Abstract
The objective of this prospective study was to determine the prevalence of echocardiographic evidence of heart disease in apparently healthy cats with heart murmurs. Thirty-two privately owned domestic cats were examined. All cats were considered healthy on the basis of history and physical examination, except for the finding of a heart murmur on auscultation. Cats on any medications (besides regular flea, tick and heartworm preventative) or that were pregnant or lactating were excluded from this study. The prevalence of echocardiographic evidence of heart disease in this population of cats was 53%. Therefore, identification of a heart murmur on routine physical examination in apparently healthy cats warrants further investigation.
Heart murmurs in apparently healthy adult cats present a dilemma to clinicians. While murmurs can be associated with cardiac disease, most commonly hypertrophic cardiomyopathy (HCM), studies have identified benign causes of murmurs in cats. 1–3 Differentiation of causes of feline cardiac murmurs is difficult by auscultation alone without additional diagnostics. Feline murmurs can be inducible (apparent only upon physical provocation, usually stress, fear or pain) or non-inducible (continuously present). 2,3 Previous studies have reported a murmur prevalence of 21–44% in overtly healthy cats. 1–3 One study determined that 15.5% of apparently healthy cats had non-inducible heart murmurs and approximately one-third of these cats were determined to have cardiac disease. 2 An additional 12% of cats in this study had inducible murmurs and several of these cats also had cardiac disease. A second study found even higher percentages of inducible (26%) and non-inducible (18%) murmurs in 100 apparently healthy cats, with 14/100 cats having cardiac disease (71% of these had murmurs). 3 Therefore, a high percentage of cats with murmurs, particularly inducible murmurs, appear to have no evidence of structural heart disease. We sought to further characterize the prevalence of heart disease and murmur etiology in apparently healthy adult cats presenting to a referral practice for evaluation of a murmur.
Materials and methods
Study design
We prospectively recruited apparently healthy cats that were presented to the Red Bank Veterinary Hospital (RBVH) cardiology service for evaluation of a murmur between March 24, 2005 and January 25, 2007. We included cats if they had no history of vomiting, diarrhea, cough, polyuria, polydipsia, or weight loss in the 4 weeks prior to evaluation. Cats had to demonstrate a heart murmur on physical examination, and could not be receiving any medications besides routine flea, tick, and/or heartworm preventative. Cats with a previous diagnosis of cardiac disease or systemic illness such as inflammatory bowel disease, hyperthyroidism, renal disease, systemic hypertension, or diabetes mellitus were excluded. All cats underwent a clinical evaluation consisting of a physical examination, packed cell volume (PCV) and total solids (TS), and echocardiogram. A complete blood count (CBC), serum chemistry profile, thyroid evaluation and systolic blood pressure were obtained from some cats at the discretion of the attending clinician. Systolic blood pressure measurement was performed in a quiet cardiology room and systolic arterial blood pressure was estimated for cats by use of the Doppler cuff-flow method as previously described. 4,5 Three consecutive measurements were performed on either the left or right forelimb and the measurement averaged. 5 Cats with serum thyroxine concentration that exceeded the upper limit of the laboratory reference interval were considered to be hyperthyroid and excluded from the study as well. All physical and echocardiographic examinations were performed by a board-certified cardiologist (CDS) or a cardiology resident (MK) with review by a cardiologist (CDS).
