1,721,202 research outputs found
Guidelines for the diagnosis and treatment of pulmonary hypertension
Task force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology and the European Respiratory Society endorsed by the International Society of Heart and Lung Transplantatio
What's new in the European Society of Cardiology/European Respiratory Society Pulmonary Hypertension Guidelines?
Comment on
2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension: The Joint Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS): Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC), International Society for Heart and Lung Transplantatio
The difficult diagnosis of pulmonary vascular disease in heart failure
Pulmonary hypertension (PH), defined as a mean pulmonary arterial pressure (PAP) ≥25 mmHg, is a well-recognised complication of left heart disease (LHD). PH prevalence is variable ranging from 25% to 80% of LHD patients according to the methods of assessment, cut-off values and characteristics of the patient population [1–3]. All aetiological types of LHD are affected, including heart failure with reduced (HFrEF) or preserved (HFpEF) left ventricular ejection fraction, and valvular LHD. The presence of PH-LHD is associated with advanced symptoms, reduced exercise capacity and impaired outcome after medical, interventional or surgical therapy [1, 3, 4].
The relevance of PH-LHD is highlighted by the recognised epidemiological predominance of this condition, which represents the most common form among the five groups included in the PH clinical classification, accounting for 65–80% of the PH cases [1, 3, 5, 6]. PH-LHD is distinctively characterised by an increase of the pulmonary artery wedge pressure (PAWP) >15 mmHg [5, 6], an accepted surrogate for left atrial pressure
Exercise training in pulmonary hypertension: improving performance but waiting for outcome
Pulmonary hypertension is a pathophysiological condition characterized by an increase of mean pulmonary arterial pressure ≥25 mmHg at rest.1 Pulmonary hypertension may complicate multiple clinical disorders and invariably it reduces exercise and functional capacity and represents a risk factor for morbidity and mortality.2 Although important progress in the pharmacotherapy of pulmonary arterial hypertension has been achieved in the past 15 years,3,4 limited functional capacity and reduced survival still characterize patient outcome. Further advances are needed in this area to improve the clinical results of a comprehensive treatment strategy.
Effects of exercise training
Ehlken and colleagues now present the data of a randomized controlled trial on the impact of exercise training on peak oxygen consumption and haemodynamics in 87 patients with pulmonary arterial hypertension or inoperable chronic thrombo-embolic pulmonary hypertension.5 The majority of subjects (91%) were on background approved pulmonary arterial hypertension therapies. The exercise training started with an in-hospital 3-week programme and was continued at home with at least 15 min/day for 5 days a week for the following 12 weeks.
After 15 weeks, the peak oxygen uptake (primary endpoint) significantly improved in the training group by +24.3% and the 6-min walk distance improved by 41 m. Haemodynamics at rest and during exercise significantly improved in the training group compared with the control group. However, the haemodynamic data were collected only in 74 patients (85%)
Treatment of pulmonary hypertension
The most common forms of pulmonary hypertension are pulmonary arterial hypertension, chronic thromboembolic pulmonary hypertension, and pulmonary hypertension due to left-sided heart and lung disease. The treatment of pulmonary arterial hypertension has advanced substantially over the past 20 years. Five different classes of drugs are now available-ie, endothelin receptor antagonists, phosphodiesterase-5 inhibitors, soluble guanylate cyclase stimulators, prostacyclin analogues, and prostacyclin receptor agonists. Long-term studies have provided evidence that various combinations of these compounds improve the progression-free survival of patients with pulmonary arterial hypertension. For patients with chronic thromboembolic pulmonary hypertension, surgical pulmonary endarterectomy is the treatment of choice. For patients who are inoperable and have chronic thromboembolic pulmonary hypertension, riociguat, a stimulator of soluble guanylate cyclase, has proven efficacious. Additionally, interventional approaches could become a treatment option for these patients. For patients with pulmonary hypertension due to left-sided heart disease or lung disease, the use of pulmonary vasodilator treatment has not been proven to be safe and effective
Pulmonary arterial capacitance in patients with heart failure and reactive pulmonary hypertension
Abstract
AIMS:
Reactive pulmonary hypertension (PH) is a severe form of PH secondary to left-sided heart failure (HF). Given the structural and functional abnormalities in the pulmonary vasculature that occur in reactive PH, we hypothesized that pulmonary artery capacitance (PAC) may be profoundly affected, with implications for clinical outcome.
