Tissue Doppler imaging for detection of radial and longitudinal myocardial dysfunction in a family of cats affected by dystrophin-deficient hypertrophic muscular dystrophy

Diagnosis of feline hypertrophic cardiomyopathy currently is based on the presence of myocardial hypertrophy detected using conventional echocardiography. The accuracy of tissue Doppler imaging (TDI) for earlier detection of the disease has never been described. The objective of this sudy was to quantify left ventricular free wall (LVFW) velocities in cats with hypertrophic muscular dystrophy (HFMD) during preclinical cardiomyopathy using TDI. The study animals included 22 healthy controls and 7 cats belonging to a family of cats with HFMD (2 affected adult males, 2 heterozygous adult females, one 2.5-month-old affected male kitten, and 2 phenotypically normal female kittens from the same litter). All cats were examined via conventional echocardiography and 2-dimensional color TDI. No LVFW hypertrophy was detected in the 2 carriers or in the affected kitten when using conventional echocardiography and histologic examination, respectively. The LVFW also was normal for 1 affected male and at the upper limit of normal for the 2nd male. Conversely, LVFW dysfunction was detected in all affected and carrier cats with HFMD when using TDI. TDI consistently detects LVFW dysfunction in cats with HFMD despite the absence of myocardial hypertrophy. Therefore, TDI appears more sensitive than conventional echocardiography in detecting regional myocardial abnormalities.     

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.     

Natural history of hypertrophic cardiomyopathy and aortic thromboembolism in a family of domestic shorthair cats

A feline domestic shorthair queen and her 3 offspring were all diagnosed with asymptomatic hypertrophic cardiomyopathy (HCM). The family has been followed for 13 years, and 3 cats have died of aortic thromboembolism (ATE). This communication documents the long-term progression of HCM in these cats that presented with mild left ventricular hypertrophy and hyperdynamic systolic ventricular function, developed progressive left atrial enlargement, and eventually resulted in hypodynamic left ventricular systolic function with relative left ventricular chamber dilation at the time of ATE.     

Reference range values of regional left ventricular myocardial velocities and time intervals assessed by tissue Doppler imaging in young nonsedated Maine Coon cats

OBJECTIVE: To describe and analyze the left ventricular free wall (LVFW) radial and longitudinal motions in a population of healthy Maine Coon cats by use of quantitative 2-dimensional color tissue Doppler imaging (TDI). ANIMALS: 23 healthy young Maine Coon cats (mean +/- SD: age, 2.1 +/- 0.9 years; weight, 5.0 +/- 1.0 kg). PROCEDURE: TDI was performed by the same trained observer (VC) on all cats. Radial LVFW velocities were recorded in endocardial and epicardial LVFW segments, and longitudinal velocities were recorded in the mitral annulus and in basal and apical LVFW segments. Isovolumic contraction and relaxation times were calculated in each myocardial segment, and the coefficients of variation (CVs; %) were determined for each TDI parameter. RESULTS: LVFW velocities were significantly higher in the endocardial layers than in the epicardial layers and also significantly higher in the basal than in the apical segments. Annular velocities were significantly higher than basal myocardial velocities in systole and early diastole. Coefficient of variation values were lower for radial velocities, particularly in systole, and were also lower for time intervals (16% to 22%) than for myocardial velocities (19% to 62%). CONCLUSIONS AND CLINICAL RELEVANCE: Because Maine Coon cats are predisposed to an inherited hypertrophic cardiomyopathy, which is a common cause of death in this breed, TDI could provide a useful tool for early detection of the disease. Tissue Doppler imaging indices may complete the conventional analysis of the left ventricular function in Maine Coon cats. However, the usefulness of TDI indices in the early detection of myocardial dysfunction needs to be clarified.     

