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Approximately one generation ago it seemed as though we were entering the Golden Age of treatment for coronary artery disease. Epidemiologic studies had identified modifiable risk factors – hypertension, cigarette smoking, hyperlipidemia, obesity, diabetes, inactivity. Coronary surgery was achieving increasingly favorable results with the introduction of internal thoracic artery grafting and dropping operative mortality. The introduction of balloon angioplasty inspired a deluge of diagnostic angiography, searching for a “dilatable lesion.” Atherosclerotic coronary artery disease was recognized as a progressive disease, and the prevailing theory was that the progressive deposition of atherosclerotic plaque would progressively obstruct the coronary lumen to the point where blood could no longer effectively flow, leading to an obstructive clot and its resultant heart attack. According to this paradigm, the angiogram was key in determining the location and degree of obstructive lesions, which information would thereby determine the need for intervention and, with some obvious controversy between surgeons and interventional cardiologists, the most appropriate approach to revascularization.

Since the pinnacle event of a heart attack was the formation of clot in the coronary lumen, thrombolytic therapy was introduced for the acute treatment of MI (myocardial infarction=heart attack). In addition to saving many lives, this treatment resulted in a remarkable revelation: once the clot was removed from the coronary artery, the underlying lesion was found on angiography most often to have a degree of disease that would not have been judged significant had the film been taken before the clot had formed! Our entire definition of what constituted significant disease – based on percentage of luminal obstruction – was not true. People were having heart attacks from thrombosis of coronary arteries in which the degree of atherosclerotic obstruction was not “significant” (i.e. did not block greater than 50% of the luminal diameter when measured on angiography). This observation revealed what we have now come to understand as two major flaws in our thinking. First of all, it is not the size of the plaque, or even necessarily the degree to which it obstructs the coronary artery, but rather the nature, composition and activity of the plaque which places the patient at risk for MI. Intensive investigation has now taught us that atherosclerotic plaque is the result of a complex, multi-faceted ongoing inflammatory response to vascular injury. It is the activity and composition of the plaque, more than its mere size which determines the patient’s heart attack risk. Secondly, in view of the above, coronary angiography, the classic “gold standard” of cardiac diagnosis, was now appreciated to be woefully inadequate to supply critical information. All that is seen is the contrast dye as it follows the course of the blood flowing through the arteries – the actual disease in the wall is appreciated only through indentation in the dye pattern. No direct visualization of wall morphology is possible.

It thus has become imperative to introduce newer imaging modalities which can define not only the lumen but the coronary wall where the disease is active. Three of these have come into more common usage, with many more innovative modalities in the preclinical development stage. Intravascular ultrasound enables the user to use echo technology at the tip of a fine catheter advanced into the coronary artery to directly visualize the wall of the artery. Although the resolution is good, this obviously requires an invasive procedure, and is thus mostly reserved for gathering additional information at the time of diagnostic and/or therapeutic coronary angiography. Magnetic resonance imaging is becoming increasing capable of capturing gated images which reveal myocardial anatomy and physiology. Resolution of the coronary arteries is somewhat confined to the more proximal larger portions of the arteries, but the technology is improving rapidly. With the ability to judge both anatomy and perfusion, this approach holds out the promise of becoming the “one stop shop” for all cardiac imaging diagnoses. Perhaps more rapidly informative is the use of fast multi-slice CT scanning, which, with the addition of dye, can rapidly assess coronary morphology, as well as revealing information which is rapidly becoming competitive with more classic invasive angiography. The dosage of radiation is being reduced with ever more rapid and strategic acquisition times. For these reasons the Florida Heart Research Institute is embarking on a study of the ability of this modality to define coronary artery disease at an early, preclinical and potentially reversible level. Perhaps with the ability to identify and prevent heart attacks before they ever happen, we will really begin to emerge into a new “Golden Age” of treatment of our nation’s leading killer, atherosclerotic coronary artery disease.