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Robert A Guyton

Publications and source records attributed to Robert A Guyton.

At least 19 recordsLinked to original sources
PubMed2006

Long-term inhibition of myocardial infarction by postconditioning during reperfusion.

Cardioprotection with postconditioning has been well demonstrated after a short period of reperfusion. This study tested the hypothesis that postconditioning reduces infarct size, vascular dysfunction, and neutrophil accumulation after a long-term reperfusion. Canines undergoing 60 min left anterior descending artery (LAD) occlusion were divided into two control groups of either 3 h or 24 h of full reperfusion and two postconditioning groups with three 30 s cycles of reperfusion and re-occlusion applied at the onset of either 3 h or 24 h of reperfusion. Size of the area at risk (AAR) and collateral blood flow during ischemia were similar among groups. In controls, infarct size as percentage of the AAR (30 +/- 3 vs. 39 +/- 2* %) by TTC staining, superoxide anion generation from the post-ischemic coronary arteries by lucigenin-enhanced chemiluminescence [(89 +/- 5 vs. 236 +/- 27* relative light units (RLU/mg)], and neutrophil (PMN) accumulation by immunohistochemical staining in the AAR (52 +/- 11 vs. 84 +/- 14* cells/mm(2) myocardium) significantly increased between 3 and 24 h of reperfusion. Postconditioning reduced infarct size (15 +/- 4 and 27 +/- 3.6 %), superoxide anion generation (24 +/- 4 and 43 +/- 11 RLU/mg), and PMN accumulation (19 +/- 6 and 45 +/- 8 cells/mm(2) myocardium) in the 3 and 24 h reperfusion groups relative to time-matched controls. These data suggest that myocardial injury increases with duration of reperfusion; reduction in infarct size and attenuation in inflammatory responses with postconditioning persist after a prolonged reperfusion. * p < 0.05 24 vs. 3 h control; p < 0.05 postconditioning vs. time-matched control.

Animals↗
PubMed2006

Neutrophil depletion reduces myocardial apoptosis and attenuates NFkappaB activation/TNFalpha release after ischemia and reperfusion.

BACKGROUND: This study tested the hypothesis that depletion of neutrophils (PMNs) reduces myocardial apoptosis via reducing oxidant generation and inhibiting NFkappaB-mediated signaling pathways after ischemia/reperfusion. METHODS: Anesthetized rats were randomly divided into one of four groups: CONTROL: 30 min ischemia and 3 h of reperfusion; PMN depletion: anti-PMN serum was injected 6 h before ischemia; N-acetylcysteine (NAC): NAC was given twice before ischemia and at reperfusion. Sham: the ligature was placed without coronary occlusion. Apoptosis was detected by TUNEL staining and DNA fragmentation. PMN accumulation was studied by immunohistochemical staining. Levels of TNF-alpha, IL-6, and caspase-3 were detected by Elisa kits. Expression in NFkappaB, Bcl-2, and Bax was assessed by Western blotting analysis. RESULTS: Relative to CONTROL, depletion of PMNs or NAC treatment reduced levels of plasma TNFalpha (567 +/- 130* and 231 +/- 72* versus 1994 +/- 447 pg/ml) and IL-6 (791 +/- 473* and 666 +/- 300* versus 3724 +/- 1233, pg/ml), accompanying a reduction in PMN accumulation (12 +/- 1* and 13 +/- 0.6* versus 20 +/- 1 mm2 myocardium) in ischemic myocardium. Both groups showed a reduction in expression of nuclear NFkappaB relative to CONTROL (62 +/- 9* and 67 +/- 8* versus 124 +/- 16 arb.u), consistent with reduced NFkappaB binding activity. The number of apoptotic cells (%) in area at risk myocardium was comparably reduced in anti-PMN and NAC groups relative to CONTROL (12 +/- 1* and 14 +/- 0.9* versus 20 +/- 1), consistent with reduced appearance of DNA ladders. Furthermore, activated caspase-3 was significantly reduced and Bcl-2 was increased relative to CONTROL. No difference in all parameters measured was detected during the course of experiment in the Sham group. CONCLUSION: These data suggest that the oxidants generated from activated PMNs after ischemia/reperfusion trigger myocardial apoptosis, which is further supported by an anti-oxidant therapy with NAC, potentially mediated by enhanced NFkappaB-TNFalpha signaling pathway, activated caspase-3 and down-regulated Bcl-2. *P < 0.05 versus CONTROL.