Echocardiography
Standard echocardiographic examinations were performed without chemical restraint using a Vivid 7 (Vingmed System 7, General Electric Medical Systems, Waukesha, Wis) echocardiograph coupled to a 10 MHz transducer. 6 We obtained both two-dimensional and M-mode measurements of the left atrium and ventricle from right parasternal short-axis and long-axis views. M-mode measurements included the interventricular septal thickness at end diastole and end systole (IVSd and IVSs, respectively), left ventricular internal dimension at end diastole and end systole (LVIDd and LVIDs, respectively), left ventricular posterior wall thickness at end diastole and end systole (LVPWd and LVPWs, respectively), left atrial dimension at end systole (LADs) and aortic root dimension (Ao). Two-dimensional measurements included IVSd, AO, LVIDd, LA (short-axis and long-axis), LVPWd. All valves and ventricular outflow tracts were examined with spectral and color Doppler. The percentage of fractional shortening (%FS) was derived using the equation [(LVIDd−LVIDs)/(LVIDd×100)]. The left atrium-to-aortic root ratio (LA:Ao) was calculated 7 and left atrial enlargement was defined as a LA:Ao ratio >1.54. 8 Systolic anterior motion of the mitral valve (SAM) was identified when mitral leaflet tissue was displaced dorsocranially during systole and spanned at least 50% of the distance from the region of leaflet coaptation to the IVS. 9 Papillary muscles were subjectively assessed as normal or enlarged and the endomyocardium was evaluated to be normal, abnormal with focal thickening or demonstrating increased echogenicity. Left ventricular concentric hypertrophy (LVCH) was defined by an end-diastolic wall thickness ≥6 mm in any region of the IVS or LVPW. 10 Dynamic right ventricular outflow tract obstruction (DRVOTO) was noted if there was a systolic jet that originated proximal to the pulmonary valve and had spectral Doppler echocardiographic characteristics that indicated late-systolic acceleration. 11 Dynamic left ventricular outflow tract obstruction (DLVOTO) was similarly defined by late-systolic acceleration. 2 An elevated aortic velocity was differentiated from DLVOTO based on normal pulsed-wave Doppler velocities within the left ventricular outflow tract but an increased velocity beyond the aortic valve and no evidence of late-systolic acceleration on spectral Doppler.
Statistical analysis
We performed descriptive statistics where appropriate.
Results
We identified 32 cats with murmurs that were eligible for inclusion. The breeds represented were domestic shorthair (n=18), domestic longhair (n=6), Persian (n=3), Siberian (n=1), Norwegian Forest Cat (n=1), Japanese Bobtail (n=1), Ragdoll (n=1), and domestic medium hair (n=1). Median weight was 5.05 kg (range 2.91–9.00 kg). Sixteen cats were castrated males, 12 were spayed females, three were intact males, and one was an intact female. Median age was 66.5 months (range 5–168 months). Median PCV was 41% (range 20–58%) and median TS were 7.5 g/dl (range 6.0–8.4 g/dl). A CBC and a serum chemistry profile were performed on 11 cats and blood work was unremarkable in all 11 cats. Only one cat demonstrated a low PCV (PCV=20%), but this cat had a normal CBC and serum chemistry profile with a hematocrit of 41% and thus the low PCV was assessed as a laboratory error. Doppler blood pressure measurements were performed in 15/32 cats, including 11/17 cats eventually diagnosed with heart disease and in all cats the mean systolic blood pressure was less than 180 mm Hg. Thyroid panels were performed on 2/17 cats diagnosed with heart disease and results of both were within normal limits.
Fifteen of the 32 cats (47%) had no identifiable echocardiographic evidence of cardiac disease (Table 1). The etiology of the murmur was identified in 5/15 of these cats (Table 2): 2/5 cats had DRVOTO; 1/5 cats had both DRVOTO and DLVOTO (velocity=3 m/s); 2/5 cats had DLVOTO (velocity=1.99 m/s and 2.9 m/s). In 10/15 cats, we could not identify a murmur etiology.
Table 1.
Characteristics of 15 normal cats with heart murmurs.
| Cat number | Comments | Murmur cause |
|---|---|---|
| 1 | WNL | Unknown |
| 2 | WNL | Unknown |
| 3 | WNL | Unknown |
| 4 | WNL | Unknown |
| 5 | DRVOTO present | DRVOTO |
| 6 | WNL | Unknown |
| 7 | WNL | Unknown |
| 8 | Aov=1.9–2.9 m/s | Aov=1.9–2.9 m/s |
| DLVOTO present | DLVOTO | |
| SAM present | ||
| 9 | Aov=1.99 m/s | Aov=1.99 m/s |
| 10 | DRVOTO present | DRVOTO |
| 11 | WNL | WNL |
| 12 | Aov=3.0 m/s | Aov=3.0 m/s |
| DLVOTO present | DLVOTO | |
| DRVOTO present | DRVOTO | |
| SAM present | ||
| 13 | WNL | Unknown |
| 14 | WNL | Unknown |
| 15 | WNL | Unknown |
WNL=within normal limits, DLVOTO=dynamic left ventricular outflow tract obstruction, DRVOTO=dynamic right ventricular outflow tract obstruction, SAM=systolic anterior motion of the mitral valve, Aov=aortic velocity. Additional notes: Cat 7: Echocardiogram was repeated 1 year later; no evidence of disease. Cat 8: Echocardiogram was repeated 4 years later; no evidence of disease was found. Cat 9: Echocardiogram repeated 2 and 4 years later; no evidence of disease was found. Cat 12: At a follow-up phone conversation 4 years after the initial echocardiogram, the owner reported no clinical signs of cardiovascular disease.
