Cardiac tamponade and electrical alternans.
Ontology highlight
ABSTRACT:
SUBMITTER: Lau TK
PROVIDER: S-EPMC101278 | biostudies-literature | 2002
REPOSITORIES: biostudies-literature
Publications
Cardiac tamponade and electrical alternans.
Lau Theodore K TK Civitello Andrew B AB Hemandez Antonieta A Coulter Stephanie A SA
Texas Heart Institute journal 20020101 1
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Project description:BackgroundT-wave alternans (TWA), a marker of electrical instability, can be modulated by cardiac resynchronization therapy (CRT). The relationship between TWA and heart failure response to CRT has not been clearly defined.Methods and resultsIn 40-patients (age 65±11 years, left ventricular ejection-fraction [LVEF] 23±7%), TWA was evaluated prospectively at median of 2 months (baseline) and 8 months (follow-up) post-CRT implant. TWA-magnitude (Valt >0μV, k≥3), its duration (d), and burden (Valt ·d) were quantified in moving 128-beat segments during incremental atrial (AAI, native-TWA) and atrio-biventricular (DDD-CRT) pacing. The immediate and long-term effect of CRT on TWA was examined. Clinical response to CRT was defined as an increase in LVEF of ≥5%. Native-TWA was clinically significant (Valt ≥1.9μV, k≥3) in 68% of subjects at baseline. Compared to native-TWA at baseline, DDD-CRT pacing at baseline and follow-up reduced the number of positive TWA segments, peak-magnitude, longest-duration and peak-burden of TWA (44±5 to 33±5 to 28±4%, p = 0.02 and 0.002; 5.9±0.8 to 4.1±0.7 to 3.8±0.7μV, p = 0.01 and 0.01; 97±9 to 76±8 to 67±8sec, p = 0.004 and <0.001; and 334±65 to 178±58 to 146±54μV.sec, p = 0.01 and 0.004). In addition, the number of positive segments and longest-duration of native-TWA diminished during follow-up (44±5 to 35±6%, p = 0.044; and 97±9 to 81±9sec, p = 0.02). Clinical response to CRT was observed in 71% of patients; the reduction in DDD-CRT paced TWA both at baseline and follow-up was present only in responders (interaction p-values <0.1).ConclusionLong-term CRT reduces the prevalence and magnitude of TWA. This CRT induced beneficial electrical remodeling is a marker of clinical response after CRT.
| S-EPMC6023131 | biostudies-literature
Project description: Not available
| S-EPMC6886137 | biostudies-literature
Project description:Cardiac action potential (AP) shape and propagation are regulated by several key dynamic factors such as ion channel recovery and intracellular Ca2+ cycling. Experimental methods for manipulating AP electrical dynamics commonly use ion channel inhibitors that lack spatial and temporal specificity. In this work, we propose an approach based on optogenetics to manipulate cardiac electrical activity employing a light-modulated depolarizing current with intensities that are too low to elicit APs (sub-threshold illumination), but are sufficient to fine-tune AP electrical dynamics. We investigated the effects of sub-threshold illumination in isolated cardiomyocytes and whole hearts by using transgenic mice constitutively expressing a light-gated ion channel (channelrhodopsin-2, ChR2). We find that ChR2-mediated depolarizing current prolongs APs and reduces conduction velocity (CV) in a space-selective and reversible manner. Sub-threshold manipulation also affects the dynamics of cardiac electrical activity, increasing the magnitude of cardiac alternans. We used an optical system that uses real-time feedback control to generate re-entrant circuits with user-defined cycle lengths to explore the role of cardiac alternans in spontaneous termination of ventricular tachycardias (VTs). We demonstrate that VT stability significantly decreases during sub-threshold illumination primarily due to an increase in the amplitude of electrical oscillations, which implies that cardiac alternans may be beneficial in the context of self-termination of VT.
| S-EPMC9054908 | biostudies-literature
Project description: Not available
| S-EPMC4900338 | biostudies-literature
Project description:Heart failure (HF) is associated with an increased propensity for atrial fibrillation (AF), causing higher mortality than AF or HF alone. It is hypothesized that HF-induced remodelling of atrial cellular and tissue properties promotes the genesis of atrial action potential (AP) alternans and conduction alternans that perpetuate AF. However, the mechanism underlying the increased susceptibility to atrial alternans in HF remains incompletely elucidated. In this study, we investigated the effects of how HF-induced atrial cellular electrophysiological (with prolonged AP duration) and tissue structural (reduced cell-to-cell coupling caused by atrial fibrosis) remodelling can have an effect on the generation of atrial AP alternans and their conduction at the cellular and one-dimensional (1D) tissue levels. Simulation results showed that HF-induced atrial electrical remodelling prolonged AP duration, which was accompanied by an increased sarcoplasmic reticulum (SR) Ca2+ content and Ca2+ transient amplitude. Further analysis demonstrated that HF-induced atrial electrical remodelling increased susceptibility to atrial alternans mainly due to the increased sarcoplasmic reticulum Ca2+-ATPase (SERCA) Ca2+ reuptake, modulated by increased phospholamban (PLB) phosphorylation, and the decreased transient outward K+ current (Ito). The underlying mechanism has been suggested that the increased SR Ca2+ content and prolonged AP did not fully recover to their previous levels at the end of diastole, resulting in a smaller SR Ca2+ release and AP in the next beat. These produced Ca2+ transient alternans and AP alternans, and further caused AP alternans and Ca2+ transient alternans through Ca2+→AP coupling and AP→Ca2+ coupling, respectively. Simulation of a 1D tissue model showed that the combined action of HF-induced ion channel remodelling and a decrease in cell-to-cell coupling due to fibrosis increased the heart tissue's susceptibility to the formation of spatially discordant alternans, resulting in an increased functional AP propagation dispersion, which is pro-arrhythmic. These findings provide insights into how HF promotes atrial arrhythmia in association with atrial alternans.
