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Background: Transcatheter aortic valve implantation (TAVI) is an established therapeutic option in patients with severe aortic valve stenosis (AS) and a high surgical risk profile. Pulmonary hypertension (PH)—often co-existing with severe AS—is associated with a limited factor for prognosis and survival. The purpose of this study was to evaluate the prevalence of PH in patients undergoing TAVI, classify these patients based on right heart catheter (RHC) measurements in different PH subtypes, and analyze prognostic values on survival after TAVI. Methods: 284 patients with severe AS underwent an RHC examination for hemodynamic assessment prior to TAVI and were categorized into subtypes of PH according to the 2015 European Society of Cardiology (ESC) guidelines. TAVI patients were followed-up with for one year with regard to 30-days and 1-year mortality as primary endpoints. Results: 74 of 284 participants showed a diastolic pressure gradient (DPG) < 7 mmHg and a pulmonary vascular resistance (PVR) > 3 Wood units (WU) and could not be formally allocated to either isolated post-capillary PH (ipc-PH) or combined pre- and post-capillary PH (cpc-PH). Therefore, a new subgroup called “borderline post-capillary PH” (borderlinepc-PH) was introduced. Compared with TAVI patients with pre-capillary PH (prec-PH), ipc-PH patients suffering from borderlinepc-PH (HR 7.114; 95% CI 2.015–25.119; p = 0.002) or cpc-PH (HR 56.459; 95% CI 7.738–411.924; p < 0.001) showed a significantly increased 1-year mortality. Conclusions: Postcapillary PH was expanded to include the so-called “borderlinepc-PH” variant in addition to the ipc-PH and cpc-PH subtypes. The one-year survival after TAVI was significantly different between the subgroups, with the worst prognosis for borderlinepc-PH and cpc-PH.

Pulmonary hypertension (PH) is a fatal condition that affects many dogs. In humans, PH is often treated with beraprost sodium (BPS). However, the effectiveness of BPS for canine PH has not been established. This study aimed to evaluate the clinical and cardiovascular response of BPS in canine patients with PH of various causes. Sixteen dogs with PH (post-capillary PH, n = 8; pre-capillary PH, n = 8) were included. BPS was continuously administered twice daily at 15 µg/kg. All dogs underwent echocardiography, including speckle-tracking analysis and blood pressure measurement, before and after BPS administration. Continuous BPS administration (range: 13.2–22.0 µg/kg) significantly decreased the pulmonary and systemic vascular impedance and increased left and right ventricular myocardial strain. In dogs with post-capillary PH, BPS administration caused no significant worsening of the left atrial pressure indicators. No side effects of BPS were observed in any dog. BPS also improved cardiac function and pulmonary circulation through pulmonary vasodilation, suggesting that BPS may be an additional treatment option for canine PH of various causes. Particularly, BPS increased left ventricular function and systemic circulation without worsening the left heart loading condition in dogs with post-capillary PH.

Pulmonary hypertension (PH) is common in patients with heart failure (HF). The role of PH in patients with HF with reduced (HFrEF) and preserved (HFpEF) left ventricular ejection fraction (LVEF) has been extensively characterized during the last years. In contrast, the pathophysiology of HF with mid-range LVEF (HFmrEF), and in particular the role of PH in this context, are largely unknown. There is a paucity of data in this field, and the prevalence of PH, the underlying mechanisms, and the optimal therapy are not well-defined. Although often studied together there is increasing evidence that despite similarities with both HFrEF and HFpEF, HFmrEF also differs from both entities. The present review provides a summary of the current concepts of the mechanisms and clinical impact of PH in patients with HFmrEF, a proposal for the non-invasive and invasive diagnostic approach required to define the pathophysiology of PH and its management, and a discussion of future directions based on insights from mechanistic studies and randomized trials. We also provide an outlook regarding gaps in evidence, future clinical challenges, and research opportunities.

The development of pulmonary hypertension (PH) in patients with heart failure is associated with increased morbidity and mortality. In this article, the authors examine recent changes to the definition of PH in the setting of left heart disease (PH-LHD), and discuss its epidemiology, pathophysiology and prognosis. They also explore the complexities of diagnosing PH-LHD and the current evidence for the use of medical therapies, promising clinical trials and the role of left ventricular assist device and transplantation.

