Short-term results of catheter-directed intrathrombus thrombolysis versus anticoagulation in acute proximal deep vein thrombosis.

BACKGROUND: Deep vein thrombosis (DVT) is a potentially progressive disease with complex clinical sequelae. The clinical practice guidelines of the American College of Chest Physicians (ACCP) recommend various treatments for all patients with objectively proven DVT. This study retrospectively compares enoxaparin with CDT on treatment efficacy and safety and the evolution of acute proximal DVT in the lower limbs. METHODS: This study comprised 53 patients with acute proximal DVT, who received either CDT followed by intravenous unfractionated heparin (UFH) or adjusted subcutaneous low-molecular-weight heparin (LMWH) (enoxaparin) for 7-14 days. Warfarin was administered to all patients for at least 6 months. The study endpoints included the evolution of DVT and treatment efficacy and safety, which were assessed with frequent duplex ultrasounds, plethysmography, and venography. The mean duration of the follow-up was 15.2 months. RESULTS: In the CDT group, patency of the iliofemoral vein segment was observed in 42.3% of the patients after 1 week (p < 0.001) and in 69.2% after 6 months. In the control group, patency was present in 15.4% of the patients after 3 months and in 38.5% after 6 months (p = 0.05). Femoral venous obstruction was found in 30.8% of CDT patients and in 61.5% of the control group (p = 0.05). Furthermore, femoral venous insufficiency was present in 46.2% of the CDT group and 53.9% of the control group after 6 months (p = 0.587). After 12 months, post-thrombotic syndrome (PTS) was found in 19.2% of the CDT patients compared to 50% of the LMWH group (p = 0.04). CONCLUSION: Duplex ultrasound analysis of thrombus progression is useful for assessing the treatment of a patient with acute proximal DVT. In this study, patients undergoing CDT experienced higher thrombus resolution and early recanalization of their veins, which may preserve venous function and further prevent development of post-thrombotic syndrome.

Brief pressure overload preconditions rabbit myocardium independent of adenosine receptor activation.

BACKGROUND: We previously reported brief pressure overload of the left ventricle reduced myocardial infarct size. The role of adenosine receptors was investigated in this study. METHODS: Pressure overload was achieved by two 10-minute partial snaring of the ascending aorta. Systolic left ventricular pressure was raised 50% above baseline value. Ischemic preconditioning was elicited by two 10-minute coronary artery occlusions. Ten minutes after different pretreatments, 60-minute occlusion of the left anterior descending coronary artery followed by 3-hour reperfusion was done to induce infarction. The area at risk and myocardial infarct size were determined by Evans blue dye injection and triphenyltetrazolium chloride staining. RESULTS: Myocardial infarct size (mean ± standard deviation), expressed as percentage of area at risk, was significantly reduced in the pressure overload group (19.3 ± 2.5 %, p < 0.001) and in the ischemic preconditioning group (18.3 ± 1.8 %, p < 0.001) versus the control group (27.3 ± 3.3 %). Pretreatment with 8-(p-sulfophenyl)-theophylline, an adenosine receptor antagonist, limited the protection by ischemic preconditioning (26.8 ± 3.7%), but not that by pressure overload (19.2 ± 2.5%, p < 0.001). The 8-(p-sulfophenyl)-theophylline did not significantly affect the extent of infarct (26.4 ± 5.4%). The hemodynamics prior to treatment, area at risk, and mortality were not significantly different among all groups of animals. CONCLUSIONS: Brief pressure overload of the left ventricle preconditioned rabbit myocardium against infarction. Because 8-(p-sulfophenyl)-theophylline had no significant effect on this response, the results are consistent with the hypothesis that the underlying mechanism does not depend on activation of adenosine receptors.

Early outcome of endovascular repair for contained ruptured abdominal aortic aneurysm.

