Electromechanical dyssynchrony can markedly worsen heart failure (HF) morbidity and mortality, independent of traditional risk factors.1–4 Depending on the metric used, current estimates of the prevalence of dyssynchrony vary from 25–30% in patients with HF (based on QRS widening) up to 60%, based on tissue Doppler or MRI measures of dyssynchronous contraction of the left ventricle (LV).5,6 Cardiac resynchronization therapy (CRT) or biventricular pacing has emerged as a promising option to treat patients with HF and dyssynchronous contraction.7–9 The past few decades have seen the rise of pharmacotherapy, primarily through agents that antagonize the effect of excessive concentrations of circulating neurohormones, yet, HF-related morbidity and mortality remain high.3–6 Biventricular stimulation has been demonstrated to improve contractile performance in patients with mechanical dyssynchrony acutely and chronically while also prolonging long-term survival—something not yet achieved by drug therapy.10 Although the clinical and mechanical effectiveness of CRT are well described, 30% of patients do not benefit from CRT and clinical criteria to identify CRT nonresponders remain elusive8,11,12 Currently, the most widely used predictor of reverse remodeling is the presence of marked mechanical dyssynchrony before CRT, as indexed by the width of the QRS.13 Mechanical dyssynchrony seems important, yet imaging-based measures have not predicted response well14 and even improvement in dyssynchrony after initiation of CRT only weakly predicts chronic response.15 Limited understanding of the molecular mechanisms underlying reverse cardiac remodeling induced by CRT has hampered the selection of potential responders. In this review, we focus on the electrophysiological aspects and molecular networks underlying the benefits of CRT. We will review how CRT homogenizes regional differences in stress kinase signaling and electric remodeling and then review its global effect on myocyte function and its …

Basic science of cardiac resynchronization therapy: molecular and electrophysiological mechanisms.

https://www.internationaljournalofcardiology.com/article/S0167-5273(14)00435-5/pdf

The predictive value of CHADS2 risk score in post myocardial infarction arrhythmias — A Cardiac Arrhythmias and RIsk Stratification after Myocardial infArction (CARISMA) substudy

An understanding of basic science is crucial for physicians who treat heart rhythm disorders. This issue summarizes the basic science of arrhythmias, including both acquired and inherited heart rhythm disorders. The basic mechanisms of arrhythmia are reviewed as are the mechanisms of atrial fibrillation. The issue is an excellent refresher for practicing cardiac electrophysiologists as well as a helpful resource for residents and fellows.

Basic science for the clinical electrophysiologist

Cardiac resynchronization therapy (CRT) is well acknowledged as an effective treatment for dyssynchronous heart failure. However, the molecular mechanism is unclear to date. Mitochondrial dysfunction and impaired energetic metabolism are two important mechanisms that lead to heart failure. Therefore, we aim to screen the changes of mitochondria-associated proteins and signaling pathways involved in heart failure and CRT treatment. A total of 24 beagle dogs were randomly assigned into control (CON), heart failure (HF), or CRT group. Myocardial mitochondria from the free wall of left ventricle was extracted for isobaric tags for relative and absolute quantitation (iTRAQ) labeling coupled with two-dimensional liquid chromatography tandem mass spectrometry analysis (2DLC-MS/MS). A total of 2190 proteins were identified, among which 234 proteins were differentially expressed in HF compared with CON group, 151 proteins were differentially expressed in CRT compared with HF group. A total of 192 of the 234 differentially expressed proteins in HF group were changed oppositely by CRT treatment, and 128 of the 151 CRT-induced differentially expressed proteins showed opposite trend of expression to HF/CON. Gene Ontology analysis of the 128 proteins revealed that 16 were localized in mitochondria, 17 were associated with calcium signaling, and 7 could be secreted extracellularly for cell-to-cell signaling. Calpain-1 (CAPN1), which is localized to mitochondria and related to calcium signaling, was upregulated in HF and downregulated after CRT treatment. CRT treatment also improved mitochondrial morphology and function and reduced collagen areas of both interstitial and perivascular fibrosis. CRT treatment significantly improved cardiac function, reduced myocardial fibrosis, and enhanced mitochondrial function in the failing heart through CAPN1 downregulation.

Protective effects of cardiac resynchronization therapy in a canine model with experimental heart failure by improving mitochondrial function: a mitochondrial proteomics study.

Wstęp: Jakość życia jest wielowymiarowym pojęciem odnoszącym się do różnych sfer funkcjonowania człowieka. Każdy proces chorobowy wpływa na życie chorego i prowadzi do rozmaitych ograniczeń. Rozwój techniki medycznej pozwolił udoskonalić stymulatory serca, które mogą spełniać różne funkcje. Umożliwiają uzyskanie czynności elektrycznej serca w sposób najbardziej zbliżony do stanu prawidłowego. Ich zadaniem jest ochrona chorego przed utratą przytomności i nagłym zgonem. Cel pracy: Ocena jakości życia chorych po wszczepieniu stymulatora serca. Materiał i metody: Grupę badanych stanowili pacjenci z wszczepionym stymulatorem serca (n = 58). Przeprowadzając badania, posłużono się kwestionariuszem ankiety własnego autorstwa oraz skalą jakości życia WHOQOL-BREF. Wyniki: Badani chorzy byli bardziej zadowoleni z jakości życia (x– = 3,60) niż ze stanu zdrowia (x– = 3,12). Zadowolonych z jakości życia było 63,79% badanych, a ze stanu własnego zdrowia 43,10% badanych. Badani najwyżej ocenili jakość życia w dziedzinie społecznej (x– = 14,15), najniżej w dziedzinie fizycznej (x– = 11,77). Wnioski: Badani chorzy przystosowali się do fun kcjonowania z wszczepionym stymulatorem serca. Jakość ich życia była zależna od: wieku, wykształcenia, aktywności zawodowej, czasu funkcjonowania z wszczepionym sty mulatorem, obecności chorób współistniejących oraz zakłóceń w funkcjonowaniu stymulatora.

https://www.termedia.pl/Journal/-50/pdf-16762-10?filename=Jakosc zycia.pdf

Martin Jan Schlij

Papers

Guidelines in cardiac pacing and resynchronization therapy

Wytyczne dotyczace stymulacji serca i resynchronizacji.