Arterial Disease

Heart Attacks




Some Topics

  • Heart Attack - Myocardial Infarction

    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

    Listen to Consequences of Arterial Disease

  • Topics from the book Heart & Arterial Disease The author is Stephen Gislason MD 2018 Edition: 190 Pages

    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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