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This article, titled "Pulmonary Complications in Patients undergoing Sternum-sparing Coronary Artery Bypass Grafting (TCRAT)," compares the occurrence of pulmonary complications in patients undergoing sternum-sparing coronary artery bypass grafting (TCRAT) versus standard coronary artery bypass grafting (CABG) via full median sternotomy (FS). The study analyzed the records of 151 TCRAT patients and 229 FS patients who underwent elective or urgent CABG. The results showed that TCRAT patients had a higher incidence of pleural effusions compared to FS patients, but this did not significantly impact clinical outcomes. The study also found that longer operation times were associated with longer ICU stays in TCRAT patients. [Extracted from the article]

Objective: The objective of this study was to describe the diastolic pressure-flow relationship and to assess critical occlusion pressure in arterial coronary bypass grafts in human beings. Methods and results: Fifteen patients were studied following elective surgical coronary artery bypass grafting. Flow in the left internal mammary artery bypass to the left anterior descending artery was measured and simultaneously, aortic pressure, coronary sinus pressure and left ventricular end-diastolic pressure were recorded. The zero-flow pressure intercept as a measure of critical occlusion pressure was extrapolated from the linear regression analysis of the instantaneous diastolic pressure-flow relationship. Mean diastolic flow was 46 ± 17 mL min-1, mean diastolic aortic pressure was 60.5 ± 10.0 mmHg. Diastolic blood flow was linearly related to the respective aortic pressure in all patients (R-values 0.7-0.99). The regression lines had a mean slope of 2.1 ± 1.2 mL min-1 mmHg-1. Mean critical occlusion pressure was 32.3 ± 9.9 mmHg and exceeded mean coronary sinus pressure and mean left ventricular end-diastolic pressure by factors of 3.1 and 2.6, respectively. Conclusions: Our data demonstrate the presence of a vascular waterfall phenomenon in the coronary circulation after internal mammary artery bypass grafting. Critical occlusion pressure in arterial grafts considerably exceeds coronary sinus pressure as well as left ventricular end-diastolic pressure and should thus be used as the effective downstream pressure when calculating coronary perfusion pressure. Our data further suggest that the slope of diastolic pressure-flow relationships provides a more rational approach to assess regional coronary vascular resistance than conventional calculations of coronary vascular resistance. [ABSTRACT FROM AUTHOR]

The effect of AT1 receptor blockade on myocardial stunning is still somewhat ambiguous. In some prior studies, coronary occlusion was of too long duration such that the effects of infarction and stunning on the recovery of contractile function could not be distinguished. In others, blood pressure was decreased such that the improved wall excursion could be the consequence of reduced afterload and/or of attenuated stunning. The present study, therefore, investigated the effect of the AT1 receptor antagonist candesartan in a pure model of myocardial stunning with controlled systemic hemodynamics. Fourteen anesthetized open-chest dogs were subjected to 15 minutes occlusion of the left circumflex coronary artery (LCx) and 4 hours subsequent reperfusion. Systemic hemodynamics (micromanometer), regional myocardial blood flow (colored microspheres), and posterior wall thickening (PWT, sonomicrometry) were measured, and data were compared between 7 placebo controls (group 1) and 7 dogs receiving 1 mg/kg candesartan i.v. before LCx occlusion (group 2). Left ventricular peak pressure was kept constant by an intra-aortic balloon, and heart rate did not change throughout the protocol. Regional myocardial blood flow was not different between the groups under control conditions, increased in response to candesartan in group 2 (posterior subendocardial blood flow from 0.99 ± 0.18 to 1.57 ± 0.45; p < 0.05 vs. control conditions), but was not different during myocardial ischemia and at 4 hours of reperfusion between the groups. Under control conditions and during myocardial ischemia, PWT was also not different between the groups. At 4 hours of reperfusion, PWT was still depressed in group 1 (−1.5 ± 3.4 % vs. 17.7 ± 5.6 % during control conditions, p < 0.05), whereas PWT had recovered in group 2 (11.4 ± 3.7 % at 4 hours reperfusion vs. 18.3 ± 2.7 during control conditions, NS, p < 0.05 vs. group 1). In conclusion, pretreatment with the AT1 receptor antagonist candesartan improved the functional recovery of reperfused myocardium. This attenuation of myocardial stunning was not based on more favorable systemic hemodynamics or regional myocardial blood flow. [ABSTRACT FROM AUTHOR]

We report a case of large paradoxical embolisms through a patent foramen ovale in a patient with acquired heparin-induced thrombocytopenia type II (HIT). One large ventricular thrombus embolizing through the aortic valve was documented on videotape for the first time while performing transesophageal echocardiography. A 56-year-old man was admitted with acute respiratory failure initially believed to have an exacerbated chronic obstructive pulmonary disease. Arterial oxygen saturation was only 33%. He received antibiotic and anti-obstructive treatments and was mechanically ventilated for 7 days. Few hours after extubation, he developed recurrent severe dyspnea accompanied by acute pain and pulselessness in his left leg. Transthoracic echocardiography revealed an enlarged right ventricle and suggested the presence of free-floating thrombi both in the right and in the left-heart cavities. During transesophageal echocardiography, a large serpentine left-heart thrombus embolized through the aortic valve and disappeared. The patient developed ventricular fibrillation and underwent successful cardiopulmonary resuscitation including emergency thrombolysis with alteplase. Four hours later, the surgeon retrieved a 20-cm long thrombus from the left femoral artery. [ABSTRACT FROM AUTHOR]

Abstract Background More than 50% of aortocoronary saphenous vein grafts are occluded 10 years after surgery. Intimal hyperplasia is the initial critical step in the progression toward occlusion. Internal mammary veins, which are physiologically prone to less hydrostatic pressure, may undergo an accelerated progression to intimal hyperplasia and thus be suitable for investigation of the mechanisms of aortocoronary vein graft disease. Methods Six minipigs underwent aortocoronary bypass grafting using standard cardiopulmonary bypass and cardioplegic arrest. Mammary vein were grafted in a reversed manner from ascending aorta to left anterior descending coronary artery (LAD). The proximal LAD was ligated, rendering the anterior left ventricle vein graft-dependent. Minipigs were killed after 4 weeks, and vein grafts were harvested. Histological and immunohistological investigation were performed with respect to morphometric analysis, endothelial damage/dysfunction (v-Willebrand-factor (vWF)), smooth muscle cells (α-smooth actin) and proliferation rate (proliferation marker Ki 67). Results Mean intimal area of vein grafts was increased compared to ungrafted mammary veins. Intimal hyperplasia in vein grafts was characterized by massive accumulation of smooth muscle cells with a high proliferation rate and endothelial perturbation. Significant (p = 0.001) intimal hyperplasia of the grafted mammary vein compared to the ungrafted mammary vein was found. These changes were absent in ungrafted mammary veins. Conclusion The present study demonstrates a pig model of aortocoronary vein graft intimal hyperplasia which is characterized by an accelerated progression within internal mammary veins. The model is suitable to investigate the pathophysiology of aortocoronary vein graft intimal hyperplasia as well as therapeutic approaches.

Objective: Cardiopulmonary bypass (CPB) via the right axillary artery (RAA) has become an alternative perfusion strategy, especially in complex aortic procedures. This study delineates our technique and outcome with direct axillary cannulation utilizing the Seldinger technique, which we adopted as the standard perfusion strategy in the sternum-sparing minimally invasive total coronary revascularization via left anterior thoracotomy (TCRAT) using CPB., Methods: From November 2019 to December 2023, a total of 413 consecutive patients underwent nonemergent isolated coronary artery bypass grafting (CABG) via left anterior minithoracotomy on CPB with peripheral cannulation via the RAA and cardioplegic cardiac arrest, using this technique as a default strategy in the daily routine. All patients had multivessel coronary artery disease. The primary outcome was intraoperative cannulation-related complications (bleeding, revision, ischemia, wound healing complications). The secondary outcome was cannulation-related events during follow-up (blood pressure differences, incidence of brachial plexus injury, clinical signs of circulatory problems of arm and hand, re-interventions). Mean midterm follow-up was 18.7 ± 12.3 [1.1-51.2] months. During follow-up, 16 patients died. Overall, a total of 397 patients (344 male; 67.6 ± 9.7 [32-88]) were included for follow-up (100%)., Results: The RAA was successfully cannulated in 100% of patients. A cannula size of 16 Fr was used in 34.6%, 18 Fr in 63.9% and 20 Fr in 1.5% of all patients. There was no intraoperative bleeding complication. In two patients, intraoperative revision of the RAA was required, necessitating a venous patch repair. At follow-up, there were no differences between the systolic and diastolic blood pressure or the pressure gradients between the right and left arm. Transient numbness of the right hand was observed in two patients. Permanent numbness was not observed. No patient needed further intervention or surgical revision of the RAA., Conclusions: The right axillary cannulation is feasible and safe in terms of vascular injury and brachial plexus injury with excellent in-hospital and follow-up outcome.

