Myocardial ischaemia: definition and causes

ESC CardioMed ◽  
2018 ◽  
pp. 1325-1329
Author(s):  
Filippo Crea ◽  
Gaetano Antonio Lanza
Keyword(s):  
Blood Flow ◽  
Coronary Artery ◽  
Myocardial Ischaemia ◽  
Coronary Artery Spasm ◽  
Coronary Vessels ◽  
Oxygen Demand ◽  
Myocardial Oxygen Demand ◽  
Clinical Settings ◽  
Variant Angina ◽  
Coronary Microvascular Function

Myocardial ischaemia is caused by a mismatch between myocardial oxygen demand and myocardial blood flow supply, which results in myocardial suffering and, when prolonged, injury. The main mechanisms of myocardial ischaemia include atherothrombotic lesions of epicardial coronary vessels, which may result in chronic and acute ischaemic syndromes; coronary artery spasm, which is mainly responsible for variant angina; and abnormalities in coronary microvascular function, which can cause or contribute to myocardial ischaemia in various clinical settings.

Myocardial ischaemia: definition and causes

ESC CardioMed ◽  
2018 ◽  
pp. 1325-1329
Author(s):  
Filippo Crea ◽  
Gaetano Antonio Lanza
Keyword(s):  
Coronary Artery ◽  
Myocardial Ischaemia ◽  
Coronary Artery Spasm ◽  
Chronic Stable Angina ◽  
Oxygen Demand ◽  
Microvascular Dysfunction ◽  
Myocardial Oxygen Demand ◽  
Coronary Microvascular Dysfunction ◽  
Coronary Artery Dissection ◽  
The Right

Myocardial ischaemia is caused by a mismatch between myocardial oxygen demand and myocardial blood flow supply, which results in reversible myocardial suffering and, when prolonged, in irreversible injury. The main causes of myocardial ischaemia include (1) atherosclerotic flow-limiting stenoses which are responsible for chronic stable angina; (2) coronary thrombus superimposed on an atherosclerotic plaque which is responsible for acute coronary syndromes; (3) coronary artery spasm which is responsible for vasospastic angina; and (4) coronary microvascular dysfunction which is responsible for microvascular angina and can also contribute to myocardial ischaemia in various clinical settings. Functional alterations (thrombus, spasm, and microvascular dysfunction) may act on angiographically normal coronary arteries or arteries presenting stenoses of variable severity. Less frequent coronary causes of myocardial ischaemia include spontaneous coronary artery dissection, myocardial bridge, coronary thromboembolism, an abnormal origin of the right or left coronary artery, and ascending aorta dissection involving coronary ostia. Finally, myocardial ischaemia can occur in the presence of severe left ventricular hypertrophy as observed in aortic stenosis and hypertrophic cardiomyopathy.

scholarly journals Pharmacotherapy of angina pectoris

1982 ◽  
Vol 63 (1) ◽  
pp. 34-39
Author(s):  
R. A. Camburg
Keyword(s):  
Coronary Artery Disease ◽  
Blood Flow ◽  
Coronary Artery ◽  
Angina Pectoris ◽  
Coronary Blood Flow ◽  
Oxygen Demand ◽  
Lipid Lowering ◽  
Myocardial Oxygen Demand ◽  
Artery Disease ◽  
Antianginal Drugs

The key to the normal functioning of the heart muscle is the delivery of metabolites to it with blood, primarily oxygen, corresponding to the needs. When the balance between the supply of oxygen to the heart and its demand is imbalanced, myocardial ischemia occurs. This condition is a central link in the pathogenesis of the so-called coronary or ischemic heart disease (IHD). In 8994% of patients with coronary artery disease, it is caused by atherosclerosis of the coronary arteries and aorta [15, 21, 26]. Regarding the pathogenetic treatment of chronic forms of coronary artery disease (CHD), namely angina pectoris, one should dwell on such points as the normalization of the psychoemotional sphere (tranquilizers), an increase in coronary blood flow and oxygen delivery (coronary active agents, -adrenoactivators), a decrease in myocardial oxygen demand (R -adrenergic blockers, cordarone, calcium antagonists), redistribution of coronary blood flow from non-ischemic zones to ischemic zones (-blockers), hemodynamic restructuring (nitrates), switching myocardial metabolism to a reserve anaerobic pathway (gliosiz, nonahlazine), effect on blood circulation antibiotics ). All these agents used for the treatment of angina pectoris are called antianginal drugs and in some cases can be combined with analgesics, cardiac glycosides, anticoagulants, antiarrhythmic, lipid-lowering and other drugs for the complex treatment of IBO.

