Overview of Equine Cardiac Disease.

Equine heart diseases can be categorized with morphologic, etiologic, and physiologic diagnoses and classified anatomically as diseases of the pericardium, myocardium, valves (endocardium), and great vessels. An appreciation of normal and pathologic physiology is a key to understanding diagnosis and therapy of heart disease. Pathophysiologic diagnoses include arrhythmias, congestive heart failure, and pulmonary hypertension. Heart rhythm disturbances can occur in isolation or with structural disease. Heart failure stems from arterial filling owing to insufficient cardiac output. Pulmonary hypertension is associated with strenuous exercise, left heart failure, bronchopulmonary diseases, and pulmonary arteriopathies. The etiopathogenesis of these disorders are incompletely understood.

Bilateral lysis of aortic saddle thrombus with early tissue plasminogen activator (BLASTT): a prospective, randomized, placebo-controlled study in feline acute aortic thromboembolism.

OBJECTIVES: The aim of this study was to investigate the impact of tissue plasminogen activator (TPA) on the treatment of feline aortic thromboembolism (FATE). METHODS: Cats diagnosed with FATE involving ⩾2 limbs were enrolled in a prospective, multicenter, double-blinded, randomized, placebo-controlled study within 6 h of an event. Diagnosis was made by clinical findings and one confirmatory criterion. Cats received placebo or TPA (1 mg/kg/h with the first 10% by bolus). All cats received pain control and thromboprophylaxis. The primary outcome was a change from baseline in a published limb score at 48 h. Secondary outcomes included 48 h survival, survival to discharge and complication proportions. Statistical analyses included pattern-mixture models, logistic regression and Fisher's exact, Student's t- and Mann-Whitney-Wilcoxon tests. RESULTS: Based on a power analysis, 40 cats were enrolled; however, only 20 survived to 48 h (TPA, n = 12; placebo, n = 8 [P = 0.34]). There was a statistically significant improvement in limb scores compared with baseline for both groups (P <0.001). Limb score at 48 h was 1 point lower (better) in the TPA group (P = 0.19). Thrombolysis had no statistically significant effect on 48 h survival (P = 0.22). Lower affected limb lactate was associated with better 48 h survival (odds ratio 1.53, 95% confidence interval 1.08-2.17; P = 0.02). The survival to discharge rates were 45% (TPA) and 30% (placebo; P = 0.51). Complications in the TPA and placebo groups included acute kidney injury (22% and 19%, respectively; P = 1.00) and/or reperfusion injuries (33% and 19%, respectively; P = 0.45). CONCLUSIONS AND RELEVANCE: Survival and complication rates of acute FATE were not different with or without thrombolysis. High in-hospital mortality decreased the statistical power to detect a statistically significant difference between treatments with regard to our primary outcome.

Detrimental effects of thyroid hormone analog DITPA in the mouse heart: increased mortality with in vivo acute myocardial ischemia-reperfusion.

There is emerging evidence that treatment with thyroid hormone (TH) can improve postischemic cardiac function. 3,5-Diiodothyropropionic acid (DITPA), a TH analog, has been proposed to be a safer therapeutic agent than TH because of its negligible effects on cardiac metabolism and heart rate. However, conflicting results have been reported for the cardiac effects of DITPA. Importantly, recent clinical trials demonstrated no symptomatic benefit in patients with DITPA despite some improved hemodynamic and metabolic parameters. To address these issues, dose-dependent effects of DITPA were investigated in mice for baseline cardiovascular effects and postischemic myocardial function and/or salvage. Mice were treated with subcutaneous DITPA at 0.937, 1.875, 3.75, or 7.5 mg·kg(-1)·day(-1) for 7 days, and the results were compared with untreated mice for ex vivo and/or in vivo myocardial ischemia-reperfusion (I/R). DITPA had no effects on baseline body temperature, body weight, or heart rate; however, it mildly increased blood pressure. In isolated hearts, baseline contractile function was significantly impaired in DITPA-pretreated mice; however, postischemic recovery was comparable between untreated and DITPA-treated groups. In vivo baseline cardiac parameters were significantly affected by DITPA, with increased ventricular dimensions and decreased contractile function. Importantly, DITPA-treated mice demonstrated high prevalence of fatal cardiac rhythm abnormalities during in vivo ischemia and/or reperfusion. There were no improvements in myocardial infarction and postischemic fractional shortening with DITPA. Myocardial sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA), phospholamban (PLB), and heat shock protein (HSP) levels remained unchanged with DITPA treatment. Thus DITPA administration impairs baseline cardiac parameters in mice and can be fatal during in vivo acute myocardial I/R.

