Python farming as a flexible and efficient form of agricultural food security.

Diminishing natural resources and increasing climatic volatility are impacting agri-food systems, prompting the need for sustainable and resilient alternatives. Python farming is well established in Asia but has received little attention from mainstream agricultural scientists. We measured growth rates in two species of large pythons (Malayopython reticulatus and Python bivittatus) in farms in Thailand and Vietnam and conducted feeding experiments to examine production efficiencies. Pythons grew rapidly over a 12-month period, and females grew faster than males. Food intake and growth rates early in life were strong predictors of total lifetime growth, with daily mass increments ranging from 0.24 to 19.7 g/day for M. reticulatus and 0.24 to 42.6 g/day for P. bivittatus, depending on food intake. Pythons that fasted for up to 4.2 months lost an average of 0.004% of their body mass per day, and resumed rapid growth as soon as feeding recommenced. Mean food conversion rate for dressed carcasses was 4.1%, with useable products (dressed carcass, skin, fat, gall bladder) comprising 82% of the mass of live animals. In terms of food and protein conversion ratios, pythons outperform all mainstream agricultural species studied to date. The ability of fasting pythons to regulate metabolic processes and maintain body condition enhances food security in volatile environments, suggesting that python farming may offer a flexible and efficient response to global food insecurity.

Psychological stress, the central nervous system and arrhythmias.

This review highlights the links between psychological stress and the neurocircuitry of cardiac-brain interactions leading to arrhythmias. The role of efferent and afferent connections in the heart-brain axis is considered, with the mechanisms by which emotional responses promote arrhythmias illustrated by inherited cardiac conditions. Novel therapeutic targets for intervention in the autonomic nervous system are considered.

Oesophageal sarcocystosis observed at slaughter provides a reliable and efficient proximate measure of Toxoplasma gondii seroprevalence in sheep.

OBJECTIVE: Successful disease management requires effective surveillance. Slaughterhouse inspections provide opportunities to efficiently collect regular disease data from many animals across large areas. Toxoplasma is a cat-borne parasite that causes reproduction failure in sheep, although it is not visually detectable at slaughterhouses. Macroscopic sarcocystosis is a disease of sheep that is visually detectable at slaughter and is caused by parasites that share a similar biology with Toxoplasma. We investigated if sarcocystosis could act as a proximate measure for Toxoplasma exposure in sheep to facilitate its efficient surveillance at large scales. DESIGN/METHODS: We compared the presence of macroscopic sarcocystosis to Toxoplasma serostatus at the animal and farm levels. RESULTS: At the animal level, we found a weak association between Toxoplasma seropositivity and sarcocysts in the oesophagus (OR = 1.76 [95% CI: 1.17, 2.65; McFadden's R2 = 0.01]) but no association between Toxoplasma seropositivity and sarcocysts in skeletal muscles. At the farm level, the seroprevalence of Toxoplasma was strongly associated with oesophageal sarcocystosis prevalence (OR = 28.59 [95% CI: 13.07, 62.57; McFadden's R2 = 0.34]) but less strongly associated with sarcocystosis prevalence in skeletal muscles (OR = 7.91 [95% CI: 1.24, 50.39; McFadden's R2 = 0.02]). CONCLUSIONS: For Toxoplasma surveillance in sheep at the farm level, routine slaughter inspection and recording of macroscopic oesophageal sarcocystosis could be are liable and efficient proximate measure. The monitoring of oesophageal sarcocystosis may be a useful passive Toxoplasma surveillance tool for guiding the timing and location of other Toxoplasma detection methods to facilitate the management of Toxoplasma impacts within the sheep industry.

No Evidence of Toxoplasma Gondii Exposure in South Australian Koalas (Phascolarctos cinereus).

Infection with the cat-borne parasite Toxoplasma gondii has been detected in numerous Australian marsupials and can lead to severe disease (toxoplasmosis) in some cases. The seroprevalence of Toxoplasma on Kangaroo Island, South Australia has been reported to be higher than the South Australian mainland in macropods, cats, and sheep, suggesting an increased risk of infection on this island. However, Toxoplasma seroprevalence in small- and medium-sized terrestrial mammals was almost zero on the island and did not differ from that on the mainland. We surveyed Toxoplasma seroprevalence in koala (Phascolarctos cinereus) populations on the island and on the mainland and assessed their risk of infection and their role in the life cycle of Toxoplasma. All screened koalas from the island (n = 94) and the mainland (n = 63) were seronegative. This represents the largest Toxoplasma seroprevalence survey in this species and provided sufficient evidence to confidently demonstrate freedom from parasite exposure in both island and mainland populations at the time of the survey. Because koalas are extensively arboreal and predominately consume tree foliage, they appear to be at negligible risk of Toxoplasma infection. Furthermore, as koalas are rarely consumed by cats, we suggest that they have a minor role in the parasite's life cycle.

