Ischemia is the leading cause of death worldwide and myocardial infarction (MI) causes well over 12 million deaths per year internationally. However, with better detections and treatments, morbidity and mortality of this disease has been lessened.

When experiencing a myocardial infarction, the most evident symptom is the pain or pressure in the chest. Other symptoms include sweating, clamminess, nausea, shortness of breath and vomiting. A study done on differences in symptoms of myocardial infarction between genders found that men reported more chest pain and diaphoresis while women had more atypical syndromes (Patel et al 2004). Atypical syndromes include increased nausea, vomiting, dyspnea, palpitations, indigestion, dizziness, fatigue, loss of appetite and syncope.

Therefore in confirming diagnosis, an electrocardiogram or measuring the serum cardiac markers is a better detection method than just depending on physical syndromes described by the patients. Common cardiac markers include C-reactive protein (CRP), cardiac troponin I and troponin T, fatty acid binding protein (FABP), myoglobin and B-type natriuetic peptide (BNP). CRP is used frequently to detect general inflammation whereas troponin is the best and most accurate for detecting myocardial damage. Cardiac markers are able to confirm diagnosis of an myocardial infarction within 3 hours by measuring leakages of myocardial enzymes. The healing process begins within 6 to 12 hours following an infarction. Coagulated necrosis occurs in which the muscle fibers become intensely eosinophilic. The infarct is then penetrated by neutrophils by the first day and then the process of replacing and repairing is done by macrophages and reparative cells within the next few days. The healing process is ultimately completed when the damaged heart muscle is replaced by a mature scar tissue.

REFERENCES

Patel H, Rosengren A, Ekman I (2004). Symptoms in acute coronary syndromes: does sex make a difference? Am Heart J.:148(1);27-33

Discuss this here

Ischemia is the leading
cause of death worldwide and myocardial infarction (MI) causes well
over 12 million deaths per year internationally. However, with better
detection and treatments, morbidity and mortality of this disease
has been lessened.  This article provides a sweeping overview of treatment options.

Early treatment include
clot bursting drugs and ballooning the arteries open. Medication used
for treatment for angina pain includes nitrates, beta-blockers and
calcium channel blockers. These drugs are either to increase or
decrease the amount of blood that gets to the heart. Nitroglycerin,
a type of nitrate is not only used for patients that has suffered a
myocardial infarction within the first 24 hours, but also prescribed
for certain cases of ischemic angina, uncontrolled hypertension and
heart failure (Landmark & Reikvam 2003).

Coronary reperfusion
therapy is done depending on the clinical condition of the patients.
The three types are coronary thrombosis, percutaneous transluminal
coronary angioplasty (PTCA) and coronary bypass surgery. Angioplasty
is done to reduce or eliminate blockages in coronary arteries which
ultimately restore normal blood flow to the heart tissue. A review
was done to compare both thrombolytic reperfusion and angioplasty to
indicate the best treatment for myocardial infarction (Nordmann et al
2005). Angioplasty fares better than thrombosis in decreasing the
incidences of death, non-fatal MI and stroke but 50% of patients that
underwent angioplasty experience restenosis (regrowth of plaque).
Primary stenting is then done following angioplasty to keep the
arteries remain open. The authors concluded that although primary
stenting does not change mortality rate compared to those that only
underwent angioplasty, reinfaction may be lessened.

REFERENCES

Patel H, Rosengren A,
Ekman I (2004). Symptoms in acute coronary syndromes: does sex make a
difference? Am Heart J.:148(1);27-33

Landmark K, Reikvam A. (2003). Nitrate
therapy during and after acute myocardial infarction. Tidsskr Nor
Laegeforen.:123(23);3377-80

Nordmann A, Bucher H, Hengstler P, Harr
T, Young J. (2005). Primary stenting versus primary balloon
angioplasty for treating acute myocardial infarction. Cochrane
Database Syst Rev.

Discuss this 'http://heartzine.com/heart-forum/Heart_Treatment_of_Mycardial_Infarction-61.html'>here

A stroke is a type of cardiovascular disease, which means it relates to the heart and the blood vessels. It affects the blood vessels that are supplying blood and therefore oxygen, within the brain. There is either a blockage or a rupture of the blood cells. The brain contains nerve cells, and if they are deprived of oxygen, they die within a few minutes.

When the nerve cells have been destroyed, then the part of the body they controlled is unable to function as well. Unfortunately brain cells cannot reproduce, and this means the effects of a stroke can be both permanent and devastating.

There are four different types of stroke; the ischemic strokes are caused by blockages, and bleeding causes the hemorrhage strokes. Clots or particles that block an artery cause cerebral thrombosis and cerebral embolism. These types of stroke are the most prevalent. Ruptured blood vessels cause cerebral and subarachnoid hemorrhages. These hemorrhaging strokes cause more deaths, than the strokes caused by blood clots.

