Heart Sounds and Murmurs: Changes Related to Severity of Chronic Valvular Disease in the Cavalier King Charles Spaniel

Auscultatory, phonocardiographic (PCG), radiographic, and echocardiographic evidence of chronic valvular disease (CVD) were studied in 79 Cavalier King Charles Spaniels with a mean age of 7.6 years (SD 2.6). Cardiac murmurs were present in 59 of the dogs and the intensity of the systolic cardiac murmur, assessed by auscultation (grade 1–6), was correlated (P < .001) to the severity of CVD (heart failure class) and to the echocardiographical dimensions of the heart (left atrial ratio, La/Ao-d, and left ventricular end diastolic diameter, LVEDD) (both P < .001). The heart sounds and duration of electromechanical systole (Q-S2) were investigated in all dogs using measurements obtained from PCG recordings. Normal regression equations describing the relation between heart rate and systolic intervals (Q-S1, Q-S2 and S1-S2) were established based on observations in 11 normal control Cavalier King Charles Spaniels. The total electromechanical systole (Q-S2), Q-S1, and S1-S2 intervals in the 59 dogs were related to the corresponding normal regression equation. A shortening of Q-S2 and S1-S2 intervals were found in dogs belonging to heart failure class I (Q-S2; P < .01 and S1 -S2; P < .05), class II, and classes III and IV (both P < .001). The ratio of the amplitudes of the first (S1) and second heart sounds (S2) measured on the PCG recordings was found to be increased in dogs belonging to class I (P < .01), class II, and classes III and IV (both P < .001). The relationship between cardiac dimensions (LVEDD and La/Ao-d) and S1a/S2a ratio was described by quadratic regression and found to be significant for both parameters (LVEDD; P < .001, R²= .54 and La/Ao-d; P < .001, R²= .63). The presence of a third heart sound (S3) was detected, using PCG, in 21 of the 68 dogs. The proportion of dogs exhibiting S3 increased with heart failure class (and increasing cardiac dimensions) (P < .001). These findings were confirmed by observations in 13 Cavalier King Charles Spaniels with cardiac failure progressing from heart failure class I to class II (Mean LVEDD from 30.2 to 35.2 mm and mean La/Ao-d from 1.09 to 1.43). An increase in intensity of the heart murmur, assessed by auscultation, increase in the ratio of the amplitudes of S1 and S2, as well as a shortening in Q-S2 and S1-S2 intervals (all P < .01) were found in these dogs. None of these dogs showed an S3 in heart failure class I, but 7 of the 13 dogs developed an S3 in class II.     

Influence of open surgical correction on intermediate-term outcome in dogs with subvalvular aortic stenosis: 44 cases (1991-1998)

OBJECTIVE: To compare outcome and intermediate-term survival for dogs undergoing open surgical correction of subvalvular aortic stenosis (SAS) with those for dogs with SAS that did not undergo surgery. DESIGN: Retrospective study. ANIMALS: 44 dogs with congenital SAS. PROCEDURE: Maximum instantaneous systolic pressure gradients were determined by use of Doppler echocardiography. Cardiopulmonary bypass and open surgical correction of SAS (membranectomy with or without septal myectomy) was performed in 22 dogs, whereas 22 dogs did not undergo surgical correction. Cumulative survival was compared between surgical and nonsurgical groups, using Kaplan-Meier nonparametric analysis and a Mantel-Cox log-rank test. RESULTS: Initial systolic pressure gradients were not significantly different for dogs undergoing surgery (128 +/- 55 mm Hg), compared with those that did not undergo surgery (117 +/- 57 mm Hg). Systolic pressure gradients were significantly decreased after surgery in dogs that underwent surgery (54 +/- 27 mm Hg). Cumulative survival was not significantly different between dogs in the surgical and nonsurgical groups. Censoring surgery-related mortality in the analysis still did not reveal a significant difference in cumulative survival between the surgical and nonsurgical groups. CONCLUSIONS AND CLINICAL RELEVANCE: Despite reductions in the systolic pressure gradient and possible associated improvement in exercise tolerance, a palliative benefit on survival was not documented in dogs undergoing surgery for SAS.     