Animals↗
PubMed2006

Impact of renal dysfunction on outcomes of coronary artery bypass surgery: results from the Society of Thoracic Surgeons National Adult Cardiac Database.

BACKGROUND: Although patients with end-stage renal disease are known to be at high risk for mortality after coronary artery bypass graft (CABG) surgery, the impact of lesser degrees of renal impairment has not been well studied. The purpose of this study was to compare outcomes in patients undergoing CABG with a range from normal renal function to dependence on dialysis. METHODS AND RESULTS: We reviewed 483,914 patients receiving isolated CABG from July 2000 to December 2003, using the Society of Thoracic Surgeons National Adult Cardiac Database. Glomerular filtration rate (GFR) was estimated for patients with the use of the Modification of Diet in Renal Disease study formula. Multivariable logistic regression was used to determine the association of GFR with operative mortality and morbidities (stroke, reoperation, deep sternal infection, ventilation >48 hours, postoperative stay >2 weeks) after adjustment for 27 other known clinical risk factors. Preoperative renal dysfunction (RD) was common among CABG patients, with 51% having mild RD (GFR 60 to 90 mL/min per 1.73 m2, excludes dialysis), 24% moderate RD (GFR 30 to 59 mL/min per 1.73 m2, excludes dialysis), 2% severe RD (GFR <30 mL/min per 1.73 m2, excludes dialysis), and 1.5% requiring dialysis. Operative mortality rose inversely with declining renal function, from 1.3% for those with normal renal function to 9.3% for patients with severe RD not on dialysis and 9.0% for those who were dialysis dependent. After adjustment for other covariates, preoperative GFR was one of the most powerful predictors of operative mortality and morbidities. CONCLUSIONS: Preoperative RD is common in the CABG population and carries important prognostic importance. Assessment of preoperative renal function should be incorporated into clinical risk assessment and prediction models.

Coronary Artery Bypass↗
PubMed2006

Infarct-sparing effect of myocardial postconditioning is dependent on protein kinase C signalling.

OBJECTIVE: Using non-selective and selective protein kinase C (PKC) epsilon and delta isoform inhibitors, we tested the hypothesis that the cardioprotective phenotype invoked by postconditioning (postcon) is dependent on PKC signalling. Furthermore, we determined whether postconditioning alters pPKCepsilon and/or pPKCdelta in cytosolic and mitochondrial fractions. METHODS: Male Sprague-Dawley rats underwent 30 min left coronary artery (LCA) occlusion followed by 3 h of reperfusion. Rats were randomised to the following groups: Untreated, no intervention either before or after LCA occlusion; Postcon, 3 cycles of 10-s full reperfusion and 10-s re-occlusion, initiated immediately at the onset of reperfusion; Chelerythrine (non-selective PKC inhibitor, 5 mg/kg)+/-postcon; Rottlerin (PKCdelta inhibitor, 0.3 mg/kg)+/-postcon; KIE1-1 (PKCepsilon inhibitor, 3.8 mg/kg)+/-postcon. A subset of rats was employed to assess pPKCepsilon and/or pPKCdelta in sham, Isch/RP (30-min LCA occlusion followed by 30-min reperfusion), and postcon-treated hearts. RESULTS: Infarct size, expressed as area of necrosis as a percentage of the area at risk, AN/AAR (%), was significantly reduced by postcon compared to control (untreated) rats (39+/-2% vs. 53+/-1% in control, P<0.001). Treatment with chelerythrine alone or the PKCepsilon antagonist KIE1-1 alone at reperfusion had no effect on infarct size compared to control. In contrast, the infarct-sparing effect of postcon was abrogated by non-selective PKC inhibition and PKCepsilon antagonism (50+/-2% and 50+/-1%, respectively, P<0.002). Inhibition of PKCdelta reduced infarct size to values comparable to that in postcon group (36+/-3% vs. 39+/-2%). However, postcon in the presence of PKCdelta inhibitor did not enhance the infarct-sparing effects (38+/-2%). In addition, pPKCepsilon in postcon hearts was significantly higher in the total cell homogenate (10338+/-1627 vs. 4165+/-608 in Isch/RP, arbitrary units), and pPKCdelta translocation to mitochondria was significantly less (>2-fold decrease) compared to Isch/RP. CONCLUSION: These data suggest that postcon modulates PKC during early reperfusion by increasing PKCepsilon expression and translocation to a site other than the outer mitochondrial membrane, and limits translocation of PKCdelta to mitochondria and associated deleterious signalling.

