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What lies ahead: he is the best physician who is the most ingenious inspirer of hope.

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In 1903, Dutch physiologist Willem Einthoven, MD, PhD invented the electrocardiograph, a machine that measures the minute electrical currents generated by the heart. Initially, it was a cumbersome and costly device, taking five technicians to operate. During the procedure, patients had to place both hands and both feet in buckets of water. But as a result of this advance cardiologists began, for the first time, to fully understand the electrical processes involved in generating the heart beat. With this knowledge, they were able to more precisely diagnosis certain cardiovascular problems.

A little more than a century later, scientific ingenuity has led to the development of many other advances. Scientists, for instance, have developed magnetic resonance imaging and other noninvasive ways to study the aging heart. Researchers have discovered a host of innovative drug treatments to help the ailing heart and arteries work better. And cardiologists and surgeons have successfully pioneered the use of cardiac catheterization, cardiovascular stents, implantable pacemakers, bypass surgery, and heart transplants.

No doubt about it, doctors know more about the heart and how to keep it healthy than at any other time in history. In just the past 30 years, gerontologists have revolutionized ideas about what happens in the older heart. They've learned, for instance, that age-related changes in the structure and function of the heart occur in virtually every person. Mounting evidence suggests that some of these changes, previously thought to be a part of normal aging, precede and predict the onset of cardiovascular diseases, even among those who do not yet have signs or symptoms of disease. But they've also learned that preventive measures, such as getting regular exercise, eating a healthy diet, and not using tobacco, can have a profound impact on the aging cardiovascular system.

In the future, interventions to slow accelerated aging of the heart and arteries in apparently healthy young and middle-age people could prevent or delay the onset of heart disease, stroke, and other cardiovascular disorders in later life, Dr. Lakatta says. These interventions may take many forms. For instance, the more we understand about the changes that take place in cells and molecules during aging, the closer we get to the possibility of designing drugs targeted to those changes. Gene therapies can also target specific cellular changes and could potentially be a way to intervene in the aging process.

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Achieving these goals will likely require considerable effort and as much, or perhaps even more, ingenuity and innovation in the coming years as has been shown in the past. NIA investigators and others are already taking steps to meet these challenges. They still have many questions to answer and mysteries to solve. But as this work progresses and scientists unravel more of the aging heart's secrets, the hope of forestalling cardiovascular disease and improving the quality of life for older people may come closer to reality.

GLOSSARY

ACTION POTENTIAL--An abrupt, transient change in the electrical charge along a heart muscle cell membrane; the first of several steps leading to the cell's contraction.

ADVENTITIA--The outermost layer of arterial wall; it is composed of connective tissue.

AFTERLOAD--The mechanical load encountered by the heart following the onset of contraction; the forces that resist the flow of blood from the heart. The afterload may increase with age due to increasingly stiff arteries and an increased tone of the smaller arteries.

ANGIOTENSIN--A chemical that constricts blood vessels, which raises blood pressure.

AORTA--The largest artery in the body. It conducts blood away from the heart, then branches into many smaller arteries that take blood to the rest of the body. The diameter of the aorta enlarges with age and its walls become stiffer.

ARTERIES--Blood vessels that carry blood away from the heart to all parts of the body. Some enlarge with age and become thicker and stiffer. Arterial walls consist of three layers: the intima, media, and adventitia.

ARTERIOLES--The very small arteries that take blood from the arteries to the capillaries.

ATHEROSCLEROSIS--A condition of the arteries in which the interior of the artery wall is made thick and irregular by deposits of fatty substances and invasive cells from the blood and arterial wall and matrix substances synthesized by the cells.

ATRIOVENTRICULAR NODE--A group of special conduction fibers at the base of the wall between the right atrium and ventricle. They relay the electrical impulses to the ventricle to initiate contraction. These electrical impulses originate in the heart's pacemaker, the sinoatrial node within the right atrium.

ATRIUM--One of the two upper chambers of the heart. The right atrium receives blood depleted of oxygen from the veins; the left atrium receives blood with fresh oxygen from the lungs. The left atrial cavity enlarges with age.

