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The Aging Heart Emily Kaditz UMMS Donald W. Reynolds Foundation Summer Intern 2012 Age-Related Changes in Cardiac Structure and Function Advancing Geriatrics.

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Presentation on theme: "The Aging Heart Emily Kaditz UMMS Donald W. Reynolds Foundation Summer Intern 2012 Age-Related Changes in Cardiac Structure and Function Advancing Geriatrics."— Presentation transcript:

1 The Aging Heart Emily Kaditz UMMS Donald W. Reynolds Foundation Summer Intern 2012 Age-Related Changes in Cardiac Structure and Function Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation

2 Why Care About Pictures of the Normal Aging Process? Images of Normal vs. Pathology Images of Aged Text on Normal vs. Aged Almost no resources available

3 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Why Should You Care?  The % of people 65 years and older is projected to rise from 13% to 20% between 2010 and 2030. Regardless of the field of medicine you choose, you will treat more patients who are 65 years or older than any previous generation of physicians.

4 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Aging ≠ Disease And disease is not inevitable with aging Normal young Normal aged Disease (sometimes) PASSAGE OF TIME However, the chance of developing some diseases increases with age… This is a function of HOMEOSTENOSIS.

5 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Homeostasis vs. Homeostenosis Homeostasis = the process through which the body maintains internal equilibrium.  With aging, more physiologic reserves are needed to maintain homeostasis when the body is not at rest. Homeostenosis = the normal decline in the body’s functional reserves.  With aging, homeostenosis increases the vulnerability of organs to certain disease states, but a homeostenotic organ is not necessarily diseased.

6 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Homeostenosis HOMEOSTASIS + STENOSIS = HOMEOSTENOSIS With homeostenosis, an insult that may be withstood in a younger person pushes the elderly beyond their functional capacity, causing decompensation, disease, or death. Physiologic reserves allow us to maintain homeostasis in the presence of environmental, emotional, or physiological stress.

7 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Homeostenosis Exertion requires the body to engage its physiologic reserves. The homeostasis line can be thought of as the state of the heart at rest. Think of the red arrow as representing the physiologic reserve required to carry 20 lbs. up a flight of stairs. You

8 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Consider a Case… A normal 78 year old woman comes in for her regular check-up. She reports feeling fine at rest, and is able to do most of her activities of daily living (ADL) without any problems. Recently, however, she has noticed that when carrying things up stairs in her home she becomes short of breath, and has even had to stop and rest if her load is too heavy. What is causing her shortness of breath? It is normal for the capacity for physical exertion to decline with aging. In the heart, normal aging brings about changes that contribute to this decreased tolerance for exertion.

9 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Homeostenosis in the Aging Heart In other words, a homeostenotic heart is one that has undergone the normal aging process. Compared with a normal young heart, the aged heart has a decreased functional capacity, but is not diseased.

10 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Homeostenosis: Visual Evidence While homeostenosis is a physiologic phenomenon, its anatomic basis can be seen on a gross and histological level. Let’s turn to consider this…

11 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Quick Review: Heart Structure & Blood Flow Inferior Superior

12 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Cardiac Homeostenosis: Changes with Normal Aging 1.Structural 2.Histologic/Cellular 3.Molecular 4.Functional a.  LV wall thickness,  LV chamber size b.Aortic valve calcification c.Mitral annulus calcification

13 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Left Ventricular Structural Changes  left ventricular (LV) wall thickness,  LV chamber size

14 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Valvular Changes Normal aortic valve Leaflet calcification Normal mitral valve Mitral annulus Annulus calcification Insert image Normal Aortic Valve image such as can be viewed via http://www.heart-valve- surgery.com/Images/normal-aortic- valve.jpg Normal aortic valve Insert image Normal Mitral Valve image such as can be viewed via http://dx.doi.org/10.1016/j.carrev.2009. 10.004 Annulus calcification Insert image Annulus Calcification image such as can be viewed via http://www.heart- valve-surgery.com/Images/mitral- valve-calcification.jpg.

15 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Cardiac Homeostenosis: Changes with Normal Aging 1.Structural 2.Histologic/Cellular 3.Molecular 4.Functional a.  # of cardiomyocytes b.(  apoptosis, necrosis) c.  myocyte size (hypertrophy) d.  lipid deposits e.  lipofuscin deposition f.  collagen deposition and fibrosis in myocardium g.Thickening of arterial intima

16 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation  Myocyte #,  Myocyte Size (Hypertrophy) NormalAged Low Power Medium Power Normal Aged High Power Muscle fibers thicken Nuclei of hypertrophic myocytes are larger and darker Note: Clear spaces between the muscle fibers are artifacts due to slide processing and are not present in living tissue, however there is a slight increase in inter-myocyte space in the aged heart.

