Female showed favorable left ventricle hypertrophy regression during post-TAVR follow-up.

Transcatheter aortic valve replacement (TAVR) is a well-established procedure using a catheter-introduced valve prosthesis for patients with severe aortic stenosis (AS). This retrospective study investigated sex-related differences in pre- and post-TAVR clinical and hemodynamic outcomes and analyzed data of the first 100 cases at Kaohsiung Medical University Chung-Ho Memorial Hospital (KMUH) between December 2013 and December 2021. Baseline characteristics, procedural outcomes, mortality rates, and echocardiographic parameters were analyzed and compared between sexes. Among the 100 patients, male (46%) and female (54%) were of similar age (mean age, male 86.0 years vs. female 84.5 years) and of the same severity of AS (mean pressure gradient, male 47.5 mmHg vs. female 45.7 mmHg) at the time receiving the TAVR procedure. Women had smaller aortic valve areas calculated by continuity equation (0.8 ± 0.3 cm2 vs. 0.7 ± 0.2 cm2, p < 0.001). In addition, women had better left ventricle ejection fraction (59.6 ± 14.0% vs. men 54.7 ± 17.2%, p < 0.01). In the post-TAVR follow-up, regression of left ventricle mass and dimension was better in women than in men. None of the patient died within 30 days after the procedure, and women tended to have a more favorable survival than men (2-year mortality and overall mortality rate in 8.3 year, women 9.1% and 22.2% vs. men 22.2% and 34.8%; p = 0.6385 and 0.1277, respectively). In conclusion, the sex-based difference in post-TAVR regression of LV remodeling suggests a need for sex-based evaluation for patients with severe AS and their post TAVR follow-up.

Significance of preoperative acute kidney injury in patients with acute type A aortic dissection.

BACKGROUND/PURPOSE: Acute type A aortic dissection (AAD) is a medical emergency with high mortality even with emergency repair. We explored the risk factors for in-hospital mortality and the impact of preoperative acute kidney injury (AKI) in patients with AAD. METHODS: Our hospital database contained records for 156 consecutive patients who underwent AAD repair between March 2000 and February 2013. They were assigned to the in-hospital mortality or the survival group. All data were collected retrospectively. RESULTS: The 30-day mortality, including intraoperative deaths, was 14.1% (22/156). Total in-hospital mortality was 19.2% (30/156). Patients who required preoperative cardiopulmonary resuscitation (CPR) (16.7 vs 3.2%; P = 0.012), or who presented with preoperative cardiac tamponade (46.7 vs 19.0%; P = 0.002), shock/hypotension (56.7 vs 21.4%; P < 0.001), or coma (20.0 vs 6.3%; P = 0.019) had a higher in-hospital mortality rate. There was no difference in in-hospital mortality rate between patients with preoperative AKI or not. Mortality and major complications were significantly correlated with the severity of AKI. Multivariate analysis confirmed that preoperative shock or hypotension (odds ratio = 5.2; 95% CI = 2.2-12.3), and preoperative AKI stage 3 (odds ratio = 4.9; 95% CI = 1.3-19.3) were independent preoperative prognostic factors of in-hospital mortality. CONCLUSION: On the basis of our results, preoperative stage 3 AKI is a crucial prognostic risk factor for patients with AAD repair, Cardiac surgeons should be aware of this condition when dealing with AAD patients.

Fate of distal aorta after acute type A aortic dissection repair: Change and persistency of postoperative false lumen status.

BACKGROUND: The role of false lumen patency related to aortic growth, re-interventions, and post-discharge mortality in the chronic phase of repaired type A acute aortic dissection (TAAAD) remains controversial. We investigated the role of postoperative false lumen patency during long-term follow-up. METHODS: Based on postoperative CT images of 70 candidates, 58 eligible patients without alteration of false lumen status were assigned into three groups: complete patency, partial patency, and complete thrombosis. Aortic growth of 7 levels was analyzed. RESULTS: Persistent complete patency in post-operative TAAAD presents faster expansion of aortic diameter (95% CI, 0.35 to 11.52; P=0.038; B=5.935) and more patients with growth rate>5mm/year (P=0.029). The persistent status of false lumen does not predict post-discharge mortality (P=0.479). History of coronary artery disease (CAD) is the only independent predictor of post-discharge mortality. CONCLUSIONS: In TAAAD patients without change of postoperative false lumen status, completely patent false lumen presents faster aortic growth and more patients with growth rate>5mm/year. False lumen status does not correlate with late survival. Here we provide an insight into persistent postoperative false lumen in TAAAD patients and may help cast light on aortic dissection in this specific subgroup to improve their late outcomes.

