Transient Myocardial Thickening in Cats: What You Need to Know About This Feline Heart “Thing”
October 2024
In today’s VETgirl online veterinary CE podcast, we discuss transient myocardial thickening (TMT) in cats. If you just had a cat diagnosed with a heart murmur and had a cardiologist echo it, how do you know if it’s TMT versus Hypertrophic Cardiomyopathy (HCM)? Tune in to find out what you need to know about this transient feline heart “thing!”
TMT stands for transient myocardial thickening. Let’s be honest, on the days when you are enjoying a caramel macchiato and daydreaming about heart disease in cats, you probably think of hypertrophic cardiomyopathy (what we’ll call HCM from now on), restrictive cardiomyopathy (what we’ll call RCM from now on), or the rare dilated cardiomyopathy (what we’ll call DCM from now on) case… and not much else. Well, there’s a newly described cardiac phenomenon in cats that – wait for it – has a MUCH better outcome than those others might. The bad news is, it will initially look exactly like HCM, and will take at least a few months to show you that it isn’t. So patience and client education are key. I’ll explain.
Transient myocardial thickening, or TMT, in cats was introduced to veterinarians in 2018 in a publication describing a small number of cases. This disease was described to have features indistinguishable from HCM on echocardiogram, specifically left ventricular concentric hypertrophy, or increased wall thickness. Unlike hypertrophic cardiomyopathy, however, TMT is reversible. Importantly, it was reported to preferentially affect young cats, who in addition to transient myocardial hypertrophy, can experience transient left atrial enlargement, congestive heart failure (CHF), and elevated serum cardiac troponin I levels. The exact pathophysiology is not yet understood but transient myocardial interstitial edema via myocarditis has been postulated, as is described in humans. What causes the myocarditis, you ask? We’re not entirely sure. Cases associated with Bartonella henselae, Streptococcus canis, feline immunodeficiency virus (FIV), panleukopenia virus, coronavirus, Sarcocystis felis, Hepatozoon silvestris, and Toxoplasma gondii have been identified, but to say that we know that a clear group of specific infectious agents, or that infectious agents alone, are responsible for TMT would be untrue.
So, Romito et al out of Italy wanted to evaluate this in a study entitled “Transient myocardial thickening: a retrospective analysis on etiological, clinical, laboratory, therapeutic, and outcome findings in 27 cats” to describe a population of cats with TMT, including the historical context of their presentation, clinical characteristics, and outcome. This was a multicenter, observational, and retrospective study over a 9-year period from 2014-2023. Cats were considered to have TMT if their initial echocardiogram demonstrated left ventricular hypertrophy (interventricular septal and/or free wall thickness > 6 mm), elevated circulating troponin I (>0.2 ng/mL), and follow-up examinations whereby reductions in left ventricular wall thickness and troponin I levels were documented. If cats were determined to have any other form of cardiac disease, or required sedation for examination, they were excluded. Cats were also excluded if they had hyperthyroidism, hypersomatotropism, or systemic hypertension, all of which can increase left ventricular wall thickness. They were also excluded if they had received corticosteroids, which can be associated with the onset of CHF in cats, or had experienced an arterial thromboembolism. Cats were also excluded if they were deemed to be clinically dehydrated at the time of echocardiogram, as this can artifactually increase left ventricular wall thickness via reduced left ventricular chamber size (think of a raisin versus a grape…).
In addition to baseline demographic and health characteristics of the cats in the study, the cat’s lifestyle (indoor, outdoor, or mixed) was determined and the presence of any events (e.g. anesthesia, stress/trauma, etc.) in the two-week period prior to diagnosis was recorded where applicable. Data from physical examination, blood pressure, radiographic and/or electrocardiographic analysis, complete blood count, serum chemistry, serum cardiac troponin I, and infectious disease testing (including PCR, antibody, cytology, or blood/urine culture) was tabulated when present.
In this study, echocardiographic images were reviewed. In addition to left ventricular wall thickness measurements to determine inclusion in the study, additional measurements were included that were both traditional (e.g., left atrial-to-aortic root ratio, or LA:Ao), or non-traditional (e.g. left atrial fractional shortening). Presence or absence of systolic anterior motion (SAM) of the mitral valve or chordal systolic anterior motion (CAM), as well spontaneous echocontrast (SEC) or thrombi were also recorded. LA:Ao was considered to be increased if 1.6. A complete description of the echocardiographic methods is beyond the scope of this podcast but appears to be consistent with current standards.
Suspected etiologies were reported when possible, as well as duration of treatment and outcome, the latter of which was subdivided into 1) number of relapses of CHF or thromboembolism, 2) time from diagnosis of increased left ventricular wall thickness to perceived resolution, and 3) clinical/diagnostic data from the time of the last recorded echocardiogram.