Assessment of a conduction-repolarisation metric to predict Arrhythmogenesis in right ventricular disorders.

BACKGROUND: The re-entry vulnerability index (RVI) is a recently proposed activation-repolarization metric designed to quantify tissue susceptibility to re-entry. This study aimed to test feasibility of an RVI-based algorithm to predict the earliest endocardial activation site of ventricular tachycardia (VT) during electrophysiological studies and occurrence of haemodynamically significant ventricular arrhythmias in follow-up. METHODS: Patients with Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) (n = 11), Brugada Syndrome (BrS) (n = 13) and focal RV outflow tract VT (n = 9) underwent programmed stimulation with unipolar electrograms recorded from a non-contact array in the RV. RESULTS: Lowest values of RVI co-localised with VT earliest activation site in ARVC/BrS but not in focal VT. The distance between region of lowest RVI and site of VT earliest site (Dmin) was lower in ARVC/BrS than in focal VT (6.8 ±â€¯6.7 mm vs 26.9 ±â€¯13.3 mm, p = 0.005). ARVC/BrS patients with inducible VT had lower Global-RVI (RVIG) than those who were non-inducible (-54.9 ±â€¯13.0 ms vs -35.9 ±â€¯8.6 ms, p = 0.005) or those with focal VT (-30.6 ±â€¯11.5 ms, p = 0.001). Patients were followed up for 112 ±â€¯19 months. Those with clinical VT events had lower Global-RVI than both ARVC and BrS patients without VT (-54.5 ±â€¯13.5 ms vs -36.2 ±â€¯8.8 ms, p = 0.007) and focal VT patients (-30.6 ±â€¯11.5 ms, p = 0.002). CONCLUSIONS: RVI reliably identifies the earliest RV endocardial activation site of VT in BrS and ARVC but not focal ventricular arrhythmias and predicts the incidence of haemodynamically significant arrhythmias. Therefore, RVI may be of value in predicting VT exit sites and hence targeting of re-entrant arrhythmias.

Mechano-electrical feedback in the clinical setting: Current perspectives.

Mechano-electric feedback (MEF) is an established mechanism whereby myocardial deformation causes changes in cardiac electrophysiological parameters. Extensive animal, laboratory and theoretical investigation has demonstrated that abnormal patterns of cardiac strain can induce alteration of electrical excitation and recovery through MEF, which can potentially contribute to the establishment of dangerous arrhythmias. However, the clinical relevance of MEF in patients with heart disease remains to be established. This paper reviews up-to date experimental evidence describing the response to different types of mechanical stimuli in the intact human heart with the support of new data collected during cardiac surgery. It discusses modulatory effects of MEF that may contribute to increase the vulnerability to arrhythmia and describes MEF interaction with clinical conditions where mechanically induced changes in cardiac electrophysiology are likely to be more relevant. Finally, directions for future studies, including the need for in-vivo human data providing simultaneous assessment of the distribution of structural, functional and electrophysiological parameters at the regional level, are identified.

Effective emotion regulation strategies improve fMRI and ECG markers of psychopathology in panic disorder: implications for psychological treatment action.

Impairments in emotion regulation are thought to have a key role in the pathogenesis of anxiety disorders, but the neurobiological underpinnings contributing to vulnerability remain poorly understood. It has been a long-held view that exaggerated fear is linked to hyperresponsivity of limbic brain areas and impaired recruitment of prefrontal control. However, increasing evidence suggests that prefrontal-cortical networks are hyperactive during threat processing in anxiety disorders. This study directly explored limbic-prefrontal neural response, connectivity and heart-rate variability (HRV) in patients with a severe anxiety disorder during incidental versus intentional emotion regulation. During 3 Tesla functional magnetic resonance imaging, 18 participants with panic disorder and 18 healthy controls performed an emotion regulation task. They either viewed negative images naturally (Maintain), or they were instructed to intentionally downregulate negative affect using previously taught strategies of cognitive reappraisal (Reappraisal). Electrocardiograms were recorded throughout to provide a functional measure of regulation and emotional processing. Compared with controls, patients showed increased neural activation in limbic-prefrontal areas and reduced HRV during incidental emotion regulation (Maintain). During intentional regulation (Reappraisal), group differences were significantly attenuated. These findings emphasize patients' ability to regulate negative affect if provided with adaptive strategies. They also bring prefrontal hyperactivation forward as a potential mechanism of psychopathology in anxiety disorders. Although these results challenge models proposing impaired allocation of prefrontal resources as a key characteristic of anxiety disorders, they are in line with more recent neurobiological frameworks suggesting that prefrontal hyperactivation might reflect increased utilisation of maladaptive regulation strategies quintessential for anxiety disorders.

