• 대한핵의학회지
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• 제38권5호
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• pp.331-337
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• 2004

Cardiac neurotransmission imaging allows in vivo assessment of presynaptic reuptake, neurotransmitter storage and postsynaptic receptors. Among the various neurotransmitter, I-123 MIBG is most available and relatively well-established. Metaiodobenzylguanidine (MIBG) is an analogue of the false neurotransmitter guanethidine. It is taken up to adrenergic neurons by uptake-1 mechanism as same as norepinephrine. As tagged with I-123, it can be used to image sympathetic function in various organs including heart with planar or SPECT techniques. I-123 MIBG imaging has a unique advantage to evaluate myocardial neuronal activity in which the heart has no significant structural abnormality or even no functional derangement measured with other conventional examination. In patients with cardiomyopathy and heart failure, this imaging has most sensitive technique to predict prognosis and treatment response of betablocker or ACE inhibitor. In diabetic patients, it allow very early detection of autonomic neuropathy. In patients with dangerous arrhythmia such as ventricular tachycardia or fibrillation, MIBG imaging may be only an abnormal result among various exams. In patients with ischemic heart disease, sympathetic derangement may be used as the method of risk stratification. In heart transplanted patients, sympathetic reinnervation is well evaluated. Adriamycin-induced cardiotoxicity is detected earlier than ventricular dysfunction with sympathetic dysfunction. Neurodegenerative disorder such as Parkinson's disease or dementia with Lewy bodies has also cardiac sympathetic dysfunction. Noninvasive assessment of cardiac sympathetic nerve activity with I-123 MIBG imaging nay be improve understanding of the pathophysiology of cardiac disease and make a contribution to predict survival and therapy efficacy.

• The Korean Journal of Physiology and Pharmacology
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• 제28권2호
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• pp.129-143
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• 2024

Sulfur dioxide (SO₂), a novel endogenous gas signaling molecule, is involved in the regulation of cardiac function. Exerting a key role in progression of hyperthyroidism-induced cardiomyopathy (HTC), myocardial fibrosis is mainly caused by myocardial apoptosis, leading to poor treatment outcomes and prognoses. This study aimed to investigate the effect of SO₂ on the hyperthyroidism-induced myocardial fibrosis and the underlying regulatory mechanisms. Elisa, Masson staining, Western-Blot, transmission electron microscope, and immunofluorescence were employed to evaluate the myocardial interstitial collagen deposition, endoplasmic reticulum stress (ERS), apoptosis, changes in endogenous SO₂, and Hippo pathways from in vitro and in vivo experiments. The study results indicated that the hyperthyroidism-induced myocardial fibrosis was accompanied by decreased cardiac function, and down-regulated ERS, apoptosis, and endogenous SO₂-producing enzyme aspartate aminotransferase (AAT)1/2 in cardiac myocytes. In contrast, exogenous SO₂ donors improved cardiac function, reduced myocardial interstitial collagen deposition, up-regulated AAT1/2, antagonized ERS and apoptosis, and inhibited excessive activation of Hippo pathway in hyperthyroid rats. In conclusion, the results herein suggested that SO₂ inhibited the overactivation of the Hippo pathway, antagonized ERS and apoptosis, and alleviated myocardial fibrosis in hyperthyroid rats. Therefore, this study was expected to identify intervention targets and new strategies for prevention and treatment of HTC.

• Korean Journal of Radiology
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• 제21권4호
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• pp.450-461
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• 2020

