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Symptom and Treatment of
Heart Disease
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Introduction to Heart Disease
Heart is one of the most important organs in our bodies.
Essentially a pump, the heart is a muscle made up of four
chambers separated by valves and divided into two
halves. Each half contains one chamber called an atrium
and one called a ventricle. The atria (plural for atrium)
collect blood, and the ventricles contract to push blood
out of the heart.
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Figure: Human heart.
The right half of the heart pumps oxygen-poor blood
(blood that has a low amount of oxygen) to the lungs
where blood cells can obtain more oxygen. Then, the
newly oxygenated blood travels from the lungs into the
left atrium and the left ventricle. The left ventricle pumps
the newly oxygen-rich blood to the organs and tissues of
the body. This oxygen provides our body with energy and
is essential to keep our body healthy.
Heart disease is a term that applies to a large number of
medical conditions relating to the heart. These medical
conditions relate to the abnormal health conditions that
directly affect the heart and all its components. Heart
disease is a major health problem within some cultures.
One theory for heart disease is the radical changes within
our lifestyles. People are often less active and eat diets
high in fats. Takeaway food is abundant today and often
people will eat it due to the increased availability. Some
takeaway outlets are now helping cater to a healthier
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lifestyle by offering a variety of healthy dishes such as
salads. People are becoming more aware of the risk of
heart disease and choosing to change their diets. Exercise
is extremely important in order to avoid heart disease.
Exercise helps to keep the heart in peak performance. By
using a combination of exercise and a balanced diet, the
risk of heart disease is greatly decreased.
The term Cardiovascular Disease covers a large number
of diseases that directly affect the heart and the blood
vessel system. It especially affects the veins and arteries
that lead to and from the heart. Research has suggested
that women who suffer with cardiovascular disease
usually suffer from forms that affect the blood vessels.
While men usually suffer from forms that affect the heart
muscle itself. Other known or associated causes of
cardiovascular disease include diabetes mellitus,
hypertension and hypercholesterolemia. Heart disease and
strokes are other common cardiovascular diseases. Two
independent risk factors that have a major impact for
heart diseases, cardiovascular diseases, are high blood
pressure and high blood cholesterol.
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Now day’s heart disease does not have to be a death
sentence. There are healthy lifestyle choices that can be
made and science has come a long way in the early
detection of heart disease.
Heart disease and strokes are other common
cardiovascular diseases. Two independent risk factors that
have a major impact for heart diseases, cardiovascular
diseases, are high blood pressure and high blood
cholesterol.
Now day’s heart disease does not have to be a death
sentence. There are healthy lifestyle choices that can be
made and science has come a long way in the early
detection of heart disease.
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A Brief History of Heart Disease:
Heart disease is the leading killer of people throughout
the world. However, health problems involving the heart
are not at all new to the human species. Although the
knowledge of the causes and effects of heart disease
began to appear in actual medical practice in the 20th
century, the history of heart disease dates back to as far
back as ancient Egypt.
Archaeological findings in ancient Egypt indicate that
Egyptians at that time thought of the heart as the seat of
human wisdom and personality. They imagined some
kinds of channels originating from the heart and carrying
its products (in which they included blood, semen, saliva,
and other fluids as well as air and nutrients) to the rest of
the body.
The history of heart disease may include the following
steps:Medieval history of heart disease.
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History of heart disease in industrials society.
Diet and the history of heart disease.
Medieval History of Heart Disease:
Research on the status of the health of the English in
medieval times indicates that people at that time suffered
from few cholesterol-related diseases (including heart
disease). People living in Briton in the middle Ages had
an infrequent history of heart disease and deaths caused
by it. The main reason underlying the healthier heart
condition of medieval English people was the use of
natural food that was not loaded with carbohydrates; was
not lacking in proteins; and was not rich in harmful fatty
compounds.
History of Heart Disease in Industrial Societies:
Studies in the history of heart disease show that the
occurrence of deaths resulting from heart problems was
rare in pre-industrial societies. After the Industrial
revolution of the 19th century, the incidence of deaths
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from heart disease went on a rise and more people became
prone to dying from heart attacks. Health professionals
hold the more relaxed and sedentary lifestyle of the
modern technological age responsible for this change.
Before the advent of sophisticated machines, most people
used to earn their living by some kind of manual work
which consumed the extra fatty deposits of the body. In
addition, manual labor was a vigorous physical activity
that kept the blood circulation high through the body.
Diet and the History of Heart Disease:
Diet also has a significant role in the history of heart
disease. While the diet of an average person in preindustrial world consisted of a higher proportion of
natural foods like whole grains and unprocessed dairy
products (milk, and curd etc.), the invention of machines
also started the trend of making rich foods.
French fries, burgers, and processed dairy foods gained
popularity. Their consumption became more a matter of
social taste than individual choice. Also contributing to
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their popularity was the economy of time in preparing
them (hence the term fast food'). All these factors
combined to make fast food the primary choice of the
general public. The result was an increased incidence of
heart disease.
Discover Heart Disease:
Heart disease was discovered by the ancient Egyptians.
During 1873–74, Georg Moritz Ebers , a German
intellectual and Egyptologist, discovered an ancient
Egyptian medical work or papyrus that proves the ancient
Egyptians were the first to discover heart disease. The
papyrus is called the Ebers papyrus in his honor. The
discovery of heart disease was described in this paper,
which is why the discovery of heart disease is attributed
to the ancient Egyptians.
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Georg Moritz Ebers
What is Heart Disease?
When people think of heart disease, a heart attack may be
the first disorder they envision. Clinically called a
myocardial infarction, a heart attack tends to be serving,
dramatic, and intense. A myocardial infarction occurs
when a section of heart tissue dies due to serve disruption
of blood flow to the area.
However, a myocardial infarction is only one type heart
disease. Under the umbrella term “Heart disease” is a
number of other conditions, including coronary heart
disease (CHD), angina pectoris (chest pain), congestive
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heart failure (a condition in which the heart loses its
ability to pump effectively), cardiomyopathy, congenital
heart disease (heart disorders that are present at birth),
arrhythmias (disorders of the heart’s rhythm),
myocarditis.
In each disorder, the health and functioning of the entire
cardiovascular system-heart, arteries, and veins, and such
vital organs as the brains, lungs and kidneys are at issue.
Definition of Heart Disease:
Any disorder that affects the heart, sometimes the term
"heart disease" is used narrowly and incorrectly as a
synonym for coronary artery disease. Heart disease is
synonymous with cardiac disease but not with
cardiovascular disease which is any disease of the heart or
blood vessels. Among the many types of heart disease,
see, for example: coronary heart disease (CHDatherosclerosis of the arteries supplying the heart), angina
pectoris (chest pain), congestive heart failure (a condition
in which the heart loses its ability to pump effectively),
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cardiomyopathy, congenital heart disease (heart disorders
that are present at birth), arrhythmias (disorders of the
heart’s rhythm), myocarditis.
Types of Heart Disease:
Heart disease is a broad term that includes all types of
diseases affecting different components of the heart. Heart
means 'cardio.' Therefore, all heart diseases belong to the
category of cardiovascular diseases.
Some types of heart diseases are:
Coronary heart disease (CHD)
Angina pectoris
Congestive heart failure
Cardiomyopathy
Congenital heart disease
Arrhythmias
Myocarditis
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Coronary Heart Disease (CHD):
Coronary heart disease (CHD) is a narrowing of the small
blood vessels that supply blood and oxygen to the heart.
CHD is also called coronary artery disease.
Causes
Coronary heart disease (CHD) is the leading cause of
death in the United States for men and women. Coronary
heart disease is caused by the buildup of plaque in the
arteries to our heart. This may also be called hardening of
the arteries.
Fatty material and other substances form a plaque
build-up on the walls of our coronary arteries. The
coronary arteries bring blood and oxygen to our heart.
This buildup causes the arteries to get narrow.
As a result, blood flow to the heart can slow down or
stop.
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Figur: Coronary heart disease.
Symptoms
Symptoms may be very noticeable, but sometimes can
have the disease and not have any symptoms. This is
especially true in the early stages of heart disease.
Chest pain or discomfort (angina) is the most common
symptom. Feel this pain when the heart is not getting
enough blood or oxygen. How bad the pain is varies from
person to person.
It may feel heavy or like someone is squeezing our
heart. We may feel it under our breast bone (sternum), but
also in your neck, arms, stomach, or upper back.
The pain usually occurs with activity or emotion, and
goes away with rest or a medicine called nitroglycerin.
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Other symptoms include shortness of breath and
fatigue with activity (exertion).
Women, elderly people, and people with diabetes are
more likely to have symptoms other than chest pain, such
as:
Fatigue
Shortness of breath
General weakness
Exams and Tests
Our doctor or nurse will examine. Doctor will often order
more than one test before making a diagnosis.
Tests may include:
Coronary angiography -- an invasive test that
evaluates the heart arteries under x-ray
Echocardiogram stress test
Electrocardiogram (ECG)
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Electron-beam computed tomography (EBCT) to
look for calcium in the lining of the arteries -- the more
calcium, the higher your chance for CHD
Exercise stress test
Heart CT scan
Nuclear stress test
Treatment
We may be asked to take one or more medicines to treat
blood pressure, diabetes, or high cholesterol levels.