Acetophenones↗
PubMed2006

Postconditioning attenuates cardiomyocyte apoptosis via inhibition of JNK and p38 mitogen-activated protein kinase signaling pathways.

A sequence of intermittent interruptions of oxygen supply (i.e., postconditioning, Postcon) at reoxygenation reduces oxidant-induced cardiomyocyte loss. This study tested the hypothesis that prevention of cardiomyocyte apoptosis by Postcon is mediated by mitogen-activated protein kinases pathways. Primary cultured neonatal rat cardiomyocytes were exposed to 3 h hypoxia followed by 6 h of reoxygenation. Cardiomyocytes were postconditioned by three cycles each of 5 min reoxygenation and 5 min hypoxia after prolonged hypoxia. Relative to hypoxia alone, reoxygenation stimulated expression of JNKs and p38 kinases, corresponding to increased activity of JNKs (phospho-c-Jun) and p38 (phospho-ATF2). The level of TNFalpha in cell lysates, activity of cytosolic caspases-8, -3, expression of Bax and the number of apoptotic cardiomyocytes were increased while expression of Bcl-2 was decreased with reoxygenation. Consistent with an attenuation in generation of superoxide anions detected by lucigenin-enhanced chemiluminescence at early period of reoxygenation, treatment of cardiomyocytes with Postcon further reduced expression and activity of JNKs and p38 kinases, level of TNFalpha, the frequency of apoptotic cells and expression of Bax. However, the inhibitory effects of Postcon on these changes were lost when its application was delayed by 5 min after the start of reoxygenation. Addition of a JNK/p38 stimulator, anisomycin into cardiomyocytes at the beginning of reoxygenation eliminated protection by Postcon. These data suggest that 1) hypoxia/reoxygenation elicits cardiomyocyte apoptosis in conjunction with expression and activation of JNK and p38 kinases, release of TNFalpha, activation of caspases, and an increase in imbalance of pro-/anti-apoptotic proteins; 2) Postcon attenuates cardiomyocyte apoptosis, potentially mediated by inhibiting JNKs/p-38 signaling pathways and reducing TNFalpha release and caspase expression.

Animals↗
PubMed2006

Early administration of clopidogrel is safe after off-pump coronary artery bypass surgery.

BACKGROUND: Patients who undergo off-pump coronary artery bypass graft surgery (OPCAB) may be hypercoagulable with an increased risk of graft thrombosis due to the lack of platelet dysfunction that accompanies "on-pump" surgery. Clopidogrel may be indicated in these patients to prevent recurrent ischemic events. The purpose of this observational study was to determine the safety of early clopidogrel administration after OPCAB. METHODS: Thirty-day follow-up of 364 consecutive OPCAB patients (January to June, 2002) was determined from a computerized database. One hundred ninety-three patients received clopidogrel 4 hours postoperatively if chest tube output was less than 100 cc/h for 4 hours, then daily for 4 weeks. Aspirin was administered preoperatively and postoperatively to all patients. Telephone follow-up was made 6 to 12 months after OPCAB. RESULTS: None of the patients who received clopidogrel in the early postoperative period required reoperation for mediastinal hemorrhage. Mean chest tube drainage at 24 hours was 1,024 +/- 563 mL in patients who received clopidogrel and 942 +/- 501 mL in patients who did not receive clopidogrel. The total number of blood units transfused and the number of patients receiving blood transfusions were similar between groups. In-hospital mortality was 1.6% in patients who received clopidogrel and 3.5% in patients who did not receive clopidogrel. No group differences in mortality or adverse cardiac events were observed at 6 months. Gastrointestinal bleeding occurred in 2.2% clopidogrel patients versus 0.7% of patients who did not receive clopidogrel. CONCLUSIONS: When administered according to our postoperative protocol, OPCAB patients can safely receive clopidogrel in the early postoperative period without increased risk for mediastinal hemorrhage.

