Left ventricular hypertrophy (LVH) refers to the expansion and the enlarged myocardium due to the increased resistance to ejection from the left ventricle to the aorta and/or the periphery, or the long-term burden imposed by the blood increase. Hypertension is a major risk factor that accounts for more than 50% of the causes of cardiovascular disease. If hypertension endure in the long term, the myocardium responds to abnormal heartbeat in the heart. Therefore, the prevalence of left ventricular hypertrophy also increases. As a result of genome-wide association study (GWAS) analysis for European people, PDGFC, MARK3, and BCL2 were related to blood pressures. In this study, the genetic polymorphisms of PDGFC, MARK3, and BCL2 were extracted and selected based on Korean genomic and epidemiologic data, and then logistic regression analysis was performed on LVH. As a result, one SNP (rs9307953) in PDGFC gene, four SNPs (rs6575983, rs17679475, rs2273703 and rs10141388) in MARK3 gene and two SNPs (rs17756073 and rs17070739) in BCL2 gene were statistically significant. The rs6575983 of the MARK3 gene showed the highest significance level ($P=7.2{\times}10^{-3}$) among the SNPs and the relative risk of 1.08 (95% confidence interval: 1.06 to 1.45). These results suggest that the polymorphisms of PDGFC, MARK3, and BCL2 not only affect European blood pressures but also correlate with LVH in Korean. These results suggest that increased understanding of the genetic correlations of the pathogenesis of LVH.
Myocardial infarction promotes cardiac remodeling and myocardial fibrosis, thus leading to cardiac dysfunction or heart failure. Peiminine has been regarded as a traditional anti-fibrotic Chinese medicine in pulmonary fibrosis. However, the role of peiminine in myocardial infarction-induced myocardial injury and fibrosis remained elusive. Firstly, rat model of myocardial infarction was established using ligation of the left coronary artery, which were then intraperitoneally injected with 2 or 5 mg/kg peiminine once a day for 4 weeks. Echocardiography and haemodynamic evaluation results showed that peiminine treatment reduced left ventricular end-diastolic pressure, and enhanced maximum rate of increase/decrease of left ventricle pressure (± dP/dt max) and left ventricular systolic pressure, which ameliorate the cardiac function. Secondly, myocardial infarction-induced myocardial injury and infarct size were also attenuated by peiminine. Moreover, peiminine inhibited myocardial infarction-induced increase of interleukin (IL)-1β, IL-6 and tumor necrosis factor-α production, as well as the myocardial cell apoptosis, in the rats. Thirdly, peiminine also decreased the myocardial fibrosis related protein expression including collagen I and collagen III. Lastly, peiminine reduced the expression of p38 and phosphorylation of extracellular signal-regulated kinase 1/2 in rat model of myocardial infarction. In conclusion, peiminine has a cardioprotective effect against myocardial infarction-induced myocardial injury and fibrosis, which can be attributed to the inactivation of mitogen-activated protein kinase pathway.
Behçet's disease is a chronic inflammatory disorder involving vessels of various sizes and organs, including the skin, joints, gastrointestinal tract, lungs, and cardiovascular system. The etiology of Behçet's disease is unclear, and clinical diagnosis is important in the absence of definitive laboratory or pathological findings diagnostic of Behçet's disease. Cardiac involvement is rare but might present as endocarditis, myocarditis, pericarditis, or intracardiac thrombosis. This report presents a case of Behçet's disease involving the heart in a 22-year-old man with unusual manifestations of right ventricular fibrosis and intracardiac thrombosis. Cardiac magnetic resonance imaging revealed multiple intracardiac thrombi and delayed diffuse subendocardial enhancement involving the right ventricle. No peripheral eosinophilia was detected. Endomyocardial biopsy showed mixed inflammatory cell infiltrates. Based on the patient's clinical history of oral ulcer and arthritis, a diagnosis of Behçet's disease was made considering the clinical, radiological, and histological findings. Intracardiac thrombi and endomyocardial fibrosis are rare manifestations of Behçet's disease, and the diagnosis is often a clinical challenge. Early diagnosis is important for appropriate management. Behçet's disease should be considered in the differential diagnosis of patients with intracardiac thrombosis and endomyocardial fibrosis of the right chamber.
