Hypertensive Heart Disease: Hypertension Curriculum Review

Hyper tension
Cur r i c u l u m
R e v i e w
Donald G. Vidt, MD, Section Editor
Hypertensive Heart Disease

L. Michael Prisant, MD
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.
ypertensive heart disease is the target organ

response of systemic arterial hypertension.
However, it is more than left ventricular hypertrophy (LVH) or heart failure (HF). It also includes
ischemic heart disease, aortic root disease, left
atrial enlargement, and arrhythmias.
From the Medical College of Georgia, Augusta, GA
Address for correspondence:
L. Michael Prisant, MD, 1120 15th Street, HB-2010,
Medical College of Georgia, Augusta, GA 30912
E-mail: mprisant@mail.mcg.edu
www.lejacq.com
VOL. 7 NO. 4 APRIL 2005
ID: 4119
LEFT VENTRICULAR HYPERTROPHY

Pathophysiology
An increase in peripheral vascular resistance, the
hallmark of established hypertension, alters wall
stress in the left ventricle (Figure 1). Concentric
LVH is the consequence of the neutralization of
wall stress associated with increased impedance to
ventricular emptying. The increase in wall thickness follows the law of Laplace (Figure 1). Wall
stress stimulates sarcomeres to proliferate in parallel by increasing protein synthesis, which increases
myocyte width. The net effect is an increase in the
wall thickness/chamber dimension or relative wall
thickness. However, when hypertrophy can no longer compensate for the increased afterload, then
LV dilatation (eccentric hypertrophy) occurs and
LV performance decreases (Figure 2).
Ambulatory blood pressure (BP) correlates better with LVH than BP measured at a single visit or
multiple office visits. However, a single ambulatory BP cannot assess the total impact of BP over
months or years. However, despite the lack of long
durations of assessment of BP, other nonhemodynamic variables (Figure 2), including body mass
index, age, physical activity, sodium, parathyroid
hormone, growth hormone, thyroid hormone, thyroid-stimulating hormone, norepinephrine, renin,
aldosterone, angiotensin II, intracellular calcium,
atrial natriuretic peptide, blood viscosity, and
arterial compliance correlate with LVH. In addition, other factors, such as obesity, can modify the
hearts response to pressure overload.
Consequences
As the ventricle becomes thicker, the elasticity
diminishes. Thus, filling during diastole becomes
more difficult and depends on atrial systole. As
a consequence, LV end-diastolic pressure and left
THE JOURNAL OF CLINICAL HYPERTENSION
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.
the acute pulmonary congestion. However, with

long-standing untreated hypertension and associated MI, fibrosis and LV dilatation contractility
diminishes and systolic HF ensues (Figure 2). The
dilated left atrium and pulmonary veins that occur
from increased LV end-diastolic pressure causes
atrial premature beats and atrial fibrillation (AF)
(Figure 2). The presence of myocardial fibrosis
predisposes patients to ventricular ectopy, as well
as potentially lethal arrhythmias that may result in
sudden cardiac death.
Figure 1. The Law of Laplace follows the formula, T=P

r/h: circumferential wall stress (T)=transmural distending pressure (P) radius of chamber (r) wall thickness
(h). To compensate for an increase in left ventricular
pressure, wall thickness increases to reduce wall stress.
Peripheral resistance
LV wall stress
Concentric LVH
Oxygen demand
Coronary flow reserve

Angina
pectoris
Myocardial
Infarction
Fibrosis
Systolic
heart failure
Obstructive epicardial
coronary artery disease
Ventricular
ectopy
Sudden
death
Nonhemodynamic
factors
Diastolic filling
LVEDP
Left atrial pressure
Atrial
fibrillation
Diastolic
heart failure
Figure 2. Pathophysiology of hypertensive heart disease.

