Materiały źródłowe

• #1 Mechanisms of cardiac pain – PubMed

  https://pubmed.ncbi.nlm.nih.gov/10099685/

  Angina pectoris often results from ischemic episodes that excite chemosensitive and mechanoreceptive receptors in the heart. Ischemic episodes release a collage of chemicals, including adenosine and bradykinin, that excites the receptors of the sympathetic and vagal afferent pathways. Sympathetic afferent fibers from the heart enter the upper thoracic spinal cord and synapse on cells of origin of ascending pathways. This review focuses on the spinothalamic tract, but other pathways are excited as well. […] Excitation of spinothalamic tract cells in the upper thoracic and lower cervical segments, except C7 and C8 segments, contributes to the anginal pain experienced in the chest and arm. Cardiac vagal afferent fibers synapse in the nucleus tractus solitarius of the medulla and then descend to excite upper cervical spinothalamic tract cells. This innervation contributes to the anginal pain experienced in the neck and jaw. The spinothalamic tract projects to the medial and lateral thalamus and, based on positron emission tomography studies, activates several cortical areas, including the anterior cingulate gyrus (BA 24 and 25), the lateral basal frontal cortex, and the mesiofrontal cortex.

• #2 Mechanisms of cardiac pain – PubMed

  https://pubmed.ncbi.nlm.nih.gov/10099685/

  Angina pectoris often results from ischemic episodes that excite chemosensitive and mechanoreceptive receptors in the heart. Ischemic episodes release a collage of chemicals, including adenosine and bradykinin, that excites the receptors of the sympathetic and vagal afferent pathways. Sympathetic afferent fibers from the heart enter the upper thoracic spinal cord and synapse on cells of origin of ascending pathways. This review focuses on the spinothalamic tract, but other pathways are excited as well. […] Excitation of spinothalamic tract cells in the upper thoracic and lower cervical segments, except C7 and C8 segments, contributes to the anginal pain experienced in the chest and arm. Cardiac vagal afferent fibers synapse in the nucleus tractus solitarius of the medulla and then descend to excite upper cervical spinothalamic tract cells. This innervation contributes to the anginal pain experienced in the neck and jaw. The spinothalamic tract projects to the medial and lateral thalamus and, based on positron emission tomography studies, activates several cortical areas, including the anterior cingulate gyrus (BA 24 and 25), the lateral basal frontal cortex, and the mesiofrontal cortex.

• #3 Mechanisms of cardiac pain – PubMed

  https://pubmed.ncbi.nlm.nih.gov/10099685/

  Angina pectoris often results from ischemic episodes that excite chemosensitive and mechanoreceptive receptors in the heart. Ischemic episodes release a collage of chemicals, including adenosine and bradykinin, that excites the receptors of the sympathetic and vagal afferent pathways. Sympathetic afferent fibers from the heart enter the upper thoracic spinal cord and synapse on cells of origin of ascending pathways. This review focuses on the spinothalamic tract, but other pathways are excited as well. […] Excitation of spinothalamic tract cells in the upper thoracic and lower cervical segments, except C7 and C8 segments, contributes to the anginal pain experienced in the chest and arm. Cardiac vagal afferent fibers synapse in the nucleus tractus solitarius of the medulla and then descend to excite upper cervical spinothalamic tract cells. This innervation contributes to the anginal pain experienced in the neck and jaw. The spinothalamic tract projects to the medial and lateral thalamus and, based on positron emission tomography studies, activates several cortical areas, including the anterior cingulate gyrus (BA 24 and 25), the lateral basal frontal cortex, and the mesiofrontal cortex.

• #4 Mechanisms of cardiac pain – PubMed

  https://pubmed.ncbi.nlm.nih.gov/10099685/

  Angina pectoris often results from ischemic episodes that excite chemosensitive and mechanoreceptive receptors in the heart. Ischemic episodes release a collage of chemicals, including adenosine and bradykinin, that excites the receptors of the sympathetic and vagal afferent pathways. Sympathetic afferent fibers from the heart enter the upper thoracic spinal cord and synapse on cells of origin of ascending pathways. This review focuses on the spinothalamic tract, but other pathways are excited as well. […] Excitation of spinothalamic tract cells in the upper thoracic and lower cervical segments, except C7 and C8 segments, contributes to the anginal pain experienced in the chest and arm. Cardiac vagal afferent fibers synapse in the nucleus tractus solitarius of the medulla and then descend to excite upper cervical spinothalamic tract cells. This innervation contributes to the anginal pain experienced in the neck and jaw. The spinothalamic tract projects to the medial and lateral thalamus and, based on positron emission tomography studies, activates several cortical areas, including the anterior cingulate gyrus (BA 24 and 25), the lateral basal frontal cortex, and the mesiofrontal cortex.