Factors associated with demoralisation syndrome in patients before and after cardiac surgery.

AIMS AND OBJECTIVES: To investigate the incidence of and contributors to demoralisation syndrome among patients before and after cardiac surgery. BACKGROUND: Demoralisation syndrome is a common but neglected phenomenon in nursing practice. Patients who require cardiac surgery experience demoralisation syndrome more often than they experience depression. DESIGN: A prospective correlational design was applied. METHODS: A convenience sample of 76 participants undergoing cardiac surgery was recruited from the cardiovascular wards of two medical centres in Taiwan. The instruments applied included the Demoralization Scale (DS), the Patient Outcome Questionnaire-9 (PHQ-9) and the Perception of Intensive Care Unit (ICU) Stay Questionnaire. RESULTS: High demoralisation was present in 44.7% of the participants before surgery but significantly decreased to 36.8% after surgery (p < .05); conversely, depression was present in 15.8% of participants before surgery and did not significantly decrease after surgery (rate after surgery, 9.2%; p > .05). A multiple regression analysis using the backward-selection method showed that depression (p < .001) and retirement (p < .05) were important predictors of pre-operative demoralisation syndrome (R2  = 0.250), whereas depression (p < .001) and perceptions of ICU stay (p > .05) remained in the regression model after surgery (R2  = 0.291). CONCLUSIONS: The study findings suggest that demoralisation syndrome is highly prevalent in patients undergoing cardiac surgery but is significantly reduced after cardiac surgery. Before surgery, depression and retirement were significant predictors of demoralisation. After surgery, depression was the only predictor. Although the perception of ICU stay was not an important predictor, it was significantly correlated with demoralisation. RELEVANCE TO CLINICAL PRACTICE: Before cardiac surgery, nurses should emphasise the importance of demoralisation development among patients who suffer from depressive symptoms and are retired. After cardiac surgery, continued follow-up is needed for the early detection and minimisation of the effect of depression and the development of demoralisation.

Epidemiology, Clinical Features, and Prescribing Patterns of Aortic Aneurysm in Asian Population From 2005 to 2011.

Aortic aneurysm (AA) is a leading cause of death in Asia and the world. The prevalence in Western countries is around 1.3% to 8%. However, it is still unclear about the incidence, prevalence, and mortality of AA in Asian population. The aim of this study is to investigate the epidemiology of AA for all subtypes in Taiwan, and describe the clinical features and prescribing patterns for AA population.A population-based study was conducted using information from National Health Insurance Research Database (NHIRD) in Taiwan. Patients who were diagnosed with AA and also received computed tomography (CT) were included in this study. Incidence, prevalence, and mortality were calculated in each year during 2005 to 2011. Prevalent comorbidities and prescribing patterns were both evaluated among study population.The average annual incidence of AA in Taiwan was 7.35 per 100,000 population, and the prevalence was 29.04 per 100,000 population. It showed an increased trend of incidence from 2005 to 2011, so as prevalence and mortality. The incidence was associated with age and sex difference. It was much higher in those older than 65 years, especially for male. Hypertension, coronary artery disease (CAD), and chronic obstructive pulmonary disease (COPD) were prevalent comorbidities. Eighty-eight percentages of patients were prescribed antihypertensive agents in acute phase, where 61.4% of calcium channel blocker (CCB) was the most one.Our study found that incidence of AA was lower in Taiwan than in other countries. Nevertheless, it showed an increased trend of AA disease for incidence, prevalence, and also mortality during 2005 to 2011.

Epidemiology and Medication Utilization Pattern of Aortic Dissection in Taiwan: A Population-Based Study.

