Show all small animal articles
Feline Hypertension- Part 1
Clarke Atkins DVM, Dipl. ACVIM - 16/06/2012
Feline Hypertension- Part 1
Hypertension is the most important cardiovascular disease of the aged cat and the most important vascular disease in cats, making up approximately 1% of NCSU admissions from 1990-1995 (Figure 1). Its recognition and appropriate treatment is therefore emerging as a critical component of small animal geriatric medicine. There are a number of target organs for systemic hypertension (Figure 2); our experience has shown that hypertensive cats have associated disease, in approximate order of clinical presentation, of the eye, kidney, heart, and central nervous system (CNS) (1). Any discussion of management of hypertension must be preceded by a discussion of the causes of hypertension, the specific target organs affected, and the mechanism by which target organs are damaged.
Hypertension in animals has largely been considered to be secondary to other diseases (e.g. renal disease and endocrinopathies), as opposed to idiopathic (primary or essential), as is the case in most human hypertensives. This has recently been questioned. One study of hypertensive cats referred for ocular disease revealed that at least 17%, and possibly as many as 50%, of cats had no identifiable cause for their systemic hypertension (1). Another study showed that approximately 20% of hypertensive cats diagnosed in “primary-care” practice were idiopathic (2). In a retrospective review of hypertensive cats, using more rigorous inclusion criteria (Atkins, Grauer, unpublished), >10% of affected cats were determined to be idiopathic. It is important to note that the average age for hypertensive cats is 14.8 years (1).
Described and potential etiologies of secondary hypertension include chronic and acute renal disease, hyperthyroidism, hypothyroidism, hyperadrenocorticism, hyperaldosteronism, pheochromocytoma, diabetes mellitus, and possibly obesity. Clearly, chronic kidney disease (CKD) has the greatest association with hypertension and may often be causal. A recent report suggested ~ 29% of elderly cats with CKD were hypertensive (3) with a further four studies giving a range of 19-65% (4).
The pathogenesis of hypertension is complex, not well understood, and beyond the scope of this paper. However, several studies have indicated that the renin-angiotensin-aldosterone system (RAAS) is probably abnormally activated in many (if not most) cats with systemic hypertension, particularly with concurrent renal disease, and certainly after therapy with drugs such as loop diuretics and vasodilators (4-6). My therapeutic approach is based on target organ damage (present vs. absent, and, if present, which organ system(s) is in peril), and a brief review of the target organs of hypertension, and how they are injured, is appropriate.
Tissues such as the eye, brain and kidney are able to protect their microcirculation from pressure fluctuation by “autoregulation”. In the normal individual the glomerular pressure is maintained between 60- 160 mmHg. However, in hypertension, this protective measure is lost and elevated systemic pressures are translated directly to the capillary beds, producing barotrauma.
The eye is the organ at greatest risk because of its vulnerability to the insult. Hypertension disrupts the “blood-ocular barriers” and produces “protective” vasoconstriction; this is followed by secondary vascular hypertrophy/hyperplasia and vascular dysfunction with leakage of blood components into ocular tissues and fluids. Clinical findings include arteriolar tortuousity, retinal edema, hemorrhage, detachment, and hyphema (Figure 3). Blindness often results from the complications of intraocular hemorrhage (tractional retinal detachment, cataract, extensive vitreal hemorrhage, and secondary glaucoma) or, more commonly, from progressive neurosensory retinal degeneration. Blindness is usually, but not inevitably, permanent. If vision returns, it may be temporary; this is because retinal degeneration from progressive ischemic injury or excitotoxicity can develop, sometimes months afterwards. Early detection of hypertensive retinopathy is imperative, arguing strongly for yearly ophthalmic examination in aged cats.
Failure of renal autoregulation results in elevated intraglomerular capillary pressure and ongoing renal destruction. This may occur with acute or chronic kidney disease and, adding to the confusion in understanding the pathogenesis of hypertensive renal disease, renal disease begets hypertension and hypertension begets renal disease. Furthermore, activation of the RAAS contributes to renal damage. Not surprisingly, ACE-Inhibitors have been shown to spare the kidney by reducing intraglomerular pressures, inhibiting mesangial cell growth and fibrosis, and possibly by reducing proteinuria. The renal arteries and arterioles are themselves damaged and contribute to the pathogenesis (see vascular damage, below).
