Intervention and risk factor

The impact of these disease and awareness is necessary in order to control this
global issue so we have to strategize how to tackle it. Reduce the possibility of
getting these conditions and advance the treatment options.

Hypetension Risk factors
1. Age. The possibility of developing high blood pressure increase with age.
Commonly men at early middle age. In Women it is more likely after
menopause low hormonal level like low progesterone and less bp antagonist
(Vascular Effects of Progesterone Mario Barbagallo,
Ligia J. Dominguez, Giuseppe Licata, Jie Shan, Li Bing, Edward Karpinski,
Peter K. T. Pang, Lawrence M. Resnick
Role of Cellular Calcium Regulation : Hypertension. 2001; 37: 142-147
. Children may also have high blood pressure is caused by problems with the
kidneys or heart, lack of exercise and diet.. same for angina and HA

Pregnancy contributes to high blood pressure because of... During pregnancy,
plasma levels of angiotensinogen increase several-fold owing to increased
estrogen. Goodman and gilman chapter 26 renin and angiotensin..( http://0-
accesspharmacy.mhmedical.com.wam.seals.ac.za/content.aspx?bookid=374&se
ctionid=41266233) therefore the prenatal care and observation is necessary step
to control this condition.

Genetics
o Race. High blood pressure is particularly common among blacks, often
developing at an earlier age than it does in whites. Serious
complications, such as stroke and heart attack, also are more common
in blacks..genetic
o Family history. High blood pressure tends to run in families.

Physical state
o Obesity and weight consideration. Having more weight than is
healthy according to the BMI as a guideline, results in the need to
transport fluids in higher quantities to maintain these extra weight. As
the volume of blood circulated through your blood vessels increases,
and results in a rise in the pressure on your artery walls. Angina and
HA
o Exercise . People who are inactive tend to have higher heart rates.
The higher your heart rate, the harder your heart must work with each
contraction and the stronger the force on your arteries. Lack of
physical activity also increases the risk of being overweight. However
this must not be blindly taken as angina of exertion may frequently
arise and discourage the patient from doing exercise. Angina and HA
Using tobacco. Tobacco contains nicotine immediately raise your blood
pressure temporarily, which is a known vasoconstrictor and the chemicals in
tobacco can damage the lining of your artery walls. This can cause your arteries
to narrow, increasing your blood pressure. Secondhand smoke also can increase
your blood pressure. Hence quitting or minimizing the use of tobacco is advised.
Through support groups prescription medication and medical advice.
secondhand smoke damage the interior walls of arteries including arteries to
your heart allowing deposits of cholesterol to collect and block blood flow.
allowing deposits of cholesterol and other substances to collect and slow blood
flow. Smoking also increases the risk of deadly blood clots forming and causing a
heart attack.Angina and HA

Diet
o sodium in your diet can cause your body to retain fluid, which
increases blood pressure. Through increase in blood fluids, increasing
therefore cardiac output and raising blood pressure, consider the
angiotensin mechanism using NaCl detection. Therefore initiatives
such as standard diet (heart foundation cookbook) Potassium.
Potassium is essential in maintaining the amount of sodium in your
cells. A deficiency of potassium, may result in a rise in sodium blood-
levels. vitamin D . It's uncertain if having too little vitamin D in your diet
can lead to high blood pressure. Vitamin D may affect an enzyme
produced by your kidneys that affects your blood pressure. The Journal
of Steroid Biochemistry and Molecular Biology
Volumes 8990, May 2004, Pages 387392
Proceedings of the 12th Workshop on Vitamin D
Vitamin D: a negative endocrine regulator of the reninangiotensin system and
blood pressure

Yan Chun Li
a,
<img alt="Corresponding author contact information"
src="http://origin-cdn.els-cdn.com/sd/entities/REcor.gif">
,
<img
src="http://origin-cdn.els-cdn.com/sd/entities/REemail.gif" alt="E-mail the
corresponding author">, Guilin Qiao
a
, Milan Uskokovic
b
, Wei Xiang
a
, Wei
Zheng
a
, Juan Kong
a

o
o Drinking too much alcohol. Over time, heavy drinking can damage
your heart. Having more than two drinks a day can raise your blood
pressure.

Stress. High levels of stress can lead to a temporary, but dramatic, increase in
blood pressure. If you try to relax by eating more, using tobacco or drinking
alcohol, you may only increase problems with high blood pressure.. as well as
anger, can also raise your blood pressure. Surges of hormones produced during
stress can narrow your arteries and worsen angina. Stress management and
support.
Certain chronic conditions. Certain chronic conditions also may increase your
risk of high blood pressure,
o including high cholesterol,
o diabetes,
o kidney disease and
o sleep apnea.