Acute aortic dissection (AD) is a catastrophic condition associated with a high rate of mortality. However, current epidemiological information regarding AD remains sparse. The objective of the present study was to investigate the current epidemiological profile and medication utilization patterns associated with aortic dissection in Taiwan.In this population-based study, we identified cases of AD diagnosed during 2005 to 2012 in the complete Taiwan National Health Insurance (NHI) Research Database. Patients with AD were identified using the International Classification of Disease, Ninth Revision (ICD-9) code 441.0, and surgical interventions were defined using NHI procedure codes.A total of 9092 individuals with a mean age of 64.4 ±â€Š15.1 years were identified. The cases were divided into 3 groups: Group A included 2340 patients (25.74%) treated surgically for type A AD; Group B included 1144 patients (12.58%) treated surgically for type B AD, and Group C included 5608 patients (61.68%) with any type of AD treated with medical therapy only. The average annual incidence of AD was 5.6 per 100,000 persons, and the average prevalence was 19.9 per 100,000 persons. Hypertension was the most common risk factor, followed by coronary artery disease and chronic obstructive pulmonary disease. Within 1 year of AD diagnosis, 92% of patients were taking antihypertensive medication. Calcium channel blockers were the most frequently prescribed antihypertensive medication for long-term observation in Taiwan.The annual trends revealed statistically significant increases in the numbers and percentages of prevalence, incidence, and mortality. Changes in patients' drug utilization in patterns were observed after AD diagnosis. Our study provides a local profile that supports further in-depth analyses in AD-affected populations.

Baicalein inhibits HMGB1 release and MMP-2/-9 expression in lipopolysaccharide-induced cardiac hypertrophy.

Myocardial dysfunction, a common complication after sepsis, significantly contributes to the death of patients with septic shock. In the search for potentially effective drugs to decrease mortality from sepsis, we investigated the cardioprotective effects of baicalein, a flavonoid present in the root of Scutellaria baicalensis, on lipopolysaccharide (LPS)-induced pro-inflammatory cytokine production and matrix metalloproteinase-2 and -9 (MMP-2/-9) expression. We found that baicalein significantly attenuated LPS-induced cardiac hypertrophy and counteracted reactive oxygen species (ROS) generation in neonatal rat cardiomyocytes. In addition, pretreatment with baicalein inhibited LPS-induced early (e.g., tumor necrosis factor-α (TNF-α) and interleukin-6) and late (e.g., high mobility group box 1 (HMGB1) pro-inflammatory cytokine release, inducible nitric oxide synthase (iNOS) expression and NO production. Finally, baicalein also significantly down-regulated the expression of MMP-2/-9 and attenuated HMGB1 translocation from the nucleus to the cytoplasm. These results suggest that baicalein can protect cardiomyocytes from LPS-induced cardiac injury via the inhibition of ROS and inflammatory cytokine production. These cardioprotective effects are possibly mediated through the inhibition of the HMGB1 and MMP-2/-9 signaling pathways.

Baicalein, an active component of Scutellaria baicalensis Georgi, prevents lysophosphatidylcholine-induced cardiac injury by reducing reactive oxygen species production, calcium overload and apoptosis via MAPK pathways.

BACKGROUND: Lysophosphatidylcholine (lysoPC), a metabolite from membrane phospholipids, accumulates in the ischemic myocardium and plays an important role in the development of myocardial dysfunction ventricular arrhythmia. In this study, we investigated if baicalein, a major component of Huang Qui, can protect against lysoPC-induced cytotoxicity in rat H9c2 embryonic cardiomyocytes. METHODS: Cell viability was detected by the MTT assay; ROS levels were assessed using DCFH-DA; and intracellular free calcium concentrations were assayed by spectrofluorophotometer. Cell apoptosis and necrosis were evaluated by the flow cytometry assay and Hoechst staining. Mitogen-Activated Protein Kinases (MAPKs), which included the ERK, JNK, and p38, and the apoptotic mechanisms including Bcl-2/Bax, caspase-3, caspase-9 and cytochrome c pathways were examined by Western blot analysis. The activation of MAPKs was examined by enzyme-linked immunosorbent assay. RESULTS: We found that lysoPC induced death and apoptosis of H9c2 cells in a dose-dependent manner. Baicalein could prevent lysoPC-induced cell death, production of reactive oxygen species (ROS), and increase of intracellular calcium concentration in H9c2 cardiomyoctes. In addition, baicalein also inhibited lysoPC-induced apoptosis, with associated decreased pro-apoptotic Bax protein, increased anti-apoptotic Bcl-2 protein, resulting in an increase in the Bcl-2/Bax ratio. Finally, baicalein attenuated lysoPC-induced the expression of cytochrome c, casapase-3, casapase-9, and the phosphorylations of ERK1/2, JNK, and p38. LysoPC-induced ERK1/2, JNK, and p38 activations were inhibited by baicalein. CONCLUSIONS: Baicalein protects cardiomyocytes from lysoPC-induced apoptosis by reducing ROS production, inhibition of calcium overload, and deactivations of MAPK signaling pathways.

