The main event of a heart attack is the occlusion of one or more
blood vessels supplying the heart muscle. Fatal heart attacks tend
to occur in the morning with an 8 AM peak and in the late afternoon
peaking at 6 PM. When blood flow is critically short, muscle cells
die. This is called a myocardial infarct and the clotting event a
thrombosis.
Thrombosis occurs in arteries narrowed by fatty lesions in the
arterial walls. Thrombosis often starts with rupture of a fatty
lesion, especially during exertion. All the surgical procedures that
increase blood flow through critically narrowed arteries may not
prevent heart attacks and strokes although placing a stent in an
obstructed artery can rescue someone who is having a heart attack.
Arterial lesions grow from the inner wall of the artery outward.
Arteries become thicker before they become narrower and plaques may
rupture in arteries that are only slightly narrowed. You cannot rely
on the measurement of narrowed arteries in an arteriogram image to
determine the risk of heart attack. While a 90% blockage of
artery looks ominous, a vessel that is 40% narrowed may thrombose because of plaque rupture. Measurements of the volume of
plaque in artery walls has become a more reliable way of assessing
the progress of arterial disease. Some suggest that intravascular
ultrasonography which determines the thickness of arterial walls is
the best measure of atherosclerosis. B-mode ultrasonography is used,
for example to measure carotid-artery intimal–medial thickness in
the neck.
Gemayel and Waters suggest: “Cardiologists have traditionally
focused on coronary narrowing as seen on angiography and have
orientated treatment towards bypassing these lesions or widening
them with angioplasty. In patients with stable coronary artery
disease, percutaneous coronary interventions reliably relieve angina
and myocardial ischemia, but do not prevent myocardial infarction or
reduce mortality. Cholesterol lowering therapy has been shown, in
several large, randomized trials reported over the past decade, to
reduce mortality and coronary events, including the need for
revascularization in a broad spectrum of patients. Mechanical and
metabolic treatments for coronary disease should be used
synergistically.”
Until recently studies of coronary artery disease focused on men
and excluded women. The impression that heart attacks remain a men's
problem is misleading. Women are protected against heart attacks until after menopause
and then rapidly catch up with men. The lifetime probability of
women in the US and Canada dying of a heart attack is 10 times
greater than dying of breast cancer. When women do have heart
attacks, their risk of dying is higher than men (Females 11.3% vs
Males 5.5%.)
Heart Attack Symptoms
Central, crushing chest pain often associated with shortness of
breath, anxiety, weakness and sweating. The classic heart attack is
unmistakable. The pain and anxiety is often severe and the weakness
profound. Many victims have the sense that they are going to die,
and some do. Other heart attacks are less obvious or occur in
escalating stages and may be missed by the patient and the doctor.
Pressure sensations in the chest, neck and left arm pain, frequent
swallowing and indigestion may be the main symptoms. Heart pain in
women is often in the back or neck and is not obviously connected to
heart problems.
Sometimes, the onset of a heart attack is sudden and dramatic
with the collapse of the victim. The heart develops irregular
rhythms and no longer pumps blood efficiently. Emergency treatment
with a defibrillator and cardiopulmonary resuscitation (CPR) may
save a life. About 300,000 people die of sudden cardiac arrest each
year in North America. In a Canadian study only 14% of heart attacks
victims who collapse get aid in time. About 4 per cent survive.
Heart attack victims who do receive CPR from strangers are three
times more likely to be alive a year later than those who had to
wait for the arrival of emergency personnel.
Cardiac arrest occurs when the electrical system of the heart
short circuits. The heart may stop or just quiver rather than pump
in a normal rhythm. Cardiac arrest is accounts for 20% to 40% of the
deaths on any single day in the USA. Ventricular fibrillation is the
most common type of cardiac arrest, while the heart stops in up to
40% of cases. The best chance of survival is shocking
the heart with a defibrillator within 5 minutes. There has been a
trend to make defibrillators more available in public places and
Phillips has introduced a device that can be kept at
home and used by inexperienced people. This is a sophisticated
device that monitors the heart, diagnoses the arrhythmia, instructs
the operator with voice messages and delivers a shock when required.
Heart attack patients who make it to the hospital often have
abnormal electrocardiograms (ECG). One of the definitive signs of
myocardial infarction in a cardiogram is ST-segment elevation
(STEMI). Another ECG sign is the development of deep Q waves.
Writing in 1995 Simmons and Willens described dramatic changes in
the management of acute myocardial infarction. Previously bed
rest was prescribed to reduce the oxygen demands in the damaged
heart. The focus changed toward interventions that could restore
blood flow to the ischemic heart muscle before permanent damage
occurred. .Blood flow can be restored with thrombolytic agents that
dissolve the obstructing clot or a cardiologist can perform
emergency coronary angioplasty (PCI). Other drugs such as
beta-blockers and angiotensin enzyme inhibitors may reduce damage to
heart muscle and preserve ventricular function. Drug
strategies for preventing arrhythmias such as prophylactic lidocaine
use and suppression of premature ventricular contractions with
antiarrhythmic drugs are no longer used.
The latest standard treatment to come under attack is the
administration of morphine to relieve the pain and fear associated
with heart attacks. A study of 57,000 heart attack patients found
patients receiving morphine had a 48 per cent higher risk of dying
than patients given nitroglycerin, and a 34 per cent greater risk of
suffering another heart attack while in hospital.
Tissue plasminogen Activator
Tissue plasminogen activator (TPA) is one of several drugs that have the
ability to dissolve the blood clots or inhibit new clot formation. Studies have
shown that TPA and other thrombolytic (clot-dissolving) agents can reduce the
amount of damage to the heart muscle and reduce the number of heart attack
deaths if they are administered within an hour or two after symptoms begin. The
sooner TPA or another appropriate treatment is begun, the better the chances for
recovery. To shorten the time between the onset of an MI and the
administration of TPA, some advocate the administration by paramedics who can
begin therapy before the patient arrives in hospital. [i]
Although TPA given within 60-minutes restored normal coronary perfusion in 57%
of patients, approximately one-half of these patients experience re-occlusion
within days. [ii] Alternative strategies are under
development. For example, Ftichett et al suggested that three agents taken
together. Aspirin, eptifibatide, and enoxaparin inhibit platelet aggregation and
thrombin formation and are associated with better short- and long-term outcomes.
[iii]
[i] Arntz HR.
Prehospital thrombolysis in acute myocardial infarction. Thromb Res 2001;103(Suppl
1):S91-6. [ii] J Invasive Cardiol 12(3s):8B-15B,
2000 [iii] David H. Fitchett, Anatoly Langer,
Paul W. Armstrong, Mary Tan, Aurora Mendelsohn, Shaun G.
Goodman. Evaluating the Efficacy of Enoxaparin vs Unfractionated Heparin
in High-Risk Patients With Non-ST-Segment Elevation Acute Coronary Syndromes
Receiving the Glycoprotein IIb/IIIa Inhibitor Eptifibatide. Am Heart J.
2006;151(2):373-379
Major diseases originate from eating too much of the wrong food and damage is
done to many organs simultaneously. The evidence does suggest that some
interventions are beneficial in terms of preventing heart attacks and strokes
and that disease progression can be halted by important changes in diet and
increased exercise. The occurrence of a heart attack or stroke confirms that
atherosclerosis is advanced, damage has been done and that the rules of
intervention have changed. We suggest that a prudent person suffering early
vascular dysfunction symptoms would be wise to pursue vigorous, thorough diet
revision at the earliest opportunity.
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