Background: The vasoconstrictive effect of epinephrine in local anesthetics affects the heart, which leads to hesitation among dentists in injecting local anesthetics into patients with cardiovascular disease. Due to its vasoconstrictive effects, the present study investigated the effects of vasopressin administration on cardiac function in rats. Methods: Experiment 1 aimed to determine the vasopressin concentration that could affect cardiac function. An arterial catheter was inserted into the male Wistar rats. Next, 0.03, 0.3, and 3.0 U/mL arginine vasopressin (AVP) (0.03V, 0.3V, and 3.0V) was injected into the tongue, and the blood pressure was measured. The control group received normal saline only. In Experiment 2, following anesthesia infiltration, a pressure-volume catheter was placed in the left ventricle. Baseline values of end-systolic elastance, end-diastolic volume, end-systolic pressure, stroke work, stroke volume, and end-systolic elastance were recorded. Next, normal saline and 3.0V AVP were injected into the tongue to measure their effect on hemodynamic and cardiac function. Results: After 3.0V administration, systolic blood pressures at 10 and 15 min were higher than those of the control group; they increased at 10 min compared with those at baseline. The diastolic blood pressures at 5-15 min were higher than those of the control group; they increased at 5 and 10 min compared with those at baseline. The preload decreased at 5 and 10 min compared to that at baseline. However, the afterload increased from 5 to 15 min compared with that of the control group; it increased at 10 min compared with that at baseline. Stroke volume decreased at 10 and 15 min compared with that of the control group; it decreased from 5 to 15 min compared with that at baseline. Stroke work decreased from 5 to 15 min compared with that of the control group; it decreased from 5 to 15 min compared with that at baseline. Conclusion: Our results showed that 3.0 U/mL concentration of vasopressin resulted in increased blood pressure, decreased stroke volume and stoke work, decreased preload and increased afterload, without any effect on myocardial contractility.
Excellent clinical results of the arterial switch operation and the limited availablity of the intraventricular rerouting has recently made an arterial switch operation to become the therapeutic method of choice for the repair of double-outlet right ventricle (DORV) with subpulmonary ventricular septal defect (VSD). The early and midterm outcomes of arterial switch operation for this anomaly were evaluated. Material and Method: Between August 1994 and July 2002, 13 patients underwent an arterial switch operation for the correction of double-outlet right ventricle with subpulmonary VSD at Dong-A university hospital.. The 50% rule was used to define DORV. Median age and mean body weight were 27 days (range, 3-120 days) and 3.8$\pm$0.7kg (range, 2.92-5.3kg) respectively. Aortic arch anomalies were associated in 6 cases (46.2%), which were all repaired through one-stage operation. The relationship of the great arteries were side-by-side in 8 cases (61.5%) and anteroposterior in 5 (38.5%). Coronary artery patterns were 1 LCx-2R in 6 cases, retropulmonary left coronary artery (LCA) in 6, and intramural LCA in 1 respectively. The enlargement of VSD was required in 1 patient and the patch enlargement of right ventricular outflow tract was performed in another one patient. The Lecompte maneuver was used in all but 3 patients with a side by side relationship of the great arteries. Result: Overall postoperative hospital mortality was 23.1 % (3/13). All operative deaths were occurred in the patients with aortic arch anomalies. There was one late death related to the postoperative complication of the central nerve system during the mean follow-up of 41.3$\pm$30.7 months. Pulmonary valvar stenosis (>30mmHg of pressure gradient) developed in 1 patient (10%) and left pulmonary artery stenosis in 2 (20%), among them, one required reoperation 52 months after repair. There was an asymptomatic patient with moderate aortic regurgitation. 5-year survival rate including operative deaths was 68.3%. Conclusion: Although the operative mortality is high in the patients with aortic arch anomaly, the arterial switch operation for DORV with supbpulmonary VSD can be performed with low operative mortality and low reoperation rate in the patients Without arch anomaly. The arterial switch operation can be considered a good option for this complex anomaly.