Renal resistive index in 55 dogs with degenerative mitral valve disease

Background

Azotemia occurs frequently in dogs with degenerative mitral valve disease (DMVD). It could indicate changes in renal hemodynamics.

Hypothesis/Objectives

To assess the renal resistive index (RI) in dogs with DMVD, and the statistical link between heart failure class, azotemia, echo‐Doppler parameters, several plasma variables, and RI.

Animals

Fifty‐five dogs with naturally occurring DVMD were used (ISACHC class 1 [n = 28], 2 [n = 19], and 3 [n = 8]).

Methods

Observational, blinded study, performed under standardized conditions. Physical examination, renal ultrasonography, and echo‐Doppler examinations were performed in awake dogs. The RI of the renal, interlobar, and arcuate arteries were measured. Plasma creatinine, urea, and N‐terminal pro‐B‐type natriuretic peptide concentrations (NT‐proBNP) were determined. Statistical links between variables and RI were tested by means of a general linear model.

Results

Although the RI of renal and arcuate arteries were unaffected by ISACHC class, the left interlobar RI increased (P < .001) from 0.62 ± 0.05 (mean ± SD) in class 1 to 0.76 ± 0.08 in class 3. It was also higher (P < .001) in azotemic (0.74 ± 0.08) than in non‐azotemic (0.62 ± 0.05) dogs. Similar findings were observed for right interlobar RI. Univariate analysis showed a positive statistical link between NT‐proBNP (P = .002), urea (P < .001), creatinine (P = .002), urea‐to‐creatinine ratio (P < .001), left atrium‐to‐aorta ratio (P < .001), regurgitation fraction (P < .001), systolic pulmonary arterial pressure (P < .001), shortening fraction (P = .035), and RI.

Conclusion and Clinical Importance

In dogs with DMVD, interlobar RI increases with heart failure severity and azotemia but a cause and effect relationship remains to be established.     

Heterotopic implantation of a porcine bioprosthetic heart valve in a dog with aortic valve endocarditis

CASE DESCRIPTION: A 5-year-old male German Shepherd Dog was evaluated because of a 5-month history of progressive lethargy, weight loss, and heart failure. CLINICAL FINDINGS: On physical examination, bounding femoral pulses and systolic and diastolic murmurs were detected. Echocardiography revealed severe aortic valve insufficiency (AVI) and a large vegetative lesion on the aortic valve consistent with aortic valve endocarditis. The AVI velocity profile half-time was 130 milliseconds; the calculated peak systolic pressure gradient across the aortic valve was 64 mm Hg. Left ventricular diameter during diastole was 63.6 mm (predicted range, 40.2 to 42 mm) and during systole was 42.9 mm (predicted range, 25.4 to 27 mm). Systolic, diastolic, and mean arterial blood pressures were 120, 43, and 65 mm Hg, respectively. TREATMENT AND OUTCOME: To palliate severe AVI, the descending aorta was occluded (duration, 16.75 minutes) and heterotopic implantation of a porcine bioprosthetic heart valve in that vessel was performed. After surgery, systolic, diastolic, and mean arterial blood pressures were 115, 30, and 61 mm Hg, respectively, in the forelimb and 110, 62, and 77 mm Hg, respectively, in the hind limb. Within 6 months, the AVI velocity profile half-time had increased to 210 milliseconds, indicating diminished severity of AVI. After 24 months, the dog was able to engage in vigorous exercise; no pulmonary edema had developed since surgery. CLINICAL RELEVANCE: Heterotopic bioprosthetic heart valve implantation into the descending aorta during brief aortic occlusion appears feasible in dogs and may provide substantial palliation for dogs with severe AVI.     

