Feline Hypertension: Diagnosis and Management
Dr Jonathan Elliott, MA, Vet MB, PhD, Cert SAC, Dip ECVPT, MRCVS
Systemic hypertension has become more frequently recognized in clinical practice as a serious problem of the ageing cat population. The reason for this is that methods for reliable measurement of arterial blood pressure in the cat have become more readily available to the practitioner. With these tools, therefore, it is possible to diagnose and treat this disease.
Measurement of systemic arterial blood pressure (SABP)
Indirect blood pressure measurement is now possible using a variety of methods. The equipment is commercially available and within the price range of many small animal practices. The three main methods available employ the oscillometric, ultrasonic Doppler, or photoplethysmographic techniques. Each has its pros and cons and developments are occurring in the technology to improve their application to the cat.
The technique used by this author is the Doppler method. We use the forelimb and apply the cuff to the antebrachium, choosing a cuff width that is about 40% of the circumference of the limb. With this method, only systolic pressure can be measured but the time required to obtain consistent readings is compatible with the practice situation. The application of a consistent routine to the measurement of SABP is important if reproducible results are to be obtained from one visit to the next. The white coat effect can be significant in the cat and measures should be taken to minimize this. These include allowing time for the cat to settle in the consultation room, measuring the blood pressure before starting the physical examination and having the owner present to gently restrain the cat if appropriate.
Criteria for the diagnosis of hypertension
Each clinic will need to develop their own criteria for diagnosing systemic hypertension based on their blood pressure measurements. This will vary according to the method and site used for measuring blood pressure. We take a SABP reading of above 175 mmHg to be abnormal. If this is coupled with clinical signs of ocular or CNS damage then a single measurement of >175 mm Hg would be sufficient evidence for us to commence treatment immediately. If there are no ocular lesions compatible with systemic hypertension then we would recheck the cat in 7 to 14 days and perform a routine plasma biochemistry screen, measure the circulating total thyroxine concentration and do a complete urinalysis. If the SABP is consistently above 175 mmHg on the second examination and the cat has an identifiable disease known to predispose to systemic hypertension, then we would commence treatment. If no underlying disease is found on the routine laboratory tests described above we may ask that the cat return for a third blood pressure measurement before recommending treatment. Most cats that are consistently hypertensive on two separate occasions remain hypertensive on the third occasion.
Risk factors for the development of systemic hypertension
Systemic hypertension in the cat is most frequently associated with chronic renal disease. The association is often said to be a secondary one with renal disease affecting the ability of the animal to regulate its blood pressure effectively. However, it is well recognized in human medicine that systemic hypertension is a significant risk factor for the development and progression of chronic renal disease. Many cats we have diagnosed with systemic hypertension are mildly azotaemic and they represent about 20% of the total population of chronic renal failure cases we diagnose in our clinical practice. Hyperthyroidism is often quoted to be a disease associated with systemic hypertension in the cat. However, although most hyperthyroid cats do have high normal SABP, the prevalence of systemic hypertension in untreated hyperthyroid cats in our clinics is around 5% and these cases tend to have concomitant azotaemia. If the blood pressure of hyperthyroid cats is examined after establishment of the euthyroid state, the prevalence of systemic hypertension increases to 20 to 25%. Thus, in some hyperthyroid cats, SABP actually increases after successful antithyroid treatment.
In other species, blood pressure seems to increase with age. The data on changes in blood pressure with age in the cat are not conclusive. Most of the cats we have diagnosed with hypertension have been 12 years or older. Nevertheless, when we compared CRF cases with hypertension and those that are normotensive, age did not appear to be a significant risk factor for hypertension.
As mentioned above, we do diagnose systemic hypertension in a proportion of animals where no underlying disease can be identified. These represent about 20% of our hypertensive caseload. Many of these non-azotaemic cases have relatively poor renal concentrating ability (urine specific gravity <1.030). It is possible that these cases represent an early stage of CRF and, if we were to measure glomerular filtration rate as a routine in our practice, we would diagnose them as such. Nevertheless, other diseases that we do not routinely test for in older cats could be underlying the systemic hypertension in these cases. Diseases such as primary hyperaldosteronism, for example, do not have established diagnostic protocols in feline practice and further work is required to establish the role of this disease in feline hypertension. Hyperadrenocorticism and pheochromocytomas are two other medical conditions which could lead to secondary hypertension and which might be considered in these cases.