Effects of pimobendan on left atrial transport function in cats.

BACKGROUND: Arterial thromboembolism is a sequela of hypertrophic cardiomyopathy (HCM) in cats related to left atrial (LA) enlargement and dysfunction. HYPOTHESIS: Pimobendan improves LA transport function in cats. ANIMALS: Twenty-two client-owned cats with HCM and 11 healthy cats. METHODS: Prospective, double-blind, randomized, placebo-controlled clinical cohort study. Cats were randomized to receive either pimobendan (0.25 mg/kg PO q12h) or placebo for 4 to 7 days. Nineteen echocardiographic variables of LA size and function were evaluated. Statistical comparisons included t tests, analysis of variance, and multivariable analyses. RESULTS: Peak velocity of left auricular appendage flow (LAapp peak; mean ± SD, 0.85 ± 0.20 vs 0.71 ± 0.22 m/s; P = .01), maximum LA volume (P = .03), LA total emptying volume (P = .03), peak velocity of late diastolic transmitral flow (A peak velocity; 0.77 ± 0.12 vs 0.62 ± 0.17 m/s; P = .05), and A velocity time integral (A VTI; 3.05 ± 0.69 vs 3.37 ± 0.49; P = .05) were increased after pimobendan. Mean change after pimobendan was larger in cats with HCM compared to healthy cats for LA fractional shortening (2.1% vs -2.1%; P = .05), A VTI (0.58 vs 0.01 cm; P = .01), LAapp peak (0.20 vs 0.02 m/s; P = .02), LA kinetic energy (3.51 vs -0.10 kdynes-cm; P = .05), and LA ejection force (1.93 vs -0.07 kdynes; P = .01) in the multivariable model. The stronger effect of pimobendan in cats with HCM was independent of LA size. CONCLUSIONS AND CLINICAL IMPORTANCE: We identified positive, albeit minor, effects of pimobendan on LA function in cats with HCM. Whether or not treatment with pimobendan decreases the risk of cardiogenic embolism deserves further study.

Detection of congestive heart failure by Doppler echocardiography in cats with hypertrophic cardiomyopathy.

BACKGROUND: Left-sided congestive heart failure (CHF) is characterized by increased filling pressures and related Doppler echocardiographic (DE) filling patterns. HYPOTHESIS: Doppler echocardiographic variables of left ventricular filling derived from transmitral flow, pulmonary vein flow, and tissue Doppler can be used to detect CHF in cats with hypertrophic cardiomyopathy (HCM). ANIMALS: Forty-seven client-owned cats. METHODS: Prospective clinical cohort study. Cats underwent physical examination, thoracic radiography, analysis of N-terminal pro-brain natriuretic peptide (NT-proBNP), and transthoracic echocardiography and were divided into 3 age-matched groups: Group 1 (apparently healthy control), Group 2 (preclinical HCM), and Group 3 (HCM and CHF). Measured and calculated variables included respiratory rate, DE estimates, serum NT-proBNP concentration, and radiographic CHF score. Groups were compared using ANOVA, and receiver operating characteristic (ROC) curve and multivariate analyses were used to identify diagnostic cutoffs for the detection of CHF. RESULTS: Fifteen cats were in Group 1, 17 in Group 2, and 15 in Group 3. The ROC analysis indicated that the ratio of peak velocity of early diastolic transmitral flow to peak velocity of late diastolic transmitral flow (area under the curve [AUC], 1.0; diagnostic cutoff, 1.77; P = .001), ratio of left atrial size to aortic annular dimension (AUC, 0.91; diagnostic cutoff, 1.96; P = .003), left atrial diameter (AUC, 0.89; cutoff, 18.5 mm; P = .004), diastolic functional class (AUC, 0.89; cutoff, class 2; P = .005), respiratory (AUC, 0.79; cutoff, 36 breaths per minute [brpm]; P = .02), and the ratio of the peak velocity of fused early and late transmitral flow velocities to the peak velocity of the fused early and late diastolic tissue Doppler waveforms (AUC, 0.74; cutoff, 15.1; P = .05) performed best for detecting CHF. CONCLUSIONS AND CLINICAL IMPORTANCE: Various DE variables can be used to detect CHF in cats with HCM. Determination of the clinical benefit of such variables in initiating treatments and assessing treatment success needs further study.