Follow our doctor's directions closely to help prevent
coronary artery disease from getting worse.
Goals for treating these conditions in people who have
coronary artery disease:
Blood pressure less than or equal to 140/90 (even
lower for patients with diabetes, kidney disease, or heart
failure)
HbA1c levels if you have diabetes at a level
recommended by our doctor
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LDL cholesterol level less than or equal to 100
mg/dL (even lower for some patients)
Treatment depends on your symptoms and how severe the
disease is. Doctor may give one or more medicines to
treat heart disease, blood pressure, diabetes, or high
cholesterol. Follow doctor's directions closely to help
prevent coronary artery disease from getting worse.
Never stop taking your medicines without talking to
doctor first. Stopping heart medicines suddenly can make
angina worse or cause a heart attack.
Angina Pectoris:
Angina pectoris–commonly known as angina–is chest
pain due to ischemia of the heart muscle, generally due to
obstruction or spasm of the coronary arteries. The main
cause of angina pectoris is Coronary Artery Disease, due
to atherosclerosis of the arteries feeding the heart. The
term derives from the Latin angina ("infection of the
throat") from the Greek ankhone ("strangling"), and the
Latin pectus ("chest"), and can therefore be translated as
"a strangling feeling in the chest".
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There is a weak relationship between severity of pain and
degree of oxygen deprivation in the heart muscle (i.e.,
there can be severe pain with little or no risk of a heart
attack, and a heart attack can occur without pain).
Worsening ("crescendo") angina attacks, sudden-onset
angina at rest, and angina lasting more than 15 minutes
are symptoms of unstable angina (usually grouped with
similar conditions as the acute coronary syndrome). As
these may herald myocardial infarction (a heart attack),
they require urgent medical attention and are generally
treated as a presumed heart attack.
Figure: Angina pectoris.
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Classification:
Stable angina
Unstable angina
Micro vascular angina
Stable angina:
Also known as effort angina, this refers to the more
common understanding of angina related to myocardial
ischemia. Typical presentations of stable angina is that of
chest discomfort and associated symptoms precipitated by
some activity (running, walking, etc.) with minimal or
non-existent symptoms at rest. Symptoms typically abate
several minutes following cessation of precipitating
activities and reoccur when activity resumes. In this way,
stable angina may be thought of as being similar to
claudicating symptoms.
Unstable angina:
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Unstable angina (UA) (also "crescendo angina;" this is a
form of acute coronary syndrome) is defined as angina
pectoris that changes or worsens.
It has at least one of these three features:
It occurs at rest (or with minimal exertion), usually
lasting >10 min;
It is severe and of new onset (i.e., within the prior 4–
6 weeks); and/or
It occurs with a crescendo pattern (i.e., distinctly
more severe, prolonged, or frequent than before).
UA may occur unpredictably at rest which may be a
serious indicator of an impending heart attack. What
differentiates stable angina from unstable angina (other
than symptoms) is the pathophysiology of the
atherosclerosis. The path physiology of unstable angina is
the reduction of coronary flow due to transient platelet
aggregation on apparently normal endothelium, coronary
artery spasms or coronary thrombosis. The process starts
with atherosclerosis, and when inflamed leads to an active
plaque, which undergoes thrombosis and results in acute
ischemia, which finally results in cell necrosis after
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calcium entry. Studies show that 64% of all unstable
anginas occur between 10 PM and 8 AM when patients
are at rest.
Instable angina, the developing thermo is protected with a
fibrous cap. This cap (atherosclerotic plaque) may rupture
in unstable angina, allowing blood clots to precipitate and
further decrease the lumen of the coronary vessel. This
explains why an unstable angina appears to be
independent of activity.
Micro vascular angina:
Micro vascular Angina or Angina Syndrome X is
characterized by angina-like chest pain, but has different
causes. The cause of Micro vascular Angina is unknown,
but it appears to be the result of poor function in the tiny
blood vessels of the heart, arms and legs. Since
microvascular angina isn't characterized by arterial
blockages, it's harder to recognize and diagnose, but its
prognosis is excellent.
Signs and symptoms:
Most patients with angina complain of chest discomfort
rather than actual pain: the discomfort is usually described
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as a pressure, heaviness, tightness, and squeezing,
burning, or choking sensation. Apart from chest
discomfort, angina pains may also be experienced in the
epigastrium (upper central abdomen), back, neck area,
jaw, or shoulders. This is explained by the concept of
referred pain, and is due to the spinal level that receives
visceral sensation from the heart simultaneously receiving
cetaceous sensation from parts of the skin specified by
that spinal nerve's dermatome, without an ability to
discriminate the two. Typical locations for referred pain
are arms (often inner left arm), shoulders, and neck into
the jaw. Angina is typically precipitated by exertion or
emotional stress. It is exacerbated by having a full
stomach and by cold temperatures. Pain may be
accompanied by breathlessness, sweating and nausea in
some cases. In this case, the pulse rate and the blood
pressure increase. Chest pain lasting only a few seconds is
normally not angina (such as pericardial catch syndrome).
Myocardial ischemia comes about when the myocardial
(the heart muscles) receive insufficient blood and oxygen
to function normally either because of increased oxygen
demand by the myocardia or by decreased supply to the
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myocardial. This inadequate perfusion of blood and the
resulting reduced delivery of oxygen and nutrients is
directly correlated to blocked or narrowed blood vessels.
Some experience "autonomic symptoms" (related to
increased activity of the autonomic nervous system) such
as nausea, vomiting and pallor.
Major risk factors for angina include cigarette smoking,
diabetes, high cholesterol, high blood pressure, sedentary
lifestyle and family history of premature heart disease.
A variant form of angina (Prinzmetal's angina) occurs in
patients with normal coronary arteries or insignificant
atherosclerosis. It is thought to be caused by spasms of
the artery. It occurs more in younger women.
Major risk factors/Causes:
Age (≥ 55 years for men, ≥ 65 for women)
Cigarette smoking
Diabetes mellitus (DM)
Dyslipidemia
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Family history of premature cardiovascular disease
(men <55 years, female <65 years old)
Hypertension (HTN)
Kidney disease (microalbuminuria or GFR<60
mL/min)
Obesity (BMI ≥ 30 kg/m2)
Physical inactivity
Decrease psychosocial stress.
Routine counseling of adults to advise them to improve
their diet and increase their physical activity has not been
found to significantly alter behavior, and thus is not
recommended.
Conditions that exacerbate or provoke angina
Medications
vasodilators
excessive thyroid replacement
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vasoconstrictors
polycythemia which thickens the blood causing it to
slow its flow through the heart muscle
One study found that smokers with coronary artery
disease had a significantly increased level of sympathetic
nerve activity when compared to those without. This is in
addition to increases in blood pressure, heart rate and
peripheral vascular resistance associated with nicotine
which may lead to recurrent angina attacks. Additionally,
CDC reports that the risk of CHD (Coronary heart
disease), stroke, and PVD (Peripheral vascular disease) is
reduced within 1–2 years of smoking cessation. In another
study, it was found that after one year, the prevalence of
angina in smoking men under 60 after an initial attack
was 40% less in those who had quit smoking compared to
those who continued. Studies have found that there are
short term and long term benefits to smoking cessation.
Other medical problems:
profound anemia
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uncontrolled HTN
hyperthyroidism
hypoxemia
Other cardiac problems:
Tachyarrhythmia
Brady arrhythmia
Valvular heart disease
Hypertrophic cardiomyopathy
Myocardial ischemia can result from:
A reduction of blood flow to the heart that can be
caused by stenosis, spasm, or acute occlusion (by an
embolus) of the heart's arteries.
Resistance of the blood vessels. This can be caused
by narrowing of the blood vessels; a decrease in radius,
Blood flow is inversely proportional to the radius of the
artery to the fourth power.
Reduced oxygen-carrying capacity of the blood, due
to several factors such as a decrease in oxygen tension
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and hemoglobin concentration. This decreases the ability
to of hemoglobin to carry oxygen to myocardial tissue.
Atherosclerosis is the most common cause of stenosis
(narrowing of the blood vessels) of the heart's arteries
and, hence, angina pectoris. Some people with chest pain
have normal or minimal narrowing of heart arteries; in
these patients, vasospasm is a more likely cause for the
pain, sometimes in the context of Prinzmetal's angina and
syndrome X.
Myocardial ischemia also can be the result of factors
affecting blood composition, such as reduced oxygencarrying capacity of blood, as seen with severe anemia
(low number of red blood cells), or long-term smoking.
Pathophysiology:
Angina results when there is an imbalance between the
heart's oxygen demand and supply. This imbalance can
result from an increase in demand (e.g. during exercise)
without a proportional increase in supply (e.g. due to
obstruction or atherosclerosis of the coronary arteries).
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Diagnosis:
Suspect angina in people presenting with tight, dull, or
heavy chest discomfort which is:
Retrosternal or left-sided, radiating to the left arm,
neck, jaw, or back.
