COMPUTED TOMOGRAPHIC CHANGES ASSOCIATED WITH THE PREPATENT AND EARLY PATENT PHASE OF DIROFILARIASIS IN AN EXPERIMENTALLY INFECTED DOG

Evolution of pulmonary arterial and parenchymal changes as assessed with computed tomography (CT) is described in a dog experimentally infected with Dirofilaria immitis. The dog was imaged 125, 168, 216, and 402 days after infection. Initial changes during the prepatent phase of infection included enlargement of the peripheral caudal lobar pulmonary arteries and intermittent periarterial interstitial infiltrates. The changes were progressive, involving additional arteries over time, but remained mild. With the presence of adult filariae a filling defect was observed in the caudal lobar pulmonary artery using CT angiography. Recognizing thoracic CT findings associated with the prepatent phase of canine heartworm infection may be important in endemic areas.     

Morphologic Changes in the Lungs of Cats Experimentally Infected With Dirofilaria immitis

The morphologic response of the pulmonary arteries and lungs in cats was studied after a five month heartworm infection produced by transplantation of four adult heartworms/cat. One group of seven heartworm infected cats was not treated, another group of seven cats was treated with 97.5 mg of aspirin given twice a week, and the third group of six cats was given aspirin at a sufficient dosage to block in vitro platelet aggregation throughout the study. A fourth group of eight noninfected cats served as controls. Five months after heartworm infection, the cats were euthanized and the lungs perfusion fixed for light microscopy and scanning electron microscopy of the pulmonary arterial surfaces. All cats in the three heartworm-infected groups had live heartworms and the typical pulmonary arterial changes of heartworm disease at necropsy. The arterial surfaces, as viewed with scanning electron microscopy, had villus proliferations that were more numerous and exuberant than similar infections in dogs. Mean percentage of arterial surface involvement with villus proliferation of the nontreated heartworm infected cats was 67.3%; the aspirin treated cats, 73.8%; and the adjusted aspirin treated cats, 75.9%. The villi were myointimal proliferations in the small and medium-sized arteries. The more elastic arteries had a predominance of fibromuscular proliferation. All heartworm infected cats had arterial muscular hypertrophy of the small arteries, in contrast to only three of eight of the nonheartworm infected cats. The caudal lobar arteries were frequently obstructed with either villus proliferation, thrombi, and/or dead heartworms. The muscular arteries had branches with marked dilation, a condition associated with pulmonary hypertension in man. However, only three cats, one in each group, had pulmonary hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)     

Heartworm migration toward right atrium following artificial pulmonary arterial embolism or injection of heartworm body fluid

Heartworms harboring in the pulmonary arteries migrated toward the right atrium following insertion of dead heartworms or heartworm-like silicone tubes, or intravenous injection of body fluid extract of a female heartworm. The migration occurred within 3 hr (early group) or 1 to 7 days (late group) after insertion of dead worms, 1 to 11 days after insertion of silicone tubes, and immediately after infusion of heartworm-body fluid. The cardiac output decreased to an unmeasurably low level, and the pulmonary arterial pressure was also reduced in the early group. Although the output decreased, the pulmonary arterial pressure and the total pulmonary resistance increased gradually in the late group. In dogs with heartworm migration, in which silicone tubes had been inserted, the changes in cardiopulmonary values were the same as those in dogs of the late group. In dogs to which the body fluid had been administered intravenously, the changes in cardiopulmonary values were well accord with those in the early group. The systemic blood pressure also fell immediately after the administration with the shock-like state. These results suggest that the death of a part of the heartworms may be closely associated with the migration of heartworms toward the right atrium through the pulmonary arterial embolism and/or shock-like reaction by heartworm body fluid.     