Hypertropic cardiomyopathy and hyperthyroidism in the cat

In a 21/2-year period, hypertrophic cardiomyopathy was found at necropsy of 23 cats that died (13 cats) or were euthanatized (10) because of problems associated with hyperthyroidism. Of these, 4 (17%) also had evidence of cardiac failure (pulmonary edema or pleural effusion). The mean body weight of the cats with hyperthyroidism and hypertrophic cardiomyopathy was significantly less (P less than 0.001) than that of clinically normal cats and cats with primary cardiomyopathy (congestive or restrictive) or excessive moderator band cardiomyopathy. In addition, the ratio of heart weight to body weight was significantly greater (P less than 0.001) in the 23 hyperthyroid cats than in the normal cats and cats with primary cardiomyopathy. Twenty (87%) of the cats had symmetric hypertrophy of the ventricular septum and left ventricular free wall, whereas the remaining 3 cats had disproportionate thickening of the ventricular septum, compared with the free wall, similar to what is found in cats with asymmetric hypertrophic cardiomyopathy. Histologic cardiac abnormalities included large, hyperchromatic nuclei, interstitial fibrosis, endocardial fibroplasia, fibrosis of the atrioventricular node, and marked disorganization of cardiac muscle cells. The study showed that hypertrophic cardiomyopathy develops in most hyperthyroid cats, some of which also develop congestive heart failure. Although the signs of heart disease in primary myocardial disease and thyrotoxic disease are similar, the characteristic signalment and clinical signs of hyperthyroidism should lead one to suspect the association of hypertrophic cardiomyopathy with the hyperthyroidism.     

猫肥厚型心肌病与心肌纤维化

肥厚型心肌病是猫最常见的原发性心脏疾病,典型特征为心脏左心室肥厚。心肌纤维化是猫肥厚型心肌病的标志性病理变化,其可导致心脏功能障碍和节律异常,是心肌病患猫预后不良的重要因素。对于猫肥厚型心肌病与心肌纤维化,目前缺乏针对性治疗,新型治疗方法亟需开发。本综述总结了猫肥厚型心肌病的病理特征以及目前关于猫心肌纤维化发病机制的研究进展,拟通过探索心肌纤维化的发病机制,从而为猫肥厚型心肌病新型治疗药物的开发寻找突破点。     

Chronic myocardial infarction due to arteriosclerosis of coronary arteries followed by acute thromboembolism of caudal abdominal aorta in a cat

A 10-year-old cat with the paresis of hind limbs was initially diagnosed as a hypertrophic cardiomyopathy followed by acute thromboembolism of caudal abdominal aorta from the findings of the medical examinations. However, this case was proved to be an chronic myocardial infarction due to arteriosclerosis of coronary arteries by the pathologic diagnosis. In the left ventricular, the hypertrophy and the narrowing were slight, and a coagulative infarction was seen obviously. The intramural coronary arteriosclerosis showed thickening of the wall due to medial hyperplasia by fibrosis, and arterial stenosis. Myocardial infarction and arteriosclerosis are scarcely any reports of these lesions in cats. This case is valuable for an extremely rare case of myocardial infarction in the cat.     

Excessive moderator bands in the left ventricle of 21 cats

Excessive numbers of moderator bands bridging the left ventricular septum and free wall and entangling papillary muscles were associated with heart failure and death in 21 cats. Clinical findings included dyspnea, anorexia, hypothermia, cardiomegaly, pleural effusion, plumonary edema, heart murmurs, gallop rhythm, electrocardiographic abnormalities (especially conduction disturbances), increased left ventricular end-diastolic pressure, angiocardiographic evidence of left ventricular restriction, and aortic thromboembolism. Pathologic changes included a morphologically distinct network of abnormal numbers of moderator bands in the left ventricle, left ventricular hypertrophy (younger cats--mean age, 4 years) or dilatation (older cats--mean age, 8.7 years), left atrial enlargement and hypertrophy, and pulmonary edema with heart failure cells in the alveoli. Heart weights of affected cats were significantly less than those of cats with congestive, hypertrophic, and restrictive cardiomyopathy (endocardial fibrosis), but were not significantly less than heart weights of clinically normal cats. Pathologic changes were characteristic of the syndrome grossly and histologically, but clinical findings were not clearly definable.     

