Chung-Yi Lee

Extracorporeal membrane oxygenation for refractory cardiogenic shock after cardiac surgery: predictors of early mortality and outcome from 51 adult patients

OBJECTIVE Extracorporeal membrane oxygenation (ECMO) offers temporary haemodynamic support for those with refractory cardiogenic shock after cardiac surgery. We review our 5-year experience regarding ECMO use on those who cannot be weaned from cardiopulmonary bypass after cardiac surgery. We analyse our cases, predict the prognostic factors of survival and compare the short-term and medium-term results. METHODS From January 2002 to December 2006, 1764 patients underwent cardiac surgery with cardiopulmonary bypass in our division. Among these, 51 patients (2.9%) required venoarterial-mode ECMO for haemodynamic support because of refractory postcardiotomy cardiogenic shock. The indication of ECMO was refractory cardiogenic shock despite adequate filling volumes, large-dose inotropes and intra-aortic balloon pump support. The following cardiac surgical procedures were performed: coronary artery bypass grafting (CABG), n=27; valvular surgery, n=11; CABG plus valvular surgery, n=7; heart transplantation, n=4 and other procedures, n=2. RESULTS Average age was 63.0+/-15.7 years. There were 36 male and 15 female patients. Average duration of ECMO was 7.5+/-6.7 days. Twenty-seven (53%) patients could be successfully weaned from ECMO. The 30-day and 3-month mortalities were 49% (25/51) and 65% (33/51). The in-hospital mortality was 67% (34/51 patients). Seventeen (33%) patients could be successfully discharged. Fifteen (29%) patients were still alive at 1-year outpatient department (OPD) follow-up. CONCLUSIONS ECMO provides a good temporary cardiopulmonary support in patients with postcardiotomy shock. The preoperative risk factors of failure to withdraw ECMO are poor left-ventricular ejection fraction, systolic blood pressure <90 mmHg and refractory severe metabolic acidosis. The peri-ECMO predictors of mortality include low serum albumin level, low platelet count, low oxygen pressure of the venous tube of the ECMO and poor cardiac systolic function.

Congenital coronary artery fistulas: clinical considerations and surgical treatment.

Background:  Coronary artery fistulas are uncommon abnormalities that can cause significant cardiac morbidity. Indications for operation vary, particularly, for asymptomatic patients. Early surgical correction is indicated because of the high incidence of late symptoms and complications.

Experience of heart transplantation from hemodynamically unstable brain-dead donors with extracorporeal support.

Yang H‐Y, Lin C‐Y, Tsai Y‐T, Lee C‐Y, Tsai C‐S. Experience of heart transplantation from hemodynamically unstable brain‐dead donors with extracorporeal support.

Infective Endocarditis from Streptococcus viridans Associated with Colonic Carcinoma: A Case Report

Abstract  Streptococcal bacteremia is an uncommon presentation for colorectal malignancy, yet most physicians would probably be aware of the association between Streptococcus bovis infection and such malignancy; however, many physicians may be unaware that other streptococcal species are also associated with colon and rectal cancers. We describe a 62‐year‐old male with adenocarcinoma of the sigmoid colon with the presentation of infective endocarditis due to infection by Streptococcus viridans, and we also report on the conditions successful treatment.

Antiarrhythmic effects of dehydroevodiamine in isolated human myocardium and cardiomyocytes

ETHNOPHARMACOLOGICAL RELEVANCE Dehydroevodiamine alkaloid (DeHE), a bioactive component of the Chinese herbal medicine Wu-Chu-Yu (Evodiae frutus), exerted antiarrhythmic effect in guinea-pig ventricular myocytes. We further characterize the electromechanical effects of DeHE in the human atrial and ventricular tissues obtained from hearts of patients undergoing corrective cardiac surgery or heart transplantation. MATERIALS AND METHODS The transmembrane potentials of human myocardia were recorded with a traditional microelectrode technique while sarcolemmal Na(+) and Ca(2+) currents in single human cardiomyocytes were measured by a whole-cell patch-clamp technique. The intracellular pH (pHi) and Na(+)-H(+) exchanger (NHE) activity were determined using BCECF-fluorescence in human atria. RESULTS In human atria, DeHE (0.1-0.3 μM) depressed upstroke velocity, amplitude of action potential, and contractile force, both in slow and fast response action potential. Moreover, the similar depressant effects of DeHE were found in human ventricular myocardium. Both in isolated human atrial and ventricular myocytes, DeHE (0.1-1 μM) reversibly, concentration-dependently decreased the Na(+) and Ca(2+)currents. Moreover, DeHE (0.1 and 0.3 μM) suppressed delayed afterdepolarizations and aftercontractions, induced by epinephrine and high [Ca(2+)]o in atria. In human ventricular myocardium, the strophanthidin-induced triggered activities were attenuated by pretreating DeHE (0.3 μM). The resting pHi and NHE activity were also significantly increased by DeHE (0.1-0.3 μM). CONCLUSIONS We concluded for the first time that, in the human hearts, DeHE could antagonize triggered arrhythmias induced by cardiotonic agents through a general reduction of the Na(+) and Ca(2+) inward currents, while increase of resting pHi and NHE activity.

