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Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgements
  9. Conflict of interest
  10. References

Objectives: To evaluate the characteristics and survival of a recent population of cats with hypertrophic cardiomyopathy.

Methods: Records at the Royal Veterinary College Queen Mother Hospital for Animals were searched for cats diagnosed with hypertrophic cardiomyopathy between 1997 and 2005. Referring veterinarians and owners were contacted to determine survival times.

Results: Cats with hypertrophic cardiomyopathy were evaluated for population characteristics (n=127) and survival times (n=109). Overall median survival from date of hypertrophic cardiomyopathy diagnosis at the Queen Mother Hospital for Animals was 1276 days. Cats with hypertrophic cardiomyopathy were younger (P=0·009), and more likely to be male (P<0·001) compared to a hospital control group (n=1473), and Ragdolls were over-represented (P<0·05). Characteristics associated with increased survival in univariate analysis included younger age (P=0·007), asymptomatic status (P<0·001), normal left atrial size (P<0·001) and presence of systolic anterior motion of the mitral valve (P=0·003). Systolic anterior motion was associated with asymptomatic status, and did not influence survival in asymptomatic cats or those in congestive heart failure. Age, left atrial size and breed were significantly associated with survival time in a multivariate analysis.

Clinical Significance: Cats with hypertrophic cardiomyopathy and left atrial enlargement have a poorer prognosis. The positive influence of systolic anterior motion on survival is likely to be linked to its association with asymptomatic status.


Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgements
  9. Conflict of interest
  10. References

Hypertrophic cardiomyopathy (HCM) is a primary myocardial disease characterised by a hypertrophied, non-dilated left ventricle (Fox 2003, Maron and others 2006). HCM is the most frequently diagnosed familial heart disease in man, occurring in approximately 1:500 in the general adult population (Maron and others 1995). It is also the most common form of heart disease seen in cats, accounting for 57·5% of feline idiopathic cardiomyopathies in one study (Ferasin and others 2003). In a recent study, HCM was found in over 15% of apparently healthy cats (Paige and others 2009). Survival has been evaluated in several previous retrospective studies of feline HCM (Atkins and others 1992, Peterson and others 1993, Fox and others 1995, Rush and others 2002). The positive prognostic factors common to more than one study were absence of clinical signs (Atkins and others 1992, Rush and others 2002) and normal left atrial (LA) size (Peterson and others 1993, Rush and others 2002). Increased heart rate was a poor prognostic sign in Atkins’ study (1992), but not in the study by Rush and others (2002). Age at diagnosis was negatively associated with prognosis in one study (Rush and others 2002). In contrast with human HCM studies (MS Maron and others 2003), systolic anterior motion (SAM) of the mitral valve was associated with improved survival in feline studies (Fox and others 1995, Rush and others 2002).

The aims of this study were to investigate contemporary characteristics and survival times of cats with HCM seen at a British referral hospital, and to identify prognostic markers of survival.

Materials and methods

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgements
  9. Conflict of interest
  10. References

Cases of feline HCM were identified by searching the electronic patient records of cats seen at the Royal Veterinary College Queen Mother Hospital for Animals (QMHA) between April 1997 and April 2005. Cats were included if a diagnosis of idiopathic HCM had been made by a board-certified cardiologist or a cardiology resident supervised by a board-certified cardiologist based on two-dimensional (2D) and/or M-mode echocardiography. Cats were excluded from the study where the diagnosis of HCM had not been made at the QMHA, where concurrent hyperthyroidism or hypertension (systolic blood pressure ≥185 mmHg) had been diagnosed, or where renal disease was present and blood pressure had not been determined.

