Pulmonary hypertension in canine degenerative mitral valve disease

Pulmonary hypertension secondary to degenerative mitral valve disease has been recognized clinically for many years in veterinary medicine, and clinical diagnosis of this syndrome in dogs has been enhanced greatly by widespread use of echocardiography and Doppler echocardiography. Medical therapy is now available to treat this clinical complication of mitral valve disease, making timely diagnosis even more important to patient longevity and quality of life.     

Neurohormonal activation in canine degenerative mitral valve disease: implications on pathophysiology and treatment

Neurohormonal systems play a critical role in canine degenerative mitral valve disease (DMVD). DMVD results in mitral regurgitation, which reduces forward cardiac output and increases intracardiac pressures. These changes trigger neurohormonal responses that ultimately result in maladaptive cardiac remodelling, congestion and heightened morbidity and mortality. Medical therapies such as ACE inhibitors and spironolactone derive their benefit by interrupting or suppressing these neurohormonal responses. Thus, knowledge of neurohormonal mechanisms can lead to a better understanding of how to treat DMVD.     

New insights into degenerative mitral valve disease in dogs.

Degenerative mitral valve disease (DMVD) is the most common cardiac disease in dogs. Although the disease is frequently described in the veterinary literature, many aspects are still unknown or controversial. Based on recent research findings, this article addresses the etiology, pathogenesis, inheritance, diagnosis of early DMVD, diagnosis of mild decompensated heart failure, and efficacy of early medical intervention in clinically compensated dogs.     

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.     

Echocardiographic estimation of mean left atrial pressure in a canine model of acute mitral valve insufficiency

High mean left atrial pressure (MLAP) due to canine degenerative mitral valve disease is associated with clinically relevant morbidity and mortality. The ability to noninvasively measure MLAP would assist in the diagnosis and treatment of disease. Doppler echocardiography allows measurement of early transmitral blood flow (E) and the velocity of the mitral valve annulus (Ea). The ratio of early mitral inflow velocity to early mitral annular velocity (E: Ea) correlates well with MLAP in human subjects. We sought to determine the ability of E: Ea to predict MLAP in dogs with experimentally induced mitral regurgitation. Nine anesthetized purpose-bred dogs underwent placement of a Swan-Ganz catheter into the left atrium and recording of MLAP. Simultaneous transthoracic echocardiographic and hemodynamic studies were performed after acute chordae tendineae rupture and during IV infusion with nitroprusside (2.5-5.0 microg x kg(-1) x min(-1)) or hydralazine (1-1.5 mg/kg). Mitral regurgitant fraction, measured by single-plane angiography and thermodilution, ranged from 17% to 81%. MLAP increased from 5.4 +/- 2.5 mm Hg to 17.4 +/- 9.4 mm Hg after creation of mitral valve regurgitation (MR; P = .018). Forty sets of echocardiographic measurements were obtained from 7 dogs, and E, as well as E: Ea, were linearly related to MLAP. The R2 value for the linear regression equation containing E: Ea as the dependent variable (0.83) was greater than that for E (0.73). The 95% confidence intervals were calculated for predicting MLAP = 20 mm Hg from E:Ea, and E:Ea >9.1 or <6.0 indicated a 95% probability that MLAP was >20 mm Hg or <20 mm Hg, respectively. Echocardiography can be used to predict MLAP in isoflurane-anesthetized dogs with experimentally induced acute mitral valve insufficiency.     

