Spectrum of M-Mode Echocardiographic Abnormalities in 75 Cats With Systemic Hypertension

Introduction

The diagnosis of systemic hypertension in cats has become more common in small animal practice. Indirect blood pressure (BP) measurement is indicated in cats with renal disease, hyperthyroidism, retinal hemorrhages and detachments, an acquired cardiac murmur, or a gallop rhythm.¹ In addition, many small animal hospitals have access to echocardiography, either in-house or by referral. Given the morphological variation in feline myocardial diseases, echocardiography is helpful in the management of cats with murmurs, arrhythmias, a gallop rhythm, cardiomegaly, or other signs of heart disease.²

During the echocardiographic examination, a two-dimensional image of the heart is evaluated qualitatively by the echocardiographer, and a cursor is positioned at standard locations for obtaining M-mode images and quantitative measurements.³⁴ Cardiac wall and chamber measurements obtained via M-mode permit comparison with normal reference ranges in order to identify abnormalities, determine differential diagnoses, and formulate a plan for additional diagnostic tests or treatment.

Published studies of echocardiographic findings in hypertensive cats have involved limited numbers of cats with disparate results.⁵⁶ In one study, 74% of 19 hypertensive cats had some form of left ventricular (LV) hypertrophy, but substantial overlap existed between normal and hypertensive cats.⁶ Another study of 15 hypertensive cats found that mean echocardiographic measurements were not significantly different from age-matched controls except for diastolic thickness of the left ventricular posterior wall (LVPW), and all mean values were within the reference ranges.⁵

The purpose of this study was to document the frequency and spectrum of M-mode echocardiographic abnormalities that occur in cats with hypertension.

Materials and Methods

Two populations of hypertensive cats were combined for this study. Medical records of cats diagnosed with systemic hypertension and having an echocardiographic examination at the University of Wisconsin-Madison School of Veterinary Medicine (UW-SVM) between 1991 and 2002 were reviewed (n=56). In addition, all echocardiographic records of cats with hypertension diagnosed at Mobile Veterinary Diagnostics from 1994 to 2001 were reviewed (n=19). Echocardiograms were performed if a murmur, gallop rhythm, arrhythmia, or radiographic evidence of cardiomegaly was present. The majority of echocardiograms at UW-SVM were performed by two of the authors (Henik, Stepien), and all echocardiograms obtained at Mobile Veterinary Diagnostics were performed by one author (Bortnowski).

Systemic arterial hypertension was defined as an indirect systolic BP ≥170 mm Hg in unsedated cats using an ultrasonic Doppler^a instrument and a 2- or 3-cm wide neonatal cuff around the median artery in the forelimb. Cuff width was within 30% to 40% of limb circumference.⁷ Measurements were made using minimal physical restraint and were obtained either before physical examination or after cage rest, to minimize stress-induced elevations in BP. Most BP measurements were made by the authors or one technician experienced in the procedure. Blood pressure readings were taken over a 5- to 10-minute period until five consecutive similar readings (i.e., <10 mm Hg variation) were obtained. The final BP value recorded at each cat’s visit was the mean of five readings.

For echocardiographic examinations, cats were placed either in right lateral recumbency on an echocardiography table or in sternal recumbency in the examiner’s lap. No sedation was used in any of the cats for the procedure. All echocardiographic measurements were performed in accordance with standards of the American Society of Echocardiography using a right parasternal approach and a 7.5-MHz or 10-MHz variable frequency probe.³⁴ M-mode measurements were obtained using two-dimensional guidance.

Information analyzed from the medical records included systolic BP values, age, gender, breed, total serum thyroxine (T₄), and serum creatinine concentrations. M-mode echocardiographic parameters assessed included dimension of the left atrium (LA), aortic root (Ao) diameter, left atrial to aortic (LA/Ao) ratio, LV internal dimension (LVID) in diastole (LVIDd) and systole (LVIDs), fractional shortening (FS) of the left ventricle, thickness of the interventricular septum (IVS) in diastole (IVSd) and systole (IVSs), thickness of the LVPW in diastole (LVPWd) and systole (LVPWs), right ventricular internal dimension in diastole (RVIDd), and mitral valve E-point to septal separation (EPSS). Fractional shortening of the LVID was calculated from the following formula: (LVID_d − LVID_s/LVID_d) × 100.