Common manifestations of hypertensive heart disease
are displayed; note the similarity of manifestations of
coronary artery disease and hypertensive heart disease.
LV=left ventricular; LVH=left ventricular hypertrophy;
LVEDP=left ventricular end-diastolic pressure
atrial pressure increases, resulting in enlargement

of the left atrium, pulmonary venous congestion,
and pulmonary congestion (Figure 2). Oxygen
demand and basal coronary blood flow increases
as myocardial hypertrophy increases; however,
coronary blood flow per unit mass of muscle at
rest is normal. Only with exercise or severe LVH
will subendocardial blood flow be jeopardized,
potentially causing myocardial infarction (MI) and
fibrosis. Intramural small vessel disease has been
shown to be present in patients with LVH.
Uncontrolled hypertension may be associated
with HF, even with preserved LV function (diastolic HF). Increased LV end-diastolic pressure
and increased impedance to LV outflow result in
232
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
the presence of left atrial enlargement, LVH, MI,

myocardial ischemia, ventricular premature beats,
and AF. Left atrial enlargementone of the earliest ECG findings of hypertensive heart diseaseis
said to be present if the terminal portion of the P
wave has a duration of 0.04 seconds and a depth
of 1 mm or more or their product is 0.04 mm
sec (Figure 3). ECG LVH with strain pattern is
the most lethal classic Framingham cardiovascular
risk factor (Figures 47).
The QRS voltage increases with both thickening
of the wall (pressure overload) and dilatation of
the chamber (volume overload) of the left ventricle.
There is significant day-to-day variability in QRS
voltage due to lead placement, respiration, and
body position. In addition, young black males may
have increased voltage in the absence of hypertension. There are various voltage criteria that have
been used to diagnose LVH, but most have a poor
sensitivity for the detection of LVH. The genderspecific Cornell voltage-QRS duration product has
emerged as the criteria with the optimum operating
characteristics. It is calculated as: men (RaVL +
SV3) (QRS duration); women: (RaVL + SV3 + 6)
(QRS duration).
LVH is present if the product exceeds 2440 mm
msec. The strain pattern is characterized by
ST depression 1 mm in lateral leads I, aVL, and
V4 to V6 (most commonly just V5 or V6 is used).
The direction of the T wave is in the opposite of
the direction of the upright QRS complex (Figure
4). Furthermore, the T wave is asymmetric with a
gradual down slope (upward convex) followed by
a rapid up slope and a terminal positive overshoot.
The presence of a strain pattern implies a poor
prognosis (Figures 5 and 7). Increased LVM and
coronary artery disease (CAD) are associated with
the strain pattern. Subendocardial ischemia may be
the cause of the strain pattern.
ECHOCARDIOGRAM
An echocardiogram provides information that
is useful in assessing symptoms of hypertensive
patients. It is not considered appropriate to order
the test for the purpose of determining the presence
of LVH in an asymptomatic patient; however, a
limited echocardiogram for that purpose has been
advocated. In addition to direct measurements of
wall thickness and chamber dimensions of the left
atrium and ventricle (Figure 8), echocardiography
offers a measurement of LV performance (ejection
fraction [EF]) as well as visualization of wallmotion abnormalities. Diastolic filling abnormalities can be determined in advanced laboratories.
Figure 3. Left atrial enlargement is one of the earliest

electrocardiographic findings of hypertensive heart disease. It is present if the terminal portion of the P wave
has a duration of 0.04 seconds and a depth of 1 mm or
more, or their product is 0.04 mm s.
Figure 4. The strain pattern with left ventricular hypertrophy conveys increased risk beyond an increased left
ventricular voltage.
An increased LVM and relative wall thickness

(>0.45) indicates concentric LVH. An abnormal
LVM index is greater than 110 g/m2 in women and
125 g/m2 in men. An increase in LVM indexed for
height appears to bestow a greater risk for women
than for men. The presence of concentric LVH
amplifies the risk associated with epicardial CAD.
Treatment
Several meta-analyses have reported superior regression of LV hypertrophy with angiotensin-converting
enzyme inhibitors than with other classes of drugs.
In contrast, two prospective, double-blind studiesthe Treatment of Mild Hypertension Study
233
Age-adjusted biennial rate/1000 men
ECG LVH absent
300
Age 3564 (yr)
234
250
200
Age 6594 (yr)
164
138
150
79
100
50
35
and stroke. Losartan was superior to atenolol by

reducing the composite end point by 13% due to
a 25% reduction in strokes. Among the enrolled
diabetic patients, total mortality was reduced.
Both ECG LVH enrollment criteria improved
more with the losartan- than the atenolol-based treatment regimen. Regression in ECG LVH by each criteria reduced cardiovascular mortality, MI, and stroke.
Approximately 10% of study participants had an
echocardiogram performed. The greatest decline
in LVM was observed between 1224 months.
Echocardiographic LVH was present in 70% of
patients at baseline and was reduced to 23% at 60
months. Associated with regression was a reduction
in left atrial diameter and improvement diastolic filling parameters. Regression of LVM index on treatment was associated with a reduction in cardiovascular mortality, stroke, and all-cause mortality.
ECG LVH present
71
27
99
83
52
29
CHF
CVA
71
23
20
0
CVD
CHD
CVD
CHD
CHF
CVA
Figure 5. Risk of cardiovascular disease with or without