http://www.mayoclinic.org/diseases-conditions/high-blood-pressure/basics/risk-
factors/con-20019580
Angina risk Factors
Diabetes. Diabetes is the inability of your body to produce enough or respond to
insulin properly. Insulin, a hormone secreted by your pancreas, allows your body
to use glucose, which is a form of sugar from foods. Diabetes increases the risk
of coronary artery disease, which leads to angina and heart attacks by speeding
up atherosclerosis and increasing your cholesterol levels.
High blood pressure. Blood pressure is determined by the amount of blood your
heart pumps and the amount of resistance to blood flow in your arteries. Over
time, high blood pressure damages arteries by accelerating hardening of the
arteries.
High blood cholesterol or triglyceride levels. Cholesterol is a major part of the
deposits that can narrow arteries throughout your body, including those that
supply your heart. A high level of the wrong kind of cholesterol, known as low-
density lipoprotein (LDL) cholesterol (the "bad" cholesterol), increases your risk of
angina and heart attacks. A high level of triglycerides, a type of blood fat related
to your diet, also is undesirable
http://www.mayoclinic.org/diseases-conditions/angina/basics/risk-
factors/CON-20031194

Heart attack risk factors
Certain factors contribute to the unwanted buildup of fatty deposits (atherosclerosis)
that narrows arteries throughout your body, including arteries to your heart. You can
improve or eliminate many of these risk factors to reduce your chances of having a
first or subsequent heart attack.
Heart attack risk factors include:
High blood pressure. Over time, high blood pressure can damage arteries that
feed your heart by accelerating atherosclerosis. High blood pressure that occurs
with obesity, smoking, high cholesterol or diabetes increases your risk even
more.
High blood cholesterol or triglyceride levels. Cholesterol is a major part of the
deposits that can narrow arteries throughout your body, including those that
supply your heart. A high level of the wrong kind of cholesterol in your blood
increases your risk of a heart attack. Low-density lipoprotein (LDL) cholesterol
(the "bad" cholesterol) is most likely to narrow arteries. A high level of
triglycerides, another type of blood fat related to your diet, also ups your risk of
heart attack. However, a high level of high-density lipoprotein (HDL) cholesterol
(the "good" cholesterol), which helps the body clean up excess cholesterol, is
desirable and lowers your risk of heart attack.
Diabetes. Diabetes is the inability of your body to adequately produce insulin or
respond to insulin need properly. Insulin, a hormone secreted by your pancreas,
allows your body to use glucose, which is a form of sugar from foods. Diabetes,
especially uncontrolled diabetes, increases your risk of a heart attack.
Family history of heart attack.
.
Illegal drug use. Using stimulant drugs, such as cocaine or amphetamines, can
trigger a spasm of your coronary arteries that can cause a heart attack.
A history of preeclampsia. This condition causes high blood pressure during
pregnancy, and increases the lifetime risk of heart disease.
http://www.mayoclinic.org/diseases-conditions/heart-attack/basics/risk-
factors/CON-20019520

Education

Resistance and pharmacovigilance

Research
Gene therapy Current Perspectives on the Use of Gene Therapy for
Hypertension
1. Craig H. Gelband,
2. Michael J. Katovich,
3. Mohan K. Raizada
Circulation Research. 2000; 87: 1118-1122


Current Perspectives on the Use of Gene Therapy for Hypertension
1. Craig H. Gelband,
2. Michael J. Katovich,
3. Mohan K. Raizada
+ Author Affiliations
1. From the Department of Physiology, College of Medicine (C.H.G., M.K.R.) and
Department of Pharmacodynamics, College of Pharmacy (M.J.K.), University
of Florida, Gainesville, Fla.
1. Correspondence to Craig H. Gelband, PhD, Department of Physiology,
University of Florida College of Medicine, PO Box 100274, Gainesville, FL
32610-0274. E-mail gelband@phys.med.ufl.edu

Next Section
Abstract
AbstractSystemic hypertension is a pathophysiological state that is manifested as
high blood pressure and is a major risk factor for stroke, ischemic heart disease,
peripheral vascular disease, and progressive renal damage. Pulmonary hypertension
occurs in 3 distinct forms: primary pulmonary hypertension, pulmonary hypertension
of the newborn, or secondary pulmonary hypertension attributable to a variety of lung
and cardiovascular diseases. This review discusses the use of gene therapy in the
control of systemic and pulmonary hypertension. Overexpression of vasodilator
genes as well as antisense knockdown of vasoconstrictor genes has been
successfully used in animal models of both forms of hypertension. Furthermore, the
use of viral vectors to deliver these constructs has achieved long-term control of
hypertension. The successful establishment of gene therapy techniques in the
animal models of hypertension coupled with the anticipated advances in the genetic
aspects of this disease would make it highly feasible to attempt gene delivery in the
control of human hypertension.
Introduction
Systemic hypertension is a complex pathophysiological state that is primarily
manifested as chronic high blood pressure. If unchecked, it is a major risk factor for
stroke, ischemic heart disease, peripheral vascular disease, and progressive renal
damage.
1

2

3
It is well established that a hyperactive renin-angiotensin system (RAS)
plays a key role in the development and maintenance of human primary
hypertension and, by some estimates, contributes to at least 10% to 30% of all cases
of hypertension.
4

5

6
It is not surprising that tremendous efforts have been directed
toward the understanding of the RAS and its involvement in the control of blood
pressure. The interruption of the RAS attenuates high blood pressure and many
pathophysiological aspects of hypertension.
1

