• Clinical and Experimental Pediatrics
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• v.52 no.7
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• pp.752-755
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• 2009

It is well known that hemodynamic load is one of the most important determinants of cardiac structure and function. Circadian variations in blood pressure (BP) are usually accompanied by consensual changes in peripheral resistance and/or cardiac output. In recent years, reduction in circadian variations in BP and, in particular, loss of nocturnal decline of BP were observed in hypertensive patients with left ventricular hypertrophy (LVH). The patients with only a slight or no loss of nocturnal decline of BP were considered "non-dippers". Regression of LVH was observed after prolonged antihypertensive therapy. Restoration of the circadian rhythm of BP was also observed. However, the classification of patients into "dippers" and "non-dippers" is arbitrary and poorly standardized and repeatable, and in the recent studies, most hypertensive patients with LVH were "dippers". Therefore, we should be particularly cautious about the conclusions drawn using this index. On the other hand, reduced activity of low-pressure cardiopulmonary baroreceptors and impaired day-to-night modulation of autonomic nervous system activity were observed in patients with only LVH. Therefore, alterations in cardiac structure may impair BP modulation. On the other hand, the reverse can also be trueprimary alterations in BP modulation, through a persistently elevated afterload, can increase cardiac mass. Thus, the interrelationship between cardiac structure and BP modulation is complex. Hence, new and more specific methods of evaluating circadian changes in BP are needed to better clarify the abovementioned reciprocal influences.

• Childhood Kidney Diseases
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• v.27 no.2
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• pp.82-88
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• 2023

Chronic kidney disease (CKD) causes numerous changes that destabilize homeostasis, of which anemia is one of its important complications. Anemia significantly reduces the quality of life in children with CKD and plays a crucial role in the progression of cardiovascular disease such as left ventricular hypertrophy, a major cause of mortality in those with advanced CKD. The treatment of anemia is a pivotal factor in reducing morbidity and mortality rates in children with CKD, representing one of the methods for enhancing patients' quality of life.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.5
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• pp.413-421
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• 2001

An impaired smooth muscle cell (SMC) relaxation of coronary artery by alteration of $K^+$ channels would be the most potential explanation for reduced coronary reserve in left ventricular hypertrophy (LVH), however, this possibility has not been investigated. We performed morphometrical analysis of the coronary artery under electron microscopy and measured $Ca^{2+}-activated\;K\;(K_{Ca})$ currents and delayed rectifier K $(K_{dr})$ currents by whole-cell and inside-out patch-clamp technique in single coronary arterial SMCs from rabbits subjected to isoprenaline-induced cardiac hypertrophy. Coronary arterial SMCs underwent significant changes in ultrastructure. The unitary current amplitude and the open-state probability of $K_{Ca}$ channel were significantly reduced in hypertrophy without open-time and closed-time kinetic. The concentration-response curve of $K_{Ca}$ channel to $Ca^{2+}$ is shifted to the right in hypertrophy. The reduction in the mean single channel current and increase in the open channel noise of $K_{Ca}$ channel by TEA were more sensitive in hypertrophy. $K_{dr}$ current density is significantly reduced in hypertrophy without activation and inactivation kinetics. The sensitivity of $K_{dr}$ current on 4-AP is significantly increased in hypertrophy. This is the first study to report evidence for alterations of $K_{Ca}$ channels and $K_{dr}$ channels in coronary SMCs with LVH. The findings may provide some insight into mechanism of the reduced coronary reserve in LVH.

• Nutrition Research and Practice
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• v.6 no.4
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• pp.315-321
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• 2012

We tested the effects of dietary intake of freeze-dried Korean traditional fermented cabbage (generally known as kimchi) with varying amounts of sodium on blood pressure and cardiac hypertrophy in spontaneously hypertensive rats (SHRs). Wistar-Kyoto rats (WKY), as a control group, received a regular AIN-76 diet, and the SHRs were divided into four groups. The SHR group was fed a regular diet without kimchi supplementation, the SHR-L group was fed the regular diet supplemented with low sodium kimchi containing 1.4% salt by wet weight, which was provided in a freeze-dried form, the SHR-M group was supplemented with medium levels of sodium kimchi containing 2.4% salt, and the SHR-H group was supplemented with high sodium kimchi containing 3.0% salt. Blood pressure was measured over 6 weeks, and cardiac hypertrophy was examined by measuring heart and left ventricle weights and cardiac histology. SHRs showed higher blood pressure compared to that in WKY rats, which was further elevated by consuming high sodium containing kimchi but was not influenced by supplementing with low sodium kimchi. None of the SHR groups showed significant differences in cardiac and left ventricular mass or cardiomyocyte size. Levels of serum biochemical parameters, including blood urea nitrogen, creatinine, glutamic-oxaloacetic transaminase, glutamic-pyruvic transaminase, sodium, and potassium were not different among the groups. Elevations in serum levels of aldosterone in SHR rats decreased in the low sodium kimchi group. These results suggest that consuming low sodium kimchi may not adversely affect blood pressure and cardiac function even under a hypertensive condition.

