1. d. local (cellular) metabolic changes e. decreased left ventricular compliance c. decreased left ventricular contractility b. increased left ventricular end-diastolic pressure a. electrocardiographic changes f angina.
The temporal sequence of events that characterize an ischemic cardiac episode is best described as a “cascade” of abnormalities which begins at a cellular level and amplifies its consequences to create regional tissue changes and eventually leads to organ dysfunction.
Interruption of adequate oxygen and fuel supply to a high metabolically active myocardial muscle fiber results in disruption of the energy dependent processes of relaxation and contraction. Local wall motion abnormalities occur within seconds following coronary occlusion. Impaired segmental diastolic and systolic functions are associated with metabolic changes which are more evident within 30-60 seconds. Changes in left ventricular function occur next, followed by electrocardiographic changes. Pain, when present, is a relatively late manifestation of coronary ischemia. As a general rule, for any given episode of myocardial ischemia, significant impairment of myocardial function is present before the pain mechanism is activated.
In some cases, however, pain may precede the development of ischemia-induced electrocardiographic abnormalities. The nature and significance of this infrequent clinical observation remains unexplained. On the other hand, the absence of electrical manifestations of ischemia in patients with clinically significant coronary artery disease with or without angina, does not exclude the diagnosis of ongoing ischemia. The limitations of surface electrocardiograms may account for the relative insensitivity of this method in detecting the electrical consequences of myocardial ischemia. Viagra Super Active
In addition to hemodynamic and neurohumerol factors, ischemia, the cardinal manifestation of coronary artery disease (whether painless or painful) may be modulated by the occurrence of concomitant disease. This is particularly true in the elderly population in which multiple disease states coexist and may have negative synergistic influence in the performance of various organs. Classic examples are anemia and chronic obstructive pulmonary disease with hypoxemia.
The spectrum of clinical manifestations of the temporary impairment of regional coronary blood flow include (alone or in combination), various forms of left ventricular dysfunction, arrhythmias, and angina and anginal equivalents.
During the last decade, the existence of totally asymptomatic myocardial ischemia has been conclusively established. Indeed, patients with silent episodes outnumber those in whom painful symptoms dominate the clinical presentation of coronary artery disease (vide infra).
Current methods for the noninvasive evaluation of the patient with known or suspected coronary artery disease detect the consequences of coronary ischemia. The most commonly used techniques provide objective evidence of myocardial ischemia by direct or indirect measurements of: electrical alterations (exercise stress test, ambulatory electrocardiography); perfusion abnormalities such as thallium- 201 scintigraphy, rubidium -82/positive emission tomography (PET); contractile dysfunction (exercise echocardiography, exercise radionuclide ventriculography); and metabolic function (PET with labeled metabolic substrates). Such techniques have allowed reliable and reproducible detection and quantification of myocardial ischemia.
2. d. alteration in the central transmission or perception of painful stimuli help to explain the lack of ischemic pain in the setting of transient myocardial ischemia
e. angina us an unreliable indicator of coronary ischemia in the diabetic patient.
The exact mechanism of cardiac pain is unknown. Several authors have attempted to establish possible differences between episodes of painful and painless ischemia; however, no consistent relationship could be established between the presence of pain and a given etiopathologic or pathophysiologic process. The coexistence of episodes of symptomatic and silent myocardial ischemia of comparable severity in the same patient is still an unexplained phenomenon.
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Studies in different patient populations with coronary artery disease have shown that there is no relationship between the cause of ischemia and the presence or absence of symptoms. Patients with vasospastic ischemia (variant angina) or ischemia due to an imbalance between supply and demand (effort angina) or with acute myocardial infarction (thrombosis) can all have silent ischemia.
Myocardial ischemia is almost always silent when episodes of ST abnormalities are brief or when minor hemodynamic changes occur. Longer duration and greater severity of ischemic episodes appear to be necessary, but do not fully explain the presence of pain. Several studies in patients with severe ischemia have failed to show a consistent relationship between the extent and duration of ischemic manifestations and the presence of angina. The finding that a subgroup of patients with silent ischemia have decreased perception of painful stimuli underscores the role of central transmission and pain threshold in determining the occurrence of symptoms. Although this hypothesis is sound and attractive, it is not a universal finding and does not appear to be a major quantitative determinant of the presence or absence of pain in most patients with myocardial ischemia. The role of central transmission and pain threshold are those of pain modulation. Most studies show overlap in sensitivity and tolerance to noxious stimuli between patients with angina and silent ischemia. In a recent study involving diabetic patients with known coronary artery disease, Nesto and coworkers found that angina was an unreliable index of myocardial ischemia. Autonomic neuropathy may account for the higher incidence of silent ischemia in the diabetic patient with coronary artery disease.
3. a. silent myocardial ischemia is the most common manifestation of ischemic heart disease c. silent ischemia is frequently detected during rest, or while smoking or while doing mental arithmetic. Coronary artery disease encompasses a variety of syndromes which can be totally asymptomatic, or associated with other clinical manifestations of ischemic heart disease or lead to sudden death. Numerous studies have shown that painless ischemia occurs three to four times more frequently than painful episodes.
The traditional interpretation of the pathophysiology of myocardial ischemia has evolved from the concept of a fixed obstructive lesion causing impairment of coronary blood supply under stress-induced increase in myocardial demand, to a concept of variable coronary obstruction in response to various stimuli. A spectrum of interactions between physical and humeral factors generated within the circulation and in the coronary artery vessel wall leads to activation of the vascular smooth muscle, which in turn causes dynamic stenosis of the coronary artery.
As previously noted, studies in various subgroups of patients with underlying coronary artery disease have shown that up to 80 percent of episodes of myocardial ischemia are asymptomatic. Silent myocardial ischemia can be simply defined as objective evidence of myocardial ischemia (such as electrocardiographic changes in stress electrocardiograph or perfusion defects in thallium-201 scintigraphy) in patients without angina or usual anginal equivalents. As a general rule, painless episodes occur at lower heart rates and during non-strenuous daily activities. Of interest is that cigarette smoking and mental arithmetic have been associated with an increased incidence of silent ischemia. tadalis sx 20
The frequency of painless vs painful ischemia among individuals is highly variable as is the frequency of ST segment shifts on a day-to-day basis. More recently, the circadian variability in the incidence of myocardial ischemia and other major cardiovascular events such as myocardial infarction, sudden death and stroke has received increasing attention. The observation that ischemic coronary events occur predominantly in the early hours of the morning with a peak incidence between 6:00 am and 12 noon, has provided new insights into the potential mechanisms responsible for these disorders. Moreover, correction of the incidence of ischemia according to time of awakening helps to substantiate an even stronger circadian periodicity.