Treatment of canine dirofilariasis: pulmonary thromboembolism caused by thiacetarsamide--microscopic changes

Light and scanning electron microscopies were used to study the pulmonary embolism occurring in Dirofilaria immitis-infected dogs after treatment with thiacetarsamide. Lesions in control dogs (nontreated) which had been infected for 4 weeks with 9 Dirofilaria immitis adults were compared with lesions occurring in infected dogs at 2 weeks and at 4 weeks after they were treated with the adulticide. Extensive thromboembolism occurred in the caudal lobar pulmonary arteries of dogs at posttreatment weeks 2 and 4. Complicated villous proliferations were present at posttreatment week 2. The characteristic myointimal proliferation of dirofilariasis showed resolution in the large pulmonary arteries of the dogs at week 4. However, the caudal lobar pulmonary arterial and lung lesions were more severe in the later group. The pathophysiology of adulticide-induced thromboembolism and associated lung parenchymal changes were discussed.     

Scintigraphic evaluation of pulmonary perfusion in dogs experimentally infected with Dirofilaria immitis

Pulmonary arterial perfusion was evaluated by perfusion lung scans in ten dogs experimentally infected with heartworm. After larval inoculation, scans were done once a month for 11 months. In 8 of 10 dogs, pulmonary arterial perfusion deficits were detected. The perfusion deficits involved the left cranial, right cranial, and right caudal lung lobes. Generally, there was a poor correlation between vascular abnormalities detected on the survey thoracic radiographs and the perfusion deficits detected by lung scanning. The perfusion deficits did not produce clinical signs or pulmonary infarction.     

RADIOGRAPHIC EVALUATION OF CANINE HEARTWORM DISEASE COEXISTING WITH RIGHT HEART FAILURE

Thoracic radiographs of 28 dogs with heartworm disease and right heart failure were evaluated subjectively and objectively. Radiographs of all dogs were abnormal. Abnormalities were consistent with those previously reported for heartworm disease but were more severe than those identified in another group of heartworm dogs that did not have right heart failure. The right ventricle and right caudal labor pulmonary artery were enlarged in every dog. The main pulmonary artery, right cranial lobar pulmonary artery, and caudal vena cava were enlarged in 24, 25, and 17 dogs, respectively. Radiographically apparent pathologic pulmonary conditions were present in 25 dogs. Pleural effusion was not identified.     

Pulmonary Arteriography and Hemodynamics During Feline Heartworm Disease

The ability of aspirin to block arterial disease and thromboembolism of the pulmonary arteries was studied in heartworm-infected cats. Three groups of cats were transplanted with four heartworms per cat and studied. One group of eight cats (aspirin group) received aspirin (97.5 mg, twice a week) for the five-month infection and another group of eight cats served as the nontreated control group (nontreated group). Based upon the results of the first two groups, the third group (adjusted aspirin group) of six cats was studied in which the aspirin dosage was adjusted in order to maintain an inhibition of in vitro platelet aggregation. Cats were studied by nonselective pulmonary arteriograms before heartworm transplantation and by selective arteriograms, aortograms, and pulmonary hemodynamics five months after heartworm transplant. Pulmonary hypertension, (mean pulmonary artery pressures greater than 16 mmHg), was discovered in three cats with one cat in each group. There were no differences in the mean pulmonary artery pressure or vascular resistance between the groups. Many of the arterial diameters for the nontreated and aspirin groups were greater after the five-month infection than before heartworm infection. All of the postinfection caudal arteries were tortuous and had aneurysms. Some of the caudal lung lobes had perfused areas that appeared to have a hypervascular microvasculature. The proportion of obstructed right and left distal caudal pulmonary arteries and the resulting nonperfused area of the caudal lung lobe in the nontreated and aspirin treated groups were each greater than in the adjusted aspirin group.(ABSTRACT TRUNCATED AT 250 WORDS)     

RADIOGRAPHIC AND ANGIOGRAPHIC EVALUATIONS OF FERRETS EXPERIMENTALLY INFECTED WITH DIROFILARIA IMMITIS

Five ferrets of each sex were each inoculated with 15 third-stage infective larvae of Dirofilaria immitis to study radiographic and angiographic changes in the cardiopulmonary system following heartworm infection; 5 additional ferrets of each sex served as noninfected controls. Prior to inoculation and every 8 weeks thereafter until 40 weeks, the infected and noninfected ferrets were radiographed; angiographic examinations were done prior to necropsy. At necropsy, the worms in the heart, lungs, and associated vessels were counted, and lung histosections were prepared and examined for changes. Radiographic changes were seen in the right side of the heart and associated vessels of infected ferrets as compared with the noninfected ferrets, but changes were less prominent than those seen in heartworm-infected dogs and cats. The changes were primarily an increase in the size of the right side of the heart, especially the right atrium. Radiographically, no changes could be visualized in the pulmonary vascular system. Worms in the enlarged cranial vena cava, azygous vein, and left caudal lobar pulmonary artery of infected animals were delineated by angiography. Histologically, no changes were seen in the pulmonary vascular tissues.     

