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Hypertensive heart disease encompasses anatomical changes and altered physiology of heart
muscle, coronary arteries, and great vessels. Left
ventricular hypertrophy is not only a target organ
response to increased afterload, but is also the
most potent cardiovascular risk factor. Regression
of hypertrophy reduces morbidity and mortality.
Heart failure may be present in the absence of a
reduction of myocardial contractility. Ischemic
heart disease occurs in the absence of epicardial
coronary disease. Left atrial size and atrial fibrillation are associated. Potentially lethal ventricular
arrhythmias and sudden cardiac death are more
common in hypertensive patients. The relationship of aortic root size to blood pressure is weaker than expected; however, the relationship to
aortic dissection is stronger. Careful attention and
treatment of left ventricular hypertrophy, heart
failure, ischemic heart disease, and atrial fibrillation will improve survival. (J Clin Hypertens.
2005:7;231238) 2005 Le Jacq Ltd.
www.lejacq.com
ID: 4119
231
The Journal of Clinical Hypertension (ISSN 1524-6175) is published monthly by Le Jacq Ltd., Three Parklands Drive, Darien, CT 06820-3652. Copyright 2005 by Le Jacq Ltd., All rights reserved. No part of this publication may be
reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publishers. The opinions
and ideas expressed in this publication are those of the authors and do not necessarily reflect those of the Editors or Publisher. For copies in excess of 25 or for commercial purposes, please contact Sarah Howell at
showell@lejacq.com or 203.656.1711 x106.
LV wall stress
Concentric LVH
Oxygen demand
Myocardial
Infarction
Fibrosis
Systolic
heart failure
Obstructive epicardial
coronary artery disease
Ventricular
ectopy
Sudden
death
Nonhemodynamic
factors
Diastolic filling
LVEDP
Atrial
fibrillation
Diastolic
heart failure
Clinical Findings
Most patients are asymptomatic with LVH.
However, dyspnea, angina, HF, syncope, and sudden death can occur. The classic physical findings
include an abnormal apical impulse and the S4 gallop. Normally, in the supine position: 1) the apical
impulse is within the midclavicular line in the forth
or fifth LV intercostal space, 2) the amplitude is
small and brief in duration, and 3) the palpable
area is less than 2.5 cm2. A sustained, enlarged
(>3 cm diameter) apical impulse, which may be
displaced outside the midclavicular line, is characteristic of isolated LVH. Using ultrafast computed
tomographic cardiac measurements, the physical
examination findings of a percussion distance
greater than 10.5 cm in the sixth left intercostal
space to detect an abnormal posterior wall thickness was 100% sensitive and 50.5% specific and
an apical impulse greater than 3 cm to detect an
increased left ventricular mass (LVM) was 100%
sensitive and 40% specific.
An S4 gallop, best heard with the bell of the
stethoscope in the left lateral decubitus position,
is common in chronic hypertension. It reflects the
decreased elasticity of a hypertrophied ventricle during the late filling of the ventricle following the atrial
contraction. Occasionally, it may be palpable.
Diagnosis
The two most common tools used to define LVH are
the electrocardiogram (ECG) and the echocardiogram. Each has prognostic significance, but provides
different data. Echocardiography supplies precise
information about LV wall thickness, left atrial size,
LV function, and wall-motion abnormalities. The
ECG provides unique information on rhythm disturbances, hyperkalemia, PR interval, and QT interval
that suggest a diagnosis or alteration of treatment.
ELECTROCARDIOGRAM
The ECG is often used as an inexpensive, initial
screening tool to assess target organ damage in
a hypertensive patient. It can be used to assess
VOL. 7 NO. 4 APRIL 2005
The Journal of Clinical Hypertension (ISSN 1524-6175) is published monthly by Le Jacq Ltd., Three Parklands Drive, Darien, CT 06820-3652. Copyright 2005 by Le Jacq Ltd., All rights reserved. No part of this publication may be
reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publishers. The opinions
and ideas expressed in this publication are those of the authors and do not necessarily reflect those of the Editors or Publisher. For copies in excess of 25 or for commercial purposes, please contact Sarah Howell at
showell@lejacq.com or 203.656.1711 x106.
Figure 4. The strain pattern with left ventricular hypertrophy conveys increased risk beyond an increased left
ventricular voltage.