Slow adaptation of ventricular repolarization as a cause of arrhythmia?

INTRODUCTION: This article is part of the Focus Theme of Methods of Information in Medicine on "Biosignal Interpretation: Advanced Methods for Studying Cardiovascular and Respiratory Systems". BACKGROUND: Adaptation of the QT-interval to changes in heart rate reflects on the body-surface electrocardiogram the adaptation of action potential duration (APD) at the cellular level. The initial fast phase of APD adaptation has been shown to modulate the arrhythmia substrate. Whether the slow phase is potentially proarrhythmic remains unclear. OBJECTIVES: To analyze in-vivo human data and use computer simulations to examine effects of the slow APD adaptation phase on dispersion of repolarization and reentry in the human ventricle. METHODS: Electrograms were acquired from 10 left and 10 right ventricle (LV/RV) endocardial sites in 15 patients with normal ventricles during RV pacing. Activation-recovery intervals, as a surrogate for APD, were measured during a sustained increase in heart rate. Observed dynamics were studied using computer simulations of human tissue electrophysiology. RESULTS: Spatial heterogeneity of rate adaptation was observed in all patients. Inhomogeneity in slow APD adaptation time constants (Δτ(s)) was greater in LV than RV (Δτ(s)(LV) = 31.8 ± 13.2, Δτ(s)(RV) = 19.0 ± 12.8 s , P< 0.01). Simulations showed that altering local slow time constants of adaptation was sufficient to convert partial wavefront block to block with successful reentry. CONCLUSIONS: Using electrophysiological data acquired in-vivo in human and computer simulations, we identify heterogeneity in the slow phase of APD adaptation as an important component of arrhythmogenesis.

Heart rate variability at limiting stationarity: evidence of neuro-cardiac control mechanisms operating at ultra-low frequencies.

This study considers the linkage of exogenously stimulated emotional stress with the neurogenic regulation of heart rate operating at very low frequencies. The objectives were three-fold: to consider the present evidence that such a linkage exists as a primary phenomenon; to compare the potential of a frequency-domain method and a time-domain method in revealing this phenomenon by characterizing heart rate variability (HRV) at frequencies of [0.0005...0.4] Hz and to design, implement and report a physiological experiment in which alternating periods of exposure to bland and high valence visual stimuli might reveal this phenomenon. A methodical challenge was to optimize the length of exposure to the stimulus such that subjects did not have time to habituate to stimuli, whilst acquiring sufficient data (heart beats) such that the ultra-low frequency (ULF) components of HRV could be described. With exposure times set to approximately 5 min, during which time the strength of the stimulus and the corresponding evoked response were considered stationary, the lowest HRV frequency component that could be characterized was 0.003 Hz. In trials with parametrically defined test data, the time-domain method based on the Ornstein­Uhlenbeck Gaussian process (OU-GP) was shown to be better than the frequency-domain method in describing the ULF components of the HRV. In an experimental cohort of 16 subjects, analysis using the OU-GP revealed evidence of cardiac regulatory mechanisms influenced by emotional valence operating in the bandwidth (ULF*) [0.002...0.01] Hz.

Brain-heart interactions and cardiac ventricular arrhythmias.

A wide range of evidence implicates the brain as playing a significant role in ventricular arrhythmias and sudden cardiac death. The mechanism is thought to involve the intermediary of the autonomic nervous system. Here we briefly consider possible mechanisms by which central neural processing may modulate the myocardial electrophysiology and hence the arrhythmia substrate.

Decreased heart rate variability during emotion regulation in subjects at risk for psychopathology.

