Hypertension 1996 :
One Medicine, Two Cultures
Primary and secondary prevention of arterial
A. De Francesco
Division of Intensive Coronary Therapy at “Addolorata” Hospital, manager
of Division Cardiology of Sport - Rome.
Arterial hypertension is a clinical condition characterized by increased
systolic/diastolic tensive values, by definition higher than 140/80-mmHg
Within such wide limits, however, several individual variations may occur,
which are used to define a necessarily rigid and schematic classification
of the different hypertension types. Based on the criteria established by
the World Health Organization (W.H.O.), all individuals with arterial hypertension
values ranging from 140/90 to 160/95 mmHg in at least two measurements out
of three, performed at five-minute intervals, may be defined as “borderline
hypertensive patients” (2).
The importance of such surveying method derives from a precise fact: a random
pressure increase may be observed in some individuals as a consequence of
an abnormally strong emotional reaction occurring as soon as the physician
approaches, but is lower in the presence of a nurse and decreases, or even
disappears, at self-measurement; indeed, tensive values in these patients
fall within a normal range at automatic 24-hour monitoring. These factors
define the so-called “white-coat hypertension”, the outbreak of a clear
alarm condition experienced by some individuals who actually do not seem
to be exposed to a true hypertensive risk: indeed the quad vitam prognosis
for these individuals fully corresponds to that of normotensive people (3,4,
The tensive condition characterized by systolic values equal to or exceeding
160 mmHg, combined with normal or reduced diastolic values, i.e. equal to
or lower than 90 mmHg, is defined as “isolated systolic hypertension”. This
type of hypertension is typically observed in elderly patients, or anyway
aged over 55, and derives from a reduced flexibility and stretching ability
of large arterial vessels (1, 6, 7, 8).
Unlike systolic hypertension, the diastolic form, characterized by tensive
values equal to or higher than 90 mmHg, progressively increases, in the
general population, up to the age of approximately 55, and remains more
or less unchanged thereafter (9).
The above definitions are obviously limited to primary or "basic" arterial
hypertension, while we will not dwell in this context on the "secondary
arterial hypertension" conditions due to other causes, discussed in the
appropriate internal medicine books.
After generally defining “arterial hypertension”, it is worth stressing
the need to adopt a scale of severity based on pressure values for all hypertensive
conditions. Starting from the lowest level, which coincides with “borderline
hypertension” (>140/90 and <160/95 mmHg), this scale moves gradually up
to “mild” (same as the “borderline” form in America) or “moderate” arterial
hypertension (160/95 and <180/110 mmHg), to the “moderate-severe” (>180/110
and <210/120 mmHg) and up to the “severe” form (>210/120 mmRg); the so-called
“malignant arterial hypertension”, now hardly ever observed, was characterized
in the past by even higher values (5).
After outlining the importance of the severity of hypertension, a further
classification is now required based on the age of the patient and/or of
the population examined, since arterial hypertension represents an important
"risk factor" for the development of cardiovascular diseases in general
and atherosclerotic ones in particular. In this respect, this classification
is based on the so-called "time/dose product" resulting from the patient's
age and/or the dating of the hypertensive condition multiplied by the latter's
The term “risk factor”, introduced by the creators and performers of the
Framingham Study and by now universally employed, is meant to fill in the
logical gap between the concepts of association and cause referring to at
least two phenomena that are assumed to be interrelated; it is better defined
as a “factor associated with a disease or clinical condition, which is suspected
to contribute to the pathogenesis of the latter” (1).
The hypothesis was formulated that the necessary conditions for the development
of atheromas at systolic pressure values as low as 120-140 mmHg be established
at an endothelial level: this assumption supports the aphorism by which
“the lower pressure values, the better; unless the individual faints every
time he/she stands up”.
On the other hand, the epidemiological data provided by the different trials
showed that a progressively higher risk of vascular accidents corresponds
to increasing arterial pressure values, even in case of an isolated increase
in systolic arterial pressure; in addition, high diastolic pressure values
seem to involve an increased relative risk of both stroke and coronary disease
(1, 2, 5, 6, 7, 9, 10).