Survival times in dogs with severe subvalvular aortic stenosis treated with balloon valvuloplasty or atenolol

OBJECTIVE: To determine survival times in dogs with severe subvalvular aortic stenosis (SAS) treated by means of balloon valvuloplasty or with atenolol, a beta-adrenoceptor blocking drug. DESIGN: Prospective study. ANIMALS: 38 dogs < 24 months old with severe SAS (peak systolic pressure gradient > or = 80 mm Hg). PROCEDURE: 10 dogs underwent balloon valvuloplasty and were reexamined 6 weeks later to determine the feasibility of the procedure. The remaining 28 dogs were randomly assigned to undergo balloon valvuloplasty (n = 15) or to be treated with atenolol long term (13) and were reexamined annually for 9 years or until the time of death. RESULTS: For the first 10 dogs, mean pressure gradient 6 weeks after balloon valvuloplasty (mean +/- SD, 119 +/- 32.6 mm Hg) was significantly decreased, compared with mean baseline pressure gradient (167 +/- 40.1 mm Hg). Median survival time for dogs that underwent balloon valvuloplasty (55 months) was not significantly different from median survival time for dogs treated with atenolol (56 months). CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that balloon valvuloplasty can result in a significant decrease in the peak systolic pressure gradient in dogs with severe SAS, at least for the short term. No clear benefit in survival times was seen for dogs that underwent balloon valvuloplasty versus dogs that were treated with atenolol.     

Pulmonic stenosis in dogs: balloon dilation improves clinical outcome

Medical records of 81 dogs with severe pulmonic stenosis from 2 referral centers were examined retrospectively. Forty dogs underwent balloon valvuloplasty (BV), which was performed by 1 operator, whereas 41 did not. The mean age at latest follow-up was 41.5 months. A statistical comparison of the clinical outcome and survival was performed. Dogs revealing clinical signs at presentation showed a 16-fold increase in risk of death compared with asymptomatic dogs (P < .001). Statistical analyses demonstrated that an increase of 1 mm Hg in transstenotic pressure gradient (PG) at presentation was associated with a 3% increase in hazard rate (P < .001). Thirty-seven dogs survived BV with a median reduction in PG of 46%. The median preoperative PG was 120 mm Hg, and median PG 24 hours postoperatively was 55 mm Hg with a median of 55 mm Hg 6 months post-BV. Twenty (49%) of the non-BV (NBV) dogs remained asymptomatic at last follow-up. Fourteen (34%) of the NBV dogs died or were euthanized because of heart disease related to pulmonic stenosis. Twelve of these dogs died suddenly, whereas only 1 of the BV dogs died suddenly. After adjusting for PG, clinical signs at presentation, and age, BV or dilation was associated with a 53% reduction in hazard rate (P = .005). This study indicates that BV, when performed by an experienced operator, appears to be successful both in alleviating clinical signs and in prolonging survival in dogs with severe pulmonic stenosis.     

EFFECTS OF INTRAVENOUS DEXMEDETOMIDINE ON CARDIAC CHARACTERISTICS MEASURED USING RADIOGRAPHY AND ECHOCARDIOGRAPHY IN SIX HEALTHY DOGS

Dexmedetomidine is a highly specific and selective α2‐adrenergic receptor agonist widely used in dogs for sedation or analgesia. We hypothesized that dexmedetomidine may cause significant changes in radiographic and echocardiographic measurements. The objective of this prospective cross‐sectional study was to test this hypothesis in a sample of six healthy dogs. Staff‐owned dogs were recruited and received a single dose of dexmedetomidine 250 μg/m² intravenously. Thoracic radiography and echocardiography were performed 1 h before treatment, and repeated 10 and 30 min after treatment, respectively. One observer recorded cardiac measurements from radiographs and another observer recorded echocardiographic measurements. Vertebral heart score and cardiac size to thorax ratio on the ventrodorsal projection increased from 9.8 ± 0.6 v to 10.3 ± 0.7 v (P = 0.0007) and 0.61 ± 0.04 to 0.68 ± 0.03 (P = 0.0109), respectively. E point‐to‐septal separation and left ventricle internal diameter in diastole and systole increased from 2.4 ± 1.1 to 6.6 ± 1.9 mm, 32.3 ± 8.1 to 35.5 ± 8.8 mm, and 19.4 ± 6 to 27.0 ± 7.2 mm, respectively (P < 0.05). Fractional shortening and sphericity index decreased from 40.7 ± 5.8 to 24.4 ± 2.9%, and 1.81 ± 0.07 to 1.58 ± 0.04, respectively (P < 0.05). Moderate‐to‐severe mitral regurgitation and mild pulmonic regurgitation occurred in all dogs after dexmedetomidine administration. Findings indicated that dexmedetomidine could cause false‐positive diagnoses of valvular regurgitation and cardiomegaly in dogs undergoing thoracic radiography and echocardiography.     

