Assessment Of Pulmonary Vascular Disease Research Articles

Assessment of Pulmonary Vascular Disease: Pulmonary Vascular Resistance, Exercise Hemodynamics, and Ventriculovascular Coupling.

Assessment of Pulmonary Vascular Disease: Pulmonary Vascular Resistance, Exercise Hemodynamics, and Ventriculovascular Coupling.

Tools of the Trade: How Do You Perform and Interpret an Exercise Test?

Background: Most pulmonary vascular disease (PVD) is poorly modifiable and incurable even with effective therapy. Therefore, adaptation to stress, the reserve of the cardiopulmonary system, is important for assessment of patient function and prognosis. Methods that assess the adaptation to stress, especially exercise, provide valuable insight into diagnosis, prognosis, and response to therapy.Implications for Clinicians: We provide a comprehensive review of the indications, methodology, and interpretation, as well as practical information of the forms of provocative testing in PVD. We include 6-minute walk testing, noninvasive cardiopulmonary exercise testing (CPET), invasive CPET, and additional forms, including volume loading.Conclusions: Through a clear understanding of the methodology in the assessment of PVD, the clinician can determine which of these “tools of the trade” are best suited to the individual patient and situation.

Noninvasive imaging in the assessment of the cardiopulmonary vascular unit.

Noninvasive imaging plays a key role in both the diagnosis and management of patients with pulmonary hypertension (PH). In recent years, there have been 2 major changes in perspective of imaging in PH. The first was the realization that imaging should focus on the evaluation of not only the pulmonary pressures but also the cardiopulmonary unit (Figure 1).1,2 The second was the emergence of multimodality imaging with a complementary role for echocardiography, magnetic resonance (MRI), computed tomography, and positron emission tomography (PET).2–7 These techniques not only help in the diagnosis of PH but also help identify factors that determine risk and prognosis and gauge therapeutic effects on right ventricular (RV) function in patients with pulmonary arterial hypertension (PAH). Although echocardiography is the mainstay in the assessment of hemodynamic and ventricular function in PH, MRI has emerged as the gold standard for quantifying volumes, function, and flow in the right side of the heart.2–7 PET is also offering novel insights into perfusion and blood flow, metabolism, neurohormonal activation, and other molecular processes in the right side of the heart but is used mainly for research at this time. Catheterization of the right side of the heart remains the gold standard for defining PH and assessing hemodynamics both at rest and with exercise. Invasive assessment of cardiac output (CO) may, however, have limited accuracy when assumed instead of measured oxygen consumption is used to derive CO (eg, using the Fick method) or when thermodilution is used in the setting of a low-CO state.8–10 Figure 1. Overview of multimodality assessment of the cardiopulmonary unit. Emphasis in evaluation has shifted for assessment of pulmonary vascular disease alone to assessment of the cardiopulmonary unit. Echocardiography, magnetic resonance imaging, positron emission tomography, computed tomography angiography …

Diagnosis and Assessment of Pulmonary Vascular Disease by Doppler Echocardiography

Pulmonary hypertension (PH) is a relatively misunderstood disease, partly related to the fact that many perceive PH to be a singular diagnosis. An unintended consequence of this is the misapplication of the role of the Doppler-Echocardiographic (DE) examination, as well as an underappreciation for its ability to help discern PH pathophysiology prior to right heart catheterization. Since DE often serves as the “gatekeeper” to invasive right heart catheterization, misinterpretation of the DE can lead to missed or delayed diagnosis with devastating consequences. Too often, the primary or nearly exclusive focus of the DE examination is placed on the pulmonary artery pressure estimation. Two main issues with this approach are that Doppler pressure estimations can be inaccurate and even when accurate, without integration of additional 2-D and Doppler information, the clinician will often still not appreciate the pathophysiology of the PH nor its clinical significance. This review will focus on the 2-D and Doppler features necessary to assess pulmonary vascular disease (PVD), discern the salient differences between PVD and pulmonary venous hypertension (PVH), and how to integrate these key DE parameters such that PH pathophysiology can be determined noninvasively and early in the patient workup. Overreliance on any single DE metric, and especially PA pressure estimation, detracts from the overall diagnostic potential of the DE examination. Integrating the relative balance of right and left heart findings, along with proper Doppler interpretation provides a wealth of clinical and pathophysiologic insight prior to invasive hemodynamic assessment. The end results are heightened awareness and improved identification of which patients should be referred for further invasive testing, as well the use of the DE information to compliment the findings from invasive testing.