Associated with exertion or emotional stress and
relieved within several minutes by rest.
Precipitated by cold weather or a meal.
Some people present with atypical symptoms, including
breathlessness, nausea, or epigastric discomfort or
burping. These atypical symptoms are particularly likely
in older people, women, and those with diabetes.
Angina pain is not usually sharp or stabbing or influenced
by respiration. Anti-acids and simple analgesia do not
usually relieve the pain. If chest discomfort (of whatever
site) is precipitated by exertion, relieved by rest, and
relieved by glyceryl trinitrate, the likelihood of angina is
increased.
In angina patients who are momentarily not feeling any
one chest pain, an electrocardiogram (ECG) is typically
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normal, unless there have been other cardiac problems in
the past. During periods of pain, depression or elevation
of the ST segment may be observed. To elicit these
changes, an exercise ECG test ("treadmill test") may be
performed, during which the patient exercises to their
maximum ability before fatigue, breathlessness or,
importantly, pain intervenes; if characteristic ECG
changes are documented (typically more than 1 mm of
flat or downsloping ST depression), the test is considered
diagnostic for angina. Even constant monitoring of the
blood pressure and the pulse rate can lead us to some
conclusion regarding the angina. The exercise test is also
useful in looking for other markers of myocardial
ischaemia: blood pressure response (or lack thereof,
particularly a drop in systolic pressure), dysrhythmia and
chronotropic response. Other alternatives to a standard
exercise test include a thallium scintigram or sestamibi
scintigram (in patients who cannot exercise enough for
the purposes of the treadmill tests, e.g:- due to asthma or
arthritis or in whom the ECG is too abnormal at rest) or
Stress Echocardiography.
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In patients in whom such noninvasive testing is
diagnostic, a coronary angiogram is typically performed
to identify the nature of the coronary lesion, and whether
this would be a candidate for angioplasty, coronary artery
bypass graft (CABG), treatment only with medication, or
other treatments. There has been research which
concludes that a frequency is attained when there is
increase in the blood pressure and the pulse rate. This
frequency varies normally but the range is 45–50 kHz for
the cardiac arrest or for the heart failure. In patients who
are in hospital with unstable angina (or the newer term of
"high risk acute coronary syndromes"), those with resting
ischaemic ECG changes or those with raised cardiac
enzymes such as troponin may undergo coronary
angiography directly.
Treatment:
The most specific medicine to treat angina is
nitroglycerin. It is a potent vasodilator that makes more
oxygen available to the heart muscle. Beta-blockers and
calcium channel blockers act to decrease the heart's
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workload, and thus its requirement for oxygen.
Nitroglycerin should not be given if certain inhibitors
such as Sildenafil (Viagra), Tadalafil (Cialis), or
Vardenafil (Levitra) have been taken within the previous
12 hours as the combination of the two could cause a
serious drop in blood pressure. Treatments are balloon
angioplasty, in which the balloon is inserted at the end of
a catheter and inflated to widen the arterial lumen. Stents
to maintain the arterial widening are often used at the
same time. Coronary bypass surgery involves bypassing
constricted arteries with venous grafts. This is much more
invasive than angioplasty.
The main goals of treatment in angina pectoris are relief
of symptoms, slowing progression of the disease, and
reduction of future events, especially heart attacks and
death. Beta blockers (e.g:- carvedilol, propranolol,
atenolol) have a large body of evidence in morbidity and
mortality benefits (fewer symptoms, less disability and
longer life) and short-acting nitroglycerin medications
have been used since 1879 for symptomatic relief of
angina. Calcium channel blockers (such as nifedipine
(Adult) and amlodipine), isosorbide mononitrate and
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nicorandil are vasodilators commonly used in chronic
stable angina. A new therapeutic class, called if inhibitor,
has recently been made available: ivabradine provides
pure heart rate reduction leading to major anti-ischemic
and antinational efficacy. ACE inhibitors are also
vasodilators with both symptomatic and prognostic
benefit and, lastly, statins are the most frequently used
lipid/cholesterol modifiers which probably also stabilize
existing athermanous plaque. Low-dose aspirin decreases
the risk of heart attack in patients with chronic stable
angina, and was previously part of standard treatment;
however, it has since been discovered that the increase in
haemorrhagic stroke and gastrointestinal bleeding offsets
this gain so they are no longer advised unless the risk of
myocardial infarction is very high.
Exercise is also a very good long term treatment for the
angina (but only particular regimens - gentle and
sustained
exercise rather
than
intense short
bursts),probably working by complex mechanisms such
as improving blood pressure and promoting coronary
artery collateralization.
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Identifying and treating risk factors for further coronary
heart disease is a priority in patients with angina. This
means testing for elevated cholesterol and other fats in the
blood, diabetes and hypertension (high blood pressure),
and encouraging smoking cessation and weight
optimization.
The calcium channel blocker nifedipine prolongs
cardiovascular event- and procedure-free survival in
patients with coronary artery disease. New overt heart
failures were reduced by 29% compared to placebo;
however, the mortality rate difference between the two
groups was statistically insignificant.
The fatty acid oxidation inhibitor mildronate is a
clinically-used anti-ischemic drug for the treatment of
angina and myocardial infarction. Mildronate shifts the
myocardial energy metabolism from fatty acid oxidation
to the more oxygen sparing glucose oxidation under
ischemic conditions, by inhibiting enzymes in the
carnitine biosynthesis pathway including gammabutyrobetaine deoxygenate. Mildronate also inhibits
carnitine acetyltransferase and therefore acts as a
myocardial energy metabolism regulator.
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Congestive heart failure:
Congestive heart failure facts
Congestive heart failure (CHF) is a condition in
which the heart's function as a pump is inadequate to meet
the body's needs.
Many disease processes can impair the pumping
efficiency of the heart to cause congestive heart failure.
The symptoms of congestive heart failure vary, but
can include fatigue, diminished exercise capacity,
shortness of breath, and swelling.
The diagnosis of congestive heart failure is based on
knowledge of the individual's medical history, a careful
physical examination, and selected laboratory tests.
The treatment of congestive heart failure can include
lifestyle modifications, addressing potentially reversible
factors, medications, heart transplant, and mechanical
therapies.
The course of congestive heart failure in any given
patient is extremely variable.
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Congestive
heart
failure:
Congestive heart failure (CHF) is a condition in which the
heart's function as a pump is inadequate to deliver oxygen
rich blood to the body. Congestive heart failure can be
caused by:
Diseases that weaken the heart muscle,
Diseases that cause stiffening of the heart muscles, or
Diseases that increase oxygen demand by the body
tissue beyond the capability of the heart to deliver
adequate oxygen-rich blood.
Figure: Congestive heart failure.
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The heart has two atria (right atrium and left atrium) that
make up the upper chambers of the heart, and two
ventricles (left ventricle and right ventricle) that make up
the lower chambers of the heart. The ventricles are
muscular chambers that pump blood when the muscles
contract. The contraction of the ventricle muscles is called
systole.
Many diseases can impair the pumping action of the
ventricles. For example, the muscles of the ventricles can
be weakened by heart attacks, infections (myocarditis) or
toxins (alcohol, some chemotherapy agents). The
diminished pumping ability of the ventricles due to
muscle weakening is called systolic dysfunction. After
each ventricular contraction (systole) the ventricle
muscles need to relax to allow blood from the atria to fill
the ventricles. This relaxation of the ventricles is called
diastole.
Diseases such as hemochromatosis (iron overload) or
amyloidosis can cause stiffening of the heart muscle and
impair the ventricles' capacity to relax and fill; this is
referred to as diastolic dysfunction. The most common
cause of this is longstanding high blood pressure resulting
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in a thickened (hypertrophied) heart. Additionally, in
some patients, although the pumping action and filling
capacity of the heart may be normal, abnormally high
oxygen demand by the body's tissues (for example, with
hyperthyroidism or anemia) may make it difficult for the
heart to supply an adequate blood flow (called high output
heart failure).
In some individuals one or more of these factors can be
present to cause congestive heart failure. The remainder
of this article will focus primarily on congestive heart
failure that is due to heart muscle weakness, systolic
dysfunction.
Congestive heart failure can affect many organs of the
body. For example:
The weakened heart muscles may not be able to
supply enough blood to the kidneys, which then begin to
lose their normal ability to excrete salt (sodium) and
water. This diminished kidney function can cause the
body to retain more fluid.
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The lungs may become congested with fluid
(pulmonary edema) and the person's ability to exercise is
decreased.
Fluid may likewise accumulate in the liver, thereby
impairing its ability to rid the body of toxins and produce
essential proteins.
The intestines may become less efficient in absorbing
nutrients and medicines.
Fluid also may accumulate in the extremities,
resulting in edema (swelling) of the ankles and feet.
Eventually, untreated, worsening congestive heart failure
will affect virtually every organ in the body.
Symptoms
of
congestive
heart
failure:
The symptoms of congestive heart failure vary among
individuals according to the particular organ systems
involved and depending on the degree to which the rest of
the body has "compensated" for the heart muscle
weakness.
