First Author: Jacek Lelakowski
All Authors: Lelakowski J
Journal Title: Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego
Abstract: Cardiac arrhythmias most often arise in the mechanism of disorders of impulse formation (automaticity, triggered activity), disorders of impulse conduction (reentry, block) or a combination of both. Atrial fibrillation (AF) most often occurs in the course of mitral stenosis and/or mitral regurgitation, rarely in the defects of the aortic valve. Ventricular arrhythmias may be associated with the most valvular heart diseases. Among the disturbances of automatism and conduction in valvular heart diseases, the most common are atrioventricular blocks (AV blocks) and intraventricular blocks. In addition to defect correction and pharmacological treatment, non-pharmacological treatment of cardiac arrhythmias (transcatheter ablative techniques, permanent pacemakers, implantable cardioverter-defibrillators, implantable cardiac resynchronization devices) plays a significant role in the treatment. It is important for the practitioner to understand about the mechanisms of arrhythmia and nonpharmacological treatment in patients with acquired valvular heart diseases.
I'm Not Sure We Had A Choice?: Decision Quality and The Use of Cardiac Implantable Electronic Devices In Older Adults With Cognitive Impairment
Better Clinical Outcome For Rehospitalization Heart Failure Patients With Reduced Left Ventricular Function in Mode of Sudden Cardiac Death
Authors: Ishikawa N, Watanabe G
Abstract: The recognition of the significant advantages of minimizing surgical trauma has resulted in the development of minimally invasive surgical procedures. Endoscopic surgery confers the benefits of minimally invasive surgery upon patients, and surgical robots have enhanced the ability and precision of surgeons. Consequently, technological advances have facilitated totally endoscopic robotic cardiac surgery, which has allowed surgeons to operate endoscopically, rather than through a median sternotomy, during cardiac surgery. Thus, repairs for structural heart conditions, including mitral valve plasty, atrial septal defect closure, multivessel minimally invasive direct coronary artery bypass grafting and totally endoscopic coronary artery bypass graft surgery (CABG), can be totally endoscopic. On the other hand, general anesthesia remains a risk in patients who have severe carotid artery stenosis before surgery, as well as in those with a history of severe cerebral infarction or respiratory failure. In this study, the potential of a new awake CABG protocol using only epidural anesthesia was investigated for realizing day surgery and was found to be a promising modality for ultra-minimally invasive cardiac surgery. We herein review robot-assisted cardiac surgery and awake off-pump coronary artery bypass grafting as ultra-minimally invasive cardiac surgeries.
Authors: Montes FR, Pardo DF, Carreño M, Arciniegas C, Dennis RJ, Umaña JP
Abstract: Antifibrinolytic agents are used during cardiac surgery to minimize bleeding and reduce exposure to blood products. Several reports suggest that tranexamic acid (TA) can induce seizure activity in the postoperative period. To examine factors associated with postoperative seizures in patients undergoing cardiac surgery who received TA. University-affiliated hospital. Case-control study. Patients undergoing cardiac surgery with cardiopulmonary bypass (CPB) between January 2008 and December 2009 were identified. During this time, all patients undergoing heart surgery with CPB received TA. Cases were defined as patients who developed seizures that required initiation of anticonvulsive therapy within 48 h of surgery. Exclusion criteria included subjects with preexisting epilepsy and patients in whom the convulsive episode was secondary to a new ischemic lesion on brain imaging. Controls who did not develop seizures were randomly selected from the initial cohort. From an initial cohort of 903 patients, we identified 32 patients with postoperative seizures. Four patients were excluded. Twenty-eight cases and 112 controls were analyzed. Cases were more likely to have a history of renal impairment and higher preoperative creatinine values compared with controls (1.39 ± 1.1 vs. 0.98 ± 0.02 mg/dL, P = 0.02). Significant differences in the intensive care unit, postoperative and total lengths of stay were observed. An association between high preoperative creatinine value and postoperative seizure was identified. TA may be associated with the development of postoperative seizures in patients with renal dysfunction. Doses of TA should be reduced or even avoided in this population.