Preoperative pulmonary hemodynamics and assessment of operability: Is there a pulmonary vascular resistance that precludes cardiac operation?

Preoperative pulmonary vascular disease remains an important risk factor for death or right-heart failure in selected children undergoing two-ventricle repair, single-ventricle palliation, or heart transplantation. Preoperative criteria for poor outcome after operation remain unclear. The purpose of this review is to critically assess both the historic and current data and make recommendations where appropriate. An extensive literature search was undertaken in October 2009. Data were analyzed by an expert multidisciplinary team and recommendations were made by consensus. PubMed was searched in October 2009. Data were analyzed and recommendations were made by consensus of a multidisciplinary team. In patients with suspected pulmonary vascular disease anticipating a two-ventricle repair, although preoperative testing via cardiac catheterization with vasodilators is reasonable, the preoperative parameters and the precise values of these parameters that best correlate with early and late outcome remain unclear. Further investigation is warranted in selected populations, such as the growing group of children with congenital heart disease complicated by chronic lung disease of prematurity, and in the developing world where patients may be more likely to present late with advanced pulmonary vascular disease. In patients with a functional single ventricle, there is growing evidence that mean pulmonary artery pressure of >15 mm Hg may be associated with both early and late mortality after the Fontan operation. The relationship of preoperative pulmonary hemodynamics to early and late morbidity remains to be defined. There most likely is a level of preoperative pulmonary vascular disease that puts an individual patient at increased risk for death or severe cyanosis after a bidirectional cavopulmonary anastomosis. It remains unclear, however, how to best assess this risk preoperatively. The limitations in obtaining an accurate assessment of pulmonary vascular disease in the complex single ventricle are discussed. In children awaiting cardiac transplantation with elevated pulmonary vascular disease of >6 U.m and/or transpulmonary gradient of >15 mm Hg, heart transplantation is deemed feasible in most transplant centers if the administration of inotropes or vasodilators can decrease the pulmonary vascular disease to <6 U.m or transpulmonary gradient to <15 mm Hg. In patients with preoperative pulmonary vascular disease, there may be contributing factors to the pulmonary vascular disease, such as the specifics of the cardiac lesion (atrioventricular valve regurgitation, low cardiac output), parenchymal and/or airway issues, and/or individual genetic predisposition. Amelioration of any reversible factors before operation and optimization of their management in the preoperative and postoperative period are recommended.

Cardiac Disease in Chronic Obstructive Pulmonary Disease

The cardiac manifestations of chronic obstructive pulmonary disease (COPD) are numerous. Impairments of right ventricular dysfunction and pulmonary vascular disease are well known to complicate the clinical course of COPD and correlate inversely with survival. The pathogenesis of pulmonary vascular disease in COPD is likely multifactorial and related to alterations in gas exchange and vascular biology, as well as structural changes of the pulmonary vasculature and mechanical factors. Several modalities currently exist for the assessment of pulmonary vascular disease in COPD, but right heart catheterization remains the gold standard. Although no specific therapy other than oxygen has been generally accepted for the treatment of pulmonary hypertension in this population, there has been renewed interest in specific pulmonary vasodilators. The coexistence of COPD and coronary artery disease occurs frequently. This association is likely related to shared risk factors as well as similar pathogenic mechanisms, such as systemic inflammation. Management strategies for the care of patients with COPD and coronary artery disease are similar to those without COPD, but care must be given to address their respiratory limitations. Arrhythmias occur frequently in patients with COPD, but are rarely fatal and can generally be treated medically. Use of beta-blockers in the management of cardiac disease, while a theoretical concern in patients with increased airway resistance, is generally safe with the use of cardioselective agents.

