• Journal of Chest Surgery
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• v.49 no.6
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• pp.413-420
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• 2016

Doctors are often faced with difficult decisions and uncertainty when patients need a certain treatment. They routinely rely on the scientific literature, in addition to their knowledge, experience, and patient preferences. Clinical practice guidelines are created with the intention of facilitating decision-making. They may offer concise instructions for the diagnosis, management (medical or surgical treatments), and prevention of specific diseases or conditions. All information included in the final version are the result of a systematic review of scientific articles and an assessment of the benefits and costs of alternative care options. The final document attempts to meet the needs of most patients in most circumstances and clinicians, aware of these recommendations, should always make individualized treatment decisions. In this review, we attempted to define the intent and applicability of clinical practice guidelines, expert consensus documents, and registry studies, focusing on the management of patients with thoracic aortic disease.

• Journal of Chest Surgery
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• v.41 no.4
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• pp.520-522
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• 2008

Aortoesophageal fistula that causes massive bleeding from the esophagus is a rare and fatal disease. The most common cause of aortoesophageal fistula is an aortic aneurysm, and the other causes are inflammatory disease and neoplasm. The treatment of choice for aortoesophageal fistula is surgery, and this surgery carries a high rate of mortality and morbidity. Stent-graft treatment is now being applied for this malady. Herein we report on a case of primary aortoesophageal fistula that was treated with primary repair of the fistula openings, and we include a review of the relevant literature.

• Journal of Chest Surgery
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• v.21 no.1
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• pp.136-142
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• 1988

Between February, 1983, and March, 1987, thirty-one systemic-pulmonary shunts were performed in 28 patients with cyanotic congenital heart disease. Age ranged from 8 months to 28 years [mean age, 5.4 years, Weight ranged from 7 kg to 48 kg [mean weight, 16kg]. There were 4 classic Blalock-Taussig shunts, 5 central polytetrafluoroethylene shunts, 1 aorta-right pulmonary artery shunt with graft, and 21 modified Blalock-Taussig shunts. One patient required another shunt immediately due to insufficient pulmonary blood flow with patent graft. There was no postoperative death. Conduit diameters included 4mm [2 cases], 5 mm [22 cases], and 6 mm [3 cases]. Long term follow up was available in 27 patients [96.4%] with mean period of 20 months [range, 4 months to 49 months]. The effectiveness of shunt was evaluated by cardiac catheterization with angiography [15 patients] or clinically. They showed improvement of systemic oxygen saturation values by 12% and decrease of hemoglobin by 2.3gm/dl [P<0.01]. There were 2 shunt occlusion in central shunts at 32 and 48 months respectively, and one narrowing of graft in modified Blalock-Taussig shunt at 12 months. The patency rate was 91.6% at 24 months for 5 mm grafts in modified Blalock-Taussig shunt.

• Preventive Nutrition and Food Science
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• v.18 no.2
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• pp.92-97
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• 2013

The calcification of vascular smooth muscle cells (VSMCs) is considered one of the major contributors for vascular disease. Phosphate is known as the inducer for VSMC calcification. In this study, we assessed whether phosphate affected cell viability and fetuin-A, a calcification inhibitor protein, both which are related to VSMC calcification. Also, VSMC viability by zinc level was assessed. The results showed that phosphate increased Ca and P deposition in VSMCs (A7r5 cell line, rat aorta origin). This phosphate-induced Ca and P deposition was consistent with the decreased A7r5 cell viability (P<0.05), which implies phosphate-induced calcification in A7r5 cells might be due to the decreased VSMC cell viability. As phosphate increased, the protein expression of fetuin-A protein was up-regulated. A7r5 cell viability decreased as the addition of cellular zinc level was decreased (P<0.05). The results suggested that zinc deficiency causes the decreased cell viability and it would be the future study to clarify how zinc does act for VSMC cell viability. The results suggest that the decreased VSMC viability by high P or low Zn in VSMCs may be the risk factor for vascular disease.