Quantification of mitral valve regurgitation in dogs with degenerative mitral valve disease by use of the proximal isovelocity surface area method

OBJECTIVE: To determine the within-day and between-day variability of regurgitant fraction (RF) assessed by use of the proximal isovelocity surface area (PISA) method in awake dogs with degenerative mitral valve disease (MVD), measure RF in dogs with MVD, and assess the correlation between RF and several clinical and Doppler echocardiographic variables. DESIGN: Prospective study. ANIMALS: 6 MVD-affected dogs with no clinical signs and 67 dogs with MVD of differing severity (International Small Animal Cardiac Health Council [ISACHC] classification). PROCEDURES: The 6 dogs were used to determine the repeatability and reproducibility of the PISA method, and RF was then assessed in 67 dogs of various ISACHC classes. Mitral valve regurgitation was also assessed from the maximum area of regurgitant jet signal-to-left atrium area (ARJ/LAA) ratio determined via color Doppler echocardiographic mapping. RESULTS: Within- and between-day coefficients of variation of RF were 8% and 11%, respectively. Regurgitation fraction was significantly correlated with ISACHC classification and heart murmur grade and was higher in ISACHC class III dogs (mean +/- SD, 72.8 +/- 9.5%) than class II (57.9 +/- 20.1%) or I (40.7 +/- 19.2%) dogs. Regurgitation fraction and left atriumto-aorta ratio, fractional shortening, systolic pulmonary arterial pressure, and ARJ/LAA ratio were significantly correlated. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that RF is a repeatable and reproducible variable for noninvasive quantitative evaluation of mitral valve regurgitation in awake dogs. Regurgitation fraction also correlated well with disease severity. It appears that this Doppler echocardiographic index may be useful in longitudinal studies of MVD in dogs.     

Malformation of the canine mitral valve complex.

Twenty-nine dogs, including 13 Great Danes and 5 German Shepherd Dogs and averaging 7.3 months age, were diagnosed clinically and radiographically as having mitral regurgitation. Alterations of the mitral valve complex included enlarged anulus; short thick leaflets, with an occasional cleft; short and stout or long and thin chordae tendineae; upward malposition of atrophic or hypertrophic papillary muscles; insertion of one papillary muscle directly into one or both leaflets; and diffuse endocardial fibrosis, occasionally with jet lesions in te left atrium. Other cardiac anomalies included dysplasia of the tricuspid valve (5 dogs), patent ductus afteriosus (2 dogs), aortic stenosis (2 dogs), and ventricular septal defect (1 dog).     

An update on treatment and prognostic indicators in canine myxomatous mitral valve disease

Mitral regurgitation caused by myxomatous mitral valve disease is the most common cause for congestive heart failure and cardiac-related mortality in dogs. Typically, it takes several years for the disease to progress from mild, clinically silent myxomatous mitral valve disease to severe disease with signs of congestive heart failure. A proportion of dogs will never progress into congestive heart failure before they die from other causes or old age. Some variables have been shown to be predictive of onset of congestive heart failure and they might be useful to identify dogs that need more frequent monitoring and eventually treatment. Results from several controlled clinical trials are available concerning medical treatment of dogs with myxomatous mitral valve disease with or without congestive heart failure. These trials provide estimates of treatment effects and also allow identification of other variables with prognostic value for the outcome after the onset of congestive heart failure. Use of prognostic variables together with qualitative and quantitative results from clinical drug trials may aid the clinician and owner to plan and decide on optimal management of the myxomatous mitral valve disease dog. The purpose of this article is to review the current knowledge of prognostic variables and therapy for this common condition in dogs.     

Caudal vena cava point-of-care ultrasound in dogs with degenerative mitral valve disease without clinically important right heart disease