• #5 Angina Pectoris: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/761889-overview

  Myocardial ischemia develops when coronary blood flow becomes inadequate to meet myocardial oxygen demand. This causes myocardial cells to switch from aerobic to anaerobic metabolism, with a progressive impairment of metabolic, mechanical, and electrical functions. Angina pectoris is the most common clinical manifestation of myocardial ischemia. It is caused by chemical and mechanical stimulation of sensory afferent nerve endings in the coronary vessels and myocardium. These nerve fibers extend from the first to fourth thoracic spinal nerves, ascending via the spinal cord to the thalamus, and from there to the cerebral cortex. […] Studies have shown that adenosine may be the main chemical mediator of anginal pain. During ischemia, ATP is degraded to adenosine, which, after diffusion to the extracellular space, causes arteriolar dilation and anginal pain. Adenosine induces angina mainly by stimulating the A1 receptors in cardiac afferent nerve endings.

• #6 Angina Pectoris: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/761889-overview

  Myocardial ischemia develops when coronary blood flow becomes inadequate to meet myocardial oxygen demand. This causes myocardial cells to switch from aerobic to anaerobic metabolism, with a progressive impairment of metabolic, mechanical, and electrical functions. Angina pectoris is the most common clinical manifestation of myocardial ischemia. It is caused by chemical and mechanical stimulation of sensory afferent nerve endings in the coronary vessels and myocardium. These nerve fibers extend from the first to fourth thoracic spinal nerves, ascending via the spinal cord to the thalamus, and from there to the cerebral cortex. […] Studies have shown that adenosine may be the main chemical mediator of anginal pain. During ischemia, ATP is degraded to adenosine, which, after diffusion to the extracellular space, causes arteriolar dilation and anginal pain. Adenosine induces angina mainly by stimulating the A1 receptors in cardiac afferent nerve endings.

• #7 Angina Pectoris: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/761889-overview

  Heart rate, myocardial inotropic state, and myocardial wall tension are the major determinants of myocardial metabolic activity and myocardial oxygen demand. Increases in the heart rate and myocardial contractile state result in increased myocardial oxygen demand. Increases in both afterload (ie, aortic pressure) and preload (ie, ventricular end-diastolic volume) result in a proportional elevation of myocardial wall tension and, therefore, increased myocardial oxygen demand. […] Myocardial ischemia can result from (1) a reduction of coronary blood flow caused by fixed and/or dynamic epicardial coronary artery (ie, conductive vessel) stenosis, (2) abnormal constriction or deficient relaxation of coronary microcirculation (ie, resistance vessels), or (3) reduced oxygen-carrying capacity of the blood.

• #8 Angina Pectoris: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/761889-overview

  Heart rate, myocardial inotropic state, and myocardial wall tension are the major determinants of myocardial metabolic activity and myocardial oxygen demand. Increases in the heart rate and myocardial contractile state result in increased myocardial oxygen demand. Increases in both afterload (ie, aortic pressure) and preload (ie, ventricular end-diastolic volume) result in a proportional elevation of myocardial wall tension and, therefore, increased myocardial oxygen demand. […] Myocardial ischemia can result from (1) a reduction of coronary blood flow caused by fixed and/or dynamic epicardial coronary artery (ie, conductive vessel) stenosis, (2) abnormal constriction or deficient relaxation of coronary microcirculation (ie, resistance vessels), or (3) reduced oxygen-carrying capacity of the blood.

• #9 Angina Pectoris: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/761889-overview

  Heart rate, myocardial inotropic state, and myocardial wall tension are the major determinants of myocardial metabolic activity and myocardial oxygen demand. Increases in the heart rate and myocardial contractile state result in increased myocardial oxygen demand. Increases in both afterload (ie, aortic pressure) and preload (ie, ventricular end-diastolic volume) result in a proportional elevation of myocardial wall tension and, therefore, increased myocardial oxygen demand. […] Myocardial ischemia can result from (1) a reduction of coronary blood flow caused by fixed and/or dynamic epicardial coronary artery (ie, conductive vessel) stenosis, (2) abnormal constriction or deficient relaxation of coronary microcirculation (ie, resistance vessels), or (3) reduced oxygen-carrying capacity of the blood.

• #10 Angina Pectoris: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/761889-overview

  Heart rate, myocardial inotropic state, and myocardial wall tension are the major determinants of myocardial metabolic activity and myocardial oxygen demand. Increases in the heart rate and myocardial contractile state result in increased myocardial oxygen demand. Increases in both afterload (ie, aortic pressure) and preload (ie, ventricular end-diastolic volume) result in a proportional elevation of myocardial wall tension and, therefore, increased myocardial oxygen demand. […] Myocardial ischemia can result from (1) a reduction of coronary blood flow caused by fixed and/or dynamic epicardial coronary artery (ie, conductive vessel) stenosis, (2) abnormal constriction or deficient relaxation of coronary microcirculation (ie, resistance vessels), or (3) reduced oxygen-carrying capacity of the blood.