In the light of the above, the wish to carry out “primary prevention” of
arterial hypertension implies pursuing the preservation of good health conditions
in order to reduce, or even eliminate, the risk of observing increased tensive
values in individual patients or, even more, in the whole population in
On the other hand, once pressure values have started increasing, the need
emerges to reduce as much as possible the relative and/or even the absolute
risk of cardiovascular complications that may result from any hypertensive
condition: thus "secondary prevention" of arterial hypertension may be carried
out (11, 12).
In order to put all this into practice, it should be considered that different
problems may affect paediatric patients compared to young adults and, even
more, aged or elderly patients, and that therefore different therapeutic
approaches should be adopted.
The problems and therapeutic approaches will therefore be different for
a young patient, for an adult patient or for an elderly patient.
Paediatric age: primary prevention
Some authors point out to the possibility to start preventing the onset
of arterial hypertension even immediately after conception, during intrauterine
life, based on the observation that a low weight at birth, combined with
the large size of the placenta, seems to be often associated, in adults,
with a high mortality rate due to cardiovascular diseases, with glucose
intolerance and, particularly, with a true hypertensive condition (13, 14,
As a consequence, physicians should be encouraged to adopt a more careful
primary prevention, especially if cardiovascular diseases and/or hypertension
may have a familial origin (13, 16). However, even if more attention is
devoted to the prevention of possible hypertensive conditions in new-born
babies, physicians should never forget that “children are not little adults”:
no drugs may and should be used for them, but rather strong and effective
hygienic and feeding principles aimed at altering, as far as possible, the
so-called familial pattern, to which both inheritance, which may not be
modified, and the environment, which instead may be thoroughly modified,
contribute in various ways and to different degrees (1, 17).
Diet control, aimed at reducing at least two of the three main cardiovascular
risk factors - hypercholesteraemia and arterial hypertension - should start
in the first two years of life, focusing on breast feeding at birth and
on delayed weaning with solid food at 4/6 months of age, while trying to
avoid adding sugar to the baby's milk, as well as cooking salt and/or seasonings
in food preparation at weaning (1).
A delayed introduction of packaged food into the feeding scheme of all babies
is also strongly recommended: indeed, such food formulas involve a four-fold
increase in sodium intake compared to normal conditions; in addition, the
energy they provide is often higher than needed as well as unbalanced in
terms of nutrients, since it involves a considerable intake of sucrose and
cholesterol along with a low polyunsaturated to saturated fats ratio. These
observations add up to the fact that the consumption of packaged food is
usually combined with a reduced intake of fruits and vegetables: the possible
integration with vitamins and mineral salts in the package does not really
change the fact that those kinds of food will hardly ever find the place
they are entitled to within the feeding schemes of adults-to-be (1).
In the first two years of life, the adoption of healthy feeding habits should
focus on moderation rather than on the elimination of some types of food,
and a wide range of nutritionally balanced food products should be introduced
while basing the energy intake on the growth requirements that allow to
preserve the desired body weight (1).
Starting from the age of 2, a maximum 30% of calories should be provided
by fats and most of the rest should be obtained from vegetal proteins and
complex carbohydrates: as for adults, saturated, polyunsaturated and monounsaturated
fatty acids should provide 10% of the total calories each, with less than
300 mg/day of cholesterol and less than 5 gr./day of sodium chloride, while
the intake of fibres, including soluble ones, should be increased (1).
In order to reduce the intake of saturated fats in children's diet schemes,
the main targets to be focused on in view of the primary prevention of atherosclerosis
and hypertension should be represented by whole milk, various kinds of sweets
and packaged snacks: the latter, like all fatty sweets, are rich in single
carbohydrates and able to provide at least twice as many calories as fruits
and vegetables at equal weight.
