Ahsan ◽  
Syed Sawkat Hossain ◽  
Md Saifullah Patwary ◽  
Md Abu Salim ◽  
Rafique Chowdhury ◽  
...  
Keyword(s):  
Subclavian Artery ◽  
Ventricular Hypertrophy ◽  
Antihypertensive Drugs ◽  
Left Subclavian Artery ◽  
Ductus Arteriosus ◽  
Coarctation Of The Aorta ◽  
Left Ventricular ◽  
Endovascular Stenting ◽  
Concentric Hypertrophy ◽  
Ct Angiogram

Narrowing of the aorta most commonly occurs in the region where the ductus arteriosus joins the aorta, i.e. at the isthmus just below the origin of the left subclavian artery. It is associated with other abnormalities, of which the most frequent are bicuspid aortic valve and ‘berry’ aneurysms of the cerebral circulation. Acquired coarctation of the aorta is rare but may follow trauma or occur as a complication of a progressive arteritis, Takayasu’s disease.A 21 years old young lady noted intermittent headache and occasionally weakness or cramps in the legs on walking from her early childhood. On examination her blood pressure in the upper limb 210 / 120 mm Hg, in lower limb was 100 / 60 mm Hg. There was radio-femoral delay and femoral pulse was weak. A systolic murmur is heard posteriorly. Radiological examination showed changes in the contour of the aorta and rib notching. ECG shows left ventricular hypertrophy. Echocardiography showed only concentric hypertrophy of LV. CT angiogram revealed coarctation of the aorta present with development of collaterals. Inspite of getting 3 different antihypertensive drugs her BP was uncontrolled. In our hospital her coarctation of the aorta was corrected by by endovascular stenting on the coarctation of the aorta. 5F, 7F & then 9F sheath, straight & J tiped terumo & J tip taflon coated 300 cm long wire was used. Predilatation was done by ballon used 3x10 mm over 0.34" J tip terumo wire @ 10 atm. Post dilatation was done by ballon used 7x20 mm @ 4 atm. Wall stent (Endoprosthesis) 9F was used. 1st Wall stent 14mm x 40mm self expanding and 2nd Wall stent 16mm x 60 mm, upper part covered the mouth of left subclavian artery. Result of stenting was good and procedure was uneventful. DOI: 10.3329/uhj.v6i2.7256University Heart Journal Vol. 6, No. 2, July 2010 pp.103-106

Coarctation of the Aorta Associated with Left Subclavian Artery Aneurysm: A Case Report

2007 ◽  
Vol 10 (3) ◽  
pp. E175-E176 ◽  
Author(s):  
Kaan Inan ◽  
Onur Goksel ◽  
Ibrahim Alp ◽  
Tuncay Erden ◽  
Melih Us ◽  
...  
Keyword(s):  
Case Report ◽  
Subclavian Artery ◽  
Left Subclavian Artery ◽  
Artery Aneurysm ◽  
Coarctation Of The Aorta ◽  
Subclavian Artery Aneurysm

scholarly journals Pulmonary atresia with a ventricular septal defect and left pulmonary artery discontinuity: a case report 

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Hyun-Hwa Cha ◽  
Hae Min Kim ◽  
Won Joon Seong
Keyword(s):  
Pulmonary Artery ◽  
Subclavian Artery ◽  
Septal Defect ◽  
Left Subclavian Artery ◽  
Ductus Arteriosus ◽  
Main Pulmonary Artery ◽  
Pulmonary Arteries ◽  
Pulmonary Atresia ◽  
Left Pulmonary Artery ◽  
Right Pulmonary Artery

