Evaluation of coagulation markers in the plasma of healthy cats and cats with asymptomatic hypertrophic cardiomyopathy

BACKGROUND: Thrombosis and arterial thromboembolism are frequent complications of feline cardiomyopathy, especially when associated with left atrial enlargement. Markers of activated coagulation may be used to evaluate the coagulation status of cats with hypertrophic cardiomyopathy (HCM) in relation to left atrial size. OBJECTIVES: The objective of this study was to compare plasma concentrations of thrombin-antithrombin complex (TAT), D-dimer, and fibrin degradation products (FDP) between clinically healthy cats and cats with HCM. Prothrombin time (PT), activated partial thromboplastin time (aPTT), and antithrombin activity were also compared and the association between left atrial (LA) size and coagulation results in cats with HCM was evaluated. METHODS: Blood samples from 19 clinically healthy cats and 20 cats with HCM were obtained. All cats with HCM were asymptomatic and had no signs of heart failure. LA diameter and LA to proximal aortic (Ao) diameter ratio (LA:Ao) were determined by echocardiography. RESULTS: Reference intervals for D-dimer and TAT concentrations in plasma of healthy cats were established as 0.09-0.32 microg/mL and 2.0-20.0 microg/L, respectively. TAT, D-dimer, and FDP concentrations were increased in 5, 3, and 2 cats with HCM, respectively. TAT and D-dimer concentrations, and PT and aPTT were not significantly different between groups. Antithrombin activity was significantly decreased in cats with HCM (P=.03) despite marked range overlap. LA and LA:Ao were not correlated with coagulation results. CONCLUSIONS: Laboratory evidence of hypercoagulability was found in 45% of cats with HCM. Left atrial size was not associated with laboratory evidence of hypercoagulability. Association between coagulation markers and risk of thrombosis has yet to be evaluated in cats with HCM.     

Prominent J wave in cats with hypertrophic cardiomyopathy

The J wave has never been documented in the electrocardiogram (ECG) of cats presenting with hypertrophic cardiomyopathy (HCM). The present study aimed to describe the presence, morphology, amplitude, and duration of J waves in cats with HCM. It included 20 apparently healthy cats and 45 cats diagnosed with HCM based on clinical, echocardiographic, ECG, and radiographic examination. The cats were of different breeds (Persian: 40, domestic short hair: 21, Siamese: 4), ages (6.01 ± 4.34 years), sexes (male: 33, female: 32), and weights (3.30 ± 1.51 kg). The J wave was absent in the ECGs of the healthy population, but was detected in 29 out of 45 cats with HCM (63%). The J waves were observed at the QRS-ST junction in more than one limb lead of the ECG. Only positive deflections with an amplitude ≥0.05 mV were included, as measured by an ECG ruler in three consecutive heart cycles. The J waves were mainly present in leads II (n=20) and III (n=16), with amplitudes of 0.06 ± 0.02 and 0.08 ± 0.03 mV; their mean (± SD) duration was 0.16 ± 0.05 msec in lead II and 0.18 ± 0.05 msec in lead III. They occurred in both notched and slurred morphologies, with the latter being more common. In conclusion, J waves were a common finding in the ECGs of cats with HCM.     

Cardiac troponin I in cats with hypertrophic cardiomyopathy

The molecular structure of cardiac troponin I (cTnI) is highly conserved across mammalian species and assays developed for its measurement in human patients have been validated in a number of veterinary species. A raised concentration of circulating cTnI is a sensitive and specific marker of cardiac myocyte injury. Raised levels have been documented in a variety of cardiac diseases in both human and veterinary patients. This study compared serum cTnI concentrations between 16 cats diagnosed with hypertrophic cardiomyopathy (HCM) using echocardiography and 18 control cats. The results show that cats with HCM have significantly higher concentration of serum cTnI (median 0.95 ng/ml, range 0.2-4.1 ng/ml) than control cats (median <0.2 ng/ml, range <0.2-0.25 ng/ml) [P<0.0001]. Furthermore in cats with cardiomyopathy a weak correlation was found between the thickness of the left ventricular freewall in diastole measured by ultrasound and serum cTnI concentration (r(2)=0.28;P=0.036). These results suggest that measurement of serum cTnI concentration may enable cats with cardiomyopathy to be distinguished from normal cats using the assay described here.     