M-mode echocardiographic measurements were compared to published reference ranges and were noted to be greater than or less than the reference range for a given parameter.⁸ These reference ranges were chosen because of their similarity to reference ranges already established in normal cats at the examiners’ institutions. In the study reported here, normal diastolic IVS and LVPW thicknesses ranged from 2.5 to 5.0 mm, and hypertrophy was defined as a diastolic IVS or LVPW thickness ≥5.5 mm.⁸ This upper limit permitted a “gray zone” (between 5.1 and 5.4 mm), in which values were above the reference range, but the cats were not considered to have a definitive diagnosis of hypertrophy. Other researchers have defined hypertrophy as a diastolic IVS or LVPW thickness >5.5 mm or >6 mm.⁶⁹¹⁰

Results

Fifty-six (74.7%) hypertensive cats had an echocardiographic examination at UW-SVM, and 19 (25.3%) were examined at Mobile Veterinary Diagnostics. Indirect systolic BP in all cats averaged 205.7±29.1 mm Hg and ranged from 170 to 300 mm Hg (median, 196.0 mm Hg). Forty-eight (64.0%) animals were domestic shorthair cats, and the remaining breed distribution included six (8.0%) domestic longhair cats, six (8.0%) Persians, five (6.7%) Burmese, four (5.3%) Siamese, and two (2.7%) Himalayans. There was also one cat each from the Balinese, Tonkinese, Somali, and Manx breeds. Gender distribution included 38 (50.7%) castrated males, one intact male, and 36 (48.0%) spayed females. The mean age of the cats was 13.8±3.6 years (range, 5 to 19 years).

Serum creatinine concentration was ≥1.8 mg/dL (reference range, 0.8 to 1.8 mg/dL) in 44 (67.7%) of the 65 cats in which it was measured. Serum T₄ concentration was determined in 69 cats. Six (8.7%) cats were hyperthyroid, and three (4.4%) cats had serum T₄ concentration below the reference range (i.e., sick euthyroid or hypothyroid).

Upon assessing echocardiographic results, 16 (21.3%) cats had measurements within the reference ranges for all M-mode echocardiographic parameters. The remaining 59 cats had at least one M-mode echocardiographic measurement or ratio outside of the reference ranges [see Table]. Thirty-six (48%) cats met the criteria for hypertrophy of the IVS or LVPW based on a diastolic measurement ≥5.5 mm.⁸ Twenty-nine (38.7%) cats had hypertrophy of the IVSd, and three cats had IVSd thickness >5.0 and <5.5 mm (i.e., IVSd was above the reference range but not considered hypertrophied). Eleven (14.7%) cats had increased IVSs, and one had a decreased IVSs. Thirty-one (41.3%) cats had hypertrophy of the LVPWd, and three cats had LVPWd thickness >5.0 and <5.5 mm. Left ventricular posterior wall thickness in systole was increased in 20 (26.7%) cats and was below the reference range in two cats. Hypertrophy of both the IVS and LVPW occurred in 24 (32%) cats and was symmetrical (i.e., measurements of IVS and LVPW within 30% of each other) in all but two cats.¹¹

Left ventricular internal dimension in diastole was within the reference range in 65 (86.7%) cats, increased in one cat, and decreased in nine (12.0%) cats. The LV systolic dimension was increased in three (4.0%) cats and decreased in nine (12.0%) cats. Left ventricular FS was increased in seven (9.3%) cats and decreased in six (8.0%) cats. One cat had increased FS as the only echocardiographic abnormality, while another cat had decreased FS as the only echocardiographic abnormality.

