What is Silent Ischemia ?
Written By : Dr.Nabil Paktin, MD.
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No discussion of silent ischemia is complete without consideration of the cardiac pain mechanism.
The afferent fibers that run in the cardiac sympathetic nerves are usually thought of as the essential pathway for the transmission of cardiac pain (Figure 1).
The atria and ventricles are abundantly supplied with sympathetic sensory innervation;
from the heart, the sensory nerve endings connect to afferent fibers in cardiac nerve bundles, which in turn connect to the upper 5 thoracic sympathetic ganglia and the upper 5 thoracic dorsal roots of the spinal cord.
Anginal pain of the heart is transferred via Cardiac nerve plexus that locate in front of the heart by sympathetic nerve and entered to the fourth and fifth sympathetic ganglions and then entered to the posterior horns ( from there passed to the sympathetic nuclei of the brain ) . cardiac sympathetic nerves connected to the stellate and cervical sympathetic ganglions , thoracic and spinal ganglions by three superior, middle and inferior nerves .Cardiac sympathetic nerves and also brachial and diaphragmatic nerves and o ulnar nerve have similar close embryologic origin and separating from one metamere . Because of close relationship between cardiac sympathetic and aforementioned nerves , chest pain in front of the thorax in addition to the sympathetic direction can be radiated to the brachial and diaphragmatic directions and exhibiting various signs .
Within the spinal cord, impulses mediated by this sympathetic afferent route probably converge with impulses from somatic thoracic structures onto the same ascending spinal neurons. This would be the basis for cardiac pain referred to the chest, wall, arm, back etc.
Ischemia without pain is called silent ischemia. Many people don’t know that they have ischemic heart disease and that’s why they could suffer a heart attack without any warning before. People with previous heart attacks , diabetes or angina are inclined to developing silent ischemia.
A-The exact explanation for a lack of symptom in the face of unequivocal ischemia remains unknown . it likely represents abnormal modulation of cardiac pain perception at different levels in the afferent pathway of the heart .
B- the association between diabetes and silent ischemia and painless infarction has been attributed to autonomic neuropathy . A higher threshold for pain has been related to increased baseline plasma Beta-endorphin levels and increased age . a potential connection exists between baroreceptor function and pain perception . this may explain the relationship among increased systolic blood pressure . reduced sensitivity to ischemic pain , and the demonstration of anginal relief with carotid sinus stimulation . results of one study suggested that the gating of afferent signals at the thalamic level is a potential mechanism for silent ischemia . patients with symptoms had activation of basal frontal , anterior , and ventral cingulated cortices and the left temporal pole . Cortical activation was limited to the right frontal region in patients with silent ischemia. it also has been proposed that , among type III patients , asymptomatic ischemia may represent shorter and less severe episodes compared with symptomatic episodes .
Myocardial ischemia is referred from :
-Transient ST-segment changes
-myocardial perfusion defects or ;
-reversible abnormalities in regional wall motion
Silent myocardial ischemia is defined as objective documentation of myocardial ischemia in the absence of angina or anginal equivalents, patients are asymptomatic lacking typical and atypical angina symptoms. Silent ischemia represents an underappreciated manifestation of coronary artery disease CAD , occurring in up to 20% to 40% of patients with stable and unstable coronary syndrome .
patients may be loosely categorized into three groups collectively representing a continuum of silent ischemia .
Detection and Prevalence
As proposed in the 1980s, a useful scheme is to consider 3 separate populations, as follows: (1) totally asymptomatic individuals; (2) those who are asymptomatic after having a myocardial infarction (MI); and (3) those with both symptomatic and asymptomatic ischemic episodes, ie, patients with stable or unstable angina. Alternatively, groups 2 and 3 can be merged so that group 1 consists of patients without known coronary artery disease and group 2 with known disease.
Type I ; have asymptomatic ischemia with no known CAD history with asymptomatic myocardial infarction patterns . clinicians may discover evidence of subclinical MI patterns from a resting ECG or a preoperative stress test . It is known that 12.5% of patients with MI had an unrecognized “silent” infarction. patients may also present with arrhythmias or sudden death from subsequent scar. These patients are considered to have an ineffective “anginal warning system” .
In addition , a subset of this group includes patients with asymptomatic ischemia without a history of infarction . silent ischemia is often discovered by stress tests after referral for aggressive primary screening .
Type II ; have symptomatic MIs but subsequent asymptomatic ischemic syndromes. Ischemia is often missed because of a lack of symptoms . patients in this category are most often encountered after a positive stress test or the rarely ordered AECG. Type II patients may have an abnormal pain threshold .
Type III ; encompasses the largest patient population with silent ischemia . these patients with known CAD have both symptomatic and asymptomatic ischemia . between 20% and 40% of patients with chronic anginal symptoms have silent ischemia . about 75% of ischemia episodes are silent , and only 25% are symptomatic .
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