5

7

8

9

10
Also, some genes encoding
members of the RAS are associated with hypertension.
11

12

13

14

15
Thus, it is
reasonable to conclude that the RAS is essential in the normal regulation of blood
pressure and pathophysiology of systemic hypertension.
Traditional agents such as diuretics, -blockers, and calcium-channel antagonists
have been used to treat systemic hypertension. Recently, a group of
antihypertensive agents targeting the RAS that act by inhibiting either the formation
of angiotensin II (Ang II) or the actions of Ang II have been used. These agents are
reliable and affordable, and their short duration of action makes them an excellent
choice for reversible drugs. However, they are not without limitations and
disadvantages. As with most antihypertensive drugs, their effects are short-lived,
have to be administered on a regular basis, and produce significant side effects.
These limitations have often led to problems with compliance with some patients.
Finally, all of the therapeutic agents are excellent in the control of blood pressure but
hold little promise in a cure, because discontinuing the drugs results in the
reappearance of high blood pressure and related cardiovascular pathophysiological
symptoms of the disease.
In addition to systemic hypertension, pulmonary hypertension is a cardiovascular
disease with significant morbidity and mortality. In pulmonary hypertension, the
mean pulmonary arterial pressure is >20 mm Hg at rest. This disorder occurs in 3
distinct forms: primary pulmonary hypertension, pulmonary hypertension of the
newborn, and secondary pulmonary hypertension.
16
The cellular and physiological
mechanisms of this form of hypertension are poorly defined; thus, there are few
effective pharmacological agents that are used clinically. The drugs presently in use
are anticoagulants, calcium-channel antagonists, intravenous prostacyclin, and
inhaled nitric oxide; however, none of these agents has significantly reduced the
mortality attributable to pulmonary hypertension. From the discussion above it can
be concluded that pharmacological regimens have reached a conceptual plateau for
the treatment and long-term prevention of hypertension and that a cure for either
systemic or pulmonary hypertension is not on the horizon.
For this reason, many investigators have turned their attention to explore a gene
therapy strategy.
17

18
They have argued that genetic manipulation may induce a
permanent correction, resulting in a possible cure for hypertension. On a conceptual
level, such an approach could offer major advantages over pharmacological therapy.
It could essentially eliminate the compliance and side-effect issues when using
conventional therapy. In addition, a genetic strategy could lead to a permanent
control of hypertension if appropriate target genes controlling hypertension could be
identified and their expression could be regulated.
Gene Therapy for Systemic Hypertension
Overexpression of Vasodilator Genes
Genes relevant to both vasodilation and vasoconstriction are successful targets for
gene therapy in systemic hypertension. Chao and colleagues
19

20

21

22

23
have
reversed systemic hypertension in adult rats by overexpressing the vasodilator
genes atrial natriuretic peptide, kallikrein, adrenomedullin, and endothelial nitric
oxide synthase (eNOS). They demonstrated that delivery of these genes, either via
naked DNA or viral delivery systems, in different rat models of hypertension
(spontaneously hypertensive rat [SHR], Dahl salt-sensitive rat, deoxycorticosterone
acetatetreated rat, and Goldblatt hypertensive rat) results in a lowering of blood
pressure that is transient in nature, lasting anywhere from 6 to 12 weeks.
Specifically, in the above models, the overexpression of kallikrein, atrial natriuretic
peptide, adrenomedullin, and eNOS caused a 22 to 50, 22, 28, and 21 mm Hg
change in blood pressure, respectively, over a period of 6 to 12 weeks after delivery.
This decrease in blood pressure is accompanied by a transient attenuation of some
pathophysiological changes observed in the major target organs (heart, kidney, and
blood vessels) associated with hypertension.
Antisense Knockdown of the RAS
The use of antisense gene therapy to target vasoconstrictor pathways has been
quite successful in lowering blood pressure and preventing or reversing the
associated cardiovascular pathophysiology of hypertension on a long-term basis.
The RAS has been the target of choice for antisense gene therapy in the treatment
of systemic hypertension. There are multiple reasons for this. First, the role of the
RAS in hypertension is well understood. Second, the RAS provides an ideal target
for gene delivery, because it is widely distributed. Third, pharmacological agents that
target the RAS exert antihypertensive effects at multiple levels (vasodilator
mechanisms and fibrinolytic and oxidative stress pathways) in addition to their
actions on Ang II.
17

Conceptual support that antisense targeting of the RAS would be effective in treating
hypertension was derived from the use of antisense oligonucleotides.
24

25

26
Studies
demonstrated that the central or peripheral injection of antisense oligonucleotides to
the RAS (angiotensinogen or angiotensin II type 1 receptor [AT
1
R]) resulted in a
transient, short-term (days), and modest, but significant, effect on lowering blood
pressure in the SHR. The amount (23 mm Hg) and duration (9 weeks) of the blood
pressurelowering effect were prolonged to weeks with the use of an adeno-
associated virus viral vector delivery system.
27

Our research group has used these studies as a basis to determine if retroviral-
vectormediated delivery of antisense targeting the AT
1
R and angiotensin-converting
enzyme (ACE) would prevent hypertension (high blood pressure) and cardiovascular
pathophysiology associated with hypertension for longer time periods.
17

28

29

30
A
single intracardiac administration of retroviral particles containing AT
1
R antisense
(AT
1
R-AS) into 5-day-old SHR results in attenuation of high blood pressure and long-
term expression of the AT
1
R-AS for at least 210 days. This attenuation of blood
pressure is similar to that seen for AT
1
R antagonists. This was associated with
complete attenuation of cardiac hypertrophy, arterial wall thickness, and perivascular
and myocardial fibrosis. AT
1
R-AS expression also resulted in significant reduction in
the amount of neointimal formation after carotid artery balloon injury in the SHR
(Figure). AT
1
R-AS prevented alterations in vascular reactivity, endothelial
dysfunction, Ca
2+
handling, and ion channel dysfunction in renal arterioles. These
studies established that AT
1
R-AS will abolish the development of hypertension in the
SHR on a long-term basis.

