Pulmonary Heart Disease: The Heart‐Lung Interaction and its Impact on Patient Phenotypes

Abstract

Pulmonary heart disease (PHD) refers to altered structure or function of the right ventricle occurring in association with abnormal respiratory function. Although nearly always associated with some degree of PH, the degree, nature, severity, and causality of PH in relation to the PHD is not necessarily linear and direct. Abnormal gas exchange is a fundamental underpinning of PHD, affecting pulmonary vascular, cardiac, renal, and neurohormonal systems. Direct and indirect effects of chronic respiratory disease can disrupt the right ventricular-pulmonary arterial (RV-PA) interaction and, likewise, factors such as sympathetic nervous system activation, altered blood viscosity, and salt and water retention can function in a feedback loop to further influence RV-PA function. Left heart function may also be affected, especially in those with pre-existing left heart disease. Thus, the physiologic interactions between abnormal respiratory and cardiovascular function are complex, with PHD representing a heterogeneous end organ effect of an integrated multisystem process. In this review, we propose to separate PHD into two distinct entities, “Type I” and “Type II” PHD. Type I PHD is most common, and refers to subjects with chronic respiratory disease (CRD) where the perturbations in respiratory function dominate over more mild cardiac and circulatory disruptions. In contrast, Type II PHD refers to the smaller subset of patients with more severe pulmonary vascular and right heart dysfunction, whom often present in a fashion similar to patients with PAH. Phenotypic differences are not made by PA pressure alone, but instead by differences in the overall physiology and clinical syndrome. Thus, key differences can be seen in symptomatology, physical signs, cardiac imaging, hemodynamics, and the cardiovascular and gas exchange responses to exercise. Such key baseline differences in the overall physiologic phenotype are likely critical to predicting response to PH specific therapy. Recognizing PHD as distinct phenotypes assists in the necessary distinction of these patients, and may also provide a key clinical and pathophysiologic framework for improved patient selection for future studies investigating the role of pulmonary hypertension-specific therapies in PHD.

Evaluation of pulmonary artery stiffness in newly diagnosed adult patients with asthma

“…8 The gold standard method in PAS evaluation is invasive measurements performed by right heart catheterization. 7,19 Recurrent hypoxia attacks in asthma lead to structural changes by triggering remodeling in the airways with chronic inflammation. Among these methods, echocardiography seems to be more advantageous in clinical use because of the ease of use, low cost, and no need for radiation and contrast agent exposure.…”

“…6,7,19,20,23,24 Pulmonary artery stiffness increases and distensibility decreases. Asthma-induced chronic inflammation and recurrent hypoxia cause structural changes and remodeling of the pulmonary vascular bed.…”

“…But in all these diseases, including asthma, the main mechanism is hypoxia-induced changes. 7,19 Recurrent hypoxia attacks in asthma lead to structural changes by triggering remodeling in the airways with chronic inflammation.…”

“…In the early stages of the disease, endothelial dysfunction develops and in the following stages, the proliferation of smooth muscle cells and the accumulation of matrix proteins in the vascular wall trigger to deteriorate the elastic structure of the pulmonary artery. 6,7,19,20,23,24 Pulmonary artery stiffness increases and distensibility decreases. The resistance in the pulmonary vascular bed increases and then pulmonary artery pressure increases.…”

Emerging Concepts in the Molecular Basis of Pulmonary Arterial Hypertension

“…Owing to the functional interrelatedness of the pulmonary vasculature and the RV, these two compartments are increasingly considered as a collective unit and assessed by examining RV-pulmonary arterial coupling in studies that focus on the pathophysiology of PAH. 1 Ideal RV-pulmonary arterial coupling is present when contractility of the RV is sufficient to match the afterload imposed by the pulmonary artery, which is determined by its distensibility or compliance, and is recognized by minimal pressure fluctuation during systole. 2 Optimal RV-pulmonary arterial coupling may be defined further based on the ratio of ventricular to arterial elastance, which typically achieves a ratio of 1.5–2.0 and reflects a balance between RV work and oxygen consumption.…”