Intracellular Acid-extruding regulators and the effect of lipopolysaccharide in cultured human renal artery smooth muscle cells.

Homeostasis of the intracellular pH (pHi) in mammalian cells plays a pivotal role in maintaining cell function. Thus far, the housekeeping Na+-H+ exchanger (NHE) and the Na+-HCO3 − co-transporter (NBC) have been confirmed in many mammalian cells as major acid extruders. However, the role of acid-extruding regulators in human renal artery smooth muscle cells (HRASMCs) remains unclear. It has been demonstrated that lipopolysaccharide (LPS)-induced vascular occlusion is associated with the apoptosis, activating calpain and increased [Ca2+]i that are related to NHE1 activity in endothelia cells. This study determines the acid-extruding mechanisms and the effect of LPS on the resting pHi and active acid extruders in cultured HRASMCs. The mechanism of pHi recovery from intracellular acidosis (induced by NH4Cl-prepulse) is determined using BCECF-fluorescence in cultured HRASMCs. It is seen that (a) the resting pHi is 7.19±0.03 and 7.10±0.02 for HEPES- and CO2/HCO3 −- buffered solution, respectively; (b) apart from the housekeeping NHE1, another Na+-coupled HCO3 − transporter i.e. NBC, functionally co-exists to achieve acid-equivalent extrusion; (c) three different isoforms of NBC: NBCn1 (SLC4A7; electroneutral), NBCe1 (SLC4A4; electrogenic) and NBCe2 (SLC4A5), are detected in protein/mRNA level; and (d) pHi and NHE protein expression/activity are significantly increased by LPS, in both a dose- and time- dependent manner, but NBCs protein expression is not. In conclusion, it is demonstrated, for the first time, that four pHi acid-extruding regulators: NHE1, NBCn1, NBCe1 and NBCe2, co-exist in cultured HRASMCs. LPS also increases cellular growth, pHi and NHE in a dose- and time-dependent manner.

Urotensin II Inhibits Doxorubicin-Induced Human Umbilical Vein Endothelial Cell Death by Modulating ATF Expression and via the ERK and Akt Pathway

Background and Purpose Regulation of the homeostasis of vascular endothelium is critical for the processes of vascular remodeling and angiogenesis under physiological and pathological conditions. Urotensin II (U-II), a potent vasoactive peptide, participates in vascular and myocardial remodeling after injury. We investigated the protective effect of U-II on doxorubicin (DOX)-induced apoptosis in cultured human umbilical vein endothelial cells (HUVECs) and the potential mechanisms involved in this process. Experimental Approach Cultured HUVECs were treated with vehicle, DOX (1 µM), U-II, or U-II plus DOX. Apoptosis was evaluated by DNA strand break level with TdT-mediated dUTP nick-end labeling (TUNEL) staining. Western blot analysis was employed to determine the related protein expression and flow cytometry assay was used to determine the TUNEL positive cells. Key Results U-II reduced the quantity of cleaved caspase-3 and cytosol cytochrome c and increased Bcl-2 expression, which results in protecting HUVECs from DOX-induced apoptosis. U-II induced Activating transcription factor 3 (ATF3) at both mRNA and protein levels in U-II-treated cells. Knockdown of ATF3 with ATF3 siRNA significantly reduced ATF3 protein levels and U-II protective effect under DOX-treated condition. U-II downregulated p53 expression in DOX-induced HUVECs apoptosis, and it rapidly activated extracellular signal-regulated protein kinase (ERK) and Akt. The DOX induced change of p53 was not affected by U-II antagonist (urantide) under ATF-3 knockdown. The inhibitory effect of U-II on DOX-increased apoptosis was attenuated by inhibitors of ERK (U0126) and PI3K/Akt (LY294002). Conclusion and Implications Our observations provide evidence that U-II protects HUVECs from DOX-induced apoptosis. ERK-Akt phosphorylation, ATF3 activation, and p53 downregulation may play a signal-transduction role in this process.