Authors: Wohlschlaeger J, Schmitz KJ, Takeda A, Takeda N, Vahlhaus C, Stypmann J, Schmid C, Baba HA
Abstract: Cyclin D1, the retinoblastoma (Rb) protein, and the E2F transcription factors are involved in the pathogenesis of cardiac hypertrophy. Cyclin D1/cdk4 complexes, by phosphorylation, inactivate Rb, thereby abrogating its growth-inhibitory effect. Ventricular unloading is associated with reversible regulation of numerous cardiomyocyte molecular systems and decreased hypertrophy. Accordingly, the hypothesis whether the Rb/E2F-1 pathway is altered by ventricular unloading was tested, and correlations with the cyclin D1 protein expression and cardiomyocyte diameters were explored.In 21 paired myocardial samples (before and after unloading) from patients with congestive heart failure (CHF), cyclin D1, phosphorylated Rb (pRb), its homologues p107 and p130 (pocket proteins), and E2F-1 were immunohistochemically investigated and morphometrically quantified. Cardiomyocyte diameters were morphometrically determined.Cyclin D1 and the proteins of the Rb/E2F-1 pathway were significantly increased during CHF compared with controls and were significantly decreased after unloading. Cyclin D1, pRb, and p130 protein expression correlated significantly with cardiomyocyte diameters. A significant positive correlation was noted between the pocket proteins, E2F-1, and cyclin D1.Increased protein expression of phosphorylated (inactivated) Rb and the pocket proteins is associated with cardiomyocyte hypertrophy in CHF. Rb inactivation might be explained by phosphorylation by increased numbers of cyclin D1/cdk4 complexes associated with cardiomyocyte hypertrophy. However, ventricular unloading can reversibly regulate this process. These data underscore the importance of cell cycle regulatory proteins in the pathogenesis of CHF-associated (maladaptive) cardiomyocyte hypertrophy and might offer novel clues for pharmacologic approaches of congestive heart failure.
Authors: Slight RD, Buell R, Nzewi OC, McClelland DB, Mankad PS
Abstract: The inadequacy of heparinization during cardiopulmonary bypass (CPB) can lead to hemostatic activation with increases in postoperative blood loss and blood product requirements after cardiac surgery. Because activated coagulation time (ACT) measurements may not be accurate during CPB, the use of a heparin management system (HMS) has been advocated. This study compared the efficacy of a modified ACT-based system versus an HMS (Hepcon; Medtronic Inc, Minneapolis, MN) for CPB anticoagulation.Randomized controlled trial.Regional cardiac surgery center.Adult elective cardiac surgical patients.Patients allocated to the HMS group (HC) received individualized heparin doses as indicated by the Hepcon system. Patients in the modified ACT group (C) received a standard weight-based heparin bolus with further doses as dictated by the ACT (Max-ACT, Helena Labs, Sunderland, UK). In addition, group C received supplemental heparin, independent of the ACT, as dictated by the volume of crystalloid added to the extracorporeal circuit. Outcome measures examined were hemostatic activation, postoperative chest tube loss, and blood product requirements.This study showed no significant difference in efficacy between the modified ACT and HMS heparinization strategies. Although the HC group received significantly greater amounts of heparin, this did not reduce hemostatic activation, postoperative blood loss, or transfusion requirements.ACT-based heparinization was found to be as efficacious as the Hepcon HMS system.
