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Objective To optimise an echocardiographic estimation of pulmonary vascular resistance (PVR e ) for diagnosis and follow-up of pulmonary hypertension (PHT). Design Cross-sectional study. Setting Tertiary referral centre. Patients Patients undergoing right heart catheterisation and echocardiography for assessment of suspected PHT. Methods PVR e ([tricuspid regurgitation velocity ×10/(right ventricular outflow tract velocity-time integral+0.16) and invasive PVR i ((mean pulmonary artery systolic pressure-wedge pressure)/cardiac output) were compared in 72 patients. Other echo data included right ventricular systolic pressure (RVSP), estimated right atrial pressure, and E/e9 ratio. Difference between PVR e and PVR i at various levels of PVR was sought using Bland–Altman analysis. Corrected PVR c ((RVSP−E/e9)/RVOT VTI ) (RVOT, RV outflow time; VTI, velocity time integral) was developed in the training group and tested in a separate validation group of 42 patients with established PHT. Results PVR e >2.0 had high sensitivity (93%) and specificity (91%) for recognition of PVR i >2.0, and PVR c provided similar sensitivities and specificities. PVR e and PVR i correlated well (r=0.77, p e underestimated marked elevation of PVR i —a trend avoided by PVR c . PVR c and PVR e were tested against PVR i in a separate validation group (n=42). The mean difference between PVR e and PVR i exceeded that between PVR c and PVR i (2.8±2.7 vs 0.8±3.0 Wood units; p i by at least one SD occurred in 10 patients over 6 months; this was detected in one patient by PVR e and eight patients by PVR c (p=0.002). Conclusion PVR e distinguishes normal from abnormal PVR i but underestimates high PVR i . PVR c identifies the severity of PHT and may be used to assess treatment response.

We thank Kerkhof et al 1 for their interest in our paper2 and are pleased they agree with our conclusion that accurate determination of end-systolic volume index (ESVI) is important in patients with reduced LVEF. 1. Table 3 and figure 2 show the entire range of ESVI values. The scatter plot of the individual data points (figure 2) and summary statistics presented in table 3 reveal the data are highly skewed to the right such that most values fall at the lower end of …

There is evidence that ultra-endurance exercise causes myocardial injury. The extent and duration of these changes remains unresolved. Recent reports have speculated that structural adaptations to exercise, particularly of the right ventricle, may predispose to tachyarrhythmias and sudden cardiac death.To quantify the extent and duration of post-exercise cardiac injury with particular attention to right ventricular (RV) dysfunction.27 athletes (20 male, 7 female) were tested 1 week before, immediately after and 1 week after an ultra-endurance triathlon. Tests included cardiac troponin I (cTnI), B-type natriuretic peptide (BNP) and comprehensive echocardiographic assessment.26 athletes completed the race and testing procedures. Post-race, cTnI was raised in 15 athletes (58%) and the mean value for the entire cohort increased (0.17 vs 0.49 microg/l, p0.01). BNP rose in every athlete and the mean increased significantly (12.2 vs 42.5 ng/l, p0.001). Left ventricular ejection fraction (LVEF) was unchanged (60.4% vs 57.5%, p = 0.09), but integrated systolic strain decreased (16.9% vs 15.1%, p0.01). New regional wall motion abnormalities developed in seven athletes (27%) and LVEF was reduced in this subgroup (57.8% vs 45.9%, p0.001). RV function was reduced in the entire cohort with decreases in fractional area change (0.47 vs 0.39, p0.01) and tricuspid annular plane systolic excursion (21.8 vs 19.1 mm, p0.01). At follow-up, all variables returned to baseline except in one athlete where RV dysfunction persisted.Myocardial damage occurs during intense ultra-endurance exercise and, in particular, there is a significant reduction in RV function. Almost all abnormalities resolve within 1 week.

