Aortic valve replacement in octogenarians: outcome and predictors of complications.

INTRODUCTION: We aimed to evaluate the outcome in octogenarians after aortic valve replacement (AVR) and to determine the perioperative parameters that were predictive of a complicated postoperative course. METHODS: The study population included 304 patients (65% male) aged 82.7 ± 3.5 years who underwent AVR alone (63%), in combination with coronary artery bypass grafting (28%) or with other procedures (9%), between 1998 and 1/2008. Most patients suffered from combined valve disease. RESULTS: Mechanical valves were implanted in 50% of the patients. The in-hospital mortality was 5.8%. The stay in the intensive care unit was 2.3 ± 0.5 days and in hospital 15.3 ± 2.6 days. After multivariate analysis we were able to identify some predictors for in-hospital mortality, such as preoperative cardiogenic shock (p<0.02), ejection fraction <0.3 (p<0.03), diameter of prosthesis <21 mm (p<0.05), and redo surgery. The most important predictors for postoperative complications after AVR were preoperative renal failure, additional surgical procedures (i.e. coronary artery bypass, mitral valve) and prolonged aortic crossclamping (all p<0.05). CONCLUSIONS: The outcome after AVR in octogenarians is satisfactory; the operative risk is acceptable and might even be reduced with an individual approach to perioperative management in high-risk patients.

Impact of prior percutaneous coronary intervention on the outcome of coronary artery bypass surgery: a multicenter analysis.

OBJECTIVES: Do prior percutaneous coronary interventions adversely affect the outcome of subsequent coronary artery bypass grafting? We investigated this effect on a multicenter basis. METHODS: Eight cardiac surgical centers provided outcome data of 37,140 consecutive patients who underwent isolated first-time coronary bypass grafting between January 2000 and December 2005. Twenty-two patient characteristics and outcome variables were retrieved. Three groups of patients were analysed for in-hospital mortality and in-hospital major adverse cardiac events: patients without a previous percutaneous coronary intervention, with 1 previous intervention, and with 2 or more previous percutaneous coronary interventions before bypass grafting. A total of 29,928 patients with complete information for prior percutaneous coronary intervention underwent final analysis. Unadjusted univariate and risk-adjusted multivariate logistic regression analysis as well as computed propensity score matching were performed, based on 14 major risk factors to correct for and minimize selection bias. RESULTS: A total of 10.3% of patients had 1 previous percutaneous coronary intervention, and 3.7% of patients had 2 or more previous interventions. Risk-adjusted multivariate logistic regression analysis revealed a significant association of 2 or more previous percutaneous coronary interventions with in-hospital mortality (odds ratio [OR], 2.0; confidence interval [CI], 1.4-3.0; P = .0005) and major adverse cardiac events (OR, 1.5; CI, 1.2-1.9; P = .0013). After propensity score matching, conditional logistic regression analysis confirmed the results of adjusted analysis. A history of 2 or more previous percutaneous coronary interventions was significantly associated with in-hospital mortality (OR, 1.9; CI, 1.3-2.7; P = .0016) and major adverse cardiac events (OR, 1.5; CI, 1.2-1.9; P = .0019). CONCLUSIONS: Multicenter analysis confirms that a history of multiple previous percutaneous coronary interventions increases in-hospital mortality and the incidence of major adverse cardiac events after subsequent coronary artery bypass grafting. Critical discussion of the treatment strategy in these patients is warranted.

The use of autologous platelet gel (APG) for high-risk patients in cardiac surgery -- is it beneficial?