The relationship of resting S-T segment depression to the severity of subvalvular aortic stenosis and the presence of ventricular premature complexes in the dog

Electrocardiograms (ECG) from 35 dogs with subvalvular aortic stenosis (SAS) with a left ventricular outflow tract pressure gradient (PG) of > or =50 mm Hg were retrospectively evaluated for S-T segment depression (STD, > or =0.2 mV in lead II). Pressure gradient, age, heart rate (HR), and number of ventricular premature complexes (VPCs) on a 24-hour ambulatory ECG for dogs with STD were not significantly different from those for dogs without STD. The S-T segment deviation did not correlate significantly with PG, age, HR, or VPCs. The significance of STD in the dog with SAS remains uncertain. Long-term prospective studies are needed to fully understand this observation.     

Nutritional Alterations and the Effect of Fish Oil Supplementation in Dogs with Heart Failure

Alterations in body composition and nutritional status are common in humans with heart failure and are related, in part, to increases in cytokine concentrations. Cytokines have not been studied previously in dogs with naturally occurring cardiac disease nor has fish oil administration been used in this population to decrease cytokine production. The purposes of this study were to characterize nutritional and cytokine alterations in dogs with heart failure and to test the ability of fish oil to reduce cytokines and improve clinical outcome. Body composition, insulinlike growth factor-1, fatty acids, and cytokines were measured in 28 dogs with heart failure and in 5 healthy controls. Dogs with heart failure then were randomized to receive either fish oil or placebo for 8 weeks. All parameters were measured again at the end of the study period. At baseline, 54% of dogs with heart failure were cachectic and the severity of cachexia correlated with circulating tumor necrosis factor-α concentrations (P= .05). Cytokine concentrations at baseline, however, were not significantly increased in dogs with heart failure compared to controls. Baseline plasma arachidonic acid (P= .02), eicosapentaenoic acid (P= .03), and docosahexaenoic acid (P = .004) concentrations were lower in dogs with heart failure than in controls. Fish oil supplementation decreased interleukin-1β (IL-1) concentrations (P= .02) and improved cachexia (P= .01) compared to the placebo group. The mean caloric intake of the heart failure dogs as a group was below the maintenance energy requirement (P < .001), but no difference was found in food intake between the fish oil and placebo groups. Insulinlike growth factor-1 concentrations (P= .01) and reductions in circulating IL-1 concentrations over the study period (P= .02) correlated with survival. These data demonstrate that canine heart failure is associated with cachexia, alterations in fatty acids, and reduced caloric intake. Fish oil supplementation decreased IL-1 concentrations and improved cachexia. In addition, reductions in IL-1 predicted survival, suggesting that anticytokine strategies may benefit patients with heart failure.     