Reduced exercise tolerance is the key symptom in chronic heart failure (CHF) leading to reductions in functional status and quality of life. The underlying mechanisms behind the muscle fatigue and dyspnoea which limit exercise capacity in heart failure are very complex, with multiple factors in the chain from the heart and lungs to the muscles contributing to the symptoms. In addition to altered cardiac function and haemodynamics as the central initiator of the heart failure syndrome, abnormalities have been identified in pulmonary function, ventilatory efficiency, peripheral vascular and in particular endothelial function, skeletal muscle structure and skeletal muscle metabolism. Over the last 20 years, the key role of the peripheral changes in skeletal muscle has been appreciated.1 Some of the changes which have been documented in the periphery and which may be important in causing reduced exercise tolerance include muscle wasting (especially in those with more advanced disease), a shift in muscle fibre type from type I fibres, which are relatively fatigue resistant, to type II fibres, and particularly type IIb fibres, which are less fatigue resistant and have reduced oxidative capacity. Ultrastructural myocyte changes have also been documented with reductions in the mitochondrial density and in oxidative enzymes. Reductions in oxygen delivery to working muscles have been identified in CHF with reduced capillary density seen in males with CHF. One of the key physiological parameters which is strongly linked to exercise capacity in almost all settings is peak oxygen consumption (peak VO2).2 This exercise-derived parameter quantifies the body's ability to take up oxygen, deliver it …

If we could give every individual the right amount of nourishment and exercise, not too little and not too much, we would have found the safest way to health.—Hippocrates circa 400 BC As eloquently described by our colleagues Ruiz et al ,1 numerous large observational and cohort studies have provided compelling evidence for the benefit of mild and moderate exercise on cardiovascular health and mortality. That the benefit of exercise intensity and duration continues to increase into the realms of intense competitive sport is more controversial. This is of importance given that endurance sporting events continue to increase in popularity. For example, over one million Americans competed in an endurance triathlon last year, and participation rates are currently increasing by 10–20% per annum.2 The last half-century has seen an increase in morbidity associated with a lack of habitual exercise and a simultaneous increase in the number of people performing exercise well in excess of recommendations. Very appropriately, the public health focus has been on addressing inactivity, but it may be presumptive to assume that there is no upper limit to what constitutes healthy exercise for the heart. There is accumulating evidence that strenuous endurance exercise may be associated with an increase in some cardiac arrhythmias and speculation that some of the structural changes associated with the ‘athlete's heart’ may not always be benign. Thus, there is a clear need to expand our understanding of the effects of greater doses of exercise. The non-standardised gradations of exercise intensity complicate interpretation of exercise studies. There is compelling evidence that ‘strenuous exercise’ is associated with improved cardiovascular outcomes, but it must be noted that the definition of ‘strenuous’ is derived from middle-aged non-athletic populations. For example, Blair et al 3 ascribed a delay in all-cause mortality to ‘high levels of fitness’, …

Background Pulmonary Arterial Hypertension (PAH) is a major cause of mortality in SSc. N-terminal pro-brain natriuretic peptide (NT-proBNP) has emerged as a candidate biomarker that may enable the early detection of systemic sclerosis-related pulmonary arterial hypertension (SSc-PAH). Objectives To incorporate N-terminal pro-brain natriuretic peptide (NT-proBNP) into a screening algorithm for systemic sclerosis-related pulmonary arterial hypertension (SSc-PAH) that could potentially replace transthoracic echocardiography (TTE) as a less costly and more convenient “first tier” test. Methods NT-proBNP levels were measured in patients from 4 clinical groups: a group with right heart catheter (RHC) diagnosed SSc-PAH prior to commencement of therapy for PAH; a group at high risk of SSc-PAH based on TTE; a group with interstitial lung disease; and systemic sclerosis (SSc) controls with no cardiopulmonary complications. NT-proBNP levels were compared using ANOVA and correlated with other clinical variables using simple and multiple linear regression. ROC curve analyses were performed to determine the optimal cut-point for NT-proBNP and other clinical variables in prediction of PAH. Results NT-proBNP was highest in the PAH group compared to other groups (p corr corr ≥1.83, had a sensitivity of 100% and specificity of 77.8% for SSc-PAH. Conclusions We have proposed a screening algorithm for SSc-PAH, incorporating NT-proBNP level and PFTs. This model has high sensitivity and specificity for SSc-PAH and if positive, should lead to TTE and confirmatory testing for PAH. This screening algorithm needs to be validated prospectively. Disclosure of Interest None Declared

We thank Magnino and colleagues for their interest in our paper1 and appreciate their comments. Their three concerns relate to the assessment of left ventricular (LV) filling pressure, the calculation of right atrial pressure (RAP) and the choice of selection of the original estimation (echocardiographic estimation of pulmonary vascular resistance (PVRe))2 versus our proposed corrected estimation (PVRc). Although imperfect, E/e' is one of the best available noninvasive tissue Doppler-based parameters for estimating LV filling pressures.3 …