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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Unstable angina is a broad clinical diagnosis that includes patients at different levels of risk for an unfavorable outcome. Although, as in other categories of coronary artery disease, the state of left ventricular function and the extent of coronary artery disease will determine long-term prognosis, recognition of clinical markers of an early unfavorable course may be of value in defining management strategies. This review focuses on the relevance of baseline clinical characteristics and noninvasive data in assessing the prognostic significance of unstable angina in light of its presenting features. Recurrence of chest pain within 48 h after admission carries a reduction in likelihood of survival of about 20% in patients with progressive or prolonged angina. Similarly, ECG changes on admission have a negative prognostic implication, particularly in rest angina, as they predict recurrence of ischemia, myocardial infarction or need for revascularization in 80% of the patients. In variant angina, determinants of prognosis are level of disease activity, as judged by recurrence of pain, ECG changes and use of calcium channel antagonists. Patients with angina after a myocardial infarction who have more than one episode of either angina or silent ischemia in 24 h have a 10% reduction in probability of survival during the 1st year compared with that of asymptomatic patients. An abrupt course, or the rapidity with which symptoms develop, is the main determinant of prognosis in new onset angina. Thus, recurrent angina and ECG changes appear to be relevant prognostic markers in the patient subsets considered; if these are present, early coronary angiography must be performed and revascularization procedures should be considered without delay.
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PMID:Unstable angina: outcome according to clinical presentation. 159 63

This study was performed to test the existing notion that an increased muscle sympathetic nerve discharge is part of the underlying mechanism for the chronic pain syndrome of primary fibromyalgia. Muscle sympathetic nerve activity was recorded in the peroneal nerve in eight patients with primary fibromyalgia and eight age-matched controls. No difference in baseline sympathetic activity was observed between patients and controls. Furthermore, patients did not show exaggerated sympathetic nerve responses to static handgrip or jaw muscle contractions, postcontraction ischemia or mental stress. Thus the results do not indicate muscle sympathetic nerve overactivity in primary fibromyalgic patients.
Pain 1992 Mar
PMID:Do patients with primary fibromyalgia have an altered muscle sympathetic nerve activity? 159 59

As our understanding of the etiology of chest pain of undetermined origin has evolved, the focus for studying this problem has switched from individual subspecialties to a multidisciplinary approach. In the subspecialties of gastroenterology and cardiology, the focus has shifted from organ-specific diagnoses to concepts of altered pain thresholds. Cardiologists began to look for functional causes of ischemia following the recognition that many patients with chest pain had normal coronary arteries. Abnormal responses of the coronary microcirculation to stress were identified in this population, and the concept of "microvascular angina" originated. Further evaluation, however, demonstrated that many of these patients did not have evidence of ischemia. In addition, a significant overlap with esophageal motility disorders was shown, and multiple sensitivities to otherwise nonirritating stimuli, whether in the heart or the esophagus, could be elicited in these patients. This finding led to the concept of abnormal visceral nociception, that is, the "sensitive heart" and the "tender esophagus," both the focus of ongoing clinical research.
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PMID:Microvascular angina and the sensitive heart: historical perspective. 159 66

Some patients with chronic arterial obstruction of the limbs may still suffer the consequences of advanced tissue ischemia, including ulceration and rest pain, and face threatened limb loss in spite of available surgical, pharmacologic, and other treatments. Additional therapeutic modalities were thus sought to accomplish limb salvage. A literature review indicated that most reports on R-wave-triggered circumferential limb compression (cardiosynchronous limb compression [CSC]) demonstrate its ability to augment limb arterial blood flow and improve ischemic limbs. To determine the device's efficacy and safety, and possibly confirm earlier positive reports, a systematic study was undertaken, using older, as well as newer, more electronically reliable CSC devices. The present study was designed to determine the following: 1. objectively, by noninvasive vascular tests, changes in limb blood flow, if any, by CSC; 2. clinical effects of CSC, if any, on the ischemic limb; 3. duration of CSC-induced limb improvements, if any; 4. side effects or safety of CSC. The study demonstrated that CSC treatments: 1. caused increased limb blood flow as determined by increased ankle/arm indices and hallux photoplethysmograph waveform amplitudes during treatments; 2. led, in most cases, to improvement in or resolution of the presenting ischemic problem (eg, ulcer, cellulitis, rest pain); 3. induced limb improvements that persist for up to seven years 4. caused no adverse side effects.
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PMID:Cardiosynchronous limb compression: effects on noninvasive vascular tests and clinical course of the ischemic limb. 159 39

The relation between coronary artery lesion morphology and associated segmental left ventricular (LV) dysfunction in patients with unstable angina is unclear. Fifty-two patients with angina occurring at rest who underwent cardiac catheterization within 3 days of the last episode of pain and had no enzymatic evidence for myocardial necrosis were evaluated. Coronary artery narrowings deemed responsible for the ischemic episodes were analyzed with regard to the artery involved, maximal diameter of the narrowing, presence of thrombus, and complex appearance. Time to catheterization, age, sex and electrocardiographic evidence of ischemia were also noted. Segmental LV dysfunction in the territory supplied by the "culprit lesion" was present in 58% of patients. It occurred significantly more often with lesion location in the left anterior descending coronary artery, and was less frequent with lesions in the left circumflex and ramus coronary arteries. Ischemic electrocardiographic changes were more sensitive in predicting LV dysfunction with culprit lesion location in the left anterior descending or right coronary artery. LV dysfunction could not be predicted by any other parameter analyzed. It is concluded that postischemic LV dysfunction occurs frequently in rest angina, especially when the severest narrowing is in the left anterior descending coronary artery.
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PMID:Frequency and predictors of left ventricular segmental dysfunction in patients with recent rest angina. 159 64