• BMB Reports
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• v.56 no.3
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• pp.160-165
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• 2023

Vascular calcification is common in cardiovascular diseases including atherosclerosis, and is associated with an increased risk of pathological events and mortality. Some semaphorin family members play an important role in atherosclerosis. In the present study, we show that Semaphorin 4D/Sema4D and its Plexin-B1 receptor were significantly upregulated in calcified aorta of a rat chronic kidney disease model. Significantly higher Sema4D and Plexin-B1 expression was also observed during inorganic phosphate-induced calcification of vascular smooth muscle cells. Knockdown of Sema4D or Plexin-B1 genes attenuated both the phosphate-induced osteogenic phenotype of vascular smooth muscle cells, through regulation of SMAD1/5 signaling, as well as apoptosis of vascular smooth muscle cells, through modulation of the Gas6/Axl/Akt survival pathway. Taken together, our results offer new insights on the role of Sema4D and Plexin-B1 as potential therapeutic targets against vascular calcification.

• Journal of Veterinary Clinics
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• v.39 no.6
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• pp.287-293
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• 2022

Radiographic left atrial dimension (RLAD) is a useful measurement to assess left atrial enlargement in dogs. There are studies on the use of RLAD on various breeds of dogs, but no study on a specific breed with myxomatous mitral valve disease (MMVD). This study was conducted to compare RLAD measurements in Maltese dogs with MMVD ACVIM stage B1 and B2, and also to investigate the correlation of RLAD with the LA:Ao ratio. A total of 29 Maltese dogs were the subjects of this study. Each dog was diagnosed with MMVD ACVIM stage B1 or B2 based on physical examination, thoracic radiography, and echocardiography. The vertebral heart size (VHS), RLAD, LVIDDn, and LA:Ao ratio were measured and compared to evaluate the differences. There were significant differences in the RLAD, LVIDDn, and LA:Ao ratio between dogs with MMVD ACVIM stage B1 and those with stage B2. There was a significant correlation between the LA:Ao ratio and both the RLAD and VHS measurements, but the correlation coefficient was higher for RLAD. The RLAD scores exhibited a significant difference between dogs with ACVIM Stage B1 and with those with B2, and these scores had a higher correlation with the LA:Ao ratio measured by echocardiography than with VHS.

• Journal of Cardiovascular Imaging
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• v.30 no.3
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• pp.202-211
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• 2022

BACKGROUND: This study aims to investigate normal changes throughout aging of the heart in cardiac magnetic resonance (CMR) imaging in healthy volunteers. While type 2 diabetes mellitus is a frequent finding in the elderly population, also the influence of this circumstance in otherwise healthy persons is part of our study. METHODS: In this prospective single-center trial, 75 healthy subjects in distinct age groups and 10 otherwise healthy diabetics were enrolled. All subjects underwent functional, flow sensitive, native T2- and T1-mapping in a 1.5T CMR scanner. RESULTS: No differences in right and left ventricular ejection fractions were observed between aging healthy groups. Bi-ventricular volumes lowered significantly (p<0.001) between the age groups. There was also a significant decrease in myocardial T1 values, aortic distensibility, and left ventricular peak diastolic strain rates. There were no differences in T2 mapping and the other deformation parameters. Patients with type 2 diabetes mellitus had lower end-diastolic volume indexes; all the other measurements were comparable. CONCLUSIONS: Aging processes in the healthy heart involve a decrease in ventricular volumes, with ejection fractions remaining normal. Stiffening of the myocardium and aorta and a decrease in T1 values are potential indications of age-related remodeling. Type 2 diabetes mellitus seems to have no major influence on aging processes of the heart.

• Journal of Chest Surgery
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• v.25 no.3
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• pp.232-239
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• 1992