BACKGROUND: Endovascular aneurysm repair (EVAR) has become a well-established technique in the treatment of elective surgery for abdominal aortic aneurysms (AAAs) due to proven benefits in mortality, hospital stay and operation time compared to open repair. The aim of this study was to report our experience in establishing the treatment protocol for EVAR of contained ruptured abdominal aortic aneurysms (rAAAs) and to illustrate the real impact of endovascular rAAA repair on surgical strategy. METHODS: Eighteen patients underwent AAA between January 2008 and October 2009. Six of them were enrolled in our study. The inclusion criteria were contained rAAA and the same anatomic consideration as in elective EVAR cases. The implant material was the Zenith AAA modular bifurcated device. Computed tomography (CT) scan was obtained in all patients pre-operatively and used as a follow-up tool. RESULTS: The mean age was 81 years (range 79-87 years). The procedural time was 259 ± 146 minutes, the maximal diameter of aneurismal sac was 8.4 ± 1.8 cm, and the pre-operative hemoglobin was 9.0 ± 1.2 mg/dL. The mean intensive care unit (ICU) stay was 10.5 ± 15 days. There was no surgical or in-hospital mortality. Complications included abdominal compartment syndrome, renal failure, wound infection and pneumonia. The mean follow-up period was 22 (range 19-29) months, with satisfactory result. CONCLUSION: Endovascular repair of rAAAs is feasible, and short-term results are promising, especially for contained and hemodynamic subgroup patients. It is indicated for elder patients with severe underlying diseases. Good logistics and adequate training of physicians or staff in an elective setting are prerequisites for this type of treatment program.

Haptoglobin phenotypes and plasma haptoglobin levels in patients with abdominal aortic aneurysm.

OBJECTIVE: Inflammation is associated with the disruption of the aortic media and appears to play a fundamental role in the progression and development of abdominal aortic aneurysm (AAA). Haptoglobin (Hp) is a genetically determined acute phase protein, the synthesis of which is increased during inflammation. This study was designed to investigate both phenotype and plasma levels of Hp in patients with AAA. METHODS: Patients with documented AAA who were admitted for elective open repair operation or endograft stent implantation, and non-AAA subjects admitted for coronary arteriography, but found to have normal or insignificant coronary artery disease, were included in the study. Plasma Hp levels were determined using a standard specific enzyme-linked immunosorbent assay, while Hp phenotype was determined by native polyacrylamide gel electrophoresis. Total cholesterol, high density lipoprotein, low density lipoprotein, and triglyceride levels were analyzed enzymatically, and C-reactive protein was analyzed by immunochemistry. RESULTS: Forty-five patients with AAA and 49 non-AAA subjects were included. The Hp 2-2 phenotype was more predominant in AAA patients compared with non-AAA subjects, but this difference was not significant (67% vs 47%; P = .141), while plasma Hp concentrations were significantly higher in AAA patients (237 ± 144 vs 163 ± 86 ng/mL; P = .024). Further analysis revealed that plasma Hp concentrations were significantly higher in AAA patients with the 2-2 phenotype compared with corresponding non-AAA subjects (238 ± 144 vs 163 ± 86 ng/mL;P = .024). CONCLUSIONS: Our findings suggest that plasma Hp concentrations are elevated in patients with AAA, particularly those with the Hp 2-2 phenotype.

Haemoglobin-induced oxidative stress is associated with both endogenous peroxidase activity and H2O2 generation from polyunsaturated fatty acids.

Patients with increased haemolytic haemoglobin (Hb) have 10-20-times greater incidence of cardiovascular mortality. The objective of this study was to evaluate the role of Hb peroxidase activity in LDL oxidation. The role of Hb in lipid peroxidation, H(2)O(2) generation and intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) was assessed using NaN(3), a peroxidase inhibitor, catalase, a H(2)O(2) decomposing enzyme and human umbilical vein endothelial cells (HUVECs), respectively. Hb induced H(2)O(2) production by reacting with LDL, linoleate and cell membrane lipid extracts. Hb-induced LDL oxidation was inhibited by NaN(3) and catalase. Furthermore, Hb stimulated ICAM-1 and VCAM-1 expression, which was inhibited by the antioxidant, probucol. Thus, the present study suggests that the peroxidase activity of Hb produces atherogenic, oxidized LDL and oxidized polyunsaturated fatty acids (PUFAs) in the cell membrane and reactive oxygen species (ROS) formation mediated Hb-induced ICAM-1 and VCAM-1 expression.

Malignancy after heart transplantation.

