In theory, echocardiography allows an accurate measurement of pulmonary artery pressure, approximate right atrial pressure, cardiac output, right ventricular diastolic function and non-volumetric assessment of systolic function, as well as some insight into the structural alterations of right ventricular architecture. Unfortunately, the vast array of possible measures complicates distillation of the few parameters that provide reproducible prognostically important information. The modest reductions in afterload achieved with current therapies (<5mmHg on average) and the unpredictability of right ventricular response, coupled with the complexity of the populations treated, means that only large-scale survival studies should be considered when determining which parameters inform patient management. Of currently widely used measures, only tricuspid annular plane systolic excursion (TAPSE) and pericardial effusion are recommended when adjusting therapy. Increased use of contrast echo, strain rate imaging, vector velocity imaging and 3D echocardiography appear to hold most hope for the future; however, none as yet has the database to support inclusion into standard clinical practice.
Contrast echocardiography, speckled tracking, strain rate imaging, vector velocity imaging, right ventricle
Disclosure: The authors have no conflicts of interest to declare.
Received: 30 April 2010 Accepted: 9 June 2010 Citation: European Cardiology, 2010;6(4):26├óÔé¼ÔÇ£30
Correspondence: John G Coghlan, Department of Cardiology, Royal Free Hospital, Pond Street, London, NW3 2QG, UK. E: Gerry.Coghlan@royalfree.nhs.uk
Goals in Pulmonary Arterial Hypertension Treatment
Pulmonary arterial hypertension (PAH) arises from pathological thickening, obstruction and constriction of the pulmonary arterioles.1 This leads to progressive elevation of pulmonary pressures initially on exertion, then at rest.2 Symptoms present late, often only when the pressures can rise little further and the cardiac output (CO) falls due to right ventricular (RV) overload.3 As the condition progresses towards the end stage, the right heart dilates and exhibits reduced function, resulting in clinical evidence of heart failure. With rare exceptions, current therapies yield modest reductions in pulmonary pressures, but by reducing pulmonary vascular resistance lead to significant increases in CO. The function and size of the right heart improves slightly and the clinical benefit is modest. As the gains in terms of RV function and pulmonary pressures are modest, techniques that focus on these aspects of cardiac function are relatively insensitive to the changes that are achieved with treatment.
The objectives of treatment have been outlined in the recent European Society of Cardiology and European Respiratory Society (ESC/ERS) guidelines. The domains identified are clinical (functional class 1 or 2, no blackouts, with no evidence of heart failure), exercise (six-minute maximum walking distance [6MWD] >500m, O2 consumption on exercise >15ml/kg/minute) and objective (normal N-terminal portion of proBNP [NTproBNP], tricuspid annular plane systolic elevation [TAPSE] >20mm, absence of pericardial effusion, right atrial pressure [RAP] <8mmHG, cardiac index >2.5l/minute). Failure to achieve these objectives is an indication to increase treatment.3 Therefore, at a simplistic level we already have echocardiographic criteria for adjusting PAH therapy. In reality, most patients do not achieve these goals, and there have been no randomised trials to demonstrate that goal-directed therapy improves survival or quality of life.
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