Left atrial diastolic dimension was above the reference range in 15 (22.1%) of the 68 cats in which it was measured and was below the reference range in two cats. Aortic root dimension was increased in four (6.0%) of 67 cats and was decreased in five (7.5%) cats. The LA/Ao ratio was above the reference range (i.e., >1.6) in 19 (28.4%) of 67 cats. No cat had an LA/Ao ratio below the reference range (i.e., <0.8).

Discussion

The response of the left ventricle to hypertension includes an increase in wall stress, a change in LV diastolic filling, thickening of the ventricular walls, and an increase in mass.¹² Echocardiographic evaluation of the LV in early hypertension has shown diastolic dysfunction prior to hypertrophy in both dogs and humans.^13–15 A lack of M-mode echocardiographic abnormalities in 21% of the hypertensive cats in the study reported here might be explained by hypertension of recent onset and by measurements taken prior to the development of hypertrophy. M-mode echocardiography in dogs with experimental hypertension allowed detection of concentric hypertrophy 6 weeks after the onset of hypertension, but the duration of hypertension in clinical cases is usually unknown.¹⁶

A recent report by Snyder, et al., evaluated echocardiographic findings in 19 hypertensive cats and found that 14 (73.7%) cats met the criteria for hypertrophy based on IVSd or LVPWd >6 mm.⁶ In that study, 10 (52.6%) cats had hypertrophy of the LVPW, one (5.3%) cat had septal hypertrophy, and three (15.8%) cats had symmetrical hypertrophy. In the study reported here, a diagnosis of hypertrophy was less common (49.3%), even with use of a less stringent criteria for hypertrophy (≥5.5 mm).⁸ If an IVS or LVPW diastolic thickness >6.0 mm was used to define hypertrophy, then septal hypertrophy would have been diagnosed in the study reported here in only 15 (20%) of 75 cats. Likewise, 15 (20%) of 75 cats would have been diagnosed with LVPW hypertrophy. Reasons for the disparity in wall hypertrophy between the study population and previous reports may be related to the large number of cats examined in the report presented here (possibly more accurate assessment of echocardiographic changes from studying 75 cats versus 19 cats), the duration of the hypertension (hypertrophy is a late myocardial change), or the presence of other factors that influence hypertrophy (e.g., neurohormonal changes, concomitant primary myocardial disease, etc.).^13–1517

Cats in the present study had similar frequencies of hypertrophy of the IVS or LVPW (38.7% and 41.3%, respectively). Hypertrophy of both the IVS and the LVPW occurred in 32% of cats, compared to only three (15.8%) of 19 cats in Snyder et al.’s study.⁶ Nelson et al. reported echocardiographic results in 15 hypertensive cats.⁵ Mean values for standard M-mode echocardiographic parameters were within the reference ranges for both hypertensive and normotensive cats. Wall thicknesses in hypertensive cats were greater than those in normotensive cats, but the absolute number of hypertensive cats with echocardiographic values outside of the reference range was not given.⁵

Systolic BP did not correlate with either LVIDd or IVSd in the study reported here, and prior studies in dogs and cats have not shown a relationship between BP and the degree of hypertrophy associated with hypertension.⁵⁶¹⁸¹⁹ A lack of correlation has also been shown in humans with hypertension and may suggest that factors other than hypertension are involved in the development of hypertrophy, or that a single BP measurement does not adequately reflect average BP over time.¹²¹⁷¹⁹ Current studies in hypertensive people suggest that neurohormones, including aldosterone, angiotensin II, and epinephrine, may contribute to the development of hypertrophy.¹⁷

Nelson et al. determined that hypertensive cats may have focal basal septal hypertrophy, which is best measured from the two-dimensional long-axis view of the heart.⁵ Standard M-mode views and measurements, which are generated from the midseptal region, do not usually detect focal hypertrophy of the LV outflow tract. Therefore, focal areas of wall thickening may be missed if the echocardiographer relies solely on M-mode measurements to detect abnormalities. Systolic wall thickness was increased in 11 cats based on IVS measurement and in 20 cats based on LVPW measurement, which may reflect hypertrophy or increased thickening from sympathetic stimulation. Systolic wall thickness was decreased in one cat on IVS measurement and in two cats on LVPW measurements. Decreased wall thickening may be associated with areas of fibrosis, or infarction with replacement of cardiac myocytes by noncontractile tissue.²

