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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Afferent fibers mediating pain from myocardial ischemia classically are believed to travel in sympathetic nerves to enter the thoracic spinal cord. After sympathectomies, angina pectoris still may radiate to the neck and inferior jaw. Sensory fibers from those regions are thought to enter the central nervous system through upper spinal cord segments. We postulated that axons from nodose ganglion cells might project to cervical cord segments. The purpose of this study was to determine the density and pathway of vagal afferent innervation to the upper cervical spinal cord. Following an injection of wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP) into the upper cervical spinal cord, approximately 5.8% of cells in the nodose ganglion contained reaction product. Cervical vagotomy did not diminish the density of WGA-HRP labeled cells in the nodose ganglion. However, a spinal cord hemisection cranial to the injection site eliminated labeling of nodose cells. These data indicate that a portion of vagal afferent neurons project from the nodose ganglion to the upper cervical spinal cord. In addition, vagal afferent fibers reach the spinal cord via a central route rather than through dorsal root ganglia.
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PMID:Projection of nodose ganglion cells to the upper cervical spinal cord in the rat. 172 Jul 4

Cardiac pains related to estrogen therapy for prostatic cancer (PC) emerged in 53% of treated patients with ischemic heart disease (IHD). The pain complaints were associated with impairment of coronary circulation in 48% of cases. This clinical condition is attributed to elevated STH levels and a trend to hypercorticism. In hypertensive PC patients estrogens provoked more frequent and severe headaches which occurred at initial stages of the treatment in 23% and after 1-year administration of hormones in 44% of patients. Hypertensive reactions may be caused by aldosterone and prolactin hyperproduction. Observation of the therapist and endocrinologist can help to prevent complications in IHD patients with PC.
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PMID:[Changes in hormonal homeostasis and development of disorders of the cardiovascular system in patients with prostatic cancer on estrogen therapy]. 172 22

Study of the detailed pathology of the myocardium and coronary arteries in ambulatory subjects dying suddenly of coronary heart disease shows that they can be divided into two groups. In one group, there is atherosclerosis with a new vascular event involving coronary thrombosis, which initiates acute myocardial ischemia. In the other group, there is chronic high-grade stenosis due to atherosclerosis, but there is no recent vascular change; the myocardium in this group shows scarring from a previously healed infarction acting as a substrate for reentrant ventricular arrhythmias. A study of 168 consecutive cases of sudden coronary death in London showed 73.3% to have had a recent coronary thrombotic lesion, giving a ratio of 2.7:1 for patients with versus patients without new acute myocardial ischemia. The widely differing ratios reported in the literature probably reflect the patterns of case selection. Prodromal pain immediately before the onset of ventricular fibrillation in a patient without previous known coronary disease selects for a thrombotic cause and acute myocardial ischemia. Absence of pain in a patient known to have had a previous infarction selects for a primary arrhythmia on the basis of preexisting myocardial hypertrophy and/or scarring.
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PMID:Anatomic features in victims of sudden coronary death. Coronary artery pathology. 172

Acute postoperative hypertension (APH) has been documented in the PACU. Over half of the patients who exhibit APH have pre-existing primary hypertension. Sustained blood pressure (BP) elevation increases the risk of myocardial ischemia, infarction, surgical site bleeding, or cerebral hemorrhage in these patients. Following surgery and anesthesia, increased sympathetic stimulation caused by a high level of circulating catecholamines can lead to APH. Some direct perioperative stimulants include pain, anxiety, hypoxia, hypercapnia, hypothermia, shivering, volume overload, and bladder distension. Nursing interventions are directed toward identifying and relieving the cause of APH. Antihypertensive drug therapy with vasodilators or adrenergic inhibitors is used if initial nursing interventions are not effective. Vasodilators frequently used are hydralazine, sodium nitroprusside, and nitroglycerin. Nicardipine has recently been introduced as an intravenous calcium channel blocker. Vasodilators are effective in BP reduction but may cause reflex tachycardia when used alone. Adrenergic inhibitors, such as esmolol and labetalol, block alpha and/or beta receptors to decrease heart rate and BP. Labetalol's effectiveness, relative freedom from side effects, and ease of administration have made it a useful drug in the treatment of APH.
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PMID:Acute postoperative hypertension in the hypertensive patient. 173 70

"Corkscrew oesophagus" is characterised on the basis of two case reports and attention is drawn to thoracic pain of oesophageal origin. Corkscrew oesophagus is a radiological diagnosis and is characterised by twisted segments in the distal third of the oesophagus. The condition can sometimes be demonstrated endoscopically and it is due to a basic disturbance in the motility of the oesophagus. Painful conditions in the oesophagus are most frequently caused by gastro-oesophageal reflux or disturbances in motility and the latter is frequently complicated by reflux oesophagitis. Pain of oesophageal origin is frequently a diagnosis by exclusion and requires exclusion of ischaemic heart disease. The initial treatment should be directed to the reflux oesophagitis. The diagnosis and information about the origin of the pain and the benign course of the condition will calm the majority of the patients and remove their fear of a possible fatal heart disease.
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PMID:[Corkscrew esophagus]. 173 62