Balloon Dilation of Congenital Subaortic Stenosis in the Dog

Balloon dilation during cardiac catheterization was evaluated for the treatment of congenital subaortic stenosis (SAS) in nine dogs. Under general anesthesia, bilateral cardiac catheterization was performed through the right jugular vein and carotid artery. Thermodilution cardiac output, and left ventricular and aortic root pressures and angiograms were obtained before and after balloon dilation. Balloons measuring 18–20 mm in diameter and 30–40 mm in length were positioned across the stenosis and three inflations 4–5 minutes apart were performed. There was no significant change in cardiac output, aortic pressure, or degree of aortic regurgitation after balloon dilation. For the entire group balloon dilation resulted in significant decreases in left ventricular systolic pressure (-61.2 ± 37.2 mm Hg [mean change ± SD], range -14 to -123), mean systolic pressure gradient (-39.6 ± 24.4 mm Hg, range –8.4 to -72.2), and peak systolic pressure gradient (-64.3 ± 46.5 mm Hg, range –17 to –143). Calculated left ventricular outflow cross-sectional area increased significantly (+.4 ± .5 cm², range –.06 to + 1.30). Clinical signs improved in the five symptomatic dogs. Individual hemodynamic responses varied widely, but the magnitude of improvement correlated with the severity of obstruction. Three dogs showed a decrease of 60% or greater (≥100 mm Hg), and six dogs showed a decrease of 25–50% (17–71 mm Hg) in peak systolic gradient after balloon dilation. Complications were frequent but most were transient and manageable. These preliminary results suggest that balloon dilation can acutely decrease outflow resistance in dogs with SAS and may be effective therapy for some affected dogs.     

Regurgitant fraction measured by using the proximal isovelocity surface area method in dogs with chronic myxomatous mitral valve disease

Previous studies have demonstrated that regurgitant fraction can be measured by using the proximal isovelocity surface area (PISA) method. For this study, we utilized this Doppler echocardiographic method to estimate the magnitude of mitral regurgitation in dogs with myxomatous mitral valve disease. Seventeen older, small dogs with chronic mitral regurgitation and no to mild myocardial failure were studied. A blinded observer judged the clinical severity of mitral regurgitation to be mild, moderate, or severe by using echocardiographic assessment of left heart size. The regurgitant fraction was calculated by using the PISA method and spectral Doppler echocardiography. The regurgitant fraction was compared to the clinical assessment of severity for each dog and to calculations of left atrial size. Five dogs had clinically mild mitral regurgitation. Four of these dogs had a regurgitant fraction between 22 and 41%, whereas 1 had a regurgitant fraction of 73%. The 3 dogs with clinical evidence of moderate mitral regurgitation had a regurgitant fraction of 46-65%. All 9 dogs with clinically severe mitral regurgitation had a regurgitant fraction greater than 75% (78-88%). The regurgitant fraction was statistically different between each group (P < .001). A good but curvilinear relationship was found between left atrial size and regurgitant fraction (r2 = 0.72). In this study, dogs with clinically severe mitral regurgitation consistently had hemodynamically severe regurgitation (regurgitant fraction > 75%), whereas dogs with clinically mild to moderate disease had lesser degrees of regurgitation. Good correlation was found between regurgitant fraction and left atrial size. We conclude that the major determinant of left atrial size and disease severity in dogs with mitrial regurgitation is the degree of mitral regurgitation.     

Intramyocardial arterial narrowing in dogs with subaortic stenosis

Earlier studies have described intramyocardial arterial narrowing based on hyperplasia and hypertrophy of the vessel wall in dogs with subaortic stenosis (SAS). In theory, such changes might increase the risk of sudden death, as they seem to do in heart disease in other species. This retrospective pathological study describes and quantifies intramyocardial arterial narrowing in 44 dogs with naturally occurring SAS and in eight control dogs. The majority of the dogs with SAS died suddenly (n=27); nine had died or been euthanased with signs of heart failure and eight were euthanased without clinical signs. Dogs with SAS had significantly narrower intramyocardial arteries (P<0.001) and more myocardial fibrosis (P<0.001) than control dogs. Male dogs and those with more severe hypertrophy had more vessel narrowing (P=0.02 and P=0.02, respectively), whereas dogs with dilated hearts had slightly less pronounced arterial thickening (P=0.01). Arterial narrowing was not related to age, but fibrosis increased with age (P=0.047). Dogs that died suddenly did not have a greater number of arterial changes than other dogs with SAS. This study suggests that most dogs with SAS have intramyocardial arterial narrowing and that the risk of dying suddenly is not significantly related to the overall degree of vessel obliteration.     