AUTONOMIC NERVOUS SYSTEM--That part of the nervous system that controls involuntary muscles, such as the heart. It uses chemicals, such as catecholamines, to send messages from the brain to the heart. With age, the body's response to cathecholamines withers.

BARORECEPTOR RESPONSE--The body's response to pressure sensitive nerves in the carotid artery that help regulate heart rate and arterial pressure; the response grows weaker with age.

BLOOD PRESSURE--The force that flowing blood exerts against artery walls. Systolic blood pressure occurs when the heart contracts and pumps blood into the aorta. Diastolic blood pressure occurs when the aortic valve closes and the heart relaxes and refills with blood.

CALCIUM PUMP PROTEINS--Proteins on the sarcoplasmic reticulum that remove calcium from the cell cytosol after a contraction. The number of these pump proteins declines with age.

CALCIUM TRANSIENT--The transient increase in calcium in the cytosol following excitation, which causes a contraction. It grows longer with age.

CAPILLARIES--The smallest blood vessels that take blood from the arterioles to cells in the body.

CARDIAC CYCLE--The cycle of synchronized activities that occurs during one heart beat.

CARDIAC OUTPUT--The amount of blood a heart pumps each minute. It is calculated by multiplying heart rate by stroke volume.

CARDIOVASCULAR--Of or pertaining to the heart and blood vessels.

CHEMOKINES--A type of cytokine that carries messages between cells. In a sense, they tell cells where to go. If chemokines are increased in a particular tissue, such as an artery, the cell with the receptor, or partner, for that particular molecule is attracted to move into that tissue.

CHOLESTEROL--A waxy, fat-like substance present in cell walls or membranes everywhere in the body, including the heart. Excess cholesterol is deposited in arteries, including the coronary arteries, where it contributes to the narrowing and blockages that cause the signs and symptoms of heart disease. Cholesterol is carried in small packages called low density (LDL) and high density (HDL) lipoproteins.

CONTRACTILE (MYOFILAMENT) PROTEINS--Proteins in myocytes that change their configuration in order to bring about a shortening or contraction of the cell. This may change with age.

CONTRACTILE STATE--The ability of the heart muscle cells to contract, also referred to as contractility.

CORONARY HEART DISEASE--Also called coronary artery disease ischemic heart disease. A narrowing of the coronary arteries due mostly to atherosclerosis resulting in a decreased flow of blood to the heart muscle and thus lower levels of oxygen reaching the heart.

CORONARY FLOW--The flow of blood through the coronary arteries that nourish the heart muscle.

CYTOKINE--Proteins that are secreted by cells and regulate the behavior of other cells by binding to receptors on their surfaces. This binding triggers a variety of responses depending on the nature of the cytokine and the target cell.

CYTOSOL--The fluid inside heart and blood vessel cells.

DIASTOLE--The period during a heart beat when the chambers are filling with blood and the heart muscle is relaxed.

DNA--Abbreviation for deoxyribonucleic acid, the molecule that contains the genetic code for all life forms except for a few viruses. It consists of two long, twisted chains of molecules in the nucleus of each cell that carries the genetic information necessary for all cellular functions, including the building of proteins.

ECHOCARDIOGRAM (ECG OR EKG)--A visual record of the heart's electrical activity.

EJECTION FRACTION--The fraction of end diastolic volume pumped out with each beat.

ELECTROCARDIOGRAPHY--A method of graphically recording the structure and movement of the heart by the echo caused by beams of ultrasonic waves.

END DIASTOLIC VOLUME--The volume of blood in the left ventricle at the end of diastole, just before the next beat.

ENDOTHELIUM--The smooth inner lining of many body structures, including the heart and blood vessels. Endothelial cells are a primary component of the intima.

END SYSTOLIC VOLUME--The volume of blood left in the heart at the end of the heartbeat.

ENZYME--A protein that promotes a specific biochemical reaction in the body without itself being permanently changed or destroyed. Enzymes may have an important role in the age-associated changes in structure and function that occur in the heart and arteries.

FRANK-STARLING LAW OF THE HEART--A phenomenon in which the more the heart muscle is stretched the more vigorously it contracts.

