Right ventricular involvement in feline hypertrophic cardiomyopathy.

OBJECTIVES: To evaluate right ventricular (RV) wall thickness and chamber dimensions in cats with hypertrophic cardiomyopathy (HCM). ANIMALS: One hundred fifty-one healthy control cats and 200 cats with HCM. METHODS: Retrospective, observational, clinical cohort study. Two-dimensional echocardiograms from all cats were analyzed. Right atrial diameter, RV free wall thickness, and RV chamber diameter were quantified using multiple imaging views. Conventional (mean ± 2 standard deviations) and allometrically scaled (Y = a × Mb) reference values were determined in normal cats and compared to values found in cats with HCM. Linear and logistic regression, multivariate regression, and mixed model analysis were performed to identify associations between RV wall thickness and severity of left ventricular (LV) hypertrophy, clinical severity of HCM, and presence of pleural effusion. RESULTS: Mean RV wall thickness was increased in HCM (p<0.001). Considering increased RV wall thickness in at least one segment, 94 (47%) and 112 (56%) cats with HCM had RV hypertrophy using upper reference limits based on mean + 2 standard deviations or allometric scaling, respectively. There was an association between severity of LV and RV hypertrophy (p<0.05). Left-sided congestive heart failure (n = 58) was associated with increased RV wall thickness in all segments compared to cats with preclinical HCM (p<0.001). Body weight had negligible effects on RV wall thickness (R2 0.08-0.17, p<0.001), whereas age and breed had no effect (p>0.05) in control cats. CONCLUSIONS: Increased RV wall thickness is common in cats with HCM and relates to severity of LV hypertrophy and clinical status.

[Congenital cardiac anomalies (pentalogy of Fallot) in a two year old ram with brachygnathia inferior]. / Kongenitale Herzanomalien (Fallotsche Pentalogie) bei einem zweijährigen Schafbock mit Brachygnathia inferior.

In a nearly two-year-old ram, descending from a breeding trial to investigate the effects of shortness of the lower jaw (brachygnathia inferior), a congenital cardiac anomaly was observed. At the age often months the affected animal, a cross breed of Cameroon Sheep and East Friesian Milk Sheep, showed exercise-induced respiratory distress for the first time. Auscultation revealed a loud systolic heart murmur (grade 5) on both sides of the thorax, most prominent over the left third intercostal space at shoulder height. Postmortem examination of the ram's heart showed a pentalogy of Fallot, consisting of a pulmonic stenosis, a ventricular septal defect, an overriding aorta, a right ventricular hypertrophy and a patent foramen ovale. A genetic defect has to be considered as a possible reason.

Right ventricular hypertrophy with heart failure in Holstein heifers at elevation of 1,600 meters.

A syndrome of progressive right-sided heart failure occurred among yearling Holsteins at a heifer-raising facility and 2 dairies on the Colorado Front Range between 2007 and 2011. Most cases were seen at the heifer-raising facility, where the disease ranked second only to pneumonia as a major cause of death in animals aged <1.5 years. The disease resulted in the death or premature sale of 55 animals over the 5-year period. Affected heifers were 4-15 months old when they developed dyspnea, tachycardia, distention and pulsation of jugular veins, lethargy, and weight loss. Clinical progression in most was rapid (2 days to 2 weeks). Ten cattle with typical clinical signs were examined postmortem between 2008 and 2010. Seven developed clinical signs after transportation 57-238 days earlier from Wisconsin (elevation: < 275 m); the remaining 3 animals were born and raised at an altitude of 1,600 m. At necropsy, the 10 cattle had marked hypertrophy of right ventricular myocardium, dilated right atria, right ventricles, and pulmonary trunks, as well as hepatomegaly, ascites, and serous atrophy of fat. The principal histological change in lungs was hypertrophied tunicae adventitia and media of muscular arteries. Hepatic changes were typical of chronic passive congestion. Ultrastructural changes in heart were consistent with uncomplicated hypertrophy of cardiocytes with no evidence of primary cardiomyopathy. The syndrome most likely represents brisket disease due to pulmonary hypertension at the modest elevation of 1,600 m.

Sodium hydrosulfide prevents hypoxia-induced pulmonary arterial hypertension in broilers.