• #11 Angina Pectoris: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/761889-overview

  Atherosclerosis is the most common cause of epicardial coronary artery stenosis and, hence, angina pectoris. Patients with a fixed coronary atherosclerotic lesion of at least 50% show myocardial ischemia during increased myocardial metabolic demand as the result of a significant reduction in CFR. These patients are not able to increase their coronary blood flow during stress to match the increased myocardial metabolic demand, thus they experience angina. […] Coronary spasm can also reduce CFR significantly by causing dynamic stenosis of coronary arteries. Prinzmetal angina is defined as resting angina associated with ST-segment elevation caused by focal coronary artery spasm. […] Approximately 30% of patients with chest pain referred for cardiac catheterization have normal or minimal atherosclerosis of coronary arteries. A subset of these patients demonstrates reduced CFR that is believed to be caused by functional and structural alterations of small coronary arteries and arterioles (ie, resistance vessels).

• #12 Angina module 3: pathophysiology – The British Journal of Cardiology

  https://bjcardio.co.uk/2020/04/angina-module-3-pathophysiology/

  Endothelial dysfunction is characterised by a reduction in the bioavailability of vasodilators, such as NO, as a result of reduced production and increased consumption of NO, and an increase in endothelium-derived contracting factors, such as endothelin and angiotensin II (AII). […] Consequently, endothelial dysfunction predisposes to atherogenesis and is a marker of atherosclerotic risk. […] The role of cigarette smoking in the development of atherosclerosis, angina and ACS has been extensively studied and reviewed. […] Smoking predisposes to atherogenesis through a number of processes including inflammation, platelet activation and fibrinolytic dysfunction, as well as modification of the lipid profile. […] The progression of atherosclerotic plaques occurs through a number of processes.

• #13 Microvascular angina and systemic hypertension

  https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-14/microvascular-angina-and-systemic-hypertension

  Myocardial ischaemia triggered by functional and/or anatomical abnormalities in the coronary microcirculation has been documented in many studies using radionuclide myocardial perfusion techniques, coronary sinus oxygen saturation measurements and coronary sinus pH changes, and/or myocardial lactate production during pacing, as well as stress-induced alterations of cardiac high-energy phosphate, as assessed by magnetic resonance spectrometry. […] Both coronary microvascular spasm and/or a reduced microvascular vasodilator capacity have been demonstrated to cause myocardial ischaemia and anginal symptoms in patients with hypertension and microvascular angina. […] The presence of endothelial dysfunction in patients with hypertension and microvascular angina has been suggested by a reduced coronary flow response to acetylcholine or atrial pacing and by inappropriate endothelial vasoconstrictor activity, mainly mediated by endothelin-1 (ET-1) production.

• #14 Microvascular angina and systemic hypertension

  https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-14/microvascular-angina-and-systemic-hypertension

  Myocardial ischaemia triggered by functional and/or anatomical abnormalities in the coronary microcirculation has been documented in many studies using radionuclide myocardial perfusion techniques, coronary sinus oxygen saturation measurements and coronary sinus pH changes, and/or myocardial lactate production during pacing, as well as stress-induced alterations of cardiac high-energy phosphate, as assessed by magnetic resonance spectrometry. […] Both coronary microvascular spasm and/or a reduced microvascular vasodilator capacity have been demonstrated to cause myocardial ischaemia and anginal symptoms in patients with hypertension and microvascular angina. […] The presence of endothelial dysfunction in patients with hypertension and microvascular angina has been suggested by a reduced coronary flow response to acetylcholine or atrial pacing and by inappropriate endothelial vasoconstrictor activity, mainly mediated by endothelin-1 (ET-1) production.

• #15 Microvascular angina and systemic hypertension

  https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-14/microvascular-angina-and-systemic-hypertension

  Myocardial ischaemia triggered by functional and/or anatomical abnormalities in the coronary microcirculation has been documented in many studies using radionuclide myocardial perfusion techniques, coronary sinus oxygen saturation measurements and coronary sinus pH changes, and/or myocardial lactate production during pacing, as well as stress-induced alterations of cardiac high-energy phosphate, as assessed by magnetic resonance spectrometry. […] Both coronary microvascular spasm and/or a reduced microvascular vasodilator capacity have been demonstrated to cause myocardial ischaemia and anginal symptoms in patients with hypertension and microvascular angina. […] The presence of endothelial dysfunction in patients with hypertension and microvascular angina has been suggested by a reduced coronary flow response to acetylcholine or atrial pacing and by inappropriate endothelial vasoconstrictor activity, mainly mediated by endothelin-1 (ET-1) production.