Minimally invasive, sternum-sparing total coronary revascularization in multivessel disease via left anterior mini-thoracotomy (TCRAT) was introduced recently. Intra-aortic balloon occlusion is a conceivable option to avoid manipulation of the ascending aorta, to reduce the risk of stroke and to be able to treat patients with severe calcifications and unfavorable aortic anatomies. Background/Objectives : The aim of our study was to show that the use of the IntraClude ® device, as part of minimally invasive coronary artery bypass grafting (CABG) via left anterior mini-thoracotomy, is feasible. Methods : From May to December 2023, CABG via left anterior mini-thoracotomy on cardiopulmonary bypass and cardioplegic arrest was successfully performed in 20 patients (17 male, 67.6 ± 8.2 (51-82) years). All patients had significant coronary artery disease (three-vessel: n = 6; two-vessel: n = 11; one-vessel: n = 3) with indication for surgical revascularization. The mean EuroScore2 was 2.6. Results : All patients successfully underwent minimally invasive CABG using endo-aortic balloon occlusion. A total of 43 distal anastomoses (2.2 ± 0.6 (1-3) per patient) were performed by using left internal artery mammary ( n = 20) and radial artery ( n = 14) for grafting the left anterior descending ( n = 19), circumflex ( n = 15) and right ( n = 6) coronary artery. There was no hospital mortality, no stroke, no myocardial infarction or repeat revascularization. A total of 15 out of 20 patients left hospital within 8 days after surgery. Conclusions : TCRAT by using the IntraClude ® device is feasible without compromising surgical principles while avoiding the external manipulation of the ascending aorta. The use of intra-aortic balloon occlusion instead of transthoracic clamps further reduces the invasiveness of the procedure.

Objective: Renal dysfunction and acute renal failure after coronary artery bypass grafting (CABG) are among the main causes of increased mortality and morbidity. A sternum-sparing concept of minimally invasive total coronary revascularization via anterior minithoracotomy (TCRAT) was introduced with promising early and midterm outcomes in multivessel coronary artery disease. There are limited data regarding renal complications in patients undergoing the TCRAT technique. The present study analyzed renal outcomes in TCRAT compared to CABG via full median sternotomy (FS). Methods: We analyzed the records of 227 consecutive TCRAT patients (from September 2021 to June 2023) and 228 consecutive FS patients (from January 2017 to December 2018) who underwent nonemergent CABG. Following propensity score matching, preoperative baseline characteristics-including age, sex, diabetes mellitus, arterial hypertension, left ventricular ejection fraction, EuroSCORE II, preoperative serum creatinine, estimated glomerular filtration rate (eGFR), serum urea, and pre-existing chronic renal insufficiency-were comparable between the TCRAT (n = 170) and the FS group (n = 170). The examined postoperative renal parameters and complications were serum creatinine, eGFR, and serum urea on the first postoperative day. Moreover, serum creatinine, eGFR and serum urea at the time of discharge, postoperative ARF, and hemodialysis were investigated. Additionally, the duration of operation, CPB time, aortic cross-clamp time, ICU and hospital stay, ECMO support, rethoracotomy and in-hospital mortality were analyzed. The parameters were compared between groups using a Student's t -test or Mann-Whitney U test. Results: The duration of operation (332 ± 66 vs. 257 ± 61 min; p < 0.05), CPB time (161 ± 40 vs. 116 ± 38 min; p < 0.05), and aortic cross-clamp time (100 ± 31 vs. 76 ± 26; p < 0.05) were longer in the TCRAT group. ICU (1.8 ± 2.2 vs. 2.9 ± 3.6 days; p < 0.05) and hospital (10.4 ± 7.6 vs. 12.4 ± 7.5 days; p < 0.05) stays were shorter in the TCRAT group. There were no differences between groups with regard to the renal parameters examined. Conclusions: Despite a prolonged duration of operation, CPB time, and aortic cross-clamp time when using the TCRAT technique, no increase in renal complications were found. In addition, ICU and hospital stays in the TCRAT group were shorter compared to CABG via full median sternotomy., Competing Interests: The authors declare no conflict of interest

Objective: A sternum-sparing approach of minimally invasive total coronary revascularization via left anterior thoracotomy demonstrated promising early outcomes in unselected patients with coronary artery multivessel disease. Follow-up data are still missing., Methods: From November 2019 to September 2023, coronary artery bypass grafting via left anterior minithoracotomy on cardiopulmonary bypass and cardioplegic cardiac arrest was performed as a routine procedure in 392 consecutive, nonemergency patients (345 men; 67.0 ± 9.9 years; range, 32-88 years). All patients had multivessel coronary artery disease (77.6% 3-vessel-disease, 22.4% 2-vessel-disease, and 32.9% left main stenosis). Patients at old age (older than a 80 years, 12.5%), with severe left ventricular dysfunction (ejection fraction <30%, 7.9%), diabetes mellitus (34.9%), massive obesity (body mass index > 35, 8.9%), and chronic lung disease (17.1%) were included. Mean European System for Cardiac Operative Risk Evaluation II score was 2.9 ± 2.8. Mean midterm follow-up (100%) was 15.2 ± 10.7 months (range, 0.1-39.5 months)., Results: Left internal thoracic artery (99.0%), radial artery (70.4%), and saphenous vein grafts (57.4%) were used, and 70.4% of patients received at least 2 arterial grafts. A total of 3.0 ± 0.8 anastomoses (range, 2-5 anastomoses) per patient were performed to revascularize the territories of left anterior descending (98.7%), circumflex (91.6%), and right coronary (70.9%) artery. Complete anatomical revascularization was achieved in 95.1%. At follow-up, all-cause-mortality, myocardial infarction, repeat revascularization, and stroke was 3.1%, 1.5%, 5.4%, and 0.7%, respectively. Overall major adverse cardiac and cerebrovascular events rate was 8.7%., Conclusions: This is the first report of midterm follow-up after routine sternum-sparing total coronary revascularization via left anterior thoracotomy for multivessel coronary artery disease with a high rate of multiple arterial grafting and complete anatomical revascularization. Outcome was favorable and similar to that of contemporary conventional coronary artery bypass grafting., Competing Interests: The authors reported no conflicts of interest. The Journal policy requires editors and reviewers to disclose conflicts of interest and to decline handling or reviewing manuscripts for which they may have a conflict of interest. The editors and reviewers of this article have no conflicts of interest., (© 2024 The Author(s).)

Objectives: Degeneration of mitral prostheses/rings may be treated by redo surgery, and, recently, by transcatheter valve-in-valve/ring implantation. This multicenter registry presents results of transcatheter valve-in-valve and repeat surgery for prostheses/rings degeneration., Methods: Data provided by 10 German heart centers underwent propensity score-matched retrospective analysis. The primary endpoint was 30-day/midterm mortality. Perioperative outcome was assessed according to the Mitral Valve Academic Research Consortium criteria. Further, the influence of moderate or greater tricuspid regurgitation (TR) on 30-day/midterm mortality was analyzed., Results: Between 2014 and 2019, 273 patients (79 transcatheter mitral valve-in-valve [TM-ViV] and 194 redo mitral valve replacement [Re-MVR]) underwent repeat procedure for mitral prosthesis/ring degeneration. Propensity score matching distinguished 79 patient pairs. European System for Cardiac Operative Risk Evaluation (EuroSCORE) II-predicted risk was 15.7 ± 13.7% in the TM-ViV group and 15.0% ± 12.7% in the Re-MVR group (P = .5336). TM-ViV patients were older (74.73 vs 72.2 years; P = .0030) and had higher incidence of atrial fibrillation (54 vs 40 patients; P = .0233). Severe TR incidence was similar (17.95% in TM-ViV vs 14.10%; P = .1741). Sixty-eight TM-ViV patients previously underwent mitral valve replacement, whereas 41 Re-MVR patients underwent valve repair (P < .0001). Stenosis was the leading degeneration mechanism in 42 TM-ViV versus 22 Re-MVR patients (P < .0005). The 30-day/midterm mortality did not differ between groups. Moderate or greater TR was a predictor of total (odds ratio [OR], 4.36; P = .0011), 30-day (OR, 3.76; P = .0180), and midterm mortality (OR, 4.30; P = .0378), irrespective of group., Conclusions: In both groups, observed mortality was less than predicted. Redo surgery enabled treatment of concomitant conditions, such as atrial fibrillation or TR. TR was shown to be a predictor of total, 30-day, and midterm mortality in both groups., (Copyright © 2022 The American Association for Thoracic Surgery. Published by Elsevier Inc. All rights reserved.)

