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

With the exception of the pain of acute aortic dissection, the thoracic aorta is not usually considered as a pain-producing organ. However, nineteenth century clinicians considered the aorta as a source of cardiovascular pain in the presence of autopsy-documented inflammatory aortitis, aortic aneurysms, and arterial hypertension, whereas early in the twentieth century, aortic pain reactions were elicited in experimental studies involving distension of the ascending aorta or the application of stimulating substances to the outer surface of the aorta. More recently, increased attention to aortic elastic properties, and to aortic vascular biology at the molecular level refocused interest on the many facets of aortic function beyond that of a simple conduit. The recognition of pain of thoracic aortic origin now extends to patients with progressive aortic syndromes such as aortic intramural hematoma, aortic intimal tears, aortic penetrating ulcers, aortic root dilatation without dissection in connective tissue disorders, inflammatory aortopathies, and abnormalities of aortic distensibility. The occurrence of pain during balloon inflation at balloon angioplasty of aortic coarctation, which disappears immediately after deflation, is the modern equivalent of the early experimental studies. The authors present a consideration of thoracic aortic pain in light of contemporary concepts in cardiovascular medicine with roots in the rich historical reservoir of information about aortic function and disease.
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PMID:Aortic pain. 964 10

Our 19th century predecessors considered the aorta as a source of cardiovascular pain associated with inflammatory aortitis, arterial hypertension, aortic aneurysms, aortic dissection, and aortic valve disease. However, during the 20th century epidemic of coronary artery disease clinicians became concerned with the syndromes associated with myocardial ischemia and infarction, relegating aortic pain syndromes to the role of a differential, "rule out", or diagnosis of exclusion rather than a primary diagnosis. We re-focus attention on a more global approach to cardiovascular pain, approaching thoracic aortic pain syndromes as primary diagnoses, while considering the dynamics and various stages of development of aortic pain syndromes, set within the clinical environment in which these syndromes arise. The central role of aortopathy is our underlying theme since the detection and clinical recognition of aortopathic disorders provide the template for identification of the population at risk for aortic pain syndromes. Clinical history, pedigree development, phenotype recognition, analysis of the elastic properties of the aorta, use of the wide range of sophisticated imaging techniques, and phenotype-genotype correlations provide the bases for the recognition, diagnosis, and management of aortopathy within the clinical setting. A futuristic anticipatory approach towards the diagnosis of aortopathy is outlined with emphasis on earlier recognition and informed clinical management ultimately leading to prevention of the acute and dynamic aortic complications.
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PMID:Aortic pain: the renaissance of cardiovascular pain and the detection of aortopathy. 1037

Background. Cardiovascular indices of pain are pervasive in the hospital setting. However, no prospective research has examined the development of cardiac responses to acutely painful procedures in the first year of life. Objectives. Our main goal was to synthesize existing evidence regarding the development of cardiovascular responses to acutely painful medical procedures over the first year of life in preterm and term born infants. Methods. A systematic search retrieved 6994 articles to review against inclusion criteria. A total of 41 studies were included in the review. Results. In response to acutely painful procedures, most infants had an increase in mean heart rate (HR) that varied in magnitude both across and within gestational and postnatal ages. Research in the area of HR variability has been inconsistent, limiting conclusions. Conclusions. Longitudinal research is needed to further understand the inherent variability of cardiovascular pain responses across and within gestational and postnatal ages and the causes for the variability.
Pain Res Manag 2016
PMID:Development of Cardiovascular Indices of Acute Pain Responding in Infants: A Systematic Review. 2744 30

In many instances, the perception of pain is disproportionate to the strength of the algesic stimulus. Excessive or inadequate pain sensation is frequently observed in cardiovascular diseases, especially in coronary ischemia. The mechanisms responsible for individual differences in the perception of cardiovascular pain are not well recognized. Cardiovascular disorders may provoke pain in multiple ways engaging molecules released locally in the heart due to tissue ischemia, inflammation or cellular stress, and through neurogenic and endocrine mechanisms brought into action by hemodynamic disturbances. Cardiovascular neuropeptides, namely angiotensin II (Ang II), angiotensin-(1-7) [Ang-(1-7)], vasopressin, oxytocin, and orexins belong to this group. Although participation of these peptides in the regulation of circulation and pain has been firmly established, their mutual interaction in the regulation of pain in cardiovascular diseases has not been profoundly analyzed. In the present review we discuss the regulation of the release, and mechanisms of the central and systemic actions of these peptides on the cardiovascular system in the context of their central and peripheral nociceptive (Ang II) and antinociceptive [Ang-(1-7), vasopressin, oxytocin, orexins] properties. We also consider the possibility that they may play a significant role in the modulation of pain in cardiovascular diseases. The rationale for focusing attention on these very compounds was based on the following premises (1) cardiovascular disturbances influence the release of these peptides (2) they regulate vascular tone and cardiac function and can influence the intensity of ischemia - the factor initiating pain signals in the cardiovascular system, (3) they differentially modulate nociception through peripheral and central mechanisms, and their effect strongly depends on specific receptors and site of action. Accordingly, an altered release of these peptides and/or pharmacological blockade of their receptors may have a significant but different impact on individual sensation of pain and comfort of an individual patient.
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PMID:Differential role of specific cardiovascular neuropeptides in pain regulation: Relevance to cardiovascular diseases. 3228 15