Vagus-preserving technique during minimally invasive esophagectomy: the effects on cardiac parameters in a swine model.

BACKGROUND: Cardiac complications are an important cause of morbidity and mortality observed after esophageal resections. We examined whether an high intrathoracic vagotomy during abdominothoracic esophagectomy would have an effect on intraoperative and early postoperative cardiac function in the setting of a minimally invasive resection. Two hypotheses were generated for this study: (1) Vagotomy would cause cardiac changes, and (2) vagus-preserving esophagectomy would prevent cardiac problems during resection and in the early postoperative phase. METHODS AND RESULTS: Thirty male pigs were operated on while cardiac parameters (heart rate [HR], cardiac index [CI], preload recruitable stroke work [PRSW], contractility speed [dp/dtmax], relaxation speed [dp/dtmin], and relaxation time [tau]) were monitored using a conductance catheter and the thermodilution method. Animals were randomized into 4 groups (each n = 7): (1) control, thoracoscopy only, (2) thoracoscopy with vagotomy, (3) esophageal resection with vagotomy, and (4) esophageal resection with vagus nerve preservation. To evaluate the first hypothesis, we compared groups 1 and 2; to evaluate the second hypothesis, we compared groups 3 and 4. HR, CI, PRSW, dp/dtmax, and tau were different in the 2 groups without resection (area under the curve; each P < .05). Vagotomy with esophagectomy resulted in nonsignificant differences between groups 3 and 4. The requirement for metoprolol administration to avoid severe tachycardia was greater in the groups that underwent vagotomy (P < .05; Fisher's exact test). CONCLUSION: An high intrathoracic vagotomy results in loss of vagal tone and a greater rate of tachycardia during thoracoscopy and esophagectomy. There were no differences, however, in cardiac dynamics between the esophagectomy groups. Thus, vagal injury is not the sole reason for cardiac dysfunction after esophagectomy.

Eprosartan improves cardiac function in swine working heart model of ischemia-reperfusion injury.

BACKGROUND: Eprosartan is an angiotensin II receptor antagonist used as an antihypertensive. We sought to evaluate the regional effect of Eprosartan on postinfarct ventricular remodeling and myocardial function in an isolated swine working heart model of ischemia-reperfusion injury. MATERIAL AND METHODS: 22 swine hearts were perfused with the Langendorff perfusion apparatus under standard experimental conditions. Myocardial ischemia was induced by a 10-min left anterior descending artery ligation. Hearts were reperfused with either saline (control group, n=11), or Eprosartan (treatment group, n=11). Left ventricular pressure (LVP) and regional heart parameters such as intramyocardial pressure (IMP), wall thickening rate (WTh), and pressure-length-loops (PLL) were measured at baseline and after 30 min of reperfusion. RESULTS: Measured parameters were statistically similar between the 2 groups at baseline. The administration of Eprosartan led to a significantly better recovery of IMP and WTh: 44.4±2.5 mmHg vs. 51.2±3.3 mmHg, p<0.001 and 3.8±0.4 µm vs. 4.4±0.3 µm, p=0.001, respectively. PLL were also significantly higher in the treatment group following reperfusion (21694±3259 units vs. 31267±3429 units, p<0.01). There was no difference in the LVP response to Eprosartan versus controls (63.6±3.0 mmHg vs. 62.5±3.1 mmHg, p=0.400). CONCLUSIONS: Pre-treatment with Eprosartan is associated with a significant improvement in regional cardiac function under ischemic conditions. Pharmacological treatment with eprosartan may exert a direct cardioprotective effect on ischemic myocardium.

Specific removal of C-reactive protein by apheresis in a porcine cardiac infarction model.

BACKGROUND: C-reactive protein (CRP) is a possible causative factor of the destructive processes observed during the weeks after myocardial infarction. METHODS: We developed a clinically relevant animal model including the removal of CRP from blood plasma utilizing a specific CRP adsorber and the visualization of the infarct scar in the living animal by cardiovascular magnetic resonance imaging as a tool to investigate the impact of CRP after acute myocardial infarction. RESULTS: We describe the facets of this model system and kinetics of clinical blood parameters like CRP and troponin. In addition, we demonstrate the potency of CRP apheresis reducing CRP levels by ~70% in the established treatment system. CONCLUSION: We showed for the first time that it is possible to conduct apheresis at the following 2 days after acute myocardial infarction in a porcine infarction model and to analyze the infarct by cardiovascular magnetic resonance imaging at day 1 and 14.

Analysis of atrial fibrillatory activity from high-resolution surface electrocardiograms: Evaluation and application of a new system.

