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Coronary Spasm Linked to Inflamed Adventitia in

Vasospastic Angina
Fran Lowry

February 06, 2018

Coronary artery spasm, an important player in ischemic heart disease, is associated with
inflammation of coronary adventitia and perivascular adipose tissue (PVAT) in patients with
vasospastic angina, a new study suggests.[1]

Japanese researchers, led by Dr Kazuma Ohyama (Tohoku University Graduate School of Medicine,
Sendai, Japan), made their finding by using 18F-fluorodeoxyglucose positron emission
tomography/computed tomography (18F-FDG PET/CT), an imaging modality that they say may be
useful in assessing disease activity.

"Although invasive methods, such as coronary angiography and provocation with acetylcholine, are
currently indispensable for diagnosis of vasospastic angina, a multimodality approach, especially 18F-
FDG PET/CT imaging, may become useful as a noninvasive tool for assessment of this disorder,"
they write.

Activation of Rho-kinase is a molecular switch for vascular smooth muscle contraction and is a
central mechanism of coronary spasm in animals and humans, the authors write.

They also note they have previously shown optical coherence tomography (OCT) permits precise
measurement of the vasa vasorum (VV) and that adventitial inflammatory changes, including the
formation of VV, play important roles in the pathogenesis of coronary spasm in pigs and humans.

To test their hypothesis that coronary artery spasm is associated with perivascular inflammation in
patients with vasospastic angina (VSA), Ohyama et al prospectively examined 27 patients with
acetylcholine-induced diffuse spasm in the left anterior descending (LAD) artery and 13 patients
suspected of having angina but without organic coronary lesions or coronary spasm.

They used CT coronary angiography and 18F-FDG PET/CT to assess coronary PVAT volume and
coronary perivascular FDG uptake in the LAD.

In addition, they used OCT to examine adventitial VV formation in the LAD, and they also measured
Rho-kinase activity in circulating leukocytes.

Patient characteristics were similar in both groups.

CT coronary angiography and 18F-FDG PET/CT showed that coronary PVAT volume and coronary
perivascular FDG uptake were significantly increased in the patients with VSA compared with
patients without VSA.

Coronary perivascular target-to-background ratio (TBR) at the spastic LAD was significantly greater
in the VSA group than in the non-VSA group (1.04 ± 0.03 vs 0.85 ± 0.04, both P<0.01).

There was a significant positive correlation between the extent of coronary perivascular TBR and
coronary vasoconstriction responses to acetylcholine in the VSA group compared with the non-VSA
group (P<0.01).

In addition, there was a significant positive correlation between the extent of coronary PVAT volume
index and that of coronary perivascular TBR in the VSA group but not in the non-VSA group.
OCT showed that adventitial VV formation significantly increased in the VSA group compared with
the non-VSA group (0.086 ± 0.006 mm2 vs 0.045 ± 0.006 mm2; P<0.01).

Rho-kinase activity in circulating leukocytes was also significantly higher in the VSA group than in the
non-VSA group. However, after medical treatment, both coronary perivascular FDG uptake and Rho-
kinase activity significantly decreased in the VSA group.

New Insights for Treatment

In an accompanying editorial,[2] Dr John F. Beltrame and Dr Peter J. Psaltis write that Ohyama et al
have provided "compelling" evidence that PVAT-associated inflammation plays a role in epicardial
coronary artery spasm.

"The pathogenetic mechanism of coronary artery spasm not only involves vascular smooth muscle
cell hyper-reactivity but also a perivascular inflammatory process," Beltrame told theheart.org |
Medscape Cardiology in email correspondence.

"This paper by international leaders in the pathophysiology of coronary artery spasm has
comprehensively demonstrated that perivascular adipose tissue–associated inflammation contributes
to the pathogenesis of coronary artery spasm, and this provides new insights into its pathogenesis
and thus a new potential target in its treatment," he said.

It has long been established that vascular smooth muscle hyper-reactivity is a fundamental cause of
the coronary artery spasm responsible for VSA, and current therapies target the inhibition of vascular
smooth muscle contraction.

Inflammation has also been implicated, but previous studies have focused on a systematic
inflammatory response, Beltrame said.

"This paper identifies that inflammation within the coronary artery wall, within the PVAT, is related to
increased coronary vasoreactivity, thus therapies that target the PVAT inflammatory response may
also modulate coronary vasoreactivity, thereby providing a new therapeutic target in the treatment of
this disabling and potentially life-threatening condition," he said.

Ohyama and Beltrame report no relevant financial relationships.

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References

1. Ohyama K, Matsumoto Y, Takanami K, et al. Coronary adventitial and perivascular adipose

tissue inflammation in patients with vasospastic angina. J Am Coll Cardiol. 2018;71:414-
425. Article
2. Beltrame JF, Psaltis PJ. The forgotten vascular layer in the forgotten coronary disorder.
2018;71:426-428. Extract

Medscape Medical News © 2018 

Cite this: Coronary Spasm Linked to Inflamed Adventitia in Vasospastic

Angina - Medscape - Feb 06, 2018.