Intravascular Ultrasound Assessment of Pulmonary Vascular Disease in Patients With Pulmonary Hypertension

BackgroundMeasurements of pulmonary pressure and resistance are still considered to be the “gold standard” in the evaluation of pulmonary hypertension (PH), despite their limitations in predicting irreversible disease. Hemodynamic assessment also only provides a global evaluation of the pulmonary vascular bed, whereas PH is an inhomogeneous disease of the vessel wall. Methods and resultsWe assessed the value of intravascular ultrasound (IVUS) in 30 patients with suspected PH and correlated the structural changes in distal pulmonary arteries found on IVUS with conventional hemodynamic data. Plasma endothelin (ET)-1 levels and pulmonary ET-1 extraction also were measured as markers of the severity of PH. The anatomic abnormalities revealed by IVUS were more severe in the lower lobes than in the upper lobes, as evidenced by the greater percentage of wall thickness (WT), the smaller lumen diameter/WT and lumen area/total vessel area (p < 0.05 for each). IVUS anatomic indexes correlated directly with hemodynamic data (eg, with pulmonary arterial systolic pressure; r = 0.56; p < 0.001) and ET-1 levels but inversely with pulmonary ET-1 extraction. ConclusionPatients with PH have greater pulmonary arterial WT that is more severe in the lower lobes than in the upper lobes. The severity of structural abnormalities found on IVUS is directly correlated with hemodynamic findings and ET-1 levels. IVUS may provide useful additional information in the assessment of patients with PH.

Intravascular ultrasound assessment of pulmonary vascular disease in patients with pulmonary hypertension: Correlation with hemodynamic data and results of interventions

Intravascular ultrasound assessment of pulmonary vascular disease in patients with pulmonary hypertension: Correlation with hemodynamic data and results of interventions

Imaging of pulmonary vascular disease by intravascular ultrasound.

To assess the ability of intravascular ultrasound (IVUS) to image changes in the pulmonary arterial wall associated with pulmonary hypertension (PHT), 10 subjects requiring diagnostic right and left heart catheterization were studied. In addition to measurements of pulmonary artery pressure and pulmonary vascular resistance and pulmonary angiography, when indicated, all underwent simultaneous IVUS imaging in the pulmonary arterial system using a 20 MHz ultrasound transducer mounted on a 2 mm diameter catheter. Four patients had normal pulmonary artery pressures and 6 had varying degrees of PHT. Satisfactory ultrasound images were obtained in 9 out of the 10 patients. In those with normal pulmonary artery pressures ultrasound showed a thin vessel wall with no distinction between separate layers. In patients with systemic PHT, a three-layered vessel wall was apparent and areas compatible with intimal proliferation were seen. In a patient with pulmonary embolic disease areas consistent with mural thrombus were detected at sites of luminal narrowing on the pulmonary angiogram. IVUS is capable of imaging some of the morphological changes in the wall of the pulmonary artery known to occur in longstanding PHT and may therefore become a useful adjunct to haemodynamic measurements and pulmonary angiography for the in vivo assessment of pulmonary vascular disease.

Indication for total correction of complete transposition of the great arteries with pulmonary hypertension

Pulmonary vascular disease (PVD) was histologically evaluated and its severity was expressed as an index of PVD in 14 autopsied and eight biopsied cases of complete transposition of the great arteries (TGA) in patients more than 6 months of age. The index varied from 1.0 to 2.3 in six patients who had survived complete surgical repair and ranged from 2.3 to 3.3 in five patients who had died of PVD postoperatively. Consequently, an index of 2.2 could be regarded as an upper limit of PVD for complete surgical repair. The index was significantly correlated to some hemodynamic factors. From the regression equation, the value 2.2 of histologic index could be translated into the clinical factors concerning hemodynamics. We consider that patients with pulmonary vascular resistance of less than 10.6 units . m2, and pulmonary arterial mean pressure less than 51 mm Hg, are suitable candidates for complete surgical repair in TGA, if more than 6 months of age. Thus histologic assessment of PVD in a lung biopsy as an indication for total correction of TGA with pulmonary hypertension appears to be useful in patients who are in borderline hemodynamic condition or in whom the hemodynamics could not be evaluated although pulmonary hypertension was suspected.