Mitral tissue inhibitor of metalloproteinase 2 is associated with mitral valve surgery outcome.

BACKGROUND: Matrix metalloproteinases play a role in regulating cardiac remodeling. We previously reported an association between tissue inhibitor of metalloproteinase 2 (TIMP-2) expression and mitral valve (MV) disease. However, the determinants and prognostic value of mitral TIMP2 after MV surgery are unknown. METHODS: This retrospective study of 164 patients after MV surgery in a tertiary medical center in Taiwan assessed mitral TIMP2 on a semiquantitative scale (0-2) by immunohistochemical staining. The primary endpoints were the composite of cardiovascular death and heart failure admission. RESULTS: Mean age was 50.4±13.7 years. After a mean follow-up period of 101±59 months, primary endpoints had occurred in 25 (15.2%) subjects. Patients with and without primary endpoint events significantly differed in terms of age (56.6±14.4 vs. 49.2±13.4 years, respectively; p = 0.013) and left ventricular end-systolic diameter (LVESD) (39.7±8.2 vs. 35.5±7.5 mm, p = 0.010) at surgery. The TIMP2 had a significant dose-dependent association with development of a primary endpoint (p = 0.002). Kaplan-Meier analysis showed that TIMP2 expression has a significant positive association with primary endpoint-free survival (log-rank test; p = 0.004). Cox regression analysis showed that independent predictors of primary endpoints were TIMP2 (hazard ratio [HR] 0.28; 95% confidence interval [CI] 0.12-0.65; p = 0.003), age (HR 1.05; 95% CI 1.02-1.09; p = 0.003) and LVESD (HR 1.05; 95% CI 1.01-1.10; p = 0.020). CONCLUSIONS: The lack of mitral TIMP2 expression is associated with increases in cardiovascular death and heart failure following MV surgery.

Acute aortic dissection type A with acute coronary involvement: a novel classification.

BACKGROUND: Acute coronary involvement (ACI) due to acute aortic dissection (AAD) type A is potentially fatal. We examined selected patients with AAD type A, which had evolved over 14 years, and acute coronary involvement. The purpose of this study was to determine the characteristics of patients with ACI due to AAD type A. METHODS: Between 1997 and 2011, we recruited 20 patients (14.1%) with ACI (14 men, 6 women; mean age: 51.8 ± 11.8 years; age range: 35-79 years) from 142 patients who had undergone surgical repair of AAD type A. RESULTS: We propose a novel 4-category classification scheme based on the surgical pathological findings. The right coronary artery was involved in 15 patients, and the left was involved in 5 patients. Fourteen patients had preoperative myocardial ischemia. In the other 6 patients, acute coronary involvement was found intraoperatively. Patients with ACI were significantly younger than those without ACI (51.8 ± 11.8 vs. 61.0 ± 11.8; p = 0.001), a lower prevalence of intramural hematoma (5.0% vs. 32.8%; p = 0.011), a higher aortic regurgitation rate (95.0% vs. 53.5%; p = 0.001). Patients presenting with ACI had an in-hospital mortality rate of 20.0% (4/20), while those without ACI had an in-hospital mortality rate of 19.7% (24/122). CONCLUSIONS: Acute coronary involvement due to AAD type A is not always associated with coronary malperfusion. Patients with ACI were much younger, had a higher aortic regurgitation rate, and, less commonly, had intramural hematoma. This new classification scheme would make it more convenient for surgeons to decide on treatment options for this special cohort.