BACKGROUND: The purpose of this study was to assess the incidence and type of malignancies after heart transplantation at a medical institute in Taiwan. METHODS: From January 1987 to December 2008, a total of 66 patients who survived more than 30 days after transplantation were enrolled in this study. RESULTS: Of the 66 heart transplant recipients, 8 (12.1%) post-transplant malignancies were diagnosed: 5 posttransplant lymphoproliferative diseases (PTLD), 1 prostate cancer, 1 lung cancer, and 1 squamous cell carcinoma of the cheek. The clinical presentations were diverse, and the diagnoses were confirmed by biopsy. Only 1 patient died of PTLD and subsequent multiple organ failure. CONCLUSION: Cancer is a limiting factor for long-term survival after heart transplantation. The most common type in this study was PTLD. Early detection and aggressive treatment results in good response and preserves the allograft.

Left ventricular aneurysm repair: a comparison of linear versus patch remodeling.

BACKGROUND: Surgical repair of left ventricular (LV) aneurysm has been performed for around 50 years. However, the most appropriate surgical approach remains undetermined. This study was undertaken to compare the efficacy of 2 established techniques, linear versus patch remodeling, for repair of dyskinetic LV aneurysms. METHODS: We retrospectively reviewed the records of 49 patients (mean age, 69.8 +/- 7.3 years) who had operation for postinfarction dyskinetic LV aneurysm between 1996 and 2006. Thirty-one patients underwent patch remodeling and 18 underwent linear repair. Short-term and mid-term outcomes, including complications, cardiac function and mortality, were assessed. RESULTS: Overall inhospital surgical mortality, major complications and early hemodynamics showed no significant differences between the 2 groups. During a mean follow-up of 44.0 +/- 34.4 months, 8 patients died, with 4 due to cardiac-related causes. Actuarial survival rates at 1, 5 and 10 years were 85.7%, 69.9% and 45.7%, respectively. Functional class improved from 2.51 +/- 0.59 to 1.66 +/- 0.54 among the mid-term survivors (p < 0.001), with no significant difference between the 2 groups. Multivariate analysis identified preoperative NYHA functional class >or= 3 as an independent risk factor for overall mortality (p = 0.008). Mid-term follow-up revealed that LV ejection fraction improved from 26.5 +/- 7.2% to 34.1 +/- 7.9% (p < 0.001) in the patch group, and from 26.3 +/- 9.0% to 32.0 +/- 9.2% in the linear group (p = 0.032). In contrast, right ventricular ejection fraction improved from 49.4 +/- 10.1% to 52.0 +/- 7.3% (p = 0.190) in the patch group, but deteriorated from 55.0 +/- 6.3% to 50.3 +/- 8.6% in the linear group (p = 0.029). CONCLUSION: These findings indicate that the 2 repair techniques have similar effectiveness with respect to short- and mid-term outcomes except for right ventricular ejection fraction. We suggest that the selection of repair technique for LV aneurysms should be individualized for each patient based on aneurysm size and extent of the scarring process into the septum and subvalvular mitral apparatus.

Cardiac myocyte progenitors from adult hearts for myocardial regenerative therapy.

BACKGROUND: The heart is a highly vascular organ and prolonged interruption of myocardial blood flow initiates events that culminate in cardiac myocyte death. Proposed experimental reparative strategies include harvesting potent cells followed by direct injection into ischemic myocardium to achieve myogenesis and angiogenesis. METHODS: Accordingly, we set out to isolate and expand a purified population of adult rat putative cardiomyocyte precursors, and to identify their characteristics in vitro. By using an acute myocardial infarction model and direct cell implantation, we further tested the hypothesis that these cells are an ideal cell source for myocardial regeneration and can enhance cardiac repair after implantation into the ischemic rat heart. RESULTS: We describe here the identification of a subpopulation of primitive cells from rat heart, processing stem cell marker, c-kit and myogenic transcriptional factors, GATA-4 and MEF 2C, and cardiac specific proteins, troponin-I, alpha-sarcomeric actinin and connexin-43. They exhibited a high in vitro proliferative potential. These findings strongly suggest that these cells are putative cardiomyocyte precursors. After transplantation, they were able to be retained and proliferate (13.63 +/- 5.97% after 2 weeks) within the ischemic heart. Progeny of implanted cells migrated along the infarcted scar, reconstituted regenerated cardiomyocytes with incorporation into host myocardium, and inhibited cardiac remodeling with decreased scar formation. CONCLUSION: Our findings suggest that putative cardiomyocyte precursors isolated from adult heart could potentially be an autologous cell source for myocardial regeneration cell therapy.

