Coronary Vasospasm
Coronary Vasospasm - Related Videos
07:03
A Low Mortality Rat Model to Assess Delayed Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage
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Cited by 22 •
2013
Aneurysmal subarachnoid hemorrhage (SAH) is bleeding that occurs into the subarachnoid space when an aneurysm ruptures. While the morbidity and mortality from this event has been on a decline due to improved treatment approaches, the risk of vasospasm after subarachnoid hemorrhage continues to be the same as it was several years ago. The importance of establishing a comprehensive and reproducible animal model to identify initiating events of cerebral vasospasm has been the focus of research...
06:39
Ultrasound Based Assessment of Coronary Artery Flow and Coronary Flow Reserve Using the Pressure Overload Model in Mice
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Cited by 20 •
2015
Coronary flow reserve (CFR) is useful for assessment of myocardial oxygen demand and evaluation of cardiovascular risk. This study establishes a step-by-step transthoracic Doppler echocardiographic (TTDE) method for longitudinal monitoring of the changes in CFR, as measured from coronary artery in mice, under the experimental pressure overload of aortic banding.
07:36
Isolation of Mouse Coronary Endothelial Cells
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Cited by 18 •
2016
This protocol is prepared to share our method of isolating mouse coronary endothelial cells for the purpose of imaging or to conduct molecular biological experiments.
13:10
Direct Re-implantation of Left Coronary Artery into the Aorta in Adults with Anomalous Origin of Left Coronary Artery from the Pulmonary Artery (ALCAPA)
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Cited by 7 •
2017
Surgical correction of ALCAPA is highly recommended, regardless of age or the degree of intercoronary collateralization. This protocol presents a technique for the direct re-implantation of adult-type ALCAPA into the aorta to re-establish the dual-coronary perfusion. Whenever feasible, direct re-implantation is preferred to other surgical correction techniques.
05:47
Modified Technique for Coronary Artery Ligation in Mice
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Cited by 8 •
2013
The surgical procedure used to induce experimental myocardial infarction in mice begins with left thoracotomy between the third and the fourth ribs in order to visualize the anterior surface of the heart and left lung. The left coronary artery is ligated, the chest is closed and the mouse is allowed to recover spontaneously.
FAQs
Abnormal contraction of coronary vascular smooth muscle is central to an episode, while endothelial dysfunction can promote impaired regulation of vessel tone. Together, these changes may sharply restrict myocardial blood flow for a limited period. This mechanism helps explain why ischemic symptoms can occur even when the underlying narrowing is transient rather than continuously present.
The clinical outcome depends on how strongly and how long the artery constricts, because reduced myocardial blood flow limits oxygen delivery. Ischemia may produce chest pain and characteristic electrocardiographic changes, while more severe or prolonged episodes can be associated with arrhythmia or infarction. These possible outcomes make recognition clinically important.
Smoking, emotional stress, cold exposure, and certain medications are associated with episodes. The pattern is also clinically notable because events may occur at rest rather than only during exertion. Identifying such circumstances can help clinicians recognize a compatible history and support evaluation of suspected variant, or Prinzmetal, angina.
Its defining clinical challenge is the temporary nature of the vessel change: blood flow can fall abruptly during an episode and improve when the contraction resolves. Symptoms therefore may not follow a constant pattern and can appear at rest. This distinction is relevant when evaluating variant angina and other ischemic syndromes with differing mechanisms.
Evaluation may identify characteristic electrocardiographic changes during an episode, reflecting transient myocardial ischemia. When additional confirmation is needed, provocative angiography can be used to assess abnormal coronary reactivity. These approaches provide complementary information: electrocardiography captures the electrical consequences of reduced blood flow, whereas angiography examines the vascular response directly.
Provocative angiography helps investigate whether the coronary arteries display an abnormal constrictive response. In the context of compatible symptoms or electrocardiographic findings, it can support recognition of a transient vascular mechanism that may not be visible continuously. Its relevance lies in linking suspected ischemia with demonstrable coronary reactivity during evaluation.
Management is directed toward relieving or preventing abnormal vessel constriction with vasodilators and reducing contributing risks through risk-factor modification. The choice to pursue these strategies follows recognition of the episodic ischemic mechanism rather than treating symptoms as unexplained chest pain alone. This approach also addresses the possibility of recurrent episodes and related complications.
Clinically, it provides an explanation for variant angina and some other ischemic presentations, including episodes occurring at rest. In research, it serves as a setting for studying vascular reactivity, meaning how coronary vessels respond by constricting or relaxing. Understanding that reactivity can support investigation of endothelial function, smooth muscle behavior, and treatment responses.