In the last decades, minimally invasive procedures have been developed in the therapy of aortic valve disorders. Recently, a novel concept of minimally invasive coronary revascularization in multivessel disease via left anterior mini-thoracotomy demonstrated promising results. Full median sternotomy, as a very invasive procedure, is the standard approach in concomitant surgical aortic valve replacement (sAVR) and coronary bypass grafting (CABG). The aim of our study was to show that the combination of minimal invasive aortic valve replacement via upper mini-sternotomy and coronary artery bypass grafting via left anterior mini-thoracotomy is feasible to avoid full median sternotomy. From 07/2022 to 09/2022, concomitant sAVR via upper partial sternotomy and CABG via left anterior mini-thoractomy on cardiopulmonary bypass and cardioplegic arrest was successfully performed in six consecutive patients (6 males; 69.8 ± 7.4 [60-79] years). All patients had severe aortic stenosis (MPG 45.5 ± 17.3 mmHg) and a significant coronary artery disease (three-vessel: 33%, two-vessel: 33%, one-vessel: 33%) with indication to cardiac surgery. Mean EuroScore2 was 3.2. All patients underwent successful less invasive concomitant biological sAVR and CABG. 67% of patients received a 25 mm, 33% received a 23 mm biological aortic valve replacement (Edwards Lifesciences Perimount). A total of 11 distal anastomoses (1.8 ± 1.0 [1-3] per patient) were performed by using left internal artery mammary (50%), radial artery (17%) and saphenous venous graft (67%) for grafting the left anterior descending (83%), circumflex (67%) and right (33%) coronary artery. Hospital mortality was 0%, stroke rate was 0%, myocardial infarction was 0% and repeat revascularization rate was 0%, ICU stay was 1 day in 83% of all patients and 50% left hospital within 8 days after surgery. Less invasive concomitant surgical aortic valve replacement and coronary artery bypass grafting using upper mini-sternotomy and left anterior mini-thoracotomy is feasible without compromises in surgical principles and complete coronary revascularization while maintaining thoracic stability by avoiding full median sternotomy., (© 2023. Springer Nature Japan KK, part of Springer Nature.)

Background: Avoidance of sternotomy while preserving complete revascularization remains challenging in multivessel coronary disease. Technical issues and in-hospital outcomes of total coronary revascularization via a small left anterior thoracotomy (TCRAT) in nonselected patients with multivessel disease are reported., Methods: From November 2019 to September 2021, coronary artery bypass grafting via left anterior minithoracotomy on cardiopulmonary bypass and cardioplegic cardiac arrest was performed in 102 patients (92 males; 67 ± 10 [42-87] years). Slings were placed around ascending aorta, left pulmonary veins, and inferior vena cava for exposure of lateral and inferior ventricular wall. All patients had multivessel coronary disease (three-vessel disease: n  = 72; two-vessel disease: n  = 30; left main stenosis: n  = 44). We included patients at old age (> 80 years, 14.7%), with severe left ventricular dysfunction (ejection fraction < 30%, 6.9%), massive obesity (body mass index > 35, 11.6%), and at increased risk (EuroSCORE II > 4, 15.7%)., Results: Left internal thoracic artery ( n  = 101), radial artery ( n  = 83), and saphenous vein ( n  = 39) grafts were used for total (61.8%) or multiple (19.6%) arterial grafting. A total of 323 distal anastomoses (3.2 ± 0.7 [2-5] per patient) were performed to revascularize left anterior descending (100%), circumflex (91.2%), and right coronary artery (67.7%). Complete revascularization was achieved in 95.1%. In-hospital mortality was 2.9%, stroke rate was 1.0%, myocardial infarction rate was 2.9%, and repeat revascularization rate was 2.0%., Conclusion: This novel surgical technique allows complete coronary revascularization in the broad majority of multivessel disease patients without sternotomy. TCRAT can be introduced into clinical routine safely. Long-term results remain to be investigated., Competing Interests: None declared., (The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/).)

Competing Interests: Disclosure The authors report no conflicts of interest in this work.

Background: Transcatheter Aortic Valve Implantation (TAVI) has emerged over time, reflected in appropriate adjustments in the European Society of Cardiology (ESC) guidelines in 2007, 2012 and 2017., Objective: The aim of this study was to analyze in-hospital outcomes after TAVI in the development within a single heart center over a period of 10 years depending on adjustments in the guidelines, infrastructural and procedural determinants., Methods: 489 consecutive patients who underwent TAVI from 2010 and 2019 at our center were analyzed retrospectively. Patients were divided into 3 groups of different treatment circumstances depending on guidelines adjustments and local infrastructural progress (group 1: 2010-2015 (n = 132), group 2: 2016-2017 (n = 155), group 3: 2018-2019 (n = 202). The primary endpoint was defined as all-cause in-hospital mortality. Secondary endpoints were selected according to the Valve Academic Research Consortium (VARC)-2 definitions. Multivariate logistic regression analysis was performed to determine predictors of in-hospital mortality. Statistical significance was assumed for p < 0.05., Results: 489 patients (346 (70.8 %) transfemoral and 143 (29.2 %) transapical) underwent TAVI. Comparing periods (group 1 vs. 2 vs. 3) age (82.1 ± 6.2 vs. 82.5 ± 4.8 vs. 81.1 ± 5.1 years, p = 0.012) and EuroSCORE II (8.4 ± 6.0 vs. 5.8 ± 4.9 vs. 5.5 ± 5.0 %, p < 0.001) declined over time. Rates of in-hospital mortality decreased significantly (9.1 % vs. 5.8 % vs. 2.5 %, p = 0.029), especially with observed-to-expected mortality ratios indicating a disproportionate decline of in-hospital mortality (1.08 vs. 1.00 vs. 0.45). Furthermore, post-procedural complications, such as acute kidney injury stage 3 (10.6 % vs. 3.2 % vs. 4.5 %, p = 0.016) and bleeding complications (14.4 % vs. 11.6 % vs 7.9 %, p = 0.165) decreased from group 1 to 3. However, rates of permanent pacemaker implantations (7.6 % vs. 11.0 % vs. 22.8 %, p < 0.001) increased, associated with a switch towards self-expanding valves (0.0 % vs. 61.3 % vs. 76.7 %, p < 0.001). Length of hospitalization as well as stay at intensive care and intermediate care unit could be reduced significantly during the observation period. In multivariate analysis age (OR: 1.103; 95 % CI: 1.013 - 1.202; p = 0.025), creatinine level before TAVI (OR: 1.497; 95 % CI: 1.013 - 2.212; p = 0.043), atrial fibrillation (OR: 2.956; 95 % CI: 1.127 - 7.749; p = 0.028) and procedure duration (OR: 1.017; 95 % CI: 1.009 - 1.025; p < 0.001) could be identified as independent predictors of in-hospital mortality., Conclusion: This study identified age, creatinine level before TAVI, the presence of atrial fibrillation and procedure duration as independent predictors for in-hospital mortality. Although these predictors decreased during the observation period, the decline in hospital-mortality was disproportionate, which was indicated by an observed-to-expected mortality ratio of 0.45 for the last observation period. However, it can be assumed that apart from patient-related factors, there were further institutional, technical and procedural developments, which ran in parallel and affected in-hospital mortality rates after TAVI., Competing Interests: Conflicts of Interest The authors state that they have no conflicts of interest.