electrocardiographic left ventricular hypertrophy after
34-year follow-up: the Framingham Study. The presence
of ECG LVH increases risk of cardiovascular disease in
younger and older persons.
ECG LVH=electrocardiographic left ventricular hypertrophy;
CVD=cardiovascular disease; CHD=coronary heart disease;
CHF=congestive heart failure; CVA=cerebrovascular accident.
Data derived from J Hypertens. 1991;9(suppl 2):S3S9.2
and the Veterans Affairs Single Drug Comparison

Study in Menfound that diuretics were associated with greater regression of LVM than other drug
classes. The Losartan Intervention For Endpoint
Reduction in Hypertension (LIFE) study specifically was designed to study hypertensive patients
5580 years of age with ECG LVH, using the
Cornell voltage-duration product (>2440 mm
msec) or the Sokolow-Lyon voltage criteria (SV1
+ RV5/6 >38 mm). Atenolol and losartan were
compared in this prospective, randomized, doubleblind study of 9193 patients. Enrollment BP was
a sitting systolic between 160200 mm Hg or a
diastolic between 95115 mm Hg. Additional
antihypertensive drugs (except blockers, angiotensin receptor blockers, or angiotensin-converting
inhibitors) could be added to achieve the target BP
after the dose of each drug was doubled and up
to 25 mg of hydrochlorothiazide supplemented.
The primary composite end point was death, MI,
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
ISCHEMIC HEART DISEASE

There are similarities between epicardial CAD
and hypertensive heart disease (Figure 2). There
None
350
Age-adjusted biennial rate/1000
Distensibility of the ventricle can be limited by

increased muscle (i.e., LVH), and collagen. To
improve filling, the left atrial pressure increases
and left atrial enlargement ensues.
Diastolic HF is common among the elderly with
hypertension, especially women. Early historical
findings include exertional fatigue and exertional
dyspnea. Although rarely performed, assessing LV
filling pressure invasively on presentation with HF
is the gold standard for proving diastolic HF.
With HF findings on physical examination or chest
x-ray that clear with diuresis, finding a preserved
EF, absent valvular (acute aortic or mitral regurgitation), and nonexistent pericardial abnormalities
(e.g., constrictive pericarditis) on echocardiography is how most clinicians make this diagnosis.
A well-trained cardiologist using cardiac Doppler
ultrasound in an advanced echocardiography laboratory can provide better information. This requires
a simultaneous assessment of mitral inflow, pulmonary venous flow, and Doppler tissue mitral annular motion. Many echocardiographic laboratories
simply report diastolic dysfunction is present when
the early mitral inflow (E wave) is less than the late
(atrial contraction) mitral inflow (A wave). This
E<A flow velocity is present with aging (probably
due to increased collagen), as well as impaired
relaxation (mild diastolic dysfunction). However,
pseudonormalization can occur with moderate diastolic dysfunction, but there are changes in pulmonary venous flow and tissue mitral annular motion.
Peak Valsalva mitral inflow distinguishes a pseudonormalized mitral inflow pattern by transforming
it into an abnormal pattern. Alternatively, radionuclide ventriculography can be used to determine
filling parameters in diastole in patients who are in
a sinus rhythm (Figure 10).
In randomized, double-blind, hypertension outcomes trials, a diuretic-based treatment regimen
prevents the development of HF. Alternatively, HF
trials with enalapril, blockers (bisoprolol fumarate, metoprolol succinate, and carvedilol, but not
metoprolol tartrate or atenolol), spironolactone,
and candesartan cilexetil have been shown to
reduce total mortality. There is only one outcome
trial that addresses borderline preserved EF (>40%)
HF, the Candesartan in Heart Failure Assessment of
Reduction in Mortality and Morbidity (CHARM)
study. As add-on therapy to routine medications,
candesartan reduced HF hospitalizations.
Voltage
X-ray LVH absent
Voltage + ST-T
X-ray LVH present
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
Figure 7. Risk of cardiovascular disease by x-ray and

