The Heart in HypertensionThe Heart in Hypertension
Jamil Mayet
Left Ventricular Hypertrophy- a historical perspective
• Association between renal disease and LVH– Richard Bright 1836
• Hypertrophy of large and small vessels related to LVH in kidney disease– George Johnson 1852
• Vascular changes and LVH without renal disease– Gull and Sutton 1872
• BP measured in life correlated with post-mortem heart weight– Evans 1921
Definition of LVH Healthy cohort of subjects No high BP, diabetes, CV disease, obesity LVH defined as LVMI > mean + 2SD
Framingham Study
LVMI > 131g/m2 males; > 100g/m2 females Cornell, New York
LVMI > 134g/m2 males; > 110g/m2 females
Levy et al. Am J Cardiol 1987;59:956-60. Devereux et al. JACC 1984;4:1222-30.
Risk factors for LVH Blood pressure
Age Gender Race Genetic factors Obesity Physical activity
Pathophysiology of LVH
High BP LV wall stress Wall stress 1/ wall thickness LV wall thickening wall stress Myocyte hypertrophy and collagen matrix Mediators:
Mechanical: preload & afterload Neurohormonal: angiotensin II, sympathetic NS
Clinic versus mean 24 hour systolic BP and LVMI
24 hour mean SBP v. LVMI (r=0.48, p<0.01)
0
50
100
150
200
250
0 100 200 300
LVMI (gm2)2
4 h
our
SB
P (
mm
Hg)
Relationship between mean 24 hour SBP and LVMI
Linear (Relationship between mean 24 hour SBP and LVMI)Linear (Relationship between mean 24 hour SBP and LVMI)Clinic SBP v. LVMI: (r=0.28,
p<0.05)
0
50
100
150
200
250
0 100 200 300LVMI (g/m2)
Clin
ic S
BP
(m
mH
g)
Mayet al et. J Cardiovasc Risk 1995;2:255-61.
Methods of detecting LVH
Clinical examination Chest radiography Electrocardiography Echocardiography (CT, MRI)
Sensitivity and specificity of ECG criteria for LVH
Sensitivity Specificity
Sokolow-Lyon 15-30 73-100
Cornell voltage 7-45 93-100
Romhilt-Estes point score 6-50 85-99
Minnesota code 3-1 3-15 88-99
Framingham criteria 3-17 98-100
Devereux et al 1983, Murphy et al 1985, Levy et al 1990, Lee et al 1992, Devereux et al 1993,Schillaci et al 1994, Crow et al 1995, Norman et al 1995, Chapman et al (in press)
Cardiothoracic ratio and CHD mortality:Whitehall study
Cardiothoracic ratio Hazard ratio for CHD*
<0.4 1.0
0.4-0.439 1.02 (0.61-1.73)
0.44-0.449 1.02 (0.60-1.74)
0.45-0.469 1.33 (0.81-2.20)
0.47- 1.65 (1.01-2.70)
*Adjusted for age, BP, HR, cholesterol, smoking, angina and ECG ischaemia
Hemingway et al. BMJ 1998; 316: 1353-4.
Cardiovascular risk in subjects with ECG-LVH: Framingham
Cardiovascular outcome
Men Women
Coronary heart disease 3.0* 4.6* Stroke 5.8* 6.2* Peripheral arterial disaese 2.7 5.3* Cardiac failure 15.0* 12.8*
Age-adjusted risk-ratio
*P<0.0001 Kannel. Eur Heart J 1992; 13 (suppl D): 82-88
Risks of X-ray and ECG LVH:Framingham
No X-ray enlargement X-ray enlargement
No ECG-LVH 171 253
ECG-LVH 669 1072
Data include men and women, aged 35-94
Age-adjusted biennial rate per 1000
Kannel. Eur Heart J 1992; 13 (suppl D): 82-88
Penn convention for M-mode measurements
Peak of QRS Endocardium excluded from SWT
and PWT Endocardium included in LVID
LV mass = 1.04[(SWT+LVID+PWT)3 - (LVID)3 - 14g
Divide by body surface area to get LV mass index
LV cavity (LVID)
Septum (SWT)
Posterior wall (PWT)
Devereux & Reichek Circulation 1977;55:613-8
ASE guidelines for M-mode measurements
Start of QRS Endocardium included in SWT and
PWT Endocardium excluded from LVID
LVM = 0.8{1.04[ (SWT+LVID+PWT)3 - (LVID)3]} + 0.6 g
Divide by body surface area to get LV mass index
LV cavity (LVID)
Septum (SWT)
Posterior wall (PWT)
Devereux et al. Am J Cardiol 1986;57:450-8
Area-length method for calculation of LV mass
LVmass=1.05[5/6(A1xL1)-5/6(A2xL2)]
Divide by body surface area to get LV mass index
Reichek et al. Circulation 1983;67:348-52
4-year age-adjusted incidence of cardiovascular disease according to LVMI
0
2
4
6
8
10
12
14
16
18
<75 75-94 95-116 117-
Males
Females
LVMI (g/m2)
Ag
e-a
dju
ste
d i n
c id
enc
e/ 1
00 s
ub
ject
s
Redrawn from Levy et al; NEJM 1990; 322: 1561-6.