Coronary artery bypass grafting (CABG) via full sternotomy remains a very invasive procedure, often requiring prolonged recovery of the patient. We describe a novel, less invasive approach for totally arterial CABG via a small left anterior thoracotomy in a pilot series of 20 unselected patients. From January to March 2020, 20 consecutive patients (mean age 65.9 ± 9.2 years, 100% male, STS-score: 1.6 ± 2) underwent CABG using only arterial conduits via a small left anterior thoracotomy. Patients were operated on cardiopulmonary bypass with peripheral cannulation and transthoracic aortic cross-clamping. Pulling tapes encircling the great vessels, the arrested empty heart was rotated and moved within the pericardium to enable conventional anastomotic techniques especially on lateral and inferior wall coronary targets. In all patients, left internal mammary artery and radial artery were utilized for bypass with 3.3 ± 0.7 distal coronary anastomoses per patient. Anterior, lateral, and inferior wall territories were revascularized in 100%, 85%, and 70% of patients, respectively. Complete anatomical revascularization was achieved in 95% of patients. ICU stay was 1 day in 17 patients, and 14 of patients left the hospital within 8 days. There was no hospital death, no stroke, no myocardial infarction, and no repeat revascularization. In this pilot series of 20 patients, minimally invasive, totally arterial CABG with avoidance of sternotomy was technically feasible with favorable patient outcomes., (© 2022. The Author(s).)

Objective and Background: We present a first description of a Heart Team (HT)-guided approach to coronary revascularization and its long-term effect on clinical events after percutaneous coronary intervention (PCI). The HT approach is a structured process to decide for coronary bypass grafting (CABG), PCI or conservative therapy in ad hoc situations as well as in HT conferences. As a hypothesis, during the long-term course after a PCI performed according to HT rules, a low number of late revascularizations, especially CABGs, are expected (F-PCI study)., Methods: In this monocentric study, the HT approach to an all-comer population was first analyzed and described in general with the help of a database. Next the use of a HT approach was described for a more homogeneous subgroup with newly detected CAD (1.CAD). Those patients in whom the HT decision was PCI (which was a 1.PCI) were then studied with the help of questionnaires for clinical events during a very long-term follow-up. Events were CABG, PCI, diagnostic catheterization (DCath) and death., Results: A significant number of patients were presented to HT conferences: 22 % out of all 11,174 catheterizations, 24 % out of all 7867 CAD cases and 35 % out of 3408 1.CAD cases. Most of these patients had multi-vessel disease (MVD). Conference decisions were isolated CABG in 46-66 %, PCI in 10-14 %, valvular surgery in 9-16 %, HTx in 10-21 % (Endstage heart failure candidates for surgery) and conservative therapy (Medical or no therapy, additional diagnostic procedures or no adherence to recommended therapy) in 2-3 %. However, most PCIs, ad hoc and elective, were performed under Heart Team rules, but without conference. During follow-up of 1.PCI patients (Kaplan-Meier analysis), CABG occurred in only 15 % of patients, PCI in 37 % and DCath in 65 %; mortality of any course was 51 %. Mortalities were similar in one-vessel disease and in a population of the same year, matched for age and sex (p < 0.057), but mortality was higher in 1.PCI patients with MVD (p < 0.001). Beyond 2 years, Kaplan-Meier curves were linear., Conclusion: The structured Heart Team approach is an effective tool for ad hoc and conference-based clinical decision-making with a sustained clinical benefit. This is demonstrated in low late CABG (and PCI) rates after a 1.PCI, without elevated mortality. The all-comer population supports the universal value of these data. Stable annual event rates late after PCI suggest a conversion to stable CAD. Heart Team conferences are also important tools in cases of valvular and end-stage heart disease.

Background: Deep sternal wound infections (DSWI) remain a devastating complication in cardiac surgery applying full sternotomy. As the risk profile in cardiac surgery changed toward an older and sicker population, the incidence of DSWI increases. Platelet rich plasma (PRP) holds promise in tissue regeneration with respect to bone regeneration, reduction of bleeding, and accelerated wound healing. The effect of PRP on DSWI was investigated in high-risk patients undergoing cardiac surgery with full sternotomy., Methods: 196 consecutive patients at risk of DSWI were randomized to application of autologous PRP before sternal wiring (n = 97) or control (n = 99). All patients underwent cardiac surgery on cardiopulmonary bypass with cardioplegic cardiac arrest. Endpoint was occurrence of DSWI requiring revision surgery., Results: Demographic, intraoperative, and perioperative variables as well as risk factors were comparable between groups. Incidence of DSWI was not different between the PRP-group and the control-group (6/97 (6.2%) vs. 3/99 (3.0%); n.s.)., Conclusions: Local application of autologous PRP in cardiac surgery patients with full sternotomy at high risk for sternal complications did not reduce the incidence of DSWI., (Georg Thieme Verlag KG Stuttgart · New York.)

Background and Aims: External support of vein grafts by fibrin glue possibly prevents overdistension, vascular remodeling, and neointimal hyperplasia. Previous animal models of neointimal hyperplasia showed conflicting results. Here, long-term effects of external fibrin glue support were studied in a new rat model of jugular vein to abdominal aorta transposition. MATERIALS AND METHODS AND METHODS: In male Wistar rats (250-300 g) right jugular vein (1.0-1.5 cm) was transposed to the infrarenal aorta. Fibrin glue (0.25 ml) covered the vein before releasing the vascular clamps (n = 6). Control vein grafts were exposed directly to blood pressure. After 16 weeks vein grafts were pressure-fixed for histology. Intima thickness, luminal and intimal area were measured by planimetry and elastic fibers demonstrated by Elastica van Giesson staining., Results: Intimal thickness (74.04 +/- 6.7 microm vs 1245 +/- 187 microm, control vs fibrin treatment; p < 0.001), intimal area (2517.16 +/- 355 mm(2) vs 18424 +/- 4927 mm(2), control vs fibrin treatment; p < 0.05) and luminal area (2184.75 +/- 347 mm(2) vs 7231.85 +/- 1782 mm(2), control vs fibrin treatment; p < 0.05) were significantly increased, elastic fibers in the vessel wall were diminished and the vessel wall infiltrated by mononuclear cells in fibrin glue supported veins., Conclusion: External support of vein grafts by fibrin glue leads to aneurysmal degeneration and intimal hyperplasia, thereby possibly jeopardizing long-term graft patency.

Invasive pulmonary aspergillosis is a severe complication in immunosuppressed patients. Surgical resection can be curative in certain patients after antifungal treatment. Over a 7-year period, ten patients with suspected invasive pulmonary aspergillosis of two university hospitals were retrospectively reviewed. A literature review was undertaken. Patient's age was 48.1 years (mean); the cause of immunosuppression was a hematological disease with consecutive therapy in seven patients and chronically corticoid therapy in three patients. After an antifungal therapy, surgical resection was performed with lobectomy/segmentectomy in 60% and with wedge-resection in 40%. Postoperative course were uneventful in seven patients, two patients died due to infectional circumstances, and one patient was reoperated because of empyema. The underlying disease marked long-term follow-up. Resection of focal pulmonary invasive aspergillosis can be curative. Clinical circumstances and dissemination must be taken into consideration to indicate surgery. To point out the best pathway randomised prospective studies are necessary.

Aims: Stretch is an important regulator of atrial function. The functional effects of stretch on human atrium, however, are poorly understood. Thus, we characterized the stretch-induced force response in human atrium and evaluated the underlying cellular mechanisms., Methods and Results: Isometric twitch force of human atrial trabeculae (n = 252) was recorded (37 degrees C, 1 Hz stimulation) following stretch from 88 (L88) to 98% (L98) of optimal length. [Na(+)](i) and pH(i) were measured using SBFI and BCECF epifluorescence, respectively. Stretch induced a biphasic force increase: an immediate increase [first-phase, Frank-Starling mechanism (FSM)] to approximately 190% of force at L88 followed by an additional slower increase [5-10 min; slow force response (SFR)] to approximately 120% of the FSM. FSM and SFR were unaffected by gender, age, ejection fraction, and pre-medication with major cardiovascular drugs. There was a positive correlation between the amplitude of the FSM and the SFR. [Na(+)](i) rose by approximately 1 mmol/L and pH(i) remained unchanged during the SFR. Inhibition of Na(+)/H(+)-exchange (3 microM HOE642), Na(+)/Ca(2+)-exchange (5 microM KB-R7943), or stretch-activated channels (0.5 microM GsMtx-4 and 80 microM streptomycin) did not reduce the SFR. Inhibition of angiotensin-II (AngII) receptors (5 microM saralasin and 0.5 microM PD123319) or pre-application of 0.5 microM AngII, however, reduced the SFR by approximately 40-60%. Moreover, stretch increased phosphorylation of myosin light chain 2 (MLC2a) and inhibition of MLC kinase (10 microM ML-7 and 5 microM wortmannin) decreased the SFR by approximately 40-85%., Conclusion: Stretch elicits a SFR in human atrium. The atrial SFR is mediated by stretch-induced release and autocrine/paracrine actions of AngII and increased myofilament Ca(2+) responsiveness via phosphorylation of MLC2a by MLC kinase.

