EFFECTS OF AGING ON THE

CARDIOVASCULAR SYSTEM.
CONGESTIVE HEART FAILURE
 Heart Failure
• Results from any structural or functional
abnormality that impairs the ability of the
ventricle to eject blood (Systolic Heart Failure)
or to fill with blood (Diastolic Heart Failure).
The Vicious Cycle of Congestive Heart
Failure

LV Dysfunction causes Decreased Blood Pressure and

Decreased cardiac output Decreased Renal perfusion

Stimulates the Release

of renin, Which allows
conversion of
Angiotensin
to Angiotensin II.
Angiotensin II stimulates
Aldosterone secretion which
causes retention of
Na+ and Water,
increasing filling pressure
 Types of Heart Failure
• Low-Output Heart Failure
– Systolic Heart Failure:
– decreased cardiac output
– Decreased Left ventricular ejection fraction
– Diastolic Heart Failure:
– Elevated Left and Right ventricular end-diastolic pressures
– May have normal LVEF
• High-Output Heart Failure
– Seen with peripheral shunting, low-systemic vascular resistance, hyperthryoidism,
beri-beri, carcinoid, anemia
– Often have normal cardiac output
• Right-Ventricular Failure
– Seen with pulmonary hypertension, large RV infarctions.
 Causes of Low-Output Heart Failure

• Systolic Dysfunction
• Coronary Artery Disease
• Idiopathic dilated cardiomyopathy (DCM)
» 50% idiopathic (at least 25% familial)
» 9 % mycoarditis (viral)
» Ischemic heart disease, perpartum, hypertension, HIV, connective tissue
disease, substance abuse, doxorubicin
• Hypertension
• Valvular Heart Disease
• Diastolic Dysfunction
• Hypertension
• Coronary artery disease
• Hypertrophic obstructive cardiomyopathy (HCM)
• Restrictive cardiomyopathy
 Clinical Presentation of Heart Failure

• Due to excess fluid accumulation:

– Dyspnea (most sensitive symptom)
– Edema
– Hepatic congestion
– Ascites
– Orthopnea, Paroxysmal Nocturnal Dyspnea (PND)
• Due to reduction in cardiac ouput:
– Fatigue (especially with exertion(
– Weakness
 Physical Examination in Heart Failure
• S3 gallop
– Low sensitivity, but highly specific
• Cool, pale, cyanotic extremities
– Have sinus tachycardia, diaphoresis and peripheral vasoconstriction
• Crackles or decreased breath sounds at bases (effusions) on lung exam
• Elevated jugular venous pressure
• Lower extremity edema
• Ascites
• Hepatomegaly
• Splenomegaly
• Displaced PMI
• Apical impulse that is laterally displaced past the midclavicular line is usually indicative of
left ventricular enlargement>
Measuring Jugular Venous Pressure
 Lab Analysis in Heart Failure
• CBC
– Since anemia can exacerbate heart failure
• Serum electrolytes and creatinine
– before starting high dose diuretics
• Fasting Blood glucose
– To evaluate for possible diabetes mellitus
• Thyroid function tests
– Since thyrotoxicosis can result in A. Fib,
and hypothyroidism can results in HF.
• Iron studies
– To screen for hereditary hemochromatosis as cause of heart failure.
• ANA
– To evaluate for possible lupus
• Viral studies
– If viral mycocarditis suspected
 Chest X-ray in Heart Failure
• Cardiomegaly
• Cephalization of the pulmonary vessels
• Kerley B-lines
• Pleural effusions
Cardiomegaly
Pulmonary vessel congestion
Kerley B lines
 Cardiac Testing in Heart Failure

• Electrocardiogram:
– May show specific cause of heart failure:
– Ischemic heart disease
– Dilated cardiomyopathy: first degree AV block, LBBB, Left
anterior fascicular block
– Amyloidosis: pseudo-infarction pattern
– Idiopathic dilated cardiomyopathy: LVH
• Echocardiogram:
– Left ventricular ejection fraction
– Structural/valvular abnormalities
EFFECTS OF AGING ON THE
CARDIOVASCULAR SYSTEM
 Hospital Mortality for
Cardiovascular Causes

Total deaths
(in thousands) Age > 65
Acute MI 78 68 (87.2%)
Arrhythmias 17 12 (70.6%)
Heart failure 42 37 (88.1%)
Cerebrovascular disease 65 49 (75.4%)

Source: National Hospital Discharge Survey, 1998.