The main source of sodium, whose quantity may hardly be assessed, is rather
represented by grains and derived products (bread and pasta), while vegetables
rank second. The shift to sodium-free or low-sodium feeding schemes (when
used, sodium and its quantity should be indicated on the appropriate package),
a reduced use of packaged food products, the purchase of fresh rather than
canned vegetables, and the use of spices instead of salt for cooking or
eating should allow a significant reduction in sodium intake with food.
In Italy, charcuterie products and sausages as well as cheese, also represent
a considerable source of sodium: such kinds of food, due often to uninformed
parents, sometimes account for a large share of daily food intake (1, 9).
Paediatric age: secondary prevention
After expressing these general introductory considerations, which apply
to any one, two possible strategies for the control of cardiovascular diseases,
even at a paediatric age, should be described: one of them concerns the
population, while the other one is defined as the "high risk" strategy.
The former, which we have been outlining so far, provides for an approach
to public health, involving both individuals at prospective risk of coronary
disease (e.g. familial origin) and people that are not deemed at risk; such
approach is adopted in view of a downward shift of risk-factor distribution
throughout the whole population. In the treatment of the paediatric and
teen-age population, efforts should focus on the onset of correct life styles,
including on-going physical exercise to be introduced into behavioural patterns,
while turning individuals accountable for their own health. The adoption
of these correct habits should also spread to include the third major cardiovascular
risk factor, i.e. cigarette smoking; in addition, nowadays, measures should
be taken against the intake of light and/or heavy drugs and the consumption
and/or excess of alcohol (1).
The "high-risk strategy", on the other hand, applies to individuals who
are subject to precise and clearly defined cardiovascular risk factors,
such as, in our case, arterial hypertension: in high-risk individuals, subject
to overt hypertensive conditions during their paediatric and/or teen-age,
a priority measure may provide for the use of drugs. In these infrequent
situations, not including secondary arterial hypertension cases due to other
causes, calcium-antagonists, ACE-inhibitors and, for the forms akin to the
so-called “hyperkinetic heart syndrome”, Beta-blockers are the least harmful
drugs that may be used: the three groups, and the latter in particular,
may benefit from a correct aerobic exercise schedule, whose effects may
add up to those provided by the drug, sometimes allowing a dose reduction:
the above-described hygienic and feeding principles will represent a correct
and inevitable integration (1, 5, 11, 12).
Adult age: primary prevention
Up to 40% of adult hypertensive patients show a cholesteraemia >240 mg
% and an approximately double incidence of obesity and diabetes compared
to normotensive people: a reduction, possibly targeted, of any of these
risk factors may turn out to be a spontaneous cause for the relevant failure
in the prevention of coronary heart diseases (18), which usually have a
Recent epidemiological and clinical data confirm that metabolic risk factors
and arterial hypertension may have a common origin, at least in some individuals:
indeed, an insulin excess is potentially able to raise pressure values by
stimulating sodium re-absorption by the kidneys, by activating the adrenergic
nervous system, by stimulating the proliferation of smooth muscle cells
of the mean arteriolar, by altering transmembrane ion exchange, by raising
triglyceridaemia, by reducing HDL cholesterol, etc. (12, 13, 18).
In addition, the plasma concentration of insulin in each individual may
be the result of an integration of 1) an excessive current and past food
intake, 2) an androgenic hormone pattern encouraging the accumulation of
a fat excess in the trunk, 3) a sedentary lifestyle, and 4) chronic stress
conditions, also including cigarette smoking which is suspected to cause
a repeated stimulation to the sympathetic nervous system. A chronically
increased insulin rate in blood brings about a downward adjustment of this
hormone's action, while chronic hyperglycaemia may reduce glucose-induced
insulin secretion. The overall effect of this homeostatic system is such
that the two variables, insulinaemia and glycaemia, will always vary proportionally,
provided that insulin secretion continues.
However, since an on-going insulin excess is not compatible with survival,
the body develops an insulin-resistance which may be either primary (of
unknown origin) or secondary (puberty, traumas, any kind of stress), in
order to mitigate the harmful effects of hyperinsulinism (12, 13, 18).