17 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Collagen deposition/ fibrosis  Lipid Deposits  Lipofuscin Deposition Lipofuscin (black arrows) is a brownish “wear and tear” pigment that accumulates with age. The pigment is a product of lipid oxidation, and is a sign of free radical damage. UMMS CC License Guido Majno

18 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Thickening of Arterial Intima Normal Aged UMMS CC License Guido Majno

19 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Cardiac Homeostenosis: Changes with Normal Aging 1.Structural 2.Histologic/Cellular 3.Molecular 4.Functional a.Altered Ca 2+ handling b.  β -adrenergic responsiveness

20 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Altered Ca 2+ Handling At rest, intracellular Ca 2+ is largely sequestered in the sarcoplasmic reticulum (SR). This is the same in the old and young heart (the figures above are mirror images of one another). Contraction of cardiac muscle depends on the release of Ca 2+ from the SR.

21 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Changes in Ca 2+ Contribute to  Contractility Changes in Ca 2+ channel activity contribute to the prolongation of APs in the aged heart. These changes also decrease the Ca 2+ stored in the SR, which means action potentials trigger a smaller rise in intracellular [Ca 2+ ]. This is important because the force of myocardial contraction is proportional to the amount of Ca 2+ released. Thus, these changes in Ca 2+ handling contribute to the decreased contractility of the aged heart. Normal shown as dashed lines

22 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation  β-adrenergic Responsiveness Isoproterenol is a β- agonist (it stimulates β- receptors), similar to epinephrine (think of an adrenaline rush). Isoproterenol increases calcium release, and thus the force of myocyte contraction. The decline in β –adrenergic responsiveness means that the aged heart gets less of a boost in contractility when stimulated by the sympathetic nervous system compared to the young heart. Normal Aged

23 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Cardiac Homeostenosis: Changes with Normal Aging 1.Structural 2.Histologic/Cellular 3.Molecular 4.Functional a.  Afterload b.Diastolic dysfunction c.Decreased contractility d.  Maximum HR

24 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation This can contribute to LV hypertrophy (LVH). Look for it in lab! Q: What happens when a muscle is forced to work harder for an extended period?  Compliance of larger arteries +  Cross-sectional area of arterioles  Systemic vascular resistance  Afterload means that during systole, the LV must work harder to eject blood into the less compliant aorta.  Afterload

25 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation LV Changes RF = risk factor for heart failure  Afterload  LV wall thickness  LV Stiffness  LV chamber size

26 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation 1.  LV filling in early diastole 2.  Importance of the LA “kick” (atrial systole) late LV filling 1 2  LV stiffness Diastolic dysfunction 2

27 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation  LV stiffness  LV compliance  EDV 65+ How would you expect decreased EDV to affect the aged heart?

28 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Determinants of Stroke Volume Recall Dr. Fahey’s lecture: Any other consequences of a decreased EDV? A smaller EDV means a smaller SV

29 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Frank Starling & PV Curves Parameters represented in the PV curve.  EDV  Preload

30 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation What about contractility? This is in part due to the molecular changes considered earlier: 1.Decreased β –adrenergic responsiveness 2. Impaired Ca 2+ handling  Contractility decreases with age.

31 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Functional Changes So far we have seen that with normal aging, the heart can not augment SV as effectively due to: 1.  Afterload 2.Diastolic dysfunction 3.  Contractility CO = SV x HR Now let’s consider the last part of the equation These changes contribute to the decline in CO max that reduces the exercise tolerance of older adults.

32 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Age-Associated Decline in Exercise Tolerance: Decreased HR max With aging, HR max decreases progressively from age 10 by about 1 bpm per year. HR max = 220 – age Why? So glad you asked! Let’s find out.

33 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation What Determines HR at Rest? Parasympathetic Tone Pacemaker cells of the sino-atrial node (SAN) depolarize spontaneously. In the young heart, the intrinsic heart rate (HR int ) of pacemaker cell depolarization is about 100 bpm. Then why is the average normal resting HR 70 bpm? The SAN is under control of the autonomic nervous system (ANS). At rest, parasympathetic input from the vagas nerve slows the rate of pacemaker cell depolarization from 100 to approximately 70 bpm. SAN Parasympathetic (vagal) input  When parasympathetic input to the SAN is removed, HR increases to HR int HR Cardiac action potential

34 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Resting HR vs. Intrinsic HR Evidence for a decreased intrinsic HR with age When vagal tone is removed from the aged heart, HR may only increase to 80 bpm. This is less than the increase to ~100 bpm seen in the young heart.  HR int decreases with aging. But… The resting HR of the aged heart is the same as that of a young heart: ~60 – 70 bpm. What does this mean?