An early symptom of congestive heart failure is
fatigue. While fatigue is a sensitive indicator of possible
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underlying congestive heart failure, it is obviously a
nonspecific symptom that may be caused by many other
conditions. The person's ability to exercise may also
diminish. Patients may not even sense this decrease and
they may subconsciously reduce their activities to
accommodate this limitation.
As the body becomes overloaded with fluid from
congestive heart failure, swelling (edema) of the ankles
and legs or abdomen may be noticed. This can be referred
to as "right sided heart failure" as failure of the right sided
heart chambers to pump venous blood to the lungs to
acquire oxygen results in buildup of this fluid in gravitydependent areas such as in the legs. The most common
cause of this is longstanding failure of the left heart,
which may lead to secondary failure of the right heart.
Right-sided heart failure can also be caused by severe
lung disease (referred to as "cor pulmonale"), or by
intrinsic disease of the right heart muscle (less common)
In addition, fluid may accumulate in the lungs,
thereby causing shortness of breath, particularly during
exercise and when lying flat. In some instances, patients
are awakened at night, gasping for air.
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Some may be unable to sleep unless sitting upright.
The extra fluid in the body may cause increased
urination, particularly at night.
Accumulation of fluid in the liver and intestines may
cause nausea, abdominal pain, and decreased appetite.
Diagnosis:
The diagnosis of congestive heart failure is most often a
clinical one that is based on knowledge of the patient's
pertinent medical history, a careful physical examination,
and selected laboratory tests.
A thorough patient history may disclose the presence of
one or more of the symptoms of congestive heart failure
described above. In addition, a history of significant
coronary artery disease, prior heart attack, hypertension,
diabetes, or significant alcohol use can be clues.
The physical examination is focused on detecting the
presence of extra fluid in the body (breath sounds, leg
swelling, or neck veins) as well as carefully
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characterizing the condition of the heart (pulse, heart size,
heart sounds, and murmurs).
Useful diagnostic tests include the electrocardiogram
(ECG) and chest X-ray to detect previous heart attacks,
arrhythmia, heart enlargement, and fluid in and around the
lungs. Perhaps the single most useful diagnostic test is the
echocardiogram, in which ultrasound is used to image the
heart muscle, valve structures, and blood flow patterns.
The echocardiogram is very helpful in diagnosing heart
muscle weakness. In addition, the test can suggest
possible causes for the heart muscle weakness (for
example, prior heart attack, and severe valve
abnormalities). Virtually all patients in whom the
diagnosis of congestive heart failure is suspected should
ideally undergo echocardiography early in their
assessment.
Nuclear medicine studies assess the overall pumping
capability of the heart and examine the possibility of
inadequate blood flow to the heart muscle. Heart
catheterization allows the arteries to the heart to be
visualized with angiography (using dye inside of the
blood vessels that can be seen using X-ray methods).
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During catheterization the pressures in and around the
heart can be measured and the heart's performance
assessed. In rare cases, a biopsy of the heart tissue may be
recommended to diagnose specific diseases. This biopsy
can often be accomplished through the use of a special
catheter device that is inserted into a vein and
maneuvered into the right side of the heart.
Another helpful diagnostic test is a blood test called a
BNP or B-type natriuretic peptid level. This level can
vary with age and gender but is typically elevated from
heart failure and can aid in the diagnosis, and can be
useful in following the response to treatment of
congestive heart failure.
The choice of tests depends on each patient's case and is
based on the suspected diagnoses.
Treatment of congestive heart failure:
Lifestyle modification
Addressing potentially reversible factors
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Lifestyle modifications
After congestive heart failure is diagnosed, treatment
should be started immediately. Perhaps the most
important and yet most neglected aspect of treatment
involves lifestyle modifications. Sodium causes an
increase in fluid accumulation in the body's tissues.
Because the body is often congested with excess fluid,
patients become very sensitive to the levels of intake of
sodium and water. Restricting salt and fluid intake is often
recommended because of the tendency of fluid to
accumulate in the lungs and surrounding tissues. An
American "no added salt" diet can still contain 4 to 6
grams (4000 to 6000 milligrams) of sodium per day. In
individuals with congestive heart failure, an intake of no
more than 2 grams (2000 milligrams) of sodium per day is
generally advised. Reading food labels and paying close
attention to total sodium intake is very important. Severe
restriction of alcohol consumption also is advised.
Likewise, the total amount of fluid consumed must be
regulated. Although many people with congestive heart
failure take diuretics to aid in the elimination of excess
fluid, the action of these medications can be overwhelmed
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by an excess intake of water and other fluids. The maxim
that "drinking eight glasses of water a day is healthy"
certainly does not apply to patients with congestive heart
failure. In fact, patients with more advanced cases of
congestive heart failure are often advised to limit their
total daily fluid intake from all sources to 2 quarts. The
above guidelines for sodium and fluid intake may vary
depending on the severity of congestive heart failure in
any given individual and should be discussed with their
physician.
An important tool for monitoring an appropriate fluid
balance is the frequent measurement of body weight. An
early sign of fluid accumulation is an increase in body
weight. This may occur even before shortness of breath or
swelling in the legs and other body tissues (edema) is
detected. A weight gain of two to three pounds over two
to three days should prompt a call to the physician, who
may order an increase in the dose of diuretics or other
methods designed to stop the early stages of fluid
accumulation before it becomes more severe.
Aerobic exercise, once discouraged for congestive heart
failure patients, has been shown to be beneficial in
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maintaining overall functional capacity, quality of life,
and perhaps even improving survival. Each person's body
has its own unique ability to compensate for the failing
heart. Given the same degree of heart muscle weakness,
individuals may display widely varying degrees of
limitation of function. Regular exercise, when tailored to
the person's tolerance level, appears to provide significant
benefits and should be used only when the individual is
compensated and stable.
Addressing potentially reversible factors:
Depending on the underlying cause of congestive heart
failure, potentially reversible factors should be explored.
For example:
In certain persons whose congestive heart failure is
caused by inadequate blood flow to the heart muscle,
restoration of the blood flow through coronary artery
surgery or catheter procedures (angioplasty, intracoronary
stenting) may be considered.
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Congestive heart failure that is due to severe disease
of the valves may be alleviated by valve surgery in
appropriate patients.
When congestive heart failure is caused by chronic,
uncontrolled high blood pressure (hypertension),
aggressive blood pressure control will often improve the
condition.
Heart muscle weakness that is due to longstanding,
severe alcohol abuse can improve significantly with
abstinence from drinking.
Congestive heart failure that is caused by other
disease states may be similarly partially or completely
reversible by appropriate measures.
Cardiomyopathy:
Cardiomyopathy (literally "heart muscle disease") is the
measurable deterioration of the function of the
myocardium (the heart muscle) for any reason, usually
leading to heart failure; common symptoms are dyspnea
(breathlessness) and peripheral edema (swelling of the
legs). People with cardiomyopathy are often at risk of
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dangerous forms of irregular heart beat and sudden
cardiac death.The most common form of cardiomyopathy
is dilated cardiomyopathy.
Figur: Dilated cardiomyopathy.
Classification:
Although in theory the term "cardiomyopathy" could
apply to almost any disease affecting the heart, in practice
it is usually reserved for "severe myocardial disease
leading to heart failure".Cardiomyopathies can be
categorized as extrinsic or intrinsic.
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An extrinsic cardiomyopathy is a cardiomyopathy
where the primary pathology is outside the myocardium
itself. Most cardiomyopathies are extrinsic; by far the
most common cause of an extrinsic cardiomyopathy is
ischemia. Ischemia can be understood as poor oxygen
supply of the heart muscle (the demand for oxygen is
higher than the current supply). The World Health
Organization calls these specific cardiomyopathies:
An intrinsic cardiomyopathy is defined as weakness
in the muscle of the heart not due to an identifiable
external cause. This definition was used to categorize
previously idiopathic cardiomyopathies although specific
external causes have since been identified for many. For
example, alcoholism has been identified as a cause for
some forms of dilated cardiomyopathy. To make a
diagnosis of an intrinsic cardiomyopathy, significant
coronary artery disease should be ruled out first (amongst
other causes). The term intrinsic cardiomyopathy does not
describe the specific etiology of weakened heart muscle.
The intrinsic cardiomyopathies consist of a variety of
disease states, each with their own causes. Many intrinsic
cardiomyopathies now have identifiable external causes
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including drug and alcohol toxicity, certain infections
(including Hepatitis C), and various genetic and
idiopathic (i.e., unknown) causes.
It is also possible to classify cardiomyopathies
functionally, as involving dilation, hypertrophy, or
restriction.
Types:
Primary/intrinsic cardiomyopathies
•
Genetic
Hypertrophic cardiomyopathy (HCM or HOCM)
Arrhythmogenic right ventricular cardiomyopathy
(ARVC)
Isolated ventricular non-compaction
Mitochondrial myopathy
•
Mixed
Dilated cardiomyopathy (DCM)
Restrictive cardiomyopathy (RCM)
•
Acquired
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Takotsubo cardiomyopathy
Loeffler endocarditis
Secondary/extrinsic cardiomyopathies
•
Metabolic/storage
amyloidosis
hemochromatosis
•
Inflammatory
Chagas disease
•
Endocrine
diabetic cardiomyopathy
hyperthyroidism
acromegaly
•
Toxicity
chemotherapy
Alcoholic cardiomyopathy
•
Neuromuscular
muscular dystrophy
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•
Nutritional diseases
Obesity-associated cardiomyopathy
•
Other
"Ischemic cardiomyopathy" is a weakness in the
muscle of the heart due to inadequate oxygen delivery to
the myocardium with coronary artery disease being the
most common cause. Not supported by current
cardiomyopathies classification schemes.