Pulsed tissue Doppler imaging in normal cats and cats with hypertrophic cardiomyopathy

Myocardial motion was quantified in normal cats (n = 25) and cats with hypertrophic cardiomyopathy (HCM) (n = 23) using the pulsed tissue Doppler imaging (TDI) technique. A physiologic nonuniformity was documented in the myocardial motion of normal cats, which was detected as higher early diastolic velocities, acceleration, and deceleration in the interventricular septum compared with the left ventricular free wall (LVFW). HCM cats exhibited lower early diastolic velocities, acceleration, and deceleration and also prolonged isovolumic relaxation time compared with normal cats. These differences were detected mainly along the longitudinal axis of the heart. A cutoff value of E' in the LVFW along the longitudinal axis >7.2 cm/s discriminated normal from HCM cats with a sensitivity of 92% and a specificity of 87%. The physiologic nonuniformity of myocardial motion during diastole was lost in affected cats. Systolic impairment (decreased late-systolic velocities in most segments along the longitudinal axis and decreased early systolic acceleration in both mitral annular sites) was evident in HCM cats irrespective of the presence of left ventricular outflow tract obstruction and congestive heart failure. Postsystolic thickening was recorded in the LVFW along the longitudinal axis only in affected cats (n = 6) and was another finding indicative of systolic impairment in the HCM of this species. This study identified both diastolic and systolic impairment in cats with HCM compared with normal cats. The study also documents the normal physiologic nonhomogeneity in myocardial motion in cats and the subsequent loss of this feature in the HCM diseased state.     

Colour M-mode tissue Doppler imaging in healthy cats and cats with hypertrophic cardiomyopathy

OBJECTIVES: To determine whether decreased diastolic and systolic myocardial velocity gradient between the endocardium and the epicardium exist in the left ventricle of cats with hypertrophic cardiomyopathy. METHODS: Myocardial velocity gradient and mean myocardial velocities were measured by colour M-mode tissue Doppler imaging in the left ventricular free wall of 20 normal cats and 17 cats with hypertrophic cardiomyopathy. RESULTS: The peak myocardial velocity gradient (sec(-1)) during the first (E1) (5.71+/-1.75 versus 11.38+/-3.1, P<0.001) and second phase (E2) (3.09+/-1.53 versus 7.02+/-3.1, P=0.005) of early diastole and also the maximum early diastolic myocardial velocity gradient (Emax) (6.12+/-2.1 versus 10.76+/-3.2, P<0.001) were reduced in cats with hypertrophic cardiomyopathy compared with normal cats. Peak myocardial velocity gradient during early systole (Se) was lower in affected cats than in normal cats (6.26+/-2.08 versus 8.67+/-2.83, P=0.006). Affected cats had a lower peak mean myocardial velocities (mm/s) during the two isovolumic periods (IVRb and IVCb) compared with normal cats (2.97+/-6.76 versus 12.74+/-5.5 and 22.28+/-9.96 versus 38.65+/-10.1, P<0.001, respectively). CLINICAL SIGNIFICANCE: This study shows that hypertrophic cardiomyopathy cats have decreased myocardial velocity gradient during both diastole and systole and also altered myocardial motion during the two isovolumic periods. Myocardial velocity gradients recorded by colour M-mode tissue Doppler imaging can discriminate between the healthy and diseased myocardium.     

Heart rate and arrhythmia frequency of normal cats compared to cats with asymptomatic hypertrophic cardiomyopathy

ObjectivesTo compare heart rate and arrhythmia frequency and complexity in a normal population of cats to a population of cats with hypertrophic cardiomyopathy (HCM).Animals17 cats with HCM and 15 cats with normal echocardiograms.MethodsResults for echocardiography, electrocardiography, Doppler blood pressure, and 24-h Holter monitoring were compared between groups.ResultsThere was no difference in heart rate between HCM cats and normal cats regardless of modality used. All (17/17) HCM cats had ventricular arrhythmias (geometric mean 124 complexes/24 h) with 82% (14/17) exhibiting complex arrhythmias (couplets, triplets, or ventricular tachycardia). Most (14/15) normal cats had ventricular arrhythmias (geometric mean 4 complexes/24 h), but only 20% (3/15) exhibited complexity. HCM cats had significantly more total ventricular complexes, ventricular premature complexes and accelerated idioventricular rhythm than normal cats (P < 0.0001, P < 0.0001, and P = 0.01, respectively). Eighty eight percent (15/17) of HCM cats had supraventricular arrhythmias (geometric mean 9 complexes/24 h) with 23% (4/17) exhibiting complexity. Sixty percent (9/15) of normal cats had supraventricular arrhythmias (geometric mean 1 complex/24 h) with 13% (2/15) exhibiting complexity. Cats with hypertrophic cardiomyopathy had significantly more supraventricular complexes than normal cats (P = 0.0148).ConclusionCats with asymptomatic HCM have more frequent and complex ventricular and supraventricular arrhythmias than normal cats but do not have different overall heart rates compared to normal cats. Further studies are needed to determine if these arrhythmias are associated with an increased risk of sudden cardiac death or influence long-term survival.     