Pulmonary hypertension in left heart disease (PH-LHD) is the most prevalent form of PH. It is classified as group 2 PH as per WHO classification. As the prevalence of left heart disease such as congestive heart failure is increasing, the number of patients with associated PH is rising, coupled with high morbidity and mortality. Pulmonary hypertension is initially passive or isolated post-capillary (Ipc-PH) due to increased left sided filling pressures. In long standing cases pre-capillary component is added due to development of pulmonary vascular disease, termed combined post- and pre-capillary PH (Cpc-PH) or reactive PH. We describe the hemodynamics, pathophysiology, role of echocardiography and right heart catheterization in PH-LHD. We discuss the significance of PH associated with congestive heart failure as well as valvular heart disease. Although there is no treatment for PH-LHD, we discuss and critically analyze various studies investigating the role of pulmonary vasodilators in this condition. As PH-LHD is an under studied disease, we highlight the areas where further research is required.

We present the rare case of a patient with pulmonary hypertension in the context of the stiff left atrial syndrome after extensive catheter ablation, a unique constellation characterized by high pulmonary artery and pulmonary artery wedge pressures due to left atrial dysfunction but normal left ventricular end‐diastolic pressure, normal mitral valve, and absence pulmonary vein stenosis. This patient was surprisingly oligosymptomatic, however, which may have been due to a persistent post‐puncture atrial septal defect, which may have allowed for controlled left atrial decompression, which is in line with the novel concept of the catheter‐based creation of an intracardiac shunt as a treatment for heart failure.

In patients with aortic and/or mitral valve disease the presence of pulmonary hypertension (PH) indicates a decompensated state of the disease with left ventricular and left atrial dysfunction and exhausted compensatory mechanism, i.e., a state of heart failure. Pulmonary hypertension in this context is the consequence of the backwards transmission of elevated left atrial pressure. In this form of PH, pulmonary vascular resistance is initially normal (isolated post-capillary PH). Depending on the extent and chronicity of left atrial pressure elevation additional pulmonary vascular remodeling may occur (combined pre- and post-capillary PH). Mechanical interventions for the correction of valve disease often but not always reduce pulmonary pressures. However, the reduction in pulmonary pressures is often modest, and persistent PH in these patients is common and a marker of poor prognosis. In the present review we discuss the pathophysiology and clinical impact of PH in patients with aortic and mitral valve disease, the comprehensive non-invasive and invasive diagnostic approach required to define treatment of PH, and recent insights from mechanistic studies, registries and randomized studies, and we provide an outlook regarding gaps in evidence, future clinical challenges, and research opportunities in this setting.

In patients with left ventricular heart failure (HF), the development of pulmonary hypertension (PH) and right ventricular (RV) dysfunction are frequent and have important impact on disease progression, morbidity, and mortality, and therefore warrant clinical attention. Pulmonary hypertension related to left heart disease (LHD) by far represents the most common form of PH, accounting for 65-80% of cases. The proper distinction between pulmonary arterial hypertension and PH-LHD may be challenging, yet it has direct therapeutic consequences. Despite recent advances in the pathophysiological understanding and clinical assessment, and adjustments in the haemodynamic definitions and classification of PH-LHD, the haemodynamic interrelations in combined post- and pre-capillary PH are complex, definitions and prognostic significance of haemodynamic variables characterizing the degree of pre-capillary PH in LHD remain suboptimal, and there are currently no evidence-based recommendations for the management of PH-LHD. Here, we highlight the prevalence and significance of PH and RV dysfunction in patients with both HF with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF), and provide insights into the complex pathophysiology of cardiopulmonary interaction in LHD, which may lead to the evolution from a 'left ventricular phenotype' to a 'right ventricular phenotype' across the natural history of HF. Furthermore, we propose to better define the individual phenotype of PH by integrating the clinical context, non-invasive assessment, and invasive haemodynamic variables in a structured diagnostic work-up. Finally, we challenge current definitions and diagnostic short falls, and discuss gaps in evidence, therapeutic options and the necessity for future developments in this context., SCOPUS: re.j, info:eu-repo/semantics/published