Commentary to: "Assessment of right ventricular-arterial coupling by echocardiography in patients with heart failure with reduced to mid-range ejection fraction: impact on survival" by Rosa et al.
Pulmonary hypertension due to left heart disease Vachiéry, Jean-Luc; Tedford, Ryan J; Rosenkranz, Stephan ...
European respiratory journal/The European respiratory journal,
01/2019, Volume:
53, Issue:
1
Journal Article
Peer reviewed
Open access
Pulmonary hypertension (PH) is frequent in left heart disease (LHD), as a consequence of the underlying condition. Significant advances have occurred over the past 5 years since the 5th World ...Symposium on Pulmonary Hypertension in 2013, leading to a better understanding of PH-LHD, challenges and gaps in evidence. PH in heart failure with preserved ejection fraction represents the most complex situation, as it may be misdiagnosed with group 1 PH. Based on the latest evidence, we propose a new haemodynamic definition for PH due to LHD and a three-step pragmatic approach to differential diagnosis. This includes the identification of a specific "left heart" phenotype and a non-invasive probability of PH-LHD. Invasive confirmation of PH-LHD is based on the accurate measurement of pulmonary arterial wedge pressure and, in patients with high probability, provocative testing to clarify the diagnosis. Finally, recent clinical trials did not demonstrate a benefit in treating PH due to LHD with pulmonary arterial hypertension-approved therapies.
In the past several decades, cardiopulmonary exercise testing (CPX) has seen an exponential increase in its evidence base. The growing volume of evidence in support of CPX has precipitated the ...release of numerous scientific statements by societies and associations. In 2012, the European Association for Cardiovascular Prevention & Rehabilitation and the American Heart Association developed a joint document with the primary intent of redefining CPX analysis and reporting in a way that would streamline test interpretation and increase clinical application. Specifically, the 2012 joint scientific statement on CPX conceptualized an easy-to-use, clinically meaningful analysis based on evidence-vetted variables in color-coded algorithms; single-page algorithms were successfully developed for each proposed test indication. Because of an abundance of new CPX research in recent years and a reassessment of the current algorithms in light of the body of evidence, a focused update to the 2012 scientific statement is now warranted. The purposes of this update are to confirm algorithms included in the initial scientific statement not requiring revision, to propose revisions to algorithms included in the initial scientific statement, to propose new algorithms based on emerging scientific evidence, to further clarify the application of oxygen consumption at ventilatory threshold, to describe CPX variables with an emerging scientific evidence base, to describe the synergistic value of combining CPX with other assessments, to discuss personnel considerations for CPX laboratories, and to provide recommendations for future CPX research.
Abstract
The contribution of the right ventricle (RV) to cardiac output is negligible in normal resting conditions when pressures in the pulmonary circulation are low. However, the RV becomes ...relevant in healthy subjects during exercise and definitely so in patients with increased pulmonary artery pressures both at rest and during exercise. The adaptation of RV function to loading rests basically on an increased contractility. This is assessed by RV end-systolic elastance (Ees) to match afterload assessed by arterial elastance (Ea). The system has reserve as the Ees/Ea ratio or its imaging surrogate ejection fraction has to decrease by more than half, before the RV undergoes an increase in dimensions with eventual increase in filling pressures and systemic congestion. RV-arterial uncoupling is accompanied by an increase in diastolic elastance. Measurements of RV systolic function but also of diastolic function predict outcome in any cause pulmonary hypertension and heart failure with or without preserved left ventricular ejection fraction. Pathobiological changes in the overloaded RV include a combination of myocardial fibre hypertrophy, fibrosis and capillary rarefaction, a titin phosphorylation-related displacement of myofibril tension–length relationships to higher pressures, a metabolic shift from mitochondrial free fatty acid oxidation to cytoplasmic glycolysis, toxic lipid accumulation, and activation of apoptotic and inflammatory signalling pathways. Treatment of RV failure rests on the relief of excessive loading.
Long-Term Use of Sildenafil in the Therapeutic Management of Heart Failure Marco Guazzi, Michele Samaja, Ross Arena, Marco Vicenzi, Maurizio D. Guazzi We tested whether chronic phosphodiesterase 5 ...inhibition by sildenafil is beneficial in heart failure. A total of 46 heart failure patients were randomly assigned to placebo (23 patients) or sildenafil (23 patients), with 3- and 6-month assessments of cardiopulmonary exercise test performance, brachial artery flow-mediated maximal dilatation, and ergoreflex responses. Sildenafil and not placebo improved flow-mediated maximal dilatation, ergoreflex effect on ventilation, exercise ventilation to CO2 production slope, and breathlessness, at both 3 and 6 months (p < 0.01). Findings suggest that benefits of sildenafil in heart failure are sustained and that an endothelium-mediated modulation of the muscle ergoreflex oversignaling may be at work.
Full text
Available for:
GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Pulmonary hypertension is a common hemodynamic complication of heart failure. Interest in left-sided pulmonary hypertension has increased remarkably in recent years because its development and ...consequences for the right heart are now seen as mainstay abnormalities that begin in the early stages of the disease and bear unfavorable prognostic insights. However, some knowledge gaps limit our ability to influence this complex condition. Accordingly, attention is now focused on: 1) establishing a definitive consensus for a hemodynamic definition, perhaps incorporating exercise and fluid challenge; 2) implementing the limited data available on the pathobiology of lung capillaries and small arteries; 3) developing standard methods for assessing right ventricular function and, hopefully, its coupling to pulmonary circulation; and 4) searching for effective therapies that may benefit lung vessels and the remodeled right ventricle. The authors review the pathophysiology, pathobiology, and emerging clinical perspectives on pulmonary hypertension across the broad spectrum of heart failure stages.
Full text
Available for:
GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
PDF
