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    The MPAP/CO slope and oxygen uptake add prognostic value in aortic stenosis

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    Background: Guidelines redefined exercise pulmonary hypertension as a mean pulmonary artery pressure/cardiac output (mPAP/ CO) slope >3 mmHg/L/min. A systolic pulmonary artery pressure (peak sPAP) >60 mmHg during exercise has been associated with an increased risk of cardiovascular events in aortic valve stenosis (AS). The prognostic value of the mPAP/CO slope in AS remains unknown

    The renin-angiotensin-aldosterone system: a crossroad from arterial hypertension to heart failure

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    The renin-angiotensin-aldosterone system (RAAS) plays a pivotal role in the regulation of blood pressure and volume homeostasis, promoting critical structural changes in every component of the cardiovascular system, including the heart and blood vessels. Consequently, the RAAS is a crucial therapeutic target for several chronic diseases of the cardiovascular system, spanning from arterial hypertension (AH) to heart failure (HF). AH represents a leading risk factor for the development of symptomatic HF, particularly with left ventricle (LV) preserved ejection fraction (HFpEF). LV diastolic dysfunction and cardiac remodelling are the first discernible manifestations of heart disease in patients with AH. Typically, AH develops many years before the diagnosis of overt HF, providing a therapeutic target for preventive strategies. Treatment of AH is based on different classes of antihypertensive drugs, which show differences in their capacity to prevent the evolution towards HF. The blockers of the RAAS are effective drugs to treat AH and prevent HF with reduced ejection fraction (HFrEF), but the evidence of the potential benefits in patients with HFpEF remains limited. In this review, the authors summarise data from several clinical trials of HFpEF and HFrEF, focusing on the mechanisms leading the transition from AH to HF and late complications

    The MPAP/CO slope and oxygen uptake add prognostic value in aortic stenosis

    No full text
    Background: Guidelines redefined exercise pulmonary hypertension as a mean pulmonary artery pressure/cardiac output (mPAP/ CO) slope >3 mmHg/L/min. A systolic pulmonary artery pressure (peak sPAP) >60 mmHg during exercise has been associated with an increased risk of cardiovascular events in aortic valve stenosis (AS). The prognostic value of the mPAP/CO slope in AS remains unknown

    Value of combined cardiopulmonary and echocardiography stress test to characterize the haemodynamic and metabolic responses of patients with heart failure and mid-range ejection fraction

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    Aims To characterize heart failure (HF) with mid-range ejection fraction (HFmrEF), combining cardiopulmonary exercise test, and exercise stress echocardiography. Methods and results We studied 169 consecutive subjects (age 62.3 ± 11 years; 74% male): 30 healthy controls, 45 patients with HF and preserved EF (HFpEF), 40 HFmrEF, and 54 with HF and reduced EF (HFrEF). Left ventricular (LV) stroke volume (SV), EF, elastance, global longitudinal strain, E/E’, oxygen consumption (VO2), and arterial-venous oxygen content difference (AVO2diff) were measured in all exercise stages. HFmrEF revealed baseline features intermediate between HFrEF and HFpEF, except for B-type natriuretic peptide levels, which was similar to HFpEF and significantly lower than HFrEF. Peak VO2 was not significantly different between HF groups. HFrEF exhibited a significantly lower peak SV as compared to either HFpEF or HFmrEF (74.3 ± 21.8 mL vs. 88.0 ± 17.4 mL and 96.5 ± 25.1 mL; P < 0.01), whereas peak heart rate was not significantly different between HF groups. A significantly reduced AVO2diff at peak exercise was apparent in HFpEF and HFmrEF (15.2 ± 3.3 mL/dL and 13.3 ± 4.2 mL/dL) vs. HFrEF (17.±6.6 mL/dL; P < 0.01), whereas no significant difference was reported between HFpEF and HFmrEF. Multivariate analysis in the overall population and all groups revealed peak parameters as independent predictors of peak VO2 (R2 = 0.90, P < 0.0001); AVO2diff showed the largest standardized regression coefficient. Conclusion In HFpEF and HFmrEF, effort intolerance is predominantly due to peripheral factors (AVO2diff), whereas in HFrEF peak VO2 is restricted by low increases in SV. Individual therapy according to which component of VO2 is more impaired is advisable

    Combining echo-derived haemodynamic phenotypes and myocardial strain for risk stratification of chronic heart failure with reduced ejection fraction

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    Echocardiography has shown to categorize heart failure (HF) patients according to haemodynamic profiles. Whether left ventricular (LV) global longitudinal strain (LV-GLS) could integrate echo-derived haemodynamic profiles to risk stratify chronic HF patients is still unknown
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