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Diastolic dysfunction and heart rate

Sonopath Forum

Diastolic dysfunction and heart rate

2 1/2-year-old spayed cat. Required butorphenol sedation. It had a mild effect. Heart rate rarely went below 200bpm. Cardiac measures were WNL. Mitral inflow was evaluated with pulsed Doppler, with the sweep speed increased to discern the E and A waves. The heart rate noted on the ECG is not correct on that picture. IVRT was normal.
Q: Would the waves noted be considered accurate and indicative of some early diastolic dysfunction or would heart rate play a significant factor in increasing the A wave amplitude during atrial systole( A wave running into E wave)? Is there value in measuring E:A in rates over 180 in cats?

Comments

Eric Lindquist

Ill let Peter answer on the wave form likely tomorrow but in lack of any structural or functional pathology my thought would be that its a benign heart as everything else looks normal.

Peter

Hi!
Basically, your M-Modes do not reveal concentric hypertrophy and the left atrial size appears normal. Regarding mitral inflow profiles: Yes, this looks like an impaired diastolic filling pattern. But note that a too far apical placement of the sample volume causes a decrease in E-wave velocity. On you’re Spectral Doppler profile there’s also some dagger-shaped downward signal (below the baseline). This could indicate some intraventricular obstruction and needs to be assessed with color Doppler interrogation of the left ventricle on apical views. An intraventricular obstruction is frequently caused by hypertrophied papillary muscles.

Peter

Regarding E-A-overlap: It is not entirely clear if this is just a function of heart rate since some cats display and overlap at a rate of 170 and some show distinct waves at 190/min. But as a general rule: at rates of > 180/min it is unlikely to see distinct waves. If they are overlapping, the summated amplitude is not of any use in terms of diastology. Note that the IVRT is heart-rate independent!. I generally advise against diagnosing any kind of “cardiomyopathy” on the basis on a single abnormal diastolic parameter, even if an impaired diastolic function pattern is not expected in a young cat. I would rather monitor the cat.

Dan lynn

Considered normal.Presented for murmur. No significant hypertrophy noted.Will look again for other LV changes.Obstructive LV outflow pattern produced at the septal base close to the end of systole with a normal pressure gradient. I assumed the cause of the murmur and possibly associated with the cats level of stress? Similar findings with better gate position too when waves seperated. Wondered if rate maybe factor of E:A reversal or would always be related to diastolic dysfunction? Would you always expect hypertrophy accompanying this flow pattern? Is LA always normal size with E:A reversal. On TDI is low E’ seen before hypertrophy?

Peter

HI
There are no studies regarding E:A reversal and heart rate, so scientifically speaking, it is unknown whether E:A changes by heart rate. In my personal experience, I have seen this sometimes (same cat, changing heart rate), but I don’t have a thorough explanation for that. In cats, LA size is mostly normal with E:A reversal (this is different in dogs!!!!). Cats with LAE usually have at least a pseudonormal pattern. And: No, I would not always expect hypertrophy with reversed E:A patterns. I see reversed E:A patterns in cats frequently with otherwise apparently normal hearts.

Peter

Re TDI: I would never ever base the diagnosis of HCM only on abnormal E’ waves. This has never been throroughly prospectively evaluated. Even though there’s some evidence that HCM is associated with lover E’ waves. Yet, it can contribute, particularly in breeding exams and borderline wall thickness.

Dan lynn

Thank you again! I was concerned with the scenario of borderline or normal measures that may be present (no HCM) with signs of early diastolic dysfunction( reversal of E:A, decreased e’ and or increased IVRT). Excluding age and hypertension, how would you weigh those diastolic findings in relation to patient/client follow up exams for an HCM phenotype or potential for emerging pathology as Dr.Lindquist would say? Would you just consider normal if the 2D and M modes are normal and there is no LVOT obstruction?

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