FREE RADICALS--Molecules with unpaired electrons that react readily with other molecules. Free radicals can damage myocytes as well as the membranes and DNA of endothelial cells in the intima and smooth muscle cells in the media. This damage can promote stiffening and thickening of arterial walls. Free radicals also can contribute to atherosclerotic plaque build up.

GENE--A segment of DNA that codes for a specific protein or other molecule. Each gene contains a specific sequence of chemicals. The sequence is referred to as a "code" because it specifies the order of amino acids (chemical building blocks of proteins) in the end product.

GENE EXPRESSION--The process by which the information contained in genes is transcribed and translated into proteins. Age-related changes in gene expression may account for some changes in heart and artery function.

HEART ATTACK--The death of a portion of heart muscle, resulting when an obstruction in one of the coronary arteries prevents an adequate oxygen supply to that muscle. Heart attacks may be referred to in terms of obstruction (coronary thrombosis) or in terms of the damage done (myocardial infarction).

HEART FAILURE--A condition in which the heart is unable to pump the amount of blood needed by the body. Heart failure can develop from many heart and circulatory disorders, such as high blood pressure heart attack. It often leads to congestion in the body tissues, with fluid accumulating in the abdomen and legs and/or in the lungs. This condition is often called congestive heart failure.

HEART RATE--The number of beats per minute.

HIGH BLOOD PRESSURE--An unstable or persistent elevation of blood pressure above the normal range. Blood pressure often increases with age. High blood pressure increases the risk of heart disease and stroke; also known as hypertension.

HIGH DENSITY LIPOPROTEINS (HDL)--The "good" cholesterol. HDL carries cholesterol in the blood from other parts of the body back to the liver, which leads to its removal from the body. HDL helps keep cholesterol from building up in the walls of the arteries.

HYPERTROPHY--Enlarge or enlargement. The myocytes that make up the walls of the heart hypertrophy with age.

ISCHEMIA--Decreased blood supply to the heart muscle.

INTIMA--The innermost layer of arterial wall closest to the blood. It is composed of a single layer of specialized cells, called endothelial cells, which sit atop the sub-endothelial space and a wall called the basement membrane.

LOW DENSITY LIPOPROTEIN (LDL)--The "bad" cholesterol.High LDL cholesterol leads to a build up of cholesterol in arteries. The higher the LDL level in your blood, the greater chance you have for getting coronary heart disease.

LUMEN--The tube-like opening in arteries and other vessels that blood flows through on its journey throughout the body.

MAXIMUM HEART RATE--The number of beats per minute during rigorous exercise. It declines by about 25 to 30 percent between the ages 20 and 80, regardless of physical fitness status. Scientists estimate maximum heart rate by subtracting your age from 220.

MAXIMUM OXYGEN CONSUMPTION--The amount of oxygen used by the body at peak exercise capacity. Also known as VO2 max, it is considered the best measure of cardiorespiratory physical fitness. Women tend to have less lean muscle mass than men, and it is lean muscle mass that needs the most oxygen. When studies compare oxygen consumption based on the amount of lean muscle rather than overall body size, the gender differences disappear. Women, in other words, use the same amount of oxygen as men.

MEDIA--The middle layer of the arterial wall. It is composed of smooth muscle cells surrounded by a network of fibers primarily made of two proteins, collagen, and elastin. The elastin forms concentric rings within the vessel wall.

MITRAL VALVE--The valve between the left atrium and ventricle. It closes more slowly with age because the rate of blood flow into the left ventricle that pushes it closed decreases with age.

MYOCARDIUM--The heart muscle.

MYOCYTE--A heart muscle cell.Myocytes decline in number but grow larger with age.

NONINVASIVE TECHNIQUES--Medical procedures that do not require needle puncture, surgery, or entering the artery.

ORGANELLE--A structure inside a cell, such as the sarcoplasmic reticulum.

OXYGEN CONSUMPTION--The amount of oxygen the entire body uses in a certain time period. It is calculated by taking the amount of oxygen in the arteries and subtracting the amount left in the veins after the body's cells have taken out oxygen. The result is then multiplied by cardiac output.