Aged↗
PubMed2006

Thoracic Surgery Directors Association Award. Cobalt chloride pretreatment attenuates myocardial apoptosis after hypothermic circulatory arrest.

BACKGROUND: Deep hypothermic circulatory arrest (DHCA) causes myocyte injury as a consequence of ischemia and reperfusion. Previous studies have shown that hypoxia or hypoxia-mimetic agents (cobalt chloride [CoCl2] or deferoxamine [DFX]) limit myocyte necrosis by upregulating the transcription factor hypoxia-inducible factor. However, it remains unknown whether these agents attenuate myocardial apoptosis after DHCA. This study tested the hypotheses (1) that hypoxia, DFX, or CoCl2 preconditioning attenuates myocardial apoptosis during DHCA; and (2) that the protective mechanism involves the altered expression of apoptosis regulatory proteins pAkt (antiapoptotic), Bcl-2 (antiapoptotic), and Bax (proapoptotic). METHODS: Anesthetized neonatal piglets were randomly assigned to four groups (n = 6 in a group): control (NaCl injection); hypoxia (pO2 of 30 to 40 mm Hg for 3 hours); DFX injection; or CoCl2 injection. Twenty-four hours later, the animals underwent cardiopulmonary bypass (CPB) and 110 minutes of DHCA. One week after CPB, percentage of apoptotic myocytes (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling [TUNEL] assay) and expression of the pAKT, Bcl-2, and Bax were assessed by Western blot. RESULTS: Although preconditioning with hypoxia and DFX failed to show a protective benefit, CoCl2 pretreatment significantly attenuated myocardial apoptosis (9.3% +/- 4.1%) versus controls (33.8% +/- 9.7%, p = 0.042). That was associated with increased myocardial pAkt expression (0.19 +/- 0.006 in CoCl2 versus 0.12 +/- 0.008 in control, p < 0.001). The expression of Bcl-2 was also significantly higher in the CoCl2 group (0.15 +/- 0.02) versus control (0.11 +/- 0.01, p = 0.007), whereas Bax expression was lower (0.34 +/- 0.04 versus 0.54 +/- 0.03 for control, p < 0.001). CONCLUSIONS: Preconditioning with CoCl2 before prolonged DHCA in neonatal piglets attenuates myocardial apoptosis by mechanisms involving phosphorylation of Akt, upregulation of the antiapoptotic protein Bcl-2, and decreased expression of the proapoptotic protein Bax.

Animals↗
PubMed2006

Coronary artery bypass is superior to drug-eluting stents in multivessel coronary artery disease.

Percutaneous intervention for the treatment of multivessel coronary artery disease continues to displace coronary artery bypass graft surgery. But controlled trials of percutaneous intervention versus coronary bypass, in meta-analysis, have shown a significant survival advantage for coronary bypass. Studies of bare metal stents have not presented any data to prompt reversal of this conclusion for all but the small portion of patients most suited for stenting. Drug-eluting stents have no survival advantage compared with bare metal stents. Data from real-world registries have shown that the current therapy of multivessel disease patients has resulted in a relative excess mortality of as much as 46% in patients with initial stenting compared with patients with initial coronary bypass. Ethical considerations demand that patients with multivessel disease be informed of the documented mortality benefit of coronary bypass graft surgery.

Angioplasty, Balloon, Coronary↗
PubMed2005

Postconditioning reduces infarct size via adenosine receptor activation by endogenous adenosine.

