Up to 25 % of LV filling is done by atrial contraction. Atrial booster function is important in LV outflow lesions. This can be critical in patients who have diastolic deformities of LV. ( an audible or even palpable S4 confirms the atrial kick in these situations ) This is how we were taught for decades right. Still, it may hold good in many left-sided condtions, but in HCM it definitely seems to be not true.
A succinct review of this topic makes a good read.
Incidence if AF in HCM is about 20% (Mostly paroxysmal 70 % , Persistent /Permanent 30 %)
Mechanism of AF IN HCM
- Increased atrial wall strain(Proven by strain echo studies)
- Atrial dilatation
- Atrial pathology (Atrial myocyte disarray, myosin is present in atria too. )
- Unrelated to HCM (SHT etc)
We can confirm with large observatory data, left ventricle handles AF so well. (Ref 1)The onset of AF, (at the least), is, expected to cause some new worsening dyspnea. Even that is not universal (very surprising isn’t it ?)
Does AF correlate with syncope? again no is the answer. So it’s the LV outflow behavior that determines the hemodynamics not what is happening at the inflow. Even hard outcomes like heart failure, sudden death, net mortality was not found to be altered much by the lesser chamber fibrillation. But, the only issue relevant here is thromboembolism that has to be taken care of.
How is that AF make little hemodynamic Impact in HCM ?
It is difficult to comprehend this scenario. For this to happen the mean LA pressure should remain within the physiological range even when the atria goes to fibrillation. But it seems distinctly possible as many patients with HCM are not aware of this arrhythmia. The LA pressure-volume loop is an enigma. It is likely LA “v” wave loop can adjust to “a” wave deficiency in an exemplary manner.
Further, the hyper-contractile left ventricle can assist itself by sucking blood in very late diastole (to be precise with the onset of systole )and so it need not really depend on the atrial kick. A similar phenomenon explains the persistence of presystolic accentuation in the murmur of mitral stenosis. The fact that rate control in AF is able to compete with rhythm control in AFFIRM/RACE study vouch for the negligible hemodynamic impact between SR/AF.
Clinical implication
- A well-tolerated AF doesn’t preclude the need for thromboprophylaxis. We must ensure NOAC/Warfarin in all those with persistent AF.
- Attempts to convert AF to sinus rhythm with all those Invasive LA mapping and Pulmonary vein is unwarranted if not contraindicated.
- When ICD is indicated additional Atrial leads to reduce AF is again becomes reductant.
Final message
Many of the hemodynamic concepts we have learned over the years could be based on logical perceptions that may not manifest at the bedside. Constant flux in our understanding of cardiovascular physiology is required.
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