New heart scanning technology opens new opportunities for the population to monitor and prevent heart attacks. The main problem is that in many cases it is difficult to predict cardiovascular changes and possible risks associated with heart failure and reductions in coronary blood flow. New heart scanning technologies allow doctors to provide patients with preventive treatment and reduce heart failures.
Heart attack (myocardial infarction (MI) occurs when severe reductions in coronary blood flow and myocardial oxygen delivery last for more than 20 minutes. The infarct begins on the inner wall or subendocardium of the heart and is confined there for the first 20 minutes to 1 hour If the coronary artery thrombosis is transient or does not cause complete coronary artery occlusion, the infarct usually remains confined to the subendocardium, and a non—Q-wave MI develops.
If the coronary artery occlusion is sustained, the myocardial necrosis progresses vertically outward toward the epicardium in the next 2 to 3 hours becoming a Q-wave, ST elevation, or transmural MI. Acute Q-wave MI is usually caused by persistent thrombotic occlusion of a coronary artery, resulting in sustained reductions in coronary blood flow and myocardial oxygen availability (Mogadan 55).
Occasionally, increases in myocardial oxygen demand above the ability of a stenotic coronary artery to deliver oxygen cause MI, often non—Q-wave MI. Such increases in oxygen demand may occur in patients with CAD who have severe systemic arterial hypertension, sustained tachycardia, or both. Sustained reductions in myocardial oxygen delivery, associated with severe systemic arterial hypotension, may also lead to MI, including non—Q-wave MI.
Approximately 30% of patients with non—Q-wave MIs have an occlusive thrombus in the infarct-related artery, usually a small coronary artery branch vessel, or in the distal portion of a larger coronary artery. When critical reductions in myocardial blood flow persist for more than 2 hours, the resultant infarct is usually a transmural, Q-wave MI.
The local accumulation of thromboxane A 2, serotonin, platelet-activating factor, adenosine diphosphate, oxygen-derived free radicals, and endothelin and thrombin activation at sites of endothelial injury contribute to vasoconstriction, platelet aggregation, Increases in systemic and local catecholamine concentrations associated with the development of unstable angina and MI also increase platelet aggregation and may contribute to coronary vasoconstriction.
Serotonin, adenosine diphosphate, thrombin, and endothelin are mitogens, and they are very likely to contribute to subsequent local fibroproliferation with increases in the neointima, further narrowing the lumen of the endotheliuminjured coronary artery (Mogadan 62).
Myocardial infarcts usually involve the left ventricle. Right ventricular infarcts occur in association with left ventricular infarcts, particularly posterior transmural left ventricular infarcts. Occasionally, they are isolated entities occurring in association with pulmonary hypertension. Most myocardial infarcts are confined to a single coronary artery and are designated anterior, anteroseptal, lateral, and posteroinferior. Multiregional infarcts also occur.
Myocardial infarcts are characterized as subendocardial when the necrosis is limited to the inner half of the ventricular wall, or transmural when the necrosis extends from the subendocardium into the outer half of the ventricular wall.
The major complications of acute myocardial infarction are infarct expansion (shape change leading to stretching and thinning of the ventricular wall), infarct extension (additional necrosis), ventricular aneurysm, cardiogenic shock, or recurrent ventricular arrhythmias related to large infarct size (generally greater than 33% to 40% of left ventricular mass), papillary muscle dysfunction, papillary muscle rupture, external cardiac rupture, ventricular pseudoaneurysm (due to sealing off of a relatively slowly evolving rupture), ventricular septal rupture, pericarditis (nonspecific and autoimmune, e.g., Dressler’s syndrome), systemic embolization from a left ventricular mural thrombus, and pulmonary thromboembolism. greater degrees of calcification in coronary arteries are consistent with greater amounts of atherosclerotic plaque and more advanced coronary luminal diameter narrowing (Mogadan 76).
Assessing coronary artery calcium can be done regardless of the patient’s ability to exercise to a maximal level and regardless of the presence or absence of resting electrocardiographic abnormalities. The most valuable finding in the symptomatic patient is a negative EBCT study for coronary calcium. The negative predictive value of such a calcium scan for significant stenosis of a major coronary artery is greater than 90% (Roberts and Zucker 92).