EFFECTS OF AGING ON THE
CARDIOVASCULAR SYSTEM
 Principal Effects of Aging on
Cardiovascular Structure and Function

• Increased vascular + myocardial

stiffness
• Decreased -adrenergic and
baroreceptor responsiveness
• Impaired sinus node function
• Impaired endothelial function

Net effect - Large reduction in CV reserve

 CV Changes: Max Exercise - Ages 20
and 80 Years
Oxygen consumption Reduced ~ 50%
AV oxygen difference Reduced ~ 25%
Cardiac output Reduced ~ 25%
Heart rate Reduced ~ 25%
LV stroke volume Reduced ~ 15% to 25%
LV end diastolic volume No change or small
decrease
LV end systolic volume Increased ~ 150%
LV ejection fraction Reduced ~ 15%
 Conduction System
 Increased elastic tissue, collagen and fat,
especially in the SA node with marked reduction
in SA node pacemaker cells
 Calcification of cardiac skeleton
 Slowed conduction throughout the heart
 Hypertension, CAD, and amyloid infiltration
amplify conduction abnormalities
 Arrhythmias
• Marked increase in frequency of supra-
ventricular and ventricular ectopic beats
• Short runs of SVT occur in 1/3 of healthy
older subjects on Holter studies
• Ventricular couplets occur in ~11% and
short runs of ventricular tachycardia
occur in ~4% of normal persons > 60 yr
• In the absence of heart disease, none of
these arrhythmias are associated with an
adverse prognosis
Source: Am J Cardiol 1992:70:748-51
 Prevalence of Nonsustained SVT
during Maximal Exercise

                                                                                    

Source: Am J Cardiol 1995;75:788-92

Prevalence of AHSD by Age and Sex in the U.S.
from 1988-94
20%
18%
Percent of Population

16%
14%
12% Male
10% Female
8%
6%
4%
2%
0%
25-44 45-54 55-64 65-74 75+
Age, years
Source: National Health and Nutrition Examination Survey
 Clinical Implications
• Increased systolic BP and pulse pressure
• Increased prevalence of atrial fibrillation,
heart failure, especially heart failure with
preserved LV function
• Increased prevalence of bradyarrhythmias
and “sick sinus syndrome”
• Worse prognosis associated with all CV
diseases
 Disease Presentation
• Atypical symptomatology
- Chest pain less frequent
- Exertional dyspnea or fatigue common
- ‘Gastrointestinal’ symptoms common
- Confusion, dizziness, other CNS sx’s
• Non-diagnostic ECG due to IVCD, LVH,
paced rhythm, electrolyte abnormalities
 GUSTO The Age-Intracranial Hemorrhage
V
Interaction
6

4
HIGHER RISK
3

LOWER RISK

0
30 40 50 60 70 80 90
Years
Source: Am Heart J 2001:142:37-42
Efficacy of Aspirin by Age: ISIS-2
Vascular Mortality at 35 Days

25%

20%

15% Placebo
Aspirin
10%

5%

0%
< 60 60-69 70+
Age, years
Source: Lancet 1988;II-349-60
 Long-term Benefits of Aspirin
25%
P < 0.00001
20%
Vascular Events

P < 0.00001
15% Aspirin
10% Control

5%
0%
< 65 65+
Age, years
Source: BMJ 1994;308:81-106
Clopidogrel in Non-ST-Elevation Acute Coronary
Syndromes: CURE

Age, Relative Lives

years Placebo Clopidogrel Risk* Saved/ 1000
< 65 7.6% 5.4% 0.71 22

> 65 15.3% 13.3% 0.87 20

*Primary endpoint: CV death, nonfatal MI or CVA

Source: N Engl J Med 2001;345:494-502

Management of Diabetes in the Older Person

Management of Diabetes in the Older

Person
Management of Diabetes in the Older Person
 Hypoglycaemia in type 2 DM

• Risk of hypo increases with increasing insulin deficiency and

duration of insulin treatment
• Regardless of treatment modality, intensive therapy associated
with increased risks of hypo
• Older patients are at increased hypo risk as a result of
diminished symptoms and altered thresholds for
counterregulatory responses
• Knowledge of hypoglycaemia is poor in the elderly and their
relatives
 Cognitive decline and
dementia

Frailty

Renal dysfunction
Increased mortality

Institutionalisatio

T2DM Old Age Hypoglycaemia

Decreased
symptoms
Tight glycaemic
Impaired counter control
regulation

Polypharmacy Decreased
microvascular
complications.
Mobility limitation and decline Falls No effect on
in physical function Fractures
macrovascular
complications.
 T2DM therapies

Targets insulin resistance Targets insulin deficiency

Diet and lifestyle Insulin secretagogues

Metformin Insulin

Glitazones (TZDs)

DPP-IV inhibitors

GLP-1 analogues

SGLT2 inhibitors: mode of action independent of beta cells

 T2DM therapies
• Pioglitazone:
– No hypos
– Wt gain, oedema, osteoporosis, ? Bladder cancer
• DPP-IV:
– No hypos, weight neutral
– Not very potent. Reduce in renal impairment
• GLP-1:
– No hypos, weight loss
– GI side effects, ? Pancreatitis, care in renal impairment, injections (but weekly
formulation available)
• SGLT2:
– No hypos, weight loss, BP,  CV death (empagliflozin)
– Need normal renal function. Not recommended in elderly
 Guidelines on glycaemic targets in older pts

European Diabetes Working Party for Older People

Clinical guidelines elderly T2DM