Concomitant intravascular and extravascular obstructive shock: a case report of cardiac angiosarcoma presenting with pericardial tamponade.

Atraumatic pericardial tamponade and intracardiac masses are both recognized etiologies of acute obstructive shock. Pericardial tamponade, is a cardiovascular emergency commonly considered by emergency physicians and, as a result, evaluation for this process has been incorporated into standardized point of care ultrasound algorithms for assessing hypotension. Obstructive shock secondary to intracardiac tumors is an atypical clinical presentation, and although it is evaluated by the same ultrasound imaging modality, it is generally not considered or evaluated for in the emergency department setting. The concomitant presentation of these two pathologic processes is an extremely rare oncologic emergency. Existing literature on the subject is found in a small number of case reports with nearly no prior descriptions in emergency medicine references. In the right clinical context this unique presentation should be considered and evaluated for in the emergency department via point of care ultrasound modality to help guide in the management of the resulting obstructive shock.

Extracellular signal-regulated kinase (ERK) activation preserves cardiac function in pressure overload induced hypertrophy.

BACKGROUND: Chronic pressure overload and a variety of mediators induce concentric cardiac hypertrophy. When prolonged, cardiac hypertrophy culminates in decreased myocardial function and heart failure. Activation of the extracellular signal-regulated kinase (ERK) is consistently observed in animal models of hypertrophy and in human patients, but its role in the process is controversial. METHODS: We generated transgenic mouse lines with cardiomyocyte restricted overexpression of intrinsically active ERK1, which similar to the observations in hypertrophy is phosphorylated on both the TEY and the Thr207 motifs and is overexpressed at pathophysiological levels. RESULTS: The activated ERK1 transgenic mice developed a modest adaptive hypertrophy with increased contractile function and without fibrosis. Following induction of pressure-overload, where multiple pathways are stimulated, this activation did not further increase the degree of hypertrophy but protected the heart through a decrease in the degree of fibrosis and maintenance of ventricular contractile function. CONCLUSIONS: The ERK pathway acts to promote a compensated hypertrophic response, with enhanced contractile function and reduced fibrosis. The activation of this pathway may be a therapeutic strategy to preserve contractile function when the pressure overload cannot be easily alleviated. The inhibition of this pathway, which is increasingly being used for cancer therapy on the other hand, should be used with caution in the presence of pressure-overload.