Recognition and therapy of systemic hypertension in cats is an important aspect of small animal geriatric medicine. Target organs of hypertension include the heart and vessels, the brain, the kidney, and probably most importantly, the eye. The etiology and pathogenesis of hypertension in cats is largely unknown, but associations with hyperthyroidism, hyperaldosteronism, and renal failure have been recognized. A recent report on 69 cases seen at North Carolina State University (NCSU) for ocular disease revealed that at least 17%, and possibly as many as 50%, of cats have no identifiable cause of systemic hypertension (primary or essential hypertension).(1) The renin-angiotensin-aldosterone system (RAAS) is probably abnormally activated in many or perhaps, most cats with systemic hypertension and certainly is activated after therapy with such drugs as loop diuretics.(2)
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, and benazepril), beta-blockers (propranolol and atenolol), and calcium channel blockers (diltiazem and amlodipine). Littman, retrospectively evaluated 24 cats with chronic renal failure (CRF), 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 similar cats and found that the response to an ACE-I or beta-blocker alone was poor.(3) Another retrospective study of 12 hypertensive cats with CRF and unresponsive to other therapy showed amlodipine to lower blood pressure by >20% in 11.(4) Snyder demonstrated blood pressure control in a randomized, blinded, placebo-controlled study of amlodipine in hypertensive cats, as well.(5) Finally, the NCSU study retrospectively found amlodipine to lower blood pressure > 20% in 30 of 32 hypertensive cats with 28 becoming normotensive.(1) 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, (6,7) and for proven effects in lowering blood pressure; (8,9) spironolactone for its aldosterone-antagonistic effects (10); and furosemide for use in heart failure accompanying hypertension.
Other therapeutic considerations include whether there is activation of the RAAS, the role of the sympathetic nervous system, renal function, and the effects of hypertension on renal function, salt intake, presence of heart failure (rare), and the presence of reversible causes of hypertension (e.g., hyperthyroidism, diabetes mellitus, pheochromocytoma). Additionally, I try to limit the number of pills to one (or 2) daily to reduce strain on the human-animal bond.
In deciding on a therapeutic approach (see Figure), 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 q24h), to reverse the cardiovascular effects of hyperthyroidism prior to or until more definitive therapy is efficacious. If unsuccessful, I would add enalapril at 0.5 mg/kg PO q24h. 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.
RAAS NOT ACTIVATED
If the RAAS is not considered to be activated (this may be an erroneous assumption) and tachycardia is not a problem, the approach is as follows: amlodipine (0.625 mg to 1.25 mg PO q24h, or even higher if unresponsive) plus a moderately salt-restricted diet and enalapril. The ACE-I is used to counteract activation of the RAAS, presumably produced by the vasodilator effect of amlodipine. If unsuccessful, I first double the dosage of amlodipine then sequentially add atenolol and finally diuretics (furosemide at 6.25–12.5 mg q24h or spironolactone at 1–2 mg/kg PO q24h), if needed. If tachycardia is present (without RAAS activation), I begin with moderate salt restriction and atenolol. If blood pressure control is unsuccessful, I, sequentially add amlodipine plus enalapril, then, if needed, double the amlodipine, and finally add a diuretic. On the other hand, if heart rate control is not initially successful, the atenolol dose is first increased. If this does not bring the exam room heart rate to < 160 or the at home heart rate to < 140, I would substitute diltiazem (DilacorR at 30 mg PO q12h) for amlodipine to better control heart rate and then follow the same sequence.
RAAS ABNORMALLY ACTIVATED
When conditions (heart failure, renal failure, or drug therapy) indicate the RAAS is inappropriately activated, I begin with amlodipine, a moderately salt-restricted diet and enalapril, followed sequentially, if blood pressure response is inadequate, with atenolol and finally diuretics (furosemide or spironolactone). If this patient were tachycardic, moderate salt restriction, atenolol, and enalapril would be used initially. If unsuccessful control of hypertension results, amlodipine is added, and followed sequentially, as needed, by a doubling of the amlodipine dosage, and finally diuretic therapy. 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 (DilacorR at 30 mg PO q12h) for amlodipine to better control heart rate and then follow the step-wise 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 cause 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 occur as a result of over-exuberant anti-hypertensive 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.(1,3)
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