Signs and symptoms:
Symptoms and signs may mimic those of almost any form
of heart disease. Chest pain is common. Mild myocarditis
or cardiomyopathy is frequently asymptomatic; severe
cases are associated with heart failure, arrhythmias, and
systemic embolization. Manifestations of the underlying
disease (e.g., Chagas' disease) may be prominent. Most
patients with biopsy-proven myocarditis report a recent
viral prodrome preceding cardiovascular symptoms.
EKG abnormalities are often present, although the
changes are frequently nonspecific. A pattern
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characteristic of left ventricular hypertrophy may be
present. Flat or inverted T waves are most common, often
with low-voltage QRS complexes. Intraventricular
conduction defects and bundle branch block, especially
left bundle branch block, are also common. An
echocardiogram is useful to detect wall motion
abnormalities or a pericardial effusion. Chest radiographs
can be normal or can show evidence of congestive heart
failure with pulmonary edema or cardiomegaly.
Treatment:
Treatment depends on the type of cardiomyopathy and
condition of disease, but may include medication
(conservative
treatment)
or
iatrogenic/implanted
pacemakers for slow heart rates, defibrillators for those
prone to fatal heart rhythms, ventricular assist devices
(LVADs) for severe heart failure, or ablation for recurring
dysrhythmias that cannot be eliminated by medication or
cardioversion. The goal of treatment is often symptom
relief, and some patients may eventually require a heart
transplant. Treatment of cardiomyopathy (and other heart
diseases) using alternative methods such as stem cell
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therapy is commercially available but is not supported by
convincing evidence.
Congenital heart disease:
A congenital heart defect (CHD) is a defect in the
structure of the heart and great vessels which is present at
birth. Many types of heart defects exist, most of which
either obstruct blood flow in the heart or vessels near it, or
cause blood to flow through the heart in an abnormal
pattern. Other defects, such as long QT syndrome, affect
the heart's rhythm. Heart defects are among the most
common birth defects and are the leading cause of birth
defect-related deaths. Approximately 9 people in 1000 are
born with a congenital heart defect. Many defects don't
need treatment, but some complex congenital heart
defects require medication or surgery.
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Figur: Congenital heart disease.
Signs and symptoms:
Signs and symptoms are related to the type and severity of
the heart defect. Symptoms frequently present early in
life, but it's possible for some CHDs to go undetected
throughout life.[3] Some children have no signs while
others may exhibit shortness of breath, cyanosis,
syncope,[4] heart murmur, under-developing of limbs and
muscles, poor feeding or growth, or respiratory infections.
Congenital heart defects because abnormal heart structure
resulting in production of certain sounds called heart
murmur. These can sometimes be detected by
auscultation; however, not all heart murmurs are caused
by congenital heart defects.
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Associated
symptoms:
Congenital heart defects are associated with an increased
incidence of some other symptoms, together being called
the VACTERL association:
V - Vertebral anomalies
A - Anal atresia
C - Cardiovascular anomalies
T - Tracheoesophageal fistula
E - Esophageal atresia
R - Renal (Kidney) and/or radial anomalies
L - Limb defects
Ventricular septal defect (VSD), atrial septal defects, and
tetralogy of Fallot are the most common congenital heart
defects seen in the VACTERL association. Less common
defects in the association are truncus arteriosus, and
transposition of the great arteries.
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Embryology:
There is a complex sequence of events that result in a well
formed heart at birth and disruption of any portion may
result in a defect.The orderly timing of cell growth, cell
migration, and programmed cell death ("apoptosis") has
been studied extensively and the genes that control the
process are being elucidated. Around day 15 of
development, the cells that will become the heart exist in
two horseshoe shaped bands of the middle tissue layer
(mesoderm),and some cells migrate from portion of the
outer layer (ectoderm), the neural crest which is the
source of a variety of cells found throughout the body. On
day 19 of development, a pair of vascular elements, the
"endocardial tubes", form. The tubes fuse when cells
between then undergo programmed death and cells from
the first heart field migrate to the tube, and form a ring of
heart cells (myocytes) around it by day 21. On day 22, the
heart begins to beat and by day 24, blood is circulating.
At day 22, the circulatory system is bilaterally
symmetrical with paired vessels on each side and the
heart consisting of a simple tube located in the midline of
the body layout. The portion that will become the atria
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and will be located closest to the head are the most distant
from the head. From days 23 through 28, the heart tube
folds and twists, with the future ventricles moving left of
center (the ultimate location of the heart) and the atria
moving towards the head.
On day 28, areas of tissue in the heart tube begin to
expand inwards; after about two weeks, these expansions,
the membranous "septum primum" and the muscular
"endocardial cushions", fuse to form the four heart
chambers of the heart. A failure to fuse properly will
result in a defect that may allow blood to leak between
chambers. After this happens, cells which have migrated
from the neural crest begin to divide the bulbus cordis, the
main outflow tract is divided in two by the growth a
spiraling septum, becoming the great vessels—the
ascending segment of the aorta and the pulmonary trunk.
If the separation is incomplete, the result is a "persistent
truncus arteriosis". The vessels may be reversed
("transposition of the great vessels"). The two halves of
the split tract must migrate into the correct positions over
the appropriate ventricles. A failure may result in some
blood flowing into the wrong vessel (e.g. overriding
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aorta). The four chambered heart and the great vessels
have features required for fetal growth. The lungs are
unexpanded and cannot accommodate the full circulatory
volume. Two structures exist to shunt blood flow away
from the lungs. Cells in part of the septum primum die
creating a hole while muscle cells, the "septum
secundum", grow along the right atrial side the septum
primum, except for one region, leaving a gap through
which blood can pass from the right artium to the left
atrium, the foramen ovale. A small vessel, the ductus
arteriosus allows blood from the pulmonary artery to pass
to the aorta.
Changes at birth:
The ductus arteriosus stays open because of circulating
factors including prostaglandins. The foramen ovale stays
open because of the flow of blood from the right atrium to
the left atrium. As the lungs expand, blood flows easily
through the lungs and the membranous portion of the
foramen ovale (the septum primum) flops over the
muscular portion (the septum secundum). If the closure is
incomplete, the result is a patent foramen ovale. The two
flaps may fuse, but many adults have a foramen ovale that
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stays closed only because of the pressure difference
between the atria.
Theories:
Rokitansky (1875) explained congenital heart defects as
breaks in heart development at various ontogenesis stages.
Spitzer (1923) treats them as returns to one of the
phylogenesis stages.Krimsky (1963), synthesizing two
previous points of view, considered congenital heart
diseases as a stop of development at the certain stage of
ontogenesis, corresponding to this or that stage of the
phylogenesis. Hence these theories can explain feminine
and neutral types of defects only.
Causes:
The cause of congenital heart disease may be either
genetic or environmental, but is usually a combination of
both.
Genetics:
Most of the known causes of congenital heart disease are
sporadic genetic changes, either focal mutations or
deletion or addition of segments of DNA. Large
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chromosomal abnormalities such as trisomies 21, 13, and
18 cause about 5-8% of cases of CHD, with trisomy 21
being the most common genetic cause.[5] Small
chromosomal abnormalities also frequently lead to
congenital heart disease, and examples include
microdeletion of the long arm of chromosome 22 (22q11,
DiGeorge syndrome), the long arm of chromosome 1
(1q21), the short arm of chromosome 8 (8p23) and many
other, less recurrent regions of the genome, as shown by
high resolution genome-wide screening (Array
comparative genomic hybridization).
The genes regulating the complex developmental
sequence have only been partly elucidated. Some genes
are associated with specific defects. A number of genes
have been associated with cardiac manifestations.
Mutations of a heart muscle protein, α-myosin heavy
chain (MYH6) are associated with atrial septal defects.
Several proteins that interact with MYH6 are also
associated with cardiac defects. The transcription factor
GATA4 forms a complex with the TBX5 which interacts
with MYH6. Another factor, the homeobox
(developmental) gene, NKX2-5 also interacts with
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MYH6. Mutations of all these proteins are associated with
both atrial and ventricular septal defects; In addition,
NKX2-5 is associated with defects in the electrical
conduction of the heart and TBX5 is related to the HoltOram syndrome which includes electrical conduction
defects and abnormalities of the upper limb. Another Tbox gene, TBX1, is involved in velo-cardio-facial
syndrome DiGeorge syndrome, the most common
deletion which has extensive symptoms including defects
of the cardiac outflow tract including tetralogy of Fallot.
