• Journal of Chest Surgery
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• v.41 no.1
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• pp.95-97
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• 2008

Ischemic ventricular rupture is one of the most fatal complications following myocardial infarction, and this requires prompt diagnosis and operation. A 75-year-old female was admitted to the ER in a semicomatous mentality with cyanotic extremities. Cardiac echography was carried out in the ER, and a $1.5{\sim}2\;cm$ thickness of effusion in the pericardium was seen. Because the patient's heart had declined to 35 times per min, an emergency operation was started while giving cardiac massage. After observing a 1 cm rupture on the right ventricular wall and a necrotic hemorrhagic scar with a rupture on the left ventricular apical wall, repair of the ruptured areas with a large Satinsky clamp was carried out to control bleeding without cardiopulmonary bypass. On the 28th day after surgery, she was discharged home with a minimal degree of dyspnea.

• Journal of Chest Surgery
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• v.44 no.2
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• pp.108-114
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• 2011

Background: Homograft cardiac valves and valved-conduits have been available in our institute since 1992. We sought to determine the long-term outcome after right ventricular outflow tract (RVOT) reconstruction using homografts, and risk factors for reoperation were analyzed. Materials and Methods: We retrospectively reviewed 112 patients who had undergone repair using 116 homografts between 1992 and 2008. Median age and body weight at operation were 31.2 months and 12.2 kg, respectively. The diagnoses were pulmonary atresia or stenosis with ventricular septal defect (n=93), congenital aortic valve diseases (n=15), and truncus arteriosus (N=8). Mean follow-up duration was $79.2{\pm}14.8$ months. Results: There were 10 early and 4 late deaths. Overall survival rate was 89.6%, 88.7%, 86.1% at postoperative 1 year, 5 years and 10 years, respectively. Body weight at operation, cardiopulmonary bypass (CPB) time and aortic cross-clamping (ACC) time were identified as risk factors for death. Forty-three reoperations were performed in thirty-nine patients. Freedom from reoperation was 97.0%, 77.8%, 35.0% at postoperative 1 year, 5 years and 10 years respectively. Small-sized graft was identified as a risk factor for reoperation. Conclusion: Although long-term survival after RVOT reconstruction with homografts was excellent, freedom from reoperation was unsatisfactory, especially in patients who had small grafts upon initial repair. Thus, alternative surgical strategies not using small grafts may need to be considered in this subset.

• Journal of Biomedical Engineering Research
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• v.23 no.1
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• pp.33-38
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• 2002

A Ventricular Assist Device(YAD) is used to support the injured natural heart So. when considering a control algorithm for YAD. it is important to reduce a natural heart's load to enhance its recovery condition. To reduce natural heart's load, a counterpulsation algorithm is used commonly. In this study, we developed a counterpulsation control algorithm for moving-actuator type VAD and tested its usefulness using in vitro MOCK circulatory system. To notice a natural heart's Pumping status, electrocardiogram(ECG) signal was used and as a result of test. the counterpulsation effect between YAD and a natural heart was occurred and Automatic Control Mode Transition was occurred properly.

• Journal of Chest Surgery
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• v.36 no.5
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• pp.363-366
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• 2003

Background: Left ventricular rupture after acute myocardial infarction is a serious complication with high mortality. Emergency operation is usually the only available treatment. A 76-year-old female with persistent chest pain and syncopal attacks was admitted. Transthoracic echocardiography showed the pericardial effusion and generalized hypokinesia of the inferolateral wall of left ventricle. Coronary angiography revealed a total occlusion of the first diagonal branch. After percutaneous transluminal coronary angioplasty with coronary stent and insertion of intraaortic balloon pump, emergency operation was performed. Under cardiopulmonary bypass and cardiac arrest with cold blood cardioplegia, coronary artery bypass graft with saphenous vein, pericardial patch covering on the rupture area with 6-0 polypropylene running sutures, and fibrin glue compression under the patch were performed. We present a case of left ventricular (free wall) rupture after acute myocardial infarction.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.6
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• pp.487-494
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• 2001