METHODS AND RESULTS:
We studied 393 HF patients of whom 124 (32%) were classified as having passive PH and 140 (36%) as having reactive PH, and 91 patients with pulmonary arterial hypertension (PAH). Mean PAC was highest in patients without PH (4.5 ± 2.1 mL/mmHg), followed by the passive PH group (2.8 ± 1.4 mL/mmHg) and was lowest in those with reactive PH (1.8 ± 0.7 mL/mmHg) (P = 0.0001). PAC and pulmonary vascular resistance (PVR) fitted well to a hyperbolic inverse relationship (PAC = 0.25/PVR, R(2) = 0.70), with reactive PH patients dispersed almost predominantly on the flat part of the curve where a reduction in PVR is associated with a small improvement in PAC. Elevated PCWP was associated with a significant lowering of PAC for any PVR (P = 0.036). During a median follow-up of 31 months, both reactive PH [hazard ratio (HR) 2.59, 95% confidence interval (CI) 1.14-4.46, P = 0.02] and reduced PAC (HR 0.72 per 1 mL/mmHg increase, 95% CI 0.59-0.88, P = 0.001) were independent predictors of mortality.
CONCLUSIONS:
The development of reactive PH is associated with a marked reduction in PAC. PAC is a strong independent haemodynamic marker of mortality in HF and may contribute to the increased mortality associated with reactive PH
Progress in the treatment of acute pulmonary embolism and chronic thrombo-embolic pulmonary hypertension/disease
The combination of an initial clinical approach aimed at evaluating the early risk of mortality with subsequent diagnostic and therapeutic approaches articulated on the overall patient's profile is recommended in acute pulmonary embolism (PE). The presence of pulmonary hypertension associated with the persistence of chronic vascular obstructions in the pulmonary arteries after one or more acute thrombo-embolic events identifies a condition defined as chronic thrombo-embolic pulmonary hypertension (CTEPH). The evolution of technology and knowledge in the field of imaging has allowed us to qualify the computed tomography angiography of the pulmonary arteries as the gold standard for the diagnostic confirmation of both acute PE and CTEPH. In both these conditions, the first therapeutic step is the immediate initiation of anticoagulant therapy. In acute high-risk PE, in addition to anticoagulant therapy, thrombolytic therapy is recommended; in the event of contraindications to thrombolysis, surgical embolectomy or percutaneous catheter-directed treatment represents viable treatment options. In CTEPH, the combination of data collected from cardiac catheterization, computed tomography angiography, and conventional angiography of pulmonary arteries allows a team of experts to identify candidates for pulmonary endarterectomy surgery. Inoperable patients should be considered for percutaneous balloon angioplasty of the pulmonary arteries which can improve patients' symptoms, quality of life, and prognosis
Balloon pulmonary angioplasty after pulmonary thromboendarterectomy
.Pulmonary thromboendarterectomy (PTE) is the treatment of choice for patients with chronic thromboembolic pulmonary hypertension (CTEPH) as it can remove the chronic, fibrotic, flow-limiting organized thrombi within the pulmonary arterial bed, addressing the primum movens of the disease (1). Despite significant improvement in all haemodynamic parameters, residual pulmonary hypertension (PH) is frequent after PTE, ranging from 17% to 31% (2,3). There is no clear definition of residual PH after PTE, and the actual incidence of this condition has been difficult to quantify. Usually, moderate residual PH is well tolerated by patients and, as shown by data from the United Kingdom cohort, clinically relevant residual PH after PTE mainly occur when the mean pulmonary arterial pressure (mPAP) is greater than 30–35 mmHg (3). The risk of persistent/recurrent PH in the long-term underlines the importance of a systematic patient follow-up, even after PTE. Balloon pulmonary angioplasty (BPA) has been developed as a compassionate procedure for symptomatic patients with CTEPH who are ineligible for surgery or with persistent/recurrent PH after PTE. BPA is not able to remove clots as PTE, but it is able to restore the flow by fragmenting the thrombotic and fibrotic material, resulting in hemodynamic and clinical improvement. Selection of good candidates for BPA, especially after PTE, includes a complete re-assessment of the patient with persistent symptomatic PH after PTE at least four to six months after surgery using high quality imaging techniques such as computed tomography pulmonary angiography (CTPA), selective pulmonary angiography (to provide fine details) and right heart catheterization (RHC) to assess the hemodynamic impairment. However, these imaging techniques are not widely available and require expertise
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