In cats with asymptomatic (preclinical/subclinical) hypertrophic cardiomyopathy, does atenolol improve survival, slow progression, or improve clinical, activity or biomarker measures compared with no treatment or placebo?
Shelf #213 · gate-verified and approved by the developer
POSSIBLE (the treatment made no difference): Every controlled look at atenolol in asymptomatic feline hypertrophic cardiomyopathy has come back null on the outcomes that matter. In the 5-year cohort (Schober 2013), atenolol-treated cats had no significant advantage in all-cause mortality (P = 0.729) or cardiac mortality (P = 0.897) over untreated cats; age and left atrial size at diagnosis, not treatment, were the only predictors of outcome. In the one double-blind, placebo-controlled randomised trial (Coleman 2020), atenolol lowered heart rate and rate-pressure product but no treatment effect on quality of life or activity was demonstrated over 6 months. A 6-cat uncontrolled pilot (Jung 2011) likewise found no fall in NT-proBNP or cardiac troponin I after 30 days of atenolol. Gaps: the survival evidence is observational and open-label, so treatment choice may have been confounded; the randomised trial is small, short, and measured soft outcomes rather than survival or echocardiographic progression over about a year; and cats with obstructive physiology were not separately tested. A modest benefit is not excluded — but none has been shown. Drafted Nov 10, 2026 (VetMed build, topic #213); all figures from abstracts fetched and verified at drafting.
Prospective, observational, open-label, clinical cohort study (record's own design wording; publication type: Controlled Clinical Trial)
Who: Cats: 63 client-owned cats with preclinical hypertrophic cardiomyopathy diagnosed by echocardiography and 31 healthy control cats of similar body weight, age, gender, and breed, in a prospective cohort study; HCM cats were treated with atenolol (6.25–12.5 mg q12h, PO; n = 42) or untreated (n = 21), and were observed for 5 years after enrollment, with death from any cause as the study end point.
Result: During the observational period, 27 cats with HCM died; 14 (22%) due to cardiac disease and 13 (21%) due to non-cardiac disease. Ten control cats (32%) died of non-cardiac disease. There was no significant difference (P = 0.307) in all-cause mortality between control and HCM cats. Cardiac mortality was higher in cats with HCM compared to control cats (P = 0.005). There was no significant difference in all-cause mortality (P = 0.729) and cardiac mortality (P = 0.897) between cats with HCM treated or untreated with atenolol. Age and left atrial size at diagnosis were the only predictors of 5-year outcome, and the authors concluded that the study failed to demonstrate an effect of atenolol on 5-year survival in cats with preclinical HCM.
Watch out: Anchor corrections: this study is NOT randomised and has no placebo or blinding — the record's own wording is a prospective, observational, open-label clinical cohort, so atenolol-treated and untreated cats may have differed at baseline (confounding by indication), and it appeared in the Journal of Veterinary Cardiology, not the Journal of Feline Medicine and Surgery as the draft tasking stated. Its endpoint is 5-year survival, longer and harder than the progression/echocardiographic framing in the topic brief.
Schober KE, Zientek J, Li X, Luis Fuentes V, Bonagura JD. Effect of treatment with atenolol on 5-year survival in cats with preclinical (asymptomatic) hypertrophic cardiomyopathy. Journal of Veterinary Cardiology. 2013;15(2):93-104. PMID: 23684504. Registry ID: none in the record. MeSH: Animals · Anti-Arrhythmia Agents/administration & dosage · Anti-Arrhythmia Agents/therapeutic use · Atenolol/administration & dosage · Atenolol/therapeutic use · Cardiomyopathy, Hypertrophic/drug therapy · Cardiomyopathy, Hypertrophic/veterinary · Cat Diseases/drug therapy · Cats · Drug Administration Schedule · Female · Male
Double-blind, placebo-controlled, randomized clinical trial (record's title wording; publication type: Randomized Controlled Trial, Veterinary)
Who: Cats: 32 client-owned cats with subclinical hypertrophic cardiomyopathy and 27 healthy control cats; QOL questionnaire responses, circulating cardiac biomarker concentrations, and accelerometer-based activity measures were compared prospectively in cats with and without HCM, and in cats with HCM before and after treatment with oral atenolol (6.25 mg/cat q 12 h) or placebo for 6 months.
Result: Owner-assessed activity of daily living score was lower in cats with HCM than in cats in controls (p = 0.0420). No differences were identified between control cats and cats with HCM for any activity variable. Compared with placebo, treatment with atenolol was associated with a lower baseline-adjusted mean ± SD heart rate (157 ± 30 vs. 195 ± 20 bpm; p = 0.0001) and rate-pressure product (22,446 ± 6,237 vs. 26,615 ± 4,623 mmHg/min; p = 0.0146). A treatment effect of atenolol on QOL or activity was not demonstrated, and the authors concluded that the findings do not support a treatment benefit of atenolol for the goal of symptom reduction in cats with subclinical HCM at the dosage evaluated.
