Cardiovascular Aging

1
Cardiovascular Aging

• Dorothy D. Sherwood, M.D.
• Health Core Physician Group
• Presbyterian Hospital of Dallas
• Division of Geriatrics
• July 26th, 2006

2
Epidemiology

• Currently, 12 of the population is gt65 years of
  age 35 million people.
• In 2030, 20 of the population will be gt65 years
  of age 71 million people one in five.
• Half of the people gt 65 years of age have after
  tax incomes at the poverty level.

3
Epidemiology

• Cardiovascular disease is the leading cause of
  death in the population gt65 years.
• One half to two thirds of the population gt 65
  years have hypertension.
• The leading discharge diagnosis forgt 65 years is
  congestive heart failure.

4
Epidemiology

• Compelling data indicates that aggressive
  treatment of hypertension, heart failure,
  coronary artery disease, and hyperlipidemia in
  those between the ages of 65 and 74 reduces
  morbidity and mortality.
• Few trials have enrolled those over 75 or those
  with co-morbid conditions.

5
Pathophysiology

• Hallmarks of cardiovascular aging include
• Increase in systolic blood pressure
• Increase in pulse pressure and pulse wave
  velocity (PWV)
• Increase in left ventricular mass
• Increase in CAD
• Increase in Atrial fibrillation

6
Pathophysiology

• Aging is associated with a
• Decrease in early left ventricular diastolic
  filling.
• Decrease in maximal heart rate
• Decrease in maximal cardiac output
• Decrease in maximal aerobic capacity
• Decreased exercise induced augmentation of LVEF
  and heart rate
• Decreased vasodilatation in response to beta
  adrenergic stimulation or endothelial mediated
  vasodilatation.

7
Pathophysiology

• Cellular, enzymatic, and molecular alterations in
  the arterial vessel
• Smooth muscle cells (SMC) migrate to the intima,
  causing intimal thickening.
• Metalloproteinases, angiotensin II, transforming
  growth factor beta, intracellular cell adhesion
  molecules, result in increased production of
  collagen, collagen cross linking, fibronectin,
  calcification, in the media with decrease in
  elastin in the media leading to stiff vessel.
• Reduced endothelial function due to apoptosis and
  senescence results in decreased NO
• Decreased vasodilatory response to beta
  adrenergic agonists and alpha adrenergic
  antagonist

8
Pathophysiology

• This results in arterial dilation with increased
  arterial stiffness and decreased NO induced
  vasodilatation.

9
Pathophysiology

• Cellular, enzymatic, and molecular alterations in
  the Heart
• Similar to those in the arterial wall with
  similar enzymatic changes resulting in increased
  collagen cross linking, increased fibronectin,
  decrease in elastin
• In the atria, decrease in sinus node cells, and
  alterations in the extracellular matrix results
  in sinus node dysfunction leading to atrial
  fibrillation similar changes occur in the AV
  node.

10
Pathophysiology

• Reduced, but hypertrophied myocytes result in
  alteration in calcium channels, leading to
• Prolongation of contraction and relaxation of the
  myocardium with aging.

11
Pathophysiology

• Changes in the intravascular environment with
  age
• Increase in prothrombotic factors s such as V,
  VIII, IX, plasminogen, resulting in impaired
  fibrinolyisis
• Increased pro-thrombotic cytokines especially
  interleukin 6
• All of these potentiate the development of
  atherosclerosis

12
Pathophysiology

• Autonomic nervous system
• Decreased number of alpha and beta adrenergic
  cells and decreased function of the cells with
  aging.
• Decreased dopaminergic responsiveness with aging
• Decreased vascular response to cholinergics, but
  increased central nervous system response

13
Pathophysiology

• The combined effect of the changes in the
  autonomic nervous system results in a decreased
  baroreceptor response in the elderly and
  decreased ability to respond to stress.

14
Pathophysiology

• We can impact some of the age related changes
• Exercise increases endothelial function
• Exercise decreases arterial wall stiffness
• ACEI, ARB, Aldosterone inhibitors, Beta blockers
  may influence remodeling of the vessels and the
  myocardium.

15
Pharmacodynamic effects of aging

• Suffice it to say, that elderly are highly
  sensitive to
• The therapeutic effects of a drug i.e. a direct
  vasodilator such a prazocin the rate effects of
  beta blockers
• The toxic effects of the drug i.e. digoxin
  toxicity occurs at a much lower dose in the
  elderly
• The drug-drug interactions ACEI and NSAID for
  example

16
Pharmacodynamic effects of aging

• Elderly patients can not take a joke!
• Look up every drug before you give it
• If renally cleared adjust the dose i.e. beta
  blockers are renally cleared.
• Know the drug-drug interactions
• Know the complications
• Start low go slow, and re-address need for drug
  at every visit.

17
Hypertension

• Measure BP in both arms, supine, sitting, and
  standing.
• Elderly patients are very susceptible to
  orthostatic hypotension.
• The risk of hypertension is greater in the
  elderly, at least up to age 80, than in the
  younger population, and the reduction in CAD and
  heart failure is greater in the elderly with
  treatment than in the young.

18
Hypertension

• Limited data from placebo controlled trials
  reveals a decrease in strokes and heart failure
  in patients over the age of 80 with treated
  hypertension, but no difference in mortality.