BACKGROUND: Wound healing in cardiac surgery has become a major problem due to the impaired risk profile of many patients. The aim of this study was to prove the influence of autologous platelet gel (APG) on wound healing in a special group of high-risk patients undergoing coronary surgery. PATIENTS AND METHODS: We performed a prospective, double-blind study in 44 patients with a special risk constellation relating to wound complications (obesity, diabetes, smoker, New York Heart Association (NYHA) III-IV and peripheral vascular disease). The study group was treated with APG, prepared using the Magellan platelet separator, the control group underwent conventional wound treatment. RESULTS: The incidence of major and minor wound complications at the thoracotomy, as well as in the area of saphenous vein harvesting, was not pronounced in either of the groups. Blood loss and pain sensations did not differ significantly either. Stay in the intensive care unit (ICU) and the in-hospital mortality were also comparable. The duration of the entire operation and the time until removing the chest-tubes were prolonged in the study group. CONCLUSION: Despite promising results in other fields of surgery, APG shows no beneficial effect in high-risk patients undergoing cardiac surgery. Probably, it depends on different types of microcirculation in atherosclerotic patients, which are quite different from those of other surgical areas. This factor may offset the existing beneficial platelet effects which could be observed, for example, in maxillo-facial surgery.

Oxygenation failure after cardiac surgery: early re-intubation versus treatment by nasal continuous positive airway pressure (NCPAP) or non-invasive positive pressure ventilation (NPPV).

BACKGROUND: Due to an increasing incidence of respiratory failure after cardiac surgery we wanted to study whether nasal continuous positive airway pressure (NCPAP) may improve pulmonary oxygen transfer and may avoid reintubation after coronary operations. Additionally, we compared this protocol to non-invasive positive pressure ventilation (NPPV). METHODS: For a period of 2 years we analyzed all patients that were extubated within 12 hours after coronary surgery, and in whom oxygen transfer (PaO2/FIO2) deteriorated without hypercapnia so that all these patients met predefined criteria for reintubation: group A=immediate reintubation (n=88), group B=NCPAP-treatment (n=173), group C=NPPV (n=18). RESULTS: 25.4% of group B- and 22.2% of group C-patients were also intubated after a period of NCPAP or NPPV. All other patients of groups B and C could be weaned from these devices (B = 34.3 +/- 5.9 hours; C = 26.4 +/- 4.4 h; p < 0.05) and were well oxygenated by face mask at ambient pressure (Ratio PaO2/FIO2: B, 138 +/- 13; C, 140 +/- 13). In group A we found a higher mortality (7.95%) compared to group B (4.04%) and group C (5.55%). NCPAP-patients suffered more frequently from an impaired sternal wound healing (A = 4.5%, B = 8.6%; p < 0.05). CONCLUSIONS: We conclude that reintubation after cardiac operations should be avoided since NCPAP and NPPV are safe and effective to improve arterial oxygenation in most patients with non hypercapnic respiratory failure.

Ca2+ sensitizer superior to catecholamine during myocardial stunning?

