Feb 18 2022 This Week in Cardiology

COMMENTARY

Feb 18, 2022 This Week in Cardiology Podcast

John M. Mandrola, MD

Disclosures

February 18, 2022

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Please note that the text below is not a full transcript and has not been copyedited. For more insight and commentary on these stories, subscribe to the This Week in Cardiology podcast on Apple Podcasts, Spotify, or your preferred podcast provider. This podcast is intended for healthcare professionals only.

In This Week’s Podcast

For the week ending February 16, 2022, John Mandrola, MD comments on the following news and features stories.

I have opined that the only way to avoid post-cardiac surgery AF was not to have cardiac surgery, because for my entire career, I’ve never seen anything work.

New research into a new avenue of therapeutics via the autonomic nervous system raises hope.

JACC published a research letter on the use of spinal cord stimulation to prevent post cardiac surgery AF. The paper was presented at the virtual ACC in 2021.

A brief background: (adapted from a nice review paper in the same issue of JACC).

Autonomic control of the heart is mediated via the neurocardiac axis, and it includes reflexes at 3 levels of cardiac neural hierarchy:

  • Central (higher forebrain structures, the brainstem, and the spinal cord),

  • In the chest but not in the heart (stellate and dorsal root ganglia),

  • intrinsic cardiac: Inputs by baroreceptors and chemoreceptors, as well as the renin-angiotensin-aldosterone system, contribute to the cardiac beat-to-beat control.

Sympathetic output to the heart is directed through the middle cervical and stellate ganglia, to postganglionic sympathetic axons, to intrinsic cardiac ganglionated plexus (GP) and the atrial and ventricular myocardium.

In parallel, parasympathetic innervation is primarily mediated by branches of the vagus nerve that synapse on ganglionic parasympathetic neurons located in the GP.

Therefore, the GP, which are mainly embedded in epicardial fat pads on the posterior surface of the atria, are composed of sympathetic and parasympathetic neurons and function as “integration centers” for cardiac autonomic input and output.

In the 1990s, Douglas. Zipes was intensely interested in this area, but for whatever reason(s), it hasn’t yielded major breakthroughs, at least until, now, possibly..

It’s a small RCT done in two centers in Russia. The intervention is spinal cord stimulation.

A standard silicone insulated wire that is routinely used in spinal cord stimulation) was placed by an experienced neurosurgeon.

Under local anesthesia and fluoroscopic guidance, a trial lead was implanted using a Tuohy needle and positioned in the posterior epidural space at the C7-T4 level left to the midline.

This position was associated with the most extensive feasible coverage of the left and middle anterior thorax.

The external segment of the lead was connected to the handheld stimulator. And patients used a hand-held controller to adjust the stimulation for comfortable but consistent paresthesias.

The stimulation was started 3 days before surgery, deactivated during surgery and restarted after.

The control arm got beta blockers and standard care.

At the end of 30 days, POAF occurred in 8 (30.7%) of 26 patients in the control group vs 1 (3.8%) of 26 patients in the SCS group (P=.012, log-rank test; HR: 0.11; 95% CI: 0.01-0.90; P=.04

Comments:

It now seems reasonable to try this in a bigger trial. I guess the most accurate assessment is I just don’t know if this works.

There are at least 8 RCTs in progress looking at the role of ANMT in AF prevention after heart surgery. These include low-level vagus stimulation from the ear; epicardial botulinum toxin, ganglionated plexus ablation and stellate ganglion blockade.

There are hopeful early signals but you have to have very pessimistic priors when it comes to AF after heart surgery, because nothing has worked before.

Statin Intolerance

We have all encountered this: patients who cannot take statin drugs due to side effects of one sort of another.

The EHJ has published a massive meta-analysis of 176 studies and more than 4 million patients in an effort to characterize statin intolerance.

The first author is Ibadete Bytyci, from Kosovo and the author list includes many noted experts in the field.

Four general statements about statin side effects.

We know that the rate of statin side effects is substantially higher in unblinded studies than it is in blinded RCTs.

In RCTs that are blinded, side effects on statins are essentially the same as placebo.

In the SAMSON trial, from the Imperial College London team, statins do indeed cause side effects, but these side effects are due to the act of taking the pill, not the statin chemical.

Finally, I mention an interaction with an orthopedic surgeon I had many years ago: he said, you cardiologists say someone’s body aches are due to statins, and I do an Xray and they are riddled with arthritis.

Older people, are going to have oodles of reasons for feeling achy and unwell.

The authors combined nearly every observational study and RCT published that reported statin intolerance symptoms. These range from 1990s to the present. 3 decades!

The worldwide prevalence of intolerance was 9.1%. Older age, female gender, Asian and African-American races, obesity, T2DM, alcohol use, hypothyroidism, chronic liver, and renal diseases were associated with a higher risk of SI, as were increased statin doses and the concomitant administration of antiarrhythmic agents.

One interesting secondary analysis comparing prevalence in studies of primary vs secondary prevention. They did not find a significant difference (8.2 vs. 9.1%).

In a press release the authors wrote statin intolerance is "overestimated and over-diagnosed" in most cases. They also wrote that their data means that "around 93% of patients on statin therapy can be treated effectively, with very good tolerability and without any safety issues," 

Comments:

I agree with their conclusions but I don’t think this data can tell them that. Go to the main figures, the Forest plots of the trials. The results of individual trials are all over the map. Some find no intolerance, some find tons.

There is a measure of this heterogeneity called I-squared. It ranges from 0-100%. When you combine studies in meta-analyses you like this to be low.

The simple point here is that the I-squared was 98-99%. I am just not sure the combination of different kinds of studies, over 30 years, tells us much that we don’t already know.

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