View larger version:
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Figure 1.
Effect of AT
1
R-AS on vascular growth after carotid artery balloon injury in the SHR.
Top, AT
1
R-AS and losartan inhibit neointima formation after arterial balloon injury.
Bar=70 m. Bottom, Mean effect of AT
1
R-AS (n>5, *P<0.05).
Intracardiac injection of virus particles containing AT
1
R-AS into the adult SHR
resulted in a 30- to 60-mm Hg reduction in blood pressure that was maintained for up
to 36 days compared with the SHR treated with virus alone.
31
This was accompanied
by a reversal of the increase in vasoreactivity and the gain of endothelial function in
renal resistance arterioles. These observations are consistent with studies that have
previously shown a similar transient reversal of high blood pressure by antisense in
the adult rat.
24

25

26

27
Collectively, these data demonstrate that virally mediated gene
delivery of AT
1
R-AS can effectively reduce blood pressure and reverse renovascular
pathophysiology associated with hypertension in the adult SHR. However, the
transient nature of the antihypertensive effect in the adult remains to be addressed
and must be improved on.
Also relevant would be determining if antisense gene targeting could clarify the role
of the tissue RAS in cardiovascular pathophysiology. This is clinically relevant in
view of the recent results from the Heart Outcomes Prevention Evaluation clinical
study.
32
This study showed that ramipril, an ACE inhibitor, produced a significant
improvement in outcomes and reduction in deaths attributable to cardiovascular
causes without a significant change in blood pressure. Introduction of ACE antisense
(ACE-AS) by a retroviral vector resulted in a modest (15 to 18 mm Hg) but significant
attenuation of high blood pressure exclusively in the SHR for 100 days.
33

34
In spite
of this modest decrease in blood pressure, ACE-AS resulted in complete attenuation
of ventricular hypertrophy and prevention of altered endothelial function, vascular
reactivity, [Ca
2+
]
i
, and ion channel dysfunction. The data provide support for the
importance of the tissue RAS emphasized in the results of the Heart Outcomes
Prevention Evaluation trial.
In summary, the above data illustrate that an interruption of the RAS activity at a
genetic level could prevent hypertension on a long-term basis. Support for this
hypothesis is provided by several experiments. The F
1
and F
2
generation offspring of
the AT
1
R-AStreated SHRs expressed a persistently lower blood pressure,
decreased cardiac hypertrophy and fibrosis, decreased medial thickness, and
normalization of renal artery excitation-contraction coupling, Ca
2+
current, membrane
potential, K
v
current, and [Ca
2+
]
i
compared with offspring derived from the virus-
treated SHRs.
30
In addition, AT
1
R-AS was found in the genomic DNA and was
expressed in cardiovascularly relevant tissue of the F
1
and F
2
offspring. The
transmission of antihypertensive phenotypes to the offspring was also seen in the
ACE-AStreated SHRs.
33

34
The mechanism of transmission of this antihypertensive
phenotype to the offspring is unknown at the present time but might involve germ line
transmission of the antisense, parental environment, transmission of a humoral
factor through the breast milk, or expression at a critical stage of SHR
development.
35

36

37

38

39
For example, cross studies have shown that SHR babies
parented by WKY mothers express a significantly lower blood pressure, while WKY
babies parented by SHR mothers are hypertensive.
36

37

Antisense Knockdown of the
1
-Adrenergic Receptors
Zhang et al
40
have used antisense oligonucleotides to the
1
receptor to provide
additional conceptual support for gene therapy in hypertension. A single intravenous
injection of
1
receptor
Previous SectionNext Section
Gene Therapy for Pulmonary Hypertension
It has only been in the last 2 years that gene therapy for treatment of pulmonary
hypertension has begun. The overexpression of vasodilator genes, eNOS, prepro-
calcitonin generelated peptide (CGRP), and prostaglandin I synthase (PGIS) has
shown great promise in the laboratory for treatment of pulmonary hypertension.
Patients with severe pulmonary hypertension have a PGIS deficiency of their
precapillary vessels, but the importance of this deficiency for lung vascular
remodeling remains unclear. Geraci et al
42
hypothesized that selective pulmonary
overexpression of PGIS may prevent the development of pulmonary hypertension.
Transgenic mice were created with selective pulmonary PGIS overexpression. The
mice overexpressing PGIS produced 2-fold more pulmonary 6-keto prostaglandin F
1

than controls, and, after exposure to chronic hypobaric hypoxia, the PGIS-
overexpressing mice showed a lower right ventricular systolic pressure than controls.
Histological examination of the lungs revealed nearly normal arteriolar vessels in the
PGIS-expressing mice in comparison with vessel-wall hypertrophy in the control
mice. These studies demonstrate that overexpression of PGIS in the lung protected
mice from the development of pulmonary hypertension after exposure to chronic
hypoxia.
Using adenoviral gene transfer of eNOS to the mouse lung, Champion et al
43