The insulin-resistance observed in basic arterial hypertension is of the
primary kind, i.e. of unknown origin, and mostly located in the skeletal
muscles, where it specifically affects glycogen synthesis causing a subsequent
endogenous hypertriglycaeridaemia and a triglyceride deposit in the fatty
tissue, especially in the abdominal region. The term insulin-resistance
derived syndrome, or polymetabolic syndrome, or X syndrome thus seems to
point out to a “risk” syndrome rather than to a true pathological condition,
which identifies an association between obesity, arterial hypertension,
hypertriglycaeridaemia, carbohydrate intolerance and hyperinsulinaemia and/or
insulin resistance, and may represent an important warning sign of diseases
that may cause accelerated atherosclerosis or ischaemic heart diseases (12,
This combination of several risk factors, including at least hypertension
and a metabolic disorder and/or obesity, heavily affects the medical record
of hypertensive patients, while encouraging the quicker development of ischaemic
coronary disease and/or an enlargement of the left ventricular mass: this
is why it should always be pursued, in view of correct diagnostic and therapeutic
approaches which should always include non-pharmacological remedies as well
Thus, before issuing any drug treatment, it may be quite useful to adopt
non-pharmacological measures to control tensive values, especially in borderline
and mild arterial hypertensive patients, but in all other patients too.
However, once it is issued, this treatment should not exclude a combination
with the hygienic and feeding principles previously recommended and implemented
A weight loss in obese patients, a decreased alcohol consumption down to
a maximum 20-30 gr. of ethanol per day, a low-sodium (allowing for a maximum
5 gr. of sodium chloride per day), low-calorie diet, with a high fibre content
(at least 30 gr./day including 50% of soluble and 50% of insoluble fibres),
regular aerobic exercise (at least 2-3 times per week with 1-hour or longer
sessions, while carefully keeping a regular heart rate of 70 to 85% of the
theoretic age-related maximum rate); discontinuing or at least sharply reducing
cigarette smoking, possibly replacing it with pipe smoking: all these measures
together may result into an outstanding fall in tensive values, at least
in some patients (2, 12). Other feeding measures, such as reduced coffee
consumption down to a maximum two cups per day, the intake of potassium,
calcium or magnesium-rich substances (i.e. some types of fruits and legumes
and hard mineral water), the increased intake of polyunsaturated fats (mainly
contained in white meat and sea fish), and a reduced saturated-fat intake
(mainly due to all animal-derived products) could be useful, even though
this has not been demonstrated for sure (1, 2, 10, 11, 12). The control
of a possibly associated diabetes or lipoidoproteinosis by means of dietary
and therapeutic measures and the discontinuing of any oestroprogestinic
contraceptive treatments represent other related measures required for hypertensive
patients of both sexes.
Adults should avoid eating afternoon snacks; if this is impossible, it could
be useful to eat season fruits or raw vegetables (cucumbers, carrots, and
fennel), while only consuming sherbets and ice-lolls occasionally and alternatively
in the summer period. The physician's and dietician's effort is very hard,
though, since it is not aimed at establishing a correct lifestyle, but rather
at encouraging behavioural changes that are often hard to achieve by individuals
who follow established bad hygienic and feeding patterns, and sometimes
even harmful, if not correctly implemented. In some rather uncommon successful
cases, especially with respect to the achievement and/or preservation of
an ideal or even just acceptable body weight, the effort required to keep
it unchanged is often even harder and stronger. However it is worth stressing
that general behavioural norms in adults may not be deemed equally important
for all types of hypertension: indeed, they represent almost all of the
possible therapeutic measures in mild and/or borderline forms, but they
gradually lose importance as more severe hypertensive conditions are observed;
notwithstanding this, even a simple weight loss in obese patients is likely
to induce a sometimes steady fall in tensive values (20, 21, 22).