Table 2.
Summary of murmur causes in 32 apparently healthy cats.
| In 15 cats with no echocardiographic evidence of heart disease: |
|
| In 17 cats with echocardiographic evidence of heart disease: |
|
DRVOTO=dynamic right ventricular outflow tract obstruction, DLVOTO=dynamic left ventricular outflow tract obstruction, Aov=aortic velocity.
Seventeen of the 32 cats (53%) had echocardiographic evidence of heart disease (Table 3). Twelve of the 17 cats had LVCH; 6/12 also had papillary muscle enlargement and 3/12 cats had focal endomyocardial thickening. Five of the 12 cats demonstrated DLVOTO and 3/12 cats had SAM. Only 1/12 cats with LVCH had mild left atrial enlargement (LA:Ao=1.6).
Table 3.
Characteristics of echocardiographic abnormalities of 17 apparently healthy cats with heart murmurs.
| Cat # | Predominant cardiac change | Other abnormalities present | Murmur cause |
|---|---|---|---|
| 1 | Focally thickened Endomyocardium | DRVOTO | DRVOTO |
| 2* | Papillary muscle enlargement | SAM present | Aov=2.0 m/s |
| Aov=2.0 m/s | |||
| 3 | Focally thickened endomyocardium | DRVOTO present | DRVOTO |
| 4 | LVCH | None | Unknown |
| 5 | LVCH | Aov=2.4 m/s | Aov=2.4 m/s |
| DLVOTO present | DLVOTO | ||
| SAM present | |||
| Enlargement of papillary muscles | |||
| 6 | LVCH | LA:Ao=1.6 | Aov=2.5 m/s |
| Aov=2.5 m/s | DLVOTO | ||
| DLVOTO present | |||
| Enlargement of papillary muscles | |||
| Focally thickened endomyocardium | |||
| 7 | LVCH | Focally thickened endomyocardium | Unknown |
| 8 | LVCH | Aov=2.0 m/s | Aov=2.0 m/s |
| DLVOTO present | DLVOTO | ||
| 9 | LVCH | Aov=2.5 m/s | Aov=2.5 m/s |
| DLVOTO present | DLVOTO | ||
| SAM present | |||
| Enlargement of papillary muscles | |||
| 10 | LVCH | Enlargement of papillary muscles | Unknown |
| 11 | LVCH | Aov=2.3 m/s | Aov=2.3 m/s |
| DLVOTO present | DLVOTO | ||
| SAM present | |||
| Enlargement of papillary muscles | |||
| 12 | LVCH | No other abnormalities identified | Unknown |
| 13 | LVCH | Aov=2.0 m/s | Aov=2.0 m/s |
| Enlargement of papillary muscles | |||
| 14 | Mitral valve disease | RVOTv=2.0 m/s | Mitral valve disease |
| DRVOTO present | DRVOTO | ||
| DLVOTO present | DLVOTO | ||
| Enlargement of papillary muscles | |||
| 15 | LVCH | SAM present | Unknown |
| Focally thickened endomyocardium | |||
| 16 | LVCH | No other abnormalities identified | Unknown |
| 17 | Mitral valve disease | No other abnormalities identified | Mitral valve disease |
Aov=aortic velocity, DRVOTO=dynamic right ventricular outflow tract obstruction, DLVOTO=dynamic left ventricular outflow tract obstruction, LVCH=left ventricular concentric hypertrophy, SAM=systolic anterior motion of the mitral valve, RVOTv = right ventricular outflow tract velocity.
Cat 2 had an echocardiogram repeated 6 months after initial examination and showed DLVOTO but other disease unchanged.
In 3/17 cats, the only abnormalities identified were mild left ventricular changes: one cat demonstrated papillary muscle enlargement only, while two cats had focal endomyocardial thickening.