Abstract Background Unilateral pulmonary artery discontinuity is a rare malformation that is associated with other intracardiac abnormalities. Cases accompanied by other cardiac abnormalities are often missed on prenatal echocardiography. The prenatal diagnosis of isolated unilateral pulmonary artery discontinuity can also be delayed. However, undiagnosed this malformation would have an effect on further prognosis. We report our case of a prenatal diagnosis of pulmonary atresia with ventricular septal defect and left pulmonary artery discontinuity. Case presentation A 33-year-old Asian woman visited our institution at 24 weeks of gestation because of suspected fetal congenital heart disease. Fetal echocardiography revealed a small atretic main pulmonary artery giving rise to the right pulmonary artery without bifurcation and the left pulmonary artery arising from the ductus arteriosus originating from the left subclavian artery. The neonate was delivered by cesarean section at 376/7 weeks of gestation. Postnatal echocardiography and multidetector computed tomography showed a right aortic arch, with the small right pulmonary artery originating from the atretic main pulmonary artery and the left pulmonary artery originating from the left subclavian artery. Patency of the ductus arteriosus from the left subclavian artery was maintained with prostaglandin E1. Right ventricular outflow tract reconstruction and pulmonary angioplasty with Gore-Tex graft patch was performed 25th day after birth. Unfortunately, the neonate died because of right heart failure 8 days postoperation. Conclusion There is a possibility that both pulmonary arteries do not arise from the same great artery (main pulmonary artery or common arterial trunk). Therefore, clinicians should check the origin of both pulmonary arteries.

scholarly journals Treatment of an Unusual Occurrence of a Complex Left Subclavian Artery/Left Internal Mammary Artery Bifurcation Stenosis in the Setting of Coronary Subclavian Steal Syndrome and Ischemic Left Ventricular Systolic Dysfunction

2018 ◽  
Vol 2018 ◽  
pp. 1-4
Author(s):  
Michael J. Martinelli ◽  
Michael B. Martinelli
Keyword(s):  
Subclavian Artery ◽  
Internal Mammary Artery ◽  
Left Subclavian Artery ◽  
Left Internal Mammary Artery ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Subclavian Steal Syndrome ◽  
Internal Mammary ◽  
Coronary Subclavian Steal Syndrome ◽  
Steal Syndrome

This case will illustrate the clinical and unique technical challenges, not previously reported, in a patient with a history of progressive left ventricular (LV) systolic dysfunction, congestive heart failure (CHF), myocardial infarction (MI), and a complex bifurcation lesion of the left subclavian artery (SA) involving the left internal mammary artery (LIMA) in the setting of coronary subclavian steal syndrome (CSSS). The approach to this lesion is complicated by significant LIMA involvement requiring intervention directed toward both the SA and the LIMA in the presence of severe LV systolic dysfunction. This clinical scenario necessitates a careful technique, utilizing bifurcation methods similar to those used in coronary intervention.

scholarly journals Serum Zinc and Selenium Concentrations in Patients with Hypertrophy and Remodelling of the Left Ventricle Secondary to Arterial Hypertension

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1803
Author(s):  
Paweł Gać ◽  
Karolina Czerwińska ◽  
Małgorzata Poręba ◽  
Adam Prokopowicz ◽  
Helena Martynowicz ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Left Ventricular Hypertrophy ◽  
Arterial Hypertension ◽  
Ventricular Hypertrophy ◽  
Serum Zinc ◽  
Left Ventricular ◽  
Left Ventricular Geometry ◽  
Serum Selenium ◽  
Hypertensive Patients ◽  
Concentric Hypertrophy

The aim of the study was to assess the relationship between serum selenium and zinc concentrations (Se-S and Zn-S) and the left ventricle geometry in patients suffering from arterial hypertension. A total of 78 people with arterial hypertension (mean age: 53.72 ± 12.74 years) participated in the study. Se-S and Zn-S were determined in all patients. The type of left ventricular remodelling and hypertrophy was determined by the left ventricular mass index (LVMI) and relative wall thickness (RWT) measured by echocardiography. Se-S and Zn-S in the whole group were 89.84 ± 18.75 µg/L and 0.86 ± 0.13 mg/L. Normal left ventricular geometry was found in 28.2% of patients; left ventricular hypertrophy (LVH) in 71.8%, including concentric remodelling in 28.2%, concentric hypertrophy in 29.5%, and eccentric hypertrophy in 14.1%. LVH was statistically significantly more frequent in patients with Se-S < median compared to patients with Se-S ≥ median (87.2% vs. 56.4%, p < 0.05), as well as in patients with Zn-S < median compared to patients with Zn-S ≥ median (83.8% vs. 60.9%, p < 0.05). In hypertensive patients, older age, higher LDL cholesterol, higher fasting glucose, lower Se-S, and lower Zn-S were independently associated with LVH. In conclusion, in hypertensive patients, left ventricular hypertrophy may be associated with low levels of selenium and zinc in the serum.

