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2014 Boston AF Symposium

Hans Kottkamp MD

Hans Kottkamp MD

Fibrotic Atrial Cardiomyopathy (FACM)

By Steve S. Ryan, PhD

Dr. Hans Kottkamp of the Hirslanden Hospital in Zurich, Switzerland presented the concept of “Fibrotic Atrial Cardiomyopathy (FACM)” in his talk entitled “Fibrotic Atrial Cardiomyopathy – Implications for Catheter Ablation of AF.”

TYPES OF A-FIB substrates

Dr. Kottkamp discussed two types of substrates (or genotypes) of how A-Fib develops:

  • “Focal” A-Fib with the trigger as the only driver and with no (or very limited) structural atrial remodeling over time (even decades or “forever”).
  • A-Fib due to a severe underlying structural heart disease, e.g. mitral stenosis which causes significant structural remodeling.

Then he proposed a third type:

  • A-Fib as a manifestation of a pre-existing “Fibrotic Atrial Cardiomyopathy (FACM)” which can be mild (I), moderate (II), or severe (III). FAMC involves structural remodeling in a potentially progressive disease process. FAMC may explain what was characterized as “Lone” A-Fib with no previously identifiable cause in an otherwise healthy patient.

(Cardiomyopathy is a heart condition or disease in which the heart muscle is weakened and the heart’s ability to pump blood is impaired. For example, fibrous tissue may partially replace the heart muscle, disabling the heart so that it no longer functions properly and blood no longer moves efficiently. Cardiomyopathy is often accompanied by atrial fibrillation. Dr. Kottkamp’s concept of “atrial cardiomyopathy” isn’t the same thing as normal cardiomyopathy in which the ventricles are impaired.) 


At last year’s Boston A-Fib Symposium (see BAFS 2013: A-Fib Produces Fibrosis—Experimental and Real-World Data), Dr. Kottkamp cited several studies which indicated that A-Fib doesn’t seem to always produce fibrosis, where there is a great variability in the degree of fibrosis.1 This is in contrast with Dr. Jose Jalife’s experimental studies of sheep where A-Fib clearly produces fibrosis (see BAFS 2013: A-Fib Produces Fibrosis—Experimental and Real-World Data). In the real, messy world it isn’t always as easy and clear how to isolate the mechanisms that produce or limit fibrosis. As Dr. Kottkamp points out, sheep are not humans. Fibrosis may work differently in humans compared to animal models like sheep. (Of course it would be unethical to experimentally produce A-Fib and fibrosis in humans as one can in animal models.)


Dr. Kottkamp cited his and other researchers’ histological data and showed slides of heart cell tissue which showed in his analysis that:

  • The hypothesis that fibrosis progresses systematically from paroxysmal to persistent A-Fib was not confirmed.
  • While there was a tendency of increased mean fibrosis level in patients with persistent vs paroxysmal A-Fib, the variation within the two groups was very high.
  • No correlation at all could be detected between patient age and increase in the extent of fibrosis or fatty changes in atrial tissue.2
  • Atrial samples taken from age-matched A-Fib-free patients contained negligibly low amounts of fibrofatty tissue despite similar clinical high-risk profiles.3

Similar to Dr. Nassir Marrouche’s Utah Stages I-IV, Dr. Kottkamp showed slides of paroxysmal patients with No Fibrosis (no FACM), Mild Fibrosis (FACM I), Moderate Fibrosis (FACM II), Severe Fibrosis (FACM III).


According to Dr. Kottkamp, what FACM means for patients:

  • In patients with “Focal” paroxysmal A-Fib (no or almost no fibrosis [No FACM], PV isolation can (almost) be considered curative. Though there are relatively rare cases of extra-PV foci in these cases.
  • In patients with  FACM I AND II (similar to Utah Stages II and III) the ablation cannot really “cure” the underlying disease FACM. However, in many of these cases, ablation can effectively treat the arrhythmia A-Fib which in many patients is the only clinical manifestation of the FACM disease.
  • While patients in FACM III (similar to Utah Stage IV) are very hard or impossible to cure with today’s standard catheter mapping and ablation techniques.