• #16 Microvascular angina and systemic hypertension

  https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-14/microvascular-angina-and-systemic-hypertension

  Myocardial ischaemia triggered by functional and/or anatomical abnormalities in the coronary microcirculation has been documented in many studies using radionuclide myocardial perfusion techniques, coronary sinus oxygen saturation measurements and coronary sinus pH changes, and/or myocardial lactate production during pacing, as well as stress-induced alterations of cardiac high-energy phosphate, as assessed by magnetic resonance spectrometry. […] Both coronary microvascular spasm and/or a reduced microvascular vasodilator capacity have been demonstrated to cause myocardial ischaemia and anginal symptoms in patients with hypertension and microvascular angina. […] The presence of endothelial dysfunction in patients with hypertension and microvascular angina has been suggested by a reduced coronary flow response to acetylcholine or atrial pacing and by inappropriate endothelial vasoconstrictor activity, mainly mediated by endothelin-1 (ET-1) production.

• #17 Ovid: Primary Care Medicine

  https://www.uky.edu/~achan2/M3/pcm-book/c20-eval-chest-pain.htm

  Chest pain may arise from chest wall, intrathoracic, abdominal, or even psychophysiologic sources. […] Angina pectoris due to occlusive coronary artery disease is the most important cardiac source of chest pain. […] The classic hallmarks of angina are its sudden onset with exertion, emotional stress, or eating (usually a very large meal) and its relief within minutes by rest or nitroglycerin. […] Unstable angina is one of the acute coronary syndromes, along with nonQ-wave myocardial infarction and Q-wave myocardial infarction. […] All are important causes of coronary chest pain and result from acute plaque rupture, which triggers platelet activation, thrombin clot formation, and active vasoconstriction. […] Myocardial infarction is typically heralded by chest pain exceeding that of unstable angina, but the presentation is often more subtle or even silent, particularly in diabetics, the elderly, and women.

• #18 Cardiac chest pain – Emergency Department Analgesia

  https://www.cambridge.org/core/books/emergency-department-analgesia/cardiac-chest-pain/C0EB4CF0789ECEF217BF223C8EC55D54

  The extensive use of short-term oxygen therapy in acute coronary syndrome (ACS), with rarely reported adverse effects and frequent cases of anecdotal benefit, supports oxygen administration as benign intervention for cardiac patients with pain and subnormal peripheral pulse oximetry. […] The pain of ACS is effectively decreased by beta-blockers. Though their exact analgesia mechanism is not known, there are several possible routes by which beta-blockers could reduce pain. […] Nitrates dilate the epicardial coronary arteries, their collaterals, and peripheral vessels, thus improving coronary perfusion and potentiating a favorable ratio of subendocardial-to-epicardial flow. […] Opioids have long been a part of the ACS treatment armamentarium. Due to its properties as a pulmonary venodilator and anxiolytic, morphine has been the analgesic of choice for ACS pain. […] Intravenous benzodiazepines should be used for patients with cocaine-associated cardiac chest pain. In this population, the risk of vasospasm from beta-blockers is such that these agents should be avoided.

• #19 Patient education: Chest pain (Beyond the Basics) – UpToDate

  https://www.uptodate.com/contents/chest-pain-beyond-the-basics

  A heart attack, or myocardial infarction (MI), occurs when the surface covering of a fatty plaque ruptures. […] A blood clot (also called a thrombus) can form on the plaque, which can partially or completely block the artery. […] If this continues for more than 15 minutes, the muscle can become damaged or „infarcted” (which means that the tissue in that area dies). […] In some cases, chest pain is caused by a heart-related problem that is not related to blood flow in the coronary arteries. […] Angina is usually not felt in any specific spot, but rather throughout the chest. […] Angina tends to come on gradually; the pain typically gets worse over several minutes. […] If the pain begins during an activity that increases physical exertion, such as walking up stairs, sexual intercourse, or raking leaves, and gets better within minutes of resting, it could be angina. […] If the pain is relieved within a minute or two with nitroglycerin, a medicine used to treat angina, it suggests (but does not prove) that ischemia is the cause.

• #20 Chest pain pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Chest_pain_pathophysiology

  Unstable angina is triggered by severe transient myocardial ischemia that occurs because changes to an atherosclerotic plaque in the coronary artery that causes platelet aggregation and vasospasm, decreasing myocardial blood supply. There is evidence that suggests unstable angina precedes myocardial infarction.

• #21 Angina – Wikipedia

  https://en.wikipedia.org/wiki/Angina

  Angina, also known as angina pectoris, is chest pain or pressure, usually caused by insufficient blood flow to the heart muscle (myocardium). It is most commonly a symptom of coronary artery disease. […] Angina is typically the result of partial obstruction or spasm of the arteries that supply blood to the heart muscle. The main mechanism of coronary artery obstruction is atherosclerosis as part of coronary artery disease. […] The pathophysiology of unstable angina is the reduction of coronary blood flow due to transient platelet aggregation on apparently normal endothelium, coronary artery spasms, or coronary thrombosis. […] The process starts with atherosclerosis, progresses through inflammation to yield an active unstable plaque, which undergoes thrombosis and results in acute myocardial ischemia, which, if not reversed, results in cell necrosis (infarction).