PRELOAD--The amount of blood in the left ventricle before contraction.

PROTEINS--Molecules composed of amino acids arranged in a specific order. Certain proteins, such as the calcium pump protein and the contractile protein myosin, appear to change with age which may account for some alterations in the function of the aging heart.

SARCOPLASMIC RETICULUM--A structure or organelle inside a myocyte. Its function is to store and release calcium for use during a contraction and to remove calcium after calcium transient causes a contraction. It removes calcium more slowly with age.

SINOATRIAL NODE--The heart's pacemaker. A group of specialized cells in the right atrium wall that give rise to the electrical impulses that initiate contractions.

STROKE VOLUME--The amount of blood pumped with each heart beat.

SYSTOLE--The period during a heart beat when the heart muscle contracts and blood is pumped out.

VEINS--The blood vessels that return blood to the heart after the body's cells have extracted oxygen.

VENTRICLE--A chamber of the heart that pumps blood out. The right ventricle pumps blood to the lungs where it picks up oxygen; the left ventricle pumps blood into the aorta, which distributes it to the rest of the body.

BIBLIOGRAPHY

Selected Readings

GENERAL

Heart and Stroke Facts, (Dallas: American Heart Association, 1992-2003).

Nuland, S.B., The Wisdom of the Body (New York: Knopf, 1997).

Zaret, B.L.; Moser M.; Cohen L.S., Yale University School of Medicine Heart Book (New York: Hearst Books, 1992).

THE AGING HEART

Anversa, P.; Annarosa, L.; Kajstura, J.; NadalGinard, B. (2002). Myocyte Growth and Cardiac Repair. Journal of Molecular and Cellular Cardiology, 34, 91-105.

Anversa, P.; Sussman, M.A.; Bolli, R. (2004). Molecular Genetic Advances in Cardiovascular Medicine: Focus on the Myocyte. Circulation Research, 109, 2832-2838.

Gerstenblith, G.; Fredricksen, J.; Yin F.C.P.; Fortuin, N.J.; Lakatta, E.G.;Weisfeldt, M.L. (1977). Echocardiographic Assessment of a Normal Adult Aging Population.Circulation Research, 56, 273-278.

Lakatta, E.G. (1993). Cardiovascular Regulatory Mechanisms in Advanced Age. Physiological Reviews, 73, 413-467.

Lakatta, E.G.; Levy,D. (2003).Arterial and Cardiac Aging: Major Shareholders in Cardiovascular Disease Enterprises: Part II: The Aging Heart in Health: Links to Heart Disease. Circulation Research, 107(2), 346-354.

Lakatta, E.G. (2002).Age-associated Cardiovascular Changes in Health: Impact on Cardiovascular Disease in Older Persons. Heart Fail Review, 7(1), 29-49.

Lakatta, E.G. (2002). Introduction: Chronic Heart Failure in Older Persons. Heart Fail Review, 7(1), 5-8.

Lakatta, E.G.; Sollott, S.J. (2002). The "Heartbreak" of Older Age.Molecular Interventions, 2(7), 431-46.

Oxenham, H.; Sharpe, N. (2002). Cardiovascular Aging and Heart Failure. The European Journal of Heart Failure, 5, 427-434.

Rodeheffer, R.J.; Gerstenblith, G.; Becker, L.C.; Fleg J.L.; Weisfeldt, M.L.; Lakatta, E.G. (1984). Exercise Cardiac Output in Healthy Human Subjects: Cardiac Dilation and Increased Stroke Volume Compensate for a Diminished Heart Rate. Circulation Research, 69, 203-213.

Schulman, S.P.; Lakatta, E.G.; Fleg, J.L.; Lakatta, L.; Becker, L.C.; Gerstenblith, G. (1992). Age-related Decline in Left Ventricular Filling at Rest and Exercise. American Journal of Physiology, 68, 28-38.

Sjogren, A.L. (1971). Left Ventricular Wall Thickness Determined by Ultrasound in 100 Subjects Without Heart Disease. Chest, 60, 341-346.