Dr. Kottkamp’s conclusions:

  • Circumferential PV isolation is a cornerstone treatment for most patients with paroxysmal A-Fib.
  • The concept of FACM as a primary atrial disease explains recurrences of paroxysmal or even persistent A-Fib after a period of stable Sinus Rhythm after a previous PV isolation by the potentially progressive nature of the FACM disease (which is independent of the arrhythmia).
  • In patients with A-Fib recurrence after durable PV isolation, the ablation strategy can be targeted to the individual substrate localization.
  • In patients with more advanced substrates (FACM II-III), additional substrate modification may be reasonable in patients with persistent A-Fib already in the first ablation session.
Editor’s Comments:
Dr. Kottkamp’s concept of Fibrotic Atrial Cardiomyopathy may become important in our understanding of A-Fib, though it needs further studies to determine how it develops and progresses, how it differs from fibrosis measurements like Utah Stages I-IV, how best to quantify and measure it, etc.
Dr. Kottkamp’s concept that Lone A-Fib may come from Cardiomyopathy, that “Lone” A-Fib isn’t really lone or idiopathic but may come from a form of Atrial Cardiomyopathy may be an important thesis for future research. It may explain why some paroxysmal A-Fib patients have extensive fibrosis, while others don’t. (Though there are other factors which may produce fibrosis as well as Cardiomyopathy.)
Dr. Platonov’s finding that age doesn’t relate to fibrosis is certainly good news for patients. It indicates that just because we are getting older, our hearts aren’t automatically developing fibrosis. (Though we do know that A-Fib is associated with aging of the heart. As patients get older, the prevalence of A-Fib increases, roughly doubling with each decade.4 This suggests that A-Fib may be related to degenerative, age-related changes in the heart.)
Contrary to Dr. Jalife’s experimental studies with sheep which showed that A-Fib produces fibrosis, Dr. Kottkamp’s studies indicate that in the real world fibrosis doesn’t progress systematically from paroxysmal to persistent A-Fib. But his studies did show that there was more fibrosis in persistent vs. paroxysmal A-Fib patients. And that people without A-Fib compared to age-matched patients with A-Fib, had “negligibly low amounts of fibrofatty tissue (fibrosis) despite similar clinical high-risk profiles.”
Even though animal models like sheep aren’t perfect, studies like Dr. Jalife’s are scientifically sound and very convincing. Sheep hearts seem very similar to human hearts for all practical purposes. As patients with A-Fib, we have to base our medical decisions on the conclusion that A-Fib produces fibrosis (Dr. Kottkamp disagrees with this conclusion); that if we stay in A-Fib over a significant period of time, we will progressively develop fibrosis which is currently irreversible. However, as Dr. Kottkamp points out, it isn’t inevitable that everyone will develop fibrosis to an equal extent. This is consistent with Dr. Jalife’s studies in which even sheep with the same environment, diet, similar gene pool, etc. did differ in how fast they developed fibrosis.

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Last updated: Saturday, February 16, 2019 

Footnote Citations    (↵ returns to text)

  1. Mahnkopk, C. et al Evolution of the left atrial substrate in patients with lone atrial fibrillation using delayed-enhanced MRI: implications for disease progression and response to catheter ablation. Heart Rhythm. 2010 Oct. 7(10):1475-81 doi: 10.1016/j.hrthm.2010.06.030. Epub 2010 Jul 1.
  2. Platonov, PG et al. Structural Abnormalities in Atrial Walls Are Associated With Presence and Persistency of Atrial Fibrillation But Not With Age. J Am Coll Cardiol 2011;58(21):2225-2232. Last accessed 4/1/14 doi:10.1016/j.jacc.2011.05.061
  3. Ibid.
  4. Calkins, H, Berger, R. Atrial Fibrillation: Management Strategies. Scientific American Special Health Reports. Last accessed August 24, 2015. URL:, p. 9.

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