Evaluation of a commercial ultrasonographic hemodynamic recording system for the measurement of cardiac output in dogs.

OBJECTIVE: To evaluate the accuracy of a commercial ultrasonographic cardiac output (CO) monitoring system (UCOMS) in anesthetized Beagles as assessed by comparison with thermodilution CO (TDCO). ANIMALS: 8 healthy anesthetized Beagles. PROCEDURES: Simultaneous UCOMS and TDCO measurements of CO were obtained during 4 hemodynamic states: baseline anesthesia (0.5% to 1.5% isoflurane), a higher depth of anesthesia (2% to 3.5% isoflurane) to yield a >or= 15% reduction in systolic arterial blood pressure, IV infusion of colloidal solution to a mean right atrial pressure of >or= 15 mm Hg, and IV infusion of dobutamine at 5 microg/kg/min. Measurements were obtained at 2 probe positions: the subxiphoid region and the right thoracic inlet. Correlation and agreement of results between methods were determined via linear regression analysis and Bland-Altman plots. RESULTS: A significant positive correlation was detected between UCOMS andTDCO measurements obtained at the subxiphoid (R = 0.86) and thoracic inlet (R = 0.83) positions. Bland-Altman plots revealed minimal bias between methods (bias +/- SD, -0.03 +/- 0.73 L/min and -0.20 +/- 0.80 L/min for subxiphoid and thoracic inlet measurements, respectively). However, the percentage error associated with UCOMS measurements made at the 2 positions was > 45%. CONCLUSIONS AND CLINICAL RELEVANCE: When compared with the results of TDCO, CO measured with the UCOMS exceeded commonly accepted limits of error in healthy dogs. The UCOMS was, however, able to track changes in CO across hemodynamic states. Additional research is needed to assess the usefulness of the UCOMS for monitoring CO in critically ill dogs.

Thrombolysis with tissue plasminogen activator (TPA) in feline acute aortic thromboembolism: a retrospective study of 16 cases.

OBJECTIVES: Thrombolytic therapy is a treatment of choice for people with acute ischemic events, but is uncommonly administered for feline aortic thromboembolism (FATE). This study reports selected clinical data and outcomes of acute FATE treated with tissue plasminogen activator (TPA). A reference group treated with current standard of care (SOC) was analyzed for comparison. METHODS: This was a retrospective study of FATE in two academic hospitals. TPA-treated cats with two or more limbs (n = 16) affected were compared with a SOC-treated group with two or more limbs affected (n = 38). A limb score based on motor function and pulse quality was calculated for each group. RESULTS: Limb score and proportion of congestive heart failure at admission was similar in both groups. Time from FATE to admission was shorter in the TPA group, with a median of 3 h (range 0-6 h) vs 6 h (range 0-48 h; P = 0.0004). The most common regimen received for TPA was 1 mg/kg over 1 h. Other treatments were similar to those of the SOC group and included analgesia, thromboprophylaxis and furosemide. Documented complications for TPA-treated cats included reperfusion injury (5/10) and acute kidney injury (AKI; 3/10). Discharge proportion rate was 44% (TPA) vs 29% (SOC; P = 0.351). There were no differences in short-term survival rate (56.2% vs 39.5%; P = 0.369), clinical improvement (56.2% vs 31%; P = 0.122), rates of reperfusion injury (50% vs 50%; P = 1.00) or AKI (30% vs 27%; P = 1.00) between the TPA-treated and SOC groups, respectively. CONCLUSIONS AND RELEVANCE: Survival and complication rates of TPA-treated cats and SOC-treated cats for acute FATE were similar.

ACVIM consensus guidelines for the diagnosis and treatment of myxomatous mitral valve disease in dogs.

This report, issued by the ACVIM Specialty of Cardiology consensus panel, revises guidelines for the diagnosis and treatment of myxomatous mitral valve disease (MMVD, also known as endocardiosis and degenerative or chronic valvular heart disease) in dogs, originally published in 2009. Updates were made to diagnostic, as well as medical, surgical, and dietary treatment recommendations. The strength of these recommendations was based on both the quantity and quality of available evidence supporting diagnostic and therapeutic decisions. Management of MMVD before the onset of clinical signs of heart failure has changed substantially compared with the 2009 guidelines, and new strategies to diagnose and treat advanced heart failure and pulmonary hypertension are reviewed.