Matrix metalloproteinase-1 mitral expression and -1607 1G/2G gene promoter polymorphism in mitral chordae tendinae rupture.

Understanding the pathogenesis of mitral chordae tendinae rupture (MCTR) is essential for identification of risk factors. Mitral matrix metalloproteinase (MMP) triggers the signal cascade that instigates cardiac fibrosis, which may be a predisposing factor in MCTR. We investigated associations among MMP1 expression, MMP1 -1607 1G/2G polymorphism and mitral chordae tendinae rupture (MCTR). This study enrolled 185 patients (group A) receiving mitral valve replacement. Group A included 65 patients with MCTR and 120 controls without MCTR. MMP1 was assessed on a semiquantitative scale (0-3) by immunohistochemical staining. For genetic association study, another 227 subjects were recruited for group B, including 75 with MCTR and 152 controls. The gene polymorphisms were analyzed by polymerase chain reaction. In group A, MCTR patients had a higher MMP1 expression compared to controls (P < 0.001). Binary regression analysis showed the variation in the MCTR patients was independently explained by MMP1 (P = 0.027). Hypertension and MMP1 staining had a synergistic effect on the MCTR occurrence (P < 0.001). In group B, MMP1 -1607 1G allele was increased in patients with MCTR compared to controls (P = 0.014). The odds ratio for the 1G/1G genotype to the 2G/2G genotype was 3.22 (P = 0.009). Univariate and logistic regression analysis showed an independent association between MCTR and MMP1 -1607 1G/2G polymorphism (P = 0.028 and 0.032, respectively). Since MMP1 mitral expression and -1607 1G/2G polymorphism were associated with MCTR independently of other baseline characteristics, MMP1 may play a role in the individual susceptibility to MCTR.

Stable haemodynamics associated with no significant electrocardiogram abnormalities is a good prognostic factor of survival for acute type A aortic dissection repair.

OBJECTIVES: Acute type A aortic dissection (AAD) is a medical emergency with high mortality even with emergency repair. We explored the prognostic factors of in-hospital mortality for AAD repair. METHODS: One hundred and thirty-three consecutive patients operated on for AAD between 1997 and 2011 were enrolled in our study. They were assigned to the in-hospital mortality or the survival group. We evaluated 101 variables to predict in-hospital mortality. All data were collected retrospectively. RESULTS: The 30-day mortality, including intraoperative deaths, was 12.8% (17/133 patients) and in-hospital mortality was 18.0% (24/133). Univariate analysis disclosed 10 significant prognostic factors. Multivariate analysis confirmed that preoperative shock or hypotension (odds ratio (OR) = 4.71; P = 0.004), an initial 24 h of bleeding >1500 ml (OR = 5.17; P = 0.01) and age ≥ 75 years (OR = 3.70; P = 0.019) were independent prognostic factors of in-hospital mortality. On the contrary, an electrocardiogram (ECG) showing no abnormalities (OR = 0.22; P = 0.008) is a good prognostic factor for survival. Interestingly, patients with stable haemodynamics without abnormal ECG findings had an excellent result of 1.6% (1/63) in-hospital mortality. CONCLUSIONS: Stable haemodynamics and no significant abnormal ECG findings predicted excellent in-hospital survival. Cardiac surgeons and cardiologists should be aware of these positive predictors when treating patients diagnosed with AAD.

Outcome and risk factors associated with surgical site infections after cardiac surgery in a Taiwan medical center.