1. The aim of the study was to determine if H(2)S is involved in the development of hypoxia-induced pulmonary hypertension in broilers, a condition frequently observed in a variety of cardiac and pulmonary diseases. 2. Two-week-old broilers were reared under normoxic conditions or exposed to normobaric hypoxia (6 h/day) with tissue levels of H(2)S adjusted by administering sodium hydrosulfide (NaHS, 10 µmol/kg body weight/day). Mean pulmonary arterial pressure, right ventricular mass, plasma and tissue H(2)S levels, the expression of cystathionine-ß-synthase (CSE) and vascular remodeling were determined at 35 d of age. 3. Exposure to hypoxia-induced pulmonary arterial hypertension was characterized by elevated pulmonary pressure, right ventricular hypertrophy and vascular remodeling. This was accompanied by decreased expression of CSE and decreased concentrations of plasma and tissue H(2)S. 4. Hypoxia-induced pulmonary hypertension was significantly reduced by administration of NaHS but this protective effect was largely abolished by D, L-propargylglycerine, an inhibitor of CSE. 5. The results indicate that H(2)S is involved in the development of hypoxia-induced pulmonary hypertension. Supplementing NaHS or H(2)S could be a strategy for reducing hypoxia-induced hypertension in broilers.

Ventricular tachycardia in English bulldogs with localised right ventricular outflow tract enlargement.

OBJECTIVES: To describe the electrocardiographic characteristics of ventricular tachycardia arising from the right ventricular outflow tract and the particular association between this arrhythmia and the presence of localised right ventricular outflow tract enlargement in English bulldogs. METHODS: Five English bulldogs were referred with a history of syncope or cardiogenic shock. In all dogs, 12-lead surface ECG, thoracic radiograph and echocardiography were collected. In all but one dog 24-hours Holter monitoring and signal-averaged ECGs was examined and in one dog electrophysiological study and radiofrequency catheter ablation of the VT substrate was performed. RESULTS: Documented arrhythmias included a single sustained monomorphic wide QRS tachycardia in four dogs, and an alternans of two different monomorphic forms in one dog. Mean QRS duration during tachy-cardia was 91·6 ±9·83 milliseconds. QRS complexes manifested a left bundle branch block morphology and an inferior axis (81 ±13·73°). R wave notching was present in the caudal (inferior) leads in three tachy-cardias. Lead I was negative in 3 of 6, positive in 1 of 6 and isodiphasic in 2 of 6. Lead aVL was negative in 5 of 6 and positive in 1 of 6. Signal-averaged electrocardiograms revealed late potentials in three dogs. Echocardiography showed a localised right ventricular outflow tract enlargement in all dogs. Cardiac map-ping established two sites of origin of ventricular tachycardia within the right ventricular outflow tract in one dog: caudal free-wall and cranial-septal. CLINICAL SIGNIFICANCE: The presence of a localised right ventricular outflow tract enlargement and ventricular tachycardia with left bundle branch block morphology could suggest segmental arrhythmogenic right ven-tricular cardiomyopathy in the English bulldog.

[Left ventricular hypertrophy in the cat - "when hypertrophic cardiomyopathy is not hypertrophic cardiomyopathy"]. / Linksherzhypertrophie bei der Katze - <>

According to WHO classification hypertrophic cardiomyopathy (HCM) is a primary genetic cardiomyopathy. Echocardiographically HCM is characterized by symmetric, asymmetric or focal left ventricular hypertrophy (LVH) without recognizable underlying physical cause. However, echocardiographically HCM in cats may not be distinguishable from other causes of a thick appearing left ventricle. Hypovolemia can look like a hypertrophied ventricle but is basically only pseudohypertrophic. Well recognized and logical physical causes of LVH include systemic hypertension and outflow obstruction. LVH similar to HCM may also be found in feline hyperthyroidism. The context of the disease helps to differentiate these physical / physiological causes of LVH. Difficult to distinguish from HCM, particularly when based on a snapshot of a single echocardiographic exam, are myocarditis and <>. Only the clinical and echocardiographic course allow a reasonably confident etiological diagnosis and the differentiation between HCM and secondary LVH.

Uni- or bi-ventricular hypertrophy and susceptibility to drug-induced torsades de pointes.