showed the beneficial effects of this gene on pulmonary hemodynamics. At 21 to 28
days after gene transfer, the pressure-flow relationship in the pulmonary vascular
bed was shifted to the right in animals transfected with eNOS, and pulmonary
pressor responses to endothelin-1, Ang II, and ventilatory hypoxia were reduced
significantly in animals transfected with the eNOS gene. In preliminary findings, this
same group demonstrated that not only did the eNOS knockout mouse have
pulmonary hypertension (pulmonary artery pressure 25 mm Hg), but when the
eNOS gene was delivered back to the lung of the knockout mouse using an
adenoviral construct, no pulmonary hypertension developed in the knockout.
44

CGRP is also believed to play an important role in maintaining low pulmonary
vascular resistance and modulating pulmonary vascular responses to chronic
hypoxia. Intratracheal administration of prepro-CGRP with an adenovirus to the
mouse lung, followed by 16 days of chronic hypoxia, caused an attenuation of the
hypoxic-induced increases in pulmonary vascular resistance, right ventricular mass,
pulmonary artery pressure, and pulmonary vascular remodeling.
45
These recent
findings suggest that the use of gene therapy targeting vasodilator agents in the lung
may be successful in the treatment of pulmonary hypertension.
Future Directions and Conclusions
It is evident from the above discussion that the use of gene therapy is an exciting
approach that is intellectually sound and, on the basis of animal experiments, may
hold great promise for a permanent treatment of hypertension. However, before
leaping to the next step (eg, clinical trials), several important issues must be resolved
and hurdles must be cleared. First, are the viral vectors the most effective means to
deliver an antihypertensive gene? Benefit versus risk consideration of viral vectors
may lead us to compromise and develop better means to deliver more effective and
highly stable naked DNA that will have prolonged duration of action of desired
effects. However, if viral vectors are the method of choice, they must meet strict
safety requirements. For example, it would be imperative that the integrations site of
the viral vector in the genome be known and that its influence on neighboring genes
be evaluated and proven to be free of immune and other adverse side effects.
Second, other gene targets that may be relevant in hypertension must be explored.
For example, the targeting of matrix proteins could be a potentially interesting site of
gene therapy for hypertension. This is relevant in view of the fact that therapies using
secreted molecules may not require as high a degree of transduction as do therapies
that require intracellular expression of proteins or antisense. Cowan et al
46
showed
that progression of pulmonary hypertension is associated with increased serine
elastase activity and the proteinase-dependent deposition of tenascin-C. In
monocrotaline-treated rats, oral administration of serine elastase inhibitors increased
survival and decreased pulmonary artery pressure and muscularization. This was
attributable to myocyte apoptosis and loss of extracellular matrix, specifically elastin
and tenascin-C. Therefore, it seems plausible that targeting extracellular matrix
proteins may also be beneficial in vascular disorders. It would also be interesting to
develop a strategy that would target antisense knockdown of Ca
2+
channels using a
smooth muscle cellspecific promoter. Finally, cell-specific overexpression of
signaling molecules that may be vasodilator in nature (ie, protein kina
In conclusion, there is sufficient evidence to indicate that gene therapy may be an
important and significant step forward in the long-term treatment and possible cure of
both systemic and pulmonary hypertension. It is quite possible that hypertension-
relevant genes could be identified in the near future. The establishment of the
conceptual basis for gene therapy in the animal models of hypertension coupled with
the anticipated advances in the genetic aspects of this disease would make it highly
feasible to attempt gene delivery in the control of human hypertension
Acknowledgments
This work was supported by National Institutes of Health grants HL-52189 (to
C.H.G.) and HL-56921 (to M.K.R. and M.J.K.) and by the American Heart
Association, Florida Affiliate.
2000 American Heart Association, Inc.


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Gelband CH, Reaves PY, Evans J, Wang H, Katovich MJ, Raizada MK.
Angiotensin II type 1 receptor antisense gene therapy prevents altered
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Hypertension. 2000;35:209213.
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Anti-anginal therapy has long been dominated by the use of beta-blockers,
Ca(2+) channel blockers and nitrates. Most recently, ranolazine was introduced
as a new anti-anginal class. This review article presents current and novel anti-
anginal strategies under development. A discussion of their molecular
mechanisms that may complement traditional therapies is presented. Medline
and PubMed scientific search tools were primarily used to identify relevant
literature dating from 1970 to 2008