BACKGROUND: Algorithms of signal processing allow the estimation of atrial fibrillation (AF) activity from surface electrocardiograms (ECGs). OBJECTIVE: To evaluate a new commercially available ECG system for AF analysis from surface potentials. METHODS: Patients (n=52, mean [+/- SD] age of 68+/-9.6 years) with persistent AF (mean duration 44+/-52.2 months), referred for cardiac surgery, underwent high-gain, high-resolution ECG preoperatively. After QRST cancellation, the frequency content of AF was identified by fast Fourier transformation. Epicardial potentials were registered at the right atrial appendage, the right atrium (RA), the left atrium (LA) and the left atrial appendage intraoperatively (nine patients). RESULTS: Mean (+/- SD) fibrillatory rate (MFR) in lead V(1) (393+/-40.4 fibrillations/min [fpm]) correlated significantly with V(2) (391+/-43.3 fpm, r=0.976; P<0.05) and II (379+/-41.1 fpm, r=0.878; P<0.05), and was stable within an interval of 13.6+/-3.8 min (27 patients). In the right atrial appendage, RA, LA and left atrial appendage, the relative difference in MFR was small (5.6%, 6.6%, 6.8% and 5.7%, respectively, compared with V(1)). The mean peak frequency component at 75% of the maximum power was significantly smaller in the LA than in the RA (13+/-4.2 fpm versus 22+/-7.2 fpm, respectively; P<0.01), and in patients with high (more than 390 fpm) compared with low (390 fpm or fewer) fibrillatory activity (14+/-7.6 fpm versus 22+/-13.3 fpm, respectively; P<0.05). There was a nonsignificant trend to higher fibrillatory activity with longer AF duration. Other characteristics (age, sex, LA size, ejection fraction, type of heart disease and medication) were not associated with the MFR. CONCLUSIONS: Using the CardioLink system, AF analysis from surface ECG is reliable and equivalent to epicardial measurements. By noninvasive assessment of individual electrical remodelling, this system certainly supports clinical AF research.

The role of atrial remodeling for ablation of atrial fibrillation.

BACKGROUND: Atrial fibrillation (AF) causes electrical, contractile, and structural remodeling of the atria. We investigated remodeling in patients undergoing AF ablation. METHODS: Concomitant ablation of permanent AF, lasting 1 to 240 months, was performed in 73 patients (49.3% men) with a mean age of 66 +/- 9.1 years undergoing mitral valve operations. Electrical (AF cycle length from surface electrocardiogram), contractile (force of contraction measured at right atrial muscle bundles), and structural (left atrial [LA] diameter from echocardiography) remodeling was assessed. Predictors for rhythm outcome were determined. RESULTS: Two patients died perioperatively, and 3 died during follow-up. The deaths were not ablation related. At the last follow-up (mean, 12 +/- 6.9 months), 47 patients (71.2%) were in sinus rhythm, 41 (62.1%) without antiarrhythmic drugs. Corresponding to cycle length (126 to 247 ms), force (2 to 18 mN/mm2), and LA diameter (37 to 79 mm), atrial remodeling exhibited a wide interindividual variability but no correlation between different remodeling levels. No relationship was found between remodeling and AF duration or LA hemodynamic load. Univariate analysis demonstrated higher force (7 +/- 4.2 vs 4 +/- 2.8 mN/mm2, p = 0.078), smaller LA diameter (51 +/- 7.1 vs 58 +/- 10.2 mm, p < 0.05), and shorter AF duration (34 +/- 48.7 vs 73 +/- 63.0 months, p < 0.05) associated with successful sinus rhythm restoration, whereas logistic regression analysis revealed AF duration (odds ratio, 1.01; 95% confidence interval, 1.00 to 1.02, p = 0.045) and LA diameter (odds ratio, 1.12; 95% confidence interval, 1.02 to 1.23, p = 0.016) as predictors. CONCLUSIONS: Atrial remodeling exhibited a high interindividual variability but no relationship within different remodeling levels, with AF duration or with LA hemodynamic load. However, AF duration and structural remodeling, but not electrical or contractile remodeling, predicted rhythm outcome.

Decellularized xenogenic heart valves reveal remodeling and growth potential in vivo.

We have developed an advanced tissue processing technique on porcine pulmonary heart valves for pulmonary valve replacement and its initial clinical application during the autograft operation according to Ross. The novel concept consists of a cell-free matrix achieved by deoxycholic acid treatment that is repopulated by host cells in vivo. Molecular biology, radioligand binding, and electron microscopy consistently showed that these valves are almost free of cellular components. Animal experiments and clinical investigations revealed excellent hemodynamic properties of the valves, no need for antithrombotic therapy, and repopulation by host cells without any signs of calcification. In juvenile sheep the internal diameter of the implanted valves significantly increased in growing animals by approximately 10 mm. The repopulation of the decellularized heart valves was found not only in sheep but also in humans, which indicates that the underlying mechanisms, presumably repair mechanisms, might be common in mammals. If these findings can be confirmed by others, they will lead to new concepts in the field of cardiovascular tissue engineering that will eliminate the need for in vitro construction of autologous heart valves.

Age-dependent chronic rejection after experimental heart transplantation.

BACKGROUND: The progressive decline of allograft function is predominantly a consequence of chronic rejection, but the etiology of this process is not fully understood. To evaluate the influence of age we performed heart transplantation in an experimental model of chronic rejection using inbred rats of different age. METHODS: Lewis rats served as donors and F344 rats were used as recipients. Young rats were 4 weeks of age, whereas adult rats were 4 months of age. Transplanted animals were grouped as follows: Group I, old to old; Group II, old to young; Group III, young to old; and Group IV, young to young. Intra-abdominal heterotopic heart transplantation was performed. Thereafter, functional evaluation was performed by daily palpation and surface electrocardiogram (ECG) to calculate the functional heart rejection index (fHRI). One month after transplantation the hearts were explanted and examined pathohistologically. RESULTS: Functional deterioration was noted in all groups, but all hearts were still beating when explanted. Young recipients and young donors showed significantly better results. Transplantation of young recipients led to a better fHRI (p < 0.001) and to a less critical chronic graft vasculopathy, especially when there was a young heart transplanted (p = 0.03). Furthermore, whenever a young donor heart was used, there was a better graft performance and less severe chronic rejection (p = 0.02). CONCLUSIONS: Experimental cardiac transplantation of young hearts leads to a better graft performance as well as to a lower incidence of a severe chronic graft disease. Thus, older donor age may adversely influence long-term performance of cardiac allografts.