Clinical Signs
Feline hypertension is most often diagnosed when a cat is presented with blindness. On examination these cats typically have retinal detachment, retinal haemorrhage, hyphema, or in most instances some combination of these findings. If fundic examinations are performed in visual cats that have been pre-emptively diagnosed with hypertension then the lesions tend to be more subtle; small retinal haemorrhages, focal retinal detachments and retinal oedema are most often observed.
Cats may also be presented for neurological signs; ataxia, weakness, disorientation, amaurosis, vestibular signs, paraparesis, decorticate posturing, stupor, seizures and sudden death have all been reported. This is considerably less frequent than presentation for ocular abnormalities.
Hypertensive cats are rarely presented with signs of congestive heart failure. More often a murmur is noted in an older cat and this increases the clinical suspicion of hypertension. However, heart murmurs are found in many normotensive older cats, so this finding alone is not enough to establish a diagnosis.
Diagnosis
The first, and most obvious reason for suspecting that a patient is hypertensive, and therefore measuring its blood pressure, is that it is exhibiting consistent clinical signs as described above. Increasingly, however, attempts are being made to measure blood pressure in a pro-active manner, prior to the development of owner-recognised abnormalities. This requires an understanding of which cats are most at risk for developing hypertension.
CKD is the problem most commonly associated with severe hypertension in the cat. In a large survey of cats presenting with ocular manifestations of hypertension 44/69 (64%) had elevated serum creatinine concentrations.1 Correspondingly, when cats with CKD are evaluated the prevalence of hypertension is high.
Estimates of the prevalence have varied considerably between studies, however (from 19–65%), which may be due to different methods of blood pressure measurement, different cut-offs taken to signify hypertension, and differences in the population studied.2,3 In particular, hypertension may be more commonly diagnosed in cats with relatively mild azotaemia; most have creatinine concentrations <300 μmol/l (3.4 mg/dl) at diagnosis. The reason for this is undocumented but may be because many cats with severe azotaemia are hypovolaemic resulting in reduced blood pressure.
Although the association between CKD and hypertension in cats is well accepted it has not been conclusively proven that the CKD causes hypertension, rather than vice versa, or even a co-incidental association due to both conditions being prevalent in the geriatric population. However, blood pressure has recently been shown to increase over time at a greater rate in azotaemic compared with non-azotaemic cats, which suggests that the azotaemia is the cause of the hypertension.4
Hyperthyroidism is commonly cited as a major cause of hypertension in the cat. Recent studies have suggested that only about 10% of hyperthyroid cats are hypertensive at the time of diagnosis and the concurrent diagnosis of hyperthyroidism and hypertensive ocular disease is infrequent. However, a significant proportion (about 20–25%) of cats actually develop hypertension with treatment for hyperthyroidism. Therefore, it is not only necessary to measure blood pressure in hyperthyroid cats at the time of initial diagnosis, but also to follow their blood pressure during treatment. Another potential (but less common) endocrine cause of hypertension is hyperaldosteronism due to an adrenal tumour.
Currently about 20% of the cats diagnosed with hypertension have no apparent underlying cause (so called idiopathic hypertensives). These are cats that are euthyroid and non-azotaemic, although it is possible that many of these cats have sub-clinical renal disease. The average age of cats diagnosed with idiopathic hypertension is 15 years, with almost all being >12 years. This observation is a good indication of the importance of measuring blood pressure in elderly cats, even if no predisposing cause for development of hypertension is identified.
Practicalities of Blood Pressure Measurement
The technique for measurement of blood pressure will be discussed in the next lecture.
Antihypertensive Therapy
There is no universally accepted cut-off for what constitutes hypertension in the cat. In cats with characteristic changes of hypertensive retinopathy/choroidopathy or hyphema the decision to implement treatment is straightforward. In patients without these signs the decision to treat hypertension is based on the probability of the patient developing target organ damage (TOD), weighed against the probability that the patient has white-coat hypertension (a transient increase in blood pressure due to the stress of being examined) for which treatment is unnecessary. The risk of TOD increases as blood pressure increases; however, there is no absolute cut-off value above which it can be said that a patient cannot have white-coat hypertension. As a result other factors must also play a role in the decision to treat.
