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Enhancing the accuracy of echocardiography in the diagnosis of pulmonary arterial hypertension: looking at the heart to learn about the lungs

imagePurpose of reviewAlthough routine use of Doppler echocardiography has led to an increased recognition of pulmonary hypertension, the role of Doppler echocardiography has largely remained as a screening tool with the primary emphasis on the presence or absence of an increased Doppler-estimated pulmonary artery systolic pressure (PASP). However, the utility of Doppler echocardiography in the workup of pulmonary hypertension extends far beyond that of a screening tool, with the integration of relevant Doppler echocardiography parameters providing a wealth of hemodynamic insight into not only if a patient has pulmonary hypertension, but why they have pulmonary hypertension. This review summarizes some of the recent advances in the use of Doppler echocardiography in evaluating the pathophysiology of pulmonary hypertension. Recent findingsDistinguishing pulmonary hypertension related to pulmonary vascular disease (i.e. pulmonary arterial hypertension, pulmonary hypertension due to lung disease, or chronic thromboembolic pulmonary hypertension; PHPVD), from those with left heart disease associated pulmonary hypertension (pulmonary venous hypertension; PVH) is crucial as workup and treatment options differ dramatically. Recent studies have identified easily obtainable Doppler echocardiography parameters that can reliably distinguish between PHPVD and PVH, allowing for rapid triage of patients with evidence of PHPVD to invasive right heart catheterization whiles avoiding invasive investigation and the inappropriate use of pulmonary hypertension specific therapy in patients with PVH. SummaryThis review highlights the importance of integrating two-dimensional and Doppler parameters in order to inform the clinician as to the hemodynamic cause of pulmonary hypertension, thus enhancing the diagnostic accuracy of Doppler echocardiography, rapidly identifying those with PHPVD and right heart dysfunction and assisting in triage of patients to further invasive hemodynamic assessment.

Clinical advances in pulmonary arterial hypertension: the year in review

imagePurpose of reviewThe purpose of this review is to summarize the last year of literature developments in the field of pulmonary arterial hypertension (PAH), with a focus on clinical research. Recent findingsPulmonary vascular research has expanded rapidly over the last decade, resulting in a change in the treatment strategy for PAH. Epidemiologic data from recent registries suggest that patients with PAH are increasing in age and comorbidities. In the modern treatment era, risk stratification for early mortality is increasingly used to guide clinicians in the choice of pulmonary vasodilator therapy. Risk-score calculators have been published and validated for PAH, currently in both the United States and Europe. In addition to increased comorbidities, pulmonary hypertension centers are encountering complicated management situations in these patients, such as pregnancy. Current data suggest that mortality for pregnant pulmonary hypertension patients remains high, although not as high as historical reports. Oral prostacyclin and prostacyclin agonist therapies are currently under investigation to aid in the management of these patients. SummaryDespite treatment advances, mortality remains high for PAH patients. Careful evaluation and risk stratification will help guide the appropriate treatment for PAH patients. Additional therapies are on the horizon for the management of this progressive disease.

Why acute pulmonary embolism becomes chronic thromboembolic pulmonary hypertension: clinical and genetic insights

imagePurpose of reviewChronic thromboembolic pulmonary hypertension (CTEPH) is a life-threatening complication that affects a small but appreciable percentage of patients after acute pulmonary embolism. The cause of CTEPH is under investigation, but no single causative mechanism has yet been identified. Recent findingsCTEPH is likely a complication of residual thrombotic material in the pulmonary arteries that becomes transformed into intravascular scars. Pulmonary artery residua are relatively common after acute pulmonary embolism, and CTEPH may be an extreme manifestation of this phenomenon. Several intriguing observations have been made in patients with CTEPH that give insights into the mechanisms responsible for its formation. Two general pathways have been investigated: resistance of thromboemboli to lysis and attenuation of cellular processes involved in thrombus resolution. This review discusses the evidence supporting each pathway as a mechanism for CTEPH formation, as well as the interaction between the two. SummaryCTEPH may be due to a complex interaction between thrombotic/thrombolytic processes and angiogenic cellular remodeling of organized thrombi. The factors involved may, in fact, vary among CTEPH patients. An understanding of the interplay between the factors that cause CTEPH may help quantify the risk of its occurrence and provide insights into how it can be prevented.

Treating large pulmonary emboli: do the guidelines guide us?

imagePurpose of reviewThe diagnosis and management of patients with large pulmonary emboli can be confusing. This review will summarize available data and suggest the areas of certainty and uncertainty in the treatment of these patients. Recent findingsPulmonary emboli can be stratified according to patient prognosis. Risk-stratification of patients with submassive pulmonary emboli is still lacking. Similarly, although the treatment of low-risk pulmonary embolism is well established, and there is consensus regarding systemic thrombolysis for unstable patients with pulmonary embolism, the management of patients with submassive pulmonary embolism is still a matter of debate. The role of novel approaches such as low-dose thrombolysis, catheter-directed therapies and advanced cardiopulmonary support is yet to be determined. Although some patients in skilled centers may benefit from pulmonary embolectomy, patient selection has yet to be refined. SummaryThe treatment of massive and submassive pulmonary embolism has yet to be standardized. The complexity in choosing appropriate treatments for these patients is due to the lack of high-quality data compounded by an expanding arsenal of therapeutic options.

Assessing recurrence risk following acute venous thromboembolism: use of algorithms

imagePurpose of reviewVenous thromboembolism (VTE) is a chronic disease, associated with a significant rate of recurrence, lower in patients with events provoked by transient risk factors and higher in unprovoked cases. Short-term treatment is indicated for provoked VTE, long-term treatment should be considered for unprovoked. The aim of this review is to evaluate the risk factors for recurrence and the decisional algorithms available to guide patients’ management. Recent findingsTo identify patients who carry a high recurrent risk and require long-term treatment, three algorithms have been proposed: the HERDOO2, the Vienna prediction model, and the DASH score. All identify male sex and elevated D-dimer levels as important risk factors for recurrence. However, important differences among the models should be outlined: in the HERDOO2 model, D-dimer levels are measured during anticoagulation and not after its withdrawal; furthermore, it indicates age greater than 65 as a risk factor for recurrence, whereas the DASH score attributes a higher risk to age less than 50. The Vienna model is complex for routine use. SummaryFurther studies are needed to clarify these discrepancies. A management study based on D-dimer levels after anticoagulation withdrawal is ongoing and could indicate a simple way to safely manage these patients.

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