Investigations CVD

Investigations

Angiography
• also known as arteriography
• X-ray examination that shows blood flow in the arteries and veins
• Shows whether blood vessels are narrow, irregular or blocked (eg. Due to arterosclerosis)
• Reveal thrombosis, aneurysm.
• Detects the development of clumps of new blood vessels (tumours, cysts)
How is it performed?
• Anaesthetic is given (usually local; children – general)
• Needle inserted into an artery (leg, arm, groin)
Femoral artery usually used
– access to heart’s left ventricle, aorta and all it’s branches
- Lowest complication rate
• Needle is in place, long thin guide wire guided into blood vessel that needs to be examined (using fluorescent screen)
• Catheter is slipped over it pushed along until tip is in the right position
• Guide wire removed and dye injected
• Image viewed on screen / rapid sequence of X-ray pictures for further investigation (flouroscopy)

Cardiac MRI
• Non-invasive test
• Uses radio waves and magnets to create pictures of organs and tissues
• No radiation
• Uses computer to create image of the heart and blood vessels (both still and moving)
• To diagnose and evaluate: -
- Coronary Artery Disease
- Damage due to Myocardial Infarction
- Heart failure
- Heart valve problem
• Sometimes dye is injected into veins to highlight heart or blood vessel in images

CT Scan
 X-ray pictures of the heart is taken (involves radiation)
 X-ray machine move around to capture images of different parts of the heart
 Each picture shows a small slice of the heart
 Computer puts picture together to make large image of the whole heart.
Use to investigate and diagnose:-
 Blocked or narrowed arteries
 Aneurysm in the aorta
 To locate a pulmonary embolism

Echocardiography
 High frequency sound wave to produce moving picture of heart
 Used to:
- detect weakened heart muscles
- measure size of the heart
- detect abnormalities in heart
(eg. Hole in septum)

Electrocardiogram
 Measure electrical activity of the heart
 used to measure:
- Any damage to the heart
- How fast your heart is beating and whether it is beating normally
- The size and position of your heart chambers

Cardiac Marker test
 To diagnose, evaluate and monitor patients with suspected acute coronary syndrome.
 Test blood for proteins which include:-
- Creatine kinase (CK)
- Creatine kinase-MB (CKMB)
- Myoglobin
- Cardiac troponin I or cardiac troponin T
 (CK, CKMB and Myoglobin found in other muscles, so troponin is usually used)
 Found in cardiac cells, released in blood after myocardial infarction

Links
http://www.nhs.uk/Conditions/Angiography
http://www.nhlbi.nih.gov/health/dci/Diseases
http://circ.ahajournals.org/cgi/content/full/109/3/e12
http://pathcuric1.swmed.edu/PathDemo/nrrt.htm#Chem
http://www.rcpamanual.edu.au/sections/pathologytest.asp?s=33&i=450
http://www.amarillomed.com/howto.htm

prevention

primary prevention
the main objective is to reduce risk of CVD. please look at risk factors and how it can cause CVD.
1) stop smoking
2) Exercise
- related to diabetes type 2
- obesity
- improved lipid profile
- improved insulin resistance
- improved endothelial function
- reduced risk of thrombogenesis
- reduced re-hospitalisations & repeat revascularizations
- lowers blood pressure
3) stress managament
- stress can increase risk of CVD
- hypertension
4) Diet
- Sugar
You should limit your sugar intake to not more than 15% of your total daily energy requirement. High intake of sugar in place of fat is accompanied by reduction in HDL cholesterol and rise in triglycerides.
- Dietary fiber
An increase in soluble or viscous fiber of 5-10g per day is accompanied by 5% reduction in LDL cholesterol.
- Lipid management. eat more omega 3 as it lowers LDL
- Salt – hypertension
- Alcohol consumption
Having one to two alcohol drinks a day may lead to a 30% reduction in heart disease, but above this level alcohol consumption will damage the heart muscle.