Watch out: The strongest design on this shelf, but its outcomes are quality of life, activity and biomarkers over 6 months — not survival or disease progression — and the atenolol dose was a fixed 6.25 mg/cat twice daily. The lower heart rate and rate-pressure product show the drug was pharmacologically active; rate control is not itself a demonstrated clinical benefit.
Coleman AE, DeFrancesco TC, Griffiths EH, Lascelles BDX, Kleisch DJ, Atkins CE, Keene BW. 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. Journal of Veterinary Cardiology. 2020;30:77-91. PMID: 32707333. Registry ID: none in the record. MeSH: Administration, Oral · Animals · Anti-Arrhythmia Agents/administration & dosage · Anti-Arrhythmia Agents/therapeutic use · Atenolol/administration & dosage · Atenolol/therapeutic use · Biomarkers/blood · Cardiomyopathy, Hypertrophic/drug therapy · Cardiomyopathy, Hypertrophic/veterinary · Cat Diseases/blood · Cat Diseases/drug therapy · Cats · Double-Blind Method · Female · Male · Quality of Life · Treatment Outcome
Pilot study with a before–after comparison (record's own wording; no control group — the record carries no design publication type)
Who: Cats: six Maine Coon or Maine Coon cross cats with severe hypertrophic cardiomyopathy and no signs of heart failure (no cat had left ventricular dynamic outflow tract obstruction caused by systolic anterior motion of the mitral valve), treated with atenolol (12.5 mg PO q12 h) for 30 days, with NT-proBNP and cardiac troponin I concentrations assayed before and on the last day of drug administration.
Result: There was no statistically significant change in NT-proBNP (median before, 394 pmol/L; range, 71–1,500 pmol/L; median after, 439 pmol/L; range, 24–1,500 pmol/L; P = .63) or in cTnI (median before, 0.24 ng/mL; range, 0.10–0.97 ng/mL; median after, 0.28 ng/mL; range, 0.09–1.0 ng/mL; P = .69) after administration of atenolol. The authors concluded that atenolol did not decrease NT-proBNP or cTnI concentrations in these cats, suggesting it did not decrease myocardial ischemia and myocyte death.
Watch out: Six cats, no untreated or placebo comparison group, and only 30 days of treatment: this uncontrolled pilot can show that the biomarkers did not fall on atenolol, not what would have happened without it. It is carded as supporting evidence alongside the two controlled records, not as a comparative trial, and its cats had severe hypertrophy without outflow obstruction — a narrower population than preclinical HCM overall.
Jung SW, Kittleson MD. The effect of atenolol on NT-proBNP and troponin in asymptomatic cats with severe left ventricular hypertrophy because of hypertrophic cardiomyopathy: a pilot study. Journal of Veterinary Internal Medicine. 2011;25(5):1044-9. PMID: 21781160. Registry ID: none in the record. MeSH: Adrenergic beta-1 Receptor Antagonists/pharmacology · Adrenergic beta-1 Receptor Antagonists/therapeutic use · Animals · Atenolol/pharmacology · Atenolol/therapeutic use · Biomarkers/blood · Cardiomyopathy, Hypertrophic/blood · Cardiomyopathy, Hypertrophic/complications · Cardiomyopathy, Hypertrophic/drug therapy · Cardiomyopathy, Hypertrophic/veterinary · Cat Diseases/blood · Cat Diseases/drug therapy · Cats · Female · Hypertrophy, Left Ventricular/blood · Hypertrophy, Left Ventricular/drug therapy · Hypertrophy, Left Ventricular/etiology · Hypertrophy, Left Ventricular/veterinary · Male · Natriuretic Peptide, Brain/blood · Peptide Fragments/blood · Pilot Projects · Troponin C/blood
Synthesis
Who: Synthesis of the cards above: Schober 2013 (63 preclinical HCM cats, 42 atenolol-treated and 21 untreated, plus 31 healthy controls, followed 5 years), Coleman 2020 (32 subclinical HCM cats randomised to atenolol or placebo for 6 months, plus 27 healthy controls) and Jung 2011 (6 cats with severe HCM, 30 days of atenolol, before–after biomarkers).
Result: (1) Survival: no significant atenolol advantage in all-cause (P = 0.729) or cardiac (P = 0.897) mortality over 5 years in the only long-term study (Schober). (2) Symptoms and activity: no demonstrated treatment effect on quality of life or activity in the only blinded placebo-controlled trial, despite clear heart-rate lowering (157 vs 195 bpm; Coleman). (3) Biomarkers: no fall in NT-proBNP or troponin I on atenolol in the pilot (Jung), and no biomarker treatment effect identified in Coleman. The consistent direction is absence of demonstrated benefit, with the caveat that the hard-outcome evidence is observational.
Watch out: No carded trial randomised cats to atenolol versus no treatment with survival or echocardiographic progression as the primary endpoint, and obstructive (systolic anterior motion) physiology — the subgroup where beta-blockade is most often rationalised — was excluded from Jung and not separately reported in the other records. Absence of demonstrated benefit is not proof of absence of a small benefit.
Synthesis of Schober KE et al. PMID: 23684504; Coleman AE et al. PMID: 32707333; Jung SW et al. PMID: 21781160. Registry IDs as on the individual cards.
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