Pathogenesis Of Chest Pain Research Articles

Exploring the Experience of Guo Yi Master Lei Zhongyi in Dialectical Treatment of Heart Failure Based on the Theory of "Yang Wei Yin Xian"

The term "heart failure" first appeared in Wang Shuhe's "Meridian: Spleen and Stomach Diseases". The related description of heart failure is recorded in the "Huangdi Neijing", which is a disease mainly characterized by palpitations, asthma, and edema. It is often the terminal stage of chronic heart disease that cannot be cured. Its basic pathogenesis is prolonged illness with deficiency of heart qi, loss of nourishment in the heart, weakness in blood circulation, prolonged stagnation of the heart meridians, cessation of water consumption, and the generation of phlegm and dampness, resulting in heart failure. The theory of "Yang Wei Yin Xian" is a highly summarized understanding by Zhang Zhongjing of the etiology and pathogenesis of chest pain and heartache. Chinese medical master Lei Zhongyi has been practicing medicine for more than 60 years and has unique insights in the prevention and treatment of heart failure, with considerable clinical efficacy. He believes that heart failure belongs to the principle of deficiency and excess, and the theory of "yang micro yin string" is also applicable to this disease. Its onset is closely related to the pathological changes of substances such as qi, blood, and body fluids. The method of treating phlegm and blood stasis together should run through the treatment process, especially for patients who consume qi and yin in the later stage. Emphasis should be placed on promoting blood circulation and nourishing qi and yin, and the treatment should focus on both attacking and tonifying, with Qi and blood regulating simultaneously. Based on clinical experience, the original Yangxin Huoxue Tang has achieved significant clinical efficacy.

Investigation of esophageal sensation and biomechanical properties in functional chest pain

There is limited and conflicting data regarding the role of esophageal hypersensitivity in the pathogenesis of functional chest pain (FCP). We examined esophageal sensori-motor properties, mechanics, and symptoms in subjects with FCP. Esophageal balloon distension test was performed using impedance planimetry in 189 (m/f = 57/132) consecutive subjects with non-cardiac, non-reflux chest pain, and 36 (m/f = 16/20) healthy controls. The biomechanical and sensory properties of subjects with and without esophageal hypersensitivity were compared with controls. The frequency, intensity, and duration of chest pain were assessed. One hundred and forty-three (75%) subjects had esophageal hypersensitivity and 46 (25%) had normal sensitivity. Typical chest pain was reproduced in 105/143 (74%) subjects. Subjects with hypersensitivity demonstrated larger cross-sectional area (P < 0.001), decreased esophageal wall strain (P < 0.001) and distensibility (P < 0.001), and lower thresholds for perception (P < 0.01), discomfort (P < 0.01), and pain (P < 0.01) compared to those without hypersensitivity or healthy controls. Chest pain scores (mean +/- SD) for frequency, intensity and duration were 2.5 +/- 0.3, 2.2 +/- 0.2, and 2.2 +/- 0.2, respectively, and were similar between the two patient groups. Seventy-five per cent of subjects with FCP demonstrate esophageal hypersensitivity. Visceral hyperalgesia and sensori-motor dysfunction of the esophagus play a key role in the pathogenesis of chest pain.

This Month in Gastroenterology

This Month in Gastroenterology

Functional chest pain of esophageal origin: hyperalgesia or motor dysfunction

OBJECTIVE: Many patients with functional (noncardiac) chest pain exhibit both hypersensitivity and motor dysfunction of the esophageal wall. We aimed to determine whether the sensory or motor dysfunction plays an important role in the pathogenesis of chest pain. METHODS: We performed graded balloon distentions of the esophagus using impedance planimetry in 16 consecutive patients with chest pain and otherwise normal cardiac and esophageal evaluations and in 13 healthy controls. In those patients who experienced chest pain with balloon distention, the test was repeated after atropine was given. Sensory and biomechanical parameters were measured. RESULTS: Balloon distention reproduced typical chest pain in 13/16 patients (81%) and at lower ( p < 0.01) sensory thresholds than controls. Pain was reproduced in all 13 patients and at lower ( p < 0.05) sensory thresholds after atropine. Also, after atropine, the esophageal cross-sectional area and wall tension increased ( p < 0.05), the tension/strain association shifted to the right ( p < 0.05), and reactivity decreased ( p < 0.002) relative to results before atropine or in healthy controls ( i.e., the esophageal wall relaxed and became more deformable). CONCLUSIONS: Even after relaxing the esophageal wall, most patients experienced chest pain and at lower sensory thresholds. Hence, hyperalgesia rather than motor dysfunction appears to be the predominant mechanism for functional chest pain of esophageal origin.

Non-cardiac, non-oesophageal chest pain: the relevance of psychological factors

Background—No cause has been determined for chest pain that is neither cardiac nor oesophageal in origin.Aims—To compare the prevalence of lifetime psychiatric disorders and current psychological distress in three consecutive...

Chest Pain of Undetermined Origin

Chest pain of undetermined origin (CPUO) can be a diagnostic dilemma for both the primary care physician and subspecialist. This article focuses on the diagnostic tools used in the evaluation of CPUO, which include: prolonged ambulatory intraesophageal pH monitoring; esophageal manometry with provocative testing; ambulatory intraesophageal pressure monitoring; the role of radiology and endoscopy in the evaluation of chest pain; the role of psychological abnormalities and abnormal nociception in the pathogenesis of chest pain; and the clinical approach and treatment rationale for CPUO.

The pathogenesis of chest pain with normal coronary arteries delineated by positron emission tomography and H 2 150 O

The pathogenesis of chest pain with normal coronary arteries delineated by positron emission tomography and H 2 150 O