Estimation of left ventricular filling pressure by use of Doppler echocardiography in healthy anesthetized dogs subjected to acute volume loading.

OBJECTIVE: To identify Doppler echocardiographic (DE) variables that correlate with left ventricular filling pressure (LVFP). ANIMALS: 7 healthy dogs (1 to 3 years old). PROCEDURES: Dogs were anesthetized and instrumented to measure left atrial pressure (LAP), left ventricular pressures, and cardiac output. Nine DE variables of LVFP derived from diastolic time intervals, transmitral and pulmonary venous flow, and tissue Doppler images were measured over a range of hemodynamic states induced by volume loading and right atrial pacing. Associations between simultaneous invasive measures of LVFP and DE measures of LVFP were determined by use of regression analysis. Receiver operating characteristic analysis was used to predict increases in mean LAP on the basis of DE variables. RESULTS: Mean LAP was correlated with several DE variables: the ratio between peak velocity during early diastolic transmitral flow and left ventricular isovolumic relaxation time (peak E:IVRT) during sinus rhythm and during right atrial pacing, IVRT, the ratio between late diastolic transmitral flow velocity and pulmonary venous flow duration, and the interval between onset of early diastolic mitral annulus motion and onset of early diastolic transmitral flow. Cutoff values of 2.20 and 2.17, for peak E:IVRT in dogs with sinus rhythm and atrial pacing predicted increases in mean LAP (> or = 15 mm Hg) with sensitivities of 90% and 100% and specificities of 92% and 100%, respectively. CONCLUSIONS AND CLINICAL RELEVANCE: Doppler echocardiography can be used to predict an increase in LVFP in healthy anesthetized dogs subjected to volume loading.

Acquired pulmonary artery stenosis in four dogs.

CASE DESCRIPTION: 4 dogs with acquired pulmonary artery stenosis (PAS) were examined for various clinical signs. One was a mixed-breed dog with congenital valvular PAS that subsequently developed peripheral PAS, one was a Golden Retriever with pulmonary valve fibrosarcoma, one was a Pembroke Welsh Corgi in which the left pulmonary artery had inadvertently been ligated during surgery for correction of patent ductus arteriosus, and one was a Boston Terrier with a heart-base mass compressing the pulmonary arteries. CLINICAL FINDINGS: All 4 dogs were evaluated with 2-dimensional and Doppler echocardiography to characterize the nature and severity of the stenoses; other diagnostic tests were also performed. TREATMENT AND OUTCOME: The mixed-breed dog with valvular and peripheral PAS was euthanized, surgical resection of the pulmonic valve mass was performed in the Golden Retriever, corrective surgery was performed on the Pembroke Welsh Corgi with left pulmonary artery ligation, and the Boston Terrier with the heart-base mass was managed medically. CLINICAL RELEVANCE: Acquired PAS in dogs may manifest as a clinically silent heart murmur, syncope, or right-sided heart failure. The diagnosis is made on the basis of imaging findings, particularly results of 2-dimensional and Doppler echocardiography. Treatment may include surgical, interventional, or medical modalities and is targeted at resolving the inciting cause.

Ischemic necrosis of the digits and hyperlipidemia associated with atherosclerosis in a Miniature American Shepherd.

CASE DESCRIPTION A 2.5-year-old 12-kg (26.4-lb) castrated male Miniature American Shepherd was referred because of a 3-week history of a localized crusted skin lesion on the digital pad of digit 3 of the right hind limb. CLINICAL FINDINGS Skin lesions were noted on the digital pads of the right hind limb. Serum biochemical analyses indicated severe hypercholesterolemia and hypertriglyceridemia. Ultrasonography of the terminal portion of the aorta and other major arterial vessels revealed substantial arteriosclerotic change. TREATMENT AND OUTCOME Medical treatments included administration of atorvastatin calcium, a low-fat diet, and omega-3 fatty acids to reduce serum lipids concentration; clopidogrel to prevent thrombosis; pentoxifylline to improve microcirculatory blood flow; clomipramine hydrochloride and trazodone hydrochloride to help with the behavioral problems; and gabapentin to help with pain management and behavioral problems. Surgical management included amputation of the initial digit involved, then eventually the entire initial limb involved. The response to treatment was poor, and euthanasia was elected. Postmortem findings revealed severe, widespread, and chronic intimal atherosclerosis; mild, widespread, and degenerative changes in the cerebral cortex; and edema and vascular congestion in the meninges. CLINICAL RELEVANCE To the authors' knowledge, this was the first report of skin necrosis secondary to atherosclerosis in a dog. Although the incidence of atherosclerosis has been considered very low in dogs, it should be investigated in dogs with severe hyperlipidemia. Primary hyperlipidemia has not been previously described in Miniature American Shepherd dogs but was the suspected underlying metabolic disorder.