Two of the 17 cats had mild degenerative mitral valve disease with mitral regurgitation. The left atrium was normal in size in both cats.
The etiology of the murmur was identified in 11/17 cats with echocardiographic evidence of heart disease (Table 3): 5/11 cats had elevated aortic velocities and DLVOTO, 2/11 had DRVOTO only, 2/11 had elevated aortic velocities only, 1/11 cats had mitral valve disease and 1/11 cats had mitral valve disease, DRVOTO and DLVOTO. We could not identify the etiology of the murmur in 6/17 cats with echocardiographic evidence of heart disease.
Discussion
We found that 53% of apparently healthy cats presenting to a cardiology service in a referral setting for evaluation of a heart murmur had echocardiographic evidence of cardiac disease. Most of these cats had LVCH with a small minority identified with degenerative mitral valve disease. Based on the high likelihood of underlying heart disease, auscultation of a heart murmur in apparently healthy cats warrants further evaluation.
Our findings are similar to those of previous investigators, although the proportion of cats with heart disease was greater in our study than prior studies. 1–3 One possible explanation is the manner in which cases were recruited in the previous and current studies – prior investigators examined 100 random apparently healthy cats, whereas we recruited apparently healthy cats in which murmurs were identified. Furthermore our exclusion criteria might have differed, resulting in exclusion of some cats with non-pathological murmurs.
All of the cats with identifiable structural heart disease in our study had mild disease, demonstrated by a normal, or mildly enlarged left atrium, and modest increases in LV wall thickness (in cases of LVCH). This is somewhat unexpected, given that a range of subclinical disease might be anticipated in a random feline population, and likely reflects the relatively small sample population of this study. Thus, clinicians should not be encouraged by this observation, as cats presenting with murmurs may harbor substantially more severe subclinical disease.
We did not evaluate papillary muscles morphometrically when making assessments about papillary muscle hypertrophy, as the technique had not yet been described at the time of data collection. 12 Only one cat in our study showed subjective evidence of isolated papillary muscle hypertrophy.
Cats frequently develop heart murmurs with structural heart disease. 13–15 However, our study and previous studies clearly demonstrate that apparently healthy cats with heart murmurs often have no underlying structural heart disease. 1–3 Furthermore, cats can develop murmurs with systemic conditions such as volume depletion, anemia, volume overload, or fever. 14,15 While we required cats to be healthy on the basis of history and physical examination for inclusion, cats with systemic illness cannot be presumed to have a murmur secondary to that illness and should receive additional testing to rule out cardiac co-morbidities.
Two-thirds of the cats (10/15) in our study without echocardiographic evidence of cardiac disease had no identifiable flow disturbance to explain the murmur. This is substantially greater than that reported in humans, where approximately 20% of humans were found to have no identifiable cause of a murmur on cardiovascular examination, 16,17 and previous reports in cats, where investigators estimated that up to 20% of cats presenting for murmur evaluation had no echocardiographically identifiable etiology. 11,18 Furthermore, we found one-third of cats (6/17) with echocardiographically identifiable structural heart disease had no identifiable flow disturbance to account for the murmur. The reason for the high proportion (50%) of cats in which murmurs were auscultated, but not echocardiographically characterized in our study, is somewhat perplexing. These results are unlikely the consequence of inappropriate probe selection, frame rate or echocardiographic interrogation, although prior investigators suggested that abnormal flows can be missed if either of these conditions are not met. 11 Furthermore, cardiologists have observed localized flow disturbances within ventricular regions that could be missed with standard imaging techniques that failed to specifically interrogate these locations (eg, placing the color Doppler gate over the apical or mid-ventricular region of the LV). A more plausible explanation, however, is that many feline murmurs are dynamic or inducible. We did not employ any maneuvers (eg, tail pinching, running a faucet, bringing a dog into the exam room) to provoke cats during the echocardiographic examination to deliberately induce a murmur by increasing sympathetic tone. 2,3 Therefore, it is possible that many inducible murmurs, detectable during a more stressful physical examination, might subside during the echocardiographic evaluation as the patient relaxes, resulting in a ‘false negative’ finding. Our findings mirror those of Drourr et al, who failed to identify flow disturbances to account for murmurs in 35/44 (79%) apparently healthy cats presenting with murmurs to a cardiology referral service, and who, like us, did not attempt to induce murmurs during the examination. 3 Thus, clinicians should be aware of the very real possibility that murmur etiology might remain undetermined even after echocardiographic evaluation by a veterinary cardiologist.
