Concomitant Transatrial and Transapical CRT-D Lead Implantation in a Patient with Chest Burn Injury.

Cardiac resynchronization therapy device with defibrillator (CRT-D) implantation is indicated for patients with a history of malignant ventricular arrhythmias, symptomatic heart failure, wide QRS, or high-degree atrioventricular block. A 67-year-old patient with dilated cardiomyopathy received a CRT-D with the conventional method but 1 month later skin necrosis was diagnosed above the device. The complete system was extracted from the patient and we utilized negative pressure wound therapy for the treatment of the remaining tissue. We decided to perform surgical reimplantation of the device using minithoracotomy: right atrial and right ventricular leads were introduced through the right atrial appendage and the left ventricular lead was inserted transapically. The device was implanted under the less scabby abdominal skin. We successfully applied the combination of transatrial and transapical lead placement, which has not been reported in the literature yet. It serves as an alternative method if the standard approach is not feasible.

Modern therapeutic approaches of cardiac arrhythmias in pregnancy / Terhességi ritmuszavarok modern terápiás megközelítései.

Összefoglaló. A ritmuszavarok elofordulása gyakoribb a terhes nok esetén, mint a nem várandósok körében. A legtöbb esetben terápiás beavatkozás nélkül is kihordható a magzat. Hemodinamikai instabilitás és magzatkárosodáshoz vezeto fetalis hypoperfusio jöhet létre, amennyiben tartós, magas kamrai frekvenciával járó epizódok jelentkeznek. Ezekben az esetekben a ritmuszavar megszüntetése indokolttá válhat. Az antiarrhythmiás gyógyszerek korlátozottan és nagy körültekintéssel alkalmazhatók a gyermeket várók körében, így a katéterablatio jelenthet biztonságos és használható alternatívát. Ezen beavatkozásokat hagyományosan röntgensugár segítségével végzik, ez azonban az ionizáló sugárzásnak a magzati fejlodésre gyakorolt hatása miatt magas rizikót jelentene. Több éve elérheto a szív-elektrofiziológiában az ún. zéró fluoroszkópiás ablatio, mely a pitvarfibrilláció kezelésében és más ritmuszavarok esetében egyaránt alkalmazható. A terheseknél alkalmazott eljárást két eseten keresztül mutatjuk be. A röntgensugár használatát, a jelen cikkben bemutatott beavatkozások esetén is, sikerült teljesen kiküszöbölnünk. Az elso, 23 hetes gravid páciensnél recidív paroxysmalis supraventricularis tachycardia miatt végeztünk elektrofiziológiai vizsgálatot. E vizsgálat során atrioventricularis nodalis reentry tachycardiát igazoltunk és abláltunk sikerrel. Második esetbemutatásunkban egy anteroseptalis járulékos köteg katéterablatiós megoldását mutatjuk be. A terhesség során jelentkezo, az anyára és/vagy magzatára veszélyt jelento ritmuszavar esetén a háromdimenziós térképezo rendszer (szükség esetén intracardialis ultrahangvizsgálattal kiegészítve) biztonságos és hatásos alternatívát jelent, olyan esetekben, ha röntgensugár nem használható. Orv Hetil. 2021; 162(41): 1643-1651. Summary. Arrhythmias are more common in pregnant women than in others. In most cases, the fetus can be delivered without therapeutic intervention. Hemodynamic instability and fetal hypoperfusion leading to fetal harm may occur if persistent episodes of high ventricular rate occur. In these cases, resolution of the arrhythmia may be advised. Antiarrhythmic drugs can be used with limitations and great caution in those expecting a child, so catheter ablation may be a safe and usable alternative. These interventions are traditionally performed using X-ray, however, due to the effect of ionizing radiation on fetal development, this would pose a high risk. Zero-fluoroscopic ablation has been available for several years in cardiac electrophysiology, which can be used both in the treatment of atrial fibrillation and in other arrhythmias. The procedure which we used in pregnant women is presented in two cases. We also managed to completely eliminate the use of X-ray during the interventions presented in this article. In the first case, a 23-week-old gravid patient underwent electrophysiological examination for recurrent paroxysmal supraventricular tachycardia. In the electrophysiological study, atrioventricular nodal reentry tachycardia was confirmed and successfully ablated. In our second case study, we present a catheter ablation for anteroseptal accessory pathway. Three-dimensional mapping system (supplemented with intracardiac ultrasound, if necessary), in the case of significant arrhythmia, is a safe and effective alternative where X-rays, which poses a risk to the mother and/or the fetus, cannot be used during pregnancy. Orv Hetil. 2021; 162(41): 1643-1651.

Implementation of a zero fluoroscopic workflow using a simplified intracardiac echocardiography guided method for catheter ablation of atrial fibrillation, including repeat procedures.