The medical records for each case were reviewed for age at diagnosis, sex, breed, date of diagnosis, heart rate, respiratory rate and presence of a murmur, gallop or arrhythmia at diagnosis, and symptomatic status at diagnosis. Cats were classified according to whether clinical signs were present at presentation (Table 1). Cats without clinical signs were classified as “asymptomatic”. Cats with clinical signs were classified as either having “congestive heart failure (CHF)” (cats showing clinical signs associated with CHF) or “clinical signs” [cats showing any clinical signs attributed to their cardiac disease, including CHF, open-mouth breathing, syncope or signs of aortic thromboembolism (ATE)]. The echocardiographic reports were reviewed for evidence of left ventricular hypertrophy, presence or absence of left atrial enlargement (LAE) and presence or absence of SAM. Left ventricular hypertrophy was defined as maximal wall thickness at least 6 mm at end diastole (Ferasin and others 2003); LAE was defined as a short axis LA:-aortic ratio >1·5 (Côté and others 2004) and SAM was defined as movement of the anterior mitral valve leaflet towards the left ventricular outflow tract observed on 2D images, supported by left ventricular outflow tract turbulence and an eccentric jet of mitral regurgitation on colour flow Doppler (Schober and Todd 2010). Any treatment initiated by the QMHA clinicians was also recorded, and analyses were carried out based on the protocol at discharge (“intention to treat”). Survival times were obtained by reviewing QMHA medical records and contacting referring practices; survival times were calculated from the day of diagnosis at the QMHA. Where practices were unable to provide details over the phone, questionnaires were sent out. Where practices were unable to provide current details, owners were contacted and asked to complete a questionnaire. For cats still alive, survival data were calculated up to May 7, 2007. A control hospital population for comparison of age, sex and breed was created to investigate risk factors for HCM amongst the referral hospital population. The control population was produced using a random number generator [Research Randomizer (1997) www.randomizer.org (accessed April 24, 2007)] to select 20% of the entire feline caseload seen by all departments in the QMHA between April 1997 and April 2005.

Table 1. Classification of symptomatic status of 127 cats with HCM
Symptomatic statusClinical signsAdditional criterian (%HCM cats)
  1. HCM Hypertrophic cardiacmyopathy, CHF Congestive heart failure.

AsymptomaticNone 59 (46·4%)
CHFRespiratory distress, tachypnoeaRadiographic evidence of pulmonary oedema/pleural effusion47 (37·0%)
  OR 
  Ultrasonographic evidence of pleural effusion 
  OR 
  Clinical response to furosemide 
Clinical signsCHF 68 (53·5%)
 OR  
 Open-mouth breathing with exertion  
 OR  
 Syncope  
 OR  
 Aortic thromboembolism  

Data were analysed using commercial software (SPSS for windows v15.0.1, SPSS, Inc., 2006 and GraphPad Prism 5, GraphPad Software, 2007) and are reported as median and range for non-normally distributed data. The Mann-Whitney test was used to compare continuous, non--normally distributed data. Categorical data were assessed with the chi-squared and Fisher’s exact tests as appropriate. Survival curves were generated using the Kaplan-Meier method and differences between groups were analysed using the Log-Rank (Mantel-Cox) test. Survival analysis was performed both with and without cats that survived less than 24 hours. Non-cardiac deaths (with survival included up to the point of death) and those cats still alive at the end of the study were right-censored. To evaluate the effects of multiple variables upon survival, multivariate analysis was performed using variables significant at P<0·20 using a forward selection stepwise Cox regression model, and hazard ratios and 95% confidence intervals were calculated. For statistical analysis within the Cox regression model, breed was collapsed into five groups – Domestic Shorthair (DSH), Domestic Longhair, Other Shorthair (containing British Shorthairs, Burmese and Oriental Shorthairs), Persian (containing Exotic Shorthairs and Persians) and Other Longhair (containing Maine Coons and Ragdolls). A value of P<0·05 was considered statistically significant.

Results

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgements
  9. Conflict of interest
  10. References

From April 1997 to April 2005, 155 cats were diagnosed with HCM. Following exclusions for hyperthyroidism (n=10), hypertension (n=9), renal disease without blood pressure measurement (n=5) and a previous diagnosis of HCM (n=4), 127 cats with HCM were included in the study. These 127 cats were all client-owned, and as far as we are aware none had been referred as part of a screening programme. The hospital population created as a control for this study contained 1473 cats.

A comparison of signalment in HCM cats versus the control population is shown in Table 2. HCM cats were significantly younger than control cats (median age 4·6 years versus 6·0 years, P=0·009) and more likely to be male (74·8% versus 58·6%, P<0·001). Of the 28 breeds in the control population, 9 were represented in the HCM population. Only Ragdolls were over-represented in the HCM population compared with the hospital population (P=0·049). No interaction of age and breed was identified, except that Ragdolls were younger [2·5 (0·5 to 4·5) years] than other HCM cats [5·0 (0·2 to 16·7) years] (P=0·038).

Table 2. Signalment of cats with HCM (n=127) versus control population (n=1473)
SignalmentHCMControlP value
  1. HCM Hypertrophic cardiomyopathy.

