QUANTITATIVE MYOCARDIAL PERFUSION IMAGING: THE BASIS OF PERSONALIZED CORONARY CARE
Overview: Myocardial Perfusion and Metabolism—Now and at the Beginning
Low coronary blood flow may cause acute coronary syndromes, angina pectoris, heart failure, arrhythmias, and even death, as reviewed in detail in Chapter 34. The capacity for increased coronary blood flow is associated with cardiovascular health, and its variations may reflect our emotional states and lifestyles, including the foods we eat—even our most recent meal. Intense risk factor treatment prevents or stabilizes atherosclerosis, thereby preserving coronary blood flow, which is the most basic vital sign of life on which blood pressure, heart rate, and respiration depend. Assessing, maintaining, or restoring coronary blood flow are the objectives of all coronary procedures and most cardiac diagnostic testing. Next to “heart,” the commonest critical word in cardiovascular practice is “ischemia,” implicitly referring to low myocardial perfusion.
Coronary blood flow is a personalized, vital sign of individual status. When severely depressed, similar to blood pressure, it heralds imminent adverse events in an individual, not just a statistical probability of adverse outcome as do risk factors or the diagnosis of coronary artery disease (CAD). Advanced imaging technology and an extensive research literature document its measurement and relevance. Yet quantitative assessment of myocardial perfusion or coronary blood flow remains largely unused and unmeasured in clinical practice; its use is restricted to a research tool in a small number of academic centers where it usually has limited impact on clinical decisions. However, in view of revascularization trials failing to improve event-free survival in patients with CAD or reduced left ventricular function, quantitative perfusion and metabolic imaging should play a larger role in selecting patients optimally benefiting from revascularization.
How does the “now” of coronary blood flow in acute coronary syndromes relate to “the beginning” of the four-chambered mammalian heart that had already evolved 200 million years ago? A stem mammal (eg, Morganucodon watsoni) was a 1-inch long weasel-like animal during dinosaurs' domination for 250 million years.1 The Chicxulub asteroid impact2 and associated Deccan volcanism blocked the sun, causing the end-Cretaceous mass extinction of most life.3,4 However, small mammals survived,5 radiating into multiple open niches and large sizes, reflecting adaptability to extreme demands and environments that required an extraordinary heart and cardiovascular system before large brains and facile limbs evolved. As documented in humans,6 canines,7 and swine,8 the branching coronary artery tree of mammals is structured in mathematically exact arterial size and length for myocardial mass.6,7
This arterial size-length-mass relationship and the branching structure of the coronary arterial tree are precisely related to coronary blood flow by a power equation for minimum energy loss. This relationship is mediated by normalized wall shear force to distribute efficiently the oxygenated coronary blood to myocardium6 while preserving capacity for high demands of coronary blood flow ...