Immunochemical property of human haptoglobin phenotypes: determination of plasma haptoglobin using type-matched standards.

OBJECTIVES: Haptoglobin (Hp) phenotypes 1-1, 2-1, and 2-2 are associated with inflammatory diseases. Since their biochemical structures are rather heterogeneous, it is necessary to accurately determine the plasma Hp levels. DESIGN AND METHODS: Immunodiffusion, immunoturbidimetric, and noncompetitive ELISA were conducted to determine the differences in immunoreactivity among Hp phenotypes and to verify that such difference may significantly affect the outcome of Hp determinations. A novel ELISA using phenotype-matched calibrators was performed to compared with a commercial GenWay ELISA kit using a single calibrator in normal healthy males. RESULTS: In immunodiffusion and immunoturbidimetric assays, the immunoreactivity of Hp 1-1 was markedly higher than 2-1 and 2-2, while an opposite result was observed using an ELISA. The latter was primarily due to the repeated antigenic epitopes in polymeric 2-1 and 2-2. Thus, Hp levels could be significantly over- or underestimated depending on the method. An accurate ELISA could be achieved when using each type-specific Hp calibrator matched to each type subject. We show the mean levels of Hp 1-1 subjects (n=16; 184+/-42 mg/dL) to be significantly and differentially greater than 2-1 (n=28; 153+/-55 mg/dL) (p<0.05) and 2-2 (n=24; 93+/-54 mg/dL) (p<0.01) subjects. CONCLUSIONS: Due to the diverse immunochemical structure among the Hp types, phenotyping should be performed in all the patients and a type-matched Hp calibrator should be used in clinical Hp determination.

Correlation between body mass index and leucopenia after administration of valganciclovir for cytomegalovirus infection in chinese cardiac recipients.

BACKGROUND: Valganciclovir (VGC) has recently been proved efficacious for the prophylaxis and treatment of cytomegalovirus (CMV) infection in transplant recipients. Leucopenia is a troublesome complication of VGC but the possible risk factors are unknown. METHODS AND RESULTS: Once a cardiac recipient's quantitative real-time CMV-polymerase chain reaction result showed positive, VGC was administered for 3 months. The 61 cardiac recipients enrolled in this study were divided into 2 groups: non-leucopenia group (n=29) and leucopenia group (n=32). The white blood cell (WBC) counts in the leucopenia group dropped approximately 55.6% in the first month after VGC therapy (pre-VGC WBC count: 5,544 cells/mm(3) vs post-VGC WBC count: 2,460 cells/mm(3), p<0.0001). The most significant difference between the 2 groups was body mass index (BMI, 23.04 vs 25.84, p=0.008), which was the impact factor of VGC-induced leucopenia. CONCLUSION: Severe leucopenia may develop after VGC therapy in Chinese cardiac recipients, especially those with lower BMI.

Endomyocardial biopsy-related tricuspid regurgitation after orthotopic heart transplantation: single-center experience.