During depolarization, extrusion of $Ca^{2+}$ from sarcoplasmic reticulum through forward-mode $Na^+-Ca^{2+}$ exchange was studied in the rat ventricular myocytes patch-clamped in whole-cell configuration. In order to confine the $Ca^{2+}$ responses in a micro-domain by limiting the $Ca^{2+}$ diffusion time, rat ventricular myocytes were dialyzed with high (14 mM) EGTA. $K^+$ current was suppressed by substituting KCl with 105 mM CsCl and 20 mM TEA in the pipette filling solution and by omitting KCl in the external Tyrode solution. $Cl^-$ current was suppressed by adding 0.1 mM DIDS in the external Tyrode solution. During stimulation roughly mimicking action potential, the initial outward current was converted into inward current, $47{\pm}1%$ of which was suppressed by 0.1 mM $CdCl_2.$ 10 mM caffeine increased the remaining inward current after $CdCl_2$ in a cAMP-dependent manner. This caffeine-induced inward current was blocked by $1\;{\mu}M$ ryanodine, $10\;{\mu}M$ thapsigargin, 5 mM $NiCl_2,$ or by $Na^+\;and\;Ca^{2+}$ omission, but not by $0.1\;{\mu}M$ isoproterenol. The $I{\sim}V$ relationship of the caffeine-induced current elicited inward current from -45 mV to +3 mV with the peak at -25 mV. Taken together, it is concluded that, during activation of the rat ventricular myocyte, forward-mode $Na^+-Ca^{2+}$ exchange extrudes a fraction of $Ca^{2+}$ released from sarcoplasmic reticulum mainly by voltage-sensitive release mechanism in a micro-domain in the t-tubule, which is functionally separable from global $Ca^{2+}{_i}$ by EGTA.

• Journal of Yeungnam Medical Science
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• v.2 no.1
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• pp.241-247
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• 1985

Bacterial endocarditis has been well recognized as an important complication of congenital heart disease, such as ventricular septal defect, patent ductus arteriosus or pulmonary stenosis. The incidence of right sided bacterial endocarditis is lesser than left sided bacterial endocarditis. Also, pulmonic valve vegetation has been thought to be relatively uncommon. And pulmonary embolism is common in the patients with right sided bacterial endocarditis. So in a patient with fever and evidence of recurrent pulmonary infarction, changing heart murmurs and scattered pneumonic infiltrates, one should direct attention to the heart as a possible source of the infection. Echocardiography with M-mode, 2-D and Doppler mode represents the only noninvasive technic available for detecting vegetations in bacterial endocarditis. In fact, the technic is more sensitive in identifying these lesions than angiography. We experienced a case of ventricular septal defect with bacterial endocarditis, pulmonic valve vegetation and multiple pulmonary embolism diagnosed with Echocardiogram and lung scan, and confirmed by operation. Patch repair of ventricular septal defect, resection of pulmonic valve and vegetation and artificial valve formation with pericardium were done.

• Biomolecules & Therapeutics
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• v.2 no.2
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• pp.114-119
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• 1994

[$^3$H]Ouabain binding parameters ( $K_{D}$ and $B_{max}$) to control rat ventricular strips and Langendorff preparations which were not previously exposed to ouabain were compared with those to both preparations that had been first exposed to a complete ouabain dose range of dose-response curve (10$^{-8}$ to 10$^{4}$M). In rat ventricular strips and Langendorff perfused heart preparations, cumulative dose-response curves of ouabain revealed biphasic positive inotropic effects, a "low-dose" effect and a "high-dose" effect with E $d_{50}$ values of 0.5 $\mu$M and 35 $\mu$M ouabain, respectively. The "low-dose" effect in ventricular strip disappeared or was diminished significantly when the ouabain dose-response curve was repeated after the washout of the effects of the first dose-response curve, whereas there were no significant differences in the maximal "high-dose"effect in both exposures to oubain. However, both of the control and ouabain-preexposed Langendorff perfused hearts revealed the same low-dose effects. The $K_{D}$ value for [$^3$H] ouabain binding and the ouabain binding site concentration ( $B_{max}$) estimated by [$^3$H]ouabain displacement assay in control preparations were 230 nM and 2 pmol/mg protein, respectively. [$^3$H]Ouabain binding parameters were not changed by repeated exposure to high concentrations of ouabain. These results suggest that digitalis receptor desensitization in the rat ventricular strip may due to the change of post-receptor events induced by ouabain binding to a high affinity site ($\alpha$$_2$isoform).).).).).