The majority of cats with echocardiographic evidence of heart disease underwent non-invasive blood pressure measurement to rule out hypertensive cardiac hypertrophy. However, some cats did not have blood pressure measured; therefore, occult hypertension could have caused the development of left ventricular hypertrophy noted in some of the cats identified with LVCH. 19–21 To increase accuracy of blood pressure measurement, three consecutive, consistent indirect measurements were obtained for cats in this study which is the minimum recommended by the American College of Veterinary Internal Medicine. 5 We took precautions to minimize stress by performing the blood pressure measurement in a quiet cardiology examination room at RBVH after the patient had visibly relaxed and become acclimated to the environment. However, given the vagaries of blood pressure measurement in cats, we cannot completely exclude the possibility that some cats were indeed hypertensive, or that others with elevated blood pressure measurements were in fact normotensive and exhibiting a white-coat effect. 22 We did not exclude cats with hypertension from the study per se, as systemic hypertension does not cause murmurs.
Only two cats underwent thyroid testing. While hyperthyroidism has been associated with cardiac disease, 23 our study specifically selected apparently healthy cats. As none of the cats exhibited clinical evidence of hyperthyroidism, we felt it unnecessary to routinely screen every cat for thyroid disease. The two cats that we screened had echocardiographic findings consistent with LVCH, which prompted us to rule out occult hyperthyroidism as a cause of these changes.
Our study does not address the issue of disease prevalence in apparently healthy cats, because we selected cats with murmurs. Previous studies have suggested that cats without murmurs can have substantial cardiac disease (HCM), 1,2,24 so clinicians should not use absence of a murmur to rule out structural heart disease.
In conclusion, our study shows that in our patient population of apparently healthy cats presenting for evaluation of a murmur, approximately 50% have detectable cardiac disease, while 50% do not. Importantly, the etiology of the murmur (echocardiographic identification of turbulent flow in a specific cardiac region) could not be determined in 50% of the cats. Clinicians should be aware that the presence of a murmur in an apparently healthy cat has a strong possibility of being physiological, but a similar probability of indicating the presence of cardiac pathology.
References
- 1.Cote E., Manning A.M., Emerson D., Laste N.J., Malakoff R.L., Harpster N.K. Assessment of the prevalence of heart murmurs in overtly healthy cats, J Am Vet Med Assoc 225, 2004, 384–388. [DOI] [PubMed] [Google Scholar]
- 2.Paige C.F., Abbott J.A., Elvinger F., Pyle R.L. Prevalence of cardiomyopathy in apparently healthy cats, J Am Vet Med Assoc 234, 2009, 1398–1403. [DOI] [PubMed] [Google Scholar]
- 3.Drourr LT, Gordon SG, Roland RM, Boggess M. Prevalence of heart murmurs and occult heart disease in apparently healthy adult cats. American College of Veterinary Internal Medicine 2010 Proceedings. Veterinary Information Network. http://beta.vin.com/Members/Proceedings/Proceedings.plx?CID=ACVIM2010&Category=8314&PID=55904&O=VIN (accessed Sept 30, 2010).