BACKGROUND: Dysfunctions in the regulation of emotional responses are related to poor psychological well-being and increased impact of cardiovascular disease. It has been suggested that the relationship between negative affect and higher morbidity could be mediated by a dysregulation of the autonomic nervous system (ANS), for example, of heart rate variability (HRV). Neuroticism is a personality trait associated with a maladaptive emotion regulation and also with alterations in ANS function. However, it is unknown whether subjects with high neuroticism present with specific biases in emotion regulation associated with reduced HRV. METHOD: In total, 33 healthy subjects (n=13, highly neurotic) performed an emotion regulation task, during which they were instructed to either passively view negative pictures or attempt to down-regulate the affect elicited by the images. During the task an electrocardiogram was recorded and HRV was measured by calculation of the high frequency spectrum (HF-HRV). RESULTS: A significant interaction between task condition and personality group was observed on HF-HRV measures (F 1,31=6.569, p=0.016). This was driven by subjects with low neuroticism presenting higher HF-HRV during down-regulation compared to passive exposure to negative stimuli, while subjects with high neuroticism reported an opposite tendency. CONCLUSIONS: Our results show reduced HF-HRV during cognitive reappraisal of negative stimuli in high neuroticism and indicate a specific link between loss of flexibility in the parasympathetic cardiovascular tone and emotion regulation, consistent with previous work. Such findings support the importance of exploring the combination of ANS adaptability and emotional dysregulation in neuroticism as different facets of a common psychosomatic vulnerability factor.

Experiment-model interaction for analysis of epicardial activation during human ventricular fibrillation with global myocardial ischaemia.

We describe a combined experiment-modelling framework to investigate the effects of ischaemia on the organisation of ventricular fibrillation in the human heart. In a series of experimental studies epicardial activity was recorded from 10 patients undergoing routine cardiac surgery. Ventricular fibrillation was induced by burst pacing, and recording continued during 2.5 min of global cardiac ischaemia followed by 30 s of coronary reflow. Modelling used a 2D description of human ventricular tissue. Global cardiac ischaemia was simulated by (i) decreased intracellular ATP concentration and subsequent activation of an ATP sensitive K⁺ current, (ii) elevated extracellular K⁺ concentration, and (iii) acidosis resulting in reduced magnitude of the L-type Ca²âº current I(Ca,L). Simulated ischaemia acted to shorten action potential duration, reduce conduction velocity, increase effective refractory period, and flatten restitution. In the model, these effects resulted in slower re-entrant activity that was qualitatively consistent with our observations in the human heart. However, the flattening of restitution also resulted in the collapse of many re-entrant waves to several stable re-entrant waves, which was different to the overall trend we observed in the experimental data. These findings highlight a potential role for other factors, such as structural or functional heterogeneity in sustaining wavebreak during human ventricular fibrillation with global myocardial ischaemia.

Minimum Information about a Cardiac Electrophysiology Experiment (MICEE): standardised reporting for model reproducibility, interoperability, and data sharing.

Cardiac experimental electrophysiology is in need of a well-defined Minimum Information Standard for recording, annotating, and reporting experimental data. As a step towards establishing this, we present a draft standard, called Minimum Information about a Cardiac Electrophysiology Experiment (MICEE). The ultimate goal is to develop a useful tool for cardiac electrophysiologists which facilitates and improves dissemination of the minimum information necessary for reproduction of cardiac electrophysiology research, allowing for easier comparison and utilisation of findings by others. It is hoped that this will enhance the integration of individual results into experimental, computational, and conceptual models. In its present form, this draft is intended for assessment and development by the research community. We invite the reader to join this effort, and, if deemed productive, implement the Minimum Information about a Cardiac Electrophysiology Experiment standard in their own work.

Heart-brain interactions in cardiac arrhythmia.

This review examines current knowledge of the effects of higher brain centres and autonomic control loops on the heart with particular relevance to arrhythmogenesis. There is now substantial evidence that higher brain function (cortex), the brain stem and autonomic nerves affect cardiac electrophysiology and arrhythmia, and that these may function as an interactive system. The roles of mental stress and emotion in arrhythmogenesis and sudden cardiac death are no longer confined to the realms of anecdote. Advances in molecular cardiology have identified cardiac cellular ion channel mutations conferring vulnerability to arrhythmic death at the myocardial level. Indeed, specific channelopathies such as long QT syndrome and Brugada syndrome are selectively sensitive to either sympathetic or vagal stimulation. There is increasing evidence that afferent feedback from the heart to the higher centres may affect efferent input to the heart and modulate the cardiac electrophysiology. The new era of functional neuroimaging has identified the central neural circuitry in this brain-heart axis. Since precipitants of sudden fatal arrhythmia are frequently environmental and behavioural, central pathways translating stress into autonomic effects on the heart might be considered as therapeutic targets. These brain-heart interactions help explain the apparent randomness of sudden cardiac events and provide new insights into future novel therapies to prevent sudden death.