INTRODUCTION: Cardiac hypertrophy is an independent risk factor for torsades de pointes (TdP), a polymorphic ventricular tachycardia that is often drug-induced, that may evolve into ventricular fibrillation and sudden death. Therefore this study was designed to determine if right (RVH), left (LVH), or biventricular (BVH) hypertrophy increases susceptibility to drug-induced TdP. METHODS: Rabbits were separated into 4 groups: control or RVH, LVH, BVH (studied 8weeks after banding of one or both great arteries). ECGs were recorded continuously under anesthesia after baseline and after rabbits received escalating doses of torsadogens (dofetilide, clofilium and terfenadine) or non-torsadogens (cilobradine, diltiazem and vehicle). The following parameters were measured [RR, PQ, QRS and QT] or calculated [QTc (F), short term variability of QT interval]. RESULTS: Generally, torsadogenicity for the compounds tested was dofetilide>clofilium>terfenadine, and there was no TdP following cilobradine, diltiazem or vehicle. In general the susceptibility to TdP was RVH>BVH>LVH>control. Rabbits with RVH developed TdP much more prevalently than for those with either LVH or BVH (p<0.05). At the low dose of dofetilide, LVH was actually protective. CONCLUSION: Rabbits with any form of hypertrophy develop prolongation of QT, QTc and increased QT instability. Rabbits with any form of hypertrophy are more prone to arrhythmia than normals in response to known torsadogens.

Evaluation of endothelial and inducible nitric oxide synthase genes expression in the heart of broiler chickens with experimental pulmonary hypertension.

1. To clarify the effect of T(3)-induced pulmonary hypertension on endothelial and inducible nitric oxide synthase (eNOS and iNOS) mRNA expression in the ventricles of the heart, semi quantitative reverse transcription-PCR was performed on total RNAs isolated from broiler chicken hearts after feeding supplementary T(3) (15 mg T3/kg) for 6 weeks. NO metabolites (nitrite/nitrate) of serum were measured. 2. The eNOS and iNOS genes were expressed in the right and left ventricles of control and T(3)-treated broilers at 12, 28 and 49 d of age. The relative amount of eNOS mRNA expression in the right and left ventricles did not significantly differ between control and T(3)-treated broilers at any age. 3. The relative amount of iNOS mRNA expression in the right and left ventricles was lower in T(3)-treated broilers than in control broilers at 49 d of age, but not at 12 or 28 d. 4. The amount of NO metabolites was reduced in the serum of T(3)-treated chickens at 49 d of age when compared with the control. 5. It is concluded that eNOS and iNOS genes are normally expressed in the heart of broilers. It is probable that impaired NO synthesis and reduction of iNOS gene expression in the heart ventricles are involved in the pathophysiology of cardiac function in broilers with pulmonary hypertension.

Comparison of the effects of candesartan cilexetil and enalapril maleate on right ventricular myocardial remodeling in dogs with experimentally induced pulmonary stenosis.

OBJECTIVE: To compare the effects of candesartan cilexetil and enalapril maleate on right ventricular myocardial remodeling in dogs with experimentally induced pulmonary stenosis. ANIMALS: 24 Beagles. PROCEDURES: 18 dogs underwent pulmonary arterial banding (PAB) to induce right ventricular pressure overload, and 6 healthy dogs underwent sham operations (thoracotomy only [sham-operated group]). Dogs that underwent PAB were allocated to receive 1 of 3 treatments (6 dogs/group): candesartan (1 mg/kg, PO, q 24 h [PABC group]), enalapril (0.5 mg/kg, PO, q 24 h [PABE group]), or no treatment (PABNT group). Administration of treatments was commenced the day prior to surgery; control dogs received no cardiac medications. Sixty days after surgery, right ventricular wall thickness was assessed echocardiographically and plasma renin activity, angiotensin-converting enzyme activity, and angiotensin I and II concentrations were assessed; all dogs were euthanatized, and collagenous fiber area, cardiomyocyte diameter, and tissue angiotensin-converting enzyme and chymase-like activities in the right ventricle were evaluated. RESULTS: After 60 days of treatment, right ventricular wall thickness, cardiomyocyte diameter, and collagenous fiber area in the PABNT and PABE groups were significantly increased, compared with values in the PABC and sham-operated groups. Chymase-like activity was markedly greater in the PABE group than in other groups. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicated that treatment with candesartan but not enalapril effectively prevented myocardial remodeling in dogs with experimentally induced subacute right ventricular pressure overload.

Further evidence for the involvement of anatomical parameters of the cardiopulmonary system in the development of ascites syndrome in broiler chickens.

