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Prevalence of PAD in primary care practices is high, yet physician awareness of the PAD diagnosis is relatively low. A simple ABI measurement identified a large number of patients with previously unrecognized PAD. Atherosclerosis risk factors were very prevalent in PAD patients, but these patients received less intensive treatment for lipid disorders and hypertension and were prescribed antiplatelet therapy less frequently than were patients with CVD. These results demonstrate that underdiagnosis of PAD in primary care practice may be a barrier to effective secondary prevention of the high ischemic cardiovascular risk associated with PAD.

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THEROTHROMBOSIS (COROnary artery disease [CAD], cerebrovascular disease [CVD], and peripheral arterial disease [PAD]) is associated with the main causes of mortality on a worldwide scale. Recent US data have confirmed that despite a decrease in agestandardized national death rates, the absolute number of deaths from these conditions continues to increase, 1 and prevalence is sharply increasing in other parts of the world. Thus, atherothrombotic diseases are, and are projected still to be, the leading cause of death worldwide by 2020. 2 Thus far, most of the information available on atherothrombosis risk has been derived from single regional locales (such as studies conducted in Europe or North America), often confined to a single subtype of patient (patients with CAD, previous stroke patients without PAD), and generally limited to hospitalized patients (as op-posed to outpatients or individuals in primary care) or to patients in clinical trials (as opposed to patients in the community).The REACH (Reduction of Atherothrombosis for Continued Health) Registry has been established to circumvent these limitations by recruit-For editorial comment see p 1253.

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We compared the activity and physiologic effects of cardiac angiotensin converting enzyme (ACE) using isovolumic hearts from male Wistar rats with left ventricular hypertrophy due to chronic experimental aortic stenosis and from control rats. In response to the infusion of 3.5 X 10-8 M angiotensin I in the isolated buffer perfused beating hearts, the intracardiac fractional conversion to angiotensin II was higher in the hypertrophied hearts compared with the controls (17.3±4.1% vs 6.8±1.3%, P < 0.01). ACE activity was also significantly increased in the free wall, septum, and apex of the hypertrophied left ventricle, whereas ACE activity from the nonhypertrophied right ventricle of the aortic stenosis rats was not different from that of the control rats. Northern blot analyses of poly(A)+ purified RNA demonstrated the expression of ACE mRNA, which was increased fourfold in left ventricular tissue obtained from the hearts with left ventricular hypertrophy compared with the controls. In both groups, the intracardiac conversion of angiotensin I to angiotensin II caused a comparable dose-dependent increase in coronary resistance. In the control hearts, angiotensin II activation had no significant effect on systolic or diastolic function; however, it was associated with a dose-dependent depression of left ventricular diastolic relaxation in the hypertrophied hearts. These novel observations suggest that cardiac ACE is induced in hearts with left ventricular hypertrophy, and that the resultant intracardiac activation of angiotensin II may have differential effects on myocardial relaxation in hypertrophied hearts relative to controls. (J. Clin.