Organization of ventricular fibrillation in the human heart: experiments and models.

Sudden cardiac death is a major health problem in the industrialized world. The lethal event is typically ventricular fibrillation (VF), during which the co-ordinated regular contraction of the heart is overthrown by a state of mechanical and electrical anarchy. Understanding the excitation patterns that sustain VF is important in order to identify potential therapeutic targets. In this paper, we studied the organization of human VF by combining clinical recordings of electrical excitation patterns on the epicardial surface during in vivo human VF with simulations of VF in an anatomically and electrophysiologically detailed computational model of the human ventricles. We find both in the computational studies and in the clinical recordings that epicardial surface excitation patterns during VF contain around six rotors. Based on results from the simulated three-dimensional excitation patterns during VF, which show that the total number of electrical sources is 1.4 +/- 0.12 times greater than the number of epicardial rotors, we estimate that the total number of sources present during clinically recorded VF is 9.0 +/- 2.6. This number is approximately fivefold fewer compared with that observed during VF in dog and pig hearts, which are of comparable size to human hearts. We explain this difference by considering differences in action potential duration dynamics across these species. The simpler spatial organization of human VF has important implications for treatment and prevention of this dangerous arrhythmia. Moreover, our findings underline the need for integrated research, in which human-based clinical and computational studies complement animal research.

A computational study of mother rotor VF in the human ventricles.

Sudden cardiac death is one of the major causes of death in the industrialized world. It is most often caused by a cardiac arrhythmia called ventricular fibrillation (VF). Despite its large social and economical impact, the mechanisms for VF in the human heart yet remain to be identified. Two of the most frequently discussed mechanisms observed in experiments with animal hearts are the multiple wavelet and mother rotor hypotheses. Most recordings of VF in animal hearts are consistent with the multiple wavelet mechanism. However, in animal hearts, mother rotor fibrillation has also been observed. For both multiple wavelet and mother rotor VF, cardiac heterogeneity plays an important role. Clinical data of action potential restitution measured from the surface of human hearts have been recently published. These in vivo data show a substantial degree of spatial heterogeneity. Using these clinical restitution data, we studied the dynamics of VF in the human heart using a heterogeneous computational model of human ventricles. We hypothesized that this observed heterogeneity can serve as a substrate for mother rotor fibrillation. We found that, based on these data, mother rotor VF can occur in the human heart and that ablation of the mother rotor terminates VF. Furthermore, we found that both mother rotor and multiple wavelet VF can occur in the same heart depending on the initial conditions at the onset of VF. We studied the organization of these two types of VF in terms of filament numbers, excitation periods, and frequency domains. We conclude that mother rotor fibrillation is a possible mechanism in the human heart.

Effect of heterogeneous APD restitution on VF organization in a model of the human ventricles.

The onset of ventricular fibrillation (VF) has been associated with steep action potential duration restitution in both clinical and computational studies. Recently, detailed clinical restitution properties in cardiac patients were reported showing a substantial degree of heterogeneity in restitution slopes at the epicardium of the ventricles. The aim of the present study was to investigate the effect of heterogeneous restitution properties in a three-dimensional model of the ventricles using these clinically measured restitution data. We used a realistic model of the human ventricles, including detailed descriptions of cell electrophysiology, ventricular anatomy, and fiber direction anisotropy. We extended this model by mapping the clinically observed epicardial restitution data to our anatomic representation using a diffusion-based algorithm. Restitution properties were then fitted by regionally varying parameters of the electrophysiological model. We studied the effects of restitution heterogeneity on the organization of VF by analyzing filaments and the distributions of excitation periods. We found that the number of filaments and the excitation periods were both dependent on the extent of heterogeneity. An increased level of heterogeneity leads to a greater number of filaments and a broader distribution of excitation periods, thereby increasing the complexity and dynamics of VF. Restitution heterogeneity may play an important role in providing a substrate for cardiac arrhythmias.

Evidence of a breakdown of corticostriatal connections in Parkinson's disease.