Spirito, P.; Maron, B.J. (1988). Influence of Aging on Doppler Echocardiographic Indices on Left Ventricular Diastolic Function. British Heart Journal, 59, 672-679.

CELLULAR CLUES

Balsam, L.B.; Wagers, A.J.; Christensen, J.L., et al. (2004).Haematopoietic Stem Cells Adopt Mature Haematopoietic Fates in Ischaemic Myocardium. Nature Cell Biology, 428, 668-673.

Beltrami,A.P.; Barlucchi, L.;Torella,D., et al. (2003). Adult Cardiac Stem Cells are Multipotent and Support Myocardial Regeneration. Cell, 114, 763-776.

Inesi, G.; Wade, R.; Rogers, T. (1998). The Sarcoplasmic Reticulum Ca2+ Pump: Inhibition by Thapsigargin and Enhancement by Adenovirus-mediated Gene Transfer. Annals of the New York Academy of Sciences, 853, 195-205.

Janczewski, A.M.; Spurgeon, H.A.; Lakatta, E.G. (2002). Action Potential Prolongation in Cardiac Myocytes of Old Rats is an Adaptation to Sustain Youthful Intracellular Ca2+ Regulation. Journal of Molecular and Cellular Cardiology, 34(6), 641-8.

Lakatta, E.G. (2003). Arterial and Cardiac Aging: Major Shareholders in Cardiovascular Disease Enterprises: Part III: Cellular and Molecular Clues to Heart and Arterial Aging. Circulation Research, 107(3), 490-497.

Lakatta, E.G.; Gerstenblith, G.; Angell, C.S.; Shock, N.W.; Weisfeldt, M.I. (1975). Prolonged Contraction Duration in Aged Myocardium. Journal of Clinical Investigation, 55, 61-68.

Lakatta, E.G.; Sollott, S.J.; Pepe, S. (2001). The Old Heart: Operating on the Edge. In: Bock, G.; Goode, J.A., eds. Ageing Vulnerability: Causes and Interventions. Novaritis Foundation Symposium, 235. New York, NY: John Wiley and Sons, Ltd., 172-201.

Lakatta, E.G. (1993), Cardiovascular Regulatory Mechanisms in Advanced Age.Physiological Review, 73, 413-467.

Long, X.; Boluyt, M.O.; O'Neill, L., et al. (1999). Myocardial Retinoid X Receptor,Thyroid Hormone Receptor, and Myosin Heavy Chain Gene Expression in the Rat During Adult Aging. Journal of Gerontology: Biological Sciences, 54A, B23-B27.

Lyons, D.; Roy, S.; Patel, M.; Benjamin, N.; Swift, C.G. (1997). Impaired Nitric Oxide-mediated Vasodilatation and Total Body Nitric Oxide Production in Healthy Old Age, Clinical Science, 93, 519-525.

Murry C.E.; Soonpaa, M.H.; Reinecke, H., et al. (2004). Haematopoietic Stem Cells do Not Transdifferentiate into Cardiac Myocytes in Myocardial Infarcts.Nature Cell Biology, 428, 664-668.

Neuss, M.; Crow, M.T.; Chesley, A.; Lakatta, E.G. (2001). Apoptosis in Cardiac Disease--What is it--How Does it Occur? Cardiovascular Drugs and Therapy, 15(6), 507-523.

O'Neill, L.; Holbrook, N.J.; Fargnoli, J.; Lakatta, E.G. (1991). Progressive Changes from Young Adult Age to Senescence in mRNA for Rat Cardiac Myosin Heavy Chain Genes, Cardioscience, 2, 1-5. Orlic, D.; Kajstura, J.; Chimen, S., et al. (2001). Bone Marrow Cells Regenerate Infracted Myocardium. Nature Cell Biology, 410, 701-705.

Phaneuf, S.; Leewenburgh, C. (2002). Cytochrome c Release from Mitochondria in the Aging Heart: A Possible Mechanism for Apoptosis with Age. American Journal of Physiology--Regulatory Integrative Comparative Physiology, 282, R423-R430.