• #22 Angina Pectoris: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/761889-overview

  Atherosclerosis is the most common cause of epicardial coronary artery stenosis and, hence, angina pectoris. Patients with a fixed coronary atherosclerotic lesion of at least 50% show myocardial ischemia during increased myocardial metabolic demand as the result of a significant reduction in CFR. These patients are not able to increase their coronary blood flow during stress to match the increased myocardial metabolic demand, thus they experience angina. […] Coronary spasm can also reduce CFR significantly by causing dynamic stenosis of coronary arteries. Prinzmetal angina is defined as resting angina associated with ST-segment elevation caused by focal coronary artery spasm. […] Approximately 30% of patients with chest pain referred for cardiac catheterization have normal or minimal atherosclerosis of coronary arteries. A subset of these patients demonstrates reduced CFR that is believed to be caused by functional and structural alterations of small coronary arteries and arterioles (ie, resistance vessels).

• #23 Angina Pectoris: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/761889-overview

  Atherosclerosis is the most common cause of epicardial coronary artery stenosis and, hence, angina pectoris. Patients with a fixed coronary atherosclerotic lesion of at least 50% show myocardial ischemia during increased myocardial metabolic demand as the result of a significant reduction in CFR. These patients are not able to increase their coronary blood flow during stress to match the increased myocardial metabolic demand, thus they experience angina. […] Coronary spasm can also reduce CFR significantly by causing dynamic stenosis of coronary arteries. Prinzmetal angina is defined as resting angina associated with ST-segment elevation caused by focal coronary artery spasm. […] Approximately 30% of patients with chest pain referred for cardiac catheterization have normal or minimal atherosclerosis of coronary arteries. A subset of these patients demonstrates reduced CFR that is believed to be caused by functional and structural alterations of small coronary arteries and arterioles (ie, resistance vessels).

• #24 Angina Pectoris: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/761889-overview

  Angina due to dysfunction of small coronary arteries and arterioles is called microvascular angina. […] The syndrome that includes angina pectoris, ischemialike ST-segment changes and/or myocardial perfusion defects during stress testing, and angiographically normal coronary arteries is referred to as syndrome X. […] A number of extravascular forces produced by contraction of adjacent myocardium and intraventricular pressures can influence coronary microcirculation resistance and thus reduce CFR. […] Myocardial ischemia can also be the result of factors affecting blood composition, such as reduced oxygen-carrying capacity of blood, as is observed with severe anemia (hemoglobin, 8 g/dL), or elevated levels of carboxyhemoglobin. […] Ambulatory ECG monitoring has shown that silent ischemia is a common phenomenon among patients with established coronary artery disease.

• #25 Pleuritic Chest Pain: Sorting Through the Differential Diagnosis | AAFP

  https://www.aafp.org/pubs/afp/issues/2017/0901/p306.html

  Pleuritic chest pain is characterized by sudden and intense sharp, stabbing, or burning pain in the chest when inhaling and exhaling. […] Pleuritic chest pain is caused by inflammation of the parietal pleura and can be triggered by a variety of causes. […] The visceral pleura does not contain pain receptors, whereas the parietal pleura is innervated by somatic nerves that sense pain due to trauma or inflammation. Inflammatory mediators released into the pleural space trigger local pain receptors. Parietal pleurae at the periphery of the rib cage and lateral hemidiaphragm are innervated by intercostal nerves. Trauma or inflammation in these regions results in pain localized in the cutaneous distribution of those nerves. In contrast, the phrenic nerve innervates the central diaphragm and can refer pain to the ipsilateral neck or shoulder.

• #26 Pleuritic Chest Pain: Sorting Through the Differential Diagnosis | AAFP

  https://www.aafp.org/pubs/afp/issues/2017/0901/p306.html

  Pleuritic chest pain is characterized by sudden and intense sharp, stabbing, or burning pain in the chest when inhaling and exhaling. […] Pleuritic chest pain is caused by inflammation of the parietal pleura and can be triggered by a variety of causes. […] The visceral pleura does not contain pain receptors, whereas the parietal pleura is innervated by somatic nerves that sense pain due to trauma or inflammation. Inflammatory mediators released into the pleural space trigger local pain receptors. Parietal pleurae at the periphery of the rib cage and lateral hemidiaphragm are innervated by intercostal nerves. Trauma or inflammation in these regions results in pain localized in the cutaneous distribution of those nerves. In contrast, the phrenic nerve innervates the central diaphragm and can refer pain to the ipsilateral neck or shoulder.