Dendritic spines are important structures which receive synaptic inputs in many regions of the CNS. The goal of this study was to test the hypothesis that numbers of dendritic spines are significantly reduced on spiny neurones in basal ganglia regions in Parkinson's disease as we had shown them to be in a rat model of the disease [Exp Brain Res 93 (1993) 17]. Postmortem tissue from the caudate and putamen of patients suffering from Parkinson's disease was compared with that from people of a similar age who had no neurological damage. The morphology of Golgi-impregnated projection neurones (medium-sized spiny neurones) was examined quantitatively. The numerical density of dendritic spines on dendrites was reduced by about 27% in both nuclei. The size of the dendritic trees of these neurones was also significantly reduced in the caudate nucleus from the brains of PD cases and their complexity was changed in both the caudate nucleus and the putamen. Dendritic spines receive crucial excitatory input from the cerebral cortex. Reduction in both the density of spines and the total length of the remaining dendrites is likely to have a grave impact on the ability of these neurones to function normally and may partly explain the symptoms of the disorder.

Physiological changes in ventricular filling alter cardiac electrophysiology in patients with abnormal ventricular function.

OBJECTIVE: To explore the hypothesis that patients with abnormal ventricular function have an altered electrophysiological response to physiological changes in ventricular filling which is not evident in people with normal ventricles. DESIGN: The influence of an acute alteration in ventricular filling on dispersion of repolarisation, measured as QT dispersion, was examined in subjects with normal (n = 9) and abnormal ventricles (n = 9). A physiological reduction in ventricular filling was achieved using dual chamber atrioventricular (AV) pacing in two different modes-AV pacing: atrial activation 120 ms before ventricular activation such that atrial contraction occurred normally in late diastole; and VA (ventriculoatrial) pacing: atrial activation 50 ms after ventricular activation, such that atrial contraction occurred after closure of the AV valves. The absence of effective atrial contraction was confirmed by echocardiography. Ventricular cycle length and sequence of excitation through the ventricle was constant throughout both VA and AV sequences within each patient. RESULTS: During AV pacing (normal ventricular filling) there was no significant difference in QT dispersion between the two groups. In contrast during VA pacing, when the atrial component to ventricular filling was abolished, there was an immediate and consistent increase in QT dispersion compared with baseline in subjects with abnormal ventricular function (p < 0.001) but not in those with normal ventricles. CONCLUSIONS: An abrupt change in ventricular filling, within the physiological range, increased QT dispersion in subjects with abnormal ventricular function but not in subjects with normal ventricles. The findings suggest an altered electrophysiological response to ventricular load in patients with abnormal ventricular function.

Soluble intercellular adhesion molecule-1 as a predictor of early adverse events in patients with chest pain compatible with myocardial ischemia.

STUDY OBJECTIVE: Inflammation plays an important role in acute coronary syndromes, and some evidence indicates that patients with a more pronounced vascular inflammatory response have a poorer outcome. Soluble intercellular adhesion molecule-1 (sICAM-1) is a specific marker for vascular endothelial cell activation. The aim of this study was to investigate the prognostic value of plasma sICAM-1 levels in patients with acute chest pain compatible with myocardial ischemia. METHODS: This prospective study was conducted at 2 urban university medical centers. The study cohort consisted of 119 consecutive patients with chest pain in whom myocardial ischemia was suspected clinically at presentation. Patients with conditions that affect sICAM-1 levels were ineligible. Cardiac troponin I (cTnI), C-reactive protein, and sICAM-1 levels were assayed at presentation to the emergency department. The primary end point was the occurrence of a serious cardiac event (death, nonfatal acute myocardial infarction, coronary revascularization) in the hospital. RESULTS: Although sICAM-1 levels tended to be higher in patients with a serious cardiac event, there was no significant association. In contrast, a cTnI level greater than 0.2 ng/mL was a powerful predictor of an in-hospital serious cardiac event (odds ratio 16.3, 95% confidence interval [CI] 4.7 to 55.9; P <.0001). Soluble ICAM-1 levels of more than 260 ng/mL at presentation had a sensitivity for predicting a serious cardiac event of 63% (95% CI 46% to 81%) but a specificity of only 47% (95% CI 38% to 57%). CONCLUSION: In a heterogeneous population of patients with chest pain compatible with myocardial ischemia, elevated sICAM-1 levels are poor predictors of an individual patient suffering a serious cardiac event in the hospital.