Contemporary evaluation of the causes of cardiac tamponade: Acute and long-term outcomes

Background: Cardiac tamponade is a life-threatening state that complicates various medical conditions. The contemporary interventional era may have led to changes in clinical characteristics, causes and outcomes of cardiac tamponade. Methods: We investigated all patients diagnosed with cardiac tamponade, based on clinical and echocardiographic findings, at a single medical center between the years 2000 and 2013. Data on medical history, index hospitalizations, pericardial fluid etiologies, and acute and long-term outcomes were collected. Results: Cardiac tamponade was observed in 83 patients (52% females). Major etiologies included complications of percutaneous cardiac interventions (36%) and malignancies (primarily lung cancer; 23%), infectious/inflammatory causes (15%) and mechanical complications of myocardial infarction (12%). Sixteen (19%) patients died during the index hospitalization. Acute presentation of symptoms and lower quantity of effusion were associated with in-hospital mortality (p = 0.045 and p = 0.007). Tamponade secondary to malignancy was associated with the most substantial increment in post-discharge mortality (from 16% in-hospital to 68% 1-year mortality). During the mean follow-up of 45 months, 39 (45%) patients died. Malignancies, mechanical complications of myocardial infarction and bleeding/coagulation abnormalities were etiologies associated with poor survival (80% mortality during follow-up). Tamponade secondary to complications of percutaneous cardiac interventions or infectious/inflammatory causes were associated with significantly lower mortality (28% and 17%; log rank p < 0.001). Conclusions: In a contemporary cohort, complications of percutaneous cardiac intervention replaced malignant diseases as the leading cause of cardiac tamponade. Nevertheless, these iatrogenic complications were associated with a relatively favorable outcome compared to tamponade induced by complications of myocardial infarction, coagulation abnormalities and malignant diseases.

A novel system for continuous, real-time monitoring of heart motion signals

Abstract Background Understanding cardiac mechanics is important for developing cardiac therapies. Current modalities for assessing cardiac mechanics sample patient’s heart at specific heart rate, contractility, preload, and afterload. The objective of this study was to test the feasibility of a novel system composed of intra-cardiac leads equipped with an inertial module chip (3D accelerometers and 3D gyroscopes) in monitoring continuous heart motion. Methods In this descriptive study, four healthy pigs were anesthetized and instrumented with motion-sensitive intra-cardiac leads; the temporal correlation between signals from motion sensors and tissue Doppler from the chest wall were studied; changes in real-time heart accelerations (ACC) and angular velocity (ANGV) were reported as percentages of change from baseline. Results Heart motion signals were sensed continuously from the right ventricular apex (RVa) and coronary sinus (CS). Volume expansion did not produce significant changes in the ACC and ANGV signals. Increasing heart rate increased the peak systolic ACC signal recorded from RVa and CS by 94 and 76%, respectively, and increased both peak systolic (61% RVa and 27% CS) and diastolic ANGV (200% CS vs. 31% RVa). Epinephrine administration increased peak systolic ACC signals at both sites (246% RVa; 331% CS). Peak systolic and diastolic ANGV increased in response to epinephrine (systolic: 198% RVa and 175% CS; diastolic: 723% CS and 89% RVa) (p = 0.125 for all changes expressed in percent). Temporal correlation between the ANGV signal and tissue Doppler signal was detected throughout all interventions. Conclusions A novel system for continuously monitoring heart motion signals from within the heart was presented. Heart motion signals in response to physiologic manipulations were characterized

Programmed electrical stimulation for risk stratification of patients with ischemic cardiomyopathy

Background: Patients with ischemic cardiomyopathy (ICM) are at an increased risk for sudden death. Although earlier trials used programmed electrical stimulation (PES) for risk stratification, more recent data demonstrate the benefit of implantable cardiac defibrillators (ICDs) in selected patients with reduced left ventricular ejection fraction (LVEF) without performing PES. However, little is known about the outcome of non-inducible patients. The purpose of this study was to evaluate the efficacy of PES for mortality risk stratification in patients with ICM. Methods: All consecutive patients who met the inclusion criteria (history of coronary artery disease, LVEF≤35%, and absence of documented spontaneous sustained ventricular tachycardia or aborted sudden cardiac death) were included in the study. The stimulation protocol involved up to three extrastimuli from two different sites in the right ventricle, with 180 ms as the shortest coupling interval. The primary endpoint was overall survival. Results: A total of 198 patients were included in the study; of these, 60 exhibited negative (−)PES, and 138 had positive (+)PES and also underwent ICD implantation. The mean follow-up duration was 4.5 years. There was no difference in age or LVEF between the patient groups. We found a trend towards an increased 5-year survival rate in the (+)PES group in whom ICD implantation had been performed (p=0.058). Survival was significantly better in patients under 68 year olds in the (+)PES group in whom ICD implantation was performed (hazard ratio=0.3, p=0.01). The survival rate of patients ≥68 years old was similar in both groups (p=0.95). Conclusions: Non-inducibility during PES does not predict the prognosis of patients with ischemic cardiomyopathy