Amlodipine is the currently recommended treatment for hypertension in cats.5-7 The cat seems to be unusual in that monotherapy in most instances results in a profound reduction in blood pressure (often 40–60 mm Hg) without attendant adverse effects. This contrasts with the situation in dogs and humans where multiple medications are often required to achieve only modest reduction in blood pressure.
Amlodipine is a dihydropyridine calcium channel blocker, with preferential affinity for the L-type channels that are found in vascular smooth muscle, rather than the calcium channels present in the myocardium or nodal tissue. Its main effect is to reduce total peripheral resistance. Since the L-type (long acting) calcium channels produce currents of long duration and inactivate slowly, drugs acting on this channel tend to have long duration and slow onset of action. This is clinically important because it means that once daily dosing is possible and patients do not suffer from initial hypotension with reflex tachycardia immediately after dosing as occurs with other classes of drugs with more rapid onset of action. Amlodipine has the potential to reduce blood pressure in both normotensive and hypertensive animals but effects in normotensive cats are modest at best; in pre-clinical safety studies amlodipine did not result in measurable reduction in blood pressure in young, healthy cats.
Amlodipine has a very long terminal elimination half-life in cats (53 hours). The drug is metabolised in the liver and then eliminated through urine and faeces and this process is not affected by reduced renal function so it can be safely used in cats with CKD. Peak plasma level of the drug is seen 3–6 hours post dosing and steady-state is reached 2 weeks after treatment is started.
The initial dose of amlodipine is 0.625 mg per cat, per day. If this dose does not reduce the blood pressure sufficiently then the dose is doubled to 1.25 mg. This dose is adequate in almost all cats. Where a poor response is noted it is generally due to poor owner or cat compliance. It is important to continue to monitor blood pressure even when the initial response to treatment is good, since in the long term the requirements for anti-hypertensive therapy may increase.
Monitoring Therapy
A common question is what constitutes optimal blood pressure for a cat receiving treatment for hypertension? In humans hypertension can result in the progression or even the development of CKD. In cats there was no difference in survival time between the cats with well controlled or poorly controlled blood pressure once other factors (primarily proteinuria) had been taken into account.8 This suggests that anti-hypertensive therapy should primarily be aimed at prevention of ocular lesions and other signs that occur with severe systemic hypertension; maintaining systolic blood pressure below 165 mm Hg is probably adequate for this. This assessment is complicated; however, since cats with the most poorly controlled blood pressure were also the ones that were most proteinuric.
References
1. Maggio F, DeFrancesco TC, Atkins CE, Pizzirani S, Gilger BC, Davidson MG. Ocular lesions associated with systemic hypertension in cats: 69 cases (1985–1998). J Am Vet Med Assoc. 2000;217(5):695–702.
2. Syme HM, Barber PJ, Markwell PJ, Elliott J. Prevalence of systolic hypertension in cats with chronic renal failure at initial evaluation. J Am Vet Med Assoc. 2002;220(12):1799–1804.
3. Stiles J, Polzin DJ, Bistner DI. The prevalence of retinopathy in cats with systemic hypertension and chronic renal failure or hyperthyroidism. J Am Anim Hosp Assoc. 1994;30:654–572.
4. Bijsmans ES, Jepson RE, Chang YM, Syme HM, Elliott J. Changes in systolic blood pressure over time in healthy cats and cats with chronic kidney disease. J Vet Intern Med. 2015;29(3):855–861.
5. Elliott J, Barber PJ, Syme HM, Rawlings JM, Markwell PJ. Feline hypertension: clinical findings and response to antihypertensive treatment in 30 cases. J Small Anim Pract. 2001;42(3):122–129.
6. Snyder PS. Amlodipine: a randomized, blinded clinical trial in 9 cats with systemic hypertension. J Vet Intern Med. 1998;12(3):157–162.
7. Huhtinen M, Derre G, Renoldi HJ, et al. Randomized placebo-controlled clinical trial of a chewable formulation of amlodipine for the treatment of hypertension in client-owned cats. J Vet Intern Med. 2015;29(3):786–793.
8. Jepson RE, Elliott J, Brodbelt D, Syme HM. Effect of control of systolic blood pressure on survival in cats with systemic hypertension. J Vet Intern Med. 2007;21(3):402–409.