Immunohistochemistry of atrial and brain natriuretic peptides in control cats and cats with hypertrophic cardiomyopathy

Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are cardiac hormones involved in electrolyte and fluid homeostasis. Our laboratory has investigated the use of ANP and BNP as diagnostic markers of cardiac disease in cats. We hypothesize that the cardiac distribution of ANP and BNP increases in cats with hypertrophic cardiomyopathy (HCM). Accordingly, we evaluated the immunohistochemical distribution of ANP and BNP in hearts of four cats with naturally occurring HCM relative to five healthy controls. Indirect immunoperoxidase was performed with polyclonal immunoglobulin G against feline ANP (1-28) and proBNP (43-56). In control cats, ANP and BNP immunoreactivity was restricted to the atria. Staining for both peptides was most intense adjacent to the endocardial surface. Auricles stained more diffusely than atria for both peptides. The interstitial capillaries and nerve fibers within the heart were positive only for BNP. Atrial immunoreactivity for ANP and BNP was more diffuse and had a less distinctly layered pattern in HCM than in control cats. Ventricular cardiomyocytes of HCM cats were negative for ANP but stained lightly and diffusely for BNP. The capillaries and nerve fibers remained positive for BNP. We conclude that in cats with HCM, the cardiac distribution of ANP and BNP is more diffuse in the atria and that novel expression of BNP in the ventricular cardiomyocytes occurs.     

Evaluation of once daily treatment with cyclosporine for anal furunculosis in dogs

Twenty-four dogs with anal furunculosis were treated with cyclosporine once daily for 13 weeks at dosages of 1.5, 3.0, 5.0 or 7.5 mg/kg, and re-examined after six and 12 months. After 13 weeks the disease in six of the dogs was in remission, 11 were controlled or improved and seven had failed to respond. The response of the dogs given the highest dose was significantly better than the response of the other groups taken together (P < 0.014), and better than the responses of the groups given 1.5 mg/kg and 5 mg/kg (P < 0.05). The dogs improved clinically during the treatment, most rapidly during the first five weeks. Of the six dogs that were in remission after 13 weeks, three relapsed after one, two and six months. The 11 dogs that were improved or controlled after 13 weeks were either left untreated or were continued on cyclosporine medication for one to three months at a dosage of 1.5 to 7.5 mg/kg; the disease went into remission in four cases and remained controlled in the other seven, but four of the 11 cases relapsed during the 12 months following the treatment. The side effects observed included increased coat turnover and transient vomiting.     

Pathology of end-stage remodeling in a family of cats with hypertrophic cardiomyopathy

End-stage hypertrophic cardiomyopathy (ES-HCM), affecting 5-10% of human hypertrophic cardiomyopathy (HCM) patients, is characterized by relative thinning of the ventricular walls and septum with dilation of the ventricular lumen, decreased fractional shortening, and progression to heart failure. C. J. Baty and others recently documented similar progressive changes to ES-HCM in a family of four cats through serial echocardiograms. At the time of heart failure, these cats exhibited changes similar to those exhibited by human ES-HCM patients. Our objectives were to describe the pathologic alterations associated with ES-HCM and investigate the pathogenesis in three of the four cats. Grossly, there was left atrial dilation with relative thinning of the interventricular septum (IVS) and left ventricular free wall (LVFW). The left atrium contained large thrombi in two of the three cats, and all three cats died following thromboembolization of the aortic bifurcation. Histologically, all three cats had subendocardial and myocardial fibrosis, predominantly of the IVS and LVFW, and one cat had acute, multifocal, myocardial infarcts with mononuclear inflammatory cell infiltrates. The pathogenesis of ES-HCM is uncertain, but theories implicate occlusion of the coronary blood flow by thickening of the coronary vessels, coronary vascular thromboembolism or coronary vessel spasm, apoptosis of myocytes, and myocardial hypertrophy beyond the ability of the vasculature to supply blood. Apoptosis assays did not reveal any apoptotic myocytes. Considering the hypercoagulative state of these cats, coronary vascular thromboembolism could be a major contributing factor. We cannot exclude apoptosis or coronary vessel spasm on the basis of the data presented.     