Authors: Suematsu N, Tsutsui H, Wen J, Kang D, Ikeuchi M, Ide T, Hayashidani S, Shiomi T, Kubota T, Hamasaki N, Takeshita A
Abstract: Tumor necrosis factor-alpha (TNF-alpha) and angiotensin II (Ang II) are implicated in the development and further progression of heart failure, which might be, at least in part, mediated by the production of reactive oxygen species (ROS). However, the cause and consequences of this agonist-mediated ROS production in cardiac myocytes have not been well defined. Recently, we demonstrated that increased ROS production was associated with mitochondrial DNA (mtDNA) damage and dysfunction in failing hearts. We thus investigated whether the direct exposure of cardiac myocytes to TNF-alpha and Ang II in vitro could induce mtDNA damage via production of ROS.TNF-alpha increased ROS production within cultured neonatal rat ventricular myocytes after 1 hour, as assessed by 2',7'-dichlorofluorescin diacetate fluorescence microscopy. TNF-alpha also decreased mtDNA copy number by Southern blot analysis in association with complex III activity, which was prevented in the presence of the antioxidant alpha-tocopherol. A direct exposure of myocytes to H2O2 caused a similar decrease in mtDNA copy number. In contrast, Ang II did not affect mtDNA copy number, despite the similar increase in ROS production. TNF-alpha-mediated ROS production and a decrease in mtDNA copy number were inhibited by the sphingomyelinase inhibitor D609. Furthermore, N-acetylsphingosine (C2-ceramide), a synthetic cell-permeable ceramide analogue, increased myocyte ROS production, suggesting that TNF-alpha-mediated ROS production and subsequent mtDNA damage were mediated by the sphingomyelin-ceramide signaling pathway.The intimate link between TNF-alpha, ROS, and mtDNA damage might play an important role in myocardial remodeling and failure.
Authors: Debreceni T, Szerafin T, Galajda Z, Miskolczi S, Péterffy A
Abstract: In the last decade a new and more effective method--the vacuum assisted wound closure (VAC)--was introduced for the treatment of the mediastinal wound infections following open heart operations. This technique gained a widespread acceptance in many countries of the world. The Centre of Cardiac Surgery of the University of Debrecen was the first to apply this treatment in Hungary. The authors evaluated the VAC therapy in a retrospective study at their institute. Between September 2002 and December 2005 62 consecutive patients were treated with this method because of wound infection in median sternotomy. Median age of 42 males and 20 females was 63,1 +/- 6,8 years (42-75). All patients had heart surgery (cardio pulmonary bypass) before they developed superficial or deep wound infection in their sternotomy site. Following exploration and radical debridement of the sternotomy wounds, VAC method was used for the treatment of infected wounds until suppuration stopped. When the wound had become macroscopically clear, reconstruction of the sternal defect was performed. This was carried out with well vascularized soft tissue flap(s) (major pectoral muscle and/or omental or pericardial fat pad) in 34 patients, sternal refixation was performed in 13 cases, while 11 patients underwent delayed secondary wound reconstruction with sutures. In one case Ley-prosthesis (sternal stabilisator metal prosthesis) was implanted. Three patients died before the sternal wound reconstruction. As a result of VAC therapy, all infected mediastinal wound cleaned up rapidly and formation of granulation tissue began. The mean period of time from the first sign of the infection to hospital discharge of the patients was 42.2 +/- 18.5 (5-185) days, while the same between sternal reconstruction and discharge was 19.9 +/- 9.6 (1-63) days. The mean duration of VAC therapy was 7.9 +/- 3.4 (1-21) days. The hospital mortality was 11.3% (7/62). Recurrence of the infection occurred in two patients (3.6%). These results suggest that Vacuum-assisted Closure system is an effective and safe method for the treatment of sternotomy wound infections following cardiac surgery. This method facilitates early clean up of infected sternotomy wounds and decreases the recurrence rate significantly.
Authors: Cvorovic V, Stankovic I, Panic M, Stipac AV, Zivkovic A, Neskovic AN, Putnikovic B
Abstract: In cardiac arrest survivors, postresuscitation myocardial stunning usually presents as either global left ventricular dysfunction or regional dyssynergy including the various forms of stress cardiomyopathy, in which rare variants may be difficult to diagnose. We present a patient with cardiac arrest during general anesthesia, in whom speckle tracking-derived myocardial strain helped to distinguish between the inverted variant of stress cardiomyopathy and global postresuscitation myocardial stunning.
