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==Pathogenesis==

==Pathogenesis==

Heartworm disease is primarily a cardiopulmonary disease. the severity and extent of lesion depends on the number and location of adult worms duration of infection, and host activity level.. The presence of parasites in the pulomnary arteries causes mechanical irritation and proliferation of the intima, redulting in narrowing and occlusion of the vessels, which leads to pulmonary hypertension. perivascular cuffing with inflammatory cells, including infiltration of high numbers of eosinophils. Severe pulmonary arterial disease may cause increased permability of the lung vessls with periarterial oedema, and intersitial and alveolar cellular infiltrate, which can result in irreversible lung fibrosis. Pulmonary thromboembolism, due to platelet aggregation induces by the parasis or in response to the deat (spontaneous or induced by adultidicat treatment) of adult worms is another possible sequela of heartworm disease. chronic lesions and subsequent scarring

Heartworm disease primarily affects the cardiopulmonary system and the severity and extent of lesions depends several factors. These include the number and location of adult worms^{merck, fera}, the duration of infection, and the level of activity of the host^merck. Parasites in the pulomnary arteries causes mechanical irritation, leading to proliferation of the intima and perivascular cuffing with inflammatory cells, particularly eosinophils. This results in narrowing and occlusion of the vessels which in turn causes pulmonary hypertension. A combination of pulmonary hypertension and inflammatory mediators can lead in an increase in permeability in pulmonary vessels, giving periarterial oedema and intersitial and alveolar infiltrates. Constriction of the pulmonary artery also increases flow velocity, especially with exertion, and resultant shear stresses further damage the endothelium. The process of endothelial damage, vasoconstriction, increased flow velocity, and local ischemia is a vicious cycle. Inflammation with ischemia can result in irreversible interstitial fibrosis., which can result in irreversible lung fibrosis. Pulmonary thromboembolism, due to platelet aggregation induces by the parasis or in response to the deat (spontaneous or induced by adultidicat treatment) of adult worms is another possible sequela of heartworm disease. chronic lesions and subsequent scarring

HW-associated inflammatory mediators that induce immune responses in the lungs and kidneys (immune complex glomerulonephritis) cause vasoconstriction and possibly bronchoconstriction. Leakage of plasma and inflammatory mediators from small vessels and capillaries causes parenchymal lung inflammation and edema. Pulmonary arterial constriction causes increased flow velocity, especially with exertion, and resultant shear stresses further damage the endothelium. The process of endothelial damage, vasoconstriction, increased flow velocity, and local ischemia is a vicious cycle. Inflammation with ischemia can result in irreversible interstitial fibrosis.

HW-associated inflammatory mediators that induce immune responses in the lungs and kidneys (immune complex glomerulonephritis) cause vasoconstriction and possibly bronchoconstriction. Leakage of plasma and inflammatory mediators from small vessels and capillaries causes parenchymal lung inflammation and edema.  

In some severe cases, worms can migreat to the right ventricle, right artrium and caudal vena cava. This retrografe migration induces incompetence of the tricuspid valve which, in association with concurrent pulmonary hypertension, is responsible for the clinical signs of right-sides heart failure (e.g. jugular distension, liver congestion, ascites). In addition, red blood cell memranes may rupture as the vells flow through the mass of parasits, causing haemolysis and haemoglobinaemia. The concomitant presence of acture right-sided heart failure and intravascular haemolysis is referred to as caval syndrome. Severe cases of caval syndrome can also be characterised by the present of adult worms in the caudal vena cava, thromboembolic events and disseminated intravascular coagulation. Caval syndrom is less common in cats due to the lighter woem burden.

In some severe cases, worms can migreat to the right ventricle, right artrium and caudal vena cava. This retrografe migration induces incompetence of the tricuspid valve which, in association with concurrent pulmonary hypertension, is responsible for the clinical signs of right-sides heart failure (e.g. jugular distension, liver congestion, ascites). In addition, red blood cell memranes may rupture as the vells flow through the mass of parasits, causing haemolysis and haemoglobinaemia. The concomitant presence of acture right-sided heart failure and intravascular haemolysis is referred to as caval syndrome. Severe cases of caval syndrome can also be characterised by the present of adult worms in the caudal vena cava, thromboembolic events and disseminated intravascular coagulation. Caval syndrom is less common in cats due to the lighter woem burden.