• Biomolecules & Therapeutics
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• v.20 no.4
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• pp.386-392
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• 2012

The endothelin (ET) signaling pathway controls many physiological processes in myocardium and often becomes upregulated in heart diseases. The aim of the present study was to investigate the effects of ET receptor upregulation on the contractile function of adult ventricular myocytes. Primary cultured adult rat ventricular myocytes were used as a model system of ET receptor overexpression in the heart. Endothelin receptor type A ($ET_A$) or type B ($ET_B$) was overexpressed by Adenoviral infection, and the twitch responses of infected ventricular myocytes were measured after ET-1 stimulation. Overexpression of $ET_A$ exaggerated positive inotropic effect (PIE) and diastolic shortening of ET-1, and induced a new twitch response including twitch broadening. On the contrary, overexpression of $ET_B$ increased PIE of ET-1, but did not affect other two twitch responses. Control myocytes expressing endogenous receptors showed a parallel increase in twitch amplitude and systolic $Ca^{2+}$ in response to ET-1. However, intracellular $Ca^{2+}$ did not change in proportion to the changes in contractility in myocytes overexpressing $ET_A$. Overexpression of $ET_A$ enhanced both systolic and diastolic contractility without parallel changes in $Ca^{2+}$. Differential regulation of this nature indicates that upregulation of $ET_A$ may contribute to diastolic myocardial dysfunction by selectively targeting myofilament proteins that regulate resting cell length, twitch duration and responsiveness to prevailing $Ca^{2+}$.

• Proceedings of the KAIS Fall Conference
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• 2011.12a
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• pp.170-173
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• 2011

Therapeutic hypothermia(TH) improves neurological outcomes and reduces mortality among survivors of out-of-hospital cardiac arrest. Animal and human studies have shown that TH results in improved salvage of the myocardium, reduced infarct size, reduced left ventricular remodeling and better long-term left ventricular function in settings of regional myocardial ischemia. This study is to investigate the effect of TH on post-resuscitation myocardial dysfunction and survival time after cardiac arrest and resuscitation in a rat model of myocardial infarction (MI). Thoracotomies were performed in 10 Male Sprague-Dawley rats weighing 450-550 g. MI was induced by ligation of the left anterior descending coronary artery (LAD). Ninety min after LAD ligation, ventricular fibrillation induction and subsequent cardiopulmonary resuscitation was performed before defibrillation attempts. Animals were randomized to two groups: a) Acute MI-Normothermia b) Acute MI-Hypothermia ($32^{\circ}C$ for 4 h). Myocardial functions, including cardiac output, left ventricular ejection fraction, and myocardial performance index were measured echocardiographically together with duration of survival. Ejection fraction, cardiac output and myocardial performance index were $54.74{\pm}9.16$, $89.00{\pm}8.89$, $1.30{\pm}0.09$ respectively and significantly better in the TH group than those of the normothermic group at the first 4 h after resuscitation($32.20{\pm}1.85$,$41.60{\pm}8.62$,$1.77{\pm}0.19$)(p=0.00). The survival time of the hypothermic group ($31.8{\pm}14.8$ h) was greater than that of the normothermic group($12.3{\pm}6.5$ h, p<0.05). This study suggested that TH attenuated post resuscitation myocardial dysfunction in acute MI and would be a potential strategy in post resuscitation care.

• Journal of Veterinary Science
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• v.22 no.5
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• pp.64.1-64.12
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• 2021

Background: Pituitary pars intermedia dysfunction (PPID), a neurodegenerative disease leading to reduced dopamine production, is a common disease in aged horses. The treatment is based on administration of the dopamine agonist pergolide. This drug has been related to valvular fibrosis in humans, but the cardiovascular effect of this drug has not yet been investigated in horses. Objectives: To determine whether pergolide induces valvular disease in horses or affects the cardiac function. Methods: Standard, tissue Doppler (TDE) and two-dimensional speckle tracking (STE) echocardiography were performed in horses with diagnosed PPID based on adrenocorticotropic hormone dosage. Measurements taken in horses treated with pergolide were compared with those from untreated horses with nonparametric t-tests. Furthermore, measurements from follow-up examinations performed at least three months after the initial exam were compared with a Wilcoxon signed rank test for repeated measurements in each group. Results: Twenty-three horses were included. None of the 12 horses under treatment developed valvular regurgitation. Furthermore, no differences in the measurements of the left ventricular systolic or diastolic function could be seen between the group of horses with treatment and those without treatment. Measurements taken in the follow-up exam did not differ compared to those taken in the initial exam in both groups. Conclusions: No changes of the left ventricular function assessed by TDE and STE could be shown in a small population of horses with confirmed PPID. Treatment with pergolide did not affect the ventricular function nor induce valvular disease.