ObjectivesCaudal vena cava (CVC) diameter and collapsibility index (CVC_D and CVC_CI) have been used to assess intravascular volume status (IVS). Maladaptations with progressive degenerative mitral valve disease (DMVD) lead to hypervolemia. We hypothesised that stages of DMVD will affect ultrasonographic CVC variables in dogs without clinically important right heart disease.Animals, materials and methodsThis retrospective study included 79 dogs with DMVD presented to the cardiology department between January 2017 and 2019. Subxiphoid views were used to obtain CVC cineloops. By visual inspection, CVC was subjectively scored as flat, normal or fat. Maximal and minimal CVC_D were measured and indexed to aortic diameter (CVC_D-max/Ao and CVC_D-min/Ao); CVC_CI was calculated as (CVC_D-max-CVC_D-min)/CVC_D-max. Fisher's exact and Kruskal–Wallis tests were used to compare CVC variables.ResultsSubjective assessment was associated with American College of Veterinary Internal Medicine (ACVIM) stages (P < 0.001). The proportion of fat CVC was greater in stages C and D. In stage D, CVC_D-max/Ao was larger compared with stages B1, B2 and C (P = 0.002, P = 0.002 and P = 0.035, respectively). In stages C and D, CVC_D-min/Ao was larger compared with B1 (P = 0.016 and P = 0.001) and B2 (P = 0.002 and P < 0.001. In stages C and D, CVC_CI was less than stage B1 (P = 0.016 and P = 0.044) and B2 (P = 0.001 and P = 0.010).ConclusionsIn dogs with DMVD without clinically important right heart disease, CVC variables differ across ACVIM stage. Subjective and objective CVC variables may be used to predict hypervolemia.     

Efficacy and safet of pimobendan in canine heart failure caused by myxomatous mitral valve disease

OBJECTIVES: To evaluate the clinical efficacy and safety of pimobendan by comparing it with ramipril over a six-month period in dogs with mild to moderate heart failure (HF) caused by myxomatous mitral valve disease (MMVD). METHODS: This was a prospective randomised, single-blind, parallel-group trial. Client-owned dogs (n = 43) with mild to moderate HF caused by MMVD were randomly assigned to one of two groups, which received either pimobendan (P dogs) or ramipril (R dogs) for six months. The outcome measures studied were: adverse HF outcome, defined as failure to complete the trial as a direct consequence of HF; maximum furosemide dose (mg/kg/day) administered during the study period; and any requirement for additional visits to the clinic as a direct consequence of HF. RESULTS: Treatment with pimobendan was well tolerated compared with treatment with ramipril. P dogs were 25 per cent as likely as R dogs to have an adverse HF outcome (odds ratio 4.09, 95 per cent confidence interval 1.03 to 16.3, P = 0.046). CLINICAL SIGNIFICANCE: R dogs had a higher overall score and thus may have had more advanced disease than P dogs at baseline (P = 0.04). These results should be interpreted cautiously but such a high odds ratio warrants further investigation.     

Polymorphism,coupling interval and prematurity index in dogs with degenerative mitral valve disease and ventricular arrhythmias

Ventricular arrhythmias (VA) are a recognized concern in dogs with degenerative mitral valve disease (DMVD). The coupling interval (CI) and the prematurity index (PI) have been shown to accurately differentiate between benign and malignant VA in people, where ventricular arrhythmias are known to be associated with an increased risk of development of signs of heart failure or sudden death. In this study, we characterized ventricular arrhythmias in dogs with symptomatic and asymptomatic DMVD. Seventy dogs with naturally-occurring DMVD and ventricular arrhythmias were retrospectively studied. A cross-sectional investigation including dogs with either symptomatic (stages C/D; n?=?41) or asymptomatic (stages B1/B2; n?=?29) DMVD was performed. Electrocardiographic tracings were reviewed to calculate both the CI and PI. In eight dogs these indices were compared with those obtained from both a Holter recording and a standard ECG tracing and no statistical differences were found (CI, p?=?0.97; PI, p?=?0.17). Even though CI and PI were determined in all animals enrolled in the study, VPC characteristics were only compared between symptomatic and asymptomatic dogs when a 24-h Holter recording was available (n?=?49). The PI was different (p?=?0.01) between symptomatic (0.65?±?0.17) and asymptomatic (0.56?±?0.18) dogs, but CI was considered similar (p?=?0.91). Also, the symptomatic dogs had more polymorphic VPC (p?=?0.002) and supraventricular arrhythmias (p?=?0.0002) than the asymptomatic animals. Polymorphism, and repeating patterns of ventricular premature complexes, were characteristics frequently present in overtly symptomatic animals affected by mitral endocardiosis.