In the end, 27 cats met the inclusion criteria in this study, with 59% being male. Median age was 3-years of age, which fits the previously reported demographics – these are predominantly young cats. In fact, not a single cat with TMT in this study was older than eight years and 70% of the cats were five years of age or younger. The vast majority (66.7%) were mixed breed cats, and indoor cats predominated (44.5%) compared with 22.2% mixed indoor/outdoor and 14.8% predominantly outdoor. In one-third of the cats (9/27), a definitive non-ordinary event was documented within the 14-day period prior to diagnosis, with a median time of five days prior. These events included spay/neuter under anesthesia, which were the majority at 7/9, or 77.8%, and abscesses, which constituted the remaining two cats.
So, what’d they find in this study? 37% of cats had a heart murmur, 33.3% were hypothermic, 18.5% were bradycardic, and 18.5% were hypothermic. Importantly, 92.6% of these cats were in congestive heart failure. So, until proven otherwise, the majority of cats with TMT are not going to be detected or diagnosed in an occult setting on routine echocardiogram. These cats come in with respiratory distress. Only seven cats, or 25.9%, had electrocardiographic abnormalities, of a wide variety. The take home from this fact is that electrocardiography is not very sensitive as a diagnostic test for TMT in these cats, which is true in dogs and cats, in general.
Cardiac troponin I was performed in all 27 cats, and the data is impressive. Troponin I was elevated in all of the cats, with a median of 5.5 ng/mL, and range of 3.1-11.9. Keep in mind that the upper end of the reference range is between 0.11-0.2 depending on the lab, and in this study, any value above 0.2 was considered elevated, so every single one of these cats had sky-high troponin levels consistent with marked myocardial inflammation at time of diagnosis. 29.6% had neutrophilic leukocytosis, either alone or combination with elevations in monocytes and/or lymphocytes. 22.2% had nonregenerative anemia. 63% of cats underwent testing for feline immunodeficiency and leukemia viruses, all of which were negative. 15 cats underwent serologic testing for Toxoplasma gondii, three of which were positive. Nine cats were PCR tested for Bartonella, with one positive result. Two cats underwent serologic testing for Bartonella, with one positive result. Small numbers of cats had blood or urine cultures, all of which were negative. In the two cats that had abscesses, both had positive bacterial cultures from the abscess.
When it came to echocardiographic findings in this study, in addition to increased left ventricular wall thickness (which was the inclusion criteria), the vast majority of cats had left atrial enlargement (96%) with normal/preserved left ventricular systolic function (96%). 40.7% of cats had reduced systolic function of the left atrium itself (a nontraditional measurement), 14.8% of cats had spontaneous echocontrast, one cat had an intracardiac thrombus, and 29.6% had reduced left atrial appendage flow velocities, the latter of which is a marker for left atrial function. Nine cats in total (one-third) had some form of systolic anterior motion of the mitral valve.
If we pause for a moment, this paints a clear picture for us as to how we are likely to encounter TMT in clinical practice; namely as a young, dyspneic cat in congestive heart failure whose echocardiogram is consistent with the parameters for a primary hypertrophic cardiomyopathy, and whose cardiac troponin I will be markedly elevated, consistent with myocarditis. Unfortunately, this will render these cats indistinguishable from a primary hypertrophic cardiomyopathy cat on this initial exam, as even the elevated cardiac troponin I is not overtly specific for TMT. Prior published studies have documented elevations in troponin I in cats with primary HCM as well – though not necessarily to such extreme elevations. So TMT would therefore have to be a consideration in any cat presenting with CHF, truthfully – but your Spidey senses should definitely be more on alert if the cat is young. And they should be even more on alert if there appears to be a recent antecedent event of suspicion, like general anesthesia, or an abscess, in this case. Unfortunately though, the number of cats in the study with a clear antecedent event was a minority, so it does not appear to be a sensitive detail, though it could prove to be reasonably specific in future studies. Although the antecedent events reported here only included spay/neuter or abscesses, I would share with you that I have had TMT cats in association with other types of stressful feline events, including recent vaccination, and even a cat whose owner simply moved to a new home an hour away!
Ok, so let’s see what data can prove useful to us to determine that this apparently young cat with CHF and suspected HCM actually has TMT. This matters, a lot. The financial and emotional toll for an owner of a cat with CHF can be high, and if the cat truly has a primary cardiomyopathy that will only progress further over time, the prognosis is poor. As a result, some owners may not even treat and will elect to euthanize. The stakes couldn’t be higher.