Examples of gene products and associated features
MYH6 GATA4 NKX2-5 TBX5
TBX1
Locus
14q11.2-q13 8p23.1-p22 5q34
12q24.1
Syndrome
Holt-Oram
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22q11.2
DiGeorge
Atrial septal defects
✔ ✔ ✔ ✔
Ventricular septal defects
✔ ✔ ✔
Electrical conduction abnormalities
✔ ✔
Outflow tract abnormalities
✔
Non-cardiac manifestations
Upper
abnormalities
Small or absent thymus
limb
Small or absent parathyroids
Facial abnormalities
The notch signaling pathway, a regulatory mechanism for
cell growth and differentiation, plays broad roles in
several aspects of cardiac development. Notch elements
are involved in determination of the right and left sides of
the body plan, so the directional folding of the heart tube
can be impacted. Notch signaling is involved early in the
formation of the endocardial cushions and continues to be
active as the develop into the septa and valves. It is also
involved in the development of the ventricular wall and
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the connection of the outflow tract to the great vessels.
Mutations in the gene for one of the notch ligands,
Jagged1, are identified in the majority of examined cases
of arteriohepatic dysplasia (Alagille syndrome),
characterized by defects of the great vessels (pulmonary
artery stenosis), heart (tetralogy of Fallot in 13% of
cases), liver, eyes, face, and bones. Though less than 1%
of all cases, where no defects are found in the Jagged1
gene, defects are found in Notch2 gene. In 10% of cases,
no mutation is found in either gene. For another member
of the gene family, mutations in the Notch1 gene are
associated with bicuspid aortic valve, a valve with two
leaflets instead of three. Notch1 is also associated with
calcification of the aortic valve, the third most common
cause of heart disease in adults.
Mutation of a cell regulatory mechanism, the Ras/MAPK
pathway are responsible for a variety of syndromes,
including Noonan syndrome, LEOPARD syndrome,
Costello syndrome and cardiofaciocutaneous syndrome in
which there is cardiac involvement.[16] While the
conditions listed are known genetic causes, there are
likely many other genes which are more subtle. It is
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known that the risk for congenital heart defects is higher
when there is a close relative with one.
Environmental:
Known antenatal environmental factors include maternal
infections (Rubella), drugs (alcohol, hydantoin, lithium
and thalidomide) and maternal illness (diabetes mellitus,
phenylketonuria, and systemic lupus erythematosus).
Maternal obesity:
As noted in several studies following similar body mass
index (BMI) ranges, prepregnant and gestating women,
who were obese (BMI ≥ 30), carried a statistically
significant risk of birthing children with congenital heart
defects (CHD) compared to normal-weight women
(BMI= 19-24.9).Although there are minor conflicting
reports, there was significant support for the risk of fetal
CHD development in overweight mothers (BMI= 2529.9). Additionally, as maternal obesity increased, the risk
of heart defects did too indicating a trend between BMI
and CHD odds. Altogether, these results present
reasonable concern for women to achieve a normalwww.AssignmentPoint.com
weight BMI prior to pregnancy to help decrease risk for
fetal heart defects.
A distinct physiological mechanism has not been
identified to explain the link between maternal obesity
and CHD, but both prepregnancy folate deficiency and
diabetes have been implicated in some studies.
Identification of the mechanism could aid health officials
to develop reduction strategies and curb CHD’s
prevalence in this preventable situation.
Classification:
A number of differing classification systems exist for
congenital heart defects. In 2000 the International
Congenital Heart Surgery Nomenclature was developed to
provide a generic classification system.
Hypoplasia:
Hypoplasia can affect the heart, typically resulting in the
underdevelopment of the right ventricle or the left
ventricle. This results in only one side of the heart capable
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of pumping blood to the body and lungs effectively.
Hypoplasia of the heart is rare but is the most serious
form of CHD. It is called hypoplastic left heart syndrome
when it affects the left side of the heart and hypoplastic
right heart syndrome when it affects the right side of the
heart. In both conditions, the presence of a patent ductus
arteriosus (and, when hypoplasia affects the right side of
the heart, a patent foramen ovale) is vital to the infant's
ability to survive until emergency heart surgery can be
performed, since without these pathways blood cannot
circulate to the body (or lungs, depending on which side
of the heart is defective). Hypoplasia of the heart is
generally a cyanotic heart defect.
Obstruction defects:
Obstruction defects occur when heart valves, arteries, or
veins are abnormally narrow or blocked. Common defects
include pulmonic stenosis, aortic stenosis, and coarctation
of the aorta, with other types such as bicuspid aortic valve
stenosis and subaortic stenosis being comparatively rare.
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Any narrowing or blockage can cause heart enlargement
or hypertension.
Septal defects:
The septum is a wall of tissue which separates the left
heart from the right heart. Defects in the interatrial septum
or the interventricular septum allow blood to flow from
the left side of the heart to the right, reducing the heart's
efficiency. Ventricular septal defects are collectively the
most common type of CHD, although approximately 30%
of adults have a type of atrial septal defect called probe
patent foramen ovale.
Cyanotic defects:
Cyanotic heart defects are called such because they result
in cyanosis, a bluish-grey discoloration of the skin due to
a lack of oxygen in the body. Such defects include
persistent truncus arteriosus, total anomalous pulmonary
venous connection, tetralogy of Fallot, transposition of
the great vessels, and tricuspid atresia.
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Defects:
Aortic stenosis
Atrial septal defect (ASD)
Atrioventricular septal defect (AVSD)
Bicuspid aortic valve
Dextrocardia
Double inlet left ventricle (DILV)
Double outlet right ventricle (DORV)
Ebstein's anomaly
Hypoplastic left heart syndrome (HLHS)
Hypoplastic right heart syndrome (HRHS)
Double inlet left ventricle
Mitral stenosis
Pulmonary atresia
Pulmonary stenosis
Transposition of the great vessels
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o
dextro-Transposition of the great arteries (d-TGA)
o
levo-Transposition of the great arteries (l-TGA)
Tricuspid atresia
Persistent truncus arteriosus
Ventricular septal defect (VSD)
Some conditions affect the great vessels or other vessels
in close proximity to the heart, but not the heart itself, but
are often classified as congenital heart defects.
Coarctation of the aorta (CoA)
Interrupted aortic arch (IAA)
Patent ductus arteriosus (PDA)
Scimitar syndrome (SS)
o Partial anomalous pulmonary venous connection
(PAPVC)
o Total anomalous pulmonary venous connection
(TAPVC)
Some constellations of multiple defects are commonly
found together.
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Tetralogy of Fallot (ToF)
Pentalogy of Cantrell
Shone's syndrome/ Shone's complex / Shone's
anomaly
Diagnosis:
Many congenital heart defects can be diagnosed
prenatally by fetal echocardiography. This is a test which
can be done during the second trimester of pregnancy,
when the woman is about 18 – 24 weeks pregnant. It can
be an abdominal ultrasound or transvaginal ultrasound.
If a baby is born with cyanotic heart disease, the diagnosis
is usually made shortly after birth due to the blue color of
their skin (called cyanosis).
If a baby is born with a septal defect or an obstruction
defect, often their symptoms are only noticeable after
several months or sometimes even after many years.
Treatment
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Sometimes CHD improves without treatment. Other
defects are so small that they do not require any
treatment. Most of the time CHD is serious and requires
surgery and/or medications. Medications include
diuretics, which aid the body in eliminating water, salts,
and digoxin for strengthening the contraction of the heart.
This slows the heartbeat and removes some fluid from
tissues. Some defects require surgical procedures to
restore circulation back to normal and in some cases,
multiple surgeries are needed.
Interventional cardiology now offers patients minimally
invasive alternatives to surgery for some patients. The
Melody Transcatheter Pulmonary Valve (TPV), approved
in Europe in 2006 and in the U.S. in 2010 under a
Humanitarian Device Exemption (HDE), is designed to
treat congenital heart disease patients with a dysfunctional
conduit in their right ventricular outflow tract (RVOT).
The RVOT is the connection between the heart and lungs;
once blood reaches the lungs, it is enriched with oxygen
before being pumped to the rest of the body.
Transcatheter pulmonary valve technology provides a
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less-invasive means to extend the life of a failed RVOT
conduit and is designed to allow physicians to deliver a
replacement pulmonary valve via a catheter through the
patient’s blood vessels.
Most patients require lifelong specialized cardiac care,
first with a pediatric cardiologist and later with and adult
congenital cardiologist. There are more than 1.8 million
adults living with congenital heart defects.
Arrhythmias:
An arrhythmia is a disorder of the heart rate (pulse) or
heart rhythm, such as beating too fast (tachycardia), too
slow (bradycardia), or irregularly.
Causes
Normally, your heart works as a pump that brings blood
to the lungs and the rest of the body.
To help this happen, your heart has an electrical system
that makes sure it contracts (squeezes) in an orderly way.
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The electrical impulse that signals your heart to
contract begins in the sinoatrial node (also called the sinus
node or SA node). This is your heart's natural pacemaker.
The signal leaves the SA node and travels through the
heart along a set electrical pathway.
Different nerve messages signal your heart to beat
slower or faster.
Arrhythmias are caused by problems with the heart's
electrical conduction system.