Quantitative assessment of velocities of the annulus of the left atrioventricular valve and left ventricular free wall in healthy cats by use of two-dimensional color tissue Doppler imaging

OBJECTIVE: To analyze velocities of the annulus of the left atrioventricular valve and left ventricular free wall (LVFW) in a large population of healthy cats by use of 2-dimensional color tissue Doppler imaging (TDI). ANIMALS: 100 healthy cats (0.3 to 12.0 years old; weighing 1.0 to 8.0 kg) of 6 breeds. PROCEDURE: Radial myocardial velocities were recorded in an endocardial and epicardial segment, and longitudinal velocities were recorded in 2 LVFW segments (basal and apical) and in the annulus of the left atrioventricular valve. RESULTS: LVFW velocities were significantly higher in the endocardial than epicardial layers and significantly higher in the basal than apical segments. For systole, early diastole, and late diastole, mean +/- SD radial myocardial velocity gradient (MVG), which was defined as the difference between endocardial and epicardial velocities, was 2.2 +/- 0.7, 3.3 +/- 1.3, and 1.8 +/- 0.7 cm/s, respectively, and longitudinal MVG, which was defined as the difference between basal and apical velocities, was 2.7 +/- 0.8, 3.1 +/- 1.4, and 2.1 +/- 0.9 cm/s, respectively. A breed effect was documented for several TDI variables; therefore, reference intervals for the TDI variables were determined for the 2 predominant breeds represented (Maine Coon and domestic shorthair cats). CONCLUSIONS AND CLINICAL RELEVANCE: LVFW velocities in healthy cats decrease from the endocardium to the epicardium and from the base to apex, thus defining radial and longitudinal MVG. These indices could complement conventional analysis of left ventricular function and contribute to the early accurate detection of cardiomyopathy in cats.     

Assessment of Left Ventricular Systolic Function by Strain Imaging Echocardiography in Various Stages of Feline Hypertrophic Cardiomyopathy

Background: Diastolic dysfunction occurs in many cats with hypertrophic cardiomyopathy (HCM). Less is known about systolic function in various stages of HCM. Myocardial strain analysis by tissue Doppler imaging (TDI) is a noninvasive echocardiographic method to assess systolic function that has not been reported previously in cats. Objectives: To evaluate systolic function in various stages of feline HCM by measurement of myocardial strain. Animals: Two hundred and sixty‐three cats. Methods: Cats were classified by echocardiography into one of the following groups: clinically healthy (control) group (n = 160), mild HCM (n = 22), moderate HCM (n = 39), and severe HCM (n = 42). Peak myocardial strain, measured by TDI in the basal and midventricular segment of the interventricular septal wall (IVS) and the left ventricular posterior wall (LVPW), was compared among different HCM and control groups. Results: Whereas conventional echocardiography demonstrated an apparently normal or supernormal contractile state based on percentage of fractional shortening, myocardial strain in all HCM groups was significantly decreased compared with the control group (P < .001). There was a significant correlation between strain values and wall thickness (P < .001). Reproducibility of strain analysis was 6.3% in the IVS and 9.7% in the LVPW. Conclusions and Clinical Importance: Myocardial strain analysis is a new, valuable, and reproducible method in cats. This method allows noninvasive detection of abnormal systolic deformation in cats with HCM despite apparently normal left ventricular systolic function as assessed by conventional echocardiography. The abnormal systolic deformation already was present in mild HCM and increased with progressive left ventricular concentric hypertrophy.     

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.     