CEREBRAL THROMBOSIS

Atherosclerosis is the build up of fatty deposits of the arteries, which leads to blood clots, this can eventually cause a cerebral thrombosis; this is the most commonly occurring stroke. They are more prevalent either at night or first thing in the morning when the blood pressure is low.

CEREBRAL EMBOLISM

A traveling clot is formed away from the brain, usually in the heart, and is transported arterially to the brain. Once it lodges in the brain it blocks the supply of oxygen, and causes immediate damage. Many of these embolic clots are formed during atrial fibrillation. This occurs when the atria does not beat methodically, they have developed a tremble. Effectively when the heart then beats it does not pump all the blood out, and the remainder forms clots.

CEREBRAL HEMORRHAGE

This occurs when an artery in the brain bursts, and floods the surrounding tissue. This is caused by a head injury of a burst aneurysm. An aneurysm is a weak spot in the artery wall, pouches filled with blood form, and then they balloon outwards. This condition is severely aggravated by high blood pressure. Because the brain has lost its supply of blood some cells will not work. There is also a resultant pressure on the surrounding brain tissue, and the severity of the pressure will determine its results. This increased pressure leads to a high mortality rate, but those that recover have a greater chance of recovery than the sufferers of strokes, which have been caused by clots. When a blood vessel bursts it compresses part of the brain, gradually the pressure is released, and the brain can take control of its prior functions. In the case of strokes, which have been caused by clots, the cells have been destroyed.

SUBARACHNOID HEMORRHAGE

This is a rupture of a blood vessel on the brains surface, and the blood leaks between the brain and the surrounding skull, nut not into the brain itself

SYMPTOMS

These very much depend on the type of stroke, and the extent of the injury.

WARNING SIGNS

• Sudden numbness or weakness of the face, arm or leg, especially on one side of the body.

• Sudden confusion, trouble with speaking or understanding.

• Sudden trouble seeing in one or both eyes.

• Sudden trouble walking, dizziness, loss of balance or coordination.

• Sudden, severe headache with no apparent cause.

A stroke is a real medical emergency and every second counts, get immediate medical assistance and note the time. Not all the warning signs will be present in every stroke, don’t waste time looking for all of them.

RISK FACTORS

• High Blood Pressure (140/90 mm Hg or higher)

• Smoking

• Diabetes Diabetes is defined as a fasting plasma glucose (blood sugar) of 126 mg/dL or more measured on two occasions. Whilst diabetes is treatable, having it still increases a person’s risk of stroke. Many people with diabetes also have high blood pressure, high blood cholesterol and are overweight. This increases their risk even more.

• Carotid or Other Artery Disease .The carotid arteries in the neck supply blood to the brain. A carotid artery narrowed by fatty deposits from atherosclerosis may become blocked by a blood clot.

• Atrial fibrillation

• Other Heart Disease. People with coronary heart disease or heart failure have more than twice the risk of stroke as those with hearts that work normally.

• Sickle cell anaemia is a genetic disorder that is prevalent in Africans "Sickled" red blood cells are less able to carry oxygen the body’s tissues and organs. They also tend to stick to blood vessel walls. This can block arteries to the brain and cause a stroke.

• Obesity and physical inactivity.

• High Blood Cholesterol .A high blood cholesterol level (240 mg/dL or higher) is bad because cholesterol can build up on the inner walls of arteries. And narrowed arteries are more likely to become blocked, causing a heart attack or stroke.

DIAGNOSIS

The tests for a stroke are complicated, a CAT scan (computerized axial tomographic) will show which type of stroke has occurred, if after an neurological examination, a stroke is suspected.

TREATMENT

Surgery, drugs, acute hospital care and rehabilitation are all accepted stroke treatments.

A WORD OF CAUTION: Please do not use this information to diagnose individual cases. Every case is unique and needs professional help to both diagnose and treatment.

GLOSSARY OF TERMS

ANEURYSM

An aneurysm is a weak spot in the artery wall, pouches filled with blood form, and then they balloon outwards.

BRAIN

One of the two components of the central nervous system, the brain is the centre of thought and emotion. It is responsible for the coordination and control of bodily activities, and the interpretation of information from the senses (sight, hearing, smell, etc.).

EMBOLISM

Embolism occurs when a travelling clot or some other particle (an embolus) forms away from the brain, usually in the heart.