Background: The regression of the left ventricular hypertrophy after prosthetic valve replacement in patients with aortic valvular stenosis is an important factor to determine the appropriateness of the replaced prosthetic valvular size. Methods: To assess the regression of myocardial hypertrophy, a retrospective analysis of Doppler echocardiographic and electrocardiographic data was undertaken before, soon after(7.5$\pm$2.1 day), and late after(10.7$\pm$1.8 months) surgery in 36 patients(22 males, 14 female, mean age 54$\pm$12.1 years, mean BSA 1.61$\pm$0.15m2) with predominant aortic valvular stenosis. The patients underwent St. Jude Medical aortic valve replacement. By the size of the valves used, the patients were divided into three groups(19, 21 and 23+). Results: The mean body surface area(1.48$\pm$0.13) in the patients with the 19 mm valve was smaller than that in the other groups(1.63$\pm$0.12)(p<0.05). No significant changes of ejection fraction were detected in all groups over time. Left ventricular muscle mass index(gm/m2) was reduced significantly in the 21 and 23+ groups over time(p<0.05), but there were no significant changes in the 19 mm valve group. The electric voltage height on EKG at the period of late after surgery was reduced significantly in all groups(p<0.05). Conclusion: Despite clinical improvement, the LVH was not reduced significantly in 19 mm valve group. Thus we suggest that more attention and additional procedures such as annular enlargement should be taken in patients who will undergo the replacement of 19 mm prosthetic valve.
Background: Obtaining precise hemodynamic and morphological information in the early postoperative period after surgical correction of congenital heart disease is important in determining the need for future medical or surgical intervention. We investigated the residual shunting after surgical repair of simple ventricular septal defect in order to know the incidence of residual shunting in the postoperative period and the natural history of small residual shunts located in the peripatch area. Material and Method: Forty three consecutive patients under one year of age who underwent patch repair of a simple ventricular septal defect were evaluated for incidence of residual shunts by echocardiography. Result: Eleven patients had echocardiographic residual shunt in the peripatch area at immediate postoperative period, however, there were no patients who needed reoperation due to deteriorated hemodynamic effect of residual shunt. The incidence of residual shunts was not significantly different with type of ventricular septal defect and material used for closure. During follow up period, two patients were lost and remaining nine patients no longer showed evidence of residual shunt. The mean time of last evidence of shunt was $4.2{\pm}3.6$ months after operation. Conclusion: Residual peripatch shunt flow was frequently noted in the immediate postoperative period following surgical repair of ventricular septal defect, however, most of them were disappeared within six months.
Kim Young Sam;Yoon Young Han;Kim Joung Taek;Kim Kwang Ho;Lim Hyun Kyoung;Kwan Jun;Baek Wan Ki
Journal of Chest Surgery
/
v.38
no.10
s.255
/
pp.717-720
/
2005
Here we report a case of posterior left ventricular (LV) free wall rupture following postinfarct ventricular septal rupture (VSR). A 58-year-old man was transferred to the hospital under the impression of acute myocardial infarction. Posterior VSR was seen on echocardiographic examination. The intraaortic balloon pump catheter was introduced percutaneously and the emergent operation was proposed. Sudden circulatory collapse was developed shortly after the anesthetic induction and the patient's chest was hurriedly opened while on cardiopulmonary resuscitation. The acute cardiac tamponade was seen and the blood was seen pumping from the longitudinal tear at the mid-level of LV posterior wall, measuring 2 cm in length. The cardiopulmonary bypass was set and LV reconstruction was done. The postoperative recovery was delayed due to the brain injury presumably caused by preoperative cardiac arrest.