Aims: To determine the strength of evidence for preoperative statin use for prevention of adverse postoperative outcomes in patients undergoing cardiac surgery., Methods and Results: After literature search in major databases, 19 studies were identified [three RCT (randomized prospective clinical trials), 16 observational] that reported outcomes of 31 725 cardiac surgery patients with (n = 17 201; 54%) or without (n = 14 524; 46%) preoperative statin therapy. Outcomes that were analysed included early all-cause mortality (30-day mortality), myocardial infarction (MI), atrial fibrillation (AF), stroke and renal failure. Odds ratio (OR) with 95% confidence intervals (95%CI) were reported using fixed or random effect models and publication bias was assessed. Preoperative statin therapy resulted in a 1.5% absolute risk reduction (2.2 vs. 3.7%; P < 0.0001) and 43% odds reduction for early all-cause mortality (OR 0.57; 95%CI: 0.49-0.67). A significant reduction (P < 0.01) in statin pretreated patients was also observed for AF (24.9 vs. 29.3%; OR 0.67, 95%CI: 0.51-0.88), stroke (2.1 vs. 2.9%, OR 0.74, 95%CI: 0.60-0.91), but not for MI (OR 1.11; 95%CI: 0.93-1.33) or renal failure (OR 0.78, 95%CI: 0.46-1.31). Funnel plot and Egger's regression analysis (P = 0.60) excluded relevant publication bias., Conclusion: Our meta-analysis provides evidence that preoperative statin therapy exerts substantial clinical benefit on early postoperative adverse outcomes in cardiac surgery patients, but underscores the need for RCT trials.

Background: Pulmonary inflammation after cardiac surgery with cardiopulmonary bypass (CPB) has been linked to respiratory dysfunction and ultrastructural injury. Whether pretreatment with methylprednisolone (MP) can preserve pulmonary surfactant and blood-air barrier, thereby improving pulmonary function, was tested in a porcine CPB-model., Materials and Methods: After randomizing pigs to placebo (PLA; n = 5) or MP (30 mg/kg, MP; n = 5), animals were subjected to 3 h of CPB with 1 h of cardioplegic cardiac arrest. Hemodynamic data, plasma tumor necrosis factor-alpha (TNF-alpha, ELISA), and pulmonary function parameters were assessed before, 15 min after CPB, and 8 h after CPB. Lung biopsies were analyzed for TNF-alpha (Western blot) or blood-air barrier and surfactant morphology (electron microscopy, stereology)., Results: Systemic TNF-alpha increased and cardiac index decreased at 8 h after CPB in PLA (P < 0.05 versus pre-CPB), but not in MP (P < 0.05 versus PLA). In both groups, at 8 h after CPB, PaO2 and PaO2/FiO2 were decreased and arterio-alveolar oxygen difference and pulmonary vascular resistance were increased (P < 0.05 versus baseline). Postoperative pulmonary TNF-alpha remained unchanged in both groups, but tended to be higher in PLA (P = 0.06 versus MP). The volume fraction of inactivated intra-alveolar surfactant was increased in PLA (58 +/- 17% versus 83 +/- 6%) and MP (55 +/- 18% versus 80 +/- 17%) after CPB (P < 0.05 versus baseline for both groups). Profound blood-air barrier injury was present in both groups at 8 h as indicated by an increased blood-air barrier integrity score (PLA: 1.28 +/- 0.03 versus 1.70 +/- 0.1; MP: 1.27 +/- 0.08 versus 1.81 +/- 0.1; P < 0.05)., Conclusion: Despite reduction of the systemic inflammatory response and pulmonary TNF-alpha generation, methylprednisolone fails to decrease pulmonary TNF-alpha and to preserve pulmonary surfactant morphology, blood-air barrier integrity, and pulmonary function after CPB.

Background: Cardiopulmonary bypass (CPB)-related inflammatory response can be attenuated by glucocorticoid treatment, but its impact on postoperative cardiopulmonary function remains controversial. It was investigated whether the systemic and myocardial antiinflammatory effects of glucocorticoids are associated with improved cardiopulmonary function in cardiac surgery patients., Methods: Eighty patients undergoing elective coronary artery bypass grafting were randomly assigned to receive a single shot of methylprednisolone (15 mg/kg) or placebo before CPB. Variables of myocardial and pulmonary function and systemic hemodynamics were measured before and 1, 4, 10, and 24 hours after CPB. Blood was sampled for measurement of proinflammatory (tumor necrosis factor-alpha, interleukin 6, interleukin 8) and antiinflammatory (interleukin 10) cytokines (by enzyme-linked immunoassay), troponin T, and C-reactive protein. Phosphorylation of inhibitory kappa-B alpha and p38 mitogen-activated protein kinase was determined in right atrial biopsies before and after CPB (phosphoprotein assay)., Results: Preoperative and intraoperative characteristics of patients were not different between groups. Methylprednisolone attenuated postoperative tumor necrosis factor-alpha, interleukin 6, interleukin 8, and C-reactive protein levels while increasing interleukin 10 release. Myocardial inhibitory kappa-B alpha was preserved with methylprednisolone (p < 0.05 versus placebo), but p38 mitogen-activated protein kinase activation occurred in both groups after CPB (p < 0.05 versus before CPB). Methylprednisolone improved postoperative cardiac index and was associated with decreased troponin T when compared with placebo (p < 0.05). Postoperative blood glucose, oxygen delivery index, and pulmonary shunt flow were increased in the methylprednisolone group (p < 0.05). There was no difference in postoperative oxygenation index, ventilation time, and clinical outcome between treatment groups., Conclusions: Glucocorticoid treatment before CPB attenuates perioperative release of systemic and myocardial inflammatory mediators and improves myocardial function, suggesting potential cardioprotective effects in patients undergoing cardiac surgery.

Vascular malformations affect 3% of neonates. Venous malformations (VMs) are the largest group representing more than 50% of cases. In hereditary forms of VMs gene mutations have been identified, but for the large group of spontaneous forms the primary cause and downstream dysregulated genes are unknown. We have performed a global comparison of gene expression in slow-flow VMs and normal saphenous veins using human whole genome micro-arrays. Genes of interest were validated with qRT-PCR. Gene expression in the tunica media was studied after laser micro-dissection of small pieces of tissue. Protein expression in endothelial cells (ECs) was studied with antibodies. We detected 511 genes more than four-fold down- and 112 genes more than four-fold up-regulated. Notably, chemokines, growth factors, transcription factors and regulators of extra-cellular matrix (ECM) turnover were regulated. We observed activation and "arterialization" of ECs of the VM proper, whereas ECs of vasa vasorum exhibited up-regulation of inflammation markers. In the tunica media, an altered ECM turnover and composition was found. Our studies demonstrate dysregulated gene expression in tunica interna, media and externa of VMs, and show that each of the three layers represents a reactive compartment. The dysregulated genes may serve as therapeutic targets.

Objective: The aim of this study was to correlate changes in regional cerebral blood flow (rCBF) to the degree of cerebral vasospasm in the canine two-hemorrhage model of subarachnoid hemorrhage (SAH)., Methods: SAH was induced in 13 adult beagle dogs using the two-hemorrhage model. Eleven beagle dogs served as controls. Angiography of the basilar artery and measurements of rCBF with colored microspheres were performed on days 1 and 8. Diameter of the basilar artery was calculated at equidistant points from the angiogram., Results: In controls, basilar artery diameter (mm) and rCBF (mL/min/g) were equal on days 1 and 8. In the SAH group, basilar artery diameter decreased significantly (1.27 +/- 0.17 [mean +/- SD]-0.84 +/- 0.15 mm). rCBF decreased significantly (P < .05) in the cerebrum (1.69 +/- 0.54 [mean +/- SD]-1.06 +/- 0.45 mL/min/g), cerebellum (1.18 +/- 0.40-0.80 +/- 0.32 mL/min/g), and brain stem (0.81 +/- 0.33-0.51 +/- 0.21 mL/min/g). However, decrements in CBF were not correlated to the reduction in vessel caliber in the corresponding vascular territory., Conclusion: Induced SAH in the canine model produces a significant impairment in rCBF irrespective of the degree of vasospasm of large cerebral vessels. The findings support the presumptive role of the microvasculature in regard to delayed cerebral ischemia after SAH.