The Tohms study, carried out on 902 patients with mild arterial hypertension,
of both sexes and aged 45 to 69, highlighted the need to adopt an aggressive
therapeutic approach to any degree of arterial hypertension, while stressing
that a combination of drug treatment and general behavioural norms is more
effective in achieving pressure values control as well as in preventing
the clinical signs of hypertensive heart diseases and abnormal ultrasound-scanning
results (6, 9, 18, 20).
Indeed, even if the absolute ictus and coronary disease risk in mild hypertensive
patients may not appear as high as in moderate and severe hypertensive patients,
clinical studies suggest that, whenever mild pressure increases are not
monitored, arterial pressure values are very likely to shift from moderate
to considerably high in the relatively short term (10).
Mature age: secondary prevention
The absolute risk of cardiovascular complications for male adults is
anyway higher than for females at all systolic pressure levels, although
the relative risk is the same for both sexes due to the above-mentioned
dose/time ratio, which may reasonably be deemed equal for individuals of
the same age. However, the absolute risk related to increased pressure values
appears much higher in elderly males and becomes even more serious as age
increases, irrespective of pressure values.
The biological role hypertension is assumed to play in cardiovascular conditions
has been clearly described: a long-term arterial pressure increase causes
a greater pressure load on the heart and ultimately produces left ventricular
hypertrophy. In addition, high-pressure levels may also cause arteriolar
smooth-muscle hypertrophy, which may even result into a functional impairment
of the kidneys. Finally, at a brain level, increased pressure values may
cause damage to the arterial wall and a subsequent haemorragic ictus. Increased
pressure levels then generally result into an accelerated atherosclerosis,
especially at a coronary level (9, 10, and 18).
Last but not least, a steady deviation (at night and day) of pressure towards
higher values may occur, a disorder, which is potentially able, in time,
to cause, left ventricle hypertrophy. This is a concentric hypertrophy due
to the addition, by myocytes, of parallel contractile proteins, which may
occur at a mere systolic pressure increase. Until recently, left ventricular
hypertrophy seemed to reflect the progressive increase of arterial pressure
and of the left ventricular post-load, in turn probably linked to a parallel
increase in total peripheral resistance; quite recent outcomes, however,
seem to point out to a reduced flexibility and stretching ability of large
vessels as the main cause for LVH (8, 18). Other authors consider the missing
pressure reduction during the night reported by a few patients as a possible
cause for LVH; in particular this could be responsible for changes in the
shape of cavities and for concentric hypertrophy, both related to an increased
rate of cardiovascular complications (24).
Indeed, many studies in very recent years highlighted that pressure levels
are not always correlated with the size of the ventricular mass, almost
as if other factors, besides pressure overloads, not necessarily of a haemodynamic
kind, could play a role in its development: humoral substances (noradrenaline,
angiotensin), intramyocyte substances, concurrent diseases, such as exogenous
obesity and/or diabetes mellitus, etc., an endothelial damage brought about
by high tension (with a subsequent defective synthesis and release of the
endothelium-derived releasing factor (EDRF) and of the endothelium-derived
constrictor factor (EDCF) or endothelia in) (1, 2, 5, 19, 24).
Whatever its origin, LVH always represents an adjustment aimed at delaying
the onset of cardiac decompensation in physiopathological terms. As a consequence,
however, the heart is subject to coronary impairment following up an intramural
arteriolar rarefaction, a reduced capillary density per heart mass unit,
and a mean hypertrophy in small coronary arteries 1 mm and, ultimately,
an increased coronary resistance. All this is combined with collagen build-up
and subendocardial fibrosis, with subsequent chronic hypoperfusion as well
as a higher risk of heart arrhythmia and/or sudden death (18).
The progressive development of atherosclerotic diseases takes a rather long
time, often longer than major trials performed in order to ascertain the
effectiveness of treatments, but the ictus risk undoubtedly rises more quickly
than the coronary disease risk. The high incidence of risk factors related
to atherosclerotic diseases in the coronary circle is very likely to reduce
the potential impact of decreased pressure values over a composite-risk
pathological process. However it is quite clear that a fall in pressure
values reduces risk and extends survival, both in mild hypertensive individuals
(moderate or borderline) and, even more so, in patients with high or very
high pressure levels (severe or serious) (10).