Chronic cardiac resynchronization therapy and reverse ventricular remodeling in a model of nonischemic cardiomyopathy.

While cardiac resynchronization therapy (CRT) has been shown to reduce morbidity and mortality in heart failure (HF) patients, the fundamental mechanisms for the efficacy of CRT are poorly understood. The lack of understanding of these basic mechanisms represents a significant barrier to our understanding of the pathogenesis of HF and potential recovery mechanisms. Our purpose was to determine cellular mechanisms for the observed improvement in chronic HF after CRT. We used a canine model of chronic nonischemic cardiomyopathy. After 15 months, dogs were randomized to continued RV tachypacing (untreated HF) or CRT for an additional 9 months. Six minute walk tests, echocardiograms, and electrocardiograms were done to assess the functional response to therapy. Left ventricular (LV) midmyocardial myocytes were isolated to study electrophysiology and intracellular calcium regulation. Compared to untreated HF, CRT improved HF-induced increases in LV volumes, diameters and mass (p<0.05). CRT reversed HF-induced prolongations in LV myocyte repolarization (p<0.05) and normalized HF-induced depolarization (p<0.03) of the resting membrane potential. CRT improved HF-induced reductions in calcium (p<0.05). CRT did not attenuate the HF-induced increases in LV interstitial fibrosis. Using a translational approach in a chronic HF model, CRT significantly improved LV structure; this was accompanied by improved LV myocyte electrophysiology and calcium regulation. The beneficial effects of CRT may be attributable, in part, to improved LV myocyte function.

Echocardiographic evidence of left atrial mechanical dysfunction after conversion of atrial fibrillation to sinus rhythm in 5 horses.

BACKGROUND: Atrial contractile dysfunction occurs in some species after conversion of atrial fibrillation (AF) to normal sinus rhythm (NSR) but has not been reported in horses with naturally occurring AF. HYPOTHESIS: Transthoracic echocardiography allows detection of left atrial (LA) mechanical dysfunction in horses after conversion of AF to NSR. ANIMALS: Five Standardbreds with AF and 6 healthy Standardbreds of similar age, weight, and athletic condition were included in this study. METHODS: Four horses were treated pharmacologically (quinidine), and 1 horse was treated by means of transvenous electrical cardioversion. Echocardiographic examinations were performed in normal horses (once) and in AF horses (24 hours and 72 hours after conversion to NSR) by means of 2-dimensional echocardiography (2DE), transmitral flow Doppler, and tissue Doppler imaging (TDI) techniques. Echocardiographic indices of LA mechanical function were compared between normal horses and AF horses. RESULTS: Two-dimensional echocardiography and TDI indices of LA mechanical function revealed significant decreases in LA contractile function and LA reservoir function 24 hours after cardioversion. This decrease was no longer statistically significant 72 hours after cardioversion, but changes in echocardiographic variables between 24 and 72 hours varied among horses. CONCLUSIONS AND CLINICAL IMPORTANCE: LA contractile dysfunction can be evaluated in horses by use of 2DE, transmitral Doppler flow velocity profiles, and analyses of LA wall motion by TDI. The results of this study are consistent with AF-induced atrial remodeling, although residual treatment effects or influence of underlying primary myopathy cannot be excluded.

Atrial, SA nodal, and AV nodal electrophysiology in standing horses: normal findings and electrophysiologic effects of quinidine and diltiazem.