N-terminal atrial natriuretic peptide immunoreactivity in plasma of cats with hypertrophic cardiomyopathy

Atrial natriuretic peptide (ANP) is an important regulator of fluid homeostasis and vascular tone. We sought to compare N-terminal ANP immunoreactivity (ANP-IR) in plasma from cats with and without hypertrophic cardiomyopathy (HCM). Secondarily, we evaluated relationships between ANP-IR and echocardiographical variables in cats with HCM and healthy cats. Venous blood samples were obtained from 17 cats with HCM and from 19 healthy cats. Plasma ANP-IR concentration was determined by an enzyme-linked immunoassay. Two cats with HCM had clinical evidence of congestive heart failure; the remainder had subclinical disease. Plasma ANP-IR concentration was higher in cats with HCM (3,808 +/- 1,406 fmol/L, mean +/- SD) than in control cats (3,079 +/- 1,233 fmol/L), but this difference was not statistically significant (P = .11; 95% confidence interval [CI] = -166 to 1,622). There was a significant, but modest correlation between plasma ANP-IR concentration and left ventricular posterior wall thickness (r = 0.42; P = .01). Additionally, plasma ANP-IR concentration was weakly correlated with left atrial size (r = 0.35; P = .03). A linear regression model was developed to further explore these relationships. Atrial size and wall thickness were included in the model; the 2 explanatory variables had an interactive effect on plasma ANP-IR concentration (R2 = 0.27; P = .02). There was no appreciable correlation between plasma ANP-IR concentration and any other echocardiographical variable. In a population that included cats with subclinical disease, those with HCM did not have significantly higher plasma ANP-IR concentration than did healthy cats. An exploratory multivariable regression analysis suggested a linear relationship between ANP-IR concentration and atrial size, wall thickness, and their interaction.     

Pharmacokinetics of controlled-release carbimazole tablets support once daily dosing in cats

Carbimazole, a prodrug of methimazole, is used in the treatment of hyperthyroidism in cats. The pharmacokinetics of methimazole was investigated in healthy cats following oral administration of 15 mg of carbimazole as a controlled-release tablet (Vidalta^®, Intervet). The controlled-release tablet did not produce a pronounced concentration peak and methimazole was present in the circulation for a sustained period, compared with a conventional tablet formulation. The time to reach peak concentrations after carbimazole administration was quite long (t_max 6 h). The absolute bioavailability of carbimazole was around 88 ± 11%. Repeated oral administration daily for 13 consecutive days did not lead to accumulation of methimazole in plasma. The extent of absorption of carbimazole was about 40% higher when administered to cats that had been fed compared to fasted cats. The relative oral bioavailability of methimazole following administration of the controlled-release tablets was similar to that of a conventional release formulation (83 ± 21%). The pharmacokinetics of this controlled-release formulation of carbimazole supports its use as a once daily treatment (both as a starting dose and for maintenance therapy) for cats with hyperthyroidism.     

Efficacy and safety of once versus twice daily administration of methimazole in cats with hyperthyroidism

OBJECTIVE: To determine whether once daily administration of methimazole was as effective and safe as twice daily administration in cats with hyperthyroidism. DESIGN: Randomized, nonblinded, clinical trial. ANIMALS: 40 cats with newly diagnosed hyperthyroidism. PROCEDURE: Cats were randomly assigned to receive 5 mg of methimazole, PO, once daily (n = 25) or 2.5 mg of methimazole, PO, twice daily (15). A complete physical examination, including measurement of body weight; CBC; serum biochemical analyses, including measurement of serum thyroxine concentration; and urinalysis were performed, and blood pressure was measured before and 2 and 4 weeks after initiation of treatment. RESULTS: Serum thyroxine concentration was significantly higher in cats given methimazole once daily, compared with cats given methimazole twice daily, 2 weeks (3.7 vs 2.0 micro +/- g/dL) and 4 weeks (3.2 vs 1.7 microg/dL) after initiation of treatment. In addition, the proportion of cats that were euthyroid after 2 weeks of treatment was lower for cats receiving methimazole once daily (54%) than for cats receiving methimazole twice daily (87%). Percentages of cats with adverse effects (primarily gastrointestinal tract upset and facial pruritus) were not significantly different between groups. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that once daily administration of methimazole was not as effective as twice daily administration in cats with hyperthyroidism and cannot be recommended for routine use.     

