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ToDay's VeTeriNary PracTice | November/December 2015 | tvpjournal.com aHs HearTWorM HoTLiNe Peer reviewed 64 infow tract to the right ventricle (Figure 3, page 63), interfering with closure of the tricuspid valve and consequently resulting in: 1-5 • significant tricuspid regurgitation • compromised right ventricular filling • in some patients, the onset of circulatory collapse. in the 1980s, a high level of scientifc interest in cs led to an expanded—albeit incomplete— understanding of the condition's etiology. Unfortunately, enthusiasm for the subject waned, and even today the etiology of cs remains incompletely defned. While it is evident that more scientifc studies are needed to completely explain this unique manifestation of a complex disease, information from earlier studies combined with more recent pictorial and clinical evidence allows formulation of a working hypothesis for the development of cs. HOW DOES CAVAL SYNDROME DEVELOP? Clinical Presentations of Heartworm Infection The pathogenesis of HWD and the chain of events that leads to illness is quite complex. Dogs with natural infection may remain asymptomatic for extended periods of time, or may present with a variety of clinical signs (Table 1 ). 6 The wide variety of clinical presentations for heartworm infection (HWi) is expected due to the complex relationship between worm numbers, extent of vascular pathology, and individuality of each dog's physiologic response, all of which result in the clinical variability observed between individual animals. Therefore, it is not surprising that trying to defne specifc causes of cs is complicated. Location of Worms in cs, heartworms are typically found in the right heart and/or vena cava, whereas in heavy HWis without cs, worms are normally found in the pulmonary arteries rather than the heart. 7 if we are to appreciate how adult worms relocate from the pulmonary arteries to the heart, as they do in cs, it may be necessary to frst understand why heartworms normally live in the pulmonary arteries. • adult heartworms live freely within the lumen of the pulmonary arteries, with no ability to attach or swim. • adult worms move quite slowly and it seems logical that they have a limited ability to freely, or at least quickly, move from one location to another. • as a result, heartworms live where blood flow forces them to live. one logical explanation as to why heartworms may normally remain in the pulmonary arteries is: • During systole, as blood is ejected into the pulmonary arteries, the volume and velocity of blood flow force heartworms to the more distal aspects of the arteries. 8-11 • Because adult heartworms move quite slowly, they may be unable to significantly move back toward the heart before the next contraction again pushes them distally, forcing them to reside in the pulmonary arteries. if we assume that blood fow is the primary factor keeping adult heartworms constrained to the pulmonary arteries, it is logical to ask what condition—or series of conditions—might allow or cause multiple heartworms to retrogradely move into the right ventricle, atrium, and/or vena cava, as they do in cs. WHY DO HEARTWORMS MIGRATE? studies in heartworm-infected dogs have shown that when hemodynamics are altered—forward fow is reduced and resistance to fow is increased— worms migrate toward the right atrium. TAblE 1. Clinical signs of Heartworm disease Weight loss Exercise intolerance Mild to severe cough Polypnea or dyspnea Hemoptysis Right-sided heart failure Signs consistent with CS* *To be discussed in Part 2 of this series TA bl E 2. d isease Processes associated with Heartworm-induced vascular obstruction • Physical obstruction by adult worms (figure 4)* • Intimal thickening of vascular walls (figure 5)* • Microvascular disease • Dead worm obstruction (figure 6) • Thrombus formation (figure 7) • Arterial fbrosis and scarring (figure 8) * Most evidence implies that presence of adult worms and intimal thickening, individually, are unlikely to have a dramatic impact on vascular fow. However, in the presence of mild to severe arterial lesions, removal and reinsertion of live heartworms has been shown to decrease and increase pulmonary arterial pressures, respectively.