Quantitative analysis of spectral Doppler clicks in assessment of aortic stenosis.

Objectives: This study was performed to evaluate an additional echocardiographic spectral Doppler marker, which would identify severe aortic stenosis (AS).

Background: Echocardiography is most commonly utilized to assess AS and has been validated against invasive measurements. However, the data obtained are not always in agreement, leaving a conundrum regarding the true severity of AS and can lead to other diagnostic procedures.

Early Diagnosis of Defibrillation Lead Dislodgement.

Objectives: This study sought to develop and evaluate an algorithm for early diagnosis of dislodged implantable cardioverter-defibrillator (ICD) leads.

Background: Dislodged defibrillation leads may sense atrial and ventricular electrograms (EGMs), triggering shocks in the vulnerable period that induce ventricular fibrillation (VF).

Methods: We developed a 2-step algorithm by using experimental lead dislodgements (LDs) at ICD implantation and a control dataset of newly implanted, in situ leads.

Permanent-temporary pacemakers in the management of patients with conduction abnormalities after transcatheter aortic valve replacement.

Background: Damage to the cardiac conduction system requiring permanent pacemaker (PPM) implantation is a known adverse outcome of transcatheter aortic valve replacement (TAVR). A permanent-temporary pacemaker (PTPM) is a device that involves an active-fixation lead attached to an external pulse generator taped to the skin. We reviewed the utility of PTPMs as a temporary bridge measure after TAVR in patients with conduction abnormalities that do not meet conventional criteria for PPM placement.

Macroreentrant Loop in Ventricular Tachycardia From the Left Posterior Fascicle: New Implications for Mapping and Ablation.

Background: The underlying mechanisms of reentry during left posterior fascicular ventricular tachycardia (LPF-VT) remain unclear. The purpose of this study is to describe the components of LPF-VT reentry circuit and their electrophysiological properties.

Methods And Results: Fourteen consecutive patients with LPF-VT underwent electrophysiology study and radiofrequency ablation.

Cellular and Molecular Mechanisms of Arrhythmia by Oxidative Stress.

Current therapies for arrhythmia using ion channel blockade, catheter ablation, or an implantable cardioverter defibrillator have limitations, and it is important to search for new antiarrhythmic therapeutic targets. Both atrial fibrillation and heart failure, a condition with increased arrhythmic risk, are associated with excess amount of reactive oxygen species (ROS). There are several possible ways for ROS to induce arrhythmia.

Increased susceptibility of spontaneously hypertensive rats to ventricular tachyarrhythmias in early hypertension.

Hypertension is a risk factor for sudden cardiac death caused by ventricular tachycardia and fibrillation (VT/VF). We hypothesized that, in early hypertension, the susceptibility to stress-induced VT/VF increases. We compared the susceptibility of 5- to 6-month-old male spontaneously hypertensive rats (SHR) and age/sex-matched normotensive rats (NR) to VT/VF during challenge with oxidative stress (H2 O2 ; 0.

c-Src kinase inhibition reduces arrhythmia inducibility and connexin43 dysregulation after myocardial infarction.

Objectives: The aim of this study was to evaluate the role of tyrosine kinase cellular-Src (c-Src) inhibition on connexin43 (Cx43) regulation in a mouse model of myocardial infarction (MI).

Background: MI is associated with decreased expression of Cx43, the principal gap junction protein responsible for propagating current in ventricles. Activated c-Src has been linked to Cx43 dysregulation.

Mitochondria oxidative stress, connexin43 remodeling, and sudden arrhythmic death.

Background: Previously, we showed that a mouse model (ACE8/8) of cardiac renin-angiotensin system activation has a high rate of spontaneous ventricular tachycardia and sudden cardiac death secondary to a reduction in connexin43 level. Angiotensin-II activation increases reactive oxygen species (ROS) production, and ACE8/8 mice show increased cardiac ROS. We sought to determine the source of ROS and whether ROS played a role in the arrhythmogenesis.