Secondary prevention
This is if you have the predisposing factors to CVD

Chronic atrial fibrillation
-Irregular pulse should be verified by an electrocardiogram. Conversion of appropriate individuals to normal sinus rhythm.
-For patients in chronic or intermittent atrial fibrillation, use warfarin anticoagulants

control of type 2 diabetes
-twice as likely to develop cardiovascular disease.
-hypoglycemic therapy – drugs (metformin), insulin
-Exercise - reduced incidence of NIDDM
-prevent/delay onset of complications of IDDM & NIDDM
-reduces insulin requirements in IDDM patients

hypertension
-Reduce salt intake
-Limit alcohol intake
-Antiplatelet agents/anticoagulants
-aspirin at 75 to 162 mg/d

hyperlipidemia
- increase physical activity
- LDL lowering drug therapy
- Fibrate, statin
- Weight reduction
- Diet- increase fiber intake

Tertiary prevention
This prevention is related to treatment and management after you have gotten myocardiac infarction.
- Beta blockers – reduces heart rate
- Renin-angiotensin-aldosterone system blockers
- Antiplatelet agents/anticoagulants
- receive higher-dose aspirin at 325 mg/d
- Statins – hyperlipidemia (lipid regulating)

Pathophysiology and Complications

Pathophysiology & Complications by Tim, Tin Yee & Me
Hypertension and Atherosclerosis

• The normal endothelium appears to exhibit an inhibitory influence on vascular smooth muscle cell growth
• Dysfunctional endothelium in hypertension contributes to or permits vascular smooth cell growth, which contributes to narrowing of the lumen
• increase the distance required for diffusion of oxygen from the lumen à would result in incomplete oxidation and lead to increased concentrations of free radicalsThis oxygen radical formation would contribute to tissue damage and lipid oxidation

Hypercholesterolemia And Atherosclerosis

• Hypercholesterolemia : an excess of cholesterol in the blood
  ¢causes increased formation of superoxide anion which causes impairment of endothelial function
• These alterations were observed in morphologically intact arteries, suggesting that impaired NO-mediated endothelium-dependent relaxation is a precursor of intimal thickening and development of atherosclerotic lesions
• Oxygen free radicals such as O2- can cause a wide spectrum of cell damage, including lipid peroxidation, inactivation of enzymes, alteration of intracellular redox state, and damage to DNA. They participate in the pathogenesis of atherosclerosis

Atherosclerosis

• As a result of endothelial injury, there is a proliferation of cells within the inner layer of the arterial(intima) and accumulation of cholesterol and other lipid within their cytoplasm
• Cholesterol seeps across the damaged endothelium and accumulates in the arterial wall, where it is ingested by macrophages and monocytes à a foamy appearance (foam cells)
• Inflammatory cells, smooth muscle cells, and macrophages migrate into the area, where cholesterol accumulates, and assemble as a soft tissue mass. Some of these cells accumulate so much cholesterol that precipitates as crystals within the cytoplasm disrupting the cells and causing cell necrosis
• Cholesterol crystals debris and enzymes escape from the disrupted cells inducing secondary fibrosis, calcification and other degenerative changes in the arterial wall.
• The end result is an irregular mass of yellow, mushy debris that encroaches on the lumen of the artery and extends more deeply into the muscular and elastic tissue of the arterial wall. The plaque like deposit of material is called and atheromatous plaque or atheroma
• This early soft atheromas obstruct flow. Often the smooth internal lining of the vessel becomes ulcerated over the surface of the fatty deposits, leaving a roughened surface that predisposes thrombus formation
  - They are unstable and especially dangerous because they may break open or haemorrhage stimulating thrombosis, acute occlusion and downstream tissue infarction
• By contrast all atherosclerosis regions tend to be scarred, hard and calcified. They may impede blood flow gradually producing downstream ischemia but they are stable and not commonly the cause of acute thrombosis and infarction because they are not as likely to occlude suddenly
• The initial stage in the development of atherosclerosis is reversible and the newly formed plaques are called unstable plaques. The latter stages, characterized by crystallization of cholesterol and secondary degenerative diseases changes, are irreversible
• The plaques, which become surrounded by fibrous tissue, are called stable plaques, and the vessel become permanently narrowed

Manifestations and complications

• atherosclerotic plaques narrow the arteries by 50 percent or more - the arteries may still be able to supply enough blood to the heart muscle if the individual is not very active and no excessive demands are placed on the heart
  -The blood supply may become inadequate if the subject exerts himself and heart requires more blood to satisfy the increased demands
• Myocardial ischemia is the term commonly used to describe a reduced blood supply to the heart muscle caused by narrowing or obstruction of the coronary arteries
• The clinical manifestations of coronary heart disease are quite variable. Although many individuals are free of symptoms, some experience bouts of oppressive chest pain that may radiate into the neck or arms. The pain, which is caused by myocardial ischemia, is called angina pectoris(“pain of the chest”)
• The usual type of angina is a midsternal pressure discomfort that occurs on exertion and subsides when the person rests. This is known as stable angina
• Unstable angina is characterized by episodes of pain that occur more frequently; last longer, and less completely relieved by nitroglycerine.
• Prinzmetal’s angina is a type of angina that characteristically occurs at rest rather than on exertion and is caused by coronary artery spasm