BACKGROUND: After open-chest cardiac surgery, ventricular function remains depressed (myocardial stunning). Catecholamines (epinephrine) improve ventricular function by increasing the intracellular Ca(2+) concentration. In parallel, the oxygen consumption is increased, so that the hitherto intact myocardium can be jeopardized. In the very insufficient ventricle, epinephrine can even become ineffective. Since Ca(2+) sensitizers provide another therapeutic avenue, the effects of epinephrine and levosimendan on postischemic hemodynamics were investigated. METHODS: After hemodynamic steady state, isolated, blood (erythrocyte-enriched Krebs-Henseleit solution)-perfused rabbit hearts were subjected to 25 min normothermic, no-flow ischemia and 20 min reperfusion. Heart rate (HR), cardiac output (CO), left ventricular pressure (LVP), coronary blood flow (CBF), and arterio-venous oxygen difference (AVDO(2)) were recorded during reperfusion and after administration of either epinephrine (n=16; 0.03 micromol), or levosimendan (n=11; 0.75 micromol) or epinephrine plus levosimendan (n=5). RESULTS: Epinephrine increased HR (19%, p=0.01) and improved hemodynamics in terms of CO (62%, p=0.0006), stroke volume SV (46%, p=0.02), stroke work W (158%, p=0.01), LVP(max) (58%, p=0.0001), maximal pressure increase dP/dt(max)(140%, p=0.0004), minimal pressure increase dP/dt(min) (104%, p=0.0002), LVP(ed) (-26%, p=0.02), and increased coronary resistance CR (31%, p=0.05). Epinephrine impaired hemodynamics in terms of AVDO(2) (+63%, p=0.003), myocardial oxygen consumption MVO(2) (+67%, p=0.0003) and MVO(2)/beat (+36%, p=0.01). External efficiency eta was increased by 92% (p=0.02). Levosimendan in postischemic hearts increased HR (32%, p=0.009) and improved hemodynamics in terms of CO (85%, p=0.01), SV (44%, p=0.03), W (115%, p=0.04), LVP(max) (95%, p=0.04), dP/dt(max) (133%, p=0.009), dP/dt(min) (121%, p=0.007), LVP(ed) (-63%, p=0.0006), and CR (-17%; n.s., p=0.1). It altered hemodynamics in terms of AVDO(2) (+7.0%; n.s., p=0.3) and MVO(2) (+32%, p=0.007) and MVO(2)/beat (+2.3%; n.s., p=0.4). External efficiency was increased by 307% (p=0.04). In five additional extremely dysfunctional rabbit hearts, epinephrine was ineffective. Additional levosimendan increased hemodynamics in terms of HR (56%; n.s., p=0.1), CO (159%, p=0.04), SV (89%, p=0.03), W (588%, p=0.02), LVP(max) (168%, p=0.03), dP/dt(max) (102%, p=0.005), dP/dt(min) (78%, p=0.006), LVP(ed) (-98%, p=0.0006), and CR (-50%, p=0.02). It altered hemodynamics in terms of AVDO(2) (-11%; n.s., p=0.05), MVO(2) (+131%, p=0.04) and MVO(2)/beat (+171%, p=0.03). External efficiency was increased by 212% (p=0.04). CONCLUSION: In contrast to epinephrine, levosimendan improves ventricular function without increasing oxygen demand, thereby considerably improving external efficiency. Even during epinephrine resistance in extremely dysfunctional hearts, levosimendan successfully improves ventricular function.

Aspirin in coronary artery bypass surgery: new aspects of and alternatives for an old antithrombotic agent.

The success of coronary artery bypass graft surgery (CABG) depends mainly on the patency of the graft vessels. Aortocoronary vein graft disease is comprised of three distinct but interrelated pathological processes: thrombosis, intimal hyperplasia and atherosclerosis. Early thrombosis is a major cause of vein graft attrition during the first month after CABG, while during the remainder of the first year, intimal hyperplasia forms a template for subsequent atherogenesis, which thereafter predominates. Platelets play a crucial role in the pathophysiology of graft thrombosis and aspirin is the primary antiplatelet drug that has been shown to improve vein graft patency within the first year after CABG. Nevertheless, a significant number of grafts still occlude in the early postoperative period despite 'appropriate' aspirin treatment. Moreover, laboratory investigations showed that the expected inhibition of platelet function is not always achieved. This has been called 'aspirin nonresponse' or 'aspirin resistance', although a uniform definition is lacking. The finding that a considerable number of patients show an impaired antiplatelet effect of aspirin after CABG brought new insight into the discussion concerning poor patency rates of bypass grafts: the early period after CABG shows a coincidence of an increased risk for bypass thrombosis (amongst others, due to platelet activation and endothelial cell disruption of the graft) and an increased prevalence of aspirin resistance. Hitherto, the underlying mechanisms of aspirin resistance are uncertain and largely hypothetical; amongst others, increased platelet turnover, enhanced platelet reactivity, systemic inflammation, and drug-drug interaction are discussed. Up to now available data concerning the clinical outcome of aspirin resistant CABG patients are limited, and there is evidence that platelets of patients with graft thrombosis are more likely to be resistant to aspirin compared with patients without thrombotic events. Many publications concerning aspirin resistance are available today, but reports addressing this topic in CABG patients are sparse. This review summarises recent insights into the antiplatelet treatment after CABG and describes the clinical benefit, but also the therapeutic failure of the well-established drug aspirin. Moreover, possible pharmacological approaches to improve antithrombotic therapy in aspirin nonresponders among CABG patients are discussed.

Coronary artery disease progression in patients who need repeat surgical revascularisation: the surgeon's point of view.