Age (median and range)4·8 (0·2 to 16·7) years6·0 (0·0 to 21·0) years0·009
Male74·8%58·6%<0·001
British Shorthair5·5%3·5%0·225
Burmese1·6%2·4%0·764
Domestic Longhair8·7%8·6%1·000
Domestic Shorthair70·1%65·0%0·285
Exotic Shorthair0·8%0·7%0·599
Maine Coon0·8%1·5%1·000
Oriental Shorthair0·8%0·5%0·529
Persian7·9%5·5%0·314
Ragdoll3·9%1·4%0·049
Other 10·9% 

Clinical findings in the HCM cats are shown in Table 3. Blood pressure was recorded in 70/127 (55·1%) of cats. Blood total thyroxine concentrations were recorded in 32/127 (25·2%) cats, and in 16/26 (61·5%) cats greater than nine years old. Auscultation was abnormal (defined as a murmur, gallop or arrhythmia) in 112/127 cats, with some cats presenting with more than one abnormality. Overall, 71·7% of cats presented with a murmur. A greater proportion of asymptomatic cats had a murmur (91·5%) than cats with CHF (42·6%, P<0·001). A gallop sound was more common in cats with CHF (31·9% versus 6·8% in asymptomatic cats, P=0·001), as were arrhythmias (19·2% with CHF versus 5·1% in asymptomatic cats, P=0·023). A normal cardiac auscultation was more likely in cats with CHF (21·3%) than in asymptomatic cats (5·1%, P=0·012). Only three asymptomatic cats were normal on auscultation; one had a familial history of HCM and the other two developed transient clinical signs (in one case jugular pulsation, the other a gallop) following administration of intravenous fluid therapy at their referring veterinarians. Of the 12 cats with clinical signs and normal auscultation, 10 had CHF. Auscultation was more likely to be abnormal in cats with SAM than those without SAM (P=0·011). There was no correlation between the presence of LAE and abnormal auscultation.

Table 3. Clinical findings in 127 cats with HCM
Clinical findingsn%Median (range)
  1. HCM Hypertrophic cardiomyopathy, CHF Congestive heart failure, SAM Systolic anterior motion.

Heart rate118 180 bpm (84 to 240)
Respiratory rate110 44 bpm (20 to 180)
Murmur12771·7 
Gallop12718·1 
Arrhythmia12710·2 
Normal auscultation12711·8 
Absence of clinical signs12746·5 
CHF12737·0 
Aortic thromboembolism12711·8 
Left atrial enlargement12748·8 
SAM12745·7 

More cats had clinical signs (53·5%) than were asymptomatic (46·5%). Not all cats with clinical signs had CHF; 16·5% had clinical signs without evidence of CHF. These signs included syncope, dyspnoea, open-mouth breathing, exercise intolerance and ATE and all of these cats had either radiographic or ultrasonographic evidence of the absence of pleural effusion or pulmonary oedema. Fifteen cats presented with ATE, 10 of which had concurrent CHF. LAE was found in 48·8% of all cats and SAM was found in 45·7%. Cats with SAM were younger [3·3 (0·2 to 11·0) years] than those without SAM [6·5 (0·4 to 16·7) years, P<0·001]. LAE was positively associated with clinical signs (P<0·001), CHF (P<0·001) and absence of SAM (P=0·004). SAM was associated with asymptomatic status (P=0·013).

Eight different treatment protocols were defined according to drug combinations (Table 4). Patients receiving aspirin, nitroglycerin or pimobendan were grouped according to their other concurrent medications. Cats presenting with SAM were more likely to receive beta blockers than cats presenting without SAM (P<0·001); however, there was no association between presenting with SAM and receiving an angiotensin converting enzyme (ACE) inhibitor (P=0·473). Cats presenting with CHF or LAE were unlikely to receive a beta blocker (P<0·001 and P=0·028, respectively) but were more likely to receive an ACE inhibitor (P<0·001 and P<0·001).

Table 4. Treatment protocols for 127 cats with HCM
Treatment protocoln (%)
  1. HCM Hypertrophic cardiomyopathy, ACE inhibitor Angiotensin converting enzyme inhibitor.