Eggs from a broiler line were incubated at two different altitudes and hatched. Relative heart and lung weights, volumes of the heart, lung and thoracic cavity, incidence of right ventricular hypertrophy and ascites, and related physiological parameters were followed in the day-old chickens hatched from the above eggs. Lung and heart weights as a percentage of body weight, lung and heart volumes relative to the volume of the thoracic cavity after removing the heart and lungs were higher in chickens hatched at high altitude. Additionally, embryonic triiodothyronine (T3) and thyroxine (T4) levels relative to cardiopulmonary parameters were higher in day-old chickens that hatched at high altitude as compared with chickens hatched at low altitude. This was associated with a lower incidence of right ventricular hypertrophy and ascites in chickens hatched at high altitude. Our data indicate that chronic hypoxia interacting with the endogenous functions of embryos during embryonic development at high altitude, as adaptation mechanisms, changed the developmental trajectories of cardiopulmonary parameters in postnatal chickens. This important development facilitates an increase in the gas exchange area in broiler chickens, thus lowering their susceptibility to pulmonary hypertension and ascites.

Increased calcium deposits and decreased Ca2+-ATPase in right ventricular myocardium of ascitic broiler chickens.

Right ventricular hypertrophy and failure is an important step in the development of ascites syndrome (AS) in broiler chickens. Cytoplasmic calcium concentration is a major regulator of cardiac contractile function and various physiological processes in cardiac muscle cells. The purpose of this study was to measure the right ventricular pressure and investigate the precise ultrastructural location of Ca(2+) and Ca(2+)-ATPase in the right ventricular myocardium of chickens with AS induced by low ambient temperature. The results showed that the right ventricular diastolic pressure of ascitic broilers was significantly higher than that of control broilers (P < 0.01), and the maximum change ratio of right intraventricular pressure (RV +/- dp/dt(max)) of ascitic broilers was significantly lower than that of the controls (P < 0.01). Extensively increased calcium deposits were observed in the right ventricular myocardium of ascitic broilers, whereas in the age-matched control broilers, calcium deposits were much less. The Ca(2+)-ATPase reactive products were obviously found on the sarcoplasmic reticulum and mitochondrial membrane of the control right ventricular myocardium, but rarely observed in the ascitic broilers. The data suggest that in ascitic broilers there is the right ventricular diastolic dysfunction, in which the overload of intracellular calcium and the decreased Ca(2+)-ATPase activity might be the important factors.

[Development and cardiomyopathy: serum response factor, a key protein]. / Développement et cardiomyopathie: le facteur de réponse au sérum, une protéine clé.

Serum response factor (SRF) is a widely expressed transcription factor involved in the transcription of various genes linked to muscle differentiation and cellular growth. Recent studies show the pivotal role of SRF in orchestrating genetic programs essential for cardiac development and function. Dominant negative isoforms of SRF resulting from caspase cleavage or alternative splicing have been identified in different forms of cardiomyopathies. This review summarizes the role of SRF, its structure, function and its role in human cardiopathies. Finally, we discuss the results of recently developed murine models which address the role of SRF in the adult heart in vivo. The existing biological data suggest that SRF could be a target of neurohumoral activation which is involved in myocardial hypertrophy. Conversely, inhibition of SRF activity in different murine models leads to dilated cardiomyopathy.

Effect of cold stress on broilers selected for resistance or susceptibility to ascites syndrome.

Genetic selection for an ascites-resistant line of broilers is seen as a permanent solution to the ascites problem. Ascites-resistant and ascites-susceptible lines have been developed using sire family selection based on mortality data taken from siblings reared in a hypobaric chamber (simulated 2,900 m above sea level). The relaxed line is representative of the original commercial pureline stock randomly mated with no artificial selection pressure. The objectives of this study were to evaluate the differences between the lines when reared in floor pens and subjected to an ascites-inducing cold stress. Seven hundred eighty three straight run broilers were reared in floor pens at local elevation (390 m above sea level). Feed and water were available ad libitum. Birds were brooded at 32 C during the first week. The second week birds were maintained at 30 degrees C. Cold stress was applied for the remaining 4 wk at 14 degrees C. Mortalities were necropsied daily to determine cause of death. Birds and feed were weighed weekly. At 6 wk, five birds per pen were bled, and half the survivors in each pen (8 to 15 birds) were killed, necropsied, and scored for ascites. Blood gases, clinical chemistries, and blood cell counts were taken. Liver, spleen, split heart, and lung weights were recorded. Body weights were not different among the resistant, susceptible, and relaxed lines (P < 0.05). Feed conversion was better in the resistant line when compared to the susceptible and relaxed lines (P < 0.05). Ascites incidence, as measured by mortality and lesion score at necropsy, was higher in the susceptible and relaxed lines when compared to the resistant line; 18.8, 12.7, and 1.6% respectively (P < 0.001). Susceptible and relaxed lines showed more right ventricular hypertrophy when compared with the resistant line (P < 0.05). The results show that under severe cold stress at local altitude (390 m above sea level), the ascites-resistant line was growing as rapidly as the other lines and was as resistant to ascites as it had been under hypobaric conditions.