OBJECTIVE: The purpose of this study was to evaluate changes in native coronary arteries in patients undergoing repeat myocardial revascularisation late (>3 years) after primary coronary artery bypass grafting (CABG). METHODS: The angiographic images of 30 patients obtained at first and redo CABG were assessed for significant (>75%), short (<1 cm) and long (>1 cm) stenosis or total occlusion in native coronary arteries. Bypass grafts were also evaluated for significant stenosis (>50%) or occlusion. RESULTS: At first CABG, a mean number of 3.3 grafts/patient (range 1-5) were implanted. The mean time interval from first CABG to reoperation was 11.4 years (range 3-21 years). All patients showed disease progression in the native coronary arteries. At redo CABG, 3 (3.5%) grafts were non-stenotic, 27 (31%) stenotic, and 57 (65.5%) occluded. In native coronary vessels, five patients developed a new left main coronary artery stenosis, and there was a four-to-six-fold increase in total occlusions. Indications for redo CABG were disease progression in non-bypassed vessels (n = 3), bypass lesions (n = 19), and both bypass lesions and disease progression in the distal segments of native coronary arteries (n = 8). CONCLUSIONS: Late after CABG, coronary artery disease is highly progressive, mainly affecting the proximal segments of native coronary arteries, with a high incidence of coronary occlusion. Conversely, a low incidence of disease progression is observed in the distal segments of native coronary arteries, except in diabetic patients. Total arterial revascularisation as a primary strategy for CABG should be highly recommended, and more aggressive risk factor management is desirable.

Aspirin-induced platelet inhibition in patients undergoing cardiac surgery.

Platelet function and response to pharmacological inhibition are altered by cardiac surgery. For example, aggregation is increased early after aortic valve replacement (AVR) and platelet response to aspirin is often insufficient after coronary artery bypass grafting (CABG). We hypothesized that the effect of aspirin administration after cardiac surgery might be impaired due to platelet activation. Therefore, the antiplatelet effect of aspirin was compared in patients (n = 20 per group) after CABG and AVR surgery (bileaflet prosthesis). Arachidonic acid-induced aggregation (turbidimetry) and thromboxane formation (radioimmunoassay) were determined before and 1, 5, and 10 days after surgery. In CABG-patients, antiplatelet treatment had been discontinued 10 days before surgery. Oral aspirin was started on day 1 after CABG. AVR-patients did not receive oral aspirin. Before surgery, platelet aggregation and thromboxane formation were significantly higher in patients with aortic stenosis. After CABG, thromboxane formation was not significantly changed from control values before surgery (66 +/- 13% on day 10) despite oral aspirin treatment, whereas thromboxane formation in patients undergoing AVR significantly increased compared to values before surgery (216 +/- 29% on day 10). In both groups of patients, 100 micromol/l aspirin in vitro largely inhibited platelet function before surgery, with markedly attenuated effects after surgery. In conclusion, thromboxane formation increased after AVR but not after CABG. The antiplatelet effect of aspirin, therefore, may be impaired after CABG by increased platelet activity. An additional in vitro "resistance" of platelets was seen after both CABG and AVR.

Beta-blocker prophylaxis for atrial fibrillation after coronary artery bypass grafting in patients with sympathovagal imbalance.

BACKGROUND: Atrial fibrillation (AF) is the most common arrhythmia after coronary bypass grafting (CABG) resulting in a prolonged hospital stay and higher costs. The withdrawal of beta-blocker and a sympathovagal imbalance were identified as risk factors for AF. METHODS: In our study we performed a measuring of standard deviation of all normal RR intervals (SDNN) among 142 consecutive patients with beta-blocker therapy before CABG in order to identify a collective who had an increased risk due to a withdrawal of beta-blocker medication. A sympathovagal imbalance was predefined as a SDNN below 30 ms. Patients were divided into four groups according to the results of SDNN and the continuous beta-blocker therapy: group I: SDNN < or = 30 ms or less and withdrawal of beta-blocker therapy (26 patients); group II: SDNN < or = 30 ms and continuously beta-blocker therapy (33 patients); group III: SDNN > 30 ms and withdrawal of beta-blocker therapy (40 patients); group IV: SDNN > 30 ms and continuous beta-blocker therapy (43 patients). RESULTS: Atrial fibrillation occurred in 39 patients (27%) after surgery. Patients of group I showed a higher incidence of AF (14 of 26 patients, 54%) than patients of group II (7 of 33 patients, 21%; p < 0.009), patients of group III (8 of 40 patients, 20%; p < 0.004), or patients of group IV (10 of 43 patients, 23%; p < 0.01). We found a significantly higher incidence of diabetes mellitus (47 vs 14% of patients; p < 0.0001) in patients with a sympathovagal imbalance than patients with a SDNN above 30 ms. CONCLUSIONS: The results of our study suggest a sympathovagal imbalance and withdrawal of a beta-blocker therapy increase the risk of postoperative AF. A continuous beta-blocker therapy reduces the risk especially in patients with a sympathovagal imbalance and should always be practiced.