Echocardiography, electrocardiography, and radiography of cats with dilatation cardiomyopathy, hypertrophic cardiomyopathy, and hyperthyroidism

The echocardiographic, ECG, and radiographic findings of sequentially examined cats with dilatation cardiomyopathy (DCM, n = 7), hypertrophic cardiomyopathy (HCM, n = 8), and hyperthyroidism (HT, n = 20) were compared with those of healthy control cats (n = 11). Cats with DCM were easily differentiated from healthy cats by echocardiography and from cats with HCM and HT by a dilated left ventricle at end-diastole with a mean +/- SD of 2.20 +/- 0.36 cm, reduced fractional shortening (2.9% +/- 3.7%), reduced aortic amplitude (0.07 +/- 0.05 cm), reduced left ventricular wall amplitude (0.09 +/- 0.09 cm), and increased E-point septal separation (0.83 +/- 0.29 cm). The cats with HCM were most consistently recognized echocardiographically by increased left ventricular wall thickness at end-diastole (0.75 +/- 0.12 cm). Some cats with HT had abnormal echocardiograms with left ventricular wall hypertrophy. These cats could usually be differentiated from the cats with HCM because of normal or increased ventricular wall amplitude, aortic amplitude, or percentage of thickening of the left ventricular wall and interventricular septum. Left atrial enlargement (left atrial diameter greater than 1.57 cm or left atrium/aorta greater than 1.75) was commonly detected by the echocardiogram in cats with DCM, HCM, or HT. The echocardiogram was helpful in differentiating the type of cardiomyopathy (DCM, HCM, or HT) when plain thoracic radiographs indicated that cardiomegaly existed. The ECG may have indicated incorrectly that there was left ventricular enlargement in some cats with HT, and it did not indicate consistently that left ventricular enlargement existed when present in cats with DCM or HCM. The ECG was a poor indicator of left atrial enlargement in all cats.     

Myocardial collagen deposition and inflammatory cell infiltration in cats with pre-clinical hypertrophic cardiomyopathy

The histological features of feline hypertrophic cardiomyopathy (HCM) have been well documented, but there are no reports describing the histological features in mild pre-clinical disease, since cats are rarely screened for the disease in the early stages before clinical signs are apparent. Histological changes at the early stage of the disease in pre-clinical cats could contribute to an improved understanding of disease aetiology or progression. The aim of this study was to evaluate the histological features of HCM in the left ventricular (LV) myocardium of cats diagnosed with pre-clinical HCM. Clinically healthy cats with normal (n = 11) and pre-clinical HCM (n = 6) were identified on the basis of echocardiography; LV free wall dimensions (LVFWd) and/or interventricular septal wall (IVSd) dimensions during diastole of 6–7 mm were defined as HCM, while equivalent dimensions <5.5 mm were defined as normal. LV myocardial sections were assessed and collagen content and inflammatory cell infiltrates were quantified objectively. Multifocal areas of inflammatory cell infiltration, predominantly lymphocytes, were observed frequently in the left myocardium of cats with pre-clinical HCM. Tissue from cats with pre-clinical HCM also had a higher number of neutrophils and a greater collagen content than the myocardium of normal cats. The myocardium variably demonstrated other features characteristic of HCM, including arteriolar mural hypertrophy and interstitial fibrosis and, to a lesser extent, myocardial fibre disarray and cardiomyocyte hypertrophy. These results suggest that an inflammatory process could contribute to increased collagen content and the myocardial fibrosis known to be associated with HCM.     

