Do beta-blockers have a place in the treatment of feline hypertrophic cardiomyopathy (HCM)?
This is one of those issues. Working in primary care practice I never really understood why people prescribed beta-blockers to cats with HCM. However, writing referral reports is good discipline: it forces you to think a bit more about what you’re suggesting. Now, I’m sure it’s complicated!
Presumably, it’s widely used in pre-clinical cases because it confers survival benefit?
J Vet Cardiol . 2013 Jun;15(2):93-104
Effect of treatment with atenolol on 5-year survival in cats with preclinical (asymptomatic) hypertrophic cardiomyopathy
Karsten E Schober 1, Jillian Zientek, Xiaobai Li, Virginia Luis Fuentes, John D Bonagura
Punchline ‘Our study failed to demonstrate an effect of atenolol on 5-year survival in cats with preclinical HCM‘
Hmm, probably not that then.
Well, maybe it relieves signs, even if they don’t live longer?
J Vet Cardiol . 2020 Aug;30:77-91
Atenolol in cats with subclinical hypertrophic cardiomyopathy: a double-blind, placebo-controlled, randomized clinical trial of effect on quality of life, activity, and cardiac biomarkers
A E Coleman 1, T C DeFrancesco 2, E H Griffiths 3, B D X Lascelles 1, D J Kleisch 1, C E Atkins 1, B W Keene
Punchline: ‘This study failed to identify an effect of subclinical HCM on owner-assessed QOL or activity or a treatment effect of atenolol on these variables at the dosage evaluated. These findings do not support a treatment benefit of atenolol for the goal of symptom reduction in cats with subclinical HCM.’
Nope. Not that either.
How about, even if it doesn’t help them live longer or relieve any signs, we might be able to find some surrogate indicator that it’s helping?
J Vet Intern Med . Sep-Oct 2011;25(5):1044-9
The effect of atenolol on NT-proBNP and troponin in asymptomatic cats with severe left ventricular hypertrophy because of hypertrophic cardiomyopathy: a pilot study
S W Jung 1, M D Kittleson
‘Atenolol administration did not decrease NT-proBNP or cTnI concentrations in cats with severe left ventricular hypertrophy caused by hypertrophic cardiomyopathy. These results suggest that atenolol did not decrease myocardial ischemia and myocyte death in these cats. A larger clinical trial is warranted to verify these findings‘
Gosh, struggling a bit here.
How about in HCM with congestive failure?
Fox P R (2003). Prospective, double- blinded, multicenter evaluation of chronic therapies for feline diastolic heart failure: interim analysis, J Vet Intern Med 17: 398 (abstract).
Punchline: ‘There was no benefit for any therapy over placebo (that is, furosemide alone) and a possible harm for beta-blocker administration‘
Well, that’s not very encouraging!
So, why are we using atenolol? Partly, I think it’s pressure to ‘do something’.
Secondly, textbooks and articles abound with anecdotal reports that heart rates and outflow tract velocities and, by implication, myocardial oxygen demand may be ‘improved’ in treated cats.
I’m really wary of mechanistic theories here. Although it’s easy to understand the ideas it’s also easy enough to come up with counter-theories. For example, HCM is largely a disease of diastolic failure. Atenolol and other beta-blockers are negative lusitropes and might thus accelerate diastolic failure.
Thirdly, beta-blockers are widely used in human medicine in analogous scenarios.
Ah, so presumably we can rely on human cardiology to come up with some proper evidence?
Eur Heart J . 2012 Jul;33(14):1724-33
Pharmacological treatment options for hypertrophic cardiomyopathy: high time for evidence
Roberto Spoladore 1, Martin S Maron, Rossella D’Amato, Paolo G Camici, Iacopo Olivotto
‘β-Blockers represent the mainstay of therapy and have proved effective in patients with angina or dyspnoea on effort, particularly when associated with LVOT obstruction, and are often employed to reduce the prevalence of non-sustained ventricular arrhythmias. These beneficial effects are mediated by sympathetic modulation of heart rate, ventricular contractility, and stiffness, leading to improved ventricular relaxation, increased time for diastolic filling, and reduced excitability. Despite these advantages, whether long-term treatment with β-blockers ultimately impacts outcome in HCM patients remains still undefined‘
I think that’s the crux: that, in human patients with angina or exertional dyspnoea, it’s difficult to deny patients beta-blockers when they clearly relieve self-reported signs regardless of lack of evidence of improved survival.
That’s essentially the rationale, I would assume, behind the feline study of Coleman et al. (cited above): to look for such benefits in cats. The lack of documented ‘quality of life (QOL)’ benefit somewhat undermines the otherwise reasonable argument that if betablockers are beneficial for QOL in people with HCM then they might also be in cats -so long as there aren’t actual negative effects on survival.
Personally, I think that in (presumed) HCM cats atenolol use is justifiable if there are signs of syncope/transient weakness/transient tachypnoea in the absence of any evidence of bradycardia (ideally Holter and document tachycardia…but I accept that it’s not always practical).
There’s a case to be made for atenolol in cases with marked hypotension associated with dynamic left ventricular outflow tract obstruction (DLVOTO)…….maybe in any cat with severe DLVOTO. There is a caveat that we don’t really know whether these cats consistently have SAM in the home environment (with normal sympathetic tone) and it has to be taken into consideration that atenolol also has potential adverse effects:
‘Common or very common
Abdominal discomfort; bradycardia; confusion; depression; diarrhoea; dizziness; dry eye (reversible on discontinuation); dyspnoea; fatigue; headache; heart failure; nausea; paraesthesia; peripheral coldness; peripheral vascular disease; rash (reversible on discontinuation); sleep disorders; syncope; visual impairment; vomiting
Atrioventricular block; bronchospasm
Rare or very rare
(Source; BNF Online)
In truth, I think we might not always know if our patients are suffering some of those. We wouldn’t be human if we didn’t suffer from confirmation bias: we overlook the negative outcomes in favour of those patients who do well.
There’s the complicating fact that some cats with apparent HCM may have other diseases (notably myocarditis) and that DLVOTO isn’t restricted to cats with primary HCM. We don’t really know that all the cats with ‘HCM-like’ echo findings have the same disease.
….and there’s financial cost and the fact that it’s never ideal to have to give medicines to a cat!
Acknowledgment: Thanks to the estimable Eoin Kilkenny for added ideas