• #27 Noncardiac Chest Pain: Epidemiology, Natural Course and Pathogenesis

  https://www.jnmjournal.org/journal/view.html?doi=10.5056/jnm.2011.17.2.110

  Gastroesophageal reflux disease is the most common esophageal cause for noncardiac chest pain in patients with and without coronary artery disease. […] Many studies have shown an association between GERD and NCCP. However, association does not confer causality. Resolution or improvement of chest pain symptoms in response to treatment with antireflux medications provides the missing causal link. […] The mechanism by which gastroesophageal reflux causes NCCP remains poorly understood. It is still unclear why esophageal exposure to gastric content in some patients causes heartburn and in others chest pain. […] Different underlying mechanisms have been suggested to result in esophageal hypersensitivity in NCCP patients. These include peripheral sensitization of esophageal sensory afferents leading to heightened responses to physiologic and pathologic stimuli and modulation of afferent neural function at the level of the spinal dorsal root or the central nervous system.

• #28 Noncardiac Chest Pain: Epidemiology, Natural Course and Pathogenesis

  https://www.jnmjournal.org/journal/view.html?doi=10.5056/jnm.2011.17.2.110

  Gastroesophageal reflux disease is the most common esophageal cause for noncardiac chest pain in patients with and without coronary artery disease. […] Many studies have shown an association between GERD and NCCP. However, association does not confer causality. Resolution or improvement of chest pain symptoms in response to treatment with antireflux medications provides the missing causal link. […] The mechanism by which gastroesophageal reflux causes NCCP remains poorly understood. It is still unclear why esophageal exposure to gastric content in some patients causes heartburn and in others chest pain. […] Different underlying mechanisms have been suggested to result in esophageal hypersensitivity in NCCP patients. These include peripheral sensitization of esophageal sensory afferents leading to heightened responses to physiologic and pathologic stimuli and modulation of afferent neural function at the level of the spinal dorsal root or the central nervous system.

• #29 Noncardiac Chest Pain: Epidemiology, Natural Course and Pathogenesis

  https://www.jnmjournal.org/journal/view.html?doi=10.5056/jnm.2011.17.2.110

  Esophageal hypersensitivity has been demonstrated in most of the non-gastroesophageal reflux disease-related noncardiac chest pain patients, regardless if esophageal dysmotility is present or absent. […] Studies have consistently documented alteration in pain perception regardless of whether dysmotility was present or absent in patients with NCCP. […] The presence of esophageal hypersensitivity can be subsequently demonstrated long after the original stimulus is no longer present and the esophageal mucosa has healed. However, it is still unclear what factors are pivotal for the persistence of such esophageal hypersensitivity. […] The relationship between NCCP and esophageal dysmotility remains an area of intense controversy because documentation of esophageal dysmotility during manometry is rarely associated with reports of chest pain symptoms. […] Overall, the disease appears to be very common, without any gender predilection, and be associated with a good prognosis. More has been learned over the years about GERD, esophageal dysmotility, esophageal hypersensitivity and psychological comorbidity as important underlying mechanisms of NCCP.

• #30 Patients with non-cardiac chest pain are reassured with brief education

  https://www.escardio.org/The-ESC/Press-Office/Press-releases/Patients-with-non-cardiacchest-pain-are-reassured-with-brief-education

  Patients diagnosed with non-cardiac chest pain are reluctant to believe they do not have heart disease. […] Studies in other centres have reported that chest pain has a non-cardiac origin in two-thirds of patients. […] Typical causes are indigestion or acid reflux, musculoskeletal disorders such as back pain or sore muscles between the ribs, and psychological issues like panic attacks and anxiety. […] Given the excellent prognostic value of coronary CT, I thought this information could be beneficial to this patient group. […] The study included 92 patients with chest pain and normal results (i.e. no sign of coronary artery disease) on CT examination of the coronary arteries. […] This included the different reasons for chest pain, low probability of inaccurate results, and very low risk of a future heart attack when CT scans show healthy arteries.

• #31 Reddit – The heart of the internet

  https://www.reddit.com/r/medicine/comments/5uetl4/what_is_the_real_cause_of_acute_atraumatic/

  It is well recognized that the majority of patients presenting with acute chest pain are not suffering from ACS. Probably a third of my patients present with chest pain of some form and I’d guess that the source of the pain is cardiac in origin for less than 5% of those. […] Personally I think that esophageal spasm is probably more common than we appreciate and is therefore underdiagnosed. Of course, I can only speculate as I do not have the tools to make the diagnosis in the ED. […] There are also probably a large number of patients with somaticized chest pain, especially the ones who tell me that they have „heart pain,” those with odd features (such as numbness in non-dermatomal patterns or other neurological symptoms), or if they have a large number of other complaints (the so-called „pan-positive ROS”). We’ve done a really good job educating patients about seeking care for the symptoms of MI in the past several decades and the unfortunate side-effect is that this effort has cemented chest pain in the public consciousness as a feared experience, which probably encourages somaticizers to report the symptom–it is a well-understood „shorthand” for having a serious problem and needing help.