Authors: Shannon R, Chaudhry M
Abstract: Compelling evidence now exists that proves adrenergic blockade is at the center of neurohormonal antagonism in heart failure (HF). Catecholamines are well known to act through both beta- and alpha-adrenergic receptors (ARs), which mediate their effects through distinct receptor pathways. Beta-AR blockers are commonly used in the treatment of HF and have distinct receptor affinity profiles. The recent COMET trial comparing 2 important beta-blocking drugs showed a distinct advantage for carvedilol in decreasing the risk of mortality from HF. The mechanism of action for carvedilol differs from metoprolol tartrate in its ability to block both alpha- and beta-ARs, leading to renewed interest in the potential role of alpha-ARs in the progression of HF. In contrast, however, the ALLHAT study discontinued use of doxazosin, an alpha1-receptor blocker because of an increase in cardiovascular events among patients using this drug. The results of these studies appear to be in contrast with respect to the role of alpha-ARs in regards to cardiovascular pathophysiology. Further study of the alpha-receptor and understanding the role of alpha-ARs in HF is necessary to understand the therapeutic effect of alpha-blockade. This article reviews our understanding of the alpha-AR in HF.
Authors: Werys K, Petryka-Mazurkiewicz J, B?aszczyk ?, Mi?ko J, ?piewak M, Ma?ek ?A, Mazurkiewicz ?, Mi?osz-Wieczorek B, Marczak M, Kubik A, D?browska A, Pi?tkowska-Janko E, Sawionek B, Wijesurendra R, Piechnik SK, Bogorodzki P
Abstract: To investigate whether magnetic resonance imaging (MRI) cine-derived dyssynchrony indices provide additional information compared to conventional tagged MRI (tMRI) acquisitions in heart failure patients undergoing cardiac resynchronization therapy (CRT).Patients scheduled for CRT (n = 52) underwent preprocedure MRI including cine and tMRI acquisitions. Segmental strain curves were calculated for both cine and tMRI to produce a range of standard indices for direct comparison between modalities. We also proposed and evaluated a novel index of "dyscontractility," which detects the presence of focal areas with paradoxically positive circumferential strain.Across conventional strain indices, there was only moderate-to-poor (R = 0.3-0.6) correlation between modalities; eight cine-derived indices showed statistically significant (P < 0.05) relations to CRT outcome compared to just two tMRI-based counterparts. The novel dyscontractility index calculated on basal slice cine images (cine dyscontractility index, "CDI") was the single best predictor of clinical response to CRT (area under the curve AUC = 0.81, P < 0.001). While poorly correlated to its tMRI counterpart (R = 0.33), CDI performed significantly better in predicting response to CRT (P < 0.005), and was also numerically better than all other tMRI indices (AUC 0.53-0.76, all P for AUC comparisons <0.17).Cine-derived strain indices offer potentially new information compared to tMRI. Specifically, the novel CDI is most strongly linked to response to cardiac resynchronization therapy in a contemporary patient cohort. It utilizes readily available MRI data, is relatively straightforward to process, and compares favorably with any conventional tagging index. J. Magn. Reson. Imaging 2016;44:1483-1492.
Authors: Wang D, Wang H, Luo P, Hwang A, Sun D, Wang Y, Zhang Z, Liu N, Wang S, Li C, Cao F
Abstract: Ghrelin is a well-characterized hormone that has protective effects on endothelial cells. Elevated HCY (homocysteine) can be a cardiovascular risk factor, but it is not known whether ghrelin can inhibit HCY-induced dysfunction and inflammatory response in rat CMECs (cardiac microvascular endothelial cells). We found that HCY treatment for 24 h inhibited proliferation and NO (nitric oxide) secretion, but with increased cell apoptosis and secretion of cytokines in CMECs. In contrast, ghrelin pretreatment significantly improved proliferation and NO secretion, and inhibited cell apoptosis and secretion of cytokines in HCY-induced CMECs. In addition, Western blot assay showed that NF-?B (nuclear factor ?B) and cleaved-caspase 3 expression were elevated, and PCNA (proliferating cell nuclear antigen) and eNOS (endothelial nitric oxide synthase) expression were decreased after treatment with HCY, which was significantly reversed by pretreatment with ghrelin. The data suggest that ghrelin inhibits HCY-induced CMEC dysfunction and inflammatory response, probably mediated by inhibition of NF-?B activation.