The kidney, like the eye, is an important target organ for hypertension, even if hypertension is secondary to renal disease. As renal disease is a major problem in the aging cat population, correction of hypertension is one way which the duration and quality of life can be improved. Yearly or more frequent fundic examination, urinalysis, microalbuminuria screening, and measurement of serum urea and creatinine, coupled with measurement of systemic blood pressure (BP), are essential in these cats.
With hypertension, the CNS also loses its ability to autoregulate. Cerebral blood pressure is normally maintained at 60-150 mmHg, but higher pressures affect the vasculature resulting in damage, leakiness, and cerebral edema, possibly with brainstem herniation (Figure 4a). Hypertension-induced over-perfusion also contributes to the edema. Vascular barotraumas may induce ischemia and brainstem or spinal cord hemorrhage (Figure 4b). Clinical signs may include cranial nerve lesions, seizures, somnolence, paralysis/ paresis and behavioral abnormalities.
Hypertension produces endothelial dysfunction with impaired vasodilation, thus worsening hypertension. Over time this results in vessel arteriosclerosis and hyperplasia of the myointimal layer, altering the vessels’ ability to protect other target organs through autoregulation. Control of BP alone does not reverse these changes, but lowering BP, while blunting the RAAS, normalizes both vascular function and anatomy (7).
Hypertension and the concomitant vascular changes produce increased cardiac afterload. This is compounded by sympathetic nervous system (SNS) activation. Cardiac hypertrophy and fibrosis is produced by the combination of hypertension (increased afterload) and RAAS and SNS activation. A review of 99 hypertensive cats (Atkins, unpublished data) revealed that the vast majority had suffered cardiac changes (Figure 5), including auscultatory abnormalities (murmur and/or gallop), cardiomegaly, left ventricular hypertrophy and/or electrocardiographic evidence of hypertensive heart disease. Despite this, only 3% of these cats developed heart failure.
Diagnosis of hypertension
Although a detailed discussion of the diagnosis of hypertension is beyond the scope of this work, a brief overview is pertinent. The veterinary profession has relied upon the Doppler method for determining BP in cats. Whilst thought to be more reliable than the oscillometric method for smaller patients, it has the distinct disadvantage of not providing diastolic or mean blood pressures in most instances. For this reason, we continue to explore the use of oscillometric equipment and newer units show promise for use in small dogs and cats. At NCSU, the tail is the appendage of choice for BP measurement, followed by the palmar surface of the front foot and finally the dorsal surface of the rear foot. Cuff width is important and should approximate to 30-40% of the circumference of the appendage used. Too small a cuff tends to over-estimate and too large a cuff to under-estimate true systemic BP. The cuff position should approximate the level of the heart. Current recommendations are that measurement should be done in a quiet area prior to examining the patient, typically in the presence of the owner and after 5-10 minutes of acclimatization. The ACVIM Panel on Hypertension suggests discarding the first measurement, then obtaining a minimum of 3, preferably 5-7, consecutive measurements with less than 20% variability in systolic BP. The conditions (including animal’s disposition, cuff size, site and all measurements) should be recorded. Many clinicians require that hypertension be documented on more than one occasion before accepting the diagnosis. Note that in animals < 10 years of age the risk of “false positive” diagnosis is increased, especially in cats because of the high prevalence of “white coat” (stressinduced) hypertension in “normotensive” animals. The possibility of misdiagnosis is reduced if concurrent predispositions (e.g. renal disease) or findings (e.g. retinopathy or murmur) are detected.
Come back next week for Part 2 covering treatment!