Schmidt, U.; del Monte, F.; Miyamoto, M.I., et al. (2000). Restoration of Diastolic Function in Senescent Rat Hearts Through Adenoviral Gene Transfer of Sarcoplasmic Reticulum Ca (2+)-ATPase. Circulation Research, 101, 790-796.

Spurgeon, H.A.; Steinbach, M.F.; Lakatta, E.G. (1983). Chronic Exercise Prevents Characteristic Age-related Changes in Rat Cardiac Contraction. American Journal of Physiology, 244, H5513-H518.

Tate, C.A.; Taffet, G.E.;Hudson, E.K., et al. (1990). Enhanced Calcium Uptake of Cardiac Sarcoplasmic Reticulum in Exercise-trained Old Rats. American Journal of Physiology, 258, H431-H435.

Vila Petroff, M.G.; Kim, S.H.; Pepe, S.; Dessy, C.; Marban, E.; Balligand, J.L.; Sollott, S.J. (2001). Endogenous Nitric Oxide Mechanisms Mediate the Stretch Dependence of Ca2+ Release in Cardiomyocytes. Nature Cell Biology, 3, 867-873.

BLOOD VESSELS AND AGING: THE REST OF THE JOURNEY

Avolio, A.P.; Chen, S.G.; Wang, R.P., et al. (1983). Effects of Aging on Changing Arterial Compliance and Left Ventricular Load in a Northern Chinese Urban Community. Circulation Research, 68, 50-58.

Avolio, A.P.; Deng, F.Q.; Li, W.Q., et al. (1985). Effects of Aging on Arterial Dispensability in Populations with High and Low Prevalence of Hypertension: Comparison Between Urban and Rural Communities in China. Circulation Research, 71, 202-210.

Bagrov, A.Y.; Lakatta, E.G. (2004). The Dietary Sodium-blood Pressure Plot "Stiffens." Hypertension, 44, 22.

Benetos, A.; Zureik, M.;Morcet, J., et al. (2000). A Decrease in Diastolic Blood Pressure Combined with an Increase in Systolic Blood Pressure is Associated with a Higher Cardiovascular Mortality in Men. Journal of the American College of Cardiology, 35, 673-680.

Bertoni, A.G.; Hundley, W.G.; Massing,M.W., et al. (2004). Heart Failure Prevalence, Incidence, and Mortality in the Elderly with Diabetes. Diabetes Care, 27, 699-703.

Carnethon, M.R.; Gidding, S.S.;Nehgme, R.; Sidney, S.; Jacobs, D.R.; Liu, K. (2003). Cardiorespiratory Fitness in Young Adulthood and the Development of Cardiovascular Disease Risk Factors. Journal of the American Medical Association, 290, 3092-3100.

Celermajer, D.S.; Sorensen, K.E.; Spiegelhalter, D.J.; Georgakopoulos, D.; Robinson, J.; Deanfield, J.E. (1994). Aging is Associated with Endothelial Dysfunction in Healthy Men Years Before the Age-related Decline in Women. Journal of the American College of Cardiology, 24, 471-476.

Chae,C.U.; Pfeffer, M.A.; Glynn, R.J.;Mitchell, G.F.; Taylor, J.O.; Hennekens, G.H. (1999). Increased Pulse Pressure and the Risk of Heart Failure in the Elderly. Journal of the American Medical Association, 281, 634-639.

Cohn, J.N.; Hoke, L; Whitman, W., et al. (2003). Screening for Early Detection of Cardiovascular Disease in Asymptomatic Individuals. American Heart Journal, 146, 572-580.

Csiszar, A.; Ungvari, Z.; Edwards, J.G., et al. (2002). Aging-induced Phenotypic Changes and Oxidative Stress Impair Coronary Arteriola Function. Circulation Research, 90, 1159-1166.

Edelberg, J.M.; Lee, S.H.; Kaur, M., et al. (2002). Platelet-derived Growth Factor-AB Limits the Extent of Myocardial Infarction in a Rat Model. Circulation Research, 105, 608-613.

Edelberg, J.M.; Reed, M.J. (2003). Aging and Angiogenesis. Frontiers in Bioscience, 8, 1199-1209.

