Evaluation of benazepril in cats with heart disease in a prospective, randomized, blinded, placebo‐controlled clinical trial

King, J. N.; Martin, Mike W.; Chetboul, Valérie; Ferasin, Luca; French, Anne; Strehlau, G.; Seewald, Wolfgang; Smith, Sarah; Swift, Simon; Roberts, Susan L; Harvey, Andrea; Little, Colin; Caney, Sarah; Simpson, Kerry; Sparkes, Andy; Mardell, E. J.; Bomassi, Eric; Sauvage, John P; Diquélou, Armelle; Schneider, Matthias; Brown, Laurence; Clarke, David D.; Rousselot, Jean-François

doi:10.1111/jvim.15572

Cited by 12 publications

(8 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In 2 randomized, placebo‐controlled studies, neither an angiotensin converting enzyme (ACE) inhibitor (ramipril) nor spironolactone had any effect on LV mass or diastolic function in cats with subclinical HCM, but study populations were small and limited to cats of a single breed that had heritable cardiomyopathy . Similarly, benazepril had no effect on time to treatment failure compared to placebo in a randomized placebo‐controlled study that included cats with subclinical heart disease . No studies have been reported of pimobendan use in cats with subclinical cardiomyopathy.…”

Section: Treatmentmentioning

confidence: 99%

“…Measurement of serum creatinine, blood urea nitrogen, and electrolyte concentrations is recommended 3‐7 days after initiating furosemide (LOE low). Angiotensin converting enzyme inhibition with benazepril did not delay the onset of treatment failure in a randomized, placebo‐controlled study of cats with CHF (LOE high) although ACE inhibitors still are used by some cardiologists. Prophylactic antithrombotic treatment with clopidogrel (18.75 mg/cat PO q24h, with food) is recommended in any cat with a history of CHF and moderate to severe LA enlargement (LOE low).…”

Section: Treatmentmentioning

confidence: 99%

“…125,126 Similarly, benazepril had no effect on time to treatment failure compared to placebo in a randomized placebo-controlled study that included cats with subclinical heart disease. 127 No studies have been reported of pimobendan use in cats with subclinical cardiomyopathy.…”

Section: Stage B2 Cardiomyopathymentioning

confidence: 99%

See 2 more Smart Citations

ACVIM consensus statement guidelines for the classification, diagnosis, and management of cardiomyopathies in cats

Fuentes

Abbott

Chetboul

et al. 2020

Veterinary Internal Medicne

Self Cite

193

236

View full text Add to dashboard Cite

Consensus Statements of the American College of Veterinary Internal Medicine (ACVIM) provide the veterinary community with up-to-date information on the pathophysiology, diagnosis, and treatment of clinically important animal diseases. The ACVIM Board of Regents oversees selection of relevant topics, identification of panel members with the expertise to draft the statements, and other aspects of assuring the integrity of the process. The statements are derived from evidence-based medicine whenever possible and the panel offers interpretive comments when such evidence is inadequate or contradictory. A draft is prepared by the panel, followed by solicitation of input by the ACVIM membership that may be incorporated into the statement. It is then submitted to the Journal of Veterinary Internal Medicine, where it is edited before publication. The authors are solely responsible for the content of the statements. AbstractCardiomyopathies are a heterogeneous group of myocardial disorders of mostly unknown etiology, and they occur commonly in cats. In some cats, they are welltolerated and are associated with normal life expectancy, but in other cats they can result in congestive heart failure, arterial thromboembolism or sudden death.Cardiomyopathy classification in cats can be challenging, and in this consensus statement we outline a classification system based on cardiac structure and function (phenotype). We also introduce a staging system for cardiomyopathy that includes subdivision of cats with subclinical cardiomyopathy into those at low risk

show abstract

Section: Treatmentmentioning

confidence: 99%

Section: Treatmentmentioning

confidence: 99%

See 1 more Smart Citation

ACVIM consensus statement guidelines for the classification, diagnosis, and management of cardiomyopathies in cats

Fuentes

Abbott

Chetboul

et al. 2020

Veterinary Internal Medicne

Self Cite

193

236

View full text Add to dashboard Cite

show abstract

“… 200 , 201 One study found no benefit; however, it included cats that were not in heart failure and so the strength of its conclusions is limited. 202 In general, the number of medications administered to a cat in heart failure should be minimized to reduce stress. In the authors’ opinion, one drug that might be safely eliminated, if elimination of a drug might be beneficial in this regard, is the ACE inhibitor.…”