233
The Journal of Clinical Hypertension (ISSN 1524-6175) is published monthly by Le Jacq Ltd., Three Parklands Drive, Darien, CT 06820-3652. Copyright 2005 by Le Jacq Ltd., All rights reserved. No part of this publication may be
reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publishers. The opinions
and ideas expressed in this publication are those of the authors and do not necessarily reflect those of the Editors or Publisher. For copies in excess of 25 or for commercial purposes, please contact Sarah Howell at
showell@lejacq.com or 203.656.1711 x106.
300
234
250
200
164
138
150
79
100
50
35
71
27
99
83
52
29
CHF
CVA
71
23
20
0
CVD
CHD
CVD
CHD
CHF
CVA
HEART FAILURE
The incidence of HF is increasing. This seems
somewhat paradoxical given the decline in ischemic heart disease and cerebrovascular events.
However, the aging of the US population is contributing to the increased incidence and prevalence
of HF. Hypertension and ischemic heart disease
are the major factors that result in HF (Figure 2).
LVH also contributes to the development of HF
(Figure 5). Hypertension is antecedent in 75% of
cases of HF. HF can be secondary to hyperthyroidism, hypothyroidism, renovascular hypertension,
and chronic kidney disease.
Diastolic dysfunction can be present in both
systolic (low EF) and diastolic (preserved EF) HF.
Preserved EF HF is associated with impaired quality of life and increased all-cause mortality (Figure
9). Diastolic dysfunction be due to an abnormality
of LV 1) distensibility, 2) filling, or 3) relaxation.
Excess risk/1000
Men
175
150
125
100
75
50
25
0
Women
129
19
36
7
Cholesterol
42
117
47
21
Hypertension
19
Diabetes
ECG LVH
Cigarette smoking
Figure 6. 36-Year follow-up Framingham Study in subjects 3564 years of age. Electrocardiographic left ventricular
hypertrophy (ECG LVH) is the most potent of traditional cardiovascular risk factors. Data derived from J Hypertens.
1991;9(suppl 2):S3S9.2
234
The Journal of Clinical Hypertension (ISSN 1524-6175) is published monthly by Le Jacq Ltd., Three Parklands Drive, Darien, CT 06820-3652. Copyright 2005 by Le Jacq Ltd., All rights reserved. No part of this publication may be
reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publishers. The opinions
and ideas expressed in this publication are those of the authors and do not necessarily reflect those of the Editors or Publisher. For copies in excess of 25 or for commercial purposes, please contact Sarah Howell at
showell@lejacq.com or 203.656.1711 x106.
None
350
Age-adjusted biennial rate/1000
Voltage
Voltage + ST-T
302
300
250
205
176
200
112
111
100
50
149
142
150
31
54
74
47 54
0
3564 yr
6594 yr
3564 yr
6594 yr
235
The Journal of Clinical Hypertension (ISSN 1524-6175) is published monthly by Le Jacq Ltd., Three Parklands Drive, Darien, CT 06820-3652. Copyright 2005 by Le Jacq Ltd., All rights reserved. No part of this publication may be
reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publishers. The opinions
and ideas expressed in this publication are those of the authors and do not necessarily reflect those of the Editors or Publisher. For copies in excess of 25 or for commercial purposes, please contact Sarah Howell at
showell@lejacq.com or 203.656.1711 x106.
200.0
No heart failure
150.0
Heart failure
154.1
115.4
88.7
87.0
100.0
51.0
50.0
0.0
25.1
0.55
0.450.54
<0.45
Ejection fraction
Figure 9. All-cause mortality in elderly patients without and with symptoms of heart failure. According to left ventricular ejection fraction, patients
with symptoms of preserved ejection fraction (>0.55) and symptoms of heart failure experience a similar event rate as asymptomatic patients with
a depressed ejection fraction (<0.45). Data derived from Gottdiener JS, McClelland RL, Marshall R, et al. Outcome of congestive heart failure in
elderly persons: influence of left ventricular systolic function. The Cardiovascular Health Study. Ann Intern Med. 2002;137(8):631639.