Treatment of systemic hypertension in the cat
The goals in managing hypertension are at least three-fold. Firstly, target organs, such as the brain and the eye should be protected from potentially catastrophic damage through blood vessel leakage. Secondly, treatment should reverse the concentric left ventricular hypertrophy that accompanies chronic hypertension. Finally, therapy should protect the remaining functioning nephrons in the kidney, lowering glomerular capillary pressure and decreasing the severity of proteinuria.
When faced with a cat with severe hypertension and the early signs of ocular damage, reducing the SABP to around 165 mm Hg seems to be protective and prevents further ocular or CNS damage. The drug that has been proven to reliably achieve this aim in the cat is the calcium channel blocker, amlodipine. Efficacy of amlodipine in the management of feline hypertension has been proven by a double blind placebo controlled clinical trial. The usual response seen to the administration of 0.625 or 1.25 mg of this drug once daily is a fall in SABP to between 130 and 170 mm Hg, almost regardless of the SABP prior to treatment.
Our approach, having diagnosed hypertension, would be to start the cat on 0.625 mg amlodipine once daily and to recheck the case in 7 to 14 days to assess response to treatment. In cats showing signs of acute onset of neurological problems or blindness due to retinal detachment, it may be advisable to hospitalize the animal and monitor the blood pressure daily to assess the response more closely. This will depend on the nature of the cat and the attitude of the owners. In routine cases, if after 7 to 14 days the SABP is still above 165 mm Hg, we would increase the dose of amlodipine to 1.25 mg and re-check again in 7 to 14 days. Most cases will respond to this treatment and SABP measured 24 hours after the last dose will be between 130 and 160 mmHg. Hypotension is very rarely a problem following this dosing regimen for amlodipine. SABP below 110 mmHg in the clinic, which is associated with clinical signs reported by the owner, would be a concern and an indication for reducing the dose.
In the cat, published data on the long-term effects of amlodipine treatment are relatively sparse. It seems to be the case that control of SABP below 165 mm Hg with amlodipine protects against ocular and CNS damage. This treatment also appears to cause left ventricular hypertrophy to regress. The renoprotective effects of monotherapy with amlodipine remain uncertain. We tend to see a decrease in protein excretion following 2 to 6 weeks of amlodipine therapy. Plasma creatinine does not change over this short time frame. This would suggest a beneficial effect on renal hemodynamics in the naturally occurring disease. Further studies are warranted, however. One biochemical change we have observed in cats treated with amlodipine is a decrease in plasma potassium concentration and some cases may require potassium supplementation to prevent severe hypokalaemia from developing. Monitoring urine protein to creatinine ratios (UPC) in response to treatment would seem logical extrapolating from human medicine. Empirically, we would suggest maintaining a UPC of below 0.5 is a logical treatment goal. It is important to ensure animals are free from inflammatory disease of the urinary tract when interpreting UPCs.
In cats that remain hypertensive despite treatment with 1.25 mg amlodipine once daily, the next step would be to add in an additional antihypertensive agent. In addition, those hypertensive animals with UPCs >0.5 following amlodipine treatment, may benefit from additional antihypertensive therapy. ACE inhibitors have been shown in many studies, to have beneficial actions on renal hemodynamics and anti-proteinuric effects. Benazepril has been shown to lower glomerular capillary pressure in experimental cats with reduced renal mass. The decrease in SABP in these animals was moderate (10 to 20 mmHg). Clinical experience would suggest that the use of ACE inhibitors alone in severely hypertensive cats is often inadequate to control SABP to a level that is protective of the eye and brain. However, in combination with amlodipine in the management of the refractory hypertensive cat or in the hypertensive cat that remains proteinuric following amlodipine treatment, the use of ACE inhibitors, such as benazepril, is logical. As these two drugs have different modes of antihypertensive action, there is a possibility that a synergistic response might occur resulting in significant hypotension. Preliminary observations in our clinic would suggest that such a response, whilst theoretically possible, seems to be rare. However, close monitoring of both SABP and plasma creatinine would be advisable following the introduction of the ACE inhibitor. A reduction in the UPC would also be a desirable response following the introduction of an ACE inhibitor to the treatment regimen.
The diagnosis of systemic hypertension in the cat is now possible for practitioners to make. The problem is relatively common, with one new case a month being diagnosed in practices with a high feline case-load. Treatment can be best achieved with amlodipine besylate which consistently lowers SABP to below a level that causes ocular or CNS damage. The most effective post-treatment target blood pressure and the most effective treatment which protects the kidneys from hypertensive damage remain to be determined.
Jonathan Elliott, MA, Vet MB, PhD, Cert SAC, Dip ECVPT,