Objective: We performed a meta-analysis to evaluate the agreement of cardiac computed tomography (CT) with cardiac magnetic resonance imaging (CMRI) in the assessment of right ventricle (RV) volume and functional parameters. Materials and Methods: PubMed, EMBASE, and Cochrane library were systematically searched for studies that compared CT with CMRI as the reference standard for measurement of the following RV parameters: end-diastolic volume (EDV), end-systolic volume (ESV), stroke volume (SV), or ejection fraction (EF). Meta-analytic methods were utilized to determine the pooled weighted bias, limits of agreement (LOA), and correlation coefficient (r) between CT and CMRI. Heterogeneity was also assessed. Subgroup analyses were performed based on the probable factors affecting measurement of RV volume: CT contrast protocol, number of CT slices, CT reconstruction interval, CT volumetry, and segmentation methods. Results: A total of 766 patients from 20 studies were included. Pooled bias and LOA were 3.1 mL (-5.7 to 11.8 mL), 3.6 mL (-4.0 to 11.2 mL), -0.4 mL (5.7 to 5.0 mL), and -1.8% (-5.7 to 2.2%) for EDV, ESV, SV, and EF, respectively. Pooled correlation coefficients were very strong for the RV parameters (r = 0.87-0.93). Heterogeneity was observed in the studies (I² > 50%, p < 0.1). In the subgroup analysis, an RV-dedicated contrast protocol, ≥ 64 CT slices, CT volumetry with the Simpson's method, and inclusion of the papillary muscle and trabeculation had a lower pooled bias and narrower LOA. Conclusion: Cardiac CT accurately measures RV volume and function, with an acceptable range of bias and LOA and strong correlation with CMRI findings. The RV-dedicated CT contrast protocol, ≥ 64 CT slices, and use of the same CT volumetry method as CMRI can improve agreement with CMRI.

• Journal of Chest Surgery
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• 제48권1호
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• pp.67-69
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• 2015

This is a report of a biatrial cardiac myxoma in a young man with a 10-month history of exertional dyspnea and palpitation. The echocardiogram revealed biatrial myxoma prolapsing through the mitral and tricuspid valves during diastole. All cardiac chambers were enlarged and dysfunctional. The electrocardiogram revealed a rapid ventricular response with atrial flutter rhythm. The masses were resected and diagnosed as myxoma by a histological examination. The follow-up echocardiogram revealed significant improvement in ventricular function and reduction in the cardiac chambers' volume. There was no evidence of myxoma recurrence. The most probable cause of the patient's heart failure was considered to be tachycardia-induced cardiomyopathy.

• Journal of Yeungnam Medical Science
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• 제22권2호
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• pp.131-140
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• 2005

Heart failure is a clinical syndrome comprised of a number of symptoms and signs associated with congestion and/or hypoperfusion. Specific pharmacologic therapies have been developed to slow disease progression from early to more advanced stages. Once symptoms have developed, aggressive multimodality interventions are instituted to alleviate symptoms and improve clinical status and quality of life; especially in those patients that present symptoms. Recently, an evolving adjunctive therapeutic modality, that involves using implanted electrical devices: cardiac resynchronization with or without implantable cardioverter defibrillators (ICD). has been used for management. Cardiac resynchronization therapy (CRT) is a proven treatment for selected patients with heart failure-induced conduction disturbances and ventricular dyssynchrony. When used in combination with stable, optimal medical therapy, CRT is designed to reduce symptoms and improve cardiac function by restoring the mechanical sequence of ventricular activation and contraction. This review summarizes the rationale, procedure, clinical trials, and clinical indications for CRT.

• 한국패류학회지
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• 제25권1호
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• pp.15-22
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• 2009

Because it is known that bivalve hearts contain various modulatory systems activated by neuroendocrine substances, it was examined whether different classes of endogenous and synthetic drugs of neuroendocrinological importance can influence cardiac functions of the Pacific oyster Crassostrea gigas. Cholinergically active agents acetylcholine and carbachol increased heart rates while diminishing cardiac contractility. Adrenergically active substances norepinephrine (NE) and epinephrine (Epi) also induced heart rate increase and contractility decrease. An $\alpha_1$-adrenergic receptor-selective agonist phenyephrine (PE) failed to modulate either parameter. The Epi-induced heart rate increase and contractile depression were both blocked significantly by non-selective $\beta_1/\beta_2$-adrenergic antagonist propranolol. A $\beta_1$-selective antagonist atenolol prevented Epi-induced heart rate decrease but not the contractile depression, suggesting possible $\beta_2$ receptors for Epi-induced contractile depression. The three autacoids examined exerted discrete responses: histamine increased heart rate and depressed contraction; $\gamma$-amino-butyric acid increased both parameters; serotonin failed to change either parameter. The 5 piscine anesthetic agents examined, MS-222, benzocaine, quinaldine, urethane, pantocaine and pentobarbital, all failed to influence the cardiac function of oysters. Collectively, activities of neuroendocrinologically acting agents in mammals showed unexpected and distinct activities from those in mammalian cardiovascular systems. These results obtained from substances of different physiological functions can serve as a basis for understanding neuroendocrine control of the heart function in Pacific oyster.