FIBRILLATION

Uncontrolled rapid contraction of the fibres in the heart that occurs in the atrial, or upper, chambers (atrial fibrillation) and in the ventricular, or lower, chambers (ventricular fibrillation)

Discuss this here

Myocardial infarction
(MI) is commonly known as heart attack. It is classified as ischemic
heart disease, together with 3 other conditions. These clinical
syndromes are also known as atherosclerosis stenosis or occlusion of
coronary arteries because of the association with narrowing of
coronary arteries. The first and the least severe of these conditions
is angina pectoris which includes stable and unstable angina.
Myocardial infarction ranks second while more extensive myocardial
scarring and heart failure is the third condition better known as
chronic ischemic heart disease. The last and most severe is sudden
cardiac death. Atherosclerosis is the main cause of most of these
ischemic heart diseases (98% of the time). Nevertheless, when a young
person is just diagnosed with myocardial infarction, the causes are
more likely among others to be infected cardiac valve or secondary
effect from cocaine.

Atherosclerosis develops
through a number of mechanisms, some of them inter-related, and
others though causes that are not yet clearly defined. One of the
main mechanisms involves dietary low density lipoprotein (LDL) and
the effects generated along its passageway.

LDL together with other
macromolecules travels into the vascular intima through the
endothelial cells. LDL gets trapped in the sub-endothelium, where it
is vulnerable to be attacked by reactive oxygen species (ROS)
(Wentworth et al 2003). These oxidized LDL is then taken up by
macrophages which give it an active form ultimately leading to
chronic inflammation (Alavi et al 2003). Inflammatory cells are
attracted to adhesion molecules expression (VCAM-1, P- and
E-selectin). These fusions enable them to travel from the blood
stream and settle at the endothelial cells. Smooth muscle cells (SMC)
are then taken up and stimulated to release collagen. Finally
atherosclerosis lesion develops which does not continue to grow but
undergoes rigorous redesigning. During these processes, intervals of
activities that might produce cardiac events occur (Scott 2004).

MI happens when the
demand of the heart muscle exceeds the supply. This process happens
when there is blockage in the coronary arteries. These blockages
might be caused by clots that are formed. Previously, it is thought
that only complete blockage causes MI but recently it was found even
minor blockages causes MI. The passage for blood flow becomes narrow
and the blood flow becomes slow. This closure of the artery causes
lack of oxygen and nutrients that is transported to the involved
heart muscle. This ultimately leads to irreversible death or necrosis
of some heart muscle.

Discuss this 'http://heartzine.com/heart-forum/Heart_Atherosclerosis_in_Mycardial_Infarction-44.html'>here

Describe the sequence of valve positions in the four phases of the cardiac cycle and the corresponding changes in volume and pressure in each chamber

Introduction

[quote]The heart provides the vital function of facilitating convective transport of nutrients and metabolites through the body.:V F Murphy[/quote]The heart provides the vital function of facilitating convective transport of nutrients and metabolites through the body. An understanding of the heart is essential for the structure function relationships of both closely associated vessels and those more distal. The understanding of the nature of pulsatile flow, for example, may be an important consideration in the understanding of trigger mechanisms for atherosclerosis.

Anatomical Aspects

The heart consists essentially of two conjoined pumps, each with two chambers. The two pumps provide for two separate circulatory systems: the pulmonary circulation, and the systemic circulation.

Referring to figure 2, below, each side of the heart consists of both an atrium (right atrium – RA, left atrium – LA), and a ventricle (right ventricle – RV, left ventricle – LV).

The right atrium is thin walled and musclar, and features the tricuspid valve (consisting of 3 cusps), and the pacemaker. The venae cavae and the coronary sinus are connected to the right atrium. The tricuspid valve leads from the right atrium to the right ventricle.

The right ventricle is about 0.5cm thick and muscular. The right ventricle leads through the pulmonary valve into the pulmonary artery.

The return from the pulmonary artery, the pulmonary vein, then enters the left atrium. The left atrium then leads to the mitral valve, which connects to the left ventricle.

The left ventricle is about 1.5cm thick and muscular. The muscle fibres change direction throughout the thickness of the ventricular wall. The left ventricle then leads to the aortic valve, leading in turn to the aorta.

Functionality

The function of the right atrium is to receive blood from the venae cavae and coronary sinus. This blood fills the atrium progressively, and is important for ventricular filling. Ventricular filling is the process by which deoxygenated blood flows through the right atrium, which is in diastole, unhindered, into the right ventricle. This takes two thirds of the cardiac cycle (500ms), starting quickly due to elasticity from previous contraction, and then further filling requires elastic deformation of the ventricular wall, hence is slower. As the filling draws to a close atrial contraction forces additional blood from the atrium into the ventricle. At rest this accounts for 15-20% of ventricular volume. The function of ventricular filling is to transfer a certain quantity of blood into the ventricle prior to its contraction and consequential expulsion through the aorta. During ventricular filling those valves opening into the ventricles are both open, and the valves permitting discharge are closed. Filling of the ventricles continues until the end-diastolic volume is achieved (EDV), or approximately 120ml in adults. Associated with the EDV is an EDP, and end diastolic pressure, 4mmHg in the right ventricle, 9mmHg in the left, an indication of the elasticity of the respective vessels.