Hypertrophic cardiomyopathy in an aged dog

A 14-year-old female Yorkshire terrier was presented with the complaint of cardiac murmur and convulsive seizure. Thickened mitral valve, left atrial enlargement, excess motions of the left ventricular (LV) free wall and the ventricular septum, and tricuspid, mitral and aortic valve regurgitations were recognized on echocardiography. Follow-up echocardiography revealed the progression of concentric LV hypertrophy and LV outflow obstruction. Clinical symptoms associated with cardiac failure did not develop during the observation period. The pathological examination of the heart revealed that the dog had the morphological hallmarks of hypertrophic cardiomyopathy: massive ventricular hypertrophy, disorganization of cardiac muscle cells, interstitial myocardial fibrosis, and abnormal intramural coronary arteries.     

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.     

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.     

Use of relaxation half-time as an index of ventricular relaxation in clinically normal cats and cats with hypertrophic cardiomyopathy

Relaxation half-time (t1/2) was evaluated as a measure of isovolumic ventricular relaxation in clinically normal cats and cats with hypertrophic cardiomyopathy. Relaxation half-time was determined directly from the left ventricular pressure tracing as the time required for the left ventricular pressure at the beginning of isovolumic relaxation to decrease by half. The value of t1/2 was unaffected by moderate changes in heart rate, inotropic state, and afterload in clinically normal cats. However, t1/2 increased significantly (P = 0.003) with increased preload. The value of t1/2 was significantly higher (P = 0.0003) in a group of cats with hypertrophic cardiomyopathy, compared with that of a group of clinically normal cats. Although t1/2 must be interpreted in the context of changes in loading conditions, the index is useful as a measure of relaxation in clinically normal cats and cats with hypertrophic cardiomyopathy.     

Tissue Doppler assessment of diastolic and systolic alterations of radial and longitudinal left ventricular motions in Golden Retrievers during the preclinical phase of cardiomyopathy associated with muscular dystrophy

OBJECTIVE: To quantify radial and longitudinal left ventricular free wall (LVFW) velocities in dogs during the preclinical phase of Golden Retriever muscular dystrophy (GRMD)-associated cardiomyopathy by use of tissue Doppler imaging (TDI). ANIMALS: 9 dogs with GRMD and 6 healthy control dogs. PROCEDURE: All dogs (< 3 years old) were examined via conventional echocardiography and 2-dimensional color TDI. Myocardial velocities in the LVFW were recorded from right parasternal ventricular short-axis (radial motion) and left apical 4-chamber (longitudinal motion) views. Cardiac assessments via TDI included maximal systolic and early and late diastolic LVFW velocities in the endocardial and epicardial layers (for radial motion) and in the basal and apical segments (for longitudinal motion) (for longitudinal motion), RESULTS:-No notable ventricular dilatation or alteration of inotropism was detected in dogs with GRMD via conventional echocardiography. Compared with healthy dogs, endocardial velocities were significantly decreased in dogs with GRMD, resulting in marked decreases in radial myocardial velocity gradients during systole and early and late diastole. Similarly, basal and apical velocities were significantly decreased in systole and the former also in early diastole, resulting in significant decreases in the 2 corresponding longitudinal myocardial velocity gradients. The radial epicardial and longitudinal late diastolic velocities were comparable in the 2 groups. CONCLUSION AND CLINICAL RELEVANCE: Results indicated that GRMD-associated cardiomyopathy in dogs is associated with early marked dysfunction of both radial and longitudinal LVFW motions. These combined regional myocardial abnormalities might be useful criteria for detection of dilated cardiomyopathy at the preclinical stage of the disease in dogs.     