PULMONARY ANGIOGRAPHY WITH 64‐MULTIDETECTOR‐ROW COMPUTED TOMOGRAPHY IN NORMAL DOGS

Pulmonary angiography using 64‐multidetector‐row computed tomography (MDCT) was used to evaluate pulmonary artery anatomy, and determine the sensitivity of pulmonary artery segment visualization in four Beagle dogs using images reconstructed to 0.625 mm and retro‐reconstructed to 1.25 and 2.5 mm slice thickness. Morphologically, characteristic features included a focal narrowing in the right cranial pulmonary artery in all dogs, which should not be mistaken as stenosis. While the right cranial pulmonary artery divided into two equally sized branches that were tracked into the periphery of the lung lobe in all dogs, only a single left cranial (cranial portion) lobar artery was present. Compared with 1.25 and 2.5 mm retro‐reconstructions, 0.625 mm reconstructions allowed for detection of significantly (P≤0.05) more pulmonary artery segments and sharper depiction of vessel margins. Clinical applications such as prevalence and significance of diameter changes, and detection of pulmonary arterial thrombembolism on lobar and sublobar level, using pulmonary angiography with 64‐MDCT applying 0.625 mm reconstruction slice thickness remain to be established.     

Improvement in pulmonary arterial lesions after heartworm removal using flexible alligator forceps

Improvement of pulmonary arterial lesions after heartworm removal using flexible alligator forceps was investigated by measuring pulmonary arterial pressure (PAP), and by angiographic and histopathological examinations in 11 dogs. PAP obtained immediately after worm removal corresponded well with angiographic abnormalities. In 2 dogs, high PAP immediately after worm removal fell gradually by 12 weeks, and obstructions on angiogram were resolved at 4 to 12 weeks. In 4 dogs, slightly high PAP fell to the normal range at 4 weeks, and angiographic abnormalities were considerably reduced at 4 to 12 weeks. In 5 dogs, PAP returned to normal range immediately after worm removal, and angiographic changes almost disappeared at 4 to 8 weeks. On biopsy immediately after worm removal, samples of the main pulmonary arteries showed severe intimal proliferations with villous or papillary protrusion into the lumen. Autopsy at 12 to 20 weeks indicated that the intimal protrusions were remarkably reduced as compared with the biopsy samples in all cases. However, villous intimal protrusions were seen in the caudal lobar arteries in cases with remaining alive worms. New vessels seemed to develop into thromboemboli with time. From these findings, it is clear that the pulmonary arterial lesions improved after heartworm removal, and the clinical signs disappeared following the improvement in hemodynamics. Aspirin therapy (5 mg/kg/day) for 4 weeks after worm removal in 5 dogs did not improve the intimal lesions as compared to 3 control dogs.     

Relationship between pulmonary arterial pressure and pulmonary thromboembolism associated with dead worms in canine heartworm disease.