Spontaneous feline hypertension: clinical and echocardiographic abnormalities,and survival rate

Systemic hypertension was diagnosed in 58 of 188 untreated cats referred for evaluation of suspected hypertension-associated ocular, neurologic. cardiorespiratory, and urinary disease, or diseases frequently associated with hypertension (hyperthyroidism and chronic renal failure). Hypertensive cats were significantly older than normotensive subjects (13.0 +/- 3.5 years versus 9.6 +/- 5.0 years; P < .01), and had a greater prevalence of retinal lesions (48 versus 3%; P < .001), gallop rhythm (16 versus 0%; P < .001), and polyuria-polydipsia (53 versus 29%: P < .01). Blood pressure was significantly higher (P < .001) in cats with retinopathies (262 +/- 34 mm Hg) than in other hypertensive animals (221 +/- 34 mm Hg). Hypertensive cats had a thicker interventricular septum (5.8 +/- 1.7 versus 3.7 +/- 0.64 mm; P < .001) and left ventricular free wall (6.2 +/- 1.6 versus 4.1 +/- 0.51 mm; P < .001) and a reduced diastolic left ventricular internal diameter (13.5 +/- 3.2 versus 15.8 +/- 0.72 mm; P < .001) than control cats. Left ventricular geometry was abnormal in 33 of 39 hypertensive subjects. No significant difference was found in age or blood pressure at the initial visit between cats that died or survived over a 9-month period after initial diagnosis of hypertension. Mean survival times were not significantly different between hypertensive cats with normal and abnormal left ventricular patterns. Further prospective studies are needed to clearly identify the factors involved in survival time in hypertensive cats.     

Nodules and masses are associated with malignant pleural effusion in dogs and cats but many other intrathoracic CT features are poor predictors of the effusion type

Thoracic CT may be used in the workup of patients with pleural effusion. In humans, certain pleural features on CT aid in diagnosing an underlying cause for pleural effusion, whereas this is not well studied in veterinary medicine. This retrospective cross‐sectional analytical study assessed pleural and other intrathoracic abnormalities on CT in dogs and cats with pleural effusion and explored potential discriminatory features between effusion types. Eighty‐nine dogs and 32 cats with pleural cytology and/or histopathology were categorized into malignant pleural disease (15 dogs and 11 cats), pyothorax (34 dogs and 7 cats), chylothorax (20 dogs and 11 cats), transudative (11 dogs and 2 cats), and hemorrhagic effusion (9 dogs and 1 cat). Multivariable logistic regression analysis comparing malignancy to other effusions found that older patient age (dogs: odds ratio 1.28, P = 0.015; cats: odds ratio 1.53, P = 0.005), nodular diaphragmatic pleural thickening (dogs: odds ratio 7.64, P = 0.021; cats: odds ratio 13.67, P = 0.031), costal pleural masses (dogs: odds ratio 21.50, P = 0.018; cats: odds ratio 32.74, P = 0.019), and pulmonary masses (dogs: odds ratio 44.67, P = 0.002; cats: odds ratio 18.26, P = 0.077) were associated with malignancy. In dogs, any costal pleural abnormality (odds ratio 47.55, P = 0.002) and pulmonary masses (odds ratio 10.05, P = 0.004) were associated with malignancy/pyothorax, whereas any costal pleural abnormality (odds ratio 0.14, P = 0.006) and sternal lymphadenopathy (odds ratio 0.22, P = 0.040) were inversely associated with transudates. There were, however, many overlapping abnormalities between effusion types, so further diagnostic testing remains important for diagnosis.     