• #32 Patients with non-cardiac chest pain are reassured with brief education

  https://www.escardio.org/The-ESC/Press-Office/Press-releases/Patients-with-non-cardiacchest-pain-are-reassured-with-brief-education

  Patients diagnosed with non-cardiac chest pain are reluctant to believe they do not have heart disease. […] Studies in other centres have reported that chest pain has a non-cardiac origin in two-thirds of patients. […] Typical causes are indigestion or acid reflux, musculoskeletal disorders such as back pain or sore muscles between the ribs, and psychological issues like panic attacks and anxiety. […] Given the excellent prognostic value of coronary CT, I thought this information could be beneficial to this patient group. […] The study included 92 patients with chest pain and normal results (i.e. no sign of coronary artery disease) on CT examination of the coronary arteries. […] This included the different reasons for chest pain, low probability of inaccurate results, and very low risk of a future heart attack when CT scans show healthy arteries.

• #33 Chest pain: MedlinePlus Medical EncyclopediaLock

  https://medlineplus.gov/ency/article/003079.htm

  Inflammation where the ribs join the breast bone or sternum (costochondritis). […] Chest pain can also be due to the following digestive system problems: Spasms or narrowing of the esophagus (the tube that carries food from the mouth to the stomach). […] Gallstones cause pain that gets worse after a meal (most often a fatty meal). […] Heartburn or gastroesophageal reflux (GERD). […] Stomach ulcer or gastritis: Burning pain occurs if your stomach is empty and feels better when you eat food.

• #34 Chest Pain: Does This Patient Have Cardiac Ischemia? | Consultant360

  https://www.consultant360.com/articles/chest-pain-does-patient-have-cardiac-ischemia

  Vasospasm (Prinzmetals angina, idiopathic, cocaine-induced). […] Next, we consider diseases that cause ischemia at the level of the microvasculature (endocardium), as opposed to the epicardium. […] Syndrome X (chest pain in the presence of normal coronary arteries on angiography, thought to be due to microvascular ischemia, endothelial cell dysfunction, and/or heightened perception of pain in the setting of any afferent stimulation. […] The prognosis is benign with respect to mortality). […] Troponin measurement is the most sensitive and specific test for the diagnosis of myocardial infarction. […] If the diagnosis remains uncertain, consider ordering a transthoracic echocardiogram. […] The differences in presentation and risk exist because an ACS is caused by unstable plaque (or, in the case of STEMI, plaque rupture) obstructing a coronary artery, whereas stable angina is caused by chronic narrowing of the coronary arteries from atherosclerotic disease.

• #35 Updated Approach to the Athlete With Chest Pain

  https://www.acc.org/Latest-in-Cardiology/Articles/2022/08/04/14/40/Updated-Approach-to-the-Athlete-With-Chest-Pain

  The workup for acute chest pain concerning for an acute coronary syndrome, aortic dissection, coronary dissection, cocaine abuse, myocarditis, pericarditis, or pulmonary embolism includes lab work, electrocardiogram (ECG), and transthoracic echocardiogram (TTE). In the intermediate to high pretest probability to groups, a stress test, CCTA, and/or cardiac catheterization may also be pursued. […] The recent guidelines distinguish coronary computed tomography angiography (CCTA) as the only Class 1A recommendation in the intermediate risk chest pain patient. […] CCTA can provide superior prognostic value of the assessment of coronary atherosclerosis, as seen in PROMISE, Scot Heart, and the CONSERVE trial. CCTA provides an opportunity to exclude obstructive coronary disease and for the early identification of non-obstructive disease and initiation of preventive strategies including statins and intensification of risk factor modification.

• #36 Updated Approach to the Athlete With Chest Pain

  https://www.acc.org/Latest-in-Cardiology/Articles/2022/08/04/14/40/Updated-Approach-to-the-Athlete-With-Chest-Pain

  The workup for acute chest pain concerning for an acute coronary syndrome, aortic dissection, coronary dissection, cocaine abuse, myocarditis, pericarditis, or pulmonary embolism includes lab work, electrocardiogram (ECG), and transthoracic echocardiogram (TTE). In the intermediate to high pretest probability to groups, a stress test, CCTA, and/or cardiac catheterization may also be pursued. […] The recent guidelines distinguish coronary computed tomography angiography (CCTA) as the only Class 1A recommendation in the intermediate risk chest pain patient. […] CCTA can provide superior prognostic value of the assessment of coronary atherosclerosis, as seen in PROMISE, Scot Heart, and the CONSERVE trial. CCTA provides an opportunity to exclude obstructive coronary disease and for the early identification of non-obstructive disease and initiation of preventive strategies including statins and intensification of risk factor modification.