myocardial gene therapy and gene expression in angina pectoris
Rck, Andreas
Date: 2006-04-21
Location: Frelsningssalen M63, Karolinska Universitetssjukhuset, Huddinge
Time: 9.00
Department: Institutionen fr medicin, Huddinge Sjukhus / Department of Medicine at
Huddinge University Hospital
Abstract:
Background Angiogenesis does not fully counteract myocardial ischemia in stable
angina pectoris. Refractory angina pectoris, with remaining symptoms despite
medication and no possibility for bypass surgery or angioplasty, is rather common.
Angiogenic gene therapy is a novel treatment strategy for these patients. Methods
and results In study I, six patients with refractory angina received intramyocardial
injections of 0.25-1 mg plasmid encoding Vascular Endothelial Growth Factor
(phVEGF-A165) via thoracotomy. The peak systolic velocity improved in all six
patients but perioperative myocardial infarction occurred in two patients. Study II was
a double-blind randomised controlled trial of the same plasmid or placebo plasmid
(0.5 mg), delivered via a percutaneous catheter system in 80 patients with refractory
angina. Reversible perfusion defects and wall motion improved in the phVEGF-
A165-treated area compared to placebo. Nitroglycerin use tended to decrease with
active treatment while symptom class and exercise capacity showed no effect
beyond placebo. Five catheter-related adverse events occurred but no adverse
effects were related to the plasmid. In study III, the prognosis of refractory angina
was assessed in all 225 patients screened for study II. The mortality was 10.6% at
three years. The baseline screening angiogram found revascularisation options in
10% of patients, although previous examinations had ruled out such possibilities.
After twelve months, 36% of the trial patients had improved by at least two symptom
classes and 37% had increased their exercise time by at least 60 seconds, with no
difference between placebo and active groups. In study IV-V, the gene expression
pattern in a reversibly ischemic myocardial area was compared to a normal area in
eight patients with stable angina pectoris. Real-time polymerase chain reaction
showed increased expression of ANP and BNP but not of VEGF and VEGF receptor
1 and 2 in reversibly ischemic myocardium. In microarray measurements, 15
additional known angiogenesis stimulators lacked differential expression. Instead, we
found increased expression of several other genes with potential angiogenic,
angiogenesis inhibiting, anti-apoptotic and muscle-related function but with yet
unknown role in the myocardium. Conclusions Intramyocardial phVEGF-A165 is safe
and increases myocardial perfusion in patients with stable angina pectoris. The
effect on symptoms should be tested in a larger trial. Patients with refractory angina
pectoris have a rather low mortality and symptomatic improvement is common.
Overexpressing VEGF (or other angiogenic factors) seems a rational strategy, as
most angiogenesis stimulators not are overexpressed in ischemic myocardium in
stable angina. The ischemia-related overexpression of ANP, BNP and other genes
with a probable anti-angiogenic function might be a limiting factor in angiogenesis.

http://publications.ki.se/xmlui/handle/10616/38926?locale-attribute=en

interventions



BACKGROUND
Salt reduction strategies are a best buy in the prevention of NCDs
Non-communicable diseases (NCDs), also known as diseases of lifestyle, are one of
the leading causes of deaths and disability in South Africa (SA), second only to
HIV/AIDS. Cardiovascular disease (CVD), which refers to heart disease and stroke,
is the most common NCD, yet up to 80% of CVD-related deaths in young people (<
65 years) are preventable though a healthy lifestyle. The incidence of CVD in SA is
increasing and is occurring more frequently in young people who are in their most
productive years. This impacts negatively on our labour force and burdens an
already flagging health-care system, posing a social and economic developmental
challenge by virtue of its costly complications, and early death.
Of the various risk factors contributing to heart disease and stroke, hypertension has
the largest impact. Hypertension is responsible for 50% of strokes, 42% of ischaemic
heart disease, 72% of hypertensive heart disease and 22% of other cardiovascular
disease burden in SA. South Africans carry a massive burden of high blood pressure
with 1 in 3 adults affected. While research shows approximately 6 million people 15
years and older are hypertensive, more than 50% are undiagnosed. It is estimated to
have caused 46 888 deaths and 390 860 disability-adjusted life years in 2000.
Hypertension alone is the leading reason for attending primary health-care, and is
the most common diagnosis (13.1%) in South Africa
1
.
The association of high salt intake on increasing blood pressure is well documented,
and in SA a key driver of the huge burden of hypertension. We consume between
two to three times the daily recommendations, which according to the World Heart
Organisation (WHO) should be less than 5 grams of salt per day. Hence the
Departments of Healths National Strategic Framework to Address NCDs aims to:
1. Reduce mean population intake of salt to < 5grams per day by 2020.
2. Reduce the prevalence of people with raised blood pressure by 20% by 2020
(through lifestyle and medication).
In a ground-breaking move in March 2013, SAs Minister of Health signed legislation
to reduce salt levels in certain foodstuffs (Government Gazette: No.R.214, under
section 15(1) of the Foodstuffs, Cosmetics and Disinfectants Act 1972 (Act 54 of
1972)). The legislation will limit salt levels in some of our most commonly consumed
foods such as bread, breakfast cereals, margarines and fat spreads, savoury
snacks, processed meats and raw-processed meat sausages, dry soup and gravy
powders and stock cubes
2
. This makes SA the first country in the world to legislate
salt levels, with the rest of the world watching SA closely.
However, global best practice shows that accompanying public education is a best
buy to change behaviors and lower salt consumption. Salt-reducing initiatives
without intensive public education generally fail. Countries like Finland and the
United Kingdom have successfully reduced their rates of hypertension, heart disease
and stroke through population-wide strategies that combined voluntary participation
from food producers and parallel public education and awareness campaigns. In
South Africa, our Health Ministry opted for a strategy combining legislation and
public education.
In addition, we know that discretionary salt is a significant source of salt amongst
South Africans. South Africans have amongst the highest use of discretionary salt in
the world, with up to 40% of salt added during cooking and at the table (compared
with 10% in the US). This strengthens the rationale for a national education and
awareness campaign to get South Africans to reduce their discretionary salt intake
3
.
The National Department of Health together with the working group tasked with the
salt-reduction regulation agreed that a massive public awareness campaign is
needed in South Africa, for greater impact of the legislation, and on public health.
Consequently, with the support of the Department of Health, Industry and scientific
experts, Salt Watch South Africa (SW) was formed to drive the national awareness
campaign and lobby stakeholders for a multisectoral collaborative approach. The
Heart and Stroke Foundation South Africa (HSF) was tasked with coordinating the
campaign, based on its independence.
Most South Africans eat more than the World Health Organisations (WHO)
recommended maximum of 5 g/day (about 1 teaspoon). Data from various studies
have shown that the average salt intake in South Africa is between 6 and 11 g/day,
double the WHO limit!
Comparing the sodium content of foods:
Look at the number for sodium in the per 100g column in the Nutritional Information
table, and compare the value for similar products.
Choose the product with the least amount of sodium.
Use the table below to decide if the food is high or low in sodium.
Foods in the low group can be eaten more often, but foods in the high group
should be eaten seldom or on special occasions.
To calculate the salt content of a product:
Take the sodium (Na) content (in milligrams) per 100g in the Nutritional Information
table.
Divide it by 1000 to get the grams of sodium.
Then multiply that by 2.5 to reach salt content of food (in grams).
Use the table below to decide if the food is high or low in salt.
Those with a salt content of less than 0.3g per 100g of salt are considered to be low
in salt, and can be eaten more often, foods with between 0.3 and 1.5 g per 100g of
salt have a moderate salt content, and can be eaten in moderation, but high salt
foods are those with more than 1.5 g per 100g of salt, and should be limited, or only
eaten seldomly.