Edelberg, J.M.; Tang, L.; Hattori, K.; Lyden, D.; Rafii, S. (2002). Young Adult Bone Marrowderived Endothelial Precursor Cells Restore Aging-impaired Cardiac Angiogenic Function. Circulation Research, 90, e89-e93.

Edelberg, J.M.; Xaymardan, M.; Rafii, S.;Hong,M.K. (2003). Adult Cardiac Stem Cells--Where do We Go From Here? Sci SAGE KE, pe17 http://sageke.sciencemag.org.

Fang, J.; Wylie-Rosett, J.; Cohen, H.W.; Kaplan, R.C.; Alderman, M.H. (2003). Exercise, Body Mass Index, Caloric Intake and Cardiovascular Mortality. American Journal of Preventive Medicine, 25, 283-289.

Fox, C.S.; Sullivan, L.; D'Agostino, R.B.; Wilson, P.W.F. (2004). The Significant Effect of Diabetes Duration on Coronary Heart Disease Mortality. Diabetes Care, 27, 704-708.

Franklin, S.S.; Khan, S.A.; Wong, N.D.; Larson, M.G.; Levy, D. (1999). Is Pulse Pressure Useful in Predicting Risk for Coronary Heart Disease. Circulation Research, 100, 354-360.

Gordon, P.A. (2004). Effects of Diabetes on the Vascular System: Current Research Evidence and Best Practice Recommendations. Journal of Vascular Nursing, 22, 2-11.

Havlik, R.J.; Simonsick, E.M.; Sutton-Tyrrell, K.; Newman, A., et al. (2003). Association of Physical Activity and Vascular Stiffness in 70- to 79-YearOlds: The Health ABC Study. Journal of Aging and Physical Activity, 11, 156-166.

Hua, C.; Griendling, K.K.; Harrison, D.G. (2003). The Vascular NAD(P)H Oxidase as Therapeutic Targets in Cardiovascular Diseases. Trends in Pharmacological Science, 24(9), 471-478.

Itescu, S.; Schuster, M.D.; Kocher, A.A. (2003). New Directions in Strategies Using Cell Therapy for Heart Disease. Journal of Molecular Medicine, 81, 288-296.

Kass, D.A.; Shapiro, E.P.; Kawaguchi, M.; Capriotti, A.R.; Scuteri, A; deGroof, R.C.; Lakatta, E.G. (2001). Improved Arterial Compliance by a Novel Advanced Glycation End-product Crosslink Breaker. Circulation Research, 104(13), 1464-1470.

Lakatta, E.G. (2000). Research Agenda for Cardiovascular Aging: Humans to Molecules. American Journal ofGeriatric Cardiology, 9(5), 51-262.

Lakatta, E.G.; Levy,D. (2003).Arterial and Cardiac Aging: Major Shareholders in Cardiovascular Disease Enterprises: Part I: Aging Arteries: a "Set Up" for Vascular Disease. Circulation Research, 107(1), 139-146.

Lakatta, E.G.; Sollott, S.J. (2002). Perspectives on Mammalian Cardiovascular Aging: Humans to Molecules.Comparative Biochemistry and Physiology. Part A,Molecular and Integrative Physiology, 132(4), 699-721.

Lakka, H.M.; Laaksonen, D.E.; Lakka, T.A., et al. (2002). The Metabolic Syndrome and Total and Cardiovascular Disease Mortality in Middle-aged Men. Journal of the American Medical Association, 288, 2709-2716.

Lassegue, B.; Clempus, R.E. (2003). Vascular NAD(P)H Oxidases: Specific Features, Expression, and Regulation. American Journal of Physiology--Regulatory, Integrative and Comparative Physiology, 285, R277-R297.

Lesnefsky, E.J.; Moghaddas, S.; Tandler, B.; Kerner, J.;Hoppel, C.L. (2002). Mitochondrial Dysfunction in Cardiac Disease: Ischemia--Reperfusion, Aging, and Heart Failure. Journal ofMolecular and Cellular Cardiology, 33. 1065-1089.