Arterial Thrombosis

• Blood flow in arteries is rapid. Therefore stasis is not involved in thrombosis of the artery.
• Main cause – injury to the wall of the vessel, secondary to arteriosclerosis
• Arteriosclerotic deposits cause ulceration and roughening of the lining of the artery, thrombi forms on the roughened area.
• Effects of the arterial thrombus formation depend on the location and size of the artery that has become obstructed.
• Blockage of :
  —Coronary artery – Leads to MI
  —Major artery in the leg – Gangrene occurs due to necrosis
  —Artery to the brain – Infarction of portion of brain, stroke

More severe and prolonged mycardial ischemia may percipitate an acute episode called a heart attack
- This event may be manifested as either cesation of normal cardiac contractions, called a cardiac arrest, or an actual necrosis of heart muscle, which is termed a myocardial infarction
Any one of the four basic mechanisms may trigger a heart attack in a patient with a coronary artery disease.
1.Sudden blockage of a coronary artery
2.Hemorrhage into an atheromatous plaque
3.Arterial spasm
4.Sudden greatly increased myocardial oxygen requirements

Myocardial Infarction

• Is a necrosis of heart muscle resulting from severe ischemia
• occurs when blood flow through one of the coronary arteries is insufficient to sustain the heart muscle and when collateral blood flow into the ischemic muscle from other coronary arteries is inadequate
• associated with severe chest pain and often with shock and collapse
• may involve the full thickness of the muscular wall (extending from endocardium to epicardium is called a transmural infarct and is usually the result of thrombosis of a major coronary artery) or only part of the muscular wall(subendocardial infarct)

Cardiac Arrest

• Myocardial ischemia increases myocardial irritability, lead to disturbances of cardiac rhythm(cardiac arrhythmias)
• Arrest occurs when an arrhythmia induced by prolonged or severe myocardial ischemia disrupts the pumping of the ventricles
• Most devastating: uncoordinated quivering of the ventricles that is called ventricular fibrillation(rapidly fatal because the normal pumping action of the ventricles ceases)
  -possible to stop the fibrillation by delivering an electric shock to the heart by means of electrodes applied to the chest
• A less common cause of cardiac arrest is complete cessation of cardiac contractions, which is called an asystole

COMPLICATIONS OF MYOCARDIAL INFARCTS

Patients who sustain a myocardial
infarction are subject to complications that fall into 7 categories:
-Disturbances of cardiac rhythm (arrhythmias)
-Heart Failure
-Intracardial Thrombi
-Pericarditis
-Cardiac rupture
-Papillary muscle dysfunction
-Ventricular aneurysm

ARRHYTHMIAS

• Disturbances of cardiac rhythm – common after Myocardial Infarct
• result from the extreme irritability of the ischemic heart muscle adjacent to the infarct and can frequently be controlled by drugs that reduce myocardial irritability
• most serious arrhythmia - ventricular fibrillation, which leads to cessation of the circulation
• Another type of disturbance of cardiac rhythm occurs if the conduction system of the heart is damaged by the infarct
• Conduction of impulses from the atria to the ventricles may be disturbed(heart block)
• The conduction disturbance may subside spontaneously as the infarct heals, but sometimes it is necessary to insert various types of electrodes directly into the heart in order to stimulate the ventricles to contract properly
• A device of this type is called a cardiac pacemaker
  - electrode is passed into a large vein in the upper arm, near the shoulder, and threaded downward into the heart until it makes contact with the wall of the right ventricle
  - then the electrode is connected to a small battery
  - the electrode stimulates the ventricles at a predetermined rate and causes them to contract at a faster, more normal rate

HEART FAILURE

• Ventricle may be so badly damaged that it is unable to maintain normal cardiac function, and the heart fails
• Heart failure may develop abruptly(acute heart failure) or a more slowly (chronic heart failure), as described in a subsequent section, and may be difficult to treat

INTRACARDIAL THROMBI

• The infarct extends to involve the endocardium, thrombi may form on the interior of the ventricular wall and cover the damaged endocardial surface(mural thrombus)
• Bits of the thrombus may break loose and be carried as emboli into the systemic circulation, causing infarctions in other organs(e.g. brain, spleen, kidneys)
• Some physicians attempt to forestall this complication by administering anticoagulants when a patient has sustained a severe infarction