Autonomic Remodeling in the Left Atrium and Pulmonary Veins in Heart Failure

BACKGROUND: Atrial fibrillation (AF) is commonly associated with congestive heart failure (CHF). The autonomic nervous system is involved in the pathogenesis of both AF and CHF. We examined the role of autonomic remodeling in contributing to AF substrate in CHF. METHODS AND RESULTS: Electrophysiological mapping was performed in the pulmonary veins (PVs) and left atrium (LA) in 38 rapid-ventricular paced dogs (CHF group) and 39 controls under the following conditions: vagal stimulation, isoproterenol infusion, β-adrenergic blockade, acetylcholinesterase (AChE) inhibition (physostigmine), parasympathetic blockade, and double autonomic blockade. Explanted atria were examined for nerve density/distribution, muscarinic receptor (MR) and beta-adrenergic receptor (βAR) densities, and AChE activity. In CHF dogs, there was an increase in nerve bundle size, parasympathetic fibers/bundle, and density of sympathetic fibrils and cardiac ganglia, all preferentially in the posterior LA/PVs. Sympathetic hyperinnervation was accompanied by increases in β(1)AR density and in sympathetic effect on ERPs and activation direction. β-adrenergic blockade slowed AF dominant frequency. Parasympathetic remodeling was more complex, resulting in increased AChE activity, unchanged MR density, unchanged parasympathetic effect on activation direction, and decreased effect of vagal stimulation on ERP (restored by AChE inhibition). Parasympathetic blockade markedly decreased AF duration. CONCLUSIONS: In this heart failure model autonomic and electrophysiologic remodeling occurs involving the posterior left atrium and pulmonary veins. Despite synaptic compensation, parasympathetic hyperinnervation contributes significantly to AF maintenance. Parasympathetic and/or sympathetic signaling may be possible therapeutic targets for AF in CHF

Autonomic Remodeling in the Left Atrium and Pulmonary Veins in Heart Failure Creation of a Dynamic Substrate for Atrial Fibrillation

Background— Atrial fibrillation (AF) is commonly associated with congestive heart failure (CHF). The autonomic nervous system is involved in the pathogenesis of both AF and CHF. We examined the role of autonomic remodeling in contributing to AF substrate in CHF. Methods and Results— Electrophysiological mapping was performed in the pulmonary veins and left atrium in 38 rapid ventricular–paced dogs (CHF group) and 39 control dogs under the following conditions: vagal stimulation, isoproterenol infusion, β-adrenergic blockade, acetylcholinesterase (AChE) inhibition (physostigmine), parasympathetic blockade, and double autonomic blockade. Explanted atria were examined for nerve density/distribution, muscarinic receptor and β-adrenergic receptor densities, and AChE activity. In CHF dogs, there was an increase in nerve bundle size, parasympathetic fibers/bundle, and density of sympathetic fibrils and cardiac ganglia, all preferentially in the posterior left atrium/pulmonary veins. Sympathetic hyperinnervation was accompanied by increases in β 1 -adrenergic receptor R density and in sympathetic effect on effective refractory periods and activation direction. β-Adrenergic blockade slowed AF dominant frequency. Parasympathetic remodeling was more complex, resulting in increased AChE activity, unchanged muscarinic receptor density, unchanged parasympathetic effect on activation direction and decreased effect of vagal stimulation on effective refractory period (restored by AChE inhibition). Parasympathetic blockade markedly decreased AF duration. Conclusions— In this heart failure model, autonomic and electrophysiological remodeling occurs, involving the posterior left atrium and pulmonary veins. Despite synaptic compensation, parasympathetic hyperinnervation contributes significantly to AF maintenance. Parasympathetic and/or sympathetic signaling may be possible therapeutic targets for AF in CHF