19
Multiple trials demonstrating benefit of
treatment of hypertension in the elderly
20
Hypertension

• Thiazides are as effective as any other drug for
  first line treatment.
• Risk of hyponatremia
• Risk of incontinence
• Risk of hypokalemia
• Never go above 25 mg, start at 6.25 mg

21
Hypertension

• To evaluate the best second line therapy for each
  patient, take into account their co-morbid
  conditions, and the drug-drug interactions that
  will occur. Use www.geriatricsatyourfingertips.c
  om.
• Or JNC 7 to determine the best choice

22
Hypertension

• Postural Hypotension a fall of 20 mm Hg with
  standing is associated with a marked increase in
  falls.
• Increases the risk associated with
  anti-depressants, anti-psychotics, and
  anti-parkinsonian medications
• Increases the risk associated with post-prandiol
  hypotension
• Greatest fall in BP is 1 hour after eating,
  returning to normal 3 to 4 hours after eating

23
CAD

• Autopsy studies show that gt 50 of the men over
  the age of 60 have significant CAD with increase
  in the incidence of multi-vessel disease and left
  main disease
• The life time risk for developing CAD is
  estimated to be 1 in 3 for men and 1 in 4 for
  women

24
CAD

• By the age of 80, 20 to 30 of men and women have
  symptomatic CAD.
• History is atypical epigastric discomfort
  shoulder pain back pain SOB nausea or no
  symptoms at all
• Symptoms not necessarily related to exertion.

25
CAD

• Testing
• Exercise stress testing has about an 80
  sensitivity and 75 specificity
• The addition of an echocardiogram or nuclear
  study improves the validity of the test
• In men and women who can not exercise, dobutamine
  or adenosine can be used.
• Due to high levels of calcification in the
  arteries, CT may not be useful in the elderly.

26
CAD

• Treatment the same as the younger population,
  unless there is less than a 2 year life
  expectancy.
• Heart Protection Study showed benefit in patients
  with disease treated with statins
• There is no data regarding statins and primary
  prevention in patients over the age of 75

27
CAD

• Age is a risk factor for myopathy with statin
  therapy. Therefore, the lowest effective dose
  should be used in this population.
• Beta blockers, ACEI, and long-acting nitrates
  should be used.
• Avoid Beta blockers in SA or AV nodal disease
• Avoid Calcium Channel Blockers

28
CAD

• Revascularization
• BARI study 109 patients ages 65 to 83.
• CABG vs. PTCA
• CABG associated with increased early mortality
  and morbidity, but less angina and less repeat
  procedures
• Stroke was more common after CABG and heart
  failure after PTCA
• 5 year survival was 86 for CABG and 81 for
  PTCA
• In hospital mortality for CABG in patients over
  75 is 6 to 8 and stroke is 3 to 6

29
CAD

• TIME trial compared re-vasularization to optimal
  medical therapy. At 6 months, revascularization
  was favored, but a 1 year there was no difference
  in outcomes
• Data is limited in the use of drug eluting stents
  and off pump bypass.

30
CAD

• Treatment of acute MI in the elderly with
  thrombolysis or primary angioplasty is associated
  with better outcomes, but also, with increased
  risk of complications including hemorrhage and
  stroke.
• Thin, black, female, prior cva, Bp gt160
  associated with increased risk of ICH

31
CAD

• Post MI treatment
• Beta Blockers, ACEI, ASA, Statins all have been
  shown to be of benefit in the elderly.
• Start with lower doses and titrate carefully

32
CHF

• Five year mortality is 50 for patients with
  systolic impairment and 25 for patients with
  diastolic HF
• There is a 4 fold increase in mortality in
  patients with diastolic dysfunction compared to
  those without HF.
• Age is associated with HF with preserved systolic
  function

33
CHF

• Exercise intolerance is the mark of heart failure
• Nocturnal cough, PND, DOE are common signs of
  heart failure, but may not be recognized
• Less than 50 of patients with moderate diastolic
  HF by doppler had the diagnosis of Hf

34
CHF

• Physical exam in the elderly is not easy they
  all have edema their neck veins are always
  distended or appear to be S3 and rales are only
  present when decompensated.
• One must rely on ECHO and BNP to diagnose heart
  failure at times.

35
CHF

• Treatment
• Not good data in the elderly most CHF studies
  are with patients with systolic dysfunction.
  Women and the frail elderly are not included at
  all.

36
CHF

• Treatment of Systolic Failure
• Control BP
• Diurese
• Control heart rate if in A fib.
• ACEI or ARB gently
• Beta blocker gently
• Exercise

37
CHF

• Diastolic Dysfunction
• Diuretics
• ACEI or ARB gently
• Beta blockers gently
• Exercise

38
Arrhythmia

• Up to 90 of the sinus node cells are lost by
  the age of 75!
• Resting heart rate is not effected by age, but
  maximal heart rate and beat to beat variability
  are both reduced.
• SN response to beta adrenergic and
  parasympathetic stimulation is reduced.

39
Arrhythmia

• EKG shows prolonged PR and LAD
• Arrhythmias requiring treatment
• Bradycardia due to SA or AV nodal dysfunction
• A Fib 8 to 10 of 80 year olds have A fib.
• 50 of patients with A fib are gt 75 years old

40
Arrhythmia

• A fib
• Focus should be on anticoagulation for stroke
  prevention and rate control. Rarely is rhythm
  control needed or possible.
• Warfarin INR 2 to 2.5
• Dont forget associated with osteoporosis
• ASA 325 mg in very elderly or very debilitated.

41
Summary

• CV aging is associated with
• Decreased arterial compliance
• Decreased cardiac compliance
• Decreased maximal heart rate and EF with
  exercise/stress
• Decreased adrenergic sensitivity
• Increased systolic hypertension
• Increased LV mass
• Increased CAD
• Increased arrhythmias

42
Summary

• Treatment
• Encourage Exercise and
• Monitor orthostatic BP.
• Start low, go slow.
• Avoid vasodilators if possible.
• May have increased sensitivity to bradycardia
  from beta blockers, calcium channel blockers.
• Watch for drug/drug interactions.
• Monitor frequently, be careful.