PERICARDITIS

• an infarct extends to involve the epicardial surface, the inflammatory process resulting from myocardial necrosis may spread to include the overlying epicardium
• lead to accumulation of fluid and inflammatory cells in pericardial sac(pericarditis)
• may cause chest pains

CARDIAC RUPTURE

• patient sustains a transmural infarct, a perforation may occur through the necrotic muscle
• permits blood to leak through the rupture into the pericardial sac
• as the blood accumulates, it compresses the heart so the ventricles cannot fill in diastole(event is called a cardiac tamponade)
• eventually the circulation ceases because the heart is no longer able to pump blood
• Less commonly, rupture occurs through the ventricular septum or papillary muscle
• Full thickness infarction of the ventricular septum may lead to septal perforation (which allows blood to leak from the left ventricle into the right ventricle during ventricular contractions instead of being ejected normally) à the output of blood from the left ventricle is reduced greatly, which often leads to severe heart failure
• An infarcted papillary muscle may tear loose from its attachment to the ventricular wall à a loss of “guy wire” support for the mitral valve leaflet to which it is attached and permits the leaflet to prolapse into the left atrium during systole. This complication results in severe mitral insufficiency, which often leads to heart failure

PAPILLARY MUSCLE DYSFUNCTION

• Normally, the papillary muscle contracts during ventricular systole along with the rest of the ventricle, exerting tension on the chordae to prevent prolapse of the mitral valve leaflets into the left atrium during systole
• If a papillary muscle becomes infarcted, it is unable to contract normally and is less able to control the movement of the attached mitral valve leaflet
• So, even if the papillary muscle does not rupture, its malfunction often allows the mitral valve to prolapse slightly into the left atrium, and a mild degree of mitral insufficiency develops

VENTRICULAR ANEURYSM

• Usually a late complication of myocardial infarction
• It is an outward bulging of the healing infarct during ventricular systole
• There are two adverse effects on ventricular function. The damaged area is unable to contract; so the overall efficiency of the left ventricular function is reduced. Moreover, as the ventricle contracts and the intraventricular pressure rises during systole, the aneurysm fills with blood and balloons out
• Consequently, part of the volume of blood within the ventricle is wasted because it fills the aneurysm rather than being ejected into the aorta, and the cardiac output is reduced correspondingly

References

1. http://hyper.ahajournals.org/cgi/content/full/25/2/155
2. http://hyper.ahajournals.org/cgi/content/full/25/2/155#SEC5
3. http://circres.ahajournals.org/cgi/content/abstract/86/1/101
4. The Nature of Disease, Pathology for the Health Professional, Thomas H Mc Connell, Lipincott.
5. An Introduction to Human Diseases, Pathology and Physiology Correlations,7th edition, Leonard V Crowley.
   

Signs and symptoms of CVD (edited)

*Note: Cardiovascular diseases include coronary heart disease (heart attacks), cerebrovascular disease, raised blood pressure (hypertension), peripheral artery disease, rheumatic heart disease, congenital heart disease and heart failure.
* there are no symptoms of the underlying disease of the blood vessels. A heart attack or stroke may be the first warning of underlying disease.

Signs
Signs found during a doctor's appointment:

high blood pressure,

Hypotension (reflect on more severe ischaemia),

a heart murmur,

Anxious and restless (common among patients with acute myocardial infarction),

Confusion (due to impaired cerebral flow),

swelling in the ankles or legs (peripheral edema),

Pulmonary edema (due to acute heart failure) which leads to acute dsypnoea,

Tachypnea (rapid breathing) or periodic breathing,

Fainting,

Cold and clammy skin or pallor,

Ascites,

Cachectic (due to severe chronic congestive heart failure)

Symptoms (Heart Attack)
Symptoms of a heart attack include:
pain or discomfort in the centre of the chest;
pain or discomfort in the arms, the left shoulder, elbows, jaw, or back.
may experience difficulty in breathing or shortness of breath;
feeling sick or vomiting;
feeling light-headed or faint;
breaking into a cold sweat;
and becoming pale.