Following atrial contraction comes isovolumetic contraction (0.05s). In this phase the muscle of the ventricle starts to contract. As it does so it increases pressure within the ventricle. The atrial valve is still closed, and the mitral valve is closed by virtue of vortexes following atrial systole. Hence the atrium at this point is essentially a closed chamber. The pressure increases until ventricular pressure is greater than arterial pressure.

Ejection (0.3s) now occurs, during which time the atrial and pulmonary valves are forced open. The blood from within the ventricle is rapidly forced out of the valve, and during the first 0.15s the rate of discharge is greater than the rate at which blood may exit via the arterial tree. This leads to a need for instantaneous dilation of the elastic arteries to take up the surplus blood. Following this the contraction becomes weaker, and pressure within the ventricle reduces until it attains a value of 2-3mm below arterial pressure. At this point the pressure gradient being reversed blood flow rapidly decelerates. Finally, the pressure difference is so low that a brief backflow into the ventricle occours, pushing the valve closed as it passes. The backflow accounts for less than 5% of the EDV. 2/3rds of the ventricular contents being expelled, the pressure falls steadily, save a small pressure wave caused by the closing of the valve.

After ejection comes a brief period of isovolumetric relaxation (0.08s). During this period the muscle of the ventricle relaxes, and ventricular pressure falls, partly driven by the elastic energy stored during contraction. As before, once the pressure gradient between the atrium and ventricle is negative, the valve opens permitting a flow from the atrium to ventricle, the ventricular filling phase repeated.

Properties of the Cardiac Cycle

Pressure within the heart during the cardiac cycle is probably the one most important parameter:V F MurphyPressure within the heart during the cardiac cycle is probably the one most important parameter, being that which drives fluid exchange between the compartments and the connective blood vessels.

At the beginning of the cardiac cycle the pressure of both the left ventricle and atrium are low, the ventricle being slightly negative due to backflow, and the atrium being slightly positive due to inflow during the final stages of ventricular systole. The pressure within the atrium increases steadily as blood is accumulated within the atrium and flows into the ventricle. The atrial systole follows and the pressure builds further as blood is forced into the ventricle. Valve closure and the relaxation of atrial systole brings about a steady drop in pressure within the atrium, whilst the ventricular pressure is rising rapidly. At this point the ventricle is acting as a closed vessel and so pressure builds until it equals arterial pressure, at which point the rate of pressure increase starts to reduce, the aortic valve opening and ejection commencing. At this point an equilibrium is sought between the ventricle and the aortic pressure �C both raising with the remains of the ventricular systole. As the arterial tree rate of removal exceeds rate of ejection pressure within both the ventricle and the aorta begin to drop, until such a point that the arterial pressure is greater than the ventricular pressure. Now, a brief period of backflow occurs and the aortic valve closes. This produces a brief increase in pressure (diacritic notch), before the pressure in the aorta starts a slow descent pending ventricular systole of the next cardiac cycle. After valve closure ventricular diastole commences and pressure drops very rapidly to zero, before again starting the slow build of ventricular filling.

The volumes moved between different parts of the heart are of further importance. It is important to note that despite differences in size and power between opposing lateral sides of the heart that the volume pumped per stroke must be essentially the same. During one stroke, 0.67 (2/3rds) of the right ventricular EDV is expelled into the aorta.:V F MurphyDuring one stroke, 0.67 (2/3rds) of the right ventricular EDV is expelled into the aorta. This equates to 70 to 80ml in an adult. The total volume within the ventricle is 120ml, and at rest 40ml remains during systole leaving the stroke volume as previously stated.

Physiological rationale for Cardiac Features

The function of the atrium is to accommodate flow of blood from the associated veins without increasing internal pressure to exceed venous pressure. It should be noted that the difference between arterial and venous pressure is what drives cardiovascular circulation, so an increase in venous pressure would necessitate an increase in arterial pressure to maintain flow rate, leading to hypertension and increased cardiac load. The function of the atrium following filling is to allow the rapid filling of the ventricle.

The function of the mitral and tricuspid valves is to prevent backflow into the atrium during ventricular contraction. Without this the stroke volume is effectively decreased leading to increased cardiac load or insufficient circulation.

The function of the pulmonary and aortic valves is to prevent back flow from the arterial network into the ventricle. This again is important for maintenance of stroke volume.

The function of the ventricle is two-fold. Firstly the ventricle must control and expel the required stroke volume into the respective artery. Secondly, the ventricle must control the arterial pressure in such a way that sufficient pressure difference exists across the cardiovascular network.