scholarly journals Left ventricular hypertrophy in patients treated with regular hemodialyses

2008 ◽  
Vol 61 (7-8) ◽  
pp. 369-374 ◽  
Author(s):  
Dejan Petrovic ◽  
Biljana Stojimirovic
Keyword(s):  
Risk Factors ◽  
Left Ventricle ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Cardiovascular Morbidity ◽  
Morbidity And Mortality ◽  
Concentric Hypertrophy ◽  
Cardiovascular Morbidity And Mortality

Left ventricular hypertrophy is the main risk factor for development of cardiovascular morbidity and mortality in patients on hemodialysis. Left ventricular hypertrophy is found in 75% of the patients treated with hemodialysis. Risk factors for left ventricular hypertrophy in patients on hemodialysis include: blood flow through arterial-venous fistula, anemia, hypertension, increased extracellular fluid volume, oxidative stress, microinflammation, hyperhomocysteinemia, secondary hyperpara- thyroidism, and disturbed calcium and phosphate homeostasis. Left ventricular pressure overload leads to parallel placement of new sarcomeres and development of concentric hypertrophy of left ventricle. Left ventricular hypertrophy advances in two stages. In the stage of adaptation, left ventricular hypertrophy occurs as a response to increased tension stress of the left ventricular wall and its action is protective. When volume and pressure overload the left ventricle chronically and without control, adaptive hypertrophy becomes maladaptive hypertrophy of the left ventricle, where myocytes are lost, systolic function is deranged and heart insufficiency is developed. Left ventricular mass index-LVMi greater than 131 g/m2 in men and greater than 100 g/m2 in women, and relative wall thickness of the left ventricle above 0.45 indicate concentric hypertrophy of the left ventricle. Eccentric hypertrophy of the left ventricle is defined echocardiographically as LVMi above 131 g/m2 in men and greater than 100 g/m2 in women, with RWT ?0.45. Identification of patients with increased risk for development of left ventricular hypertrophy and application of appropriate therapy to attain target values of risk factors lead to regression of left ventricular hypertrophy, reduced cardiovascular morbidity and mortality rates and improved quality of life in patients treated with regular hemodialyses.

COARCTATION OF THE AORTA WITH CONGESTIVE HEART FAILURE IN INFANCY—MEDICAL TREATMENT

PEDIATRICS ◽  
1956 ◽  
Vol 17 (1) ◽  
pp. 45-57
Author(s):  
Henry T. Lang ◽  
Alexander S. Nadas
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Medical Treatment ◽  
Ventricular Hypertrophy ◽  
Failure To Thrive ◽  
Coarctation Of The Aorta ◽  
Left Ventricular ◽  
Late Childhood ◽  
Feeding Problems ◽  
Left And Right

Nine infants with uncomplicated coarctation of the aorta in congestive heart failure are presented. The symptomatology was dominated by feeding problems, failure to thrive, dyspnea, and cyanosis. On physical examination, in addition to signs referable to the coarctation, signs of both left and right-sided congestive heart failure were noted. The roentgenographic survey revealed marked generalized cardiomegaly and pulmonary congestion. Electrocardiograms in the infants less than 6 months of age showed left, right, or combined ventricular hypertrophy, whereas those more than 6 months of age all showed left ventricular hypertrophy. Medical treatment, consisting of digitalis, oxygen, mercurial diuretics, diet low in sodium, and antibiotics, was successful in all instances. Digitalization was maintained throughout infancy. Operative intervention can be safely postponed until late childhood unless medical management is not successful. A review of the pertinent literature is presented.

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