Several large studies have shown a substantial increase in the incidence and mortality of heart attacks in diabetics (Roberts and Zucker 93). In some studies, the rise in incidence and mortality was higher in women than in men. Premenopausal women have a much lower incidence and mortality of heart attacks than both men and postmenopausal women who are not receiving estrogen replacement therapy. Earlier in life, these rates are much lower in women than in men.
However, the difference between men and women narrows with increasing age. By the sixth to seventh decade of life, the incidence and mortality of heart attacks in men and women are similar. Large studies have shown that risk factors for the development of heart attacks are similar in men and women. However, the interactions between those risk factors are more important in women (Roberts and Zucker 91).
The main advantage of new technology is that “the scans can largely replace diagnostic angiograms, the expensive, onerous way of looking for blockages in arteries, and can make diagnosis so easy that doctors would not hesitate to use them. They are expected to cost about $700, compared with about $4,000 for an angiogram” (Kilata 2004).
Fortunately, many of the risk factors for heart attack (i.e., cigarette smoking, diabetes, high lipid levels, and hypertension) are under the direct control of the patient and physician. Women should therefore be encouraged to reduce these risk factors whenever possible. new technology shows increases in mean pulmonary capillary wedge pressure during episodes of angina pectoris. With the onset of myocardial ischemia, the initial hemodynamic change in the left ventricle is a decrease in myocardial compliance and an increase in stiffness.
This results in a sharp increase in mean pulmonary capillary wedge pressure during angina, with a return to baseline as angina resolves. The change in compliance is followed by ST- to T-wave changes on the ECG, a decline in regional systolic wall thickening, and finally the development of chest pain, with this entire sequence occurring within a few seconds.
Asymptomatic patients differ from symptomatic patients in that the risk of subsequent morbid events is relatively small. Data available at this time are not conclusive regarding whether coronary calcification in asymptomatic individuals can predict short-term risks. The chest discomfort is typically milder than that which occurs with acute MI.
The pain is usually not severe and is described as recurrent chest or epigastric tightness or pressure. Typically, the episodes of angina last less than 30 minutes; they may or may not be associated with nausea. On occasion, however, unstable angina is associated with more severe and prolonged chest pain and nausea, making its differentiation from acute MI at the bedside difficult (Roberts and Zucker 33).
The new scanning technology is as highly variable as those in patients with stable angina, but they may include reversible or fixed reductions in regional wall motion or global left ventricular functional abnormalities. In some patients, reductions in regional wall motion occur with episodes of rest angina and resolve as angina resolves.
For a cardiologist focused on “significant” stenosis and binary decision making concerning revascularization procedures, ultrafast CT is of little value except to increase the number of diagnostic arteriograms, many of which show little obstructive disease. However, according to a new paradigm for the primarily noninvasive management of coronary atherosclerosis (see next section), there is substantial merit to screening for coronary calcification using ultrafast CT.
Patients with a high calcium score would then be evaluated with definitive PET to assess the effects of endothelial dysfunction, diffuse CAD, or regional flow-limiting stenosis on myocardial perfusion.
Evaluation of the severity and size of regional perfusion defects or a longitudinal perfusion gradient provides a noninvasive basis for either instituting lifelong intense treatment of risk factors or proceeding to arteriography. In the latter case, revascularization would be highly likely in patients with large, life-threatening perfusion defects that objectively indicate severe stenosis of a major proximal coronary artery (Kilata 2004).
In sum, the new technology allows to prevent of heart attacks at the early possible stages and evaluate risk factors and possible changes in heart functions. Patients with chest pain syndromes are usually not seen by a cardiologist initially but instead, present to the office of a primary care physician or an emergency room.
In the emergency room setting, men with chest pain are more often admitted to the hospital than women. Patients who are not admitted to the hospital for evaluation of chest pain syndrome may be referred for heart scanning. Again, the data are conflicting concerning stress test results and referral for cardiac catheterization.
Mogadan, M. Every Heart Attack is Preventable. LifeLine Press, 2001.
Roberts, J. C., Zucker, M Reverse Heart Disease Now: Stop Deadly Cardiovascular Plaque Before It’s Too Late. Wiley, 2008.
Kilata, G. Heart Scanner Stirs New Hope and a Debate. the New York Times 2004. Web.