OBJECTIVE: Pulmonary vein isolation (PVI) is the cornerstone of the interventional treatment of atrial fibrillation (AF). Traditionally, during these procedures the catheters are guided by fluoroscopy, which poses a risk to the patient and staff by ionizing radiation. Our aim was to describe our experience in the implementation of an intracardiac echocardiography (ICE) guided zero fluoroscopic (ZF) ablation approach to our routine clinical practice. METHODS: We developed a simplified ICE guided technique to perform ablation procedures for AF, with the aid of a 3D electroanatomical mapping system. The workflow was implemented in two phases: (1) the Introductory phase, where the first 16 ZF PVIs were compared with 16 cases performed with fluoroscopy and (2) the Extension phase, where 71 consecutive patients (including repeat procedures) with ZF approach were included. Standard PVI (and redoPVI) procedures were performed, data on feasibility of the ZF approach, complications, acute and 1-year success rates were collected. RESULTS: In the Introductory phase, 94% of the procedures could be performed with complete ZF with a median procedure time of 77.5 (73.5-83) minutes. In one case fluoroscopy was used to guide the ICE catheter to the atrium. There was no difference in the complication, acute and 1-year success rates, compared with fluoroscopy guided procedures. In the Extension phase, 97% of the procedures could be completed with complete ZF. In one case fluoroscopy was used to guide the transseptal puncture and in another to position the ICE catheter. Acute success of PVI was achieved in all cases, 64.4% patients were arrhythmia free at 1-year. Acute major complications were observed in 4 cases, all of these occurred in the redo PVI group and consisted of 2 tamponades, 1 transient ischemic attack and 1 pseudoaneurysm at the puncture site. The procedures were carried out by all members of the electrophysiology unit in the Extension phase, including less experienced operators and electrophysiology fellows (3 physicians) under the supervision of the senior electrophysiologist. Consequently, procedure times became longer [90 (75-105) vs 77.5 (73.5-85) min, p = 0.014]. CONCLUSIONS: According to our results, a ZF workflow of AF ablations can be successfully implemented into the routine practice of an electrophysiology laboratory, without compromising safety and effectivity.

The issue of permanent pacemaker implantation following cardiac surgery / A szívmutétet követo végleges pacemaker-implantáció kérdésköre

The issue of postoperative arrhythmias requiring pacemaker therapy is widely studied in the field of cardiac surgery and it is a complex perioperative problem. The aim of this paper is to summarize the relevant international guidelines and recommendations and to present our hospital's experience. We present the current, decisive recommendations and important studies, and present patients who underwent pacemaker implantation within one month after cardiac surgery between 01. 01. 2014 and 31. 12. 2018 in our hospital and compare them with the international findings. According to the international literature, the rate of permanent pacemaker implantation after cardiac surgery ranges from about 1.5% to 5%, and this rate seems to increase later. We have detailed information and many identified predictors about the development of conduction disturbances, but the current guidelines provide only weak recommendations. In the early perioperative period (1 month), pacemaker implantation was required in 15 cases (0.55%); in the course of long-term follow-up, 6 patients were still pacemaker-dependent. Perioperative arrhythmias are frequent and serious complications after cardiac surgery, prolong patient recovery time and put financial burden on the hospitals. The rate of need for a permanent pacemaker is low in our hospital, and in the late follow-up we can find only a small part of patients with pacemaker dependency. It would be necessary to start a prospective study and to develop a standardized protocol based on the information currently available. This would be a useful and authoritative help for the postoperative care in cardiac surgery. Orv Hetil. 2020; 161(31): 1271-1280.

Cardioprotective Effect of Resveratrol in a Postinfarction Heart Failure Model.

Despite great advances in therapies observed during the last decades, heart failure (HF) remained a major health problem in western countries. In order to further improve symptoms and survival in patients with heart failure, novel therapeutic strategies are needed. In some animal models of HF resveratrol (RES), it was able to prevent cardiac hypertrophy, contractile dysfunction, and remodeling. Several molecular mechanisms are thought to be involved in its protective effects, such as inhibition of prohypertrophic signaling molecules, improvement of myocardial Ca2+ handling, regulation of autophagy, and the reduction of oxidative stress and inflammation. In our present study, we wished to further examine the effects of RES on prosurvival (Akt-1, GSK-3ß) and stress signaling (p38-MAPK, ERK 1/2, and MKP-1) pathways, on oxidative stress (iNOS, COX-2 activity, and ROS formation), and ultimately on left ventricular function, hypertrophy and fibrosis in a murine, and isoproterenol- (ISO-) induced postinfarction heart failure model. RES treatment improved left ventricle function, decreased interstitial fibrosis, cardiac hypertrophy, and the level of plasma BNP induced by ISO treatment. ISO also increased the activation of P38-MAPK, ERK1/2Thr183-Tyr185, COX-2, iNOS, and ROS formation and decreased the phosphorylation of Akt-1, GSK-3ß, and MKP-1, which were favorably influenced by RES. According to our results, regulation of these pathways may also contribute to the beneficial effects of RES in HF.

Doxycycline protects against ROS-induced mitochondrial fragmentation and ISO-induced heart failure.

