Pulmonary circulation
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Pulmonary circulation · Mar 2015
Derivation of a screening tool to identify patients with right ventricular dysfunction or tricuspid regurgitation after negative computerized tomographic pulmonary angiography of the chest.
Many dyspneic patients who undergo computerized tomographic pulmonary angiography (CTPA) for presumed acute pulmonary embolism (PE) have no identified cause for their dyspnea yet have persistent symptoms, leading to more CTPA scanning. Right ventricular (RV) dysfunction or overload can signal treatable causes of dyspnea. We report the rate of isolated RV dysfunction or overload after negative CTPA and derive a clinical decision rule (CDR). ⋯ Logistic regression found only normal CTPA scanning significant. The final rule (persistent dyspnea + normal CTPA scan) had a positive predictive value of 53% (95% CI: 37%-69%). We conclude that a simple CDR consisting of persistent dyspnea plus a normal CTPA scan predicts a high probability of isolated RV dysfunction or overload on echocardiography.
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Pulmonary circulation · Dec 2014
The Sugen 5416/hypoxia mouse model of pulmonary hypertension revisited: long-term follow-up.
The combination of a vascular endothelial growth factor receptor antagonist, Sugen 5416 (SU5416), and chronic hypoxia is known to cause pronounced pulmonary hypertension (PH) with angioobliterative lesions in rats and leads to exaggerated PH in mice as well. We sought to determine whether weekly SU5416 injections during 3 weeks of hypoxia leads to long-term development of angioobliterative lesions and sustained or progressive PH in mice. Male C57BL/6J mice were injected with SU5416 (SuHx) or vehicle (VehHx) weekly during 3 weeks of exposure to 10% oxygen. ⋯ In conclusion, SU5416 combined with 3 weeks of hypoxia causes a more profound PH phenotype in mice than hypoxia alone. PH persists over 10 weeks of normoxic follow-up in SuHx mice, but significant angioobliterative lesions do not occur, and neither PH nor RV dysfunction worsens. The SuHx mouse model is a useful adjunct to other PH models, but the search will continue for a mouse model that better recapitulates the human phenotype.
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Pulmonary circulation · Dec 2014
Vascular stiffening in pulmonary hypertension: cause or consequence? (2013 Grover Conference series).
Recent studies have indicated that systemic arterial stiffening is a precursor to hypertension and that hypertension, in turn, can perpetuate arterial stiffening. Pulmonary artery (PA) stiffening is also well documented to occur in pulmonary hypertension (PH), and there is evidence that pulmonary vascular stiffness (PVS) may be a better predictor of outcome than pulmonary vascular resistance (PVR). We have hypothesized that the decreased flow-damping function of elastic PAs in PH likely initiates and/or perpetuates dysfunction of pulmonary microvasculature. ⋯ Current therapeutic treatments do not provide a realistic approach to destiffening arteries and, thus, to potentially abrogating the effects of high pulsatile flow on the distal pulmonary vasculature or the increased work imposed by stiffening on the RV. Scrutinizing the effect of PA stiffening on high pulsatile flow-induced cellular and molecular changes, and vice versa, might lead to important new therapeutic options that abrogate PA remodeling and PH development. With a clear understanding that PA stiffening may contribute to the progression of PH to an irreversible state by contributing to chronic microvascular damage in lungs, future studies should be aimed first at defining the underlying mechanisms leading to PA stiffening and then at improved treatment approaches based on these findings.
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Pulmonary circulation · Dec 2014
Pulmonary hypertension and the right ventricle-thinking outside the box (Third International Right Heart Failure Summit, part 1).
The Third International Right Heart Failure Summit (Boston, MA) convened a group of international clinical and scientific experts in pulmonary vascular disease and right heart disease to explore cutting-edge developments in the mechanisms and clinical management of right-sided cardiovascular disease. The symposium was organized into three distinct sessions, the first of which was titled "Pulmonary Hypertension and the Right Ventricle-Thinking outside the Box" and will be the focus of this review. Three internationally renowned experts in pulmonary hypertension and right heart disease-Drs. ⋯ Finally, Dr. Bogaard provided a lecture titled "Treating Right Heart Failure: Why Does the Art of Medicine Lead the Science?" Bogaard provided a stimulating review of cutting-edge translational research of right ventricular function and dysfunction. In particular, he described a variety of molecular and cellular changes that occur in the hypertrophied right ventricle and contrasted those changes that may be adaptive from those that are maladaptive and may be potential therapeutic targets.
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Pulmonary circulation · Sep 2014
ReviewBiomechanics of the right ventricle in health and disease (2013 Grover Conference series).
Right ventricular (RV) function is a major determinant of the symptomatology and outcome in pulmonary hypertension. The normal RV is a thin-walled flow generator able to accommodate large changes in venous return but unable to maintain flow output in the presence of a brisk increase in pulmonary artery pressure. The RV chronically exposed to pulmonary hypertension undergoes hypertrophic changes and an increase in contractility, allowing for preserved flow output in response to peripheral demand. ⋯ The molecular mechanisms of RV systolic failure are currently being investigated. It is important to refer biological findings to sound measurements of function. Surrogates for E max and E a are being developed through bedside imaging techniques.