BACKGROUND/PURPOSE: Surgical site infection (SSI) after cardiac surgery leads to morbidity and mortality. Identifying SSI risk factors, which vary between populations, is important in preventing infection. METHODS: A retrospective chart review of adult cases receiving cardiac surgery in a Taiwan medical center in 2004 and 2005. RESULTS: Of the 260 cases included in the study, 169 (65.0%) received a coronary artery bypass graft, 65 (25.0%) cardiac valvular surgery and 26 (10.0%) aortic or septal defect operations. The SSI rate was 13.5%. Univariate analysis showed that chronic obstructive pulmonary disease (COPD) (p = 0.008), congestive heart failure New York Heart Association class IV (p = 0.048), longer preoperative hospital stay, preoperative nosocomial infection, higher volume of blood loss and larger packed red blood cell transfusions during the operation were significantly related to SSI. Logistic regression analysis further identified COPD, pre-operative nosocomial infection and emergency surgery as being independently associated with SSI (odds ratios of 4.96, 5.88 and 9.77, respectively). Obesity and diabetes mellitus were not associated with SSI. CONCLUSION: COPD is an independent underlying illness associated with SSI after cardiac surgery. Minimizing preoperative hospitalization and nosocomial infection, and awareness of cases presenting with relevant risk factors, are useful in reducing SSI.

Shock wave therapy effectively attenuates inflammation in rat carotid artery following endothelial denudation by balloon catheter.

BACKGROUND: This study investigates the effectiveness of extracorporeal shock wave (ECSW) in ameliorating inflammatory mediator expression and neointimal formation in a rat model of vascular injury. METHODS AND RESULTS: Male Sprague-Dawley rats with left carotid artery (LCA) injury induced by balloon dilatation (BD; group 1) were compared with group 2 [LCA injury plus ECSW-181 (defined as 181 total shocks given in LCA at 0.011 mJ/mm(2)) on day 2 post-LCA injury], and group 3 (normal controls). The rats in each group were further divided into 3 subgroups (n = 6, each) that were sacrificed on postoperative day 3, 7 and 14, respectively. The results demonstrated that, compared to groups 2 and 3, group 1 had significantly increased cellular expression of CD40, interleukin-18, and connexin 43 at each analyzed time point (all p < 0.001). Additionally, LCCA macrophage (CD68) recruitment was substantially increased in group 1 compared to groups 2 and 3 (all p < 0.001). Furthermore, LCA neointimal proliferation and media thickness were markedly higher in group 1 than in groups 2 and 3 on days 7 and 14 post-BD (all p < 0.001). CONCLUSIONS: ECSW markedly attenuates inflammatory responses, proliferation of neointima and smooth muscle cells in a rat vascular injury model.

Synergistic effect of mitral expression of tissue inhibitor of metalloproteinase-2 with hypertension on the occurrence of mitral chordae tendinae rupture.

OBJECTIVES: We previously found the association between mitral chordae tendinae ruptures (MCTR) and hypertension. Tissue inhibitor of metalloproteinase-2 (TIMP2), which expresses differently under pressure loads, could trigger a signal cascade instigating cardiac fibrosis, possibly predisposing to MCTR. We aimed to elucidate the relationship between the TIMP2 and hypertension and the effect they may have on the occurrence of MCTR. METHODS: Using a cross-sectional study in a tertiary medical center in Taiwan, we enrolled 186 patients who had received mitral valve replacements and classified them into two groups: 64 (34%) with MCTR and 122 (66%) without MCTR. Expression of mitral TIMP2 was assessed on a semiquantitative scale (grade 0-3) by immunohistochemical staining using antibodies against TIMP2. RESULTS: TIMP2 expression was significantly higher in MCTR patients (P < 0.001). Multiple logistic regression analysis showed four independent risk factors: TIMP2 [odds ratio (OR) = 1.82, 95% confidence interval (CI) = 1.18-2.81, P = 0.007], hypertension (OR = 2.40, CI = 1.08-5.34, P = 0.032), rheumatic heart disease (OR = 0.18, CI = 0.05-0.70, P = 0.014), and left ventricular end-diastolic dimension (OR = 1.10, CI = 1.05-1.15, P < 0.001). Among nonhypertensive patients, the higher expression of TIMP2 (grade 2 and 3 vs. 0 and 1) was associated with a 3.27-fold risk. However, hypertensive patients with higher TIMP2 expression had a significantly 10-fold higher risk (P < 0.001 for interaction). CONCLUSION: Mitral TIMP2 expression is higher in patients with MCTR and there is a synergistic effect of mitral TIMP2 staining with hypertension on the occurrence of MCTR.