To verify whether plasma beta-endorphin and bradykinin affects the pathophysiology of myocardial ischemia and the perception of cardiac pain, 35 patients with coronary artery disease were subjected to treadmill testing and 48-hour Holter ECG monitoring to measure their pain thresholds. Patients were divided into two groups during exercise testing: group 1 (N = 19) who had ST segment depression, and group 2 (N = 16), who had chest pain. Both groups were then compared with 12 age-matched control subjects. Pain thresholds were measured after Holter ECG monitoring, and blood samples were drawn before and immediately after exercise. No statistical differences were noted between groups 1 and 2 with regard to the severity of myocardial ischemia as assessed by ST segment depression or exercise tolerance time. The frequency of the episodes of silent myocardial ischemia in group 1 was found to be significantly (p less than 0.05) higher than that in group 2. The duration of the episodes of silent myocardial ischemia in group 1 was 41.9 minutes (range 3 to 343 minutes), which was significantly (p less than 0.05) longer than that in group 2 (11.5 minutes; range 0 to 74). The pain threshold in group 1 was a statistically (p less than 0.05) higher value than that in group 2. Although the resting plasma beta-endorphin level in group 1 was not statistically significantly different from values in either group 2 or the control group, during exercise the plasma beta-endorphin levels in both group 1 and the control group were significantly (p less than 0.05) elevated in comparison with their resting levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differences in plasma beta-endorphin and bradykinin levels between patients with painless or with painful myocardial ischemia. 173 63

The prognostic value of silent ischemia during a symptom-limited predischarge exercise test (ET) was evaluated in 740 men after an episode of unstable angina or non-Q wave myocardial infarction. The 51% of patients with ST depression at the ET had a higher rate of myocardial infarction or death after 1 year (18%) compared with those without ST depression (9%; p less than 0.01). This increased risk was not influenced by the presence or absence of pain at the ET: 18.3% in patients with painful ischemia compared with 18.1% in patients with silent ischemia. However, ST depression combined with pain at the ET predicted a higher incidence of class III or IV angina at follow-up (43.9% compared with 16.7% in the group with asymptomatic ST depression; p less than 0.001). Because revascularization in addition to alleviating symptoms also enhances the prognosis in certain groups of patients, selections for coronary angiography and possible revascularization should not be made only on the basis of symptoms but also on the presence of myocardial ischemia, whether symptomatic or not.
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PMID:The predictive value of silent ischemia at an exercise test before discharge after an episode of unstable coronary artery disease. RISC Study Group. 173 66

A sample of 45 patients with a history of coronary heart disease and documented myocardial ischemia during exercise testing were evaluated in an investigation of the possible relationships between psychological factors (depression and Type A behavior pattern), plasma beta-endorphin response and pain experience during maximal exercise-induced ischemia. Depression was assessed using the MMPI-D subscale, while Type A was evaluated using the Structured Interview. All patients developed ischemia during exercise as defined by ST-segment depression; however, only 18 patients reported anginal pain. Patients with high depression scores (MMPI-D greater than or equal to 70; n = 13) showed lesser increases in plasma beta-endorphin levels, tended more often to report anginal pain and rated pain as more severe during exercise than patients with low depression scores (MMPI-D less than 60; n = 18). Hemodynamic responses and severity of ischemia (assessed by ejection fraction changes and wall-motion abnormalities) did not differ between depression groups. Even after adjustment for group differences in exercise duration, depression was significantly associated with a lesser beta-endorphin response in the sample as a whole and, among patients reporting angina, with earlier pain onset and greater pain duration and severity. In contrast, when Type A versus B/X subgroups were compared, no differences in pain experience, beta-endorphin response or measures of ischemia were obtained. These findings suggest that in patients with ischemic heart disease, there may be a relationship between depression and anginal pain which may in part involve a blunted or absent beta-endorphin response.
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PMID:Depression and type A behavior pattern in patients with coronary artery disease: relationships to painful versus silent myocardial ischemia and beta-endorphin responses during exercise. 175 50

Silent myocardial ischemia (SMI) is divided into 3 groups: type I: completely asymptomatic patients, type II: patients after acute myocardial infarction with SMI, type III: patients with angina pectoris (AP) and SMI. Pathophysiology on the lack of pain-perception and the cause for high tolerance against pain in SMI-patients has not yet been cleared up. It is most likely that more than one mechanism is involved in every patient, e.g. generally lower pain-perception in SMI-patients, physically counter-regulation in pain, duration and strength of myocardial ischemia. Diagnosis of SMI can be made by exercise- and long-term-ECG, thalliumszintigraphy and coronary angiography, in doing so the pros and cons of the 4 established methods have to be noted. The summary of the findings together with the lack of pain leads to the diagnosis of SMI.
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PMID:[Silent myocardial ischemia. Current concepts of pathophysiology and diagnosis]. 176 83

The authors observed for a long-period 453 patients with the ischemic heart disease after the operation of aorto-coronary shunting (ACS). At discharge from the hospital, in 96.9% of the patients operated on, the clinical improvement of the state was noted, in 78.4% of them, the attacks of angina disappeared. Five years later, in 46.1% of the patients examined, there were no stenocardia, in 53.9%, retrosternal pain was noted. According to the findings of repeated coronarography, development of the stenocardiac syndrome is caused by insufficient function of the venous shunts and aggravation of stenosing atherosclerosis. By means of twin pharmacodynamic tests, it was established that monotherapy and combined therapy with calcium antagonists were the optimal ones.
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PMID:[Coronary surgery from the aspect of ambulatory care follow-up]. 177 56


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