Independency of myocardial stunning of endothelial stunning?

BACKGROUND AND OBJECTIVE: Vascular endothelial cells play an important role in the control of vascular tone. The reasons for coronary endothelial dysfunction are complex and may involve ischemia/reperfusion injury. We investigated whether endothelial, smooth muscle, and myocardial dysfunction are independent phenomena. METHODS: Rabbit hearts were rapidly excised without intermittent ischemia, connected to a modified Langendorff apparatus, and perfused with a modified Krebs-Henseleit solution containing bovine erythrocytes. Normoxic control hearts (n = 16) were perfused for 125 min. Postischemic hearts (n = 15) were perfused for 45 min, submitted to global ischemia (20 min) and reperfused (60 min). Both the normoxic and the postischemic hearts were divided into three groups that received either 0.9% NaCl (placebo), or 3-morpholinosydnonimine (SIN-1; 100 microM),or substance P (SP; 5 nM). RESULTS: After SIN-1, CBF in the normoxic hearts was increased by maximum 63% and after SP by 62%. 60 min after the onset of reperfusion, the postischemic hearts of both groups had recovered to 95% LVP(max). In the postischemic hearts, SIN-1 increased CBF still by 58%, while the endothelium-dependent vasomotion was impaired: SP improved CBF by only 9%. SUMMARY AND CONCLUSIONS: The particular protocol permitted differentiation between myocardial and vascular stunning. The results show that, while myocardial function has already recovered, endothelial cells are more severely impaired than smooth muscle cells, and that this injury persists beyond myocardial stunning. Thus, endothelial-dependent dysfunction can still impair vasodilatation while ventricular dysfunction has already resolved.

Surgery for severe aortic stenosis with low transvalvular gradient and poor left ventricular function -- a single centre experience and review of the literature.

BACKGROUND: A retrospective comparative study was designed to determine whether the transvalvular gradient has a predictive value in the assessment of operative outcome in patients with severe aortic stenosis and poor left ventricular function. METHODS: From a surgical database, a series of 30 consecutive patients, who underwent isolated aortic valve replacement for severe aortic stenosis with depressed left ventricular (LV) function (EF < 40%), were enrolled in the study and divided into two groups according to the mean transvalvular gradient (TVG): LG(low gradient)-Group < 40 mmHg (n = 13), and HG(high gradient)-Group > 40 mmHg (n = 17). Both groups were then comparatively assessed with respect to perioperative organ functions and mortality. RESULTS: Both groups were well matched with respect to the preoperative clinical status. LG-Group had a larger aortic valve area, higher LVEDP, larger LVESD and LVEDD, and higher mean pulmonary pressures. The immediate postoperative outcome, hospital morbidity and mortality did not differ significantly among the groups. CONCLUSION: In patients with severe aortic stenosis and poor LV function, the mean transvalvular gradient, although corresponds to reduced LV performance, has a limited prognostic value in the assessment of surgical outcome. Generally, operating on this select group of patients is safe.

Is size-reducing ascending aortoplasty with external reinforcement an option in modern aortic surgery?

