• Journal of Chest Surgery
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• v.20 no.2
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• pp.241-250
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• 1987

We scrutinized the preoperative electrocardiographic and hemodynamic findings in adult atrial septal defects older than 15 years, and then followed up the postoperative electrocardiographic changes sequentially. In preoperative electrocardiographs, the mean PR interval [0.17 sec] was prolonged than normal adults [M;0.13,F;0.15], and the mean QRS axis [93.1*] was deviated to rightward than normal [M;63.7*,F;64.4*], and 122 cases of all 159 patients [77.8%] were in RAD quadrant. The QRS morphology was classified into three groups; a] crista supraventricularis hypertrophy, 25 cases, b] right ventricular outflow tract hypertrophy, 89 cases, c] right ventricular hypertrophy, 44 cases, and normal rs pattern, 1 case. Comparing the QP/QS, Pp/Ps, Rp/Rs in these three groups, Qp/Qs increased a] 2.65 to b] 2.97 and decreased b] 2.97 to c] 2.55, Pp/Ps increased a] 0.27 to b] 0.35 to c] 0.44, and Rp/Rs increased a] 0.1 to b] 0.14 to c] 0.2. In comparing the atrial fibrillation with sinus rhythm, the patient`s mean age was increased [26.4 to 45.7], the mean Qp/Qs was decreased [2.97 to 2.7], the mean Pp/Ps was increased [0.35 to 0.46], the mean Rp/Rs increased [0.14 to 0.2], and the QRS morphology was RVOT hypertrophy;7 cases, RVH;2 cases in all 11 cases. Therefore, the atrial fibrillation was appeared in progressed status. Increasing the mean pulmonary arterial pressure, size of the R` wave in Vl lead increased, and the QRS morphology tended to become severe patterns. Postoperatively, the PR interval shortened and QRS axis tended to normal axis quadrant, and size of R` wave decreased sequentially, atrial fibrillation disappeared in 4 cases. Conclusively, by use of the conventional surface electrocardiography, we could anticipate the hemodynamic changes and the prognosis at outpatient department.

• Childhood Kidney Diseases
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• v.15 no.1
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• pp.14-21
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• 2011

Although left Left ventricular hypertrophy (LVH) is not only an adaptive response of the heart to increased cardiac workload in hypertension, it surelybut also is the most potent risk factor of overt cardiovascular complications such as coronary heart disease, heart failure, arrhythmia and stroke in the hypertensive population. Also it has become generally accepted that subclinical cardiovascular disease begins in childhood and LVH is the most readily assessed marker for that. As LVH can be seen in children and adolescents with even mild blood pressure elevation with the reported prevalence of 10 to 47%, aggressive antihypertensive treatment is critical in preventing the development of hypertensive heart disease in that those cases.

• 한국생물공학회:학술대회논문집
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• 2005.10a
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• pp.880-880
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• 2005

• Journal of Cardiovascular Imaging
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• v.31 no.1
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• pp.41-48
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• 2023

BACKGROUND: The function of left atrium (LA) is difficult to assess because of its ventricle-dependent, dynamic movement. The aim of this study was to assess LA function using velocity vector imaging (VVI) and compare LA function in patients with hypertrophic cardiomyopathy (HCMP) and left ventricular hypertrophy (LVH) with normal controls. METHODS: Fourteen patients with HCMP (72% male, mean age of 52.6 ± 9.8), 15 hypertensive patients with LVH (88% male, mean age of 54.0 ± 15.3), and 10 age-matched controls (83% male, mean age of 50.0 ± 4.6) were prospectively studied. Echocardiographic images of the LA were analyzed with VVI, and strain rate (SR) was compared among the 3 groups. RESULTS: The e' velocity (7.7 ± 1.1; 5.1 ± 0.8; 4.5 ± 1.3 cm/sec, p = 0.013), E/e' (6.8 ± 1.6; 12.4 ± 3.3; 14.7 ± 4.2, p = 0.035), and late diastolic SR at mid LA (-1.65 ± 0.51; -0.97 ± 0.55; -0.82 ± 0.32, p = 0.002) were significantly different among the groups (normal; LVH; HCMP, respectively). The e' velocity, E/e', and late diastolic SR at mid LA were significantly different between normal and LVH (p = 0.001; 0.022; 0.018), whereas LA size was similar between normal and LVH (p = 0.592). The mean late diastolic peak SR of mid LA was significantly correlated with indices of diastolic function (E/e', e', and LA size). CONCLUSIONS: The SR is a useful tool for detailed evaluation of LA function, especially early dysfunction of LA in groups with normal LA size.

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.3
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• pp.203-210
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• 2015

AMP-activated protein kinase (AMPK) is a key regulator of energy metabolism. Previous studies have shown that activation of AMPK results in suppression of cardiac myocyte hypertrophy via inhibition of the p70S6 kinase (p70S6K) and eukaryotic elongation factor-2 (eEF2) signaling pathways. Epigallocatechin-3-gallate (EGCG), the major polyphenol found in green tea, possesses multiple protective effects on the cardiovascular system including cardiac hypertrophy. However, the molecular mechanisms has not been well investigated. In this study, we found that EGCG could significantly reduce natriuretic peptides type A (Nppa), brain natriuretic polypeptide (BNP) mRNA expression and decrease cell surface area in H9C2 cardiomyocytes stimulated with phenylephrine (PE). Moreover, we showed that AMPK is activated in H9C2 cardiomyocytes by EGCG, and AMPK-dependent pathway participates in the inhibitory effects of EGCG on cardiac hypertrophy. Taken together, our findings provide the first evidence that the effect of EGCG against cardiac hypertrophy may be attributed to its activation on AMPK-dependent signaling pathway, suggesting the therapeutic potential of EGCG on the prevention of cardiac remodeling in patients with pressure overload hypertrophy.