Abnormal (extra) signals may occur
Electrical signals may be blocked or slowed
Electrical signals travel in new or different pathways
through the heart
Some common causes of abnormal heartbeats are:
Abnormal levels of potassium or other substances
Heart attack, or a damaged heart muscle from a past
heart attack
Heart disease that is present at birth (congenital)
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Heart failure or an enlarged heart
Overactive thyroid gland
Arrhythmias may also be caused by some substances or
drugs, including:
Alcohol, caffeine,
amphetamines
or
stimulants
such
as
Beta-blockers
Cigarette smoking (nicotine)
Drugs that mimic the activity of your nervous system
Medicines used for depression or psychosis
Sometimes anti-arrhythmic medications -- prescribed to
treat one type of arrhythmia -- will cause another type of
arrhythmia.
Some of the more common abnormal heart rhythms are:
Atrial fibrillation or flutter
Atrioventricular nodal reentry tachycardia (AVNRT)
Heart block or atrioventricular block
Multifocal atrial tachycardia
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Paroxysmal supraventricular tachycardia
Sick sinus syndrome
Ventricular fibrillation or ventricular tachycardia
Wolff-Parkinson-White syndrome
Symptoms:
When we have an arrhythmia, our heartbeat may be:
Too slow (bradycardia)
Too quick (tachycardia)
Irregular, uneven, or skipping beats
An arrhythmia may be present all of the time or it may
come and go. We may or may not feel symptoms when
the arrhythmia is present. Or, we may only notice
symptoms when we are more active.
Symptoms can be very mild, or they may be severe or
even life-threatening.
Common symptoms that may occur when the arrhythmia
is present include:
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Chest pain
Fainting
Light-headedness, dizziness
Paleness
Shortness of breath
Sweating
Exams and Tests:
The doctor will listen to your heart with a stethoscope and
feel your pulse. Our blood pressure may be low or
normal.
Heart monitoring devices are often used to identify the
rhythm problem, such as a:
Holter monitor (used for 24 hours)
Event monitor or loop recorder (worn for 2 weeks or
longer)
Other tests may be done to look at heart function:
Coronary angiography
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ECG (electrocardiogram)
Echocardiogram
A special test, called an electrophysiology study (EPS), is
done to take a closer look at the heart's electrical system.
Treatment:
When an arrhythmia is serious, you may need urgent
treatment to restore a normal rhythm. This may include:
Electrical
cardioversion)
"shock"
therapy
(defibrillation
or
Implanting a short-term heart pacemaker
Medications given through a vein (intravenous) or by
mouth
Sometimes, getting better treatment for your angina or
heart failure will decrease the chance of having an
arrhythmia.
Medications called anti-arrhythmic drugs may be used:
To prevent an arrhythmia from happening again
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To keep heart rate from becoming too fast or too
slow
Some of these medicines can have side effects. Take them
as prescribed by your health care provider. Do not stop
taking the medicine or change the dose without first
talking health care provider.
Other treatments to prevent or treat abnormal heart
rhythms include:
Cardiac ablation used to destroy areas in heart that
may be causing heart rhythm problems
An implantable cardiac defibrillator is placed in
people who are at high risk of sudden cardiac death
Pacemaker, a device that senses when heart is beating
irregularly, too slowly, or too fast. It sends a signal to
heart that makes heart beat at the correct pace.
Myocarditis:
Myocarditis or inflammatory cardiomyopathy
inflammation of heart muscle (myocardium).
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is
Myocarditis is most often due to infection by common
viruses, such as parvovirus B19, less commonly nonviral
pathogens such as Borrelia burgdorferi (Lyme disease) or
Trypanosoma cruzi, or as a hypersensitivity response to
drugs.
The definition of myocarditis varies, but the central
feature is an infection of the heart, with an inflammatory
infiltrate, and damage to the heart muscle, without the
blockage of coronary arteries that define a heart attack
(myocardial infarction) or other common noninfectious
causes.Myocarditis may or may not include death
(necrosis) of heart tissue. It may include dilated
cardiomyopathy.
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Figur: Myocarditis
Myocarditis is often an autoimmune reaction.
Streptococcal M protein and coxsackievirus B have
regions (epitopes) that are immunologically similar to
cardiac myosin. During and after the viral infection, the
immune system may attack cardiac myosin.
Because a definitive diagnosis requires a heart biopsy,
which doctors are reluctant to do because they are
invasive, statistics on the incidence of myocarditis vary
widely.
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The consequences of myocarditis thus also vary widely. It
can cause a mild disease without any symptoms that
resolves itself, or it may cause chest pain, heart failure, or
sudden death. An acute myocardial infarction-like
syndrome with normal coronary arteries has a good
prognosis. Heart failure, even with dilated left ventricle,
may have a good prognosis. Ventricular arrhythmias and
high-degree heart block have a poor prognosis. Loss of
right ventricular function is a strong predictor of death.
Signs and symptoms:
The signs and symptoms associated with myocarditis are
varied, and relate either to the actual inflammation of the
myocardium, or the weakness of the heart muscle that is
secondary to the inflammation. Signs and symptoms of
myocarditis include:Chest pain (often described as "stabbing" in
character)
Congestive heart failure (leading
breathlessness and hepatic congestion)
Palpitations (due to arrhythmias)
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to
edema,
Sudden death (in young adults, myocarditis causes up
to 20% of all cases of sudden death)
Fever (especially when infectious, e.g. in rheumatic
fever)
Symptoms in infants and toddlers tend to be more
nonspecific, with generalized malaise, poor appetite,
abdominal pain, and/or chronic cough. Later stages of the
illness will present with respiratory symptoms with
increased work of breathing, and is often mistaken for
asthma.
Since myocarditis is often due to a viral illness, many
patients give a history of symptoms consistent with a
recent viral infection, including fever, rash, diarrhea, joint
pains, and easy fatigueability.
Myocarditis is often associated with pericarditis, and
many patients present with signs and symptoms that
suggest concurrent myocarditis and pericarditis.
Causes:
A large number of causes of myocarditis have been
identified, but often a cause cannot be found. In Europe
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and North America, viruses are common culprits.
Worldwide, however, the most common cause is Chagas'
disease, an illness endemic to Central and South America
that is due to infection by the protozoan Trypanosoma
cruzi.
Infections:
Viral (parvovirus B19, coxsackie virus, HIV,
enterovirus, rubella virus, polio virus, cytomegalovirus,
human herpesvirus 6 and possibly hepatitis C)
Protozoan (Trypanosoma cruzi causing Chagas
disease and Toxoplasma gondii)
Bacterial (Brucella, Corynebacterium diphtheriae,
gonococcus, Haemophilus influenzae, Actinomyces,
Tropheryma whipplei, Vibrio cholerae, Borrelia
burgdorferi, leptospirosis, and Rickettsia)
Fungal (Aspergillus)
Parasitic
(ascaris,
Echinococcus
granulosus,
Paragonimus westermani, schistosoma, Taenia solium,
Trichinella spiralis, visceral larva migrans, and
Wuchereria bancrofti)
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Bacterial myocarditis is rare in patients without
immunodeficiency.
Toxins:
Drugs (ethanol, anthracyclines and some other forms
of chemotherapy, and antipsychotics, e.g. clozapine, also
some designer drugs such as mephedrone)[5]
Immunologic:
Allergic (acetazolamide, amitriptyline)
Rejection after a heart transplant
Autoantigens
(scleroderma,
systemic
lupus
erythematosis, sarcoidosis, systemic vasculitis such as
Churg-Strauss syndrome, and Wegener's granulomatosis)
Toxins (arsenic, toxic shock syndrome toxin, carbon
monoxide, or snake venom)
Heavy metals (copper or iron)
Physical agents:
Electric shock, hyperpyrexia, and radiation
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Diagnosis:
Endomyocardial biopsy specimen with extensive
eosinophilic infiltrate involving the endocardium and
myocardium (hematoxylin and eosin stain)
Myocarditis refers to an underlying process that causes
inflammation and injury of the heart. It does not refer to
inflammation of the heart as a consequence of some other
insult. Many secondary causes, such as a heart attack, can
lead to inflammation of the myocardium and therefore the
diagnosis of myocarditis cannot be made by evidence of
inflammation of the myocardium alone.
Myocardial inflammation can be suspected on the basis of
electrocardiographic (ECG) results, elevated C-reactive
protein (CRP) and/or Erythrocyte sedimentation rate
(ESR) and increased IgM (serology) against viruses
known to affect the myocardium. Markers of myocardial
damage (troponin or creatine kinase cardiac isoenzymes)
are elevated.
The ECG findings most commonly seen in myocarditis
are diffuse T wave inversions; saddle-shaped ST-segment
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elevations may be present (these are also seen in
pericarditis).
The gold standard is still biopsy of the myocardium,
generally done in the setting of angiography. A small
tissue sample of the endocardium and myocardium is
taken, and investigated by a pathologist by light
microscopy and—if necessary—immunochemistry and
special staining methods. Histopathological features are
myocardial interstitium with abundant edema and
inflammatory infiltrate, rich in lymphocytes and
macrophages. Focal destruction of myocytes explains the
myocardial pump failure.
