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Low coronary blood flow causes acute coronary syndromes (ACS), angina pectoris, myocardial infarction, impaired left ventricular (LV) function, heart failure, arrhythmia, and death. High coronary blood flow capacity associates with cardiovascular health; its variations, reflecting our emotional states, lifestyles, and food, even the postprandial lipid surge of the last meal, are all documented to alter coronary blood flow and risk factors, symptoms, and outcomes of coronary artery disease. Evolving from 200 million years ago, concepts regarding the mammalian heart—coronary blood flow, human gender evolution, fluid dynamic equations, coronary pressure flow measurements, quantitative perfusion imaging, diagnostic tests, coronary artery disease in women versus men, and how poor coronary flow is optimally treated—constitute a highly integrated continuum, a syncytium of knowledge immediately relevant to current cardiovascular medicine and patient well-being.
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Resurgent interest in coronary blood flow related to myocardial “ischemia” derives, in part, from substantial disconnects in cardiovascular medicine. Immediate percutaneous coronary intervention (PCI) in ACS reduces myocardial infarction and cardiovascular mortality.1 However, all elective revascularization trials driven by “ischemia” on diagnostic testing fail to reduce myocardial infarction or cardiovascular deaths despite relief of angina2,3,4,5,6,7,8,9 (Fig. 34–1).
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This disconnect even reaches into the legality of fully informed consent wherein “cardiologists (95%) in this sample did not inform the patient that PCI would not lower the risk of death or MI [myocardial infarction], or that the symptom benefit is gone after 5 years.”10,11 This issue is particularly relevant in view of only half of procedures being classified as appropriate out of 145,000 elective PCIs of the National Cardiovascular Data ...