OBJECTIVE: Enlargement of the ascending aorta is often combined with valvular, coronary, or other cardiac diseases. Reduction aortoplasty can be an optional therapy; however, indications regarding the diameter of aorta, the history of dilatation (poststenosis, bicuspid aortic valve), or the intraoperative management (wall excision, reduction suture, external reinforcement) are not established. METHODS: In a retrospective study between 1997 and 2005, we investigated 531 patients operated for aneurysm or ectasia of the ascending aorta (diameter: 45-76mm). Of these, in 50 patients, size-reducing ascending aortoplasty was performed. External reinforcement with a non-coated dacron prosthesis was added in order to stabilize the aortic wall. RESULTS: Aortoplasty was associated with aortic valve replacement in 47 cases (35 mechanical vs 12 biological), subvalvular myectomy in 29 cases, and CABG in 13 cases. The procedure was performed with low hospital mortality (2%) and a low postoperative morbidity. Computertomographic and echocardiographic diameters were significantly smaller after reduction (55.8+/-9mm down to 40.51+/-6.2mm (CT), p<0.002; 54.1+/-6.7mm preoperatively down to 38.7+/-7.1mm (echocardiography), p<0.002), with stable performance in long-term follow-up (mean follow-up time: 70 months). CONCLUSIONS: As demonstrated in this study, size reduction of the ascending aorta using aortoplasty with external reinforcement is a safe procedure with excellent long-term results. It is a therapeutic option in modern aortic surgery in patients with poststenotic dilatation of the aorta without impairment of the sinotubular junction of the aortic valve and root.

[Postconditioning: a brief review]. / Postkonditionierung: ein kurzer Uberblick.

Preconditioning is the most effective form of cardioprotection that can be induced via different interventions before a longer-lasting ischemia (= index ischemia). Preconditioning can be induced by short bouts of ischemia, several pharmaceuticals (e.g., adenosine), and volatile anesthetics. A brief ischemia of an organ other than the heart can likewise initiate protection of the heart, which has been called preconditioning at a distance or remote preconditioning. According to the more recent literature, short bouts of ischemia after an index ischemia can also initiate cardioprotection, e.g., improve postischemic dysfunction or reduce infarct size, which has been called postconditioning. Such a postconditioning can also be elicited at a distant organ, termed remote postconditioning. It is the aim of this short review to characterize preconditioning and in particular postconditioning, describe possible mechanisms, and call attention to the clinical relevance.

Delayed preconditioning via Angiotensin-converting enzyme inhibition: pros and cons from an experimental study.

1. Bradykinin B(2) receptor activation confers preconditioning from ischaemic injury. In the present study, we tested whether an angiotensin-converting enzyme (ACE) inhibitor (captopril) could mediate delayed preconditioning and, thus, cardioprotection. 2. New Zealand white rabbits received 15 mL infusion of either saline (control group; n = 7) or drugs (0.3 mg/kg captopril (CAP group; n = 7) or 0.3 mg/kg captopril + 0.1 mg/kg HOE 140 (CAPHOE group; n = 7)) via a marginal ear vein over 30 min. After 24 h, hearts were connected to a Langendorff apparatus and buffer perfused. The experimental protocol consisted of 20 min global normothermic hypoxia, followed by 120 min reperfusion. 3. Compared with baseline, the mean (SEM) contractile state (= dP/dt(max)) at 120 min reperfusion was decreased to 42 +/- ;23, 72 +/- ;16 (*P < 0.05 vs control) and 49 +/- ;22% in the control, CAP and CAPHOE groups, respectively. Early relaxation (= dP/dt(min)) was reduced to 55 +/- ;28, 73 +/- ;15 (*P < 0.05 vs control) and 52 +/- ;19% in the control, CAP and CAPHOE groups, respectively. The estimate for myocardial oxygen consumption (MVO(2)= rate-pressure product) was decreased to 52 +/- ;15, 69 +/- ;24 (*P < 0.05 vs control) and 56 +/- ;15% in the control, CAP and CAPHOE groups, respectively. Similarly, coronary flow was decreased in the control, CAP and CAPHOE groups to 49 +/- ;20, 67 +/- ;18 and 46 +/- ;19%, respectively. In contrast, ventricular extrasystoles during reperfusion were significantly elevated in both the CAP and CAPHOE groups (1.3 +/- ;0.2 and 1.1 +/- ;0.3 /min, respectively) compared with control (0.4 +/- ;0.2 /min). 4. Captopril confers delayed preconditioning against stunning via a B(2) receptor-mediated pathway. This pharmacological preconditioning protects against systolic and diastolic stunning, against vascular stunning and preserves cardiac metabolism. In addition to its accepted cardioprotective effects in early preconditioning, captopril should induce delayed preconditioning (e.g. for routine interventional cardiology or in elective cardiac surgery).