Meaume, S.; Bentos, A.; Henry,O.F.; Rudnichi, A.; Safar, M.E. (2001). Aortic Pulse Wave Velocity Predicts Cardiovascular Mortality in Subjects >70 Years of Age. Arteriosclerosis, Thrombosis, and Vascular Biology, 21, 2046-2050.

Miake, J.;Marban, E.;Nuss, H.B. (2002). Biological Pacemaker Created by Gene Transfer. Nature Cellular Biology, 419, 132-133.

Nadal-Ginard, B.; Kajstura, J.; Annarosa, L.; Anversa, P. (2003). Myocyte Death, Growth and Regeneration in Cardiac Hypertrophy and Failure. Circulation Research, 92, 139-150.

National Library of Medicine. Genetics Home Reference: Help Me Understand Genetics, Chapter 5, Gene Therapy, July 2004, http://ghr.nlm.nih.gov/dynamicImages/understandGenetics/genetherapy.pdf.

Newman, A.B.; Arnold, A.M.; Naydeck, B.L., et al. (2003). "Successful Aging:" Effect of Subclinical Cardiovascular Disease. Archives of Internal Medicine, 163, 2315-2322.

Olivetti, G.; Abbi, R.; Quaini, F.; Kajstura, J., et al. (2003). Apoptosis in the Failing Heart. New England Journal of Medicine, 336, 1131-1141.

Pastor-Barriuso, R.; Banegas, J.R.; Damian, J.; Appel, L.J.; Guallar, E. (2003). Systolic Blood Pressure, Diastolic Blood Pressure, and Pulse Pressure: An Evaluation of Their Joint Effect on Mortality. Annals of Internal Medicine, 139, 731-739.

Piepoli, M.F.; Davos, C.; Francis, D.P.; Coats, A.J. (2004). ExTraMATCH Collaborative, Exercise Training Meta-analysis of Trials in Patients with Chronic Heart Failure (ExTraMATCH). British Medical Journal, 328 (7433), 189.

Pina, I.L.; Apstein, C.S.; Balady, G.J., et al. (2003). Exercise and Heart Failure: A Statement from the American Heart Association Committee on Exercise,Rehabilitation, and Prevention.Circulation Research, 107, 1210-1225.

Ramachandran, S.V.; Beiser, A.; Seshadri, S., et al. (2002). Residual Lifetime Risk for Developing Hypertension in Middle-aged Women and Men: The Framingham Study. Journal of the American Medical Association, 287 (8), 1003-1010.

Rasucher, F.M.; Goldschmidt-Clermont, P.J.; Davis, B.H., et al. (2003). Aging, Progenitor Cell Exhaustion, and Atherosclerosis. Circulation Research, 108, 457-463.

Sacks, F.M.; Svetkey, L.P.; Vollmer, W.M., et al. (2001). Effects on Blood Pressure of Reduced Dietary Sodium and the Dietary Approaches to Stop Hypertension (DASH) Diet. The New England Journal of Medicine, 244(1), 3-10.

Safar, M.E. (2001). Systolic Blood Pressure, Pulse Pressure, and Arterial Stiffness as Cardiovascular Risk Factors. Current Opinion in Nephrology and Hypertension, 10, 257-261.

Scuteri, A.; Najjar, S.S.; Muller, D.C.; Andres, R.; Hougaku, H.; Metter, E.J.; Lakatta, E.G. (2004). Metabolic Syndrome Amplifies the Age-associated Increases in Vascular Thickness and Stiffness. Journal of the American College of Cardiology, 43 (8), 1396-1398.

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SAMUEL TAYLOR COLERIDGE, ENGLISH POET AND PHILOSOPHER, 1772-1834
COPYRIGHT 2007 National Institute on Aging
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Title Annotation:Aging Hearts & Arteries: A Scientific Quest
Author:Coleridge, Samuel Taylor
Publication:Pamphlet by: National Institute on Aging
Article Type:Glossary
Geographic Code:1USA
Date:Nov 1, 2007
Words:4832
Previous Article:Blood vessels and aging: the rest of the journey: a man is as old as his arteries.
Next Article:Introduction.
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