To examine effects of thromboemboli due to dead worms on pulmonary arterial pressure (PAP), 20 to 50 dead heartworms were inserted into the pulmonary arteries of 4 heartworm uninfected dogs (uninfected group) and 11 dogs infected with heartworms (infected group). In the uninfected group, the mean PAP rose 1 week after worm insertion (10.9 to 166. mmHg), but it recovered by the 4th week. Clinical signs, hemodynamics and blood gas findings also deteriorated at the 1st week, but recovered at the 4th week. Angiographic and pathological findings indicated that blood flow recovered through the spaces between thromboemboli and vessel walls at the 4th week. The infected dogs were divided into three groups. In the infected-I group (5 dogs), the intimal lesions of the pulmonary arteries were slight, and clinical and laboratory findings showed changes similar to those of the uninfected group. In the infected-II group (4 dogs), the pulmonary arterial lesions were severe and the mean PAP was higher (25.7 mmHg) than in the uninfected group before worm insertion. An increase in PAP (34.1 mmHg) and worsening of clinical and laboratory findings were noticed till the 4th week. Thromboemboli adhered extensively to the vessel walls. Two dogs in the infected-III group died of severe dyspnea on the 9th and 10th day, and the mean PAP rose remarkably at the 1st week (from 19.4 to 28.2 mmHg). Severe pulmonary parenchymal lesions with edema or perforation were observed. From the above results, it was clarified that effects of dead worms on PAP and clinical signs depended on the severity of pulmonary arterial lesions before worm insertion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Aberrant migration and surgical removal of a heartworm (Dirofilaria immitis) from the femoral artery of a cat

A cat was evaluated for an acute‐onset of right pelvic limb paresis. Thoracic radiographs revealed normal cardiac size and tortuous pulmonary arteries. Abdominal ultrasound identified a heartworm (HW) extending from the caudal abdominal aorta into the right external iliac artery and right femoral artery. The cat was HW‐antigen positive. Echocardiography revealed a HW within the right branch of the main pulmonary artery and evidence of pulmonary hypertension. An agitated‐saline contrast echocardiogram revealed a small right to left intracardiac shunt at the level of the atria. Surgical removal of the HW was performed with no substantial postoperative complications. There was return of blood flow and improved motor function to the limb. The cat remains mildly paretic on the affected limb with no other clinical signs.     

CARDIAC AND PULMONARY ARTERY MENSURATION IN FELINE HEARTWORM DISEASE

A retrospective study was undertaken to quantify thoracic radiographic changes in cats with heartworm diseases, ( Dirofilaria immitis ). Using a blinded study format, the cardiac silhouette, thoracic cavity and pulmonary arteries were measured from thoracic radiographs of 21 cats with feline heartworm disease and 30 cats without known cardiac or pulmonary vessel pathology. Measured data were normalized to the thoracic cavity or bony structures within the radiographic field of view. The measurements were compared between the two groups of cats using an unpaired, two-tailed Student's t -test, with a p value of < 0.05 being considered significant. Cats with feline heartworm disease had enlargement of the craniocaudal aspect of the cardiac silhouette and normalized cardiac:thoracic ratio (p < 0.05) on the lateral view. Also, there was significant enlargement of the central and peripheral caudal lobar pulmonary arteries and their normalized ratios (p < 0.05) in the heartworm infected cats as visualized on the ventrodorsal projection. Tortuosity of the pulmonary arteries was seen in three of the 21 infected cats. Eleven of the 21 cats with feline heartworm disease had pulmonary parenchymal changes. Based on the present study, central and peripheral pulmonary artery enlargement as viewed on the ventrodorsal radiograph was the single best radiographic indicator of feline heartworm disease.     

MEASUREMENTS OF THE PULMONARY VASCULATURE ON THORACIC RADIOGRAPHS IN HEALTHY DOGS COMPARED TO DOGS WITH MITRAL REGURGITATION

This study reassessed the previously reported radiographic method of comparing pulmonary vessels versus rib diameter for differentiating healthy dogs and dogs with mitral regurgitation. The width of the right cranial pulmonary artery and vein at the fourth rib level, right caudal pulmonary artery and vein at the ninth rib level, and the diameters of the fourth rib and ninth rib were measured in prospectively recruited healthy dogs (n = 40) and retrospectively recruited dogs with mitral regurgitation (n = 58). In healthy dogs, the pulmonary arteries and accompanying veins were similar in size. The cranial lobar vessels were smaller than the fourth rib. However, 67.5% of right caudal pulmonary artery diameters and 65% of vein diameters were larger than the ninth rib in healthy dogs. The right caudal pulmonary vein diameter in dogs with mitral regurgitation, particularly those within moderate and severe grades, was significantly larger than that in healthy dogs (P < 0.001). The comparative method used to detect enlargement of the right caudal pulmonary vein relative to the accompanying pulmonary artery had the highest sensitivity (80.2%) and specificity (82.5%) for predicting mitral regurgitation. A cut‐off of 1.22 when applying the ninth rib criterion had better specificity (73%) than the most used value ≤ 1 (89.7% sensitivity and 63.8% specificity), although it has less sensitivity (73%). We recommend using the accompanying pulmonary artery and 1.22 × the diameter of the ninth rib as a radiographic criterion for assessing the size of the right caudal pulmonary vein and differentiating healthy dogs from those with mitral regurgitation.     