Further evidence for the involvement of cardiac beta-adrenergic receptors in right ventricle hypertrophy and ascites in broiler chickens.

The present study was carried out to determine, first, the cardiac beta-adrenergic receptor characteristics of broiler chick embryos exposed to two different CO(2) levels during the last stage of embryonic development, and second, the prophylactic effect of beta(1)-adrenoceptor blocker on right ventricular hypertrophy in broiler chickens. High CO(2) embryos showed significantly higher haematocrit values, higher partial pressure of CO(2) levels and lower partial pressure of O(2) levels than those of normal CO(2) embryos. Exposure of chick embryos to high CO(2) levels reduced the binding capacity of myocardial beta-adrenergic receptors compared with those embryos incubated at the normal CO(2) level. Atenolol-supplemented diet numerically reduced ascites incidence in broiler chickens (7%) compared with birds fed the control diet (15%). In conclusion, these data support the important role of the beta-adrenergic receptor in the cardiovascular system for cardiac output, and secondary to pulmonary hypertension syndrome.

Surgical correction of double-chambered right ventricle in dogs.

Double-chambered right ventricle (DCRV) is possibly an emerging congenital cardiac anomaly in dogs. The defect causes clinical and pathophysiologic signs similar to those of congenital pulmonic stenosis in dogs but has distinct diagnostic features, breed predilections, and implications for treatment. The defect is often associated with clinical signs early in life. Surgical correction of DCRV can be undertaken with the aid of cardiopulmonary bypass and offers the prospect of an improved clinical outcome.

Plasma taurine levels in broilers with pulmonary hypertension syndrome induced by unilateral pulmonary artery occlusion.

Low plasma levels of taurine are associated with losses of cardiac sarcomeric proteins, leading to heart failure in mammals. Recently, it was proposed that cardiac taurine depletion serves to defend the heart against injury caused by regional ischemia in mammals. The role of taurine has not been well documented in broilers, particularly in relation to pulmonary hypertension syndrome (PHS; ascites). Three independent experiments evaluated plasma taurine in male broilers by utilizing the following treatments: unoperated controls (CONTROL; n = 10 in each experiment); sham operated (SHAM; n = 11, 12, and 10); or, unilaterally pulmonary artery clamped (PAC; n = 18, 29, and 24) that did (PAC-ascites) or did not (PAC-normal) develop ascites within 12 d postsurgery. Plasma samples were collected 9 and 11 d postsurgery in Experiments 1 and 2, respectively, and 2 d before and 4, 8, and 12 d after surgery in Experiment 3. Plasma taurine was analyzed by HPLC. Twelve days postsurgery, the birds were euthanatized, and ventricles were weighed for calculating the right:total ventricular weight ratio (RV:TV). The RV:TV of PAC birds (>0.35) consistently was higher (P < 0.01) than that of CONTROL and SHAM birds (<0.27 and 0.25, respectively). In Experiments 1 and 2, plasma taurine was higher (P < 0.05) in PAC-ascites (380 and 370 nmol/mL) than in SHAM broilers (183 and 186 nmol/mL), whereas CONTROL (262 and 278 nmol/mL) and PAC-normal (362 and 300 nmol/mL) broilers tended to have intermediate plasma taurine levels. In Experiment 3, PAC birds had higher (P < 0.05) plasma taurine at 8 and 12 d postsurgery when compared with presurgery levels, whereas plasma taurine was unchanged over time in CONTROL and SHAM birds. These results suggest cardiac taurine may be released into the plasma as a protective mechanism in response to the induction of pulmonary hypertension, hypoxemia, and right-side heart failure, similar to the mechanism reported for protecting cardiac muscle from ischemia in mammals.