35 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Resting HR vs. Intrinsic HR In a 20 y.o., HR int is ~100 bpm.  At rest, vagal tone decreases HR by ~30 – 40 bpm. In an 80 y.o., HR int may be ~70 bpm.  The effect of vagal tone is to decrease HR by ~5-10 bpm.  Vagal tone diminishes with aging. This is important because it means the aged heart gets a smaller increase in CO by removing vagal tone than the younger heart.

36 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Maximum HR HR rises above HR int when the SAN is stimulated by the sympathetic nervous system. The decreased HRint, vagal tone, and – adrenergic responsiveness all contribute to the decreased HR max of the aged heart. This may be a more familiar depiction of the same concept.

37 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Back to Our Case… Why is our 75 year old patient becoming short of breath during an activity that she used to be able to do without difficulty? What changes have we considered that might account for her decreased tolerance for exertion?

38 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Summary of Normal Physiological Changes During Exercise

39 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Age-Related Cardiac Changes that Decrease Exercise Tolerance CO = SV x HR Note: Ejection fraction is the clinically measured index of contractility.  Ejection Fraction  Myocardial Contractility  β -adrenergic Responsiveness  LV Filling Altered Myocardial Ca 2+ Handling  Preload  Cardiac Output  Max HR  Systemic Vascular Resistance  Afterload  Stroke Volume  Aortic Compliance  Intrinsic HR  LV Stiffness

40 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Homeostenosis Any exertion requires the body to engage its physiologic reserves. The homeostasis line can be thought of as the state of the heart at rest. Think of the red arrow as representing the physiologic reserve required to carry 20 lbs. up a flight of stairs. So, what is going on with our patient? Normal aging! You

41 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Bibliography Arbab-Zadeh A., et al. (2004). Effect of aging and physical activity on left ventricular compliance. Circulation 110:1799-1805. [American Heart Association © ]. Bluhm, S., Wicking, A., and Benedict, S. (2004). The Heart (image). Biology Guide, The. United Kingdom. Retrieved June 2012, from http://www.biologyguide.net/biol1/5a_heart.htm#A1 (public domain). Bonavitacola, P., Blanchard, G., McGee, S., Johansen, K., Vanguri, V., Cornejo, K., Khan, A., Gurwitz, J. and Pugnaire, M.. Anatomy Image Atlas on Aging: Kidney. POGOe - Portal of Geriatric Online Education. Retrieved September 27, 2012 from http://www.pogoe.org/productid/21017. Cardiovascular Revascularization Medicine, Volume 11, Issue 4, October–December 2010, Pages 249–259 http://dx.doi.org/10.1016/j.carrev.2009.10.004 Carrick-Ranson, G., Hastings, J., Bhella, P., Shibata, S., Fujimoto, N., Palmer, N. D., et al. (2012 (in press)). The effect of healthy aging on left ventricular relaxation and diastolic suction. American Journal of Physiology(In Press). Retrieved September 27, 2012, from http://ajpheart.physiology.org/content/early/2012/05/31/ajpheart.00142.2012.full.pdf. Cheng, S., Xanthakis, V., Sullivan, L., Lieb, W., Massaro, J., Aragaam, J., et al. (2010, August 10). Correlates of echocardiographic indices of cardiac remodeling over the adult life course: Longitudinal observations from the Framingham heart study. Circulation, 570-578. Retrieved September 27, 2012, from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2942081/ (LV graphs). Christou, D. and Seals, D. (2008). Decreased maximal heart rate with aging is related to reduced β-adrenergic responsiveness but is largely explained by a reduction in intrinsic heart rate. J Appl Physiol 105:24-29. Cuenoud, H. (n.d.). Aortic Calcification (image). Cuenoud, H. F. (n.d.). Personal Communication. Department of Health and Human Services. (2010, June 23). Projected Future Growth of Older Population (data). Retrieved June 2012, from Administration on Aging: http://www.aoa.gov/AoARoot/Aging_Statistics/future_growth/docs/By_Age_Total_Population.xls. Elderly #114. (2012, February). Heather's Animations. Retrieved June 2012, from http://www.heathersanimations.com/elderly/114.gif. Fahey, M. (2011, October 19). The heart as a pump: Understanding cardiac mechanics. Retrieved September 27, 2012, from UMMS Blackboard Learning System: RESTRICTED https://learning.umassonline.net/webct.../HeartasPump.pdf. Indoor Cycle Instructor Podcast. (2010, December 30). The Cardio Zone: Heart Rate Training Guide (image). Why we need a standard method to describe heart rate training zones part 1. WishList Member. Retrieved September 27, 2012, from http://www.indoorcycleinstructor.com/wp- content/uploads//2010/12/fat-burning-zone.jpg. Interactive Pathology Laboratory. (n.d.). Heart: Myocardial Hypertrophy. IPLAB.NET The Online Interactive Pathology Laboratory. Retrieved September 27, 2012, from IPLAB.NET: http://peir.path.uab.edu/iplab/messages/598/442.html. Kappagoda, T. and Amsterdam, E. (2012). Exercise and heart failure in the elderly. Heart Failure Reviews, 17(4-5), 635-662. Koeppen, B., and Stanton, B. (Eds.) (2010) Berne and Levy Physiology, 6 th ed. Philadelphia: Mosby Elsevier.