Reactive oxygen species-targeted therapeutic interventions for atrial fibrillation.

Atrial fibrillation (AF) is the most common arrhythmia that requires medical attention, and its incidence is increasing. Current ion channel blockade therapies and catheter ablation have significant limitations in treatment of AF, mainly because they do not address the underlying pathophysiology of the disease. Oxidative stress has been implicated as a major underlying pathology that promotes AF; however, conventional antioxidants have not shown impressive therapeutic effects.

The predictive power of depression screening procedures for veterans with coronary artery disease.

Depression leads to a worse outcome for patients with coronary artery disease (CAD). Thus, accurately identifying depression in CAD patients is imperative. In many veterans affairs (VA) hospitals, patients are screened for depression once a year using the patient health questionnaire (PHQ-9).

Enhanced sensitivity of aged fibrotic hearts to angiotensin II- and hypokalemia-induced early afterdepolarization-mediated ventricular arrhythmias.

Unlike young hearts, aged hearts are highly susceptible to early afterdepolarization (EAD)-mediated ventricular fibrillation (VF). This differential may result from age-related structural remodeling (fibrosis) or electrical remodeling of ventricular myocytes or both. We used optical mapping and microelectrode recordings in Langendorff-perfused hearts and patch-clamp recordings in isolated ventricular myocytes from aged (24-26 mo) and young (3-4 mo) rats to assess susceptibility to EADs and VF during either oxidative stress with ANG II (2 μM) or ionic stress with hypokalemia (2.

Inhibition of c-Src tyrosine kinase prevents angiotensin II-mediated connexin-43 remodeling and sudden cardiac death.

Objectives: The aim of this study was to test whether c-Src tyrosine kinase mediates connexin-43 (Cx43) reduction and sudden cardiac death in a transgenic mouse model of cardiac-restricted overexpression of angiotensin-converting enzyme (ACE8/8 mice).

Background: Renin-angiotensin system activation is associated with an increased risk for arrhythmia and sudden cardiac death, but the mechanism is not well understood. The up-regulation of c-Src by angiotensin II may result in the reduction of Cx43, which impairs gap junction function and provides a substrate for arrhythmia.

Metabolic stress, reactive oxygen species, and arrhythmia.

Cardiac arrhythmias can cause sudden cardiac death (SCD) and add to the current heart failure (HF) health crisis. Nevertheless, the pathological processes underlying arrhythmias are unclear. Arrhythmic conditions are associated with systemic and cardiac oxidative stress caused by reactive oxygen species (ROS).

Inhibition of renin-angiotensin system (RAS) reduces ventricular tachycardia risk by altering connexin43.

Renin-angiotensin system (RAS) activation is associated with arrhythmias. We investigated the effects of RAS inhibition in cardiac-specific angiotensin-converting enzyme (ACE) overexpression (ACE 8/8) mice, which exhibit proclivity to ventricular tachycardia (VT) and sudden death because of reduced connexin43 (Cx43). ACE 8/8 mice were treated with an ACE inhibitor (captopril) or an angiotensin receptor type-1 blocker (losartan).

Suppression of re-entrant and multifocal ventricular fibrillation by the late sodium current blocker ranolazine.

Objectives: The purpose of this study was to test the hypothesis that the late Na current blocker ranolazine suppresses re-entrant and multifocal ventricular fibrillation (VF).

Background: VF can be caused by either re-entrant or focal mechanism.

Methods: Simultaneous voltage and intracellular Ca(+)² optical mapping of the left ventricular epicardial surface along with microelectrode recordings was performed in 24 isolated-perfused aged rat hearts.

Atrial fibrillation: the emerging role of inflammation and oxidative stress.

Atrial fibrillation (AF) remains the most commonly encountered sustained arrhythmia in clinical practice and contributes to increased morbidity and mortality. Management of AF poses a challenge due to the refractory nature of the arrhythmia and the associated thromboembolic complications. Recent studies have implicated both systemic and local cardiac inflammation in the development as well as persistence of AF.