In addition to their anti-bacterial action, tetracyclines also have complex biological effects, including the modification of mitochondrial protein synthesis, metabolism and gene-expression. Long-term clinical studies have been performed using tetracyclines, without significant side effects. Previous studies demonstrated that doxycycline (DOX), a major tetracyclin antibiotic, exerted a protective effect in animal models of heart failure; however, its exact molecular mechanism is still unknown. Here, we provide the first evidence that DOX reduces oxidative stress-induced mitochondrial fragmentation and depolarization in H9c2 cardiomyocytes and beneficially alters the expression of Mfn-2, OPA-1 and Drp-1 -the main regulators of mitochondrial fusion and fission-in our isoproterenol (ISO)-induced heart failure model, ultimately decreasing the severity of heart failure. In mitochondria, oxidative stress causes a shift toward fission which leads to mitochondrial fragmentation and cell death. Protecting mitochondria from oxidative stress, and the regulation of mitochondrial dynamics by drugs that shift the balance toward fusion, could be a novel therapeutic approach for heart failure. On the basis of our findings, we raise the possibility that DOX could be a novel therapeutic agent in the future treatment of heart failure.

Chronic PARP-1 inhibition reduces carotid vessel remodeling and oxidative damage of the dorsal hippocampus in spontaneously hypertensive rats.

Vascular remodeling during chronic hypertension may impair the supply of tissues with oxygen, glucose and other compounds, potentially unleashing deleterious effects. In this study, we used Spontaneously Hypertensive Rats and normotensive Wistar-Kyoto rats with or without pharmacological inhibition of poly(ADP-ribose)polymerase-1 by an experimental compound L-2286, to evaluate carotid artery remodeling and consequent damage of neuronal tissue during hypertension. We observed elevated oxidative stress and profound thickening of the vascular wall with fibrotic tissue accumulation induced by elevated blood pressure. 32 weeks of L-2286 treatment attenuated these processes by modulating mitogen activated protein kinase phosphatase-1 cellular levels in carotid arteries. In hypertensive animals, vascular inflammation and endothelial dysfunction was observed by NF-κB nuclear accumulation and impaired vasodilation to acetylcholine, respectively. Pharmacological poly(ADP-ribose)polymerase-1 inhibition interfered in these processes and mitigated Apoptosis Inducing Factor dependent cell death events, thus improved structural and functional alterations of carotid arteries, without affecting blood pressure. Chronic poly(ADP-ribose)polymerase-1 inhibition protected neuronal tissue against oxidative damage, assessed by nitrotyrosine, 4-hydroxinonenal and 8-oxoguanosine immunohistochemistry in the area of Cornu ammonis 1 of the dorsal hippocampus in hypertensive rats. In this area, extensive pyramidal cell loss was also attenuated by treatment with lowered poly(ADP-ribose)polymer formation. It also preserved the structure of fissural arteries and attenuated perivascular white matter lesions and reactive astrogliosis in hypertensive rats. These data support the premise in which chronic poly(ADP-ribose)polymerase-1 inhibition has beneficial effects on hypertension related tissue damage both in vascular tissue and in the hippocampus by altering signaling events, reducing oxidative/nitrosative stress and inflammatory status, without lowering blood pressure.

PARP-inhibitor treatment prevents hypertension induced cardiac remodeling by favorable modulation of heat shock proteins, Akt-1/GSK-3ß and several PKC isoforms.

Spontaneously hypertensive rat (SHR) is a suitable model for studies of the complications of hypertension. It is known that activation of poly(ADP-ribose) polymerase enzyme (PARP) plays an important role in the development of postinfarction as well as long-term hypertension induced heart failure. In this study, we examined whether PARP-inhibitor (L-2286) treatment could prevent the development of hypertensive cardiopathy in SHRs. 6-week-old SHR animals were treated with L-2286 (SHR-L group) or placebo (SHR-C group) for 24 weeks. Wistar-Kyoto rats were used as aged-matched, normotensive controls (WKY group). Echocardiography was performed, brain-derived natriuretic peptide (BNP) activity and blood pressure were determined at the end of the study. We detected the extent of fibrotic areas. The amount of heat-shock proteins (Hsps) and the phosphorylation state of Akt-1(Ser473), glycogen synthase kinase (GSK)-3ß(Ser9), forkhead transcription factor (FKHR)(Ser256), mitogen activated protein kinases (MAPKs), and protein kinase C (PKC) isoenzymes were monitored. The elevated blood pressure in SHRs was not influenced by PARP-inhibitor treatment. Systolic left ventricular function and BNP activity did not differ among the three groups. L-2286 treatment decreased the marked left ventricular (LV) hypertrophy which was developed in SHRs. Interstitial collagen deposition was also decreased by L-2286 treatment. The phosphorylation of extracellular signal-regulated kinase (ERK)1/2(Thr183-Tyr185), Akt-1(Ser473), GSK-3ß(Ser9), FKHR(Ser256), and PKC ε(Ser729) and the level of Hsp90 were increased, while the activity of PKC α/ßII(Thr638/641), ζ/λ(410/403) were mitigated by L-2286 administration. We could detect signs of LV hypertrophy without congestive heart failure in SHR groups. This alteration was prevented by PARP inhibition. Our results suggest that PARP-inhibitor treatment has protective effect already in the early stage of hypertensive myocardial remodeling.