Dobutamine stress for evaluation of right ventricular reserve in pulmonary arterial hypertension.

Right ventricular contractile response to pharmacological stress in pulmonary arterial hypertension (PAH) has not been characterised. We evaluated right ventricular contractile reserve in adults with PAH using dobutamine stress echocardiography. 16 PAH patients and 18 age-matched controls underwent low-dose dobutamine stress echocardiography. Contractile reserve was assessed by the change (Δ; peak stress minus rest value) in tricuspid annular plane systolic excursion (TAPSE) and tricuspid annular systolic velocity (S'). A subgroup of 13 PAH patients underwent treadmill cardiopulmonary exercise testing for peak oxygen uptake (V'O2peak). At rest, TAPSE and S' were reduced in the PAH group compared with controls (1.7 ± 0.4 versus 2.4 ± 0.2 cm and 9.7 ± 2.6 versus 12.5 ± 1.2 cm · s(-1), respectively; p<0.05). Contractile reserve was markedly attenuated in PAH compared to controls (ΔTAPSE 0.1 ± 0.2 versus 0.6 ± 0.3 cm and ΔS' 4.6 ± 2.8 versus 11.2 ± 3.6 cm · s(-1); p<0.0001). In the sub-group of PAH patients with preserved right ventricular systolic function at rest, contractile reserve remained depressed compared to controls. V'O2peak was significantly correlated with ΔS' (r=0.87, p=0.0003) and change in stroke volume (r=0.59, p=0.03). Dobutamine stress can reveal sub-clinical reduction in right ventricular contractile reserve in patients with PAH. A correlation with exercise capacity suggests potential clinical value beyond resting measurements.

Dobutamine stress echocardiography for the assessment of pressure-flow relationships of the pulmonary circulation.

BACKGROUND: Stress testing of the pulmonary circulation (via increasing pulmonary blood flow) can reveal abnormal mean pulmonary artery pressure-cardiac output (mPpa-Q) responses, which may facilitate early diagnosis of pulmonary vascular disease. We investigated the application of dobutamine stress echocardiography (DSE) for the noninvasive assessment of mPpa-Q relationships. METHODS: DSE using an incremental dose protocol (≤ 20 µg/kg/min) was performed in 38 subjects (16 patients with pulmonary arterial hypertension [PAH] and 22 healthy control subjects). An additional 22 healthy control subjects underwent exercise stress echocardiography as a comparator group. Multipoint mPpa-Q plots were analyzed, and the pulmonary vascular distensibility coefficient α was calculated. RESULTS: DSE was feasible and informative in 93% of subjects. The average dobutamine-induced mPpa-Q slope was 1.1 ± 0.7 mm Hg/L/min in healthy control subjects and 5.1 ± 2.5 mm Hg/L/min in patients with PAH (P < .001). The dobutamine-induced α was markedly reduced in patients with PAH (0.003 ± 0.001 mm Hg vs 0.02 ± 0.01 mm Hg in control subjects, P < .001). When exercise and dobutamine stress were compared in healthy control subjects, the exercise-induced mPpa-Q slope was modestly higher (1.6 ± 0.7 mm Hg/L/min, P = .03 vs dobutamine). In patients with PAH, lower functional class status was associated with lower dobutamine-induced mPpa-Q slopes (P = .014), but not with resting total pulmonary vascular resistance. CONCLUSIONS: Noninvasive assessment of mPpa-Q relationships is feasible with dobutamine stress. DSE may potentially be a useful noninvasive technique for stress testing of the pulmonary vasculature.

Steroid-induced diabetes: is it just unmasking of type 2 diabetes?

Aims. We compared the demographic profile and clinical characteristics of individuals with new onset steroid-induced diabetes (NOSID) to Type 2 diabetes (T2DM) patients with and without steroid treatment. Methods. The demographic profile and clinical characteristics of 60 individuals who developed NOSID were examined and matched to 60 type 2 diabetes patients receiving steroid therapy (T2DM+S) and 360 diabetic patients not on steroids (T2DM) for age, duration of diabetes, HbA1c, gender, and ethnicity. Results. Patients who developed NOSID had less family history of diabetes (P ≤ 0.05) and were less overweight (P ≤ 0.02). NOSID was more commonly treated with insulin. Despite a matching duration of diabetes and glycaemic control, significantly less retinopathy was found in the group of patients with NOSID (P < 0.03). Conclusions. It appears that steroid treatment primarily precipitated diabetes in a group of individuals otherwise less affected by risk factors of diabetes at that point in time, rather than just opportunistically unmasking preexisting diabetes. Furthermore, the absence of retinopathy suggests that patients with NOSID had not been exposed to long periods of hyperglycaemia. However, the impact of the underlying conditions necessitating steroid treatment and concomitant medications such as immunosuppressants on diabetes development remain to be defined.