- 4.Grandy J.L., Dunlop C.L., Hodgson D.S., Curtis C.R., Chapman P.L. Evaluation of the Doppler ultrasonic method of measuring systolic arterial pressure in cats, Am J Vet Res 53, 1992, 1166–1169. [PubMed] [Google Scholar]
- 5.Brown S., Atkins C., Bagley R., et al. Guidelines for identification, evaluation and management of systemic hypertension in dogs and cats, J Vet Intern Med 21, 2007, 542–548. [DOI] [PubMed] [Google Scholar]
- 6.Thomas W.P., Gaber C.E., Jacobs G.J., et al. Recommendations for standards in transthoracic two-dimensional echocardiography in the dog and cat. Echocardiography Committee of the Specialty of Cardiology, American College of Veterinary Internal Medicine, J Vet Intern Med 7, 1993, 247–252. [DOI] [PubMed] [Google Scholar]
- 7.Boon J.A. Evaluation of size, function, and hemodynamics. Cann C., Brown P. Manual of veterinary echocardiography, 1998, Williams & Wilkins: Baltimore, 151–260. [Google Scholar]
- 8.Abbott J.A., MacLean H.N. Two-dimensional echocardiographic assessment of the feline left atrium, J Vet Intern Med 20, 2006, 111–119. [DOI] [PubMed] [Google Scholar]
- 9.Sahn D.J., DeMaria A., Kisslo J., Weyman A. Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements, Circulation 58, 1978, 1072–1083. [DOI] [PubMed] [Google Scholar]
- 10.Fox P.R., Liu S.K., Maron B.J. Echocardiographic assessment of spontaneously occurring feline hypertrophic cardiomyopathy. An animal model of human disease, Circulation 92, 1995, 2645–2651. [DOI] [PubMed] [Google Scholar]
- 11.Rishniw M., Thomas W.P. Dynamic right ventricular outflow obstruction: a new cause of systolic murmurs in cats, J Vet Intern Med 16, 2002, 547–552. [DOI] [PubMed] [Google Scholar]
- 12.Adin D.B., Diley-Poston L. Papillary muscle measurements in cats with normal echocardiograms and cats with concentric left ventricular hypertrophy, J Vet Intern Med 21, 2007, 737–741. [DOI] [PubMed] [Google Scholar]
- 13.Harpster N.K. Cardiovascular diseases of the domestic cat, Adv Vet Sci Comp Med 21, 1977, 39–74. [PubMed] [Google Scholar]
- 14.Harpster N.K. Cardiovascular diseases. Holzworth J. Diseases of the cat: medicine and surgery, 1987, WB Saunders: Philadelphia, 820–933. [Google Scholar]
- 15.Bonagura J.D. Cardiovascular diseases. Sherding R.G. The cat: diseases and clinical management, 2nd edn, 1994, Churchill Livingstone: St Louis, 824. [Google Scholar]
- 16.Attenhofer Jost C.H., Turina J., Mayer K., et al. Echocardiography in the evaluation of systolic murmurs of unknown cause, Am J Med 108, 2000, 614–620. [DOI] [PubMed] [Google Scholar]
- 17.Roldan R.A., Shively B.K., Crawford M.H. Value of cardiovascular physical examination for detecting valvular heart disease in asymptomatic subjects, Am J Cardiol 77, 1996, 1327–1331. [DOI] [PubMed] [Google Scholar]
- 18.Bonagura J.D. Feline echocardiography, J Fel Med Surg 2, 2000, 147–151. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 19.Henik R.A., Stepien R.L., Bortnowski H.B. Spectrum of M-Mode echocardiographic abnormalities in 75 cats with systemic hypertension, J Am Anim Hosp Assoc 40, 2004, 359–363. [DOI] [PubMed] [Google Scholar]
- 20.Chetboul V., Lefebvre H.P., Pinhas C., Clerc B., Boussouf M., Pouchelon J.L. Spontaneous feline hypertension: clinical and echocardiographic abnormalities and survival rate, J Vet Intern Med 17, 2003, 89–95. [DOI] [PubMed] [Google Scholar]
- 21.Nelson O.L., Reidesel E., Ware W.A., Christensen W.F. Echocardiographic and radiographic changes associated with systemic hypertension in cats, J Vet Intern Med 16, 2002, 418–425. [DOI] [PubMed] [Google Scholar]
- 22.Belew A.M., Barlett T., Brown S.A. Evaluation of the white coat effect in cats, J Vet Intern Med 13, 1999, 134–142. [DOI] [PubMed] [Google Scholar]
- 23.Jacobs G., Hutson C., Dougherty J., Kirmayer A. Congestive heart failure associated with hyperthyroidism in cats, J Am Vet Med Assoc 188, 1986, 52–56. [PubMed] [Google Scholar]
- 24.Rush J.E., Freeman L.M., Fenollosa N.K., Brown D.J. Population and survival characteristics of cats with hypertrophic cardiomyopathy: 260 cases (1990–1999), J Am Vet Med Assoc 220, 2002, 202–207. [DOI] [PubMed] [Google Scholar]