electrocardiographic left ventricular hypertrophy in a 34year Framingham Study follow-up in men. The presence
of ST-T changes (i.e., strain pattern) on an electrocardiogram conveys additional risk beyond excess voltage.
LVH=left ventricular hypertrophy. Data derived from
J Hypertens. 1991;9(suppl 2):S3S9.2
Figure 8. M-mode echocardiogram; direct measures of

wall thickness and chamber dimensions in diastole and
systole are measured.
are multiple potential reasons why hypertensive

patients experience ischemia (Table I). Ischemic
heart disease events are numerically the most common cardiovascular event among hypertensive
patients. The presence of LVH increases the probability of a cardiovascular event (Figure 5).
Coronary flow reserve refers to the increment
in coronary blood flow measured by an intracoronary Doppler catheter due to coronary vasodilators such as papaverine, dipyridamole, or adenosine. Impaired coronary reserve (ratio <3:1) refers
to a less than expected increase in coronary blood
flow. Coronary vasodilator reserve is lower and
LVM index is higher in patients who have positive
thallium stress test without significant CAD. Since
MI is the most common potentially preventable
235
Event rate/1000 person-years
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.
Figure 10. Radionuclide angiography is a highly reproducible

method for determining ejection fraction for patients in a sinus
rhythm. The top panel shows a background-corrected timeactivity curve over a cardiac cycle. The bottom panel shows
the first derivative of those counts: diastolic function is determined by evaluating the time-activity curves during diastole;
time-to-peak filling rate (TPFR) and the peak-filling rate (PFR)
are calculated as measures of diastolic dysfunction.
dv/dt=the derivitave of ventricular volume over time;
EDV=end-diastolic volume
236
cardiovascular event in hypertensive patients, it

would be useful to have a noninvasive test to
distinguish significant obstructive large conduit
epicardial CAD from other causes of myocardial
ischemia in hypertensive patients. However, there
is no such test at present.
Routine exercise stress testing in hypertensive
patients is associated with a 62% false-positive
rate and 53% false-negative rate for significant
obstructive CAD (Table II). Exercise radionuclide
angiography has been shown to be associated with
a 49% positive predictive accuracy in hypertensive
compared with an 89% predictive accuracy in normotensive patients. Thallium (with dipyridamole
if the target heart rate is not achieved) stress testing is useful as a test of exclusion in hypertensive
patients, since the negative predictive value is 98%
and the sensitivity is 94.4%. Newer, noninvasive tests, including dipyridamole and dobutamine
echocardiography, have higher false-negative rates
and a high interobserver variability; whereas, that
is not the case with exercise dipyridamole thallium or technetium-99m sestamibi nuclear scans.
These tests should be used to exclude those with
significant obstructive epicardial CAD. Although
coronary arteriography is considered the gold
standard for defining anatomical coronary disease, there are problems evaluating the degree and
significance of luminal stenosis by this method.
Intravascular ultrasound with Doppler has been
useful to elucidate a better understanding.
blockers and angiotensin-converting enzyme
inhibitors are usually recommended for patients
with CAD. The recently completed International
Verapamil-Sustained Release Trandolapril Study
(INVEST) examined over 22,000 hypertensive
Men
Women
Age-adjusted odds ratio
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
with ECG LVH is associated with greater LVM,

eccentric hypertrophy, and reduced circumferential
end-systolic stress/end-systolic volume index. In
the Framingham Study, echocardiographic aortic
root size was determined primarily by age, height,
weight, and gender. There was a weaker (but significant) direct association with mean arterial and
diastolic BP and an inverse association with systolic BP and pulse pressure. More data are needed
to better understand these relationships. Modern
management of aortic dissection requires an emergency imaging study and cardiology and thoracic
surgery consultations.
CONCLUSIONS
The various components of hypertensive heart
disease increase overall morbidity and mortality. Careful attention and treatment of LVH,
heart failure, ischemic heart disease, and AF will
improve survival.
Table I. Potential Mechanisms of Ischemia With
Hypertension
Increased coronary arteriolar resistance

Impaired coronary flow reserve
Endothelial dysfunction
Epicardial coronary artery atherosclerosis
Compression of coronary arterioles by muscle and fibrosis
Arteriolar wall thickening
Coronary artery size mismatch
Increased blood viscosity
Abstracted from Hypertension. 1999;34:782789.5
237
Table II. Predictive Value of Various Noninvasive Tests in Hypertensive Patients