  2. Other – not included in analyses – died in first 24 hours (n=6), just diltiazem (n=2), just spironolactone> (n=1).

ACE inhibitor6 (4·7)
Beta blocker27 (21·3)
ACE inhibitor and beta blocker13 (10·2)
Furosemide6 (4·7)
Furosemide and ACE inhibitor30 (23·6)
Furosemide and beta blocker4 (3·1)
Furosemide, ACE inhibitor and beta blocker4 (3·1)
No treatment28 (22·0)
Other9 (7·1)

At the time of the study, survival data were available for 109 cats (39 cats were still alive, 70 had died or been euthanised). Eighteen were lost to follow-up and these were excluded from all survival analysis. Of the 70 cats that died, 18 were for non-cardiac reasons, including neoplasia (n=4), neurological abnormalities (n=3), renal disease (n=3), road traffic accidents (n=3), gastrointestinal disease (n=2), urinary disease (n=1) and unknown cause (n=2). Median follow-up was 397 days and median survival for all HCM cats was 1276 (0 to 3617) days. The survival analysis was repeated excluding cats that survived less than 24 hours, but yielded similar results and so is not reported here. Kaplan-Meier survival curves are shown of the effect on survival of CHF (Fig 1), LAE (Fig 2), SAM (Fig 3), SAM in asymptomatic cats (Fig 4), SAM in cats with clinical signs (Fig 5) and SAM in cats with CHF (Fig 6). Median survival for other groups is listed in Table 5.

image

Figure 1. Survival (cardiac mortality): hypertrophic cardiomyopathy (HCM) +/− congestive heart failure (CHF). Median survival was greater than 3617 (0 to 3617) days in cats without CHF and 194 (0 to 2899) days for cats with CHF

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image

Figure 2. Survival (cardiac mortality): hypertrophic cardiomyopathy (HCM) +/− left atrial enlargement (LAE). Median survival was greater than 3617 (0 to 3617) days in cats with normal LA size and 229 (0 to 2190) days in cats with LAE

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image

Figure 3. Survival (cardiac mortality): hypertrophic cardiomyopathy (HCM) +/− systolic anterior motion (SAM). Median survival was 372 (0 to 2899) days in cats without SAM and greater than 3617 (0 to 3617) days in cats with SAM

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image

Figure 4. Survival (cardiac mortality): asymptomatic hypertrophic cardiomyopathy (HCM) +/− systolic anterior motion (SAM). For asymptomatic cats, median survival was greater than 2574 (2 to 2574) days for cats without SAM and greater than 3617 (0 to 3617) days for cats with SAM

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image

Figure 5. Survival (cardiac mortality): hypertrophic cardiomyopathy (HCM) with clinical signs +/− systolic anterior motion (SAM). For cats presenting with clinical signs, median survival was 194 (0 to 2899) days for cats without SAM and greater than 2791 (0 to 2791) days for cats with SAM

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image

Figure 6. Survival (cardiac mortality): hypertrophic cardiomyopathy (HCM) with congestive heart failure (CHF) +/− systolic anterior motion (SAM). For cats with CHF, median survival was 218 (0 to 2899) days for cats without SAM and 191 (0 to 2190) days for cats with SAM

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Table 5. Median survival times (cardiac mortality, days) for 109 cats with HCM
 YesNoP value
  1. HCM Hypertrophic cardiomyopathy, CHF Congestive heart failure, LAE Left atrial enlargement, SAM Systolic anterior motion.

Age >6 years370 (0 to 1616)1941 (0 to 3617)0·007
Ragdoll19 (4 to 40)1297 (0 to 3617)<0·001
Clinical signs229 (0 to 2899)>3617 (0 to 3617)<0·001
CHF194 (0 to 2899)>3617 (0 to 3617)<0·001
LAE229 (0 to 2190)>3617 (0 to 3617)<0·001
SAM (all HCM cats)>3617 (0 to 3617)372 (0 to 2899)0·003
SAM (asymptomatic cats only)>3617 (0 to 3617)>2574 (2 to 2574)0·345
SAM (cats with clinical signs only)>2791 (0 to 2791)194 (0 to 2899)0·004
SAM (cats with CHF only)191 (0 to 2190)218 (0 to 2899)0·303

In the univariable analysis, young cats (≤6 years) lived longer than older cats (>6 years, P=0·007). Ragdolls had shorter survival times when compared to all other cats in the study, with a median survival of 19 days compared with 1297 days for other cats (P<0·001). No other breed had a significantly different survival.

Factors associated with increased survival times included asymptomatic status, normal LA size and presence of SAM. Nevertheless, SAM did not have a significant influence on survival in the asymptomatic cats, nor in cats with CHF (Table 5, Figs 4 and 5). SAM remained a positive prognostic indicator in those cats presenting with clinical signs (a group that included cats with intermittent open-mouth breathing, CHF and ATE) (Fig 6). Survival time was not significantly influenced by sex, heart rate or respiratory rate. Treatment protocol was strongly associated with the presence or absence of CHF, and there was no effect of treatment on survival within these groups.