BACKGROUND: Damage of tricuspid valve (TV) with resultant tricuspid regurgitation (TR) induced by endomyocardial biopsy (EMB) following heart transplantation has been reported in several studies. This study tried to determine the prevalence of EMB-related iatrogenic damage over tricuspid apparatus following orthotopic heart transplantation and to evaluate its impact on the patients. METHODS: Fifty patients received orthotopic heart transplantation between July 1987 and March 2005. Eleven patients were excluded from the study due to early postoperative mortality or inadequate follow-up. The medical records of the remaining 39 patients were reviewed retrospectively for basic characteristics as well as each attempted EMB. The iatrogenic damage of tricuspid apparatus and serial change of TR were accessed with 2-D and Doppler echocardiography. The obtained data were analyzed for their statistical significance with SPSS (version 12.0). RESULTS: A total of 373 biopsies were performed on the 39 patients between 1987 and 2005. The follow-up duration was 42.9+/-26.7 months. The prevalence of TR immediately following heart transplantation was 84.6%, with only 25.6% of patients having moderate or severe TR. At the end of the follow-up, the prevalence of TR increased to 92.3% and 61.5% of patients having moderate or severe TR, respectively. Eight patients (20.5%) had small chordae rupture (SCR) noted after 6.6+/-3.2 biopsies, and 10 patients (25.6%) had flail tricuspid valve (FTV) after 5.7+/-5.1 biopsies. Of patients with SCR, 62.5% had progression of TR, and 70% of patients with FTV showed significant TR change. CONCLUSION: The prevalence of iatrogenic tricuspid apparatus damage was high in this study. It contributed to the progression of TR significantly regardless of the damage severity. Measurements should be taken for prevention of iatrogenic tricuspid apparatus damage induced by EMB.

Endoaneurysmorrhaphy and cryoablation for postinfarction left ventricular aneurysm with ventricular tachycardia.

BACKGROUND: Early reperfusion in the acute phase of myocardial infarction and better medical treatment of consequent heart failure and tachyarrhythmia have decreased the incidence of massive myocardial infarction, left ventricular (LV) aneurysm and also postinfarction-sustained ventricular tachycardia (VT). However, for a number of patients, surgical ablation combined with aneurysm resection and myocardial revascularization remains a possible curative procedure. In this study, the efficacy of endoaneurysmorrhaphy and cryoablation was evaluated in patients with postinfarction LV aneurysm with VT. METHODS: The medical records of 9 patients who underwent LV endoaneurysmorrhaphy and cryoablation for VT at Taipei Veterans General Hospital between January 1995 and August 2005 were reviewed retrospectively. RESULTS: There were 8 men and 1 woman, with a mean age of 69.7 years (range, 52-77 years). Preoperative VT and LV aneurysm were found in all patients, who underwent extensive cryoablation at the transitional zone of scar and viable tissue without intraoperative mapping and LV remodeling with prosthetic patch. Associated procedure included coronary artery bypass grafting in 8 patients. During follow-up, no surgical or in hospital mortality were noted. There was 1 late sudden death at home 1.7 months after the operation. No recurrent VT was detected, and all patients showed improvement in New York Heart Association functional class (mean, 2.33 vs.1.67; p=0.025) and LV ejection fraction (mean, 26.3% vs.34.1%; p=0.021). CONCLUSION: In patients suffering from postinfarction LV aneurysm complicated with VT, combining cryoablation and endoaneurysmorrhaphy offers good arrhythmia control and clinical outcome.

Coronary artery bypass grafting in patients with left ventricular dysfunction.

BACKGROUND: Coronary artery bypass grafting surgery (CABG) remains a challenge for patients with coronary artery disease and left ventricular (LV) dysfunction. The aim of this study was to evaluate the result of CABG in patients with LV dysfunction. METHODS: Medical records of 1,847 patients who underwent primary, isolated CABG at Taipei Veterans General Hospital from January 1, 1991 to December 31, 2002, were reviewed. The mortality rate associated with clinical and operative variables was compared between patients with LV ejection fraction (LVEF) > or = 35% and patients with LVEF < 35%. RESULTS: Patients with LVEF < 35% had more episodes of myocardial infarction (57.5% vs 28.9%, p < 0.001) and history of congestive heart failure (18.1% vs 3.2%, p < 0.001), higher New York Heart Association (NYHA) class, and higher angina class. Longer cardiopulmonary bypass time (147 +/- 44 minutes vs 137 +/- 40 minutes, p < 0.001) but fewer left internal mammary artery (LIMA) grafts (46.8% vs 65.7%, p < 0.001) were used in patients with LVEF < 35%. Patients with LVEF < 35% had significantly higher hospital mortality (6.6% vs 2.2%, p < 0.001), higher major morbidity (23.3% vs 16.1%, p < 0.01), and longer hospital stay (25 +/- 23 days vs 21 +/- 16 days, p < 0.01). CONCLUSION: Although patients with LV dysfunction had higher mortality and morbidity, CABG could be done in these high-risk patients with acceptable results.