Objective: Cardiac surgery on cardiopulmonary bypass (CPB) results in progressive myocardial dysfunction, despite unimpaired coronary blood flow, and is associated with increased myocardial tumor necrosis factor-alpha (TNFalpha) expression. We investigated whether anti-inflammatory treatment prevents increased TNFalpha expression and myocardial dysfunction after CPB., Methods and Results: Baseline systemic hemodynamics, myocardial contractile function, aortic and coronary blood flow were measured in anesthetized pigs. Then, placebo (PLA; saline; n=7) or methylprednisolone (MP; 30 mg/kg; n=6) was infused intravenously and CPB was instituted. Global ischemia was induced for 10 min by aortic cross-clamping, followed by 1 h of cardioplegic cardiac arrest. After declamping and reperfusion, CPB was terminated after a total of 3 h. Measurements were repeated at 15 min, 4 h, and 8 h following termination of CPB. Systemic TNFalpha-plasma concentrations and left ventricular TNFalpha expression were analyzed. With unchanged coronary blood flow in both groups, a progressive loss of myocardial contractile function to 38+/-2% of baseline (p<0.01) and cardiac index to 48+/-6% of baseline (p<0.01) at 8 h after CPB in PLA was attenuated in MP (myocardial function: 72+/-3%, p<0.01 vs PLA; cardiac index: 78+/-6%, p<0.05 vs PLA). Systemic TNFalpha was increased at 8 h in PLA compared to MP (243+/-34 vs 90+/-34 pg/ml, p<0.05). Myocardial TNFalpha was increased at 8 h after CPB compared to baseline and MP (p<0.05). Myocardial TNFalpha immunostaining was more pronounced in PLA than in MP (p<0.05), with TNFalpha-mRNA localization predominantly to cardiomyocytes., Conclusions: Methylprednisolone attenuates both systemic and myocardial TNFalpha increases and progressive myocardial dysfunction induced by cardiac surgery, suggesting a key role for TNFalpha.

Background: Differences in vascular reactivity have been associated with variable NO release due to 894G/T and -786C/T polymorphisms of the eNOS gene. Carriers of the 894T and -786C alleles are known to have enhanced vascular responsiveness to vasoconstrictor stimulation due to decreased NO generation. Thus, we hypothesized that eNOS gene polymorphism could influence perioperative hemodynamics and catecholamine support in patients undergoing cardiac surgery with CPB., Methods: In 105 patients undergoing elective CABG with CPB, systemic hemodynamics, cardiac index (CI), systemic and pulmonary vascular resistance indices (SVRI, PVRI) and catecholamine support were measured at baseline and 1 h, 4 h, 10 h and 24 h after CPB. Genotyping for the 894G/T and -786C/T eNOS gene polymorphisms was performed by polymerase chain reaction amplification. Patients were divided according to their genotype (894G/T: GG=group 1, GT and TT=group 2; -786C/T: TT=group 3, CT and CC=group 4)., Results: Genotype distribution for 894G/T polymorphism was 41% (GG), 52.4% (GT), 6.6% (TT) and for -786C/T polymorphism 37.1% (TT), 41.9% (CT) and 21% (CC). Pre- and intraoperative characteristics and systemic hemodynamics did not differ between groups. CI, SVRI and PVRI remained unaffected by genotype distribution. Statistical analysis of postoperative data revealed no difference between groups, especially for pharmacologic inotropic or vasopressor support. Also, coexistence of the 894T and -786C alleles had no impact on perioperative variables compared to homozygous 894G and -786T allele carriers., Conclusions: In contrast to current suggestions, the 894G/T and -786C/T genetic polymorphisms of the eNOS gene do not influence early perioperative hemodynamics after cardiac surgery with CPB.

Introduction: In addition to their lipid-lowering action, it has been demonstrated that statins can exert direct anti-inflammatory effects. We investigated the effect of preoperative statin therapy on systemic inflammatory markers and myocardial NF-kappaB inhibitor IkappaB-alpha after cardiac surgery., Methods: Thirty-six patients undergoing elective coronary artery bypass grafting with cardiopulmonary bypass (CPB) with cardioplegia were divided into two groups (statin group, n = 18; control group, n = 18). Plasma concentrations of pro-inflammatory cytokines (tumor necrosis factor alpha [TNFalpha], interleukin [IL]-6, IL-8) and anti-inflammatory IL-10 were measured before and 1, 4, 10, and 24 hours (h) after CPB. Phosphorylated IkappaB-alpha/total IkappaB-alpha ratio was assessed before and after CPB in right atrial biopsies., Results: Baseline and operative data did not differ between groups. Statin therapy was associated with lower preoperative low-density lipoprotein levels compared to control (73+/-6 vs. 92+/-6 mg/dL; P=0.03). Release of IL-6 was attenuated in the statin group at 4 h (2270+/-599 vs. 5120+/-656 pg/ml; P<0.01) and 10 h (1295+/-445 vs. 3116+/-487 pg/ml; P<0.05) compared to the control group. IL-10 increased after surgery in both groups (P<0.05), but was higher in the statin group at 1 h (66+/-15 vs. 26+/-16 pg/mL; P<0.01). Phosphorylated IkappaB-alpha/total IkappaB-alpha ratio before CPB did not differ between groups, but was elevated after CPB in both groups (P<0.05), indicating enhanced degradation of IkappaB-alpha. Statin therapy had no effect on TNFalpha and IL-8., Conclusions: Preoperative statin therapy attenuates the release of pro-inflammatory IL-6 and up-regulates anti-inflammatory IL-10 after cardiac surgery with cardioplegia, but fails to inhibit phosphorylation of myocardial IkappaB-alpha.

Neonatal rat hearts are more tolerant to ischemia compared to adult rat hearts. We hypothesized that opioid receptors and mitochondrial potassium channels are involved in the elevated ischemia tolerance of neonatal rats. Newborn rats were treated by an intraperitoneal injection with sodium chloride (placebo, Pla; n = 7), naloxone (Nal; n = 8), or K+ (ATP) channel blocker 5-hydroxydecanoate (HD; n = 8), or were left untreated (sham; n = 8). Thirty minutes after injection, the rats were sacrificed and hearts were arrested cardioplegically and fixed with aldehyde fixative 90 min after global ischemia at room temperature. For control, newborn rat hearts were fixed immediately after sacrifice. Ventricular tissue blocks were prepared for electron microscopy. Mitochondrial (volume-weighted mean volume of mitochondria) and cardiomyocyte volume (cellular edema index, CEI) were estimated to quantify the ischemic injury. Compared to control myocardium, CEI was increased by 244% +/- 39% in sham, 173% +/- 28% in Nal, 142% +/- 25% in HD, and 101% +/- 24% in Pla (P < 0.05 between groups). Volume-weighted mean volume of mitochondria was increased by 514% +/- 235% in sham, 341% +/- 110% in Nal, 458% +/- 149% in HD, and 175% +/- 70% in Pla. Differences between Pla and other groups were significant (P < 0.01 for all). No significant difference was observed between the other groups. Thus, ischemic injury was smallest with placebo, indicating a mechanism similar to preconditioning induced by the intraperitoneal injection. This response was attenuated by blockade of opioid receptors and mitochondrial potassium channels, suggesting their involvement in the elevated ischemia tolerance of newborn rat hearts.