Compared with cats that survived less than one year, cats surviving greater than three years were younger (P=0·012), more likely to be asymptomatic (P=0·005), to have normal LA size (P<0·001) and to have SAM of the mitral valve (P=0·003) at presentation.

Age, breed, asymptomatic status (yes/no), presence of CHF, LAE and SAM were taken forward to the multivariable model. Age (>6 years), LAE and breed (Other Longhair) remained negative predictors of survival in multivariable analysis (Table 6). Older cats had a 2·96-fold increase in hazard of death compared to young cats, Other Longhair (Ragdolls and Maine Coon) had an 8·75-fold hazard of death compared to the DSH reference category and the presence of LAE increased the hazard of death 6·65-fold.

Table 6. Final model of the Cox proportional hazards multivariable analysis of survival in 109 cats with HCM
 HR95% Confidence interval of HRP value
  1. HCM Hypertrophic cardiomyopathy, HR Hazard ratio, LAE Left atrial enlargement, DSH Domestic Shorthair (n=80), DLH Domestic Longhair (n=8).

  2. *British Shorthair (n=5), Burmese (n=2) and Oriental Shorthair (n=1).

  3. Exotic Shorthair (n=1) and Persian (n=7).

  4. Maine Coon (n=1) and Ragdoll (n=4).

LAE6·653·32 to 13·34<0·001
Breed   
 DSHReference 0·002
 DLH1·130·47 to 2·760·782
 Other Shorthair*0·520·12 to 2·220·379
 Persian2·120·76 to 5·870·149
 Other Longhair8·752·96 to 25·88<0·001
Age   
 ≤6 Years  0·001
 >6 Years2·961·52 to 5·76 

Discussion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgements
  9. Conflict of interest
  10. References

Although there have been other reports of outcome in cats with HCM (Atkins and others 1992, Peterson and others 1993, Fox and others 1995, Rush and others 2002, Ferasin and others 2003), this is the largest European study to date. Median survival (1276 days) in this study was longer than in previous studies [492 days (Ferasin and others 2003) and 732 days (Atkins and others 1992)], despite similar proportions of cats with CHF. This could reflect different treatment protocols, differences in euthanasia recommendations or genuine differences in the populations.

In this study, cats with HCM were younger than control cats, and slightly younger (median age 4·8 years) than previously reported for HCM (5·9 to 6·5 years, Atkins and others 1992, Ferasin and others 2003). We also found cats with SAM were younger than those without SAM, which has not been previously reported. As in previous reports, males were over-represented (74·8%) but sex did not affect the survival. It is likely that there is a true male bias in the feline HCM population, although there is no such male predisposition in human HCM (Maron and others 2000).

Thirty-seven per cent of cats had CHF in this study, which is comparable with previous studies; 16·5% of cats in the study presented with clinical signs in the absence of CHF. These signs included open-mouth breathing and dyspnoea, clinical signs which are normally due to CHF. One possible explanation is that these cats were suffering from angina-like chest pains, a presentation reported in human patients with HCM (BJ Maron and others 2003). The proportion of cats without clinical signs (46·5%) was also similar to previous studies. In this study only 11·8% of HCM cats were normal on auscultation, whereas Rush and others (2002) found 22% of cats with HCM had no gallop or murmur. Auscultatory abnormalities appeared to be more common in asymptomatic cats than in those with CHF, as an asymptomatic cat might not otherwise be submitted for further investigations in the absence of a murmur. An alternative explanation is that murmurs become less common in cats with CHF. In this study, we did find that SAM was less common in cats with CHF, although the proportion overall (45·7%) was mid-way between other studies [28·8% (Rush and others 2002) to 67·4% (Fox and others 1995)].

Although our finding that cats up to six years lived longer than older cats is consistent with the findings of Rush and others (2002), even in the general cat population one would expect young cats to live longer than old cats. Nonetheless, it was important to adjust the other variables identified in the multivariable model by age.