Assessment of the Risk Factors and Outcomes for Postoperative Atrial Fibrillation Patients Undergoing Isolated Coronary Artery Bypass Grafting.

BACKGROUND Atrial fibrillation is the most common complication of cardiac surgery and is associated with significant morbidity and mortality. Recognizing patients at high risk for developing postoperative atrial fibrillation (POAF) may help identify those who could benefit from strategies to prevent POAF. This study was conducted to delineate outcomes and to assess risk factors for POAF among Taiwanese patients undergoing coronary artery bypass grafting (CABG). METHODS From January 2009 until February 2012, this prospective study included 266 consecutive patients admitted to our hospital with coronary artery disease. All patients underwent isolated CABG. Patients with preoperative permanent atrial fibrillation and concomitant surgery were excluded. Multiple risk factors associated with the incidence of POAF were collected and evaluated. RESULTS POAF occurred in 126 of 226 patients (47.37%). Univariate analysis revealed that significant risk factors for the condition were age, gender, diabetes, dyslipidemia, smoking, impaired renal function, impaired cardiac function, and increased serum electrolytes. Multivariate analysis showed dyslipidemia [hazard ratio (HR): 0.418; 95% confidence interval (Cl): 0.190-0.915, p = 0.029], impaired renal function as indicated by an estimated glomerular filtration rate < 60 mL/min/1.73 m(2) (HR: 3.174; 95% CI: 1.432-7.037, p = 0.004), and serum sodium (HR: 1.112; 95% Cl: 1.047-1.182, p = 0.001) prior to cardiopulmonary bypass as significant. Moreover, POAF was associated with lower 30-day, 1- and 3-year cumulative survival rates and higher early postoperative complications. CONCLUSIONS Patients with isolated CABG who were administered β-blockers, angiotensin converting enzyme inhibitor/angiotensin receptor blockers treatment, and lipid therapy before CABG were associated with reduced POAF, while those with impaired renal function and higher serum sodium before CABG predisposed POAF in a Taiwanese population. KEY WORDS Atrial fibrillation (AF); Coronary artery bypass grafting (CABG); Coronary artery disease (CAD); Postoperative atrial fibrillation (POAF).

Left Atrial Appendage Aneurysm with Paroxysmal Atrial Fibrillation

Aneurysm of the left atrial appendage is extremely rare, and afflicted patients most commonly present with atrial tachyarrhythmia or thromboembolism. For these patients, resection of the aneurysm is the recommended and preferred therapy. We present the case of a 57-year-old woman who was found incidentally to have a large aneurysm of the left atrial appendage presenting as atrial fibrillation. After surgical intervention with resection of the aneurysm and a Cox maze III procedure, the patient recovered and was discharged in sinus rhythm.

Functional characterization of transmembrane intracellular pH regulators and mechanism of alcohol-induced intracellular acidosis in human umbilical cord blood stem cell-like cells.

Abstract Changing intracellular pH (pHi) exerts considerable influence on many cellular functions. Different pHi regulators, such as the Na+-H+ exchanger (NHE), Na+/ symporter, and Cl−/OH− exchanger (CHE), have been identified in mature mammalian cells. The aims of the present study were to investigate the physiological mechanisms of pHi recovery and to further explore the effects of alcohol on the pHi in human umbilical cord blood CD34+ stem cell–like cells (HUCB-CD34+STs). HUCB-CD34+STs were loaded with the pH-sensitive dye, 2′,7′-bis(2-carboxethyl)-5(6)-carboxyfluorescein, to examine pHi. In isolated HUCB-CD34+STs, we found that (1) the resting pHi is 7.03 ± 0.02; (2) 2 Na+-dependent acid extruders and a Cl−-dependent acid loading carrier exist and are functional; (3) alcohol functions in a concentration-dependent manner to reduce pHi and increase NHE activity, but it does not affect CHE activity; and (4) fomepizole, a specific alcohol dehydrogenase inhibitor, does not change the intracellular acidosis and NHE activity–induced by alcohol, whereas 3-amino-1, 2,4-trizole, a specific catalase inhibitor, entirely abolishes these effects. In conclusion, we demonstrate that 2 acid extruders and 1 acid loader (most likely NHE, NBC, and CHE, respectively) functionally existed in HUCB-CD34+STs. Additionally, the intracellular acidosis is mainly caused by catalase-mediated alcohol metabolites, which provoke the activity of NHE.