Cardiomyopathy in Dystrophin-Deficient Hypertrophic Feline Muscular Dystrophy

A colony of cats affected with hypertrophic feline muscular dystrophy was used to study the occurrence of cardiomyopathy associated with dystrophin deficiency. Affected male and female cats, obligate carrier females, and unaffected healthy littermates were followed from 12 weeks of age into adulthood. Thoracic radiography, 2-D echocardiography, and 2-D-derived M-mode echocardiography were performed at 3-month intervals until 12 months of age and regularly thereafter. From 9 months of age, all affected cats had larger hearts than normal and carrier animals. Left ventricular wall thickness in systole and in diastole and interventricular septal thickness in systole were greater in affected cats 12 months and older when compared with normal or heterozygous animals (P < .05). The myocardium of affected cats was diffusely hypoechoic and thickened. Multiple hyperechoic foci were in the myocardium and papillary musculature. Shortening fraction was normal in all cats. Changes seen in carrier females included enlargement and hyperechogenicity of the papillary musculature after the age of 2 years. Gross and light microscopic examination revealed left ventricular wall thickening with multiple foci of mineralization in 2 of 5 hearts from dystrophin-deficient cats. Although approximately 10% of the normal dystrophin amount was present in the skeletal muscle, dystrophin could not be detected in the myocardium. Early onset concentric myocardial hypertrophy was present in all adult cats. Lesions were mainly localized in the myocardium of the left ventricular free wall and interventricular septum, papillary musculature, and the endocardium. Clinical signs of heart failure developed only infrequently in cats with hypertrophic feline muscular dystrophy.     

Canine hypertrophic cardiomyopathy.

Necropsy findings in 10 dogs with naturally occurring cardiac disease closely resembled hypertrophic cardiomyopathy in human beings and cats. Each dog had marked cardiac hypertrophy, and 8 dogs had disproportionate thickening of the ventricular septum with respect to the left ventricular free wall (compared with dogs with normal hearts or with cardiac hypertrophy due to acquired or congenital heart disease). Ratios of septum to free wall thickness in the 10 dogs ranged from 1.1 to 1.5, and 6 had ratios greater than or equal to 1.3. Marked cardiac muscle cell disorganization in the ventricular septum, characteristic of human patients with hypertrophic cardiomyopathy, was found in only 2 of the 10 dogs. Death occurred while the dogs were under anesthesia during the course of operative procedures (5 dogs) or unexpectedly in animals without previous manifestations of cardiac disease (3 dogs). Four dogs had clinical signs of congestive heart failure, including 2 with marked cardiac decompensation. Two of these 4 dogs with heart failure and 1 dog that died during unrelated surgery, but without prior signs of heart disease, had electrocardiographic evidence of complete heart block.     

M-MODE ECHOCARDIOGRAPHY AS A DIAGNOSTIC AID FOR FELINE CARDIOMYOPATHY

Normal cats and cats with congestive cardiomyopathy (CCM) and hypertrophic cardiomyopathy (HCM) were examined using M-mode echocardiography to determine its diagnostic capabilities. Sixteen normal cats were examined to verify previously reported data and to add further echocardiographic inforamtion (left atrial/aortic root ratio, left posterior wall thickness at end systole and end diastole, amplitude of mitral valve excursions, and velocity of valve opening and closure) to aid in differential diagnosis. Significant (p<0.05) changes were detected between the normal cats and those with cardiomyopathy. In each type of cardiomyopathy, alterations in left atrial dimension, left atrial/aortic root ratio, left ventricular dimension, left ventricular wall thickness and percentage of ventricular dimensional change were identified. Altered mitral valve motion was found with HCM. Echocardiography was found to be an accurate technique for definitive diagnosis of feline cardiomyopathy.     

Syncope associated with hypertrophic cardiomyopathy in a dromedary camel

A case of hypertrophic cardiomyopathy in a dromedary camel (Camelus dromedarius) is described for the first time. The patient, a castrated 9-year-old animal, presented with a 6-month history of several episodes of syncope after moderate exercise and later at rest. The syncope had a sudden onset and a duration of 30 to 45 seconds. After clinical, electrocardiographical and echocardiographical examination, a tentative diagnosis of hypertrophic cardiomyopathy was made. At necropsy, the heart had a globose shape and was firm on palpation. The left ventricular free wall and the interventricular septum were thickened in cross-section and the left ventricular lumen was small. The clinical diagnosis was confirmed by histologic examination of heart tissue that demonstrated hypertrophy of myocardial fibres with vesicular nuclei and the presence of diffuse interstitial fibrosis.