Objective: Mild to moderate transient contractile dysfunction is frequently observed after cardiac surgery on cardiopulmonary bypass (CPB) but may also lead to low-cardiac-output (LCO) failure especially in patients with unstable angina, and is often referred to represent myocardial stunning. Whether time course of contractile dysfunction after cardiac surgery is similar to that of myocardial stunning was investigated in pigs., Methods: After baseline measurements of systemic hemodynamics (micromanometry), myocardial contractile function (sonomicrometry), cardiac output and coronary flow (ultrasonic probe), CPB was instituted. Control animals (n = 7) were weaned after 3 h from CPB. In LCO animals (n = 8), global ischemia was induced for 10 min by aortic crossclamping, followed by 1 h of cardioplegic cardiac arrest. After declamping and reperfusion, CPB was terminated after a total of 3 h. Measurements were repeated at 15 min, 4 h and 8 h after CPB. Systemic TNFalpha-plasma concentrations were measured (ELISA) and left ventricular biopsies were analyzed with respect to myocardial TNFalpha (immunohistochemistry) and irreversible cellular damage (light/electron microscopy)., Results: Contractile function decreased in LCO (75 +/- 12%) and control (83 +/-17%) at 15 min compared to baseline (p < 0.05). Thereafter, contractile function remained unchanged in control, but progressively decreased in LCO (52 +/- 12% at 4 h; 36 +/- 5% at 8 h; p < 0.05). Coronary flow remained unchanged in both groups. Cardiac output progressively decreased to 2.8 +/- 0.9 l/min at 8 h in the LCO group compared to baseline (5.9 +/- 1.1 l/min, p < 0.05) and control (5.7 +/- 1.4 l/min, p < 0.05). There was no evidence for myocardial infarction. TNFalpha-plasma concentrations and myocardial TNFalpha-staining were increased at 8 h after CPB in the LCO group compared to baseline and control (p < 0.05)., Conclusions: The progressive pattern of myocardial dysfunction apart from ongoing ischemia after cardiac surgery suggested underlying mechanisms at least partially different from those of myocardial stunning.

Background: Surgical correction of hypertrophic obstructive cardiomyopathy in severely symptomatic patients has been proven to be effective over the long term. The introduction of catheter-based procedures restricts surgical therapy to a subset of patients not suitable for septal ablation or requiring concomitant cardiac surgery., Methods: Between 8/2001 and 8/2003, 25 patients (58 +/- 15 years) underwent extended transaortic septal myectomy with partial excision and mobilization of the papillary muscles. Concomitant surgical procedures were performed in 40 % (CABG n = 9, aortic valve replacement n = 2). In 24 %, prior septal ablation was ineffective. Intraventricular gradient was 80 +/- 29 mm Hg at rest and 143 +/- 35 mm Hg during exercise. Mitral regurgitation affected 72 % of patients, and 88 % were NYHA functional class III or IV., Results: No hospital death, no postsurgical ventricular septal defect, and no complete atrioventricular block occurred. Severe nonfatal complications occurred in 24 % of patients. Intensive care was necessary for 1.8 +/- 1.7 days; total hospital stay was 11.8 +/- 3.8 days. Early follow-up was complete in 100 % (15 +/- 6 months, total of 376 months) with no late deaths, no relevant mitral regurgitation, or intraventricular gradients. Functional status was markedly improved (NYHA class I 40 %, class II 56 %, class III 4 %)., Conclusions: Early results of extended surgical myectomy and reconstruction of the subvalvular mitral apparatus in hypertrophic obstructive cardiomyopathy remain excellent with respect to mortality, morbidity, and functional capacity even when restricting surgery to patients earlier supposed to be at high risk.

Background: Ultrastructural data on acute right ventricular pressure load in pigs are rare., Materials and Methods: In control (n = 7) and banding groups (n = 6), right ventricular pressure (micromanometry) and function (sonomicrometry) were measured. Right ventricular pressure was increased 2.5-fold in the banding group by pulmonary artery constriction. Right ventricular biopsies were taken at baseline and after 6 h and processed for electron microscopy. Parameters of cellular injury were determined stereologically. Three perfusion -fixed hearts were investigated qualitatively in each group., Results: Stereology revealed an increase in the sarcoplasmic volume fraction and the cellular edema index in the banding group ( p < 0.05). Mitochondrial surface-to-volume ratio and volume fraction did not show significant alterations. Subendocardial edema and small amounts of severely injured myocytes were observed in the perfusion-fixed hearts after banding. Ultrastructure was normal in controls. After an initial increase, the right ventricular work index declined progressively in the banding group but remained unchanged in controls., Conclusions: Ultrastructural alterations resulting from acute right ventricular pressure load were characterized by edema of subendocardial myocytes and single cell necrosis. Focal adrenergic overstimulation and mechanical stress are probably more relevant in the pathogenesis of these lesions than ischemia.

Background: The frequency and importance of microembolization in patients with acute coronary syndromes and during coronary interventions have recently been appreciated. Experimental microembolization induces immediate ischemic dysfunction, which recovers within minutes. Subsequently, progressive contractile dysfunction develops over several hours and is not associated with reduced regional myocardial blood flow (perfusion-contraction mismatch) but rather with a local inflammatory reaction. We have now studied the effect of antiinflammatory glucocorticoid treatment on this progressive contractile dysfunction., Methods and Results: Microembolization was induced by injecting microspheres (42-microm diameter) into the left circumflex coronary artery. Anesthetized dogs were followed up for 8 hours and received placebo (n=7) or methylprednisolone 30 mg/kg IV either 30 minutes before (n=7) or 30 minutes after (n=5) microembolization. In addition, chronically instrumented dogs received either placebo (n=4) or methylprednisolone (n=4) 30 minutes after microembolization and were followed up for 1 week. In acute placebo dogs, posterior systolic wall thickening was decreased from 20.0+/-2.1% (mean+/-SEM) at baseline to 5.8+/-0.6% at 8 hours after microembolization. Methylprednisolone prevented the progressive myocardial dysfunction. Increased leukocyte infiltration in the embolized myocardium was prevented only when methylprednisolone was given before microembolization. In chronic placebo dogs, progressive dysfunction recovered from 5.0+/-0.7% at 4 to 6 hours after microembolization back to baseline (19.1+/-1.6%) within 5 days. Again, methylprednisolone prevented the progressive myocardial dysfunction., Conclusions: Methylprednisolone, even when given after microembolization, prevents progressive contractile dysfunction.

Background: The prognostic value of elevated serum levels of procalcitonin (PCT) in patients early after cardiac surgery on cardiopulmonary bypass (CPB) remains unclear. In a prospective study, we investigated whether PCT is useful as a prognostic marker in cardiac surgery with respect to mortality, complications and infections, and whether PCT is a specific marker for occurrence of infections., Methods: Within 8 months, a subset of 80 high-risk patients (APACHE II-score: 25.1 +/- 4.7 (mean +/- SD)) out of a consecutive cohort of 776 patients was investigated. Demographic data, operative data and clinical endpoints (mortality, infection, severe complication) were documented. Serum levels of PCT were analyzed preoperatively and at postoperative day 1., Results: Hospital mortality in this high-risk group was 21.3 %, infections occurred in 33.8 % and complications in 58.8 % of the patients. Preoperative PCT was normal in all patients. Postoperative PCT was increased in non-survivors compared to survivors (34.3 +/- 7.0 ng/ml vs. 15.9 +/- 4.9 ng/ml; p < 0.05), in patients with severe complications (30.3 +/- 6.7 ng/ml vs. 5.5 +/- 1.4 ng/ml; p < 0.05) and in patients with infections (38.4 +/- 11.3 ng/ml vs. 10.8 +/- 1.6 ng/ml; p < 0.05). Area under receiver operating characteristic curve for PCT as predictor of mortality, infections and complications was 0.772 (95 %-confidence-interval (CI): 0.651 - 0.894), 0.720 (95 %-CI: 0.603 - 0.837) and 0.861 (95 %-CI: 0.779 - 0.943), respectively. PCT was not different with infectious compared to non-infectious complications., Conclusions: High levels of PCT are associated with mortality, infections, and severe complications early after cardiac surgery using cardiopulmonary bypass and therefore provide a valuable prognostic marker. However, PCT does not discriminate between infectious and non-infectious complications.

Coronary microembolization results in progressive myocardial dysfunction, with causal involvement of tumor necrosis factor-alpha (TNF-alpha). TNF-alpha uses a signal transduction involving nitric oxide (NO) and/or sphingosine. Therefore, we induced coronary microembolization in anesthetized dogs and studied the role and sequence of NO, TNF-alpha, and sphingosine for the evolving contractile dysfunction. Four sham-operated dogs served as controls (group 1). Eleven dogs received placebo (group 2), 6 dogs received the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME, group 3), and 6 dogs received the ceramidase inhibitor N-oleoylethanolamine (NOE, group 4) before microembolization was induced by infusion of 3000 microspheres (42-microm diameter) per milliliter inflow into the left circumflex coronary artery. Posterior systolic wall thickening (PWT) remained unchanged in group 1 but decreased progressively in group 2 from 20.6+/-4.9% (mean+/-SD) at baseline to 4.1+/-3.7% at 8 hours after microembolization. Leukocyte count, TNF-alpha, and sphingosine contents were increased in the microembolized posterior myocardium. In group 3, PWT remained unchanged (20.3+/-2.6% at baseline) with intracoronary administration of L-NAME (20.8+/-3.4%) and 17.7+/-2.3% at 8 hours after microembolization; TNF-alpha and sphingosine contents were not increased. In group 4, PWT also remained unchanged (20.7+/-4.6% at baseline) with intravenous administration of NOE (19.5+/-5.7%) and 16.4+/-6.3% at 8 hours after microembolization; TNF-alpha, but not sphingosine content, was increased. In all groups, systemic hemodynamics, anterior systolic wall thickening, and regional myocardial blood flow remained unchanged throughout the protocols. A signal transduction cascade of NO, TNF-alpha, and sphingosine is causally involved in the coronary microembolization-induced progressive contractile dysfunction.