Use the table below as a guide to make shopping easier

- See more at: http://www.heartfoundation.co.za/salt-
watch#sthash.GN9Ms06m.dpuf


http://www.heartfoundation.co.za/salt-watch

Endocrine Hypertension
Hypertension - or high blood pressure - affects millions of Americans. Endocrine
hypertension is a subset of hypertension caused by hormone imbalance, most
frequently involving the pituitary or adrenal gland. Patients who develop hypertension
before the age of 30 who have a strong family history of hypertension, adrenal
tumors, or develop a low potassium level (hypokalemia) should be screened for
endocrine hypertension. Patients who have poor blood pressure control despite
taking three or more blood pressure medications (resistant hypertension) should also
be screened.
Endocrine Hypertension Disorders
Endocrine hypertension can be caused when glands produce too much or not
enough hormone, or when they are affected by tumors.
Primary Aldosteronism
The most common form of endocrine hypertension, primary aldosteronism affects an
estimated 5 percent to 10 percent of all patients with hypertension and is often under
diagnosed. Excessive aldosterone production by the adrenal glands leads to fluid
retention, loss of potassium and hypertension. If untreated, hyperaldosteronism may
cause an enlarged heart.
Primary aldosteronism is diagnosed through blood and urine tests, and a CT scan of
the adrenal glands. In some cases, adrenal vein sampling may be necessary to help
differentiate the cause of the primary aldosteronism.
Forms of the disorder include:
Conn's syndrome a common subtype caused by a single adrenal tumor.
Surgery to remove the tumor is an effective treatment.
Bilateral adrenal hyperplasia a common subtype caused by enlarged adrenal
glands. This disorder is best treated with medications such as spironolactone and
eplerenone.
Primary adrenal hyperplasia a rare subtype in which only one gland is
enlarged. Surgery is the preferred treatment.
Glucocorticoid remediable aldosteronism (GRA) a rare subtype caused by a
genetic mutation, often occurring in many family members.
Familial hyperaldosteronism a rare subtype in which about half of each
generation develops hyperaldosteronism.
Cushings Syndrome
Cushing's syndrome occurs when too much cortisol is produced by the adrenal
glands. People with Cushings syndrome often have other endocrine-related
disorders, including diabetes, obesity, hypertension, kidney stones and osteoporosis.
Many patients also suffer from depression.
Pheochromocytoma
Phecohromocytoma is a rare syndrome caused by tumors of the adrenal glands.
These tumors produce excessive amounts of adrenaline, noradrenaline or other
catecholamines. Though rare, patients with adrenal tumors should be tested for
pheochromocytoma as about 10 percent of tumors are malignant.
Common symptoms are sweating, palpitations and headache, though patients can
also have many other symptoms. Patients with a pheochromocytoma may have
episodic or sustained hypertension. Some patients experience very high blood
pressure readings known as hypertensive crisis, which is a medical emergency.
One in 10 people with pheochromocytoma has tumors located outside the adrenal
glands. These extra-adrenal pheochromocytomas are also known as
paragangliomas.
Acromegaly
Acromegaly is a tumor of the pituitary gland that leads to excess growth hormone.
Symptoms include joint and muscle problems, headache and vision problems.
Affected patients tend to have very large hands, feet and tongue, and a prominent
jaw. They can develop hypertension and diabetes.
Hyperthyroidism or Hypothyroidism
These disorders, if severe and untreated, can be associated with elevated blood
pressure. Treatment of the thyroid disorder usually lowers the blood pressure to
normal.
Other Causes of Endocrine Hypertension and Related Syndromes:
Pseudohypoaldosteronism type 2 (Gordons syndrome) patients develop
hypertension and have high potassium levels (hyperkalemia)
Liddles syndrome a rare genetic form of hypertension in which patients have
very low levels of aldosterone (pseudoaldosteronism)
Apparent mineralocorticoid excess (AME) a rare genetic form of
hypertension
Licorice ingestion high blood pressure and low potassium triggered by eating
licorice (usually black).
Bartters syndrome detected in infancy or childhood with symptoms of severe
low potassium (hypokalemia) and other birth defects. No associated hypertension.
Gitelmans syndrome milder form of hypokalemia occurring in young adults,
often with low magnesium levels as well. No associated hypertension.