• Journal of Veterinary Clinics
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• v.18 no.4
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• pp.452-454
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• 2001

A two-month-old female Yorkshire terrier was referred to the Veterinary Teaching Hospital, College of Veterinary Medicine, Kyungpook national University. The patient was presented with a history of dyspnea, cough, exercise intolerance and abdominal distension, but she was appetence. In physical examination the puppy was coughed on slight tracheal compression. Rectal temperature, pulse and respiratory rate were normal, and grade 3/6 systolic murmur heard at the left heart base. The murmur was crescendo-decrescendo. Electrocardiography showed sinus arrhythmia, right-ventricular hypertrophy pattern, and right axis deviation. Thoracic radiography revealed cardiomegaly, bulging of the main pulmonary artery, and enlarged left side heart. Abdominal radiography revealed abdkominal distention. Echocardiography showed hypertrophy of right ventricle and turbulence in the pulmonary artery in parasternal oblique view. Subvalvular pulmonic stenosis was diagnosis based upon the clinical signs, physical examination, electrocardiography, radiography and echocardiography. We treated the patient with furosemide, enalapril and $\beta$-blocker. After the clinical signs of cough, abdominal distension and dyspnea were disappeared, she was on just $\beta$-blocker for prevention of occurrence of congestive heart failure. Now she was recovered her health, and she is not on any medication.

• The Journal of the Korea Contents Association
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• v.16 no.2
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• pp.666-672
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• 2016

We extracted 50 LVH patients out of 30'~80's who performing ECG and echocardiography examination. We used Devereux's theory to examinate LVH with echocardiography and used Sokolow-Lyon's theory to examinate LVH with ECG. We used regression and correlation analysis by SPSS, used ROC curve analysis to decide predominance of two ways of .Age, BMI, SBP and DBP whice are the danger factors of LVH and standard value of LVH diagnosis examination seems correlated. Out of 50 LVH patients, 50 patients were diagnosed LVH by echcardiography examination and only 21 patients were diagnosed LVH by ECG examination. Also echocardiography was AUC 99%, sensitivity 96%, singularity 95%, accuracy 95.5%. And ECG was AUC 76%, sensitivity 62%, singularity 76%, accuracy 68%.By comparing accuracy between echocardiography and ECG in diagnosing LVH, we could tell echocardiography was examination with higher accuracy. Therefore, if one was diagnosed with summit on 1st examination with ECG, considering age, body mass index, systolic blood pressure and dilator blood pressure, should offer echocardiography examination.

• Journal of Yeungnam Medical Science
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• v.27 no.1
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• pp.52-56
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• 2010

Idiopathic peripartum cardiomyopathy is an uncommon malady disease. Making the diagnosis is often difficult and it is always necessary to exclude other prior heart disease and other causes of left ventricular dysfunction in pregnant women. Heart failure in these women ensues when the cardiovascular demands of normal pregnancy are further amplified when the common complications of pregnancy complications superimposed upon these underlying conditions that cause compensated ventricular hypertrophy. This may be aggravated by making a late diagnosis and providing inappropriate treatment. We experienced a 38-year-primigravida who has diagnosed with idiopathic peripartum cardiomyopathy and underwent elective cesarean section with general anesthesia.

• Biomolecules & Therapeutics
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• v.28 no.5
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• pp.482-489
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• 2020

G protein-coupled receptor kinase 5 (GRK5) has been considered as a potential target for the treatment of heart failure as it has been reported to be an important regulator of pathological cardiac hypertrophy. To discover novel scaffolds that selectively inhibit GRK5, we have identified a novel small molecule inhibitor of GRK5, KR-39038 [7-((3-((4-((3-aminopropyl)amino)butyl)amino)propyl)amino)-2-(2-chlorophenyl)-6-fluoroquinazolin-4(3H)-one]. KR-39038 exhibited potent inhibitory activity (IC₅₀ value=0.02 µM) against GRK5 and significantly inhibited angiotensin II-induced cellular hypertrophy and HDAC5 phosphorylation in neonatal cardiomyocytes. In the pressure overload-induced cardiac hypertrophy mouse model, the daily oral administration of KR-39038 (30 mg/kg) for 14 days showed a 43% reduction in the left ventricular weight. Besides, KR-39038 treatment (10 and 30 mg/kg/day, p.o.) showed significant preservation of cardiac function and attenuation of myocardial remodeling in a rat model of chronic heart failure following coronary artery ligation. These results suggest that potent GRK5 inhibitor could effectively attenuate both cardiac hypertrophy and dysfunction in experimental heart failure, and KR-39038 may be useful as an effective GRK5 inhibitor for pharmaceutical applications.