The aims of this study were to examine the release speed of the ball in maximal instep kicking with the preferred and the non-preferred leg and to relate ball speed to biomechanical differences observed during the kicking action. Seven skilled soccer players performed maximal speed place kicks with the preferred and the non-preferred leg; their movements were filmed at 400 Hz. The inter-segmental kinematics and kinetics were derived. A coefficient of restitution between the foot and the ball was calculated and rate of force development in the hip flexors and the knee extensors was measured using a Kin-Com dynamometer. Higher ball speeds were achieved with the preferred leg as a result of the higher foot speed and coefficient of restitution at the time of impact compared with the non-preferred leg. These higher foot speeds were caused by a greater amount of work on the shank originating from the angular velocity of the thigh. No differences were found in muscle moments or rate of force development. We conclude that the difference in maximal ball speed between the preferred and the non-preferred leg is caused by a better inter-segmental motion pattern and a transfer of velocity from the foot to the ball when kicking with the preferred leg.

Coronary microembolization is a frequent complication of atherosclerotic plaque rupture in acute coronary syndromes and during coronary interventions. Experimental coronary microembolization results in progressive contractile dysfunction associated with a local inflammation. We studied the causal role of tumor necrosis factor-alpha (TNF-alpha) in the progressive contractile dysfunction resulting from coronary microembolization. Anesthetized dogs were subjected to either coronary microembolization with infusion of 3.000 microspheres (42 microm diameter) per ml coronary inflow into the left circumflex coronary artery (n=9), or to intracoronary infusion of recombinant human TNF-alpha without microembolization (n=4), or to treatment with anti-murine TNF-alpha sheep antibodies prior to microembolization (n=4). Posterior systolic wall thickening (PWT; sonomicrometry) decreased from 21.1+/-5.3% (s.d.) at baseline to 5.5+/-2.2% (P<0.05) at 8 h after microembolization. Infarct size (1.8+/-1.9%; TTC and histology) and the amount of apoptosis (<0.1%; TUNEL and DNA-laddering) were small. TNF-alpha at the protein level (WEHI cytolytic assay) was increased and localized to leukocytes (immunostaining), which were increased in number (quantitative histology). In situ hybridization for TNF-alpha mRNA identified viable cardiomyocytes surrounding the microinfarcts as the major source of TNF-alpha. Supporting the role of TNF-alpha, infusion of TNF-alpha without microembolization decreased PWT from 27.3+/-6.9% at baseline to 10.1+/-4.9% after 8 h (P<0.05); in contrast, in the presence of TNF-alpha antibodies, microembolization no longer reduced PWT (19.3+/-7.0% at baseline v 16.9+/-5.0% at 8 h). In conclusion, TNF-alpha is the mediator responsible for the profound contractile dysfunction following coronary microembolization., (Copyright 2002 Academic Press.)

Background: Cytomegalovirus (CMV), Chlamydia pneumoniae (C. pneumoniae), and Helicobacter pylori (H. pylori) have been implicated in atherosclerosis and restenosis after angioplasty. The patterns of distribution within coronary lesions and possible coinfections of these pathogens in the coronary vasculature had not previously been evaluated., Design: A prospective, observational clinical study., Methods: Large coronary specimens (9-105 mm long) were obtained by endatherectomy of 53 patients undergoing aortocoronary bypass surgery. Samples were taken from two different sites of every lesion, resulting in a total of 106 probes. Presence of each pathogen was determined by polymerase chain reaction, subsequent hybridization, and DNA sequencing., Results: Cytomegalovirus and C. pneumoniae were detected in 30 and 32% of the samples, respectively; H. pylori was not detectable. The pathogens were not homogeneously distributed. A concurrent infection with both pathogens was observed in five of 106 (5%) lesions and five of 53 (9%) patients. Restenotic lesions were more often found in specimens in which cytomegalovirus was detected (five of 16 versus two of 37). Patients with C. pneumoniae-positive coronary lesions more commonly presented with unstable angina., Conclusions: Inhomogeneous infections with cytomegalovirus and C. pneumoniae of coronary atherosclerotic lesions are found to be prevalent when serial analysis is performed. Concurrent infection with both pathogens occurs coincidentally; however, possible clinical implications of this new observation and the pathogenic impact on atherosclerosis need further investigation.

A close relationship exists between regional myocardial blood flow (RMBF) and function during acute coronary inflow restriction (perfusion-contraction matching). However, the relationship of flow and function during coronary microvascular obstruction is unknown. In 12 anesthetized dogs, the left circumflex coronary artery was perfused from an extracorporeal circuit. After control measurements, 3,000 microspheres (42 micrometer diameter) per milliliter per minute inflow were injected to cause a microembolism (ME, n = 6). With unchanged systemic hemodynamics and RMBF, posterior systolic wall thickening (PWT) decreased from 19.8 +/- 1.9% SD at control to 13.3 +/- 4.0, 10.3 +/- 3.8, and 6.9 +/- 4.7% (P < 0.05 vs. control) at 1, 4, and 8 h, respectively. For comparison, inflow was progressively reduced to match PWT to that of the ME group at 1, 4, and 8 h (stenosis, STE, n = 6). RMBF in the STE group was reduced in proportion to PWT. Infarct size was not different among groups (6.5 +/- 4.5 vs. 3.4 +/- 3.2%). However, the number of leukocytes infiltrating the area at risk was significantly greater in the ME group than in the STE group. Coronary microembolization results in perfusion-contraction mismatch and is associated with an inflammatory response.

Background: New onset of atrial fibrillation is a frequent complication after coronary artery bypass grafting and is a major cause of postoperative morbidity. Preoperative oral treatment with amiodarone hydrochloride has been shown to be efficacious as prophylaxis. The present study investigated whether intraoperative use of intravenous amiodarone has a preventive effect on the incidence of atrial fibrillation after coronary revascularization., Methods: In a prospective study, 150 consecutive patients (mean age, 63 +/- 8 years; 132 men and 18 women) undergoing coronary artery bypass grafting were randomly assigned to one of three groups. Two groups received different doses of intravenous amiodarone (group I, 300-mg bolus and 20 mg x kg(-1) x day(-1) for 3 days; group II, 150-mg bolus and 10 mg x kg(-1) x day(-1) for 3 days) after aortic cross-clamping and one group, placebo (group III). Continuous electrocardiographic online monitoring was performed for 10 days. Arrhythmias were analyzed with respect to type, frequency, duration, and clinical relevance., Results: New onset of atrial fibrillation occurred in 24% of patients in group I, 28% in group II, and 34% in group III (p = not significant). Atrial fibrillation with a rapid ventricular response (>120 beats per minute) was significantly more frequent in the control group (group I, 14%; group II, 24%; group III, 32%; p < 0.05, group I versus group III) and appeared significantly earlier (group I, day 4.3 +/- 2.5; group II, day 4.8 +/- 2.9; group III, day 2.6 +/- 1.3; p < 0.05, group III versus groups I and II). Temporary atrial pacing because of bradycardia (<60 beats per minute) was necessary significantly more often in group I (group I, 48%; group II, 40%; group III, 28%; p < 0.05, group I versus group III). Early mortality rate (group I, 4%; group II, 2%; group III, 4%), rate of perioperative complications (group I, 14%; group II, 20%; group III, 14%), and duration of hospital stay (group I, 14.0 days; group II, 14.4 days; group III, 14.7 days) were not different between groups., Conclusions: Intraoperative prophylactic use of amiodarone does not prevent new onset of atrial fibrillation in patients undergoing coronary artery bypass grafting and had no effect on outcome. Therefore, intraoperative prophylactic treatment with amiodarone at the tested doses does not appear to be justified.