Hyperbaric oxygen therapy with topical negative pressure: an alternative treatment for the refractory sternal wound infection.

Sternal osteomyelitis is a potentially lethal complication after cardiac surgery. It may be the cause of postoperative morbidity and mortality. We present a case of deep sternal wound infection after sternotomy. The patient received three treatments of surgical debridement, irrigation, topical negative pressure (TNP) dressing, and hyperbaric oxygen (HBO) therapy. Forty-five HBO therapy sessions were administered. After nine weeks, the sternal wound was healed and completely epithelialized. This conservative therapy can be an alternative and inexpensive method for the difficult sternal wound infection patient.

Displacement of the beating heart induces an immediate and sustained increase in myocardial reactive oxygen species.

BACKGROUND: Heart manipulation and displacement are common maneuvers during beating heart surgery to expose coronary arteries for revascularization. Effects of heart displacement on free radical generation, reactive oxygen species (ROS) have not been previously described. METHODS AND RESULTS: Seven adult male dogs were anesthetized, a left lateral thoracotomy performed to expose the heart, and the coronary sinus cannulated for ROS sampling during different manipulation protocols: (1) heart in normal position; (2) 90 degree manual heart displacement; (3) Trendelenburg position while the heart displaced 90 degrees and (4) return heart to normal resting anatomical position and plus the operating table returned to horizontal. Heart displacement followed by anatomical re-positioning significantly increased the ROS signal as measured by EPR (50-fold compared with control values; p<0.01). CONCLUSION: Trendelenburg positioning and/or repositioning the heart during cardiac surgery may induce acute reperfusion injury and increase ROS.

The effects of debanding on the lung expression of ET-1, eNOS, and cGMP in rats with left ventricular pressure overload.

Pulmonary hypertension (PH) usually develops secondary to left ventricular (LV) dysfunction; therefore, it is also called retrograde PH. To investigate our hypothesis that PH is at least partially reversible, as in some congenital heart diseases, in a rat model we investigated whether release of constriction could attenuate pulmonary vascular remodeling and change the expression of endothelin (ET)-1 and endothelial nitric oxide synthase (eNOS). We used rats with LV dysfunction produced by an ascending aortic banding. In this study, there were four groups enrolled: 4-weeks banded (AOB(1-28); n = 7), 7-weeks banded (AOB(1-49); n = 7), debanded groups (AOB(1-28)/DeB(29-49); n = 7), and rats receiving a sham operation (n = 7). Subsequently, there was significant attenuation of medial hypertrophy in pulmonary arterioles and reversal of PH in the AOB(1-28)/DeB(29-49) group (sham, 19 +/- 1.3 mm Hg; AOB(1-28), 31 +/- 2.7 mm Hg; AOB(1-49), 32 +/- 2.7 mm Hg; and AOB(1-28)/DeB(29-49), 20 +/- 1.3 mm Hg). PreproET-1 mRNA and eNOS mRNA were measured by competitive reverse transcriptase (RT) polymerase chain reaction (PCR), and eNOS was measured by Western blotting. Compared with the banded groups, debanding significantly decreased pulmonary preproET-1 mRNA, pulmonary ET-1 (sham, 210 +/- 12 pg/g protein; AOB(1-28), 242 +/- 12 pg/g protein; AOB(1-49), 370 +/- 49 pg/g protein; and AOB(1-28)/DeB(29-49), 206 +/- 1.9 pg/g protein), and plasma ET-1 levels (sham, 10.1 +/- 1.5 pg/ml; AOB(1-28), 13.4 +/- 2.0 pg/ml; AOB(1-49), 15.4 +/- 2.0 pg/ml; and AOB(1-28)/DeB(29-49), 10.3 +/- 0.9 pg/ml protein). Debanding could not, however, alter pulmonary eNOS, eNOS mRNA, or cGMP. These findings suggest that pulmonary vascular remodeling, increased pulmonary arterial pressure, and upregulation of ET-1 gene expression are all reversible. We infer that it is the upregulated gene expression of ET-1, not eNOS, that is closely related to the development of the PH secondary to 4 weeks of aortic banding.