Detection of Congestive Heart Failure in Dogs by Doppler Echocardiography

Background: Echocardiographic prediction of congestive heart failure (CHF) in dogs has not been prospectively evaluated. Hypothesis: CHF can be predicted by Doppler echocardiographic (DE) variables of left ventricular (LV) filling in dogs with degenerative mitral valve disease (MVD) and dilated cardiomyopathy (DCM). Animals: Sixty‐three client‐owned dogs. Methods: Prospective clinical cohort study. Physical examination, thoracic radiography, analysis of natriuretic peptides, and transthoracic echocardiography were performed. Diagnosis of CHF was based upon clinical and radiographic findings. Presence or absence of CHF was predicted using receiver‐operating characteristic (ROC) curve, multivariate logistic and stepwise regression, and best subsets analyses. Results: Presence of CHF secondary to MVD or DCM could best be predicted by E : isovolumic relaxation time (IVRT) (area under the ROC curve [AUC]=0.97, P < .001), respiration rate (AUC=0.94, P < .001), Diastolic Functional Class (AUC=0.93, P < .001), and a combination of Diastolic Functional Class, IVRT, and respiration rate (R²=0.80, P < .001) or Diastolic Functional Class (AUC=1.00, P < .001), respiration rate (AUC=1.00, P < .001), and E : IVRT (AUC=0.99, P < .001), and a combination of Diastolic Functional Class and E : IVRT (R²=0.94, P < .001), respectively, whereas other variables including N‐terminal pro‐brain natriuretic peptide, E : Ea, and E : Vp were less useful. Conclusion and Clinical Importance: Various DE variables can be used to predict CHF in dogs with MVD and DCM. Determination of the clinical benefit of such variables in initiating, modulating, and assessing success of treatments for CHF needs further study.     

Cardiac troponin-I concentration in dogs with cardiac disease

Cardiac troponin-I (cTnI) is a highly sensitive and specific marker of myocardial injury and can be detected in plasma by immunoassay techniques. The purpose of this study was to establish a reference range for plasma cTnI in a population of healthy dogs using a human immunoassay system and to determine whether plasma cTnI concentrations were high in dogs with acquired or congenital heart disease, specifically cardiomyopathy (CM), degenerative mitral valve disease (MVD), and subvalvular aortic stenosis (SAS). In total, 269 dogs were examined by physical examination, electrocardiography, echocardiography, and plasma cTnI assay. In 176 healthy dogs, median cTnI was 0.03 ng/mL (upper 95th percentile = 0.11 ng/mL). Compared with the healthy population, median plasma cTnI was increased in dogs with CM (0.14 ng/mL; range, 0.03-1.88 ng/mL; P < .001; n = 26), in dogs with MVD (0.11 ng/mL; range, 0.01-9.53 ng/mL; P < .001; n = 37), and in dogs with SAS (0.08 ng/mL; range, 0.01-0.94 ng/mL; P < .001; n = 30). In dogs with CM and MVD, plasma cTnI was correlated with left ventricular and left atrial size. In dogs with SAS, cTnI demonstrated a modest correlation with ventricular wall thickness. In dogs with CM, the median survival time of those with cTnI >0.20 ng/mL was significantly shorter than median survival time of those with cTnI <0.20 ng/mL (112 days versus 357 days; P = .006). Plasma cTnI is high in dogs with cardiac disease, correlates with heart size and survival, and can be used as a blood-based biomarker of cardiac disease.     

Cardiac Troponin‐I Concentration,Myocardial Arteriosclerosis,and Fibrosis in Dogs with Congestive Heart Failure because of Myxomatous Mitral Valve Disease

Background

Few previous studies have investigated the association between biomarkers and cardiac disease findings in dogs with naturally occurring myxomatous mitral valve disease (MMVD).

Aim

To investigate if histopathological changes at necropsy could be reflected by in vivo circulating concentrations of cTnI and aldosterone, and renin activity, in dogs with naturally occurring congestive heart failure because of MMVD.

Animals

Fifty privately owned dogs with MMVD and heart failure.

Methods

Longitudinal Study. Dogs were prospectively recruited and examined by clinical and echocardiographical examination twice yearly until time of death. Blood was stored for batched analysis of concentrations of cTnI and aldosterone, and renin activity. All dogs underwent a standardized necropsy protocol.

Results

cTnI were associated with echocardiographic left ventricular end‐diastolic dimension (P < .0001) and proximal isovolumetric surface area radius (P < .004). Furthermore, in vivo cTnI concentrations reflected postmortem findings of global myocardial fibrosis (P < .001), fibrosis in the papillary muscles (P < .001), and degree of arterial luminal narrowing (P < .001) Aldosterone or renin activity did not reflect any of the cardiac disease variables investigated.

