The manner in which an individual presents with coronary artery disease depends upon the location of the interruption in the coronary artery, how quickly the interruption occurs, and the nutrient demands of the myocardium at the time. Acutely damaged heart muscle appears as a red purple bruise which has a reduced amount or no contraction.
The individual may have chest pain that is better described as chest discomfort, chest tightness or a constricting sensation. The discomfort may travel to the shoulders and arms including elbows and wrists. It also may travel to the lower jaw including the teeth, to the back between the shoulder blades and to the upper abdomen. The discomfort is not affected by breathing in or out. It may be accompanied by shortness of breath, sweating, and nausea and vomiting.
If complete occlusion (blockage) is within the proximal or main portion of the coronary artery, a significant amount of heart muscle may be destroyed. Enough blood may not be ejected and blood pressure will not be supported. Fainting with unconsciousness may occur if the blood pressure drops. If recovery from an acute event such as this occurs, a remaining large area of non contracting scar which does not eject blood may leave an individual easily fatigued and possibly short of breath, even at rest. This known as congestive heart failure.
Before the actual heart attack (myocardial infarction or MI) occurs, the individual may have warning signs. These are the above described symptoms known as angina pectoris and occur with the increased myocardial nutrient demands of exertion or anxiety. These symptoms indicate that the coronary artery is only partially closed by the cholesterol plaque. Plaques can completely occlude a coronary artery suddenly by causing tiny particles in the blood called platelets to clog up the remaining part of the narrowed channel, or the plaques can hemorrhage into themselves increasing their size causing complete coronary occlusion.
If complete coronary occlusion never occurs, or if it occurs slowly, the individual may never have the unremitting chest discomfort of a classic heart attack, but rather just periodic chest discomfort described as angina pectoris above. In this situation the appearance of the myocardium may appear normal but also may reveal patchy areas of scar or fibrous tissue which does not contract very well. If the scarred area is extensive, the amount of ejected blood from each beat may be significantly reduced causing symptoms of congestive heart failure.
A significant percent of individuals never have chest discomfort at all. The classic warning signs of angina pectoris or impending heart attack are absent. This is especially noted in the elderly or diabetics. One of the challenges in cardiology is to identify these people.
Besides the mechanical contraction problems of the myocardium with a heart attack, the ability of the mitral valve to close may be impaired resulting in a leak between the left ventricle and left atrium when the left ventricle contracts. Also a rupture of heart muscle between the 2 ventricular chambers can occur, and the heart muscle can rupture into the fibrous sac (pericardium) which contains the heart.
All living cells are electrically active, and this activity is
determined by a balance of chemicals within each cell and across the cell membrane which separates it from other cells. In mammals these chemicals are sodium, potassium, chlorine, and calcium. They create a measurable mini- potential across the cell membrane just like a battery. The myocardium therefore consists of millions of cells that have electrical potential. When a myocardial cell contracts it is the temporary interchange of these chemicals across the membrane that cause the myocardial protein elements within each cell to inter connect and change the shape of the cell; ie, making it shorter. In cardiac muscle this whole system is coordinated by a nerve conduction system that may be compared to conductive wires that extend from the atria to the ventricles. This nerve conduction system is located just beneath the inner surface of the cardiac chambers and ensures that the atria and ventricles contract on time and in a coordinated manner. It is this
conduction system that can be recorded by the electrocardiogram (EKG). The wire network works automatically, and in an adult at rest, it emits chemical electric current thru its distribution at 72 times per minute.
A heart attack not only damages heart muscle, it damages the electrical activity of the heart. If one of the myocardial cell membranes is injured, the chemical balance maintaining potential across its membrane is disturbed. This cell may then contract independently of the networked coordinating system, and in addition, the damaged cell will transmit its irritability to many contiguous cells. The entire myocardium may then be affected causing potentially fatal heart rhythms as ventricular tachycardia and ventricular fibrillation. These rhythm disturbances cause rapid, uncoordinated and weak myocardial contractions and can lead to full cardiac arrest.
Cardiac rhythm disturbances are a frequent cause of complications from a heart attack, including death. It is one of the major reasons for dealing with chest pain as a possible life or death situation.