International journal of cardiology
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In patients presenting to the Emergency Department (ED) with potential acute myocardial infarction (AMI), elevated cardiac troponin (cTn) levels are indicative of myocardial necrosis. We assessed the accuracy of 'delta cTn' at 2h or 6h compared to the cTn concentration above the 99th percentile reference value for AMI in a prospective study of adult patients presenting to ED with symptoms suggestive of possible acute coronary syndrome. ⋯ An algorithm incorporating cTnI concentration and delta cTn values with a sensitive troponin assay allows accurate diagnosis of AMI within 2h from presentation and earlier rule-out of AMI in the majority of patients.
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Few studies have had the opportunity to examine a broad range of predictors of pre-hospital delay from a multivariate perspective that includes not only sociodemographic and clinical features but also atypical symptoms, patient appraisal and behavior, across the acute coronary syndrome (ACS) spectrum. ⋯ Multivariable analyses found that although sociodemographic, clinical history or situational predictors contributed to the variance in pre-hospital delay, the main predictors of pre-hospital delay were behavioral and symptom presentation factors. These factors should therefore be incorporated into patient education and interventions, to further improve patient pre-hospital delay time.
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To further understand the pathophysiology of concomitant cardiac and renal dysfunction, we investigated molecular, structural and functional changes in heart and kidney that occur when a kidney insult (5/6 nephrectomy-STNx) follows myocardial infarction (MI). ⋯ STNx accelerated cardiac changes post-MI whilst MI accelerated STNx-induced renal fibrosis, supporting bidirectional interactions in cardiorenal syndrome (CRS). This animal model may be of use in assessing the impact of therapies to treat CRS.
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Stress-induced cardiomyopathy (SIC), also known as Takotsubo cardiomyopathy, is an acute cardiac syndrome with substantial morbidity and mortality. The unique hallmark of SIC is extensive ventricular akinesia involving apical segments with preserved function in basal segments. Adrenergic overstimulation plays an important role in initiating SIC but the pathophysiological pathways and receptors involved are unknown. ⋯ We provide a novel rat model of SIC that supports the hypothesis of circulating catecholamines as initiators of SIC. We propose that the β-adrenoreceptor pathway is important in the setting of severe catecholamine overstimulation and that perturbations of cardiac metabolism occur in SIC.