In cases requiring drug treatment, the global clinical conditions of patients
and the side effects of drugs should be taken into account: if the patient
also shows metabolic disorders, the potential effects on metabolic parameters,
on which Beta-blockers and thiazide diuretics seem to exert the strongest
effects (5, 18), should be particularly monitored. Administration of the
former, especially if they are not heart-selective and have no intrinsic
sympatheticomimetic activity, may block the effects of hyperinsulinaemia,
so that hypertriglycaeridaemia and a reduced HDL cholesterol value may be
observed during chronic treatment (18).
In a strictly metabolic sense, ACE-inhibitors and calcium-antagonists appear
as the drugs of choice, since they may also positively affect the development
of atheromatous plaques as well as a reduction of the left ventricular mass
which, as mentioned, may alone influence the outcome for hypertensive patients
(5, 18, 19, 24).
However, based on current knowledge, it does not seem correct to consider
the drug-related heart mass reduction as beneficial, at least as long as
it is not possible to establish precisely whether this reduction occurs
in the collagen-fibrotic part or in the muscular part; therefore it is not
acceptable to charge with an increased risk drugs that do not cause a heart
mass reduction (19).
Alpha-blockers and the new Alpha-beta-blockers, like carvedilole, show no
undesired effects on glycoside and lipid metabolism, just like anti serotoninergic
drugs, which however are not even able to reduce the left ventricular mass;
especially the former produce positive metabolic effects, such as an HDL
increase and a reduced triglyceride and total cholesterol rate. Physicians
are responsible for the choice of the most appropriate drug for each case
Primary prevention is not applicable in elderly patients (>60), unless
it has been undertaken in the previous years, but secondary prevention is
still possible: indeed, arterial hypertension in individuals clearly showing
a progression of arteriosclerotic processes, usually only at a systolic
level, represents an important risk factor for the onset of brain vascular
diseases and of all the major types of stroke. On the other hand, arterial
hypertension also seems to be deeply involved in the pathogenesis and development
of atheromatous injuries in extracranial vessels and in the hyaline degeneration
of arterial walls, along with a subsequent aneurysm dilatation, of the small
arteries entering the brain.
Data drawn from the Framingham cardiovascular study seem to confirm that
the death risk of long-term hypertensive patients with other important associated
cardiovascular risk factors (age, sex, cigarette smoking, cholesterol levels
and glucose intolerance), due to any cause, is reportedly 31% lower and
the cardiovascular death risk is 60% lower in patients submitted to long-term
treatment compared to untreated ones (4, 25, 26).
This is the reason why arterial hypertension and all other possibly related
important risk factors should be treated early and in an appropriate manner.
In the SHEP (Systolic Hypertension in the Elderly Program) study, chlorthali
done alone, even at low doses (12.5 mg/day), turned out effective for a
reduction in the percent rate of lethal and non-lethal stroke in patients
over 55 suffering from isolated systolic hypertension. Recently introduced
drugs of a different kind, such as ACE-inhibitors and calcium-antagonists,
are assumed to provide more substantial benefits (4, 6, and 27). However
it is a good practice to use great caution in coping with hypertension in
elderly patients, both in the isolated systolic and in the systolic-diastolic
form, whether or not associated with other cardiovascular risk factors.