Incidence of cardiovascular mortality according to presence or absence of LVH
00.5
11.5
22.5
33.5
44.5
5
Men Women
No LVH
LVH
4-y
ea
r ag
e-a
dju
ste
dca
rdio
vasc
ula
r m
ort
ality
P<0.001 P=ns
Redrawn from Levy et al, NEJM 1990; 322: 1561-6.
Risks associated with LVM and geometry
0
10
20
30
40
>125 <125 >125 <125
<0.45
>0.45
LVMI (g/m2) LVMI (g/m2)
RWT
Total mortality* Cardiovascular events†
% p
atie
nts
Koren et al. Ann Int Med 1991; 114: 345-352.*P<0.001, †P=0.03
Regression of LVH by drug treatment:meta-analysis of RCTs
-14
-12
-10
-8
-6
-4
-2
0
Diuretics B-blockers CCB's ACE-I
Schmieder et al. JAMA 1996; 275: 1507-1513
Mea
n %
in
LV
MI
Between treatment P<0.01
Prognostic significance of Echo LVM regression
0
1
2
3
4
5
6
7
All LVH
Regressors Non-regressors
Eve
nts/
100
pat
ient
yea
rs
Verdecchia et al. Circulation 1998; 97: 48-54
*
†
*P=0.04, †P=0.0004 after adjustment for age.
Prognostic significance of ECG voltage
changes: Framingham
0
0.5
1
1.5
2
Decreased voltage Increased voltage
Males FemalesOR
for
CV
eve
nts
(2 y
ears
)
*
*
*P<0.05Levy et al. Circulation 1994; 90: 1786-1793
Age-adjusted risk of congestive heart failure by hypertensive status
0
20
40
60
80
100
Ann
ual i
ncid
ence
/ 10
,000
Women Men
NormotensiveBorderlineHypertensive <140/90
>160/90
Kannel WB.Framingham
The progression from hypertension to congestive heart failure
• 5143 subjects in Framingham study• 392 new cases of clinical CCF after mean
follow up of 20 years • In 91% hypertension antedated CCF• MI present in 52% of hypertensive men and
34% of hypertensive women with CCF• Median survival after CCF diagnosis in ht
1.37 years in men and 2.48 in women
Levy et al. JAMA 1996;275:1557-62
Age-adjusted BP parameters and CHF risk
0
0.5
1
1.5
2
2.5
SBP (mmHg) DBP (mmHg) PP (mmHg)<120 120-
139140-159>159 <70 70-7980-89>89 <54 54-
67>67
Hazard
Ratio
Chae et al. JAMA199;281:634-9
Arterial stiffening in hypertension
• Increased PW velocity with early wave reflection
• Increased central systolic pressure and lower diastolic pressure
• Discrepancy between central and peripheral pressures lessened
• Therefore peripheral BP underestimates central effects
Reducing arterial stiffness as a therapeutic goal
• Later wave reflection reduces peak central pressure which is caused by summation of systolic wave and reflected wave
• In periphery peak pressure is not a summation wave and so there is less of a decrease
• Reducing stiffness causes preferential decrease in central compared with peripheral pressures
Non-pharmacological approaches to reducing arterial stiffness
• Increased arterial stiffness in obese subjects with improvement following weight reduction
• Moderate aerobic exercise increases arterial compliance
• Subjects with high salt intake have better arterial distensibility than those with low intake.
• Improvement following salt restriction
Stiffnessimpact
LVregression
Outcomedata
-blockers ?+ + No
ACE-inhibitors +++ +++ No
-blockers + + Yes
-blockers ‘extra’ ++ ?? No
Ca++ antagonists +++ ++ Yes
thiazides + +/++ Yes +
Relation between vascular and LV impacts of antihypertensives
Diastolic heart failure
• Symptoms/signs of heart failure with normal or mildly impaired LV systolic function
• Prevalence depends on clinical definition of heart failure
• May be up to 30% of cases with heart failure
• Diastolic dysfunction in hypertensives is very common, particularly in those with LVH
Pathophysiology of diastolic dysfunction
• Impaired relaxation– Energy dependent and sensitive to ischaemia
• Coronary artery disease• Microvascular ischaemia (arteriolar rarefaction,
arteriole wall thickening, perivascular fibrosis, endothelial dysfunction, relative myocyte hypertrophy)
• Decreased compliance– Increase in myocardial collagen
Echocardiographic assessment
• 2D echo to assess systolic function
• Doppler echo– Transmitral flow
• E/A wave ratio• E wave deceleration time
– IVRT
Doppler patterns of diastolic dysfunction
• Impaired relaxation– Reduced E/A ratio– Increased EDT– Increased IVRT
• Restriction– LA pressure increases due to myocardial stiffness– High peak E wave velocity– Short EDT– Very short IVRT
Treatment of diastolic heart failure
• Treat underlying cause eg ischaemia
• Impaired relaxation– Theoretically rate-limiting agents effective
• Beta-blockers, verapamil• Reduce HR and prolong diastole• Reduce myocardial oxygen demand• Lower BP and reduce LVH
Treatment of diastolic heart failure
• Restriction– Drugs which reduce fibrosis and lower LA
pressure theoretically should be effective• ACEI• AII blockers• Diuretics
– If LA pressure lowered too much cardiac output significantly worsened
• Can cause significant morbidity
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