Ten-year experience with surgical repair of mycotic aortic aneurysms.

BACKGROUND: Mycotic aneurysm remains a lethal pathologic entity, especially when rupture occurs. It may result from primary aortitis, be induced by septic emboli, or be secondary to an adjacent infection, such as pancreatitis or a psoas muscle abscess. Surgical intervention is the only way to treat such disease. Even when successful repair is achieved by insertion of an interposition in situ graft or by performance of an extra-anatomic bypass, the prognosis is poor. The aim of this study was to present our experience of managing mycotic aortic aneurysms during the past 10 years. METHODS: From January 1994 to June 2004, a total of 734 patients with aortic aneurysms underwent surgical repair at our institution. Among these cases, 17 (2.3%) were shown to be mycotic aneurysms of the ascending aorta (n = 1), aortic arch (2), thoracic and thoracoabdominal aorta (3), or abdominal aorta (11); 14 patients (mean age, 58.8 years) were male. Preoperative imaging studies were performed in all patients. Mycotic aortic aneurysms were suspected in 12 of the 17 patients (70.6%) preoperatively, and 4 of these 12 patients were found to have ruptures on imaging. At the time of surgery, 9 of the 17 aneurysms (52.9%) were ruptured. Fifteen patients had an interposition graft inserted after meticulous debridement, 1 underwent an aorto-aortic bypass, and 1 underwent an extra-anatomic (axillo-femoral) bypass. An omentum patch was applied to wrap the graft in 8 of 11 mycotic aortic aneurysms of the abdominal aorta. The most common pathogens were Salmonella spp. (n = 7) and Staphylococcus spp. (4). All patients received antibiotic therapy, according to the culture report, for about 4-6 weeks postoperatively. RESULTS: In-hospital mortality was 11.8% (n = 2). Another patient died from massive upper gastrointestinal bleeding 6 months after operation because of complications involving an aorto-duodenal fistula, and another died from stomach cancer 6 years after surgery. Long-term follow-up (mean, 37 months; range, 3-111 months) revealed that, at the time of writing, the remaining 13 patients were alive and well, without any recurrence of aneurysm. CONCLUSION: Mycotic aneurysm of the aorta is a life-threatening disease, especially when rupture occurs. The high mortality rate is due not only to the high rupture rate, but also to sepsis. When mycotic aortic aneurysm is diagnosed, early surgical intervention is mandatory.

beta(2)-glycoprotein I protects J774A.1 macrophages and human coronary artery smooth muscle cells against apoptosis.

beta(2)-Glycoprotein I (beta(2)-GPI) is a plasma glycoprotein with multifactorial relevance to clinical consequences. It was previously indicated that beta(2)-GPI can selectively bind to apoptotic cells. This study was designed to determine the role of beta(2)-GPI in apoptosis. Using an immunohistochemical study, we observed that beta(2)-GPI was co-localized with the apoptotic macrophages and smooth muscle cells (SMCs) of human coronary arteries. The contribution of beta(2)-GPI to apoptotic death was then investigated in vascular cells. Two nitric oxide (NO) donors, S-nitrosoglutathione (GSNO) and S-nitroso-N-acetyl penicillamine (SNAP) were used in this study to trigger apoptosis in J774A.1 macrophages and human coronary artery smooth muscle cells (HCASMC). Cell viability was significantly improved in beta(2)-GPI-treated cells. It was also possible to detect a remarkable inhibitory effect by beta(2)-GPI on the NO-induced apoptosis by preventing nuclear shrinkage. Furthermore, the NO-induced apoptosis was associated with increase in caspase-3 activity and in the protein levels of caspase-3, c-Fos, and c-Jun. However, all these apoptosis-related events were inhibited in vascular cells treated with 200 microg/ml beta(2)-GPI. This is the first study to show that beta(2)-GPI may be important in the prevention of apoptosis in vascular cells.

The value of plasma levels of tumor necrosis factor-alpha and interleukin-6 in predicting the severity and prognosis in patients with congestive heart failure.