Indeed no brain flow self-regulation disorders following up a reduced vascular
compliance should be induced, although they may always occur if related
to possible changes in the anatomical structure of the vessel wall of elderly
hypertensive patients. In this kind of patients there is no need to reach
ideal arterial pressure values, but rather a satisfactory and gradual fall
in arterial pressure values should be achieved: such results may often be
obtained by simply reducing salt intake with the diet. Systolic hypertension
in elderly people seems to be highly sensitive to this measure due to a
reduced activation of the adrenergic and the renin-aldosterone systems (5,
7, 20, 22, and 27). Sodium restrictions should be combined with reduced
alcohol consumption and calorie intake, in order to obtain a non-dramatic
weight loss, however sufficient to keep the body weight within values not
exceeding 15% of the ideal weight; cigarette smoking should also be reduced,
while reduced cholesterol levels have not proved useful. On the other hand,
a potentially effective increased potassium and fibre intake with the diet
should be achieved through a more frequent consumption of fresh fruits and
vegetables (5, 6).
A motor rehabilitation programme, strictly based on aerobic principles and
correctly supported by expert staff according to typical heart rehabilitation
measures, may also prove effective in these patients to achieve a better
tensive value control (6, 27).
At the end of this discussion on such an irksome subject as prevention,
which any physician tends to approach with great efforts and somewhat mistrustfully,
we hope we have succeeded in contributing, however slightly, to throw light
upon such a wide and complicated field as hypertension, in which practitioners
tend to get lost if they are not correctly directed and driven: all this
in view of an effective co-operation between specialized cardiologists and
- J. STOKES: Fattori di Rischio Cardiovascolari. In: “FATTORI DI RISCHIO
E PREVENZIONE DELLE CORONAROPATIE” di E.D. FROHLICK, CAP.I: pagg. 3-20.
Ed. MENARINI - MOMENTO MEDICO, SALERNO, 1992.
- F. AGABITI ROSEI, C. FERNANDEZ, F. RIOLO: Ii mio paziente iperteso
in ambulatorio. Ed. SICEX, ROMA, 1995.
- P. VERDEOCHIA, C. PORCELLATI: L'ipertensione da camice bianco. G.
ITAL. CARDIOL. 25: 899-909, 1995.
- L. PELLEGRINO, G. PRENCIPE: Ipertensione arteriosa da camice bianco;
studio ultrasonografico delle arterie carotidi. CARDIOLOGIA, 41, 8:
- R.L. BLOOMFIELD, M. HARPER, H. UHL: Ipertensione; Un approccio muitidisciplinare.
Pagg. 35-70, 106-122, 147-167. ED. GUIDOTTI, FIRENZE, 1993.
- J.L. PROBSTFIELS, C.D. FURBERO: Ipertensione sistolica nell' anziano.
In: FATTORI DI RISCHIO E PREVENZIONE DELLE CORONAROPATIE di E.D. FROHLICK,
cap.IV: pagg. 65-84. Ed. MOMENTO MEDICO MENARINI, SALERNO, 1992.
- A. RAPPELLI: Ipertensione e malattie cerebrovascolari. Da: CLINICA
DELL'IPERTENSIONE di A. ZANCHETTI. ED. CENTRO SCIENTIFICO EDITORE, TORINO,
- A. FERRARO, C. PALOMBO, A. DISTANTE, A. L'ABBATE: Ipertensione arteriosa
e arterie dl grosso calibro. 0. ITAL. CARDIOL., 23: 921-932, 1993.
- F. MAGRINI: Ipertensione e cardiopatia ischemica. Da: CLINICA DELL'IPERTENSIONE
di A. ZANCHETTI. Ed. CENTRO SCIENTIFICO EDITORE, TORINO, 1993.
- E.J. ROCCELLA, A.E. BOWLR: L'ipertensione come fattore di rischio.
In: FATTORI DI RISCHIO E PREVENZIONE DELLE CORONAROPATIE di E.D. FROHLICH,
Cap.III: pagg. 49-63. Ed. MOMENTO MEDICO MENARINI, SALERNO, 1992.
- H.B. SADLO, N.K. WENGER: Ruolo dell'esercizio fisico nella prevenzione
primaria e secondaria della malattia coronarica ateroscierotica. In:
FATTORI DI RISCHIO E PREVENZIONE DELLE CORONAROPATIE di E.D. FROHLICH,
CAP.XII: pagg. 177-190, ED., MOMENTO MEDICO MENARINI, SALERNO, 1992.
