NAVC - How I Treat Feline Hypertension
World Small Animal Veterinary Association World Congress Proceedings, 2014
Clarke Atkins, DVM, DACVIM (Internal Medicine and Cardiology); Jane Lewis Seaks, Distinguished Professor Emeritus
College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA

Hypertension is the most important cardiovascular disease of the aged cat and the most important vascular disease in cats. Hence, its recognition and appropriate treatment are emerging as a critical component of small animal geriatric medicine. There is a host of target organs of hypertension. Our experience has shown that hypertensive cats have associated disease, in order of prevalence, of the eye, kidney, heart, and central nervous system.


Therapies for feline hypertension have varied and have not often been systematically evaluated. Therapies that have been employed and reported upon include diuretics (furosemide and spironolactone), angiotensin-converting enzyme inhibitors (ACE-I; captopril, enalapril, lisinopril, and benazepril), beta-blockers (propranolol and atenolol), and calcium-channel blockers (diltiazem and amlodipine). Littman retrospectively evaluated 24 cats with chronic renal failure (CRF) and found that the most effective antihypertensive therapy was the combination of a beta-blocker and an ACE-I and that there was a poor response to furosemide. Jensen prospectively studied 12 similarly affected cats and found that the response to an ACE-I or beta-blocker alone was poor. Another retrospective study of 12 hypertensive cats with CRF and unresponsive to other therapy, showed amlodipine to lower blood pressure by ≥ 20% in 11. Snyder demonstrated blood pressure control in a randomized, blinded, placebo-controlled study of amlodipine in hypertensive cats as well. Finally, the NCSU study retrospectively found amlodipine to lower blood pressure ≥ 20% in 30 of 32 hypertensive cats with 28 of 32 becoming normotensive. Diltiazem and beta-blockers alone or with ACE-I also lowered blood pressure in the majority of cats so treated. The literature and clinical experience would, nevertheless, lead one to appropriately conclude that amlodipine is the single best agent for the management of feline systemic hypertension. This said, beta-blockers have a specific role in slowing heart rate and blocking the cardiovascular effects of T3 in hyperthyroidism; ACE-I in combating drug-induced or spontaneous activation of the RAAS, for preserving renal function, and for proven effects in lowering blood pressure; spironolactone for its aldosterone-antagonistic effects; and furosemide (possibly with nitroglycerin) for use with concurrent heart failure (See Table).

Other therapeutic considerations include whether there is activation of the RAAS (initially or iatrogenically), the role of the sympathetic nervous system, renal function and the effects of hypertension on renal function, salt intake, presence of heart failure (uncommon), and the presence of reversible causes of hypertension (e.g., hyperthyroidism, diabetes mellitus, adrenal tumors). Additionally, I try to limit the number of pills to 1 (or 2) daily to reduce strain on the human-animal bond. In deciding on a therapeutic approach, the author divides cats as follows: reversible cause - yes or no; with or without presumed RAAS activation (renal failure, heart failure, or treatment with vasodilators or loop diuretics); and by presence or absence of tachycardia (> 200 bpm). The only common treatable cause of feline hypertension is hyperthyroidism, which is treated with methimazole, surgery, or 131I. In these cats, because of the effects of T3 on beta receptors, I employ a beta-blocker, such as atenolol (6.25–12.5 mg PO daily), to reverse the cardiovascular effects of hyperthyroidism prior to or until more definitive therapy is efficacious. If unsuccessful, I add enalapril at 0.5 mg/kg/day PO. In all cases, I employ a moderately salt-restricted diet (one designed for kidney patients) to lessen total body sodium without worsening renal function or severely activating the RAAS. Another method of evaluation is by target organ damage and thereby urgency of treatment (see Figure below). This thought process suggests that BP-dependent organs (brain, eye) are at greater immediate risk than RAAS-dependent target organs (kidney, heart, vessels), so the approach can be different.


Figure 1. Risk of target organs dictates type and urgency of treatment
Figure 1. Risk of target organs dictates type and urgency of treatment


In the euthyroid, non-tachycardic cat with hypertension, the somewhat complex algorithm described below can be avoided by merely administering amlodipine and enalapril each day. I advise 1 tablet in the AM and 1 in the PM, if the owners' schedule allows. If blood pressure control is not successful, see the material below.

Algorithmic Approach to Hypertension

RAAS Abnormally Activated (Most Cases)

When conditions (heart failure, renal failure, or drug therapy) indicate the RAAS is inappropriately activated, I begin therapy with amlodipine, a moderately salt-restricted diet and enalapril. If a normotensive state does not result, I add, sequentially, atenolol and finally diuretics (furosemide or spironolactone).

Alternatively, if tachycardia is a concern, moderate salt restriction, atenolol, and enalapril would be used initially. If unsuccessful control of hypertension results, amlodipine would be added and followed sequentially, as needed, by a doubling of the amlodipine dosage, and finally diuretic therapy if needed. If after initial therapy, heart rate control is inadequate, the atenolol dose is first increased. If this does not adequately control heart rate, I would substitute long-acting diltiazem (Dilacor® at 30 mg PO BID) for amlodipine to better control heart rate and then follow the stepwise sequence mentioned above for blood pressure control, if needed.

Heart failure secondary to hypertension is rare and will not be discussed, except to say that diuretics will likely be necessary in such patients to control signs and that enalapril is indicated. Lastly, if renal failure or significant renal disease is present, the etiology should be sought (at least by urinalysis and culture) in the hopes of finding a reversible cause. Otherwise, treatment of renal disease is standard and beyond the scope of this manuscript. It is wise to consider the routes of excretion of the drugs being used in deciding dosage and dosing interval in the face of renal insufficiency. Lastly, hypotension may infrequently result from over-exuberant antihypertensive therapy; this should be avoided, as it may further compromise renal function.

The prognosis, overall, for hypertension is guarded but not grave. Vision lost rarely returns but survival averages have ranged from 18–21 months from the date of diagnosis.

Cardiovascular formulary for the hypertensive cat


Trade name*






1.25 mg tablets

0.625 PO SID–BID




30 mg tablets

7.5 mg PO TID

Lusitrope, vasodilator, negative chronotrope


Dilacor XR

180, 240 mg caps

30 mg PO BID


Cardizem CD

180, 240 mg caps

45 mg PO SID



Enacard (Vasotec)

1, 2.5, & 5 mg tablets

0.5 mg/kg PO SID

ACE-I (CHF, hypertension)


Lotensin (Fortekor)

5 & 10 mg tablets

0.25–0.5 mg/kg PO SID–BID




25 mg tablets

6.25–12.5 mg PO SID

Negative chronotrope, antiarrhythmic, lusitrope, antihypertensive


Nitrol, Nitro-Bid

2% ointment

1/8–¼ inch topically TID for 24 hours

Venodilator (CHF)

LMW Heparin


2500 U/0.2 ml

100 U/kg SQ qd




81 mg

40–80 mg q 72 h




75 mg

17.5 mg SID



Speaker Information
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Clarke Atkins, DVM, DACVIM (Internal Medicine and Cardiology)
College of Veterinary Medicine
North Carolina State University
Raleigh, NC, USA

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