BACKGROUND: High plasma levels of pro-inflammatory cytokines play an important role in the pathophysiology of congestive heart failure (CHF). Therefore, we conducted a case-control study to determine the correlations between plasma levels of cytokines, i.e., tumor necrosis factor-alpha (TNF-alpha) and interleukin (IL)-6, and the severity and mortality in patients with CHF. METHODS: One-hundred and 18 cases (62+/-15 years old) were classified into 3 groups: group 1 comprised 44 control cases with normal coronary arteriogram and left ventriculography and without valvular disorders or cardiomyopathy; group 2 comprised of 37 cases with mild CHF in New York Heart Association (NYHA) functional class (FC) II; group 3 had 37 cases with moderate/severe CHF in NYHA FC III or IV. Pre-catheterization plasma levels of TNF-alpha and IL-6 along with clinical and hemodynamic variables and follow-up data of cardiac death were assessed. RESULTS: Patients of group 3 had smaller body mass index, lower systolic and diastolic blood pressures, faster heart rates, higher left ventricular end-diastolic pressure and lowered triglyceride levels than the patients of groups 1 and 2. The plasma levels of TNF-alpha and IL-6 increased significantly in patients of group 3 in comparison with patients of groups 1 and 2 (both p < 0.001). Over the following 1.5 years, 13 patients died. Univariate analysis identified the following variables to be associated with poor prognosis: NYHA FC (p < 0.001), plasma TNF-alpha (p = 0.013), plasma IL-6 (p < 0.001), systolic blood pressure (p = 0.001), heart rate (p = 0.045) and left ventricular end-diastolic pressure (p = 0.021). Multivariate Cox regression analysis identified the independent predictors of cardiac death as FC (p = 0.007) and plasma IL-6 (p = 0.021). CONCLUSIONS: Our findings indicate that the plasma levels of IL-6 and TNF-alpha and especially the former, is a useful marker to correlate the progression of severity and late cardiac death in patients with CHF.

Brief pressure overload of the left ventricle preconditions rabbit myocardium against infarction.

BACKGROUND: Several nonischemic stimuli have been shown to precondition myocardium. We investigated cardioprotective effects and underlying mechanisms of brief pressure overload of the left ventricle in this study. METHODS: Brief pressure overload of the left ventricle was achieved by two 10-minute partial snaring of the ascending aorta so that systolic left ventricular pressure was raised 50% above the baseline value. Ischemic preconditioning was elicited by two 10-minute coronary artery occlusions. Ten minutes after different pretreatments, myocardial infarction was induced by a 60-minute coronary artery occlusion followed by 3-hour reperfusion. Area at risk and myocardial infarct was determined by blue dye injection and triphenyl tetrazolium chloride staining. RESULTS: The myocardial infarct size, expressed as percentage of area at risk, was significantly reduced in the pressure overload group (15.9% +/- 2.9%, p < 0.001, n = 9) as well as in the ischemic preconditioning group (14.9% +/- 1.9%, p < 0.001, n = 9) versus the control group (30.0% +/- 6.9%, n = 10). Pretreatment with a blocker of stretch-activated ion channels (gadolinium, 40 micromol/kg, intravenous) abolished the protection induced by pressure overload and ischemic preconditioning. Gadolinium itself did not alter the extent of infarct. There was no significant difference in hemodynamics, area at risk, and mortality among all groups of animals. CONCLUSIONS: Brief pressure overload of the left ventricle by partial snaring of the ascending aorta preconditioned rabbit myocardium against infarction. The underlying mechanism might be related to activation of stretch-activated ion channels.

Results of surgical treatment for peripheral arterial occlusive disease in women.

BACKGROUND: The incidence and prevalence of peripheral arterial occlusive disease (PAOD) in women is more prevalent than generally appreciated, and the results of surgical treatment are not certain. The purpose of this study was to investigate the result of surgical treatment of PAOD in female patients in our service. METHODS: Medical records of female patients undergoing surgical treatment for PAOD in Taipei Veteran General Hospital from January 1, 1997 to July 31, 1998 were reviewed retrospectively. The clinical variables were evaluated, including age, smoking, diabetes mellitus, hypertension, renal function, coexistent coronary disease, history of stroke, Fontaine stages, surgical procedures and results. RESULTS: There were 20 female patients undergoing surgical treatment for PAOD during the study period, aged from 57 to 91 years, with an average of 73.7 +/- 2.2. Four patients presented with rest pain. Twelve patients presented with gangrene of lower limbs. Ten patients underwent bypass surgery. Three patients received embolectomy. One patient underwent below knee amputation after femoro-popliteal bypass. One patient underwent below knee amputation after embolectomy. Five patients underwent above knee amputation without bypass surgery or embolectomy. Four patients (20%) died after surgery. CONCLUSIONS: The female patients of PAOD presented with severe symptoms and advanced Fontaine stages. The delay in diagnosis and referral resulted in an unsatisfying outcome of surgical treatment. An aggressive approach in diagnosis and referral is necessary for better results.