236
The Journal of Clinical Hypertension (ISSN 1524-6175) is published monthly by Le Jacq Ltd., Three Parklands Drive, Darien, CT 06820-3652. Copyright 2005 by Le Jacq Ltd., All rights reserved. No part of this publication may be
reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publishers. The opinions
and ideas expressed in this publication are those of the authors and do not necessarily reflect those of the Editors or Publisher. For copies in excess of 25 or for commercial purposes, please contact Sarah Howell at
showell@lejacq.com or 203.656.1711 x106.
Men
Women
4
3
2
1
0
Cigarettes
Diabetes
ECG LVH
Hypertension
BMI
Alcohol
Risk factors
Figure 11. Risk factors for the development of atrial fibrillation: 38-year follow-up of the Framingham Study.
Hypertension, electrocardiographic left ventricular hypertrophy, and diabetes were predictors for the development of
atrial fibrillation; in contrast, body mass index, alcohol, and cigarettes in men were not.
ECG LVH=electrocardiographic left ventricular hypertrophy; BMI=body mass index. Data derived from Kannel WB,
Wolf PA, Benjamin EJ, et al. Prevalence, incidence, prognosis, and predisposing conditions for atrial fibrillation: population-based estimates. Am J Cardiol. 1998;82:2N9N.
patients with stable CAD using verapamil-sustained release or atenolol as initial therapy to
control BP utilizing a prospective, open-label,
blinded end point design. Trandolapril and hydrochlorothiazide could be added to each group to
achieve the target BP. There was no difference
between the treatment approaches in achieving
the composite end point of death, MI, or stroke.
There were more new cases of diabetes mellitus in
the atenolol group.
ARRHYTHMIAS
Hypertensive patients are more likely have both
atrial and ventricular arrhythmias. Both hypertension and ECG LVH are potent risk factors for the
development of AF (Figure 11). Systolic BP and
pulse pressure are associated increased left atrial
size. The echocardiographic findings of left atrial
enlargement, LVH, and reduced EF are predictors of AF. Cardiac conditions predisposing to
AF include HF, MI, and valve disease. Given the
potential embolic risk for cerebrovascular events,
prompt identification and treatment is mandatory.
Even without LVH, ventricular arrhythmias
are more common in hypertensive compared with
normotensive patients. If LVH is present, then
ventricular ectopy, ventricular tachycardia, and
sudden cardiac death occur more frequently.
AORTA
Hypertension is a known predictor of proximal
aortic dissection. The LIFE Study reported that
aortic root dilatation in hypertensive patients
237
The Journal of Clinical Hypertension (ISSN 1524-6175) is published monthly by Le Jacq Ltd., Three Parklands Drive, Darien, CT 06820-3652. Copyright 2005 by Le Jacq Ltd., All rights reserved. No part of this publication may be
reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publishers. The opinions
and ideas expressed in this publication are those of the authors and do not necessarily reflect those of the Editors or Publisher. For copies in excess of 25 or for commercial purposes, please contact Sarah Howell at
showell@lejacq.com or 203.656.1711 x106.
SUGGESTED READING
Prisant LM, Frank MJ, Carr AA, et al. How can we
diagnose coronary heart disease in hypertensive patients?
Hypertension. 1987;10:467472.
Kannel WB. Left ventricular hypertrophy as a risk factor:
the Framingham experience. J Hypertens Suppl. 1991;9:
S3S8; discussion S8S9.
Frohlich ED, Apstein C, Chobanian AV, et al. The heart in
hypertension. N Engl J Med. 1992;327:9981008.
Prisant LM, Houghton JL, Bottini PB, et al. Hypertensive
heart disease. How does blood pressure affect left ventricular mass? Postgrad Med. 1994;95:5962, 6676.
Frohlich ED. State of the art lecture. Risk mechanisms in
hypertensive heart disease. Hypertension. 1999;34:782789.
238
The Journal of Clinical Hypertension (ISSN 1524-6175) is published monthly by Le Jacq Ltd., Three Parklands Drive, Darien, CT 06820-3652. Copyright 2005 by Le Jacq Ltd., All rights reserved. No part of this publication may be
reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publishers. The opinions
and ideas expressed in this publication are those of the authors and do not necessarily reflect those of the Editors or Publisher. For copies in excess of 25 or for commercial purposes, please contact Sarah Howell at
showell@lejacq.com or 203.656.1711 x106.