December 2017 at a Glance: Left Ventricular Ejection Fraction, Exercise Capacity, Peripartum Cardiomyopathy

The 2016 European Society of Cardiology (ESC) guidelines on heart failure (HF) introduced the term of HF with mid-range ejection fraction (HFmrEF) for those patients with a left ventricular ejection fraction (LVEF) of 40–49%.1 This new classification has fostered studies describing these patients' characteristics.2 Analyses from the ESC-HF Long-Term Registry, the Trial of Intensified versus standard Medical therapy in Elderly patients with congestive HF (TIME-CHF) and the Swedish HF registry show a prevalence of HFmrEF of 17–24% among HF patients.3-5 Compared to patients with HF and preserved ejection fraction (HFpEF), patients with HFmrEF had a higher prevalence of coronary artery disease, similar to that of patients with HF and reduced ejection fraction (HFrEF), and had a similar prognosis, better than that of patients with HFrEF.3, 4 The impact of chronic kidney disease on outcomes was also larger in patients with HFrEF and HFmrEF than in those with HFpEF.6 The assessment of the temporal changes of LVEF shows that most patients with HFmrEF have recovered from a lower LVEF whereas the decline from HFpEF to HFmrEF is much less common.7, 8 Thus, these studies show that the characteristics of HFmrEF patients are similar to those of HFrEF patients. Their better prognosis, similar to that of HFpEF patients, is consistent with a mild impairment of LVEF and with the inverse relationship of LVEF with mortality when LVEF is <50%.9 The prognostic value of high-sensitivity troponin plasma levels has been widely shown.10, 11 Less known is their interaction with LVEF and the value of high-sensitivity troponin I (hsTnI), compared with troponin T (hsTnT). Gohar et al.12 have measured hsTnI and hsTnT plasma levels in 1096 patients with HF, divided according to their LVEF. Similar to natriuretic peptides, plasma troponin levels were higher in patients with HFrEF, compared with those with HFpEF. Patients with HFmrEF had intermediate values. Independently of LVEF, both hsTnI and hsTnT values had an additive prognostic value and this was even higher in patients with HFpEF.12 The limitations of echocardiographic measurements, including the E/e' ratio alone, for the estimation of left ventricular end-diastolic pressure or pulmonary artery pressure in patients with HFpEF are shown by Hummel et al.13 Bosch et al.14 confirm the independent prognostic value of right ventricular (RV) dysfunction, measured by RV longitudinal strain or tricuspid annular plane systolic excursion (TAPSE), in patients with either HFrEF or HFpEF. RV dysfunction was related with left ventricular systolic function and atrial fibrillation but not with pulmonary artery pressure. Increased chemoreflex sensitivity is a determinant of the excessive ventilatory response, leading to low arterial carbon dioxide (CO2) tension (PaCO2) at peak exercise, in patients with HFrEF.15 Van Iterson et al.16 compared the determinants of the ventilator response to exercise, measured by the slope of the relationship between ventilation and CO2 production (VE/VCO2 slope) in HFpEF and HFrEF patients. The VE/VCO2 slope was increased in both patient groups, although with higher values in HFrEF vs. HFpEF patients. Determinants of VE/VCO2 differed in patients with HFrEF vs. those with HFpEF. They were mainly related with peak exercise PaCO2 in HFrEF patients, consistent with their relation with abnormal chemoreflexes.15 In contrast, the variability of VE/VCO2 slope values in HFpEF patients was mainly related with the increased pulmonary dead space to the tidal volume ratio (Vd/Vt) than with PaCO2.16 The role of reflex mechanisms arising from the skeletal muscles is also shown by Giannoni et al.17 They studied 25 patients with mitochondrial disease and no known cardiac involvement. Compared with normal subjects, these patients had reduced exercise capacity, as shown by both a lower peak oxygen consumption and an increased VE/VCO2 slope, and these values correlated with increased ergoreflex sensitivity, consistent with the role of skeletal muscle abnormalities as major determinants of exercise intolerance.17, 18 Ersbøll et al.19 report the first population-based estimate of the incidence of peripartum cardiomyopathy (PPCM) from a European country, Denmark. PPCM had an incidence of 1 in 10 149 deliveries, which is intermediate between the American and the Japanese estimates. Complete recovery of left ventricular function occurred in 52.5% of patients. Major adverse events, including death, mechanical circulatory support or heart transplantation and persistent severe HF, occurred in 14.8% of cases. In 54.1% of cases, PPCM was associated with hypertensive disorder of pregnancy and these cases had better outcomes.19 The outcomes of subsequent pregnancies in 34 patients with previous PPCM were analysed by Hilfiker-Kleiner et al.20 Pregnancy ended prematurely in 4/34 (12%) cases. Relapse rate of PPCM was 56% with 4/34 (12%) deaths. Reduced LVEF before subsequent pregnancy was associated with higher mortality (25% vs. 0%).20

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