Oxford Journals
Medicine
Cardiovascular Research
Volume 53, Issue 3
Pp. 688-708.
Gender has an important influence on blood pressure, with premenopausal women
having a lower arterial blood pressure than age-matched men. Compared with
premenopausal women, postmenopausal women have higher blood pressures,
suggesting that ovarian hormones may modulate blood pressure. However, whether
sex hormones are responsible for the observed gender-associated differences in
arterial blood pressure and whether ovarian hormones account for differences in
blood pressure in premenopausal versus postmenopausal women remains unclear.
In this review, we provide a discussion of the potential blood pressure regulating
effects of female and male sex hormones, as well as the cellular, biochemical and
molecular mechanisms by which sex hormones may modify the effects of
hypertension on the cardiovascular system.

https://www.nhlbi.nih.gov/health/health-topics/topics/angina/
at Is Angina?
Angina (an-JI-nuh or AN-juh-nuh) is chest pain or discomfort that occurs if an area of
your heart muscle doesn't get enough oxygen-rich blood.
Angina may feel like pressure or squeezing in your chest. The pain also can occur in
your shoulders, arms, neck, jaw, or back. Angina pain may even feel like indigestion.
Angina isn't a disease; it's a symptom of an underlying heart problem. Angina usually
is a symptom of coronary heart disease (CHD).
CHD is the most common type of heart disease in adults. It occurs if a waxy
substance called plaque (plak) builds up on the inner walls of your coronary arteries.
These arteries carry oxygen-rich blood to your heart.
Plaque Buildup in an Artery

Figure A shows a normal artery with normal blood flow. The inset image shows a
cross-section of a normal artery. Figure B shows an artery with plaque buildup. The
inset image shows a cross-section of an artery with plaque buildup.
Plaque narrows and stiffens the coronary arteries. This reduces the flow of oxygen-
rich blood to the heart muscle, causing chest pain. Plaque buildup also makes it
more likely that blood clots will form in your arteries. Blood clots can partially or
completely block blood flow, which can cause a heart attack.
Angina also can be a symptom of coronary microvascular disease (MVD). This is
heart disease that affects the hearts smallest coronary arteries. In coronary MVD,
plaque doesn't create blockages in the arteries like it does in CHD.
Studies have shown that coronary MVD is more likely to affect women than men.
Coronary MVD also is called cardiac syndrome X and nonobstructive CHD.
Types of Angina
The major types of angina are stable, unstable, variant (Prinzmetal's), and
microvascular. Knowing how the types differ is important. This is because they have
different symptoms and require different treatments.
Stable Angina
Stable angina is the most common type of angina. It occurs when the heart is
working harder than usual. Stable angina has a regular pattern. (Pattern refers to
how often the angina occurs, how severe it is, and what factors trigger it.)
If you have stable angina, you can learn its pattern and predict when the pain will
occur. The pain usually goes away a few minutes after you rest or take your angina
medicine.
Stable angina isn't a heart attack, but it suggests that a heart attack is more likely to
happen in the future.
Unstable Angina
Unstable angina doesn't follow a pattern. It may occur more often and be more
severe than stable angina. Unstable angina also can occur with or without physical
exertion, and rest or medicine may not relieve the pain.
Unstable angina is very dangerous and requires emergency treatment. This type of
angina is a sign that a heart attack may happen soon.
Variant (Prinzmetal's) Angina
Variant angina is rare. A spasm in a coronary artery causes this type of angina.
Variant angina usually occurs while you're at rest, and the pain can be severe. It
usually happens between midnight and early morning. Medicine can relieve this type
of angina.
Microvascular Angina
Microvascular angina can be more severe and last longer than other types of angina.
Medicine may not relieve this type of angina.
Overview
Experts believe that nearly 7 million people in the United States suffer from angina.
The condition occurs equally among men and women.
Angina can be a sign of CHD, even if initial tests don't point to the disease. However,
not all chest pain or discomfort is a sign of CHD.
Other conditions also can cause chest pain, such as:
Pulmonary embolism (a blockage in a lung artery)
A lung infection
Aortic dissection (tearing of a major artery)
Aortic stenosis (narrowing of the hearts aortic valve)
Hypertrophic cardiomyopathy (KAR-de-o-mi-OP-ah-thee; heart muscle
disease)
Pericarditis (inflammation in the tissues that surround the heart)
A panic attack
All chest pain should be checked by a doctor.