Cardiac magnetic resonance imaging (cMRI or CMR) has
been shown to be very useful in diagnosing myocarditis
by visualizing markers for inflammation of the
myocardium. Recently, consensus criteria for the
diagnosis of myocarditis by CMR have been published.
Treatment:
As most viral infections cannot be treated with directed
therapy, symptomatic treatment is the only form of
therapy for those forms of myocarditis. In the acute
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phase, supportive therapy, including bed rest, is indicated.
For symptomatic patients, digoxin and diuretics provide
clinical improvement. For patients with moderate to
severe dysfunction, cardiac function can be supported by
use of inotropes such as Milrinone in the acute phase,
followed by oral therapy with ACE inhibitors (Captopril,
Lisinopril) when tolerated. People who do not respond to
conventional therapy are candidates for bridge therapy
with left ventricular assist devices. Heart transplantation
is reserved for patients who fail to improve with
conventional therapy.
In several small case series and randomized control trials,
systemic corticosteroids have shown to have beneficial
effects in patients with proven myocarditis. However,
data on the usefulness of corticosteroids should be
interpreted with caution, since 58% of adults recover
spontaneously, while most studies on children and infants
lack control groups.
Epidemiology:
The exact incidence of myocarditis is unknown. However,
in series of routine autopsies, 1–9% of all patients had
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evidence of myocardial inflammation. In young adults, up
to 20% of all cases of sudden death are due to
myocarditis.
Among patients with HIV, myocarditis is the most
common cardiac pathological finding at autopsy, with a
prevalence of 50% or more.
Heart Disease Risk Factors:
Some conditions as well as some lifestyle factors can put
people at a higher risk for developing heart disease. All
persons can take steps to lower their risk of heart disease
and heart attack by addressing these risk factors. Control
of risk factors is especially need by people who already
have heart disease.
Conditions
Behavior
Heredity
Heart Disease Conditions:
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Blood cholesterol levels
High blood pressure
Diabetes mellitus
Blood
Cholesterol
Levels:
Cholesterol is a waxy substance produced by the liver or
consumed in certain foods. It is needed by the body, and
the liver makes enough for the body's needs. When there
is too much cholesterol in the body—because of diet and
the rate at which the cholesterol is processed—it is
deposited in arteries, including those of the heart. This
can lead to narrowing of the arteries, heart disease, and
other complications.
Some cholesterol is often termed "good," and some often
termed "bad." A higher level of high–density lipoprotein
cholesterol, or HDL, is considered "good," and gives
some protection against heart disease. Higher levels of
low–density lipoprotein, or LDL, are considered "bad"
and can lead to heart disease. A lipoprotein profile can be
done to measure several different forms of cholesterol, as
well as triglycerides (another kind of fat) in the blood.
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High
Blood
Pressure:
High blood pressure is another major risk factor for heart
disease. It is a condition where the pressure of the blood
in the arteries is too high. There are often no symptoms to
signal high blood pressure. Lowering blood pressure by
changes in lifestyle or by medication can lower the risk of
heart disease and heart attack.
Diabetes
Mellitus:
Diabetes also increases a person's risk for heart disease.
With diabetes, the body either doesn't make enough
insulin, can't use its own insulin as well as it should, or
both. This causes sugars to build up in the blood. About
three–quarters of people with diabetes die of some form
of heart or blood vessel disease. For people with diabetes,
it is important to work with a healthcare provider to help
in managing it and controlling other risk factors.
Heart Disease Behavior:
Tobacco use
Diet
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Physical inactivity
Obesity
Alcohol
Tobacco Use
Tobacco use increases the risk of heart disease and heart
attack. Cigarette smoking promotes atherosclerosis and
increases the levels of blood clotting factors, such as
fibrinogen. Also, nicotine raises blood pressure, and
carbon monoxide reduces the amount of oxygen that
blood can carry. Exposure to other people's smoke can
increase the risk of heart disease even for nonsmokers.
Diet
Several aspects of peoples' dietary patterns have been
linked to heart disease and related conditions. These
include diets high in saturated fats and cholesterol, which
raise blood cholesterol levels and promote atherosclerosis.
High salt or sodium in the diet causes raised blood
pressure levels.
Physical Inactivity
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Physical inactivity is related to the development of heart
disease. It also can impact other risk factors, including
obesity, high blood pressure, high triglycerides, a low
level of HDL (good) cholesterol, and diabetes. Regular
physical activity can improve risk factor levels.
Obesity
Obesity is excess body fat. It is linked to higher LDL
(bad) cholesterol and triglyceride levels and to lower
HDL (good) cholesterol, high blood pressure, and
diabetes.
Alcohol
Excessive alcohol use leads to an increase in blood
pressure, and increases the risk for heart disease. It also
increases blood levels of triglycerides which contribute to
atherosclerosis.
Heart Disease Heredity:
Heart disease can run in the family. Genetic factors likely
play some role in high blood pressure, heart disease, and
other vascular conditions. However, it is also likely that
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people with a family history of heart disease share
common environments and risk factors that increase their
risk. The risk for heart disease can increase even more
when heredity is combined with unhealthy lifestyle
choices, such as smoking cigarettes and eating a poor diet.
Prevention of Heart Disease:
We can help prevent heart disease by making healthy
choices and managing any medical conditions you may
have.
Live a Healthy Lifestyle
Guidelines and Recommendations
Live a Healthy Lifestyle
Eat a healthy diet. Choosing healthful meal and snack
options can help avoid heart disease and its
complications. Be sure to eat plenty of fresh fruits and
vegetables.
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Eating foods low in saturated fat and cholesterol and high
in fiber can help prevent high blood cholesterol. Limiting
salt or sodium in diet can also lower blood pressure.
For more information on healthy diet and nutrition, see
CDC's Nutrition and Physical Activity Program Web site.
Maintain a healthy weight. Being overweight or
obese can increase your risk for heart disease. To
determine whether your weight is in a healthy range,
doctors often calculate a number called the body mass
index (BMI). Doctors sometimes also use waist and hip
measurements to measure a person's excess body fat.
If you know your weight and height, you can calculate
your BMI at CDC's Assessing Your Weight Web site.
Exercise regularly. Physical activity can help you
maintain a healthy weight and lower cholesterol and
blood pressure. The Surgeon General recommends that
adults should engage in moderate-intensity exercise for at
least 30 minutes on most days of the week.
For more information, see CDC's Nutrition and Physical
Activity Program Web site.
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Don't smoke. Cigarette smoking greatly increases
your risk for heart disease. So, if you don't smoke, don't
start. If you do smoke, quitting will lower your risk for
heart disease. Your doctor can suggest ways to help you
quit.
For more information about tobacco use and quitting, see
CDC's Smoking & Tobacco Use Web site.
Limit alcohol use. Avoid drinking too much alcohol,
which causes high blood pressure. For more information,
visit CDC's Alcohol and Public Health Web site.
Prevent or Treat Medical Conditions
If we have high cholesterol, high blood pressure, or
diabetes, there are steps we can take to lower risk for
heart disease.
Have cholesterol checked. Our health care provider
should test cholesterol levels at least once every five
years. Talk with doctor about this simple blood test.
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Monitor blood pressure. High blood pressure has no
symptoms, so be sure to have it checked on a regular
basis.
Manage diabetes. If we have diabetes, closely
monitor blood sugar levels. Talk with health care provider
about treatment options.
Take medicine. If taking medication to treat high
cholesterol, high blood pressure, or diabetes, follow
doctor's instructions carefully. Always ask questions if we
don't understand something.
Talk with health care provider. Doctor can work
together to prevent or treat the medical conditions that
lead to heart disease. Discuss treatment plan regularly and
bring a list of questions to
appointments.
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Guidelines and Recommendations:
Recommendations of Aspirin for Prevention of
Cardiovascular Disease.
The Seventh Report of the Joint National Committee
on Prevention, Detection, Evaluation, and Treatment of
High Blood Pressure.
This report provides evidence-based guidelines about
preventing and managing high blood pressure. From the
National Heart, Blood, and Lung Institute.
Third Report of the Expert Panel on Detection,
Evaluation, and Treatment of High Blood Cholesterol in
Adults (Adult Treatment Panel III).
Provides evidence-based guidelines about screening for
and treating high cholesterol. From the National Heart,
Blood, and Lung Institute.
Clinical Guidelines on the Identification, Evaluation,
and Treatment of Overweight and Obesity in Adults.
Provides evidence-based guidelines about screening for
and treating overweight and obesity. From the National
Heart, Lung, and Blood Institute.
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Physical Activity and Health: A Report of the
Surgeon General
the first Surgeon General’s Report specifically addressing
physical activity and health.
2008 Physical Activity Guidelines for Americans.
These science-based guidelines provide strategies for
Americans to improve their health through physical
activity.
Surgeon General's Reports Related to Tobacco Use
Links to reports concerning smoking and health, including
reports on involuntary exposure to tobacco smoke and on
tobacco use among ethnic minority groups.
Dietary Guidelines for Americans.
Provides authoritative advice about good dietary habits
that can promote health and reduce risk of disease.
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