Combining the antecedent history data with infectious disease testing, a suspected cause could be established in just over half (14) of the cats. All cats were hospitalized and treated appropriately for CHF, which included furosemide for all, and pimobendan (64%), clopidogrel (44%), benazepril, spironolactone, enoxaparin, and sotalol for some, depending on the clinician. Cats with positive infectious disease testing or abscesses received therapies appropriate for the infection. 48% of the cats were initially oxygen dependent. Cats spent an average of four days in the hospital, and of course they all survived, otherwise the diagnosis of TMT would not have been possible. VETgirl has personally had to ventilate several of these young, myocarditis cats during her residency at PennVet too! (which is why she published the paper “Indications for and outcome of positive-pressure ventilation in cats: 53 cases (1993-2002) as she wanted to stop venting these cases!
Here’s the cool part. Echocardiographic normalization of left ventricular wall thickness occurred between days 18-96 from initial presentation, with a median of 43 days. These cats had a notable number of follow-up visits in the weeks and months that followed discharge from the hospital which allowed for this determination. Four cats experienced relapse of CHF at least one time during the period from initial diagnosis to resolution of echocardiographic wall thickness changes. At the time of resolution of left ventricular wall thickness changes, none of the cats had clinical signs, and heart murmurs had resolved in all but one of the cats that had them initially. Cardiac troponin I was noted to have a statistically significant decrease by that time as well, including normalization in 24 cats, representing 88.9%. In the three cats where troponin I did not completely normalize, the highest residual elevation reported was only 0.41 ng/mL.
By the time of the final echocardiogram performed in the study cats, virtually all other echocardiographic abnormalities documented on initial examination had normalized, as well, including LA:Ao, left atrial functional parameters, presence of spontaneous contrast or thrombi, and systolic anterior motion of the anterior mitral valve leaflet or chordae tendinae. Medications were discontinued altogether in 66.7% of cats, furosemide was tapered to lower doses in those where it was continued, and four cats (14.8%) were maintained on pimobendan monotherapy. None of the cats experienced recurrent CHF, thromboembolic events, or arrhythmias thereafter in the records available for review.
Though still a small number of cats overall, this study does represent the description of characteristics in the largest number of cats with TMT to date, and the data is consistent with prior reports. A notable number of cats in the study had access to outdoors, and as reported earlier some cats eventually had diagnostic testing confirmatory of an infectious disease.
Whether these two facts are related is not entirely clear, but may be a relationship to be explored in the future. The presence of a clear antecedent event was notably lower in this group of cats than reported in the 2018 study (Novo Matos, et al). It is not clear why this was the case, but the take home message is that while the presence of an event shortly prior to onset of CHF in a young cat should raise suspicion for TMT, the absence of one should by no means exclude it. The authors were upfront in stating that the pathophysiology behind the antecedent events as cause for TMT is not known, despite postulations in the human literature about catecholamine-driven myocarditis.
So, what are some limitations of this study? The authors acknowledge some straightforward limitations, including retrospective design, small sample size, potential confounding influence of dehydration if not accurately assessed, and limitations of standard two-dimensional echocardiography when compared with more advanced modalities (e.g. tissue Doppler, speckle-tracking, etc.) that might provide more detailed assessment of myocardial structure and function across serial examinations. Though a small group of cats, I think this study provided good data that concurs with the small volume of data already available on TMT.
So, what do we take away from this VETgirl podcast? For the everyday practitioner, TMT must be on our radar when any dyspneic cat arrives at our clinic and is ultimately diagnosed with CHF and suspected HCM, but in particular the index of suspicion for TMT should rise significantly with young cats, especially those less than five years of age. Markedly elevated cardiac troponin I levels and/or recent historical stressful event, illness, or medical intervention should further increase our suspicion for TMT, and the former would warrant basic feline infectious disease testing, at minimum. For those thinking “I don’t have troponin I testing in my clinic, I’ll just use an NT-proBNP,” not so fast – that NT-proBNP will be elevated in all cats with significant cardiomegaly, and is not a specific marker for myocardial inflammation like troponin I.
Given the marked difference in outcome and long-term prognosis for cats with CHF vs TMT, it’s critical we keep our eyes out for potential TMT cases, and educate our cat owners. Although in some cases this may result in owners who wait 2-4 months only to be told that, in fact, their young cat appears to truly have irreversible hypertrophic cardiomyopathy, for others they will learn that their cat has a normalized heart, no longer requires cardiac therapy, and likely to live a long, healthy life – and that is not an opportunity we want to miss.
References:
1. Romito G, Elmi A, Guglielmini C et al. Transient myocardial thickening: A retrospective analysis on etiological, clinical, laboratory, therapeutic, and outcome findings in 27 cats. J Vet Cardiol 2023;50, 51-62.
2. Lee JA, Drobatz KJ, Koch MW, King LG. Indications for and outcome of positive-pressure ventilation in cats: 53 cases (1993-2002). J Am Vet Med Assoc 2005; 15;226(6):924-31.
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