Abdominal complications following open-heart surgery: a report of 12 cases and review of the literature.

INTRODUCTION: Abdominal complications following open-heart surgery remain serious events as the mortality is reported to be tremendously high. The clinical presentation, the diagnostic strategy and the therapeutic management varies. We reviewed all records of those patients who developed abdominal complications with surgical consequences during the last five years, recorded a complete follow-up and compared the findings to a current view of the literature. PATIENTS AND METHODS: Altogether 5720 patients underwent open-heart surgery at our institution between 1/98 and 12/02. Out of these 12 (10 men, 2 women) developed severe gastrointestinal complications with surgical consequences. The mean age was 73.17 +/- 8.1 I1 years. Seven patients underwent isolated coronary artery bypass grafting (CABG), two patients combined aortic valve replacement (AVR) and CABG, one isolated AVR, one mitral valve replacement (MVR) and yet another one combined MVR and CABG. The clinical records of all these patients were examined and a complete follow-up was recorded. RESULTS: The duration of the entire cardiac operation was a mean of 212.67 +/- 36.97 min, perfusion time 103 +/- 29.32 min and myocardial ischaemic time 52.25 +/- 24.56 min. Length of ICU-stay was between I and 5 days after cardiac surgery. Concerning gastrointestinal complications nine patients suffered from ischaemic intestinal disease, two from gastrointestinal ulcer bleeding and one from a preoperatively unknown bowel tumour with subsequent ileus. Four patients died in the immediate postoperative course, one patient within two years and seven patients show a satisfactory status at follow-up. CONCLUSIONS: A review from the literature shows an enormous mortality from abdominal complications following open-heart surgery. This was also found in our series. As many of these patients have a history of abdominal disease more attention should be paid to such anamnestic hints in the preparation before cardiac surgery. Hence we recommend early diagnostic measures and explorative laparotomy in doubtful situations in patients with positive anamnesis.

Gene expression in acute Stanford type A dissection: a comparative microarray study.

BACKGROUND: We compared gene expression profiles in acutely dissected aorta with those in normal control aorta. MATERIALS AND METHODS: Ascending aorta specimen from patients with an acute Stanford A-dissection were taken during surgery and compared with those from normal ascending aorta from multiorgan donors using the BD Atlas Human1.2 Array I, BD Atlas Human Cardiovascular Array and the Affymetrix HG-U133A GeneChip. For analysis only genes with strong signals of more than 70 percent of the mean signal of all spots on the array were accepted as being expressed. Quantitative real-time polymerase chain reaction (RT-PCR) was used to confirm regulation of expression of a subset of 24 genes known to be involved in aortic structure and function. RESULTS: According to our definition expression profiling of aorta tissue specimens revealed an expression of 19.1% to 23.5% of the genes listed on the arrays. Of those 15.7% to 28.9% were differently expressed in dissected and control aorta specimens. Several genes that encode for extracellular matrix components such as collagen IV alpha2 and -alpha5, collagen VI alpha3, collagen XIV alpha1, collagen XVIII alpha1 and elastin were down-regulated in aortic dissection, whereas levels of matrix metalloproteinases-11, -14 and -19 were increased. Some genes coding for cell to cell adhesion, cell to matrix signaling (e.g., polycystin1 and -2), cytoskeleton, as well as several myofibrillar genes (e.g., alpha-actinin, tropomyosin, gelsolin) were found to be down-regulated. Not surprisingly, some genes associated with chronic inflammation such as interleukin -2, -6 and -8, were up-regulated in dissection. CONCLUSION: Our results demonstrate the complexity of the dissecting process on a molecular level. Genes coding for the integrity and strength of the aortic wall were down-regulated whereas components of inflammatory response were up-regulated. Altered patterns of gene expression indicate a pre-existing structural failure, which is probably a consequence of insufficient remodeling of the aortic wall resulting in further aortic dissection.