This article was kindly provided by Royal Canin, makers of a range of veterinary diets for dogs and cats. For the full range please visit www.RoyalCanin.co.uk or speak to your Veterinary Business Manager:
1. Maggio F, DeFrancesco TC, Atkins CE, et al. Ocular lesions associated with systemic hypertension in cats: 69 cases (1985-1998). J Am Vet Med Assoc 2000; 217: 695-702.
2. Elliott J, Fletcher M, Syme H. Idiopathic feline hypertension: Epidemiological study. J Vet Intern Med 2003;17:254.
3. Elliott J, Rawlings PJ, Markwell PJ, et al. Incidence of hypertension in cats with naturally-occuring chronic renal failure. J Vet Intern Med 1999; 13:251.
4. Brown S, Atkins C, Bagley R, et al. Guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats. J Vet Intern Med 2007;21:542-558.
5. Haggstrom J, Hansson K, Karlberg BE, et al. Effects of long-term treatment with enalapril or hydralazine on the renin-angiotensin-aldosterone system and fluid balance in dogs with naturally acquired mitral valve regurgitation. Am J Vet Res 1996;57:1645-1652.
6. Atkins CE, Rausch WP, Gardner SY, et al. The effect of amlodipine and the combination of amlodipine and enalapril on the renin-angiotensinaldosterone system in the dog. J Vet Pharm Ther 2007;30:394-400.
7. Schiffrin EL, Park JB, Intengan HD, et al. Correction of arterial structure and endothelial dysfunction in human essential hypertension by the angiotensin receptor antagonist losartan. Circulation 2000;101:1653-1659.
8. Littman MP. Spontaneous systemic hypertension in 24 cats. J Vet Intern Med 1994;8:79-86.
9. Jensen J, Henik RA, Brownfield M, et al. Plasma renin activity and angiotensin I and aldosterone concentrations in cats with hypertension associated with chronic renal disease. Am J Vet Res 1997;58:535-540.
10. Henik RA, Snyder PS, Volk LM. Treatment of systemic hypertension in cats with amlodipine besylate. J Am Anim Hosp Assoc 1997;33:226-234.
11. Snyder PS. Amlodipine: a randomized, blinded clinical trial in 9 cats with systemic hypertension. J Vet Intern Med 1998;12:157-162.
12. Maschio G, Alberti D, Janin G, et al. Effect of the angiotensin convertingenzyme inhibitor benazepril on the progression of chronic renal insufficiency. The Angiotensin-Converting-Enzyme Inhibition in Progressive Renal Insufficiency Study Group. N Eng J Med 1996;334: 939-945.
13. Brown SA, Brown CA, Jacobs G, et al. Effects of the angiotensin converting enzyme inhibitor benazepril in cats with induced renal insufficiency. Am J Vet Res 2001;62:375-383.
14. Miller RH, Lehmkuhl LB, Smeak DD, et al. Effect of enalapril on blood pressure, renal function, and the renin-angiotensin-aldosterone system in cats with autosomal dominant polycystic kidney disease. J Vet Intern Med 1999;60:1516-1525.
15. Grauer GF, Greco DS, Getzy DM, et al. Effects of enalapril versus placebo as a treatment for canine idiopathic glomerulonephritis. J Vet Intern Med 2000;14:526- 33.
16. Brilla CG ML, Weber KT. Antifibrotic effects of spironolactone in preventing myocardial fibrosis in systemic arterial hypertension. Am J Cardiol 1993;71:12-16.
17. Ligtenberg G, Blankestijn PJ, Oey PL, et al. Reduction of sympathetic hyperactivity by enalapril in patients with chronic renal failure. N Engl J Med 1999;340:1321-1328.
18. Atkins CE, Gallo AM, Kurzman ID, et al. Risk factors, clinical signs, and survival in cats with a clinical diagnosis of idiopathic hypertrophic cardiomyopathy: 74 cases (1985-1989). J Am Vet Med Assoc 1992;201:613- 618.
19. Rush JE, Atkins CE. Vascular Disease. Small Animal Medicine. D.G. Allen (ed), J.B. Lippincott Co., Philadelphia, 1991;323-340.
Show all small animal articles