Pulmonary hypertension: prevalence and mortality in the Armadale echocardiography cohort.

BACKGROUND: Pulmonary hypertension (PHT) lacks community prevalence and outcome data. OBJECTIVE: To characterise minimum 'indicative' prevalences and mortality data for all forms of PHT in a selected population with an elevated estimated pulmonary artery systolic pressure (ePASP) on echocardiography. DESIGN: Observational cohort study. SETTING: Residents of Armadale and the surrounding region in Western Australia (population 165 450) referred to our unit for transthoracic echocardiography between January 2003 and December 2009. RESULTS: Overall, 10 314 individuals (6.2% of the surrounding population) had 15 633 echo studies performed. Of these, 3320 patients (32%) had insufficient TR to ePASP and 936 individuals (9.1%, 95% CI 8.6% to 9.7%) had PHT, defined as, ePASP>40 mm Hg. The minimum 'indicative' prevalence for all forms of PHT is 326 cases/100 000 inhabitants of the local population, with left heart disease-associated PHT being the commonest cause (250 cases/100 000). 15 cases of pulmonary arterial hypertension/100 000 inhabitants were identified and an additional 144 individuals (15%) with no identified cause for their PHT. The mean time to death for those with ePASP >40 mm Hg, calculated from the first recorded ePASP, was 4.1 years (95% CI 3.9 to 4.3). PHT increased mortality whatever the underlying cause, but patients with PHT from left heart disease had the worst prognosis and those with idiopathic pulmonary arterial hypertension receiving disease-specific treatment the best prognosis. Risk of death increased with PHT severity: severe pulmonary hypertension shortened the lifespan by an average of 1.1 years compared with mild pulmonary hypertension. CONCLUSIONS: In this cohort, PHT was common and deadly. Left heart disease was the most common cause and had the worst prognosis and treated pulmonary arterial hypertension had the best prognosis.

Reduced ventricular flow propagation velocity in elite athletes is augmented with the resumption of exercise training.

Chronic exercise induces physiological enlargement of the left ventricle ('athlete's heart'), but the effects of current and long-term exercise training on diastolic function have not been investigated. Echocardiography and Doppler imaging were used to assess left ventricular (LV) dimensions and indices of diastolic filling in 22 elite athletes at the end of their 'off-season' (baseline) and, subsequently, following 3 and 6 months of training. Twelve matched controls were also studied at baseline, 3 and 6 months. Compared to controls at baseline, athletes exhibited significantly higher LV mass (235.7 +/- 7.1 g versus 178.1 +/- 14.5 g, P < 0.01) and reduced flow propagation velocity (V(P): 50.21 +/- 1.7 versus 72.2 +/- 3.6 cm s(-1), P < 0.01), a measure of diastolic function. Three months of training further increased LV mass in athletes (253.2 +/- 7.1 g; P < 0.01 versus baseline), and significantly increased their V(P) (66.7 +/- 2.5 cm s(-1); P < 0.05 versus baseline). These trends for increased mass and diastolic filling persisted following 6 months of training (LV mass 249.0 +/- 8.7 g P < 0.05 versus baseline; V(P) 75.7 +/- 3.0 cm s(-1); P < 0.01 versus baseline, and P = 0.01 versus 3 months). This study suggests that following a period of relative inactivity the rate of ventricular relaxation during early diastole may be slowed in athletes who exhibit ventricular hypertrophy, whilst resumption of training increases the speed of ventricular relaxation in the presence of further hypertrophy of the left ventricle.