OBJECTIVE: This study tested the hypothesis that brief cycles of iterative ischemia-reperfusion at onset of reperfusion (termed "postconditioning", post-con) delays washout of intravascular adenosine and thereby increases endogenous adenosine receptor (AR) activation during the early moments of reperfusion (R). METHODS: Isolated mouse hearts were subjected to 20 min global ischemia (I) and 30 min R with or without post-con (3 or 6 cycles of 10 s R&I). Intravascular purines in coronary effluent were analyzed by HPLC. To assess the functional role of endogenous AR activation in post-con, an open-chest rat model of myocardial infarction was employed. Rats were randomly divided into 11 groups: control, no intervention at R; post-con, three cycles of 10 s R followed by 10 s LCA re-occlusion immediately upon R. In the following interventions, drugs (or vehicle) were administered 5 min before R in the absence or presence (+/-) of post-con. Vehicle (DMSO < 300 microl/kg); 8-SPT (non-selective AR antagonist, 10 mg/kg) +/- post-con; DPCPX (A(1A)R antagonist, 0.1 mg/kg) +/- post-con; ZM241385 (A(2A)AR antagonist, 0.2 mg/kg) +/- post-con; MRS1523 (A(3)AR antagonist, 2 mg/kg) +/- post-con. RESULTS: In isolated mouse hearts, post-con reduced diastolic pressure during both early (26+/-3* vs. 37+/-3 mmHg at 5 min) and late (22+/-3* vs. 34+/-3 mmHg at 30 min) R. Post-con also hastened the early recovery of contractile function (developed pressure 39+/-6* vs. 16+/-2 mmHg at 5 min R), although differences did not persist at 30 min R. Importantly, post-con was associated with reduced adenosine washout (58+/-5* vs. 155+/-16 nM/min/g) at 2 min R suggesting greater retention time of intravascular adenosine. In rats, post-con significantly attenuated infarct size compared to control (40+/-3% vs. 53 +/- 2%* in control), an effect that was unaltered by DPCPX (42 +/- 2%) but was abrogated by 8-SPT (50 +/- 2%), ZM241385 (49 +/- 3%) or MRS1523 (52 +/- 1%) (P < 0.02). CONCLUSION: These data suggest that post-con involves endogenous activation of A(2A) and A3 but not A1AR subtypes. This activation may be linked to the delay in the washout of intravascular adenosine during the early minutes of R during which post-con is applied.

Adenosine↗
PubMed2005

Emergency coronary artery bypass grafting can be performed safely without cardiopulmonary bypass in selected patients.

BACKGROUND: Patients requiring emergency surgical revascularization are often not considered for off-pump coronary artery bypass grafting (OPCAB). METHODS: From 1996 to 2003, 614 patients underwent emergency coronary artery bypass grafting (Society of Thoracic Surgeons definition) at an academic institution. Forty-four (7%) of these procedures were performed without cardiopulmonary bypass, while 570 were conventional coronary artery bypass procedures with cardiopulmonary bypass (CABG/CPB). Data were collected prospectively into a computerized database and reviewed retrospectively. RESULTS: Though a greater proportion of CABG/CPB patients had critical left main stenosis (15.9% vs 38.3%, p = 0.005), other preoperative risk factors were similar between groups. Completeness of revascularization (No. distal anastomoses/No. diseased vessel systems) was significantly greater in the CABG/CPB group (1.51 +/- 0.03 vs 1.25 +/- 0.07, p = 0.003). There were no differences among individual complication rates (death, cardiac reoperation, postoperative myocardial infarction, permanent cerebral vascular accident, deep sternal wound infection, renal failure requiring hemodialysis, and respiratory failure requiring reintubation). However, the combined incidence of these endpoints was significantly lower in the OPCAB group (6.8% vs 21.1%, p = 0.038). OPCAB patients received fewer blood transfusions (65.9% vs 84.9%, p = 0.004) and had a significantly shorter intensive care unit stay (1.47 vs 3.20 days, p = 0.016). In-hospital mortality (0% vs 6.3%, p = 0.168) and mean postoperative length of stay (5.48 vs 7.03 days, p = 0.414) favored OPCAB, but did not reach statistical significance. CONCLUSIONS: Off-pump coronary artery bypass can be performed safely and effectively and should be considered in selected patients with acceptable hemodynamics undergoing emergency coronary revascularization.

Coronary Artery Bypass↗
PubMed2005

Early experience with activated recombinant factor VII for intractable hemorrhage after cardiovascular surgery.