• Journal of Cardiovascular Imaging
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• v.26 no.4
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• pp.214-216
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• 2018

• Korean Circulation Journal
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• v.54 no.4
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• pp.187-188
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• 2024

• Journal of Chest Surgery
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• v.19 no.1
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• pp.1-11
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• 1986

Using an experimental model of pulmonary hypertension, the effects of anticonstrictive drugs on the development of pulmonary vascular remodeling and right ventricular hypertrophy were studied. Male Sprague-Dawley rats weighing 200~250 gm were used. For the experimental model of pulmonary hypertension, a group of animal was given by a subcutaneous injection of monocrotaline on a dose of 20mg, 40mg, or 60mg per kg of body weight. After 4 weeks of injection, all animals were sacrificed. Another group of animal was given by a subcutaneous injection of monocrotaline in a dose of 40 mg per kg of body weight. The animals were sacrificed, in which they were kept alive for 1, 2, 3 and 4 weeks, respectively. For the effects of anticonstrictive drugs on the development of pulmonary vascular remodeling and right ventricular hypertrophy, the animals treated with monocrotaline were given daily by an intraperitoneal injection of phenoxybenzamine in a dose of 1.3mg/kg of body weight, and were given propranolol via their drinking water at a concentration of 400mg/liter. The animals were sacrificed after 4 weeks of administration. The hearts and lungs were examined histopathologically and morphometrically. The results obtained were summarized as follows: 1. The rats treated with monocrotaline showed an interstitial pneumonitis, medial thickening of the pulmonary small arteries and hypertrophy of the right ventricular wall. 2. The medial thickening of the pulmonary arteries in rats treated with monocrotaline was due to muscular hypertrophy and hyperplasia, and the right ventricular hypertrophy was due to hypertrophy of cardiac muscles. Both medial thickening of the pulmonary arteries and hypertrophy of right ventricular wall were more marked with time and with dose. 3. The daily intraperitoneal injection of phenoxybenzamine suppressed significantly the percentage medial thickness of pulmonary small arteries and the index of right ventricular hypertrophy in rats given a single subcutaneous injection of monocrotaline, but propranolol has shown no protective effect on the development of medial thickening of pulmonary arteries and right ventricular hypertrophy in treated with monocrotaline. The results described above suggested that monocrotaline is an alkaloid selectively inducing pulmonary hypertension and that a-adrenergic receptor is responsible for the pathogenesis of monocrotaline induced pulmonary hypertension in rat.

• Reproductive and Developmental Biology
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• v.35 no.2
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• pp.159-165
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• 2011

To explore the role of histone deactylase (HDAC) activation in an in vivo model of hypertrophy, we studied the effects of Trichostatin A (TSA). TSA subjected to thoracic aortic banding (TAB)-induced pressure stress in mice. In histological observations, TAB in treated mice showed a significant hypertrophic response, whereas the sham operation remained nearly normal structure with partially blunted hypertrophy. TSA treatment had no effect (measured as HW/BW) on sham-operated animals. TAB animals treated with vehicle manifested a robust ~50% hypertrophic response (p<0.05 vs sham). TAB mice treated with 2 mg/kg/day TSA manifested a blunted growth responses, which was significantly diminished (p<0.05) compared with vehicle-treated TAB mice. TAB mice treated with a lower dose of TSA (0.5 mg/kg/day) manifested a similar blunting of hypertrophic growth (~25% increase in heart mass). Furthermore, to determine activity duration of TSA in vitro, 1 nM TSA was added to H9c2 cells. Histone acetylation was initiated at 4 hr after treatment, and it was peak up to 18 hr, then followed by significantly reduced to 30 hr. We also analyzed the expression of p53 following TSA treatment, wherein p53 expression was elevated at 4 hr, and it was maintained to 24 hr after treatment. ERK was activated at 8 hr, and maintained till 30 hr after treatment suggesting an intracellular signaling interaction between TSA and p53 expression Taken together, it is suggested that HDAC activation is required for pressure-overload growth of the heart. Eventually, these data suggest that histone acetylation may be a novel target for therapeutic intervention in pressure-overloaded cardiac hypertrophy.

• Korean Journal of Veterinary Research
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• v.45 no.4
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• pp.537-544
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• 2005

We have examined distribution and expression of caveolin-3 (cav-3), one of three caveolin isoforms from 16-wks-old spontaneously hypertensive rats (SHR) compared with age-matched control wistar-kyoto (WKY) rats. The expression of cav-3 was increased, whereas expression of PKB/Akt and calcineurin (Cn) was not changed in cardiac tissues of SHR compared to WKY rats. Interestingly, expression of cav-3, PKB/Akt and Cn were decreased in plasma membrane fraction in SHR compared to WKY rats. In H9c2 cardiomyoblast cells treated with phenylephrine ($50{\mu}M$, 48hr) or isoproterenol ($10{\mu}M$, 48hr), the expression of cav-3 was markedly enhanced compared to nontreated cells. Upon immunofluorescence analysis, cav-3 was localized in plasma membrane of control H9c2 cells. However phenylephrine or isoproterenol treatment caused translocation of cav-3 to perinuclear region. These results suggest that cav-3 plays as positive regulators in the development of hypertrophy in cardiac tissues of SHR rats.