Approximately 87% of cats in this study had LVIDd within the reference range; therefore, measurable volume overload associated with chronic renal failure, mitral valvular insufficiency, myocardial failure, or hyperthyroidism was not present in most of the cats. One cat had LVIDd >18 mm. Nine (12.0%) cats had decreased LVIDd, perhaps as a result of impingement of the LV lumen by hypertrophic walls or dehydration associated with renal failure. Echocardiographic studies in hypertensive people have shown normal LV dimensions, but a study in hypertensive dogs revealed decreased LV lumen size.²⁰²¹

Left ventricular internal dimension in systole was within the reference range in 84% of the hypertensive cats. Decreased LVIDs was present in eight cats, and it was associated with a normal LVIDd in five cats and a decreased LVIDd in three cats. A decreased lumen during systole with a normal diastolic dimension may reflect increased sympathetic tone (e.g., fear or hyperthyroidism).² When associated with a decreased diastolic dimension, a decreased systolic dimension may result from dehydration or decreased lumen size from hypertrophy.²

Fractional shortening of the LV, an index of contractility and systolic function, was within the reference range in 62 (82.7%) of the 75 cats. Seven (9.3%) cats had increased FS, and one of these cats was hyperthyroid. Six (8.0%) cats had low FS (<35%), suggesting myocardial failure. None of the cats with myocardial failure were hyperthyroid, but four of the six were azotemic. Other myocardial diseases (e.g., idiopathic cardiomyopathies), in addition to hypertensive heart disease, may have been present in those cats with myocardial failure, or a decreased FS may have reflected disease chronicity.¹² Fractional shortening has been shown to be normal to increased in hypertensive humans and dogs.^131620–23 Six months of experimental hypertension in dogs did not result in deterioration of LV function, although in the later stages of hypertension, hypertrophy may no longer compensate for increased wall stress, and systolic function may deteriorate.¹²¹⁶

Left atrial dimension was increased (>15 mm) in 22.1% of cats in the present study. It is difficult to compare these findings to prior studies, because Snyder et al. used more stringent criteria for LA enlargement (≥18 mm). In Snyder et al., however, the hypertensive cats did have a statistically larger LA than the normal cats.⁶ Left atrial size was not reported in the study by Nelson et al.⁵ Left atrial dilatation in cats in the present study may be a result of ventricular remodeling with subsequent mitral valve regurgitation or a result of concomitant mitral valve degenerative changes.²⁴

Widening of the ascending aorta has been documented in hypertensive cats, but standard M-mode measurements, which are at the level of the aortic valve leaflets, usually are normal.⁵ In the cats of this study, four (6.0%) of 67 cats with Ao measurements had an increased aortic diameter. In five cats, aortic diameter was decreased, which may have reflected dehydration or another cause of decreased cardiac output (e.g., myocardial failure).

Right ventricular internal dimension is measured in diastole, and dilatation may reflect primary or secondary disease of the right side of the heart, or it may suggest fluid overload.²⁵ Increased EPSS may indicate volume overload of the LV and decreased transvalvular flow of the mitral valve.²⁵ Conclusions regarding these parameters in hypertension could not be made, because abnormalities of each occurred in only one cat.

Conclusion

Variable changes in the structure of the heart were seen in cats with systemic hypertension as measured by M-mode echocardiography. One in five hypertensive cats had a normal echocardiogram based on M-mode measurements, and in the cats with echocardiographic abnormalities, changes were inconsistent. The marked variability of echocardiographic findings in hypertensive cats made echocardiography an unreliable indicator of the need for BP assessment and an unreliable screening test for hypertension in cats. Based on these findings, the absence of echocardiographic abnormalities does not rule out systemic hypertension as a cause of cardiovascular disease in cats.