Novo Matos J, Pereira N, Glaus T, Wilkie L, Borgeat K, et al. Transient Myocardial Thickening in Cats Associated with Heart Failure. J Vet Intern Med. 2018 Jan;32(1):48-56. PubMed PMID: 29243322.
Congestive heart failure (CHF) is a common clinical syndrome in cats that has been discussed extensively on this blog. CHF is an end-stage result of heart disease characterized by the buildup of fluid within or around the lungs. Most CHF in cats is caused by hypertrophic cardiomyopathy (HCM) and is generally considered to be an irreversible and fatal process. While various therapies have come forward to prolong the course of disease and manage symptoms, most cats with CHF die within 3-6 months of diagnosis.
It has been noted by many veterinarians that a small portion of cats with CHF due to apparent HCM have prolonged survival and may be eventually weaned off of medications. The authors of this study looked into this demographic of cats to determine if an alternate process was at play. The study was designed as a retrospective case-control study. Cats from 4 referral centres presenting for CHF (pulmonary edema and pleural effusion) were included. Included cats were required to have at least 2 echocardiograms with one showing myocardial thickening and left atrial enlargement, and the second showing normalization of these values. Cats with thin or dyskinetic myocardial segments were excluded. Cats with similar signs but echocardiographic evidence of persistent wall thickening were selected to use as control cats. Exclusion criteria included hypertension, hyperthyroidism, CKD, or diabetes mellitus.
Standard echocardiographic views were reviewed by board certified cardiologists. Some cats also had assessment of blood Cardiac Troponin I levels, infectious disease serology, and blood chemistries.
21 cats were identified with Transient Myocardial Thickening (TMT). Males were over represented in the HCM group but not the TMT group. Most of the TMT cats had an identified “antecedent event” occur within days before presentation. These included general anesthesia, traffic accidents, vaccination, bite wounds, pneumonia, fevers, and others. Cats received many drugs including opioids, steroids, NSAIDs, antibiotics, or others.
On initial echocardiogram, cats with HCM had higher left ventricular thickness than cats with TMT (8.1mm vs 6.8mm), and larger LA/Ao ratios (2.4 vs 1.8). No other differences were seen. The median time to resolution of cardiac values in TMT cats was 3.3 months. At the final echocardiogram, cats with TMT had decreased wall thickness to 4.8mm while HCM cats had remained statistically unchanged at 7.9mm. TMT LA/Ao had decreased to 1.45 while HCM cats increased to 2.6.In cats with cardiac troponin I measured, HCM cats were higher than TMT (2.1ng/mL vs 1.2ng/mL). In TMT cats this normalized as CHF resolved.
Congestive heart failure only recurred in 1 of 21 cats with TMT compared to 15 of 21 with CHF. 20 of 21 TMT cats had all CHF dugs discontinued by 4.6 months after initiation (the other cat remained on clopidogrel due to a mitral valve thrombus).
The authors suggest several possible etiologies for this transient myocardial thickening. These may include myocarditis or myocardial edema (due to infections such as toxoplasma or FIV, neoplastic infiltration, or other processes), or transient cardiomyopathies such as the stress induced “Takotsubo cardiomyopathy” seen in humans or the “capture myopathy” seen in confined wildlife. The elevated troponin I levels seen in TMT cats suggests that some degree of myocardial damage is present. The history of antecedent events in many patients and similarity to steroid-induced CHF suggests that some degree of catecholamine or corticosteroid induced effect may have been present.
Several limitations to this study exist. Not all cats were evaluated with the same methodologies (ie Troponin I assessment, tissue Doppler) at the same time points relative to disease onset. Cats had been administered various therapies prior to echocardiography and were in various states of hydration and systemic stability. These variables may have hindered accurate comparison of cats. Further testing, such as cardiac MRI or histopathology, may be needed to fully characterize cats with TMT.
At the present time, differentiation of HCM from TMT is difficult. While TMT cats were younger, had thinner ventricular walls, and higher troponin I levels, significant overlap in values makes differentiation from a point measurement difficult to impossible. Perhaps the main takeaway from this study is the need for careful monitoring and recheck echocardiography in cats with CHF, especially in younger cats with a known antecedent event due to the possibility of remission of signs. (MRK)
Hiramitsu S, Morimoto S, Kato S, et al. Transient ventricular wall thickening in acute myocarditis: A serial echocardiographic and histopathologic study. Jpn Circ J 2001;65:863–866.