Establishing monitoring guidelines is important for identification of electrophysiologic changes in critically ill patients. Inclusion of continuous ST monitoring can alert critical care nursing staff to ischemia, electrolyte changes, and activity intolerance, as well as provide an objective measurement of the efficacy of nursing interventions. This simple technology, a software addition to the current bedside hardware, can assist in salvaging myocardium, decreasing anxiety by reducing pain episodes and their duration, and identifying early electrophysiologically significant drug and electrolyte changes. Nursing research is essential in establishing additional indications for continuous ST monitoring and in evaluating the usefulness of the continuous 12-lead ST-segment monitoring systems as they come into use.
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PMID:Clinical significance of ST-segment monitoring. 159 54

Objective signs of myocardial ischemia without angina pectoris or its equivalents define the syndrome of silent myocardial ischemia. Its significance lies in the prevalence and prognostic implications. As a prevalence, asymptomatic coronary heart disease can be found in 2.5% of men 40 to 60 years old. Silent myocardial ischemia is frequently found in patients with unstable coronary syndromes. The Framingham Study showed 25% of all myocardial infarctions as unrecognized by patients and physicians. The prognostic implications of silent myocardial ischemia are shown in large studies on prognosis of pathologic exercise-ECG's. Asymptomatic patients with pathologic exercise-ECG have always been recognized as having a significantly increased risk of myocardial infarction and death. Recently, many studies showed a worse prognosis for patients with asymptomatic transient ischemia on Holter-ECG. This can be found in patients with stable angina pectoris, unstable angina pectoris, patients with peripheral arterial disease, and patients after myocardial infarction. It becomes clear that prognosis is not defined by the pain, but by the severity of ischemia. Silent ischemia has to be viewed together with the severity of the underlying coronary heart disease. This synopsis will define the necessary steps for further diagnosis and treatment.
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PMID:[Clinical importance of silent ischemia]. 160 22

The clinical diagnosis must be enriched by quantifiable parameters when a new therapeutic method must be tested. We analyse the role of vascular explorations for epidural stimulation and limb arteriopathies. Four different fields of investigations can be defined. Accuracy of the diagnosis: The tests are useful to rule out some differential diagnoses of arterial involvement, and to establish the functional severity (stage III). 1--Treadmill test: nonischemic pain is ruled out: the evolution can be followed up. 2--Doppler velocimetry demonstrates the extent of the dominant arterial involvement in cases of associated lesions. 3--Arterial pressure gradients: their presence demonstrates significant lesions and allows detecting the affected levels. Quantification of severity: After detecting the lesions, their impact must be appreciated. From a macrocirculatory point of view, the measurement of pressures and flow rates is more sensitive than the Doppler study. From a microcirculatory point of view, the tcpO2 is very useful. 1--Arterial pressure: measured in the ankle and the first toe. There are three degrees: non-threatening ischemia (pulsatile Doppler, distal pressure exceeding 30 mm Hg), threatening ischemia (non pulsatile Doppler, distal pressure exceeding 30 mm Hg), irreversible ischemia (no more pulse, no more capillary flow). If there are arterial calcifications, the pressure in the toe must be measured. 2--Arterial flow rate: the average flow rate may be preserved in an arteriopathy, while the pulsatile rate is already degraded. Non invasive electromagnetic or nuclear magnetic resonance flowmeters measure the total muscular flow. Laser Doppler shows the cutaneous flow rate. 3--The tcpO2: normally greater than 60 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Vascular exploration tests. Importance for the indications and monitoring of epidural medullary neuro-stimulation]. 161 3

Most spinal dural arteriovenous malformations are located in the thoracic and lumbar regions. The symptoms include pain, weakness, sensory disturbances, and sphincter dysfunction, which are usually gradual in onset. They are attributed to venous hypertension with a resultant ischemia of the cord, and hemorrhage from them is rare. The authors report an unusual case of a patient with a dural arteriovenous malformation in the cervical spine who was admitted with a sudden onset of severe headache and dysesthesia due to subarachnoid hemorrhage.
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PMID:Dural arteriovenous malformation in the cervical spine presenting with subarachnoid hemorrhage: case report. 164 Oct 89

A case report of a patient with persistent left anterior hemiblock admitted with acute ischemic heart disease is described. At effort during follow-up evaluation, the patient complained of retrosternal pain when the heart rate was 124 beats/min. No pathological ST-T changes were demonstrated at this time. At 133 beats/min, the precordial pain increased, the QRS axis displayed a marked shift to the right, and ischemic ST-T depression was recorded. In discussing this unreported phenomenon, it is pointed out that left anterior hemiblock does not necessarily represent an anatomical block of the atrioventricular bundle but may simply reflect a relative delay in conduction. In addition, acute ischemia may change the physiological behavior of the system resulting in slower conduction through the posterior rather than through the anterior atrioventricular bundle. The influence of left anterior and left posterior hemiblock on ischemic ST-T changes and on the coronary flow distribution is discussed.
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PMID:Shift from left to right axis deviation during ischemia. 761 50


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