Electrocardiographic and genetic evaluation of giant jungle fowl, broilers, and their reciprocal crosses following unilateral bronchus occlusion.

Electrocardiography is useful as a noninvasive technique for detecting right ventricular hypertrophy in birds developing pulmonary hypertension (PH) and pulmonary hypertension syndrome (PHS, ascites). The objective of this study was to identify every aspect of the Lead II ECG wave form (amplitude or duration) that can be correlated with right ventricular hypertrophy [increased right:total ventricular weight ratios (RV:TV)] indicative of PH across a broad genetic background. Sham operations were conducted, or PH was induced by occluding one extrapulmonary primary bronchus in 14-d-old chicks produced from matings of broilers (B x B), Giant Jungle Fowl (J x J), and their reciprocal crosses (B x J and J x B). Standard three-lead electrocardiograms (ECG) were recorded on Days 28 and 42, and final necropsies were conducted to evaluate the incidence of ascites, confirm sex, and obtain ventricular weights for calculating RV:TV. Ascites did not develop in the J x J, and one each of the B x J and J x B chicks developed ascites; consequently, only data from birds that did not develop ascites were compared. Heart rate was recorded, and the following amplitudes and durations were measured or calculated for three consecutive wave cycles of the Lead II ECG: base of R to the peak of R (RbR), peak of R to base of S (RS), base of S to peak of R' (SR'), S, peak of R' to base of R' (R'R'b), and base of S to peak of T (ST). Differences between the ECG of sham and bronchus clamp groups were more prominent in B x B and B x J than in J x B, and bronchus occlusion did not affect the ECG, growth, or RV:TV ratios of J x J. In contrast, sex influences were more prominent in J x J and J x B than in B x J and B x B. These observations suggest a paternal pattern of inheritance for Lead II ECG wave forms, with crosses sired by broilers (B x B, B x J) exhibiting susceptibility to PH and few ECG differences related to sex, whereas crosses sired by Giant Jungle Fowl U x J, J x B) exhibited resistance to PH and numerous ECG differences related to sex.

[A case of interatrial communication in a dog]. / Un case de communication interatriale (CIA) chez le chien.

A 4 month old female German Shepherd was presented for the work-up of a heart murmur that has been detected by the referring veterinarian. Clinical examination and thoracic radiography showed an enlargement of the right ventricle, and an increased pulmonary perfusion. Echocardiography showed an interatrial communication (atrial septum defect), and colour Doppler allowed the confirmation of a left to right shunt. The article discusses the diagnostic possibilities of this rare congenital cardiac malformation in the dog.

Isolated right-ventricular hypertrophy associated with severe pulmonary vascular apolipoprotein A1-derived amyloidosis in a dog.

A 12-year-old dachshund was referred for respiratory distress, coughing, and weight loss. Cyanosis, dyspnea, tachypnea, and harsh lung sounds were noted on physical examination. Polycythemia with an increased number of nucleated red blood cells; right atrial enlargement; severe interstitial-to-alveolar pattern in all lung fields; and peripheral, echogenic, pulmonary masses were observed. Cytological examination of pulmonary aspirates indicated possible pulmonary carcinoma. The dog was euthanized at the owner's request. Isolated right-ventricular hypertrophy and pulmonary arteriopathy with amyloid deposits of apolipoprotein A1 were identified upon necropsy and histopathology. Pulmonary vascular amyloidosis should be considered in the differential diagnoses of respiratory distress in aged dogs.

Hypertrophic cardiomyopathy in a common wombat (Vombatus ursinus).

A case of hypertrophic cardiomyopathy (HCM) in a common wombat (Vombatus ursinus) is described. At necropsy, the heart showed symmetrical ventricular hypertrophy, a narrow left ventricular cavity, and dilatation of the left atrium. Microscopical findings in the ventricular myocardium included a strikingly disordered arrangement of cardiac muscle cells, in which adjacent cells were aligned perpendicularly and obliquely to each other, interstitial myocardial fibrosis, and arteriosclerosis of small intramural coronary arteries (fibromuscular hyperplasia). The changes, which were widespread in both ventricles, resembled those of HCM in man and other animals.