Women are more likely than are men to also have symptoms unrelated to chest pain, such as:
Neck, jaw, shoulder, upper back or abdominal discomfort
Shortness of breath
Nausea or vomiting
Abdominal pain or "heartburn"
Sweating
Lightheadedness or dizziness
Unusual or unexplained fatigue

Sensation of rapid heartbeats = palpitations
swelling caused by an abnormal accumulation of fluid in body tissues = Edema
Difficult, labored breathing,; shortness of breath = Dyspnea
Light-headedness or fainting caused by insufficient blood supply to the brain = syncope
Difficulty breathing related to body position, especially shortness of breath while lying on the back = orthopnea

Symptoms (cerebrovascular) Most common symptom of a stroke:
sudden weakness of the face, arm, or leg, most often on one side of the body.

Other symptoms:
sudden onset of numbness of the face, arm, or leg, especially on one side of the body;
confusion, difficulty speaking or understanding speech;
difficulty seeing with one or both eyes;
difficulty walking, dizziness, loss of balance or coordination;
severe headache with no known cause;
and fainting or unconsciousness.

Symptoms (hypertension)
High blood pressure usually has no symptoms, but it can cause serious problems such as stroke, heart failure, heart attack and kidney failure. You can control high blood pressure through healthy lifestyle habits and taking medicines, if needed.

Symptoms (Peripheral artery disease)
-The most common early symptom is intermittent claudication (IC) - discomfort or pain in your legs that happens when you walk and goes away when you rest.
-May not always feel pain; instead you may feel a tightness, heaviness, cramping, or weakness in your leg with activity.
-With critical limb ischemia, you may experience pain in your feet or in your toes even when you are not walking.
-In severe peripheral artery disease, you may develop painful sores on your toes or feet. If the circulation in your leg does not improve, these ulcers can start as dry, gray, or black sores, and eventually become dead tissue (called gangrene).

Symptoms ( Rheumatic Heart Disease)
-a condition in which the heart valves are damaged by rheumatic fever.
-Rheumatic fever begins with a strep throat (also called strep pharyngitis), caused by Group A Streptococcus bacteria - most common bacterial infection of the throat.

symptoms of strep throat?
sudden onset of sore throat
pain on swallowing
fever, usually 101–104°F
headache
red throat/tonsils
abdominal pain, nausea and vomiting may also occur, especially in children

symptoms of rheumatic fever?
Fever
painful, tender, red swollen joints
pain in one joint that migrates to another one
heart palpitations
chest pain
shortness of breath
skin rashes
Fatigue
small, painless nodules under the skin
Symptoms (Congenital Heat Disease)
Symptoms can include:
Rapid breathing 
Cyanosis (a bluish tint to the skin, lips, and fingernails)
Fatigue (tiredness) 
Poor blood circulation
*Congenital heart defects DON’T cause chest pain or other painful symptoms.
Babies with congenital heart defects may have cyanosis or tire easily when feeding. Sometimes they have both problems. As a result, they may not gain weight or grow as they should
Older children may get tired easily or short of breath during exercise or activity.

Due to congenital heart disease, Heart works harder -> Heart Failure (*a condition in which the heart can't pump blood strongly throughout the body)

Symptoms (Heart Failure)
Fatigue with exercise
Shortness of breath
A buildup of blood and fluid in the lungs
A buildup of fluid in the feet, ankles, and legs
Cough with frothy sputum
increased urination at night
confusion and/or impaired memory
chronic lack of energy
difficulty sleeping at night due to breathing problems


Reference links:

http://images.google.com.my/imgres?imgurl=http://www.southwestlondoncardiacnetwork.nhs.uk/Images/HF_symptoms.gif&imgrefurl=http://www.southwestlondoncardiacnetwork.nhs.uk/Task%2520Groups/HeartFailure.html&usg=__k6-5BVZPwlABvKmQZ4DzBW4DaT0=&h=258&w=382&sz=35&hl=en&start=5&um=1&tbnid=6JkmTRecbm22JM:&tbnh=83&tbnw=123&prev=/images%3Fq%3Dheart%2Bfailure%26hl%3Den%26client%3Dfirefox-a%26rls%3Dorg.mozilla:en-US:official%26sa%3DN%26um%3D1

http://www.americanheart.org/presenter.jhtml?identifier=4709

http://www.medicinenet.com/congenital_heart_disease/page3.htm#6whatare

http://www.who.int/entity/cardiovascular_diseases/en/

http://www.genderandhealth.ca/en/modules/cardiovascular/cvd-case-mrs-heart-05.jsp

http://content.nhiondemand.com/psv/HC2.asp?objID=100610&cType=hc

http://www.vascularweb.org/patients/NorthPoint/Leg_Artery_Disease.html

Book: —Epstein et al (2008), Clinical Examination, 4th Edition, Mosby Elsevier, London.