• Journal of Chest Surgery
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• v.20 no.2
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• pp.404-410
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• 1987

An 18-day-old male neonate with hypoplastic left heart syndrome underwent surgical intervention by modification of the Norwood procedure on September 23, 1986. Hypoplastic left heart syndrome is a serious congenital cardiac anomaly that has a fatal outlook if left untreated. Included in this anomaly are [1] aortic valve atresia, and hypoplasia of the ascending aorta and aortic arch, [1] mitral valve atresia or hypoplasia, and [3] diminutive or absent left ventricle. Patent ductus arteriosus is essential for any survival, and there is usually a patent foramen ovale. Coarctation of the aorta is frequently associated with the lesion.z With a limited period of cardiopulmonary bypass, deep hypothermia, and circulatory arrest, the ductus arteriosus was excised. The main pulmonary artery was divided immediately below its branches, and the distal stump of the divided pulmonary artery was closed with a pericardial patch. The aortic arch was incised, and a 1 5mm tubular Dacron prosthesis was inserted between the main pulmonary artery and the aortic arch. A 4mm shunt of polytetrafluoroethylene graft was established between the new ascending aorta and the right pulmonary artery to provide controlled pulmonary blood flow. Following rewarming, the heart started to beat regularly, but the patient could not be weaned from cardiopulmonary bypass. At autopsy, the patient was found to have hypoplasia of the aortic tract complex with mitral atresia and aortic atresia. A secundum atrial septal defect was noted. Right atrial and ventricular hypertrophy was present, and the left ventricle was entirely absent. Although unsuccessful in this case report, continuing experience with hypoplastic left heart syndrome will lead to an improvement in result.

• Journal of Chest Surgery
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• v.12 no.3
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• pp.281-288
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• 1979

For years, physicians and anatomists have been interested in the heart that has one functioning ventricle. Various terms have been suggested for this entity including single ventricle, common ventricle, double-inlet left ventricle, cor biatriatum triloculare, and primitive ventricle. In this report, the term "single ventricle" is utilized as suggested by Van Praagh, and is defined as that congenital cardiac anomaly in which a common or separate atrioventricular valves open into a ventricular chamber from which both great arterial trunks emerge. An outlet chamber, or infundibulum, may or may not be present and give rise to the origin of either of the great arteries. This definition excludes the entity of mitral and tricuspid atresia. An 11 year old cyanotic boy was admitted chief complaints of exertional dyspnea and frequent upper respiratory infection since 2 weeks after birth. He was diagnosed as inoperable cyanotic congenital heart disease, and remained without any corrective treatment up to his age of 11 year when he suffered from aggravation of symptoms and signs of congestive heart failure for 2 months before this admission. On 22nd of May 1979, he was admitted for total corrective operation under the impression of tricuspid atresia suggested by a pediatrician. Physical check revealed deep cyanosis with finger and toe clubbing, and grade V systolic ejection murmur with single second heart sound was audible at the left 3rd intercostal space. Development was moderate in height [135 cm] and weight[28Kg]. Routine lab findings were normal except increased hemoglobin [21.1gm%], hematocrit [64 %], and left axis deviation with left ventricular hypertrophy on EKG. Cardiac catheterization and angiography revealed 1-transposition of aorta, pulmonic valvular stenosis, double inlet of a single ventricle with d-loop, and normal atriovisceral relationship [Type III C solitus according to the classification of Van Praagh]. At operation, longitudinal incision at the outflow tract of right ventricle in between the right coronary artery and its branch [LAD from RCA] revealed high far anterior aortic valve which had fibrous continuity with mitral annulus, and pulmonic valve was stenotic up to 4 mm in diameter positioned posterolaterally to the aorta. Ventricular septum was totally defective, and one markedly hypertrophied moderator band originated from crista supraventricularis was connected down to the imaginary septum of the ventricular cavity as a pseudoseptum of the ventricle. Size of the defect was 3X3 cm2 in total. Patch closure of the defect with a Teflon felt of 3.5 x 4 cm2 was done with interrupted multiple sutures after cut off of the moderator band, which was resutured to the artificial septum after reconstruction of the ventricular septum. Pulmonic valvotomy was done from 4 mm to 11 mm in diameter thru another pulmonary arteriotomy incision, and right ventriculotomy wound was closed reconstructing the right ventricular outflow tract with pericardial autograft of 3 x 4 cm2. Atrial septal defect of 2 cm in diameter was closed with 3-0 Erdeck suture, and atrial wall was sutured also when rectal temperature reached from 24`C to 35.5`C. Complete A-V block was managed with temporary external pacemaker with a pacing rate of 110/min. thru myocardial wire, and arterial blood pressure of 80/50 mmHg was maintained with Isuprel or Dopamine dripping under the CVP of 25-cm saline. Consciousness was recovered one hour after the operation when his blood pressure reached 100 /70 mmHg, but vital signs were not stable, and bleeding from the pericardial drainage and complete anuria were persisted until his heart could not capture the pacemaker impulse, and patient died of low output syndrome 320 min after the operation.