Bruce treadmill
Exercise radionuclide ventriculography
Planar exercise thallium ( dipyridamole)
SPECT technetium-99m sestamibi
Dipyridamole echocardiography
Dobutamine echocardiography
POSITIVE PREDICTIVE VALUE (%)

41
46
39
67
90
85
NEGATIVE PREDICTIVE VALUE (%)

43
56
98
94
64
83
OVERALL ACCURACY (%)

42
49
70
71
74
84
SPECT=single-photon emission computed tomography
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
Lorell BH, Carabello BA. Left ventricular hypertrophy:

pathogenesis, detection, and prognosis. Circulation.
2000;102:470479.
Okin PM, Devereux RB, Jern S, et al. Regression of
electrocardiographic left ventricular hypertrophy during
antihypertensive treatment and the prediction of major
cardiovascular events. JAMA. 2004;292:23432349.
Devereux RB, Wachtell K, Gerdts E, et al. Prognostic significance of left ventricular mass change during treatment
of hypertension. JAMA. 2004;292:23502356.
Aurigemma GP, Gaasch WH. Clinical practice. Diastolic
heart failure. N Engl J Med. 2004;351:10971105.
Zile MR, Baicu CF, Gaasch WH. Diastolic heart failure
abnormalities in active relaxation and passive stiffness of
the left ventricle. N Engl J Med. 2004;350:19531959.

Hypertensive Heart Disease: Hypertension Curriculum Review

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Hypertensive Heart Disease: Hypertension Curriculum Review

Uploaded by

Copyright:

Available Formats

Hyper tension

Donald G. Vidt, MD, Section Editor

Hypertensive Heart Disease

ypertensive heart disease is the target organ

VOL. 7 NO. 4 APRIL 2005

LEFT VENTRICULAR HYPERTROPHY

THE JOURNAL OF CLINICAL HYPERTENSION

the acute pulmonary congestion. However, with

Figure 1. The Law of Laplace follows the formula, T=P

Coronary flow reserve

Left atrial pressure

Figure 2. Pathophysiology of hypertensive heart disease.

atrial pressure increases, resulting in enlargement

THE JOURNAL OF CLINICAL HYPERTENSION

the presence of left atrial enlargement, LVH, MI,

VOL. 7 NO. 4 APRIL 2005

Figure 3. Left atrial enlargement is one of the earliest

An increased LVM and relative wall thickness

THE JOURNAL OF CLINICAL HYPERTENSION

Age-adjusted biennial rate/1000 men

ECG LVH absent

Age 3564 (yr)

Age 6594 (yr)

and stroke. Losartan was superior to atenolol by

ECG LVH present

Figure 5. Risk of cardiovascular disease with or without

and the Veterans Affairs Single Drug Comparison

THE JOURNAL OF CLINICAL HYPERTENSION

VOL. 7 NO. 4 APRIL 2005

ISCHEMIC HEART DISEASE

VOL. 7 NO. 4 APRIL 2005

Distensibility of the ventricle can be limited by

X-ray LVH absent

X-ray LVH present

Figure 7. Risk of cardiovascular disease by x-ray and

Figure 8. M-mode echocardiogram; direct measures of

are multiple potential reasons why hypertensive

THE JOURNAL OF CLINICAL HYPERTENSION

Event rate/1000 person-years

Figure 10. Radionuclide angiography is a highly reproducible

THE JOURNAL OF CLINICAL HYPERTENSION

cardiovascular event in hypertensive patients, it

VOL. 7 NO. 4 APRIL 2005

Age-adjusted odds ratio

VOL. 7 NO. 4 APRIL 2005

with ECG LVH is associated with greater LVM,

Increased coronary arteriolar resistance

THE JOURNAL OF CLINICAL HYPERTENSION

Table II. Predictive Value of Various Noninvasive Tests in Hypertensive Patients

POSITIVE PREDICTIVE VALUE (%)

NEGATIVE PREDICTIVE VALUE (%)

OVERALL ACCURACY (%)

SPECT=single-photon emission computed tomography

THE JOURNAL OF CLINICAL HYPERTENSION

Lorell BH, Carabello BA. Left ventricular hypertrophy:

VOL. 7 NO. 4 APRIL 2005

You might also like