BACKGROUND: Intractable hemorrhage after complex cardiovascular operations is a serious and potentially lethal complication. We report our experience with the use of activated recombinant factor VIIa (rFVIIa) as rescue therapy for patients with refractory postoperative hemorrhage. METHODS: From April 2002 through December 2003, 9 patients received rFVIIa for intractable hemorrhage after cardiovascular surgery. Patients underwent aortic surgery (2), coronary artery bypass graft surgery (4), double valve operations (2), and mitral valve replacement (1). Four of these procedures were reoperations. Intraoperative aprotinin was used in all patients. All patients underwent standard heparinization (300 IU/kg) before cardiopulmonary bypass and reversal with protamine. RESULTS: Five patients underwent reexploration for mediastinal hemorrhage before treatment; 2 were reexplored twice. The average transfusion requirement before rFVIIa administration was 9 U of blood, 7 U of plasma, 22 U of platelets, and 19 U of cryoprecipitate. rFVIIa was administered as an intravenous bolus at 68 to 120 mug/kg. Mean time of administration from the first operation was 10.9 +/- 7.2 hours. At the time of activated rFVIIa administration, chest tube drainage averaged 640 mL/h. In all patients, chest tube drainage was dramatically reduced to less than 100 mL/h within 5 hours after drug delivery. None of the patients required reexploration after treatment. There were no postoperative neurologic or cardiovascular complications. CONCLUSIONS: When used as rescue therapy for intractable hemorrhage after cardiovascular surgery, rFVIIa may be effective in promoting hemostasis, preventing reexploration, and reducing transfusion requirements.

Cardiovascular Surgical Procedures↗
PubMed2005

Intraoperative radiofrequency ablation for the treatment of atrial fibrillation during concomitant cardiac surgery.

BACKGROUND: Radiofrequency ablation has been recently introduced as an alternative to the surgical maze procedure to eliminate atrial fibrillation (AF). The purpose of this study was to examine the effectiveness of unipolar radiofrequency ablation in patients with AF undergoing open heart surgery. METHODS: A retrospective review was performed on 54 patients undergoing radiofrequency ablation with concomitant cardiac operations from March 2002 through July 2003. Forty-two patients (77.8%) received left atrial ablation, and 12 (22.2%) received biatrial ablation. RESULTS: Mean duration of preoperative AF was 46.3 +/- 44 months; 23 (42.6%) had AF 5 years or more, 32 (59.3%) had continuous AF, and 12 (22.6%) had a preoperative left atrial diameter of 6.0 cm or greater. At discharge, 33 patients (70.2%) were free from AF, 30 (62.5%) were in normal sinus rhythm, and 6 (12.7%) required a new pacemaker. Mid-term follow-up was available in 44 (93.6%) patients, with a median follow-up of 8.7 months (range, 3 to 22 months). At follow-up, 34 (77.3%) patients were free from AF. There were no significant differences in freedom from AF in patients with continuous versus intermittent AF or duration of 5 or greater years versus less than 5 years. In patients with isolated mitral valve surgery and radiofrequency ablation, 22 (88.0%) were free from AF compared with 12 (63.2%) with other operations (p = 0.074). In patients with left atrial diameter less than 6.0 cm, 30 (88.2%) were free from AF compared with 4 (40%) with left atrial diameter of 6.0 cm or greater (p = 0.006). CONCLUSIONS: Radiofrequency ablation is an effective surgical option for the treatment of continuous or intermittent AF. The elimination of AF using radiofrequency ablation is most successful in patients undergoing isolated mitral valve surgery with preoperative left atrial diameter less than 6.0 cm.

Aged↗
PubMed2005

Incidence of deep sternal wound infections after tracheostomy in cardiac surgery patients.