| S-EPMC7402519 | biostudies-literature
Project description:We present a previously healthy young man with cardiac tamponade. He underwent emergency pericardiocentesis. The pericardial fluid was exudative, and Salmonella sp. was grown on both pericardial and blood cultures. Further investigations revealed that this patient had classical Hodgkin lymphoma, which explains his immunocompromised state predisposing him to this infection. (Level of Difficulty: Advanced.).
| S-EPMC9666747 | biostudies-literature
Project description:Cardiac tamponade is a rare and life-threatening condition that can be caused by trauma and various medical conditions. Failure to recognize and repair it quickly could lead to significant morbidity or even death. This case demonstrates the electrocardiogram (ECG) findings of low voltage QRS and electrical alternans in cardiac tamponade. It also highlights the classic ultrasound (US) findings of pericardial effusion and right ventricular collapse during diastole in cardiac tamponade. Classic physical exam findings of cardiac tamponade include Beck's Triad (jugular venous distention, hypotension, and muffled heart sounds) and pulsus paradoxus. This patient only had jugular venous distention and pulsus paradoxus. The case is centered on a 52-year-old male who presented with shortness of breath, wheezing, and a productive cough with streaks of blood. A CT chest was performed which revealed a large pericardial effusion, right upper lobe lung mass, and bilateral pulmonary emboli. A bedside transthoracic echocardiogram was then performed which confirmed the large effusion as well as right ventricular collapse during diastole. Cardiothoracic surgery and interventional cardiology were consulted and both agreed to take the patient to the cardiac catheterization lab for percutaneous drainage of the effusion. Pericardiocentesis was performed and 1.7 liters of serosanguinous fluid was removed and a drain was left in place. He recovered well from the procedure and had an uneventful admission. After reviewing this case, learners should be able to recognize the diagnostic features and various causes of pericardial effusion and cardiac tamponade.TopicsElectrocardiography, echocardiography, cardiac tamponade.
| S-EPMC10332784 | biostudies-literature
Project description:ContextCardiac tamponade (CT) following cardiac surgery is a potentially fatal complication and the cause of surgical reintervention in 0.1%-6% of cases. There are two types of CT: acute, occurring within the first 48 h postoperatively, and subacute or delayed, which occurs more than 48 h postoperatively. The latter does not show specific clinical signs, which makes it more difficult to diagnose. The factors associated with acute CT (aCT) are related to coagulopathy or surgical bleeding, while the variables associated with subacute tamponade have not been well defined.AimsThe primary objective of this study was to identify the factors associated with the development of subacute CT (sCT).Settings and designThis report describes a case (n = 80) and control (n = 160) study nested in a historic cohort made up of adult patients who underwent any type of urgent or elective cardiac surgery in a tertiary cardiovascular hospital. Methods: The occurrence of sCT was defined as the presence of a compatible clinical picture, pericardial effusion and confirmation of cardiac tamponade during the required emergency intervention at any point between 48 hours and 30 days after surgery. All factors potentially related to the development of sCT were taken into account.Statistical analysis usedFor the adjusted analysis, a logistical regression was constructed with 55 variables, including pre-, intra-, and post-operative data.ResultsThe mortality of patients with sCT was 11% versus 0% in the controls. Five variables were identified as independently and significantly associated with the outcome: pre- or post-operative anticoagulation, reintervention in the first 48 h, surgery other than coronary artery bypass graft, and red blood cell transfusion.ConclusionsOur study identified five variables associated with sCT and established that this complication has a high mortality rate. These findings may allow the implementation of standardized follow-up measures for patients identified as higher risk, leading to either early detection or prevention.
| S-EPMC5914216 | biostudies-literature
Project description:Cardiac repolarization alternans is an arrhythmogenic rhythm disturbance, manifested in individual myocytes as a beat-to-beat alternation of action potential durations and intracellular calcium transient magnitudes. Recent experimental studies have reported "subcellular alternans," in which distinct regions of an individual cell are seen to have counterphase calcium alternations, but the mechanism by which this occurs is not well understood. Although previous theoretical work has proposed a possible dynamical mechanism for subcellular alternans formation, no direct evidence for this mechanism has been reported in vitro. Rather, experimental studies have generally invoked fixed subcellular heterogeneities in calcium-cycling characteristics as the mechanism of subcellular alternans formation.In this study, we have generalized the previously proposed dynamical mechanism to predict a simple pacing algorithm by which subcellular alternans can be induced in isolated cardiac myocytes in the presence or absence of fixed subcellular heterogeneity. We aimed to verify this hypothesis using computational modeling and to confirm it experimentally in isolated cardiac myocytes. Furthermore, we hypothesized that this dynamical mechanism may account for previous reports of subcellular alternans seen in statically paced, intact tissue.Using a physiologically realistic computational model of a cardiac myocyte, we show that our predicted pacing algorithm induces subcellular alternans in a manner consistent with theoretical predictions. We then use a combination of real-time electrophysiology and fluorescent calcium imaging to implement this protocol experimentally and show that it robustly induces subcellular alternans in isolated guinea pig ventricular myocytes. Finally, we use computational modeling to demonstrate that subcellular alternans can indeed be dynamically induced during static pacing of 1D fibers of myocytes during tissue-level spatially discordant alternans.Here we provide the first direct experimental evidence that subcellular alternans can be dynamically induced in cardiac myocytes. This proposed mechanism may contribute to subcellular alternans formation in the intact heart.
| S-EPMC2740370 | biostudies-literature