BACKGROUND: Although atrial arrhythmias are clinically important in horses, atrial electrophysiology has been incompletely studied. HYPOTHESES: Standard electrophysiologic methods can be used to study drug effects in horses. Specifically, the effects of diltiazem on atrioventricular (AV) nodal conduction are rate-dependent and allow control of ventricular response rate during rapid atrial pacing in horses undergoing quinidine treatment. ANIMALS: Fourteen healthy horses. METHODS: Arterial blood pressure, surface electrocardiogram, and right atrial electrogram were recorded during sinus rhythm and during programmed electrical stimulation at baseline, after administration of quinidine gluconate (10 mg/kg IV over 30 minutes, n = 7; and 12 mg/kg IV over 5 minutes followed by 5 mg/kg/h constant rate infusion for the remaining duration of the study, n = 7), and after coadministration of diltiazem (0.125 mg/kg IV over 2 minutes repeated every 12 minutes to effect). RESULTS: Quinidine significantly prolonged the atrial effective refractory period, shortened the functional refractory period (FRP) of the AV node, and increased the ventricular response rate during atrial pacing. Diltiazem increased the FRP, controlled ventricular rate in a rate-dependent manner, caused dose-dependent suppression of the sinoatrial node and produced a significant, but well tolerated decrease in blood pressure. Effective doses of diltiazem ranged from 0.125 to 1.125 mg/kg. CONCLUSIONS AND CLINICAL IMPORTANCE: Standard electrophysiologic techniques allow characterization of drug effects in standing horses. Diltiazem is effective for ventricular rate control in this pacing model of supraventricular tachycardia. The use of diltiazem for rate control in horses with atrial fibrillation merits further investigation.

Methods and reliability of echocardiographic assessment of left atrial size and mechanical function in horses.

OBJECTIVE: To assess the feasibility, describe the techniques, and determine the reliability of transthoracic echocardiography for characterization of left atrial (LA) size and LA mechanical function in horses. ANIMALS: 6 healthy adult horses. PROCEDURES: Repeated echocardiographic examinations were performed independently by 2 observers in standing, unsedated horses by use of 2-dimensional echocardiography, pulsed-wave flow Doppler, and tissue Doppler imaging (TDI) techniques. Test reliability was determined by estimating measurement variability, within-day interobserver variability, and between-day inter- and intraobserver variability of all echocardiographic variables. Variability was expressed as the coefficient of variation (CV) and the absolute value below which the difference between 2 measurements will lie with 95% probability. RESULTS: Most echocardiographic variables of LA size had low overall variability (CV, < 15%). Among the 2-dimensional indices of LA mechanical function, area-based and volume-based ejection phase indices had moderate between-day variability (CV usually < 25%). Transmitral Doppler flow indices were characterized by low to high between-day variability (CV, 6% to 35%). The TDI wall motion velocities had high between-day variability (CV, > 25%), whereas most TDI-derived time intervals had low variability (CV, < 15%). CONCLUSIONS AND CLINICAL RELEVANCE: LA size and mechanical function can be reliably assessed in standing, unsedated horses by use of 2-dimensional echocardiography, transmitral blood flow velocity profiles, and analyses of LA wall motion by use of TDI. These results may provide useful recommendations for echocardiographic assessment of LA size and function in horses.

Cutting balloon and high-pressure balloon dilation for palliative treatment of congenital double-chambered right ventricle and primary infundibular stenosis in a Golden retriever dog.

Combined cutting balloon and high-pressure balloon dilation was performed in a dog with a double-chambered right ventricle and severe infundibular stenosis of the right ventricular outflow tract. The peak systolic pressure gradient across the stenosis decreased by 65% after dilation (from 187 mmHg before to 66 mmHg after) affirming the intervention as successful. However, early re-stenosis occurred within 3 months leading to exercise intolerance, exercise-induced syncope, and right-sided congestive heart failure. Cutting balloon followed by high-pressure balloon dilation provided temporary but not long-term relief of right ventricular obstruction in this dog.

Quantification of myocardial stiffness using magnetic resonance elastography in right ventricular hypertrophy: initial feasibility in dogs.

