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<\/a><\/p>\nIn humans, causes of PH were historically categorized as either primary or secondary. More recently, they have been further classified into 5 groups based on similarities in pathology, hemodynamic consequences, and therapeutic approaches.10<\/sup> A recent American College of Veterinary Internal Medicine (ACVIM) consensus statement on PH in dogs proposed a similar 6-group classification scheme for use in veterinary medicine.1<\/sup><\/span><\/p>\nGroup 1<\/h3>\n
Group 1 is composed of causes capable of increasing PVR, including heritable diseases, certain drugs or toxins (e.g., dexfenfluramine, fenfluramine), systemic-to-pulmonary (left-to-right) congenital shunts, and idiopathic causes. In cases of systemic-to-pulmonary congenital shunt, the increase in Qp, which in some cases can be more than double the systemic blood flow, increases shear stress on the pulmonary vascular endothelium. This subsequently stimulates vascular remodeling in the pulmonary circulation, leading to increased PVR and, when severe, Eisenmenger\u2019s physiology (shunt reversal).6<\/sup><\/span><\/p>\nGroup 2<\/h3>\n
Group 2 describes PH secondary to left-sided heart disease, the estimated most common cause of PH in dogs.8,11<\/sup> Any heart disease severe enough to progress to significant left-sided volume overload, left atrial hypertension, and enlargement can cause pulmonary venous hypertension and postcapillary PH. Chronically, the pulmonary arteries may \u201creact\u201d to this increase in pressure as well as hypoxia (in patients with pulmonary edema) and undergo structural changes that increase PVR, resulting in combined (pre- and postcapillary) PH.8 <\/sup>Although PH is most commonly seen in dogs with myxomatous mitral valve degeneration, additional causes include dilated cardiomyopathy and mitral valve dysplasia.8,11<\/sup><\/span><\/p>\nGroup 3<\/h3>\n
Group 3 describes PH secondary to respiratory disease, hypoxia, or both. In contrast to what happens in the systemic circulation, when the pulmonary circulation is faced with hypoxia, it undergoes vasoconstriction to improve ventilation-perfusion matching. Disease processes such as chronic obstructive airway disorders or primary pulmonary parenchymal disease, or chronic exposure to high altitude, can result in chronic hypoxia and pulmonary vasoconstriction.12,13<\/sup> Excessive volume in vessels receiving diverted blood may result in vascular structural remodeling and increased PVR, worsening PH.2<\/sup> These disorders are thought to be an underestimated cause of PH due to the difficulty of their definitive diagnosis in veterinary medicine.1<\/sup><\/span><\/p>\nGroup 4<\/h3>\n
Group 4 describes PH resulting from pulmonary emboli, thrombi, or thromboemboli, in either the acute or chronic setting. Occlusion of part of the pulmonary arteries increases PVR. Many diseases have been associated with thromboembolic disease, including immune-mediated diseases, neoplasia, sepsis, pancreatitis, protein-losing diseases, and infectious diseases.14,15<\/sup><\/span><\/p>\nGroup 5<\/h3>\n
Group 5 is unique to veterinary medicine and describes PH induced by heartworm disease (Dirofilaria<\/i>) or Angiostrongylus<\/i> infection. PVR increases after worm-induced myointimal proliferation, inflammation, fibrosis, and thromboembolism develop within the pulmonary arteries.16,17<\/sup><\/span><\/p>\nGroup 6<\/h3>\n
Group 6 describes PH with multifactorial mechanisms, including masses that compress the pulmonary vasculature and combinations of diseases in groups 1 through 5.<\/span><\/p>\nDiagnosis of Pulmonary Hypertension<\/h2>\n
Given the wide variety of diseases that can lead to the development of PH, systemic evaluation is warranted to investigate the cause in an individual patient. However, diagnosis of the underlying cause is often challenging and can be elusive in some cases despite thorough evaluation. Diagnostic efforts should concentrate on identifying severity of PH, presence of right-sided CHF, and other factors that may affect prognosis. Many patients are classified as having \u201cidiopathic\u201d PH, but it is more likely that the cause is not clinically identified due to the limitations of diagnostics in veterinary medicine compared to human medicine.1<\/sup> For example, diagnostics such as ventilation-perfusion lung scan, pulmonary function testing (e.g., <\/span>spirometry, exercise testing), and computed tomography pulmonary angiography are commonly included in the diagnostic approach to PH in humans but not <\/span>routinely performed or practical in most veterinary patients.18<\/sup><\/p>\nRight Heart Catheterization<\/h3>\n