BACKGROUND: Tracheostomy after median sternotomy is associated with an increased risk of deep sternal wound infection (DSWI). However, associated comorbidities in these patients make the exact risk of tracheostomy difficult to discern. Therefore, we performed a retrospective review to determine the risk of DSWI in our cardiac surgery patients who underwent postoperative tracheostomy. METHODS: Our cardiac surgery database was queried from January 1996 to July 2003. Perioperative morbidities were identified for all patients who underwent tracheostomy after cardiac surgery. Statistical analysis was performed using chi2 analysis and Fisher's exact test. RESULTS: During the study period, 16,277 cardiac procedures were performed through a median sternotomy. Tracheostomy was performed in 291 patients (1.8%). Deep sternal wound infections occurred in 0.8% of all patients and in 3.4% of patients (9 of 268) who underwent tracheostomy. Mean number of days to tracheostomy was 14.2 in the DSWI group and 15.8 in the non-DSWI group (p = 0.45). In patients with a tracheostomy, preoperative renal failure was the only perioperative comorbidity found to be significantly associated with DSWI (p = 0.03). Overall operative mortality was 3.6%. Mortality was 16.5% for patients with DSWI, 22.7% for patients requiring tracheostomy, and 55% for patients with DSWI and tracheostomy. CONCLUSIONS: The incidence of DSWI after tracheostomy, in our experience, is not as high as previously reported. Tracheostomy can be performed safely after median sternotomy with a low morbidity and mortality rate. However, if DSWI occurs after tracheostomy, mortality is significant.

Aged↗
PubMed2005

Impact of unstable angina on outcomes of transmyocardial laser revascularization combined with coronary artery bypass grafting.

BACKGROUND: For sole therapy transmyocardial laser revascularization (TMR), unstable angina has been demonstrated to be a significant independent predictor of operative mortality. The objective of this study was to investigate the preoperative risk profile of patients undergoing TMR plus coronary artery bypass graft surgery (CABG) and to determine the impact of unstable angina on outcomes. METHODS: Using The Society of Thoracic Surgeons National Cardiac Database from 1998 to 2003, 5,618 patients underwent TMR plus CABG. These patients were compared with 932,715 patients who underwent CABG only operations. RESULTS: The TMR plus CABG patients had a significantly higher incidence of diabetes (50% versus 34%), renal failure (7% versus 5%), peripheral vascular disease (20% versus 16%), reoperative surgery (26% versus 9%), three-vessel coronary artery disease (80% versus 71%), hyperlipidemia (73% versus 62%; p < 0.001 for all comparisons). The incidence of preoperative unstable angina was similar (46% versus 47%). The unadjusted perioperative mortality was 3.8% for TMR plus CABG patients. When unstable angina patients were removed, the observed mortality for TMR plus CABG was decreased to 2.7%. CONCLUSIONS: It is likely that patients who undergo TMR plus CABG have a higher prevalence of diffuse coronary disease based on their preoperative demographics. Despite the increased risk associated with such anatomy, the mortality rate was not significantly increased when TMR was added to CABG in an effort to provide a more complete revascularization. As was noted from the outcomes of sole therapy TMR, in unstable angina patients, TMR plus CABG carries a higher risk, but this risk is not significantly different from that of such patients treated with CABG alone.

Angina, Unstable↗
PubMed2005

Polarized arrest with warm or cold adenosine/lidocaine blood cardioplegia is equivalent to hypothermic potassium blood cardioplegia.

BACKGROUND: Hypothermic depolarizing hyperkalemic (K + 20 mEq/L) blood cardioplegia is the "gold standard" in cardiac surgery. K + has been associated with deleterious consequences, eg, intracellular calcium overload. This study tested the hypothesis that elective arrest in a polarized state with adenosine (400 micromol/L via adenosine triphosphate-sensitive potassium channel opening) and the Na + channel blocker lidocaine (750 micromol/L) as the arresting agents in blood cardioplegia provides cardioprotection comparable to standard hypothermic K + -blood cardioplegia. METHODS: Anesthetized dogs were placed on cardiopulmonary bypass and assigned to 1 of 3 groups receiving antegrade cardioplegia delivered every 20 minutes for 1 hour of arrest: cold (10 degrees C) K + -blood cardioplegia (n = 6), cold (10 degrees C) adenosine/lidocaine blood cardioplegia (n = 6), or warm (37 degrees C) adenosine/lidocaine blood cardioplegia (n = 6). After an hour of arrest, cardiopulmonary bypass was discontinued, and reperfusion was continued for 120 minutes. RESULTS: Time to arrest was longer with cold and warm adenosine/lidocaine blood cardioplegia (175 +/- 19 seconds and 143 +/- 19 seconds, respectively) compared with K + -blood cardioplegia (27 +/- 2 seconds; P < .001). Postcardioplegia left ventricular systolic function (slope of the end-systolic pressure/dimension relationship) was comparable among the 3 groups (K + -blood cardioplegia, 15.2 +/- 2.1 mm Hg/mm; cold adenosine/lidocaine blood cardioplegia, 15.9 +/- 3.4 mm Hg/mm; warm adenosine/lidocaine blood cardioplegia, 14.1 +/- 2.8 mm Hg/mm; P = .90). Plasma creatine kinase activity in cold and warm adenosine/lidocaine blood cardioplegia was similar to that in K + -blood cardioplegia at 120 minutes of reperfusion (cold adenosine/lidocaine blood cardioplegia, 11.5 +/- 2.1 IU/g protein; warm adenosine/lidocaine blood cardioplegia, 10.1 +/- 0.9 IU/g protein; K + -blood cardioplegia, 7.6 +/- 0.8 IU/g protein; P = .17). Postcardioplegia coronary artery endothelial function was preserved in all groups. CONCLUSIONS: Intermittent polarized arrest with warm or cold adenosine/lidocaine blood cardioplegia provided the same degree of myocardial protection as intermittent hypothermic K + -blood cardioplegia in normal hearts.