PULMONARY ANGIOGRAPHY USING 16 SLICE MULTIDETECTOR COMPUTED TOMOGRAPHY IN NORMAL DOGS

We report a canine computed tomography (CT) pulmonary angiography technique using multidetector CT (MDCT). CT pulmonary angiography using a 16 slice MDCT was performed on five healthy, anesthetized beagles. A helical acquisition with pitch of 1.4 was used. The time delay for the angiographic study was determined using a bolus‐tracking program. A dose of 400 mg I/kg of nonionic contrast medium (Iohexol 300 mg I/ml) was administered to each dog via a cephalic catheter using an angiographic power injector at a rate of 5 ml/s. In two dogs a second study, using a contrast medium dose of 200 and 600 mg I/kg was performed. Arterial enhancement of transverse and reformatted images was classified subjectively as excellent, good, or poor, and assessed objectively by measuring Hounsfield units at the right main pulmonary artery. Angiographic studies were evaluated by two radiologists to determine the number of subsegmental arterial branches visualized. The median number of subsegmental arterial branches identified was five (range: 2–7). Based on the time attenuation curve obtained by the bolus‐tracking program, there was consistent enhancement of the right main pulmonary artery beginning at 6 s and peaking at 8 s in 4/5 dogs. The contrast medium dose of 400 mg I/kg produced good to excellent vascular enhancement in the same 4/5 dogs. A dose of 200 mg I/kg resulted in poor enhancement. CT pulmonary angiography using MDCT and an automated bolus‐tracking program allows rapid, consistent evaluation of the pulmonary vasculature using a single dose of 400 mg I/kg of contrast medium.     

THORACIC RADIOGRAPHIC ABNORMALITIES IN 200 DOGS WITH SPONTANEOUS HEARTWORM INFESTATION

Thoracic radiographs of 200 dogs with spontaneously occurring heartworm disease were reviewed. Radiographs of 28 dogs (14%) were normal. In the remaining 172 dogs various combinations of cardiopulmonary abnormalties were found. The most frequently observed combination, noted in 61 of 200 dogs, was right ventricular, main pulmonary, and right cranial lobar pulmonary artery enlargemetn. Dogs with severe increse of one parameter generally had severe increase of the other two parameters also. One hundred five of the 200 dogs had a right cranial lobar pulmonary artery of normal size. Thus, right cranial lobar pulmonary artery size, when normal, is not a sensitive indicator of the absence of heartworm disease. There was a statistically significant positive relation between the size of the caudal vena cava and that of the right ventricle.     

Computed tomography features of bronchial and non-bronchial collateral arterial circulation development in a dog diagnosed with multiple chronic pulmonary thrombi

A 5 year-old female Lhasa Apso was diagnosed with a large right pulmonary artery thrombus, multiple smaller pulmonary thrombi, and pulmonary hypertension. In addition, thoracic computed tomography angiography revealed numerous periesophageal arterial vessels, tortuous and dilated bronchial arteries, and an enlarged tortuous left phrenic artery, consistent with systemic bronchial and non-bronchial collateral arterial circulation development. These features of chronic pulmonary arterial thrombi have not been described in dogs but are recognized in people. One year after the diagnosis, the dog was still alive and there were no clinical signs reported.     

Cardiopulmonary function in dogs with serious chronic heartworm disease.