• 한국산학기술학회논문지
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• 제14권7호
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• pp.3319-3325
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• 2013

본 논문에서는 일상생활에서 생활 의학의 한 방편으로 사용되고 있는 수지침이 실제 인체장기에 어떤 영향을 미치는지에 대해 IT 기술을 적용하여 이를 규명하는 연구를 행하고자 한다. 이를 위해 우선적으로 수지침 요법을 기반으로 인체에 있어 가장 중요한 장기인 심장을 대상으로 심장과 관련된 손 반사점인 A16 혈자리를 5분간 자극하여 전과 후의 얼굴 영상을 수집하고 Lab 색체계를 적용하여 심장과 연관된 이마와 입술 영역에 대한 색상 측정을 통해 상호간의 비교, 분석을 수행하였다. 최종적으로 생체 영상신호의 변화량 측정에 의해 A16 혈자리 자극으로 심장기능에 미치는 효과를 규명하는 연구를 수행하였으며 실험 결과 자료들에 대해 유의성 분석을 통해 실험 결과 자료가 유효한 결과 자료인지 여부에 대한 규명을 행하고자 한다.

• 한국정보통신학회논문지
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• 제17권4호
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• pp.959-964
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• 2013

본 논문에서는 스완-간즈 카테터(Swan-Ganz catheter)를 사용하여 심장질환 중환자의 상태를 정확하게 파악하기 위해 기존의 모듈들보다 더 정밀한 데이터 측정이 가능한 모듈을 구현한다. 기존 방식은 차가운 수액을 심장에 주입하여 혈액의 온도변화와 회복시간을 측정하는 CO(Cardiac Output)를 측정하던 Bolus타입의 CO모듈이 존재하였지만, 지속적 환자 징후 관찰이 어렵다는 한계 때문에 현재는 대부분의 병원에서 사용하지 않는 상태이다. 이러한 한계를 극복하기 위해 지속적 심박출량 측정 플랫폼을 통해 효율적인 환자 징후관찰 및 상태파악이 가능 하도록 한다. 또한, 현재 기존 병원에서 심폐기능 이상 중환자의 징후관찰 및 상태파악을 위해 고가의 해외기기 도입으로 낭비되는 비용 문제를 해결하고 정밀한 데이터 수집으로 정확한 환자의 진단이 이루어 질 수 있도록 기존 모듈들의 문제점을 보완하였다.

• Biomolecules & Therapeutics
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• 제28권5호
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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 Ginseng Research
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• 제45권6호
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• pp.683-694
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• 2021

Background: Ginsenoside Rg1 (Rg1) has been well documented to be effective against various cardiovascular disease. The aim of this study is to evaluate the effect of Rg1 on mechanical stress-induced cardiac injury and its possible mechanism with a focus on the calcium sensing receptor (CaSR) signaling pathway. Methods: Mechanical stress was implemented on rats through abdominal aortic constriction (AAC) procedure and on cardiomyocytes and cardiac fibroblasts by mechanical stretching with Bioflex Collagen I plates. The effects of Rg1 on cell hypertrophy, fibrosis, cardiac function, [Ca²⁺]_i, and the expression of CaSR and calcineurin (CaN) were assayed both on rat and cellular level. Results: Rg1 alleviated cardiac hypertrophy and fibrosis, and improved cardiac decompensation induced by AAC in rat myocardial tissue and cultured cardiomyocytes and cardiac fibroblasts. Importantly, Rg1 treatment inhibited CaSR expression and increase of [Ca²⁺]_i, which similar to the CaSR inhibitor NPS2143. In addition, Rg1 treatment inhibited CaN and TGF-b1 pathways activation. Mechanistic analysis showed that the CaSR agonist GdCl₃ could not further increase the [Ca²⁺]_i and CaN pathway related protein expression induced by mechanical stretching in cultured cardiomyocytes. CsA, an inhibitor of CaN, inhibited cardiac hypertrophy, cardiac fibrosis, [Ca²⁺]_i and CaN signaling but had no effect on CaSR expression. Conclusion: The activation of CaN pathway and the increase of [Ca²⁺]_i mediated by CaSR are involved in cardiac hypertrophy and fibrosis, that may be the target of cardioprotection of Rg1 against myocardial injury.