Epicardial Spasm
Epicardial Spasm - Related Videos
07:44
Epicardial Outgrowth Culture Assay and Ex Vivo Assessment of Epicardial-derived Cell Migration
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Cited by 9 •
2016
Here, we describe methods for isolating primary mouse epicardial cells by an outgrowth culture assay and assessing the functional migration of epicardial-derived cells (EPDC) using an ex vivo heart culture system. These protocols are suitable for identifying genetic and chemical modulators of epicardial epithelial-to-mesenchymal transition (EMT) and motility.
01:16
Vascular Spasm
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2025
The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last for...
06:31
In Vitro Culture of Epicardial Cells From Mouse Embryonic Heart
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Cited by 13 •
2016
The epicardium is an essential source of multipotent cardiovascular progenitor cells and paracrine factors that are required for cardiovascular development and regeneration. We describe here a method to culture mouse embryonic epicardial cells.
09:17
High-Resolution Endocardial and Epicardial Optical Mapping in a Sheep Model of Stretch-Induced Atrial Fibrillation
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Cited by 20 •
2011
This report provides a detailed description of the methodology and results of simultaneous endocardial and epicardial optical mapping of electrical excitation in the intact left atrium of a Langendorff-perfused sheep heart during stretch-induced atrial fibrillation.
06:18
Measurement of Myocardial Lactate Production for Diagnosis of Coronary Microvascular Spasm
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Cited by 15 •
2021
Myocardial lactate production (coronary arterial-venous difference in serum lactate level) during coronary spasm provocation testing is considered as a highly sensitive marker that reflects acetylcholine-induced myocardial ischemia due to microvascular spasm. This article presents the procedures to assess myocardial lactate production for the diagnosis of coronary microvascular spasm.
FAQs
Impaired endothelial regulation can allow coronary vascular smooth muscle to contract abnormally. This abnormal contractile response narrows the artery temporarily and reduces blood flow to the myocardium. The endothelial contribution is clinically important because it points to a dynamic vascular mechanism rather than a continuously narrowed vessel, helping explain why episodes may resolve after occurring at rest.
When a major coronary artery constricts, myocardial blood flow can fall temporarily. If the reduction is sufficient, the heart muscle may become ischemic, meaning it receives inadequate blood flow for its needs. That transient ischemia can produce chest pain and electrocardiographic changes, giving clinicians objective evidence that an episode affects myocardial perfusion.
Vasospastic angina reflects a temporary change in coronary vessel caliber, whereas fixed coronary obstruction represents a persistent limitation to blood flow. The distinction matters because symptoms and ischemic findings may occur even when a lasting blockage does not explain them. Recognizing the dynamic mechanism supports evaluation and prevention strategies directed at recurrent spasm.
Resolution of the constriction does not eliminate the potential significance of an episode. A marked, temporary reduction in myocardial blood flow can produce ischemia and, in severe cases, arrhythmias. These consequences explain why clinicians must consider both the transient vascular event and its effects on cardiac function when assessing suspected vasospastic angina.
Evaluation combines the symptom pattern with electrocardiography and coronary imaging. Symptoms can suggest an episodic process, while an electrocardiogram may show changes associated with transient ischemia. Coronary imaging helps assess the arteries and distinguish a dynamic narrowing mechanism from fixed obstruction. Together, these approaches provide complementary information rather than relying on one finding alone.
Pharmacologic provocation testing may be used when clinicians need additional evidence that symptoms and ischemic findings arise from a spasm mechanism. It is performed when appropriate as part of the diagnostic evaluation, alongside symptom assessment, electrocardiography, and coronary imaging. Its role is to help clarify a suspected dynamic coronary response when routine evaluation is not sufficient.
Once the mechanism is recognized, treatment strategies focus on preventing recurrent episodes and protecting cardiac function. This approach addresses more than the immediate chest pain because repeated or severe transient reductions in myocardial blood flow may have clinically important consequences. Management therefore follows the identified vascular mechanism rather than treating the presentation solely as fixed coronary obstruction.
Chest pain occurring at rest can reflect a transient coronary vascular event rather than only a persistent arterial blockage. Considering Epicardial Spasm encourages clinicians to correlate resting symptoms with electrocardiographic changes, coronary findings, and, when appropriate, provocation testing. This broader assessment improves recognition of vasospastic angina and supports mechanism-directed prevention.