Cardiopulmonary function was examined in 18 dogs with serious chronic heartworm disease showing ascites, subcutaneous edema, prostration, weakness, jaundice and so on. After surgical heartworm removal from the pulmonary arteries, 10 dogs recovered (surviving group), and 8 dogs died or were euthanatized because of poor prognosis (nonsurviving group). The number of live heartworms residing in the pulmonary arteries of the surviving group tended to be larger than that in the nonsurviving group. At necropsy, severe pulmonary arterial lesions such as thromboembolism including dead heartworms, proliferative and villous lesions and intimal hyperplasia were noticed in all dogs examined, and tended to be severer in the nonsurviving group. Heartworm-coiling around the tricuspid valve chord was found in 1 dog of the surviving group and 4 dogs of the nonsurviving group. Before heartworm removal, there was no significant difference in the mean pulmonary arterial pressure (MPAP) between the surviving and nonsurviving group. Right atrial pressure (v-wave) was higher, and the cardiac index (CI) was lower in the nonsurviving group. Arterial oxygen tension was lower in the surviving group than in the heartworm-free group, and it was lower in the nonsurviving group than in the surviving group. Carbon dioxide tension was lower in the surviving group than in the heartworm-free group. Bicarbonate concentration (HCO3-) was lower both in the surviving and nonsurviving groups than in the heartworm-free group. One week after heartworm removal, MPAP decreased (P less than 0.05), and CI and HCO3- tended to increase in the surviving group.     

MULTIDETECTOR‐ROW COMPUTED TOMOGRAPHY PATTERNS OF BRONCHOESPHAGEAL ARTERY HYPERTROPHY AND SYSTEMIC‐TO‐PULMONARY FISTULA IN DOGS

Anomalies involving arterial branches in the lungs are one of the causes of hemoptysis in humans and dogs. Congenital and acquired patterns of bronchoesophageal artery hypertrophy have been reported in humans based on CT characteristics. The purpose of this retrospective study was to describe clinical, echocardiographic, and multidetector computed tomography features of bronchoesophageal artery hypertrophy and systemic‐to‐pulmonary arterial communications in a sample of 14 dogs. Two main vascular patterns were identified in dogs that resembled congenital and acquired conditions reported in humans. Pattern 1 appeared as an aberrant origin of the right bronchoesophageal artery, normal origin of the left one, and enlargement of both the bronchial and esophageal branches that formed a dense network terminating in a pulmonary artery through an orifice. Pattern 2 appeared as a normal origin of both right and left bronchoesophageal arteries, with an enlarged and tortuous course along the bronchi to the periphery of the lung, where they communicated with subsegmental pulmonary arteries. Dogs having Pattern 1 also had paraesophageal and esophageal varices, with the latter being confirmed by videoendoscopy examination. Authors conclude that dogs with Pattern 1 should be differentiated from dogs with other congenital vascular systemic‐to‐pulmonary connections. Dogs having Pattern 2 should be evaluated for underlying pleural or pulmonary diseases. Bronchoesophageal artery hypertrophy can be accompanied by esophageal venous engorgement and should be included in the differential diagnosis for esophageal and paraesophageal varices in dogs.     

COLLATERAL PULMONARY CIRCULATION IN DOGS EXPERIMENTALLY INFECTED WITH DIROFILARIA IMMITIS: ITS ANGIOGRAPHIC EVALUATION*

Collateral pulmonary circulation was evaluated angiographically 11 months after experimental infection of dogs with either 25 or 100 infective larvae of Dirofilaria immitis. In both groups, collateral pulmonary circulation developed from bronchial arteries and esophageal branches of the left gastric artery. Of the four dogs receiving 25 larvae, one had no detectable collateral circulation, one developed collateral pulmonary circulation from the bronchial arteries only, and two had collateral pulmonary circulation from the bronchial arteries and esophageal branches of the left gastric artery. Of the three dogs receiving 100 larvae, all had collateral pulmonary circulation from the bronchial arteries and the esophageal branches of the left gastric artery. Bronchial artery collateral pulmonary circulation was more extensive in the 100-larvae dogs than in the 25-larvae dogs. Collateral pulmonary circulation from the left gastric artery esophageal branches was similar in both dog groups. Angiographically detectable collateral pulmonary circulation developed within the first year of heaertworm infection. In some respects, the extent of collateral pulmonary circulation development was related to the severity of heartworm infection.