• #37 Angina Pectoris: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/761889-overview

  Myocardial ischemia develops when coronary blood flow becomes inadequate to meet myocardial oxygen demand. This causes myocardial cells to switch from aerobic to anaerobic metabolism, with a progressive impairment of metabolic, mechanical, and electrical functions. Angina pectoris is the most common clinical manifestation of myocardial ischemia. It is caused by chemical and mechanical stimulation of sensory afferent nerve endings in the coronary vessels and myocardium. These nerve fibers extend from the first to fourth thoracic spinal nerves, ascending via the spinal cord to the thalamus, and from there to the cerebral cortex. […] Studies have shown that adenosine may be the main chemical mediator of anginal pain. During ischemia, ATP is degraded to adenosine, which, after diffusion to the extracellular space, causes arteriolar dilation and anginal pain. Adenosine induces angina mainly by stimulating the A1 receptors in cardiac afferent nerve endings.

• #38 Angina module 3: pathophysiology – The British Journal of Cardiology

  https://bjcardio.co.uk/2020/04/angina-module-3-pathophysiology/

  Endothelial dysfunction is characterised by a reduction in the bioavailability of vasodilators, such as NO, as a result of reduced production and increased consumption of NO, and an increase in endothelium-derived contracting factors, such as endothelin and angiotensin II (AII). […] Consequently, endothelial dysfunction predisposes to atherogenesis and is a marker of atherosclerotic risk. […] The role of cigarette smoking in the development of atherosclerosis, angina and ACS has been extensively studied and reviewed. […] Smoking predisposes to atherogenesis through a number of processes including inflammation, platelet activation and fibrinolytic dysfunction, as well as modification of the lipid profile. […] The progression of atherosclerotic plaques occurs through a number of processes.

• #39 ‘Primary’ Microvascular Angina: Clinical Characteristics, Pathogenesis and Management | ICR Journal

  https://www.icrjournal.com/articles/primary-microvascular-angina-clinical-characteristics-pathogenesis-and-management?language_content_entity=en

  The causal mechanisms of CMVD in patients with primary stable MVA are not fully understood and are likely to be several. Traditional cardiovascular risk factors for CAD are known causes of CMVD, although there is no clear evidence of a direct relationship among risk factors and the severity of CMVD in MVA patients. Increased adrenergic activity and/or abnormal function of cardiac sympathetic nerve fibres have been also suggested as causal factors in some studies, and inflammatory mechanisms were reported to have a role in MVA. Also importantly, oestrogen deficiency has been advocated as a causal mechanism in women with MVA. […] CMVD, presenting as abnormal coronary microvascular dilation, microvascular spasm, or both, is the pathogenic mechanism underlying MVA.

• #40 Long-term cardiac pathology in individuals with mild initial COVID-19 illness | Nature Medicine

  https://www.nature.com/articles/s41591-022-02000-0

  Cardiac symptoms are increasingly recognized as late complications of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in previously well individuals with mild initial illness, but the underlying pathophysiology leading to long-term cardiac symptoms remains unclear. […] Ongoing inflammatory cardiac involvement may, at least in part, explain the lingering cardiac symptoms in previously well individuals with mild initial COVID-19 illness. […] Lingering cardiac symptoms, including exercise intolerance, tachycardia and chest pain, are increasingly recognized late complications of COVID-19. […] It remains uncertain whether persistent symptoms, at least in part, relate to cardiovascular involvement and what are the underlying pathophysiological correlates. […] At baseline, participants with cardiac symptoms had higher mapping values, suggesting diffuse myocardial inflammation, and more frequent pericardial enhancement, suggesting pericardial inflammatory involvement compared to asymptomatic participants.

• #41 Noncardiac Chest Pain: Epidemiology, Natural Course and Pathogenesis

  https://www.jnmjournal.org/journal/view.html?doi=10.5056/jnm.2011.17.2.110

  Esophageal hypersensitivity has been demonstrated in most of the non-gastroesophageal reflux disease-related noncardiac chest pain patients, regardless if esophageal dysmotility is present or absent. […] Studies have consistently documented alteration in pain perception regardless of whether dysmotility was present or absent in patients with NCCP. […] The presence of esophageal hypersensitivity can be subsequently demonstrated long after the original stimulus is no longer present and the esophageal mucosa has healed. However, it is still unclear what factors are pivotal for the persistence of such esophageal hypersensitivity. […] The relationship between NCCP and esophageal dysmotility remains an area of intense controversy because documentation of esophageal dysmotility during manometry is rarely associated with reports of chest pain symptoms. […] Overall, the disease appears to be very common, without any gender predilection, and be associated with a good prognosis. More has been learned over the years about GERD, esophageal dysmotility, esophageal hypersensitivity and psychological comorbidity as important underlying mechanisms of NCCP.

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