Adenosine↗
PubMed2005

Replacement of mechanical mitral valve prosthesis due to patient intolerance of clicking noise: case report.

A 55-year-old male underwent combined coronary artery bypass grafting and mitral valve replacement with a No. 31 St. Jude Medical mechanical prosthetic valve. Over the next few months, the patient experienced severe difficulty with the 'clicking' noise of the mechanical valve, to the extent that it affected his daily activities. At approximately four months after the first operation, and at the patient's insistence, he underwent redo sternotomy and replacement of the mechanical mitral valve with a Mosaic porcine bio-prosthesis, with an uneventful recovery. While this case represents an unusual indication for valve replacement, it illustrates the importance of considering non-traditional factors when choosing the optimal prosthetic valve.

Bioprosthesis↗
PubMed2004

Hypoxic postconditioning reduces cardiomyocyte loss by inhibiting ROS generation and intracellular Ca2+ overload.

We have shown that intermittent interruption of immediate reflow at reperfusion (i.e., postconditioning) reduces infarct size in in vivo models after ischemia. Cardioprotection of postconditioning has been associated with attenuation of neutrophil-related events. However, it is unknown whether postconditioning before reoxygenation after hypoxia in cultured cardiomyocytes in the absence of neutrophils confers protection. This study tested the hypothesis that prevention of cardiomyocyte damage by hypoxic postconditioning (Postcon) is associated with a reduction in the generation of reactive oxygen species (ROS) and intracellular Ca(2+) overload. Primary cultured neonatal rat cardiomyocytes were exposed to 3 h of hypoxia followed by 6 h of reoxygenation. Cardiomyocytes were postconditioned after the 3-h index hypoxia by three cycles of 5 min of reoxygenation and 5 min of rehypoxia applied before 6 h of reoxygenation. Relative to sham control and hypoxia alone, the generation of ROS (increased lucigenin-enhanced chemiluminescence, SOD-inhibitable cytochrome c reduction, and generation of hydrogen peroxide) was significantly augmented after immediate reoxygenation as was the production of malondialdehyde, a product of lipid peroxidation. Concomitant with these changes, intracellular and mitochondrial Ca(2+) concentrations, which were detected by fluorescent fluo-4 AM and X-rhod-1 AM staining, respectively, were elevated. Cell viability assessed by propidium iodide staining was decreased consistent with increased levels of lactate dehydrogenase after reoxygenation. Postcon treatment at the onset of reoxygenation reduced ROS generation and malondialdehyde concentration in media and attenuated cardiomyocyte death assessed by propidium iodide and lactate dehydrogenase. Postcon treatment was associated with a decrease in intracellular and mitochondrial Ca(2+) concentrations. These data suggest that Postcon treatment reduces reoxygenation-induced injury in cardiomyocytes and is potentially mediated by attenuation of ROS generation, lipid peroxidation, and intracellular and mitochondrial Ca(2+) overload.

Animals↗