Right heart catheterization is the gold standard for the diagnosis of PH.7,19<\/sup> It is seldom performed in veterinary medicine due to the invasiveness of the procedure, cost, and inherent risks. Nevertheless, it is considered indicated in some patients, particularly animals with congenital heart disease when intervention is being planned and accurate assessment of the PVR is necessary.<\/span><\/p>\nImaging<\/h3>\n
Echocardiography<\/b><\/p>\n
In most veterinary patients with suspected PH, hemodynamic parameters are estimated with Doppler echocardiography, a minimally invasive method with acceptable reliability despite its limitations.19,20<\/sup> Numerous quantitative echocardiographic parameters are used to assess the severity of PH, with the peak tricuspid regurgitation velocity being the most used and relied upon. Briefly, quantification of the peak tricuspid regurgitation velocity is used to estimate the pressure difference, or pressure gradient (PG), between the right atrium and right ventricle during ventricular systole, using the simplified Bernoulli equation (PG<\/span>\u2009<\/span>=<\/span>\u2009<\/span>4V2<\/sup>; V<\/span>\u2009<\/span>=<\/span>\u2009<\/span>peak tricuspid regurgitation velocity in m\/s). In the absence of a right ventricular outflow tract obstruction such as a double-chamber right ventricle or pulmonic stenosis, the PG plus the estimated right atrial pressure yields the estimated systolic pulmonary artery pressure.7,8<\/sup> Echocardiography can also be used to estimate the mean and diastolic pulmonary artery pressures by quantifying the velocity of the pulmonic valve insufficiency, with the early and end-diastolic peak velocities used to estimate the mean and diastolic pulmonary artery pressures, respectively.7,8<\/sup><\/span><\/p>\nIn addition to estimation of systolic, mean, and diastolic pulmonary artery pressures, echocardiography is used to evaluate for additional changes suggestive of PH (<\/span>BOX 1<\/b><\/span>). A recent ACVIM consensus statement recommended the use of both tricuspid regurgitation velocity and the number of echocardiographic signs of PH to determine the echocardiographic probability of PH (low, moderate, or high).1<\/sup> Echocardiography is also used to evaluate for the presence of left-to-right shunting defects, left atrial hypertension, heartworm disease, thromboembolic disease, and compressive mass lesions.<\/span><\/p>\nBOX 1 Echocardiographic Signs Suggestive of Pulmonary Hypertension<\/div>
\n
\n- Right ventricular hypertrophy (concentric, eccentric, or mixed)<\/li>\n
- Systolic interventricular septal flattening<\/li>\n
- Decreased left ventricular size<\/li>\n
- Right ventricular systolic dysfunction<\/li>\n
- Right atrial enlargement<\/li>\n
- Enlargement of the caudal vena cava without respiratory variation<\/li>\n
- Pulmonary artery enlargement<\/li>\n
- Right pulmonary artery distensibility<\/li>\n
- Doppler-derived right ventricular outflow acceleration time and acceleration time\/ejection time ratio<\/div><\/div><\/li>\n<\/ul>\n
Radiography<\/b><\/p>\n
Thoracic radiographs may show right atrial, ventricular, and pulmonary artery enlargement (reverse D sign) in cases of moderate to severe PH (FIGURE<\/b><\/span><\/span>\u00a02<\/b><\/span>). Changes to the pulmonary vasculature (arteries versus both arteries and veins), as well as left-sided heart changes and changes in the aspect of the lung parenchyma, depend on the type of PH. It is important to note that some dogs may develop pulmonary infiltrates consistent with noncardiogenic pulmonary edema as a direct result of severe PH.2<\/sup> Additional radiographic features of pulmonary hypertension are discussed in a recent review article.21<\/sup><\/span><\/p>\n