James B Herrick in the year 1912 published a paper in JAMA on Clinical features of sudden obstruction of the coronary arteries. 1912;LIX(23):2015-2022 doi:10.1001/jama. 1912. 04270120001001. The concept presented shows the presence of intracoronary thrombus in acute myocardial infarction.

it has been an age old controversy regarding whether or not thrombi were responsible for acute myocardial infarction, crescendo angina or sudden ischemic death. Please see references below. The media behind plaque becomes very much vascularized and these vessels enter the intima is well known. Bleeding from these vessels crossing the media causes few red cells to lie free within the lipid pool of several plaques. in large lipid rich plaques, no fibrin or platelets may be found.

1. Geiringer E. Intimal vascularisation and atherosclerosis.J Pathol

Bacteriol 1951; 63: 201-11.

2. Barger AC, Beeuwkes R III, Lainey LL, Silverman KJ.

Hypothesis: vasa vasorum and neovascularization of human coronary

arteries. A possible role in the pathophysiology of atherosclerosis.

N Engl I Med 1983; 310: 175-7.

Please refer to paper on Plaque fissuring - the cause of ischemic acute myocardial infarction, sudden ischemic death, and crescendo angina. Br heart J 1985;53:363-373 by Michael JDavis, Anthony C Thomas.

You may want to consider inflammatory and/or vasoconstriction etiologies around pre-existing plaques as a cause for MI without thrombus formation.

You may find these articles interesting:

Libby P, et al: Inflammation and atherosclerosis. Circulation. 2002;105:1135-1143

Maseri A. From syndromes to specific disease mechanisms. The search for the causes of myocardial infarction. Ital Heart J. 2000;1: 253–257.

It is possible to have a Coronary Artery spasm in a sclerotic vessels. It occurs normaly in coronary arteries that have not become hardened but can occur in arteries with plaque stoping blood-flow.

I think this one can help

http://circinterventions.ahajournals.org/cgi/pmidlookup?view=long&pmid=20031702

I agree with some of the previous answers; the appearance of a severe vasospasm due to multiple reasons, on an artery probably affected by a significant degree of atherosclerosis can produce a temporary closing of the blood flow. IN these cases a coronariografy is would not revealing the existence of an trombotic occlusion ..

Prof. (ret.) Alexander Nedok: Yes, it is possible. Late prof. S. Trifunović from Novi Sad University scool of medicine, as I independently, in Belgrade, we had more than 30 yrs ago, ex-sportsmen individuals with hypertophied hearts, which, after strenouous effort during recreation,, have had myocardial infaction without local thrombosis in the infarct-related coronary artery.

According to the European Society of Cardiology (and other societies) universal definition of myocardial infarction, there are five type of MI. Type 1 is your conventional MI related to plaque erosion or rupture leading to thrombus formation. Type 3 is defined by the circumstance of sudden death, but could also be related to thrombus formaiton. Type 4a is MI related to PCI and Type 5 is MI related to CABG. Type 4b is the detection of stent thrombosis. All types are related to thrombosis except type 2. Type 2 is MI secondary to ischemia due to increased oxygen demand or decreased supply (e.g. coronary artery spams, coronary embolism, anaemia, arrhythmias, hypertension or hypotension.

So in conclusion, a type 2 MI occurs without thrombosis.

Reference attached

Subendocardial infarctions usually occur without thrombosis-I wrote my thesis already in 1974 about differences' between various types of AMI. Erhardt LR. Clinical and pathological observations in different types of acute myocardial infarction. Thesis. Acta Medica Scaninavia Suppl 560, 1974.

Underperfusion of the endocardium including the papillary muscles is the cause of this type of MI

I totally agree with the  Julio F Marchini's opinion and underline that type 2 MI is frequent in young people (drug addiction - ipercatecholaminergic syndrome etc)

Excellent info above. 

Collectively in our ongoing studies and anecdotes of routine clinical use, we are finding that

Absolutely YES! I had in my great series of more than 14.000 AMI or ACS patients in my CCU 1969-1990 a lot of such examples in the case of various situations of discrepancy between myocardial oxygen demand and support, now presented in the ESC group 2