Section: Treatmentmentioning

confidence: 99%

The Feline Cardiomyopathies: 2. Hypertrophic cardiomyopathy

Kittleson

Côté

2021

Journal of Feline Medicine and Surgery

View full text Add to dashboard Cite

Practical relevance: Hypertrophic cardiomyopathy (HCM) is the most common form of feline cardiomyopathy observed clinically and may affect up to approximately 15% of the domestic cat population, primarily as a subclinical disease. Fortunately, severe HCM, leading to heart failure or arterial thromboembolism (ATE), only occurs in a small proportion of these cats. Patient group: Domestic cats of any age from 3 months upward, of either sex and of any breed, can be affected. A higher prevalence in male and domestic shorthair cats has been reported. Diagnostics: Subclinical feline HCM may or may not produce a heart murmur or gallop sound. Substantial left atrial enlargement can often be identified radiographically in cats with severe HCM. Biomarkers should not be relied on solely to diagnose the disease. While severe feline HCM can usually be diagnosed via echocardiography alone, feline HCM with mild to moderate left ventricular (LV) wall thickening is a diagnosis of exclusion, which means there is no definitive test for HCM in these cats and so other disorders that can cause mild to moderate LV wall thickening (eg, hyperthyroidism, systemic hypertension, acromegaly, dehydration) need to be ruled out. Key findings: While a genetic cause of HCM has been identified in two breeds and is suspected in another, for most cats the cause is unknown. Systolic anterior motion of the mitral valve (SAM) is the most common cause of dynamic left ventricular outflow tract obstruction (DLVOTO) and, in turn, the most common cause of a heart murmur with feline HCM. While severe DLVOTO is probably clinically significant and so should be treated, lesser degrees probably are not. Furthermore, since SAM can likely be induced in most cats with HCM, the distinction between HCM without obstruction and HCM with obstruction (HOCM) is of limited importance in cats. Diastolic dysfunction, and its consequences of abnormally increased atrial pressure leading to signs of heart failure, and sluggish atrial blood flow leading to ATE, is the primary abnormality that causes clinical signs and death in affected cats. Treatment (eg, loop diuretics) is aimed at controlling heart failure. Preventive treatment (eg, antithrombotic drugs) is aimed at reducing the risk of complications (eg, ATE). Conclusions: Most cats with HCM show no overt clinical signs and live a normal or near-normal life despite this disease. However, a substantial minority of cats develop overt clinical signs referable to heart failure or ATE that require treatment. For most cats with clinical signs caused by HCM, the long-term prognosis is poor to grave despite therapy. Areas of uncertainty: Genetic mutations (variants) that cause HCM have been identified in a few breeds, but, despite valiant efforts, the cause of HCM in the vast majority of cats remains unknown. No treatment currently exists that reverses or even slows the cardiomyopathic process in HCM, again despite valiant efforts. The search goes on.

show abstract

“…7,8 Unlike ACE, which cleaves 2 amino acids, ACE2 removes a single amino acid from AT1 and AT2, forming angiotensin 1-9 (Ang1-9) and angiotensin 1-7 (Ang1-7), respectively ( Figure 1). Despite a structural difference of just 1 amino acid, Ang1-7, Ang1-9, and other APs such as angiotensin [1][2][3][4][5] are vasodilatory, natriuretic, and cardioprotective. 9 This discovery has expanded our understanding of the AP system and use of traditional RAASi drugs, such as ACEI, beyond just AT1 and AT2.…”

Section: Introductionmentioning

confidence: 99%

Effect of angiotensin receptor blockers and angiotensin‐converting enzyme 2 on plasma equilibrium angiotensin peptide concentrations in cats with heart disease

Larouche‐Lebel

Loughran

Huh

et al. 2020

Veterinary Internal Medicne

View full text Add to dashboard Cite

Background Little is known about the effect of renin angiotensin aldosterone system‐inhibiting (RAASi) drugs on alternative angiotensin peptides (APs) such as angiotensin 1‐7 (Ang1‐7), which are mediated by angiotensin‐converting enzyme 2 (ACE2). Hypothesis/Objectives Angiotensin receptor blockers (ARBs) would alter balance of APs and differences would be magnified in vitro by incubation of plasma samples with recombinant human ACE2 (rhACE2). Animals Six cats with cardiomyopathy (CM), 8 healthy cats. Methods Prospective open label trial. Plasma equilibrium concentrations of APs were measured in healthy cats as well as in CM cats that first received no RAASi drugs (CMnoRAASi) and then after 14 days of PO telmisartan (CMARB). Plasma APs also were measured after in vitro incubation with rhACE2. Results No significant differences were found between healthy and CMnoRAASi groups. Concentrations of several APs, including angiotensin I (AT1) and angiotensin II (AT2) were significantly different between CMnoRAASi and CMARB groups. Incubation with rhACE2 decreased AT1 and AT2 in both groups. The geometric mean concentration of Ang1‐7 was significantly higher in CMARB (4.9 pg/mL; 95% confidence interval [CI], 3.7‐6.4 pg/mL) vs CMnoRAASi (3.2 pg/mL; 95% CI, 2.2‐4.7 pg/mL; P = .01) and in CMARB + ACE2 (5.0 pg/mL; 95% CI, 3.9‐6.4 pg/mL) vs CMnoRAASi + ACE2 (3.0 pg/mL; 95% CI, 1.7‐5.5 pg/mL; P = .01). The most favorable theoretical AP profile that maximized Ang1‐7 and other alternative APs was CMARB + ACE2. Conclusions and Clinical Importance Balance between traditional and alternative APs can be favorably shifted using ARBs and in vitro incubation with rhACE2. These data shed light on new AP‐targeting strategies in cats with CM.

show abstract

Evaluation of benazepril in cats with heart disease in a prospective, randomized, blinded, placebo‐controlled clinical trial

Cited by 12 publications

References 29 publications

ACVIM consensus statement guidelines for the classification, diagnosis, and management of cardiomyopathies in cats

ACVIM consensus statement guidelines for the classification, diagnosis, and management of cardiomyopathies in cats

The Feline Cardiomyopathies: 2. Hypertrophic cardiomyopathy

Effect of angiotensin receptor blockers and angiotensin‐converting enzyme 2 on plasma equilibrium angiotensin peptide concentrations in cats with heart disease

Contact Info

Product

Resources

About