Author + information
- S. David Gertz, MD, PhD∗ (, )
- Gideon Uretzky, MD,
- Lilach Gavish, PhD and
- Mervyn S. Gotsman, MD
- ↵∗Institute for Medical Research, The Hebrew University–Hadassah Medical School, P.O. Box 12272, Jerusalem, Israel 91120
In their study of optical coherence tomography (OCT)-defined morphological characteristics of coronary artery spasm sites in vasospastic angina, Shin et al. (1) found thrombi at only 23 (29%) of 80 sites of spasm in patients with vasospastic angina and in only one-half of patients with a diagnosis of acute myocardial infarction. They reported a reduction in coronary flow at only 40 (50%) of 80 sites of spasm in patients with vasospastic angina and in only 31% of patients with acute myocardial infarction.
The authors point out that it is thought that thrombosis is the result of grossly reduced blood flow secondary to critical vascular constriction and suggest that the lack of a correlation between frequency of thrombus and clinical presentation in their study may be related to the relatively small size of the thrombi as seen on OCT. Triple therapy with aspirin, clopidogrel, and unfractionated heparin and “spontaneous” fibrinolysis should be considered among the possible explanations for the low number and/or size of the thrombi in these patients.
They then cite our animal study that showed, by scanning electron microscopy and arterial flow monitoring, that endothelial damage and thrombosis can occur even in circumstances of partial arterial constriction (40% to 60% luminal diameter reduction), especially if superimposed on pre-existing arteriosclerosis (2). However, they did not mention a critically important controlled finding of that study that the hemodynamic forces at such sites of partial coronary constriction can be sufficiently severe to exceed what has been calculated to be the “yield stress” of the endothelial lining. This hemodynamically induced damage was found to range from focal vacuolar injury to cellular fragmentation and desquamation with exposure of highly thrombogenic subendothelial tissues. These animal studies suggested that coronary spasm may cause myocardial ischemia not just by total obstruction of the artery at the site of spasm, but also by endothelial damage and thrombus formation that may occur at sites of spasm even, and perhaps particularly, when the reduction in luminal diameter is insufficient to reduce the rate of distal coronary flow (2,3). Indeed, the endothelial damage, whether hemodynamically or otherwise induced, would also be expected to promote or exacerbate underlying atherosclerosis.
By showing with correlative quantitative angiography that blood flow at sites of coronary spasm was reduced in only one-half of patients with angina and in less than one-third of patients with acute myocardial infarction, the study by Shin et al. (1) provides strong clinical support for the experimentally demonstrated role of hemodynamic forces in vascular damage and thrombosis in patients with vasospastic angina.
Please note: This work is supported in part by the Rosetrees Trust Fund of the UK and The Brandman Foundation. The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- American College of Cardiology Foundation
- Shin E.-S.,
- Ann S.H.,
- Singh G.B.,
- et al.
- Gertz S.D.,
- Uretzky G.,
- Wajnberg R.S.,
- Navot N.,
- Gotsman M.S.