Since January 1977 to the end of September 1982, total 60 Ionescu-Shiley pericardial xenograft heart valves were implanted for valve replacement in 50 patients at the Han Yang University Hospital. The operative procedures were as follow: Mitral valve replacement [MVR] in 25 patients, Mitral valve replacement [MVR] and Tricuspid valve [TV] annuloplasty in 7 patients, Aortic valve replacement [AVR] in 8 patients, Aortic valve replacement [AVR] and Mitral valve replacement [MVR] in 8 patients. Aortic valve replacement [AVR] and Mitral valve replacement [MVR] and Tricuspid valve [TV] annuloplasty in 2 patients. To evaluate the immediate hemodynamic changes after valve replacements, the pressures of each cardiac chamber and ulmonary artery were checked before and after valve replacement on the operation table. Right ventricle [RV] pressure was decreased from 52.09\ulcorner6.71 to 45.57\ulcorner5.03 mmHg, Pulmonary artery [PA] pressure was decreased from 45.97\ulcorner2.69 to 41.00\ulcorner3.99 mmHg, and Left atrium [LA] pressure was decreased from 30.33\ulcorner13.02 to 22.76\ulcorner.97 mmHg before and after valve replacement. In MVR group, RV pressure was decreased from 49.17\ulcorner7.89 to 43.14\ulcorner4.14 mmHg, PA pressure was decreased from 44.67\ulcorner3.18 to 38.67\ulcorner2.85 mmHg, and LA pressure was decreased from 31.46\ulcorner13.47 to 21.91\ulcorner.17 mmHg. In AVR group, RV pressure was decreased from 53.0\ulcorner7.44 to 44.71 \ulcorner3.24 mmHg, PA pressure was decreased from 34.83\ulcorner0.73 to 31.86\ulcorner.36 mmHg, and LA pressure was not changed. In double valve replacement [MVR and AVR] group, RV pressure was decreased from 57.50\ulcorner3.82 to 42.50\ulcorner.80 mmHg, PA pressure was decreased from 51.17\ulcorner1.42 to 43.33\ulcorner4.53mmHig, and LA pressure was decreased from 34.33\ulcorner2.09 to 25.50\ulcorner0.21 mmHg. But in the group where MVR and TV annuloplasty were performed, preoperative RV and PA pressure were markedly increased and no pressure decrease in RV and PA noticed after valve replacement. This study shows good immediate postoperative hemodynamic results after valve replacement using Ionescu-Shiley xenograft valve except in the cases of MVR and TV annuloplasty and advanced disease with pulmonary hypertension.
Between May 1991 and September 1995, 7 patients underwent surgical repair of ventricular septal defect (VSD) complicated with myocardial infarction in Asan Medical Center. The patients included two male and five female. The ages of patients were ranged from 54 years to 76 years with a mean of 65 years. The sites of postinfarction ventricular septal defect were consist of anterior septal defect in 6 patients and anteroposterior septal defect in 1 patient. Preoperative 2D-echocardiography & angiography were performed in all patients in order to measure ventricular function and evaluate the extent of coronary artery disease. The operations were delayed till mean 24 $\pm$ 12days after myocardial infarction. All patients underwent infarctectomy and Teflon patch closures through the area of the left ventricle infarction or aneurysm in the anterior or apical aspect of postinfarction ventricular septal defect. The ventricular septal defect repaired simultaneously with coronary artery b pass graft in 3 patients, with ventricular aneurysmectomy in 5 patients, and with left ventricular thrombectomy in 1 patient. Patch fixation in the left side of interventricular septum by tracts-septal interrupted pledget suture reduced the recurrence rate of VSD. There were 2 postoperative complications : One with pneumonia, 1 patient with the skin necrosis of left thigh. There was ilo early death. The 6 patients except for one emigrant were followed up postoperatively between 3 and 63 months(mean .28 months), without any sequelae and late death. They are in New York Heart Association functional class I-II.
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