Conclusion and clinical importance

Cardiac fibrosis and arteriosclerosis in dogs with MMVD are reflected by circulating cTnI concentration, but not by aldosterone concentration or renin activity. Cardiac troponin I could be a valuable biomarker for myocardial fibrosis in dogs with chronic cardiac diseases.     

Pulmonary function in dogs with mitral valve regurgitation

Mitral valve regurgitation was created in 2 groups of dogs. Groups were selected on absence (group 1) or presence (group 2) of clinical signs of congestive left ventricular failure. Group-2 dogs, in which mean left atrial pressures were greater than 30 mm of Hg, had increases in heart rate, pulmonary arterial mean pressure, left atrial diameter, and left ventricular diastolic diameter. These changes were associated with decreased arterial O2 tension, decreased static and dynamic compliance, reduced lung volumes, and increased pulmonary resistance. Group-1 dogs, in which mean left atrial pressure was less than 30 mm of Hg, had moderate changes in hemodynamics, but no changes in pulmonary function, except during exercise when arterial O2 tension decreased.     

Prediction of first onset of congestive heart failure in dogs with degenerative mitral valve disease: The PREDICT cohort study

ObjectiveTo identify risk factors for first-onset congestive heart failure (CHF) in dogs with degenerative mitral valve disease (DMVD).AnimalsEighty-two dogs with and without CHF secondary to DMVD were retrospectively assigned to a derivation cohort. Sixty-five dogs with asymptomatic DMVD were recruited into a prospective validation cohort.MethodsVariables associated with risk of CHF in dogs were identified in a derivation cohort and used to construct a predictive model, which was then prospectively tested through longitudinal examination of a validation cohort.ResultsLogistic regression analysis of the derivation cohort yielded a predictive model that included the left atrial to aortic root dimension ratio (LA:Ao) and plasma concentration of N-terminal pro-B-type natriuretic peptide (NT-proBNP). When this model was prospectively applied to the validation cohort, it correctly predicted first-onset of CHF in 69.2% of cases. Analysis of the validation cohort revealed that plasma NT-proBNP concentration and indexed left ventricular end-diastolic diameter (LVIDd:Ao) were independent risk factors for development of first-onset CHF in dogs with DMVD (NT-proBNP ≥1500 pmol/L, odds ratio (OR), 5.76, 95% confidence interval (CI), 1.37–24.28, P = 0.017; LVIDd:Ao ≥3, OR, 6.11, 95% CI, 1.09–34.05, P = 0.039).ConclusionsMeasures of left heart size and plasma NT-proBNP concentration independently estimate risk of first-onset of CHF in dogs with DMVD. These parameters can contribute to the management of dogs with DMVD.     

Long-term follow-up after transvenous single coil embolization of patent ductus arteriosus in dogs

Background: Long‐term follow‐up studies after interventional therapy of patent ductus arteriosus (PDA) in dogs are rare. Hypothesis: Transvenous PDA embolization with a single detachable coil is a highly effective method in patients with an angiographically determined PDA ≤ 4.0 mm. Animals: Twenty‐eight dogs with an angiographic PDA ≤ 4.0 mm were included. Methods: Prospective follow‐up study after PDA coil embolization. Results: The median follow‐up time was 792 days (range, 2–3, 248 days). The rate of complete closure demonstrated by Doppler color flow was 54% at day 3 after intervention and the final cumulative rate was 71%. The rate of complete closure was significantly different between small and moderately sized PDA over the study period (P < .0001) and finally was 100 and 50%, respectively. In 16 dogs with complete closure, no recanalization was found. Disappearance of the continuous heart murmur was found in 89% after 3 days, and this increased to a final cumulative rate of 96%. Indexed left ventricular internal diameter in diastole (LVDd‐I) decreased significantly (P < .0001). In the group with moderately sized PDA, a significant difference (P= .0256) was seen in LVDd‐I between patients with and without residual shunt after exclusion of patients with persistent severe mitral valve regurgitation. Conclusion and Clinical Importance: Long‐term follow‐up after single coil embolization showed complete closure in all small PDA but a residual shunt with mild hemodynamic consequences was present in half of the moderately sized PDA.