Ragdolls (but not Maine Coons) were over-represented in this study, and were younger at presentation than the general HCM population. They also had significantly shorter survival times compared to other breeds. This supports previous findings (Lefbom and others 2001) where they were reported to suffer from a more severe type of the disease and to be diagnosed at a mean age of 15 months in a series of 10 Ragdolls with HCM. Although Ragdolls were grouped with Maine Coons for multivariable analysis and remained an independent prognostic variable, most of this effect can be attributed to the contribution of the Ragdolls rather than the Maine Coons. Whilst the number of Ragdolls in the study is very small, the briefness of their survival postdiagnosis was felt to be worthy of mention. As HCM is known to have a genetic cause in the Ragdoll (Meurs and others 2007) and as we have no information on whether or not these cats were related, we cannot rule out a particularly malignant mutation within a family line rather than a breed associated effect. However, as there have been previous reports of Ragdolls developing severe disease (Lefbom and others 2001), it is likely that this is a breed-related effect. Other breed associations should be interpreted in the context of breeder screening, which could result in a relative increase in the proportion of less clinically severe cases.

As in the study of Rush and others (2002), no significant relationship was found between heart rate and survival. This is in contrast to the reported findings of Atkins and others (1992) where survival was improved in cats with a heart rate of less than 200 beats/minute.

Asymptomatic cats had longer survival times than symptomatic cats, with the asymptomatic cats failing to reach a survival probability of less than 50% by the end of the study (median survival time >3617 days). Improved survival for cats without clinical signs was recognised in Atkins and others’ (1992) study (median survival time 1129 days) and Rush and others’ (2002) study (median survival time >1830 days). Survival times for cats with CHF (194 days) were shorter than previously reported [563 days (Rush and others 2002)] but longer than first reported [92 days (Atkins and others 1992)].

As in previous studies (Peterson and others 1993, Rush and others 2002), LAE was a negative prognostic indicator and associated with clinical signs and CHF. LAE has also been associated with ATE (Rush and others 2002), and cats with ATE have generally poor survival times, with median survival time varying from 61 days (Atkins and others 1992) to 184 days (Rush and others 2002). This could be another reason for the strong link between LAE and poor survival (Fig 2).

SAM was an overall positive prognostic indicator in both this study (Fig 3) and in previous studies (Fox and others 1995, Rush and others 2002). However, in human HCM patients SAM is a negative prognostic indicator, and is linked to worsening of New York Heart Association stage classification and increased risk of sudden death (MS Maron and others 2003). We found SAM was less common in symptomatic cats, in cats with CHF and in cats with LAE. It is not possible to determine from a retrospective study whether this is because a disproportionate number of asymptomatic cats with SAM are detected as a result of their murmur, or because cats stop demonstrating SAM when they develop CHF. SAM was not a prognostic indicator of survival in cats with CHF (Fig 6), nor in asymptomatic cats (Fig 4). Although SAM was associated with a better prognosis in cats with clinical signs (Fig 5), this may be because CHF was linked to absence of SAM and to increased risk of death. Those cats with SAM were more likely to be suffering from non-CHF clinical signs (e.g. syncope or open-mouth breathing with exertion) and would thus have had a reduced risk of death compared to the CHF cats.

Study limitations

There are certain weaknesses within this study. The population characteristics were obtained retrospectively, so it was not possible to rule out every cause of left ventricular hypertrophy in every case. Cases were investigated by clinicians according to their clinical judgement and the financial constraints of owners. Blood pressure was not measured in every case, so that some hypertensive cats may have been included in the study, despite excluding cats with known renal disease. Conversely, some cats may have been excluded from the study as a result of falsely elevated blood pressure measurements due to stress. Thyroxine concentrations were not measured in every cat. The control population may not be representative of all normal cats as it represents a population at a referral institution rather than the population of cats in the community. As a retrospective study, certain weaknesses are inherent. Reliance is placed on previous clinical records and on the memories of owners. Cats were treated by multiple clinicians using different treatment protocols. A prospective study would help eliminate the variation in these factors.

Conclusion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgements
  9. Conflict of interest
  10. References

We found that cats with HCM were younger than the hospital population and were more likely to be male. Ragdolls appeared to be predisposed and had a particularly poor prognosis. Younger age, lack of clinical signs and normal LA size were all associated with improved survival. SAM was associated with improved survival in cats with clinical signs, but not in asymptomatic cats or cats with CHF. A prospective study would be necessary to clarify the effect of SAM on prognosis.

Acknowledgements

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgements
  9. Conflict of interest
  10. References

We would like to thank all the practices who referred cats included in this study, and particularly those who kindly supplied follow-up information. We would also like to thank all the clinicians at the QMHA who wrote referral letters for the cats included in this study.

Conflict of interest

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgements
  9. Conflict of interest
  10. References

None of the authors of this article has a financial or personal relationship with other people or organisations that could inappropriately influence or bias the content of the paper.

References

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgements
  9. Conflict of interest
  10. References
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