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1.  Right and Left Heart Failure in Severe H1N1 Influenza A Infection 
Influenza infection can affect cardiac function. The recent pandemic of H1N1 influenza A provided an opportunity to study echocardiographic findings in critically ill infected patients.
We hypothesized that critically ill patients with H1N1 infection would have a higher incidence of right and left heart failure than is seen in unselected populations of patients with septic shock and/or Acute Respiratory Distress Syndrome (ARDS).
We retrospectively studied all patients admitted to four ICUs at three hospitals in Salt Lake County, Utah, USA with laboratory-confirmed H1N1 infection in whom a clinical echocardiogram was available.
Twenty-three of 48 patients had qualifying echocardiograms. Right ventricular (RV) dilatation (50–80%) and at least moderate systolic impairment (23%) were common, higher than the range described in general populations with ARDS. Left ventricular systolic dysfunction was present in 17% of patients. No single echocardiographic parameter was associated with 28-day mortality or ventilator-free days to 28 days.
Critically ill patients with H1N1 infection frequently exhibit right heart dilatation and failure. RV basal dilatation was extremely common. These patients have less left heart failure than expected on the basis of prior descriptions of influenza myopericarditis or of general populations of septic patients.
doi:10.1183/09031936.00008210
PMCID: PMC3170697  PMID: 20516055
Acute Respiratory Distress Syndrome; Echocardiography; Heart Failure; Influenza A Virus; Pulmonary Heart Disease
2.  A Predictive Instrument Using Contrast Echocardiography in Patients Presenting to the Emergency Department With Chest Pain and Without ST-segment Elevation 
Aims
Risk stratification of patients presenting to the emergency department (ED) with suspected cardiac chest pain (CP) and an undifferentiated electrocardiogram (ECG) is difficult. We hypothesized that in these patients a risk score incorporating clinical, ECG, and myocardial contrast echocardiography (MCE) variables would accurately predict adverse events occurring within the next 48 hours.
Methods and Results
Patients with CP lasting for ≥30 min who did not have ST segment elevation on the ECG, were enrolled. Regional function (RF) and myocardial perfusion (MP) were assessed by MCE. A risk model was developed in the initial 1166 patients (cohort 1), and validated in subsequent 720 patients (cohort 2). Any abnormality or ST changes on ECG (OR 2.5, 95% CI:1.4–4.5, p=0.002, and OR 2.9, 95% CI:1.7–4.8, p<0.001, respectively), abnormal RF with normal MP (OR 3.5, 95% CI:1.8–6.5, p<0.001), and abnormal RF with abnormal MP (OR 9.6, 95% CI:5.8–16.0, p<0.001) were found to be significant multivariate predictors of non-fatal myocardial infarction or cardiac death. The estimate of the probability of concordance for the risk model was 0.82 for cohort 1 and 0.83 for cohort 2. The risk score in both cohorts stratified patients into 5 distinct risk groups with event rates ranging from 0.3% to 58%.
Conclusions
A simple predictive instrument has been developed from clinical, ECG, and MCE findings obtained at the bedside that can accurately predict events occurring within 48 hours in patients presenting to the ED with suspected cardiac CP and an ECG that is not diagnostic for acute ischemic injury. Its application could enhance care of CP patients in the ED. For instance, patients with a risk score of 0 could be discharged from the ED without further work-up. However, this needs to be validated in a multi-center study.
doi:10.1016/j.echo.2010.03.013
PMCID: PMC2876194  PMID: 20418056
chest pain; emergency department; myocardial contrast echocardiography
3.  Randomized controlled trial of the efficacy of aerobic exercise in reducing metabolic risk in healthy older people: The Hertfordshire Physical Activity Trial 
Background
While there are compelling observational data confirming that individuals who exercise are healthier, the efficacy of aerobic exercise interventions to reduce metabolic risk and improve insulin sensitivity in older people has not been fully elucidated. Furthermore, while low birth weight has been shown to predict adverse health outcomes later in life, its influence on the response to aerobic exercise is unknown. Our primary objective is to assess the efficacy of a fully supervised twelve week aerobic exercise intervention in reducing clustered metabolic risk in healthy older adults. A secondary objective is to determine the influence of low birth weight on the response to exercise in this group.
Methods/Design
We aim to recruit 100 participants born between 1931–1939, from the Hertfordshire Cohort Study and randomly assign them to no intervention or to 36 fully supervised one hour sessions on a cycle ergometer, over twelve weeks. Each participant will undergo detailed anthropometric and metabolic assessment pre- and post-intervention, including muscle biopsy, magnetic resonance imaging and spectroscopy, objective measurement of physical activity and sub-maximal fitness testing.
Discussion
Given the extensive phenotypic characterization, this study will provide valuable insights into the mechanisms underlying the beneficial effects of aerobic exercise as well as the efficacy, feasibility and safety of such interventions in this age group.
Trial Registration
Current Controlled Trials: ISRCTN60986572
doi:10.1186/1472-6823-9-15
PMCID: PMC2708167  PMID: 19545359
4.  Casq2 deletion causes sarcoplasmic reticulum volume increase, premature Ca2+ release, and catecholaminergic polymorphic ventricular tachycardia  
Journal of Clinical Investigation  2006;116(9):2510-2520.
Cardiac calsequestrin (Casq2) is thought to be the key sarcoplasmic reticulum (SR) Ca2+ storage protein essential for SR Ca2+ release in mammalian heart. Human CASQ2 mutations are associated with catecholaminergic ventricular tachycardia. However, homozygous mutation carriers presumably lacking functional Casq2 display surprisingly normal cardiac contractility. Here we show that Casq2-null mice are viable and display normal SR Ca2+ release and contractile function under basal conditions. The mice exhibited striking increases in SR volume and near absence of the Casq2-binding proteins triadin-1 and junctin; upregulation of other Ca2+-binding proteins was not apparent. Exposure to catecholamines in Casq2-null myocytes caused increased diastolic SR Ca2+ leak, resulting in premature spontaneous SR Ca2+ releases and triggered beats. In vivo, Casq2-null mice phenocopied the human arrhythmias. Thus, while the unique molecular and anatomic adaptive response to Casq2 deletion maintains functional SR Ca2+ storage, lack of Casq2 also causes increased diastolic SR Ca2+ leak, rendering Casq2-null mice susceptible to catecholaminergic ventricular arrhythmias.
doi:10.1172/JCI29128
PMCID: PMC1551934  PMID: 16932808

Results 1-4 (4)