INTRODUCTION: Myocardial stiffness is an important determinant of cardiac function and is currently invasively and indirectly assessed by catheter angiography. This study aims to demonstrate the feasibility of quantifying right ventricular (RV) stiffness noninvasively using cardiac magnetic resonance elastography (CMRE) in dogs with severe congenital pulmonary valve stenosis (PVS) causing RV hypertrophy, and compare it to remote myocardium in the left ventricle (LV). Additionally, correlations between stiffness and selected pathophysiologic indicators from transthoracic echocardiography (TTE) and cardiac magnetic resonance imaging were explored. METHODS: In-vivo CMRE was performed on nine dogs presenting severe congenital PVS using a 1.5T MRI scanner. T1-MOLLI, T2-prepared-bSSFP, gated-cine GRE-MRE and LGE (PSIR) sequences were used to acquire a basal short-axis slice. RV and LV-free-wall (FW) stiffness measurements were compared against each other and also correlated to ventricular mass, RV and LV FW thickness, T1 and T2 relaxation times, and extracellular volume fraction (ECV). Peak transpulmonary pressure gradient and myocardial strain were also acquired on eight dogs by TTE and correlated to RV-FW systolic stiffness. Potential correlations were evaluated by Spearman's rho (rs). RESULTS: RV-FW stiffness was found to be significantly higher than the LV-FW stiffness both during end-systole (ES) (p=0.002) and end-diastole (ED) (p=0.029). Significant correlations were observed between RV-FW ES and LV-FW ED stiffness versus ECV (rs=0.75; p-value=0.05). Non-significant moderate correlations were found between LV-FW ES (rs=0.54) and RV-FW ED (rs=0.61) stiffness versus ECV. Furthermore, non-significant correlations were found between RV or LV-FW stiffness and the remaining variables (rs<0.54; p-value>0.05). CONCLUSION: This study demonstrates the feasibility of determining RV stiffness. The positive correlations between stiffness and ECV might indicate some interdependence between stiffness and myocardial extracellular matrix alterations. However, further studies are warranted to validate our initial observations.

Tei index of myocardial performance applied to the right ventricle in normal dogs.

Right ventricular (RV) dysfunction is a cause of exercise intolerance, hypotension, syncope, and heart failure in dogs with cardiac and respiratory disorders. The study objective was to determine Doppler-derived reference values that reflect global RV function in healthy dogs. We measured systolic time intervals and an RV index of myocardial performance (IMP) in 45 healthy dogs between 8 months and 8 years of age. Pulsed-wave Doppler recordings of mitral, tricuspid, aortic, and pulmonic were acquired. Pre-ejection period (PEP), ejection time (ET), PEP/ET, and IMP were determined for both ventricles by separate cardiac cycles. Compared to the mean left ventricular (LV) IMP (0.410; 95% confidence intervals [CI] 0.378-0.442), mean RV IMP (0.250; 95% CI 0.222-0.278) was significantly smaller, and mean ET for the RV (187 millisecond [ms]; 95% CI 182-192) was significantly longer than the LV (173 ms; 95% CI 168-179). A clinically relevant correlation was not found among RV IMP and body weight, heart rate, RV ET, RV PEP, or RV PEP/ET. Calculation of LV IMP with 2 separate sample volumes yielded smaller values than from a single sample volume, with a difference in means of 0.040. We conclude that the RV IMP is relatively independent of body weight and heart rate within the ranges studied and is consistently lower than values derived from the LV in healthy dogs. This study provides additional reference values for RV function in dogs and may be useful for identification of RV dysfunction in dogs.

Effects of diltiazem on hemodynamic variables and ventricular function in healthy horses.

Quinidine is effective for treatment of atrial fibrillation (AF) in horses, but often accelerates ventricular response rate. Diltiazem effectively controls heart rate response to AF in other species. This investigation determined the effects of diltiazem on cardiac rate and rhythm, left ventricular (LV) function, central hemodynamics, and peripheral blood flow in normal, standing, nonsedated horses. A dose-finding study was performed. Afterward, 8 healthy horses were treated with diltiazem IV every 30 minutes to achieve cumulative dosages of 0 (saline control), 1, 1.5, and 2 mg/kg. Plasma diltiazem concentration, heart rate and rhythm (by electrocardiography), LV function and central hemodynamics (by cardiac catheterization), LV dimensions (by echocardiography), and forelimb blood flow (by Doppler sonography) were determined during each treatment period. Diltiazem plasma concentrations between 390 and 910 ng/mL were achieved, with considerable variation among horses. Cardiac effects of diltiazem included intermittent depression of the sinus and atrioventricular (AV) nodes and mild impairment of systolic and diastolic LV function. Vascular effects of diltiazem included arterial vasodilatation, increased limb blood flow, and decreased systemic vascular resistance. Baroreceptor reflex-mediated sympathetic activation increased sinus node rate and presumably blunted the depressive effects of diltiazem on myocardial and nodal tissues. Two horses developed transient high-grade sinus arrest with severe systemic hypotension. Diltiazem appears relatively safe in healthy horses, but dosage may be limited by hypotension from vasodilatation and direct suppression of sinus node discharge. Because of its inhibitory effects on AV nodal conduction, diltiazem may prove useful for heart rate control in horses with AF.

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.