Operative results of coronary artery bypass grafting in women.

BACKGROUND: The relative mortality of coronary artery bypass grafting (CABG) surgery in women is not certain. The purpose of this study was to examine the results of primary, isolated CABG in a series of Taiwanese female patients. METHODS: Medical records of 2055 patients (188 women and 1867 men), who underwent primary, isolated CABG at Taipei Veterans General Hospital from January 1, 1991 to December 31, 1999, were reviewed. The mortality rate, associated with clinical and operative variables, was compared between female and male patients. RESULTS: The female patients had more diabetes (51.6% vs. 29.9%, P<0.01), more hypertension (77.1% vs. 65.0%, P<0.01), and more hypercholesterolemia (39.4% vs. 29.6%, P<0.01), as compared with men. Fewer women consumed cigarette smoking (17.0% vs. 52.1%, P<0.001). Fewer internal mammary artery grafts were used in women (43.1% vs. 57.3%, P<0.001). Nine female (4.8%) and 93 male patients (5.0%) died. There was no significant difference in hospital mortality between women and men. Other variables, including age, angina class, NYHA class, incidence of peripheral arterial occlusive disease, stenosis of left main coronary artery, number of stenotic coronary arteries, incidence of emergent operations, anastomosis number, aortic cross-clamping time, cardiopulmonary bypass time, and left ventricular ejection fraction, were not significantly different between female and male patients. CONCLUSIONS: Although the female patients were more frequently diabetic, hypertensive, and hypercholesterolemic, the hospital mortality of CABG in women was not significantly different from that in men. This result supports an aggressive surgical treatment for women with coronary artery disease.

The effect of pathophysiology on the outcome of mitral valve repair for mitral regurgitation.

The advantages of mitral valve repair in mitral regurgitation are well established. The aim of this study was to analyze retrospectively the early and mid-term results of primary mitral valve repair. Between January 1995 and August 2001, primary mitral valve repair operations were performed on 112 patients (76 men and 36 women) with mitral regurgitation; the mean age was 59.8 +/- 16.5 years. Mitral valve repair was performed for rheumatic heart disease (13), degenerative disease (60), infective endocarditis (2), ischemic heart disease (26), congenital heart disease (2), and dilated cardiomyopathy (9). The degree of mitral regurgitation was moderate in 28 patients, moderately severe in 17 patients, and severe in 67 patients, as determined by echocardiography. Left ventricular ejection fraction (mean 41.2% +/- 13.5%) was measured by radionuclide ventriculography. Fifty percent of patients underwent additional procedures (e.g., coronary artery bypass grafting). The mortality rate was 8.9% (10/112) for hospitalized patients, 19.2% (5/26) for ischemic disease, and 5% (3/60) for degenerative disease. Follow-up duration ranged from 0.37 to 84.03 months. All survivors were evaluated with serial echocardiography. At the final follow-up echocardiography of 94 patients without reoperation and 6 patients at the time of reoperation, 84% had no or mild mitral regurgitation. The survival rate at 5 years was 92.68 +/- 3.57% for degenerative disease and 44.47% +/- 10.89% for ischemic disease. The risk of infective endocarditis (1.78%), thromboembolism (1.78%), and anticoagulant-related complications (0.8%) was very low during the follow-up period. The pathophysiological mechanism resulting in mitral regurgitation was the most important determinant of outcome after mitral valve repair. Excellent results were achieved with mitral valve repair for degenerative disease. Because of low morbidity and acceptable mortality, we strongly recommend mitral valve repair for mitral regurgitation due to degenerative disease.