Systolic and diastolic myocardial dysfunction in cats with hypertrophic cardiomyopathy or systemic hypertension

BACKGROUND: Hypertrophic cardiomyopathy (HCM) and chronic systemic hypertension (SHT) can both lead to left-ventricular hypertrophy (LVH) in cats. Assessment of LVH-associated myocardial dysfunction could provide new insights in the understanding of the pathophysiology of these diseases. HYPOTHESIS: Quantification of left-ventricular free-wall (LVFW) motion using tissue Doppler imaging (TDI) could permit differentiation of feline HCM from SHT-related LVH (LVH-SHT). ANIMALS: A total of 108 cats of different breeds were enrolled in this study: 35 cats with HCM, 17 with concentric LVH and SHT, and 56 healthy cats as a control group. METHODS: All cats were examined by conventional echocardiography and 2-dimensional color TDI. RESULTS: Radial and longitudinal diastolic LVFW velocities were similarly altered in cats with HCM and LVH-SHT, compared to controls. Systolic velocities were also lower in the groups with hypertrophy than in the controls, for longitudinal but not radial motion. To determine whether these diastolic and systolic alterations could also be observed in cats without LVFW hypertrophy, we performed a subgroup analysis in cats with a normal M-mode examination, that is, with only a localized subaortic interventricular septum hypertrophy. A significant radial and longitudinal diastolic dysfunction was still observed in both the HCM and LVH-SHT groups compared to controls, and systolic dysfunction was detected in the longitudinal motion. CONCLUSIONS: LVFW motion is similarly altered in cats with HCM and LVH-SHT. This dysfunction occurs independently of the presence of myocardial hypertrophy, demonstrating that TDI is capable of detecting systolic and diastolic segmental functional changes in nonhypertrophied wall segments in cats with HCM and SHT.     

Azotemia in cats with feline hypertrophic cardiomyopathy: Prevalence and relationships with echocardiographic variables

ObjectivesThe prevalence of renal azotemia in cats with acquired heart disease is not well documented. The aims of this study were therefore (1) to determine the prevalence of azotemia within a hospital population of cats with hypertrophic cardiomyopathy (HCM), and (2) to evaluate the relationship between echocardiographic variables and plasma urea and creatinine.Animals, materials and methods134 client-owned cats were retrospectively studied including 102 cats with HCM and 32 control cats. A complete physical examination, electrocardiography, systolic arterial blood pressure measurement, thoracic radiographs, and echocardiography were performed. Plasma creatinine and urea were determined in all cats. The animal was considered azotemic if plasma creatinine was >1.8 mg/dL and/or urea >65 mg/dL (i.e. BUN> 30 mg/dL).ResultsThe prevalence of azotemia was lower in control cats (25.0%) than in cats with HCM (58.8%) (P = 0.003). No significant differences in plasma urea and creatinine were observed between the HCM and control cats. There was no effect of plasma creatinine and urea on conventional echocardiographic variables in cats with HCM.ConclusionsAzotemia is a frequent finding in cats with HCM but is not dependent on echocardiographic variables.     

Comparison of myocardial contrast enhancement via cardiac magnetic resonance imaging in healthy cats and cats with hypertrophic cardiomyopathy

OBJECTIVE: To quantify myocardial contrast enhancement (MCE) of the left ventricle (LV) by use of cardiac magnetic resonance imaging (CMRI) in healthy cats and cats with hypertrophic cardiomyopathy (HCM) and to compare MCE between the 2 groups. ANIMALS: 10 healthy cats and 26 Maine Coon cats with moderate to severe HCM but without clinical evidence of congestive heart failure. PROCEDURE: Anesthetized cats underwent gradient echo CMRI examination. Short-axis images of the LV were acquired before and 7 minutes after IV administration of gadolinium dimeglumine. Regions of interest were manually traced in the quadrants of 5 mid-LV slices acquired at end systole, and the MCE percentage was calculated from summed weight-averaged data from all slices. Doppler tissue imaging echocardiography was performed to measure the early diastolic myocardial velocity (Em) as an index of diastolic function. Three-way repeated-measures ANOVA was used to determine differences in MCE between cats with HCM and healthy cats. Simple linear regression was used to assess whether MCE was correlated with LV mass, LV mass index (LVMI), or Em. A Student t test was used to compare the SDs of the postcontrast myocardial signal intensity between the 2 groups. RESULTS: There was no difference in MCE between cats with HCM and healthy cats. There was no correlation of MCE with LV mass, LVMI, or Em. There was no difference in heterogeneity of signal intensities of LV myocardium between the 2 groups. CONCLUSIONS AND CLINICAL RELEVANCE: Contrast-enhancement CMRI was not useful in detecting diffuse myocardial fibrosis in cats with HCM.