Acute renal failure is a well known serious complication following open heart surgery and is associated with a significant increase in morbidity and mortality rate. From 1984 to 1990, 33 patients who had acute renal failure following cardiopulmonary bypass received renal replacement therapy. PD[Peritonial dialysis] was employed in 11 patients and CAVH[continous arteriovenous hemofiltration] was employed in 22 patients. Their age ranged from 3 months to 64 years[mean 25.5$\pm$7.8 years]. The disease entities included congenital cardiac anomaly in 18, valvular heart disease in 15 and aorta disease in 2 cases. Low cardiac output was thought as a primary cause of ARF except two redo valve cases who showed severe Aemolysis k depressed renal function preoperatively. Mean serum BUN and creatinine level at the onset renal replacement therapy were 65$\pm$8 mg/dl and 3.5$\pm$0.4 mg/dl respectively, declining only after reaching peak level 7&10 days following the onset of therapy. Overall hospital mortality was 72.7%[24/33]; 81%[9/11] in PD group and 68.2% [15/22] in CAVH group respectively. The primary cause of death was low cardiac output & hemodynamic depression in all the cases. The fatal complications included multiorgan failure in 7, disseminated intravascular coagulation and sepsis in 6, neurologic damage in 4 and mediastinitis in 3 cases. No measurable differences were observed between CAVH and PD group upon consequence of acute renal failure and disease per se. The age at operation, BUN/Cr level at the onset of bypass and highest BUN/Cr level and the consequence of low output status were regarded as important risk factors, determining outcome of ARF and success of renal replacement therapy. Thus, we concluded that althoght the prognosis is largely determined by severity of low cardiac output status and other organ complication, early institution of renal replacement therapy with other intensive supportive measures could improve salvage rate in established ARF patients following CPB.

• Korean Journal of Clinical Pharmacy
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• v.21 no.1
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• pp.6-13
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• 2011

Bolus intravenous injection of adenosine resulted the temporal decrease of systemic blood pressure and heart rate in the anesthetized rats. Adenosine also resulted the persistent decrease of contractility and heart rate in the isolated spontaneously beating rat right atria. Both of the above inhibition effets of adenosine were increased by the pretreatment of NBI (nitrobenzylthioinosine), whitch is an adenosine transport inhibitor, but decreased by the pretreatment of 8- phenyltheophy1line, which is an adenosine antagonist. In isolated thoracic aorta ring segment of normotensive rats, intact rings were relaxed by adenosine ($42.3{\pm}8.7%$) and ATP ($85.9{\pm}15.8%$) in the concentration of $10^{-4}M$, but rubbed rings were relaxed by adenosine ($35.2{\pm}1.9%$) and ATP ($11.3{\pm}9.0%$) in $10^{-4}M$. After pretreatment of L-NAME (N-Nitro-Larginine methyl ester), which is an NO inhibitor, adenosine-induced relaxation was not affected, but ATP-induced relax ation was significantly inhibited (P<0.01). Meanwhile, adenosine resulted almost same as vasorelaxation in isolated thoracic aorta of SHR comparing to those of normotensive rats. But, vasodilation responses of ATP in intact rings of SHR are significantly inhibited comparing to those of normotensive rats. Adenosine-induced relaxation is attenuated after 8-phenyltheophylline pretreatment, but increased after NBI pretreatment. However, ATP-induced relaxations are not affected by 8-phenyltheophylline or NBI pretreatment. These results suggested that the hypotensive effects of adenosine was due to the decrease of contractile force and heart rate through the A1 receptor and vasodilation are mediated by A2 receptor of the vascular smooth muscle. And, the heart protective and vasodilation effects of adenosine might suggest that it would be useful in the acute treatment of coronary artery disease.

• Clinical and Experimental Pediatrics
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• v.45 no.2
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• pp.267-272
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• 2002

Typical hypoplastic left heart syndrome(HLHS) is a distinct pathologic entity with aortic atresia, mitral atresia, very hypoplastic or absent left ventricle and thread like ascending aorta. Occasionally, the lesser degree of hypoplasia is found and is called hypoplastic left heart complex(HLHC) by some authors. This HLHC is often associated with critical aortic stenosis. Fetal echocardiography has enabled us to observe human fetal heart in-utero and to diagnose congenital heart disease prenatally over the last 20 years. The diagnosis of HLHS in fetal echocardiography is based on 2-dimensional echocardio -graphic evidence of a diminutive ascending aorta, aortic atresia, mitral atresia or severe stenosis and a hypoplastic left ventricle. Abnormal flow direction through atrial septum or through isthmus greatly aids the diagnosis. This report shows a fetal case who showed hypoplastic left side chambers and retrograde isthmic flow and was diagnosed with hypoplastic left heart syndrome. After birth, although the baby had tachy-dyspnea for the first 3 weeks, she finally recovered without any intervention and showed catch up growth of left side chambers. This case illustrates the extreme difficulty of assessing left ventricle in a fetus.