years, and 4, in patients aged 90 to 99 years of age. None were 100 or older. Each of the 6 patients in- cluded in this study aged 100 or older had been studied from 1970 to 1992 when the author lived in the Washington, DC, area. Thus, these 6 patients were from among approximately 12,000 hearts personally examined by the author during that 22-year period. In summary, cardiac findings at necropsy have been described in 6 patients aged 100 to 103 years of age. Although 4 had considerably narrowed cor- onary arteries at necropsy, none had had apparent clinical evidence of myocardial ischemia or conges- tive heart failure during life. Two had small grossly visible left ventricular scars. Two of the 6 had histologic evidence of cardiac amyloidosis. Un- steadiness of gait, cerebral insufficiency, and falls may be more of a danger to centenarians than atherosclerotic coronary artery disease. Three of the 6 died within days of a fall, and the other 3 died from consequences of intestinal problems. 1. Wyke A. 21st Century Miracle Medicine: Robosurgery, Wonder Cures, and the Quest for Immortality. New York: Plenum Publishing Corp., 1997:352. 2. Fries JF. Aging, natural death, and the compression of morbidity. N Engl J Med 1980;303:130 –135. 3. Comfort A. The Biology of Senescence, 3rd ed. New York: Elsevier 1979: 81– 86. 4. Waller BF, Roberts WC. Cardiovascular disease in the very elderly. Analysis of 40 necropsy patients aged 90 years or over. Am J Cardiol 1983;51:403– 421. 5. Lie JT, Hammond PI. Pathology of the senescent heart: anatomic observations on 237 autopsy studies of patients 90 to 105 years old. Mayo Clinic Proc 1988;63:552–564. 6. Gertz SD, Malekzadeh S, Dollar AL, Kragel AH, Roberts WC. Composition of atherosclerotic plaques in the four major epicardial coronary arteries in patients 90 years of age. Am J Cardiol 1991;67:1228 –1233. 7. Roberts WC. Ninety-three hearts 90 years of age. Am J Cardiol 1993;71: 599 – 602. 8. Shirani J, Yousefi J, Roberts WC. Major cardiac findings at necropsy in 366 American octogenarians. Am J Cardiol 1995;75:151–156. Effects of Acute Cigarette Smoking on Endothelium- Dependent Arterial Dilatation in Normal Subjects John Lekakis, MD, Christos Papamichael, MD, Costas Vemmos, MD, Kimon Stamatelopoulos, MD, Anastassios Voutsas, MD, and Stamatios Stamatelopoulos, MD I t is well known that cigarette smoking increases the risk of atherosclerosis in coronary, cerebral, and peripheral arteries, and its effects on endothelial func- tion have received considerable interest. Endothelial dysfunction, an early phenomenon in atherogenesis, has been described in brachial arteries of healthy chronic and passive smokers 1,2 ; endothelium-depen- dent vasodilatation is also impaired in systemic arter- ies after acute cigarette smoking. 3 There are no data on how long the deleterious effect of acute smoking on endothelium lasts. Many of the effects of nicotine are attenuated with repeat exposure. 4,5 Data on the possible development to tolerance regarding endothe- lial dysfunction after cigarette smoking are lacking. The present study evaluates the duration of the dele- terious effect of acute smoking on endothelium and investigates the possible development of tolerance produced by repeated nicotine exposure. ••• The study group was composed of 10 healthy vol- unteers (6 men and 4 women, mean age 36  7 years, range 22 to 46). All subjects were nonsmokers; no participant had systemic hypertension, serum total cholesterol level 240 mg/dl, diabetes mellitus, or any cardiac disease. They were taking no cardiovas- cular medications. All subjects gave informed consent before entering the study. From the Department of Clinical Therapeutics, Alexandra University Hospital, Athens, Greece. Dr. Lekakis’s address is: John Lekakis, MD, 86 Alkionis Street, P. Faliron 175 62, Athens, Greece. Manuscript received October 1, 1997; revised manuscript received and ac- cepted January 2, 1998. TABLE I Certain Findings in the Six Centenarians Pt. Age (yr) Race Gender HW (g) LV N LV Fi Dilated Calcium (0–4+) Number of 4 Major CAs 75% in 2 CSA Number of 5-mm Coronary Segments Number of Coronary Segments Narrowed to 4 Categories of CSA Narrowing Cardiac Adiposity Cardiac Amyloid RV LV CAs AV MVA PM 0–25% 26–50% 51–75% 76–100% 1 100 W F 280 0 0 0 0 4+ 2+ 2+ + 2 40 0 24 (60%) 12 (30%) 4 (10%) 0 0 2 100 W M 335 0 + + 0 2+ 1+ 0 + 1 47 18 (38%) 21 (45%) 6 (13%) 2 (4%) + + 3 100 B F 240 0 0 + 0 2+ 1+ 0 + 0 — — — — — 0 0 4 103 B F 320 0 0 0 0 0 0 0 + 0 45 45 (100%) 0 0 0 0 + 5 103 B F 385 0 0 0 0 2+ 1+ 1+ + 2 — — — — — + 0 6 103 W M 410 0 + 0 0 2+ 1+ 0 + 1 — — — — — 0 0 AV = aortic valve; B = black; CAs = coronary arteries; CSA = cross-sectional area; F = female; Fi = fibrosis; HW = heart weight; LV = left ventricle; M = male; MVA = mitral valve annulus; N = necrosis; PM = papillary muscle; RV = right ventricle; W = white. ©1998 by Excerpta Medica, Inc. 0002-9149/98/$19.00 1225 All rights reserved. PII S0002-9149(98)00098-8