- A. DE FRANCESCO, E. SEVERINI: Diagnosi e prevenzione cardiovascolare
nello sportivo; cap. 17-22. CAPOZZI EDITORE, Roma, 1995.
- E. FERRANNINI, S. VICHI: La sindrome da insulino-resistenza. QUON,
1, 3: 24-37, 1994.
- D.J.P. BARKER, A.R. ULL, C. OSMOND, S.J. SIMMONDS: Fatal and placental
size and risk of hypertension in adult life. BMJ, 301: 259-262, 1990.
- C.N. HALES, D.J.P. BARKER, P.M.S. CLARK et al.: Fatal and infant
growth and impaired glucose tolerance at age 64. BMJ, 303: 1019-1022,
- M.C. BRESCHI, G. SEGHIERI, G. BARTOLOMEI, A. GIRONI, S. BALDI, E.
FERRANNINI: relation of birth-weigh to maternal plasma glucose and insulin
concentrations during normal pregnancy. DIABETOLOGIA, 36: 1315-1321,
- F. FONDA: I bambini non sono piccoli adulti. G. ITAL. CARDIOL.,
24: 1261-1263, 1994.
- M. MANCINI: Ipertensione, diabete e malattie metaboliche. Da: CLINICA
DELL'IPERTENSIONE di A. ZANCHETTI. Ed. CENTRO SCIENTIFICO EDITORE, TORINO,
- E.D. FROHLICH: Ipertrofia ventricolare sinistra; un fattore indipendente
di rischio. In: FATTORI DI RISCHIO E PREVENZIONE DELLE CORONAROPATIE
di E.D. FROHLICH, cap. V: pagg. 85-94, ED. MOMENTO MEDICO MENARINI,
- E. AMBROSIONI Ipertensione borderline. Da: CLINICA DELL'IPERTENSIONE
di A. ZANCHETTI. Ed. CENTRO SCIENTIFICO EDITORE, TORINO, 1993.
- M.F. GOLDSMITH: Ipertensione arteriosa lieve; terapia farmacologica
e stile di vita. JAMA Ed. It. 5, 8: 409-410, 1993.
- G.L. WOLLAM, W. DALLAS HALL: Trattamento dell'ipertensione; pratica
clinica e dilemmi terapeutici: pagg. 3-102. COPYRIGHT HAROFARMA V.K.
LTD, CHICAGO, 1989.
- D. MARTINEZ CARO: Cuore ed esercizio fisico. COLLANA DI CARDIOLOGIA
CLINICA: pagg. 106-126. ED. LUSOFARMACO, DOYMA ITALIA, MILANO, 1993.
- P. VERDECCHIA, S. PEDE: E possibile identificare un tipo di ipertrofia
ventricolare sinistra associato ad un significativo rischio di complicanze
cardiovascolari nel paziente con ipertensione arteriosa essenziale?
G. ITAL. CARDIL., 26: 231-240, 1996.
- L. PELLEGRINO, G. PRENCIPE: Studio ecotomografico ad alta risoluzione
delle lesioni ateroscierotiche delle arterie carotidi nella ipertensione
arteriosa essenziale borderline. G. ITAL. CARDIOL. 24: 1199-1210, 1994.
- P.A. SYTOWSKI, A.B. D'AGOSTINO, A.J- BELANGER, W.B. KANNEL: tendenze
secolari nell'ipertensione arteriosa “sustained” a lungo termine, nel
trattamento a lungo termine e nella mortalita cardiovascolare; lo studio
di Framingham dal 1950 al 1990. CIRCULATION ed. It. 1, 3: 160-169, 1996.
- GRUPPO DI RICERCA COOPERATIVA SHEP: Prevenzione dell'ictus con la
terapia antipertensiva negli anziani con ipertensione sistolica isolata.
Risultati finali del programma sulla ipertensione sistolica negli anziani
(SEEP) . JAMA, 265: 3255-3264, 1991.
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