Traditionally, an MI has been viewed as an obliga- tory event in the transition to depressed systolic function. Because MI occurs in 16% of those who develop depressed LV ejection fraction compared with 3% of those who do not, it is an important risk factor.224 However, there must be other mechanisms because increased LV mass remains associated with the development of depressed LV ejection fraction even in patients free of clinically manifest CAD, including MI. With antihypertensive treatment, the incidence of LV hyper- trophy is reduced by 35%, and the development of HF is reduced by 52%.222 The mechanisms for the progression from hypertension to clinical HF with preserved ejection fraction represent an area of ongoing investigation.225 Potential mechanisms include progressive changes in the myocardial extracellular matrix and elevation in LV filling pressures.226-231 6.4. CAD and Acute HF Ischemia may trigger acute pulmonary edema. The majority of patients with flash pulmonary edema have preserved systolic These patients are generally elderly and have severe CAD, typically with 1 occluded vessel and a severely stenosed coronary artery supplying collateral flow.234-236 Patients with preserved systolic function and LV hypertrophy are particularly susceptible to this type of episode because of their reduced ventricular distensibility, in which small changes in ventricular volume status can lead to large changes in filling pressures. This abnormal diastolic pressure volume relationship may also explain why these patients frequently improve quickly with diuresis and lowering of BP.237 In terms of management, the same principles apply when this occurs in the setting of ischemic cardiomyopathy as in ACS. Refer to the Management of Hypertension in Patients With ACS section above. 6.5. 