42 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Bibliography Lilly, L. (Ed). (2011). Pathophysiology of Heart Disease, 5 th Ed. Philadelphia: Wolters Kluwer. Lin, J., Lopez, E., Jin, Y., Van Remmen, H., Bauch, T., Han, H., and Lindsey, M. (2008, April). Age-related cardiac muscle sarcopenia: Combining experimental and mathematical modeling to identify mechanisms. Experimental Gerontology, 43(4): 296-306 retrieved September 27, 2012 from http://www.sciencedirect.com/science/article/pii/S0531556507003002 Majno, G. (n.d.). University of Massachusetts Medical School. (virtual microscopy). Mills, S. (2004). Normal mitral valve (image) Histology for Pathologists, 3 rd ed. Philadelphia: Lippincott Williams and Wilkins. Moslehi, J., DePinho, R., Sahin, E. (2012). Telomeres and mitochondria in the aging heart. Circ Res 110:1226-1237. Musclemanheart. (n.d.). Office Clip Art Gallery. Microsoft Corporation. Retrieved September 27, 2012, from http://office.microsoft.com/en- us/images/results.aspx?qu=muscleandex=1#ai:MC900151949|. Old man viewing microscope. (n.d.) Automation for instrumentation [website]. Retrieved 11.22.2011 from http://www.automationforinstrumentation.com/old%20man%20viewing%20microscope.jpg. Oldie 00014. (2012, February). Heather's Animations. Retrieved June 2012, from http://www.heathersanimations.com/elderly/oldie00014.gif. Oxenham H, and Sharpe N. (2003). Cardiovascular aging and heart failure. Euro J Heart Fail 5:427-434. Pick, A. (n.d.). Adam's Heart Valve Surgery Blog: Aortic Valve - Normal Size (image). HeartValveSurgery.com: Patient and Caregiver Resources. Retrieved June 29, 2012, from Adam's Heart Valve Surgery Blog: http://www.heart-valve-surgery.com/heart-surgery-blog/2010/07/02/aortic-valve-size- normal/. Pick, A. (n.d.). Adam's Heart Valve Surgery Blog: Mitral Annulus Structure (image). Retrieved June 9, 2012, from HeartValveSurgery.com: Patient and Caregiver Resources: http://www.heart-valve-surgery.com/heart-surgery-blog/2010/07/02/aortic-valve-size-normal/. Pick, A. (n.d.). Adam's Heart Valve Surgery Blog: mitral valve calcification (image). Retrieved August 17, 2012, from HeartValveSurgery.com Patient and Caregiver Resources: http://www.heart-valve-surgery.com/Images/mitral-valve-calcification.jpg. Rhodes, R., Bell, D. (2009). Medical Physiology: Principles for Clinical Medicine. Philadelphia: Lippincott Williams and Wilkins. Senescence - Medical Definition and More from Merriam-Webster. (2012). Merriam-Webster Online. Springfield, MA. Retrieved June 2012, from http://www.merriam-webster.com/medical/senescence Sport2 new1. (2012, February). Heather's Animations. Retrieved June 2012, from http://www.heathersanimations.com/Sport2/new1.gif. Taffet, G. (2008). Homeostenosis. POGOe - Portal of Geriatric Online Education. Retrieved September 28, 2012 from http://www.pogoe.org/productid/20197. Taffet, G., and Teasdale, T. (2007). Homeostenosis: Trans-sarcolemmal Calcium Flux. Self-Instructional Modules in Geriatric Medicine. Retrieved September 27, 2012, from http://www.ouhsc.edu/geriatricmedicine/Education/Homeostenosis/Homeostenosis.htm#HomeostenosisIndex.htm. Torella, D., et al. (2004). Cardiac stem cell and myocyte aging, heart failure, and insulin-like growth factor-1 overexpression. Circ Res 95:514-524.

43 Advancing Geriatrics Education (AGE): A UMMS initiative funded by the Donald W. Reynolds Foundation Acknowledgements Gary Blanchard, MD Colleen Burnham, MBA* Henri Cuenoud, MD* Michael Fahey, MD Jerry Gurwitz, MD Megan Janes, MS2 Krista Johansen, MD* Mary Ellen Keough, MPH Sarah McGee, MD* Erica Oleson, DO * author


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