Amiodarone prophylaxis for atrial fibrillation of high-risk patients after coronary bypass grafting: a prospective, double-blinded, placebo-controlled, randomized study.

AIMS: Atrial fibrillation (AF) occurs often in patients after coronary artery bypass grafting (CABG) and can result in increased morbidity and mortality. Previous studies using P-wave signal-averaged electrocardiogram (P-SAECG) have shown that patients with a longer filtered P-wave duration (FPD) have a high risk of AF after CABG. We have shown that patients with an FPD > or = 124 ms and a root-mean-square voltage of the last 20 ms of the P-wave 20 < or = 3.7 microV have an increased risk of AF after surgery. Accordingly, the aim of this study was to investigate whether or not prophylactic peri-operative administration of amiodarone could reduce the incidence of AF in this high-risk group undergoing CABG identified by P-SAECG. METHODS AND RESULTS: In this prospective, double-blinded, placebo-controlled, randomized study, 110 patients received either amiodarone (n = 55) or placebo (n = 55). During CABG, two patients of both groups died. Amiodarone was given as 600 mg oral single dose one day before and from days 2 through 7 after surgery. In addition, amiodarone was also administered intravenously during surgery in a 300-mg bolus for 1 h and as a total maintenance dose of 20 mg/kg weight over 24 h on the first day following surgery. The primary endpoint was the occurrence of AF after CABG. The secondary endpoint was the hospitalization length of stay after CABG. The baseline characteristics were similar in both treatment groups. The incidence of post-operative AF was significantly higher in the placebo group compared with the amiodarone group (85 vs. 34% of patients, P < 0.0001). The prophylactic therapy with amiodarone significantly reduced the intensive care (1.8 +/- 1.7 vs. 2.4 +/- 1.5 days, P = 0.001) and hospitalization length of stay (11.3 +/- 3.4 vs. 13.0 +/- 4.3 days, P = 0.03). In the amiodarone group, concentrations of amiodarone and desethylamiodarone differed significantly between patients with AF and sinus rhythm (amiodarone: 0.96 +/- 0.5 vs. 0.62 +/- 0.4 microg/mL, P = 0.02; desethylamiodarone: 0.65 +/- 0.2 vs. 0.48 +/- 0.1 microg/mL, P = 0.04). CONCLUSION: The incidence of post-operative AF among high-risk patients was significantly reduced by a prophylactic amiodarone treatment resulting in a shorter time of intensive care unit and hospital stay. Our data supports the prophylactic use of amiodarone in peri-operative period in patients at high risk for AF after CABG.

In vivo echocardiographic imaging of transplanted human adult stem cells in the myocardium labeled with clinically applicable CliniMACS nanoparticles.

OBJECTIVES: Intramyocardial transplantation of bone marrow-derived cells is currently under clinical evaluation as a therapy of heart failure. A major limitation of all clinical studies dealing with myocardial cell engraftment is the inability to track the fate of the transplanted cells. We present a clinically applicable technique using transesophageal echocardiography (TEE) of CliniMACS nanoparticle labeled transplanted CD133+ cells in ischemic hearts. METHODS AND RESULTS: CD133+ cells were isolated from human bone marrow by CliniMACS magnetic bead selection. Positive (5 x 10(6) cells) cells were transplanted into porcine ischemic myocardium (n = 6). Control animals (n = 5) received medium injection. TEE was performed to demonstrate the distribution of the cells during and 8 weeks after the procedure. Accumulations of labeled CD133+ cells of adjacent injections in the myocardium were discriminatively identified by TEE. CONCLUSIONS: TEE is an elegant method for real-time documentation of successful transplantation and cell colony localization of magnetically labeled CD133+ cells in the ischemic myocardium. Our method should be of special interest for TEE-guided transcatheter injection of cells.