scholarly journals A Case of Spontaneous Multivessel Coronary Artery Spasm That Underwent Stent Implantation Accompanying ST Segment Elevation on Inferior Electrocardiographic Leads

2016 ◽  
Vol 2016 ◽  
pp. 1-3
Author(s):  
Nuray Kahraman Ay ◽  
Muharrem Nasifov ◽  
Ömer Goktekin
Keyword(s):  
Blood Flow ◽  
Coronary Artery ◽  
Myocardial Ischaemia ◽  
Coronary Artery Spasm ◽  
Coronary Spasm ◽  
St Segment Elevation ◽  
St Segment ◽  
Coronary Artery Segment ◽  
Artery Segment ◽  
Electrocardiographic Leads

Coronary artery spasm is usually defined as a focal constriction of a coronary artery segment, which is reversible, and causes myocardial ischaemia by restricting coronary blood flow. A coronary spasm may rarely compromise all three epicardial arteries simultaneously. We present a case of severe coronary spasm afflicting all coronary arteries accompanying an ST segment elevation in leads D2-D3 and aVF.

Endothelin-1 limits increases in blood flow to native and collateral-dependent myocardium

1997 ◽  
Vol 273 (1) ◽  
pp. R41-R48 ◽  
Author(s):  
J. D. Symons ◽  
S. V. Rendig ◽  
L. W. Fu ◽  
J. C. Longhurst
Keyword(s):  
Blood Flow ◽  
Coronary Artery ◽  
Oxygen Demand ◽  
Control Group ◽  
Myocardial Oxygen Demand ◽  
Receptor Antagonism ◽  
Time Control ◽  
Eta Receptor ◽  
Group 2 ◽  
Group 1

We hypothesized that blood flow to collateralized and noncollateralized myocardium is improved by antagonism of endothelin (ET) A receptors. Coronary collateral development was stimulated by placing an ameroid constrictor around the left circumflex coronary artery (LCx; collateralized region) in 11 swine. After 35 +/- 2 days, the left anterior descending coronary artery (LAD; noncollateralized region) was autoperfused at constant pressure using blood from a femoral artery. In group 1 (n = 6) transmural blood flow was measured using radioactive microspheres in the LAD, LCx, and border regions (i.e., area between LAD and LCx) during pacing stress while vehicle (phosphate-buffered saline) was infused into the LAD coronary artery (pace 1). Approximately 55 min later, a second period of pacing (pace 2) was performed in the presence of ETA receptor antagonism (BQ-123; 5 mg.ml-1.min-1 ic). In the time control group (group 2, n = 5) vehicle was infused during both pacing periods. Indexes of myocardial oxygen demand were similar between paces 1 and 2 in each group. Compared with the first pacing period, transmural blood flow (ml.100 g-1.min-1) was higher (P < 0.05) during ETA receptor antagonism (i.e., pace 2) in the LAD (105 +/- 8 vs. 139 +/- 9), border (51 +/- 5 vs. 83 +/- 7), and LCx regions (22 +/- 3 vs. 41 +/- 4, respectively) in group 1. In group 2, while perfusion in the border (98 +/- 17 vs. 103 +/- 16) and LCx regions (19 +/- 4 vs. 27 +/- 6) was similar in paces 1 and 2, LAD transmural flow was greater (134 +/- 9 vs. 160 +/- 13; P < 0.05) during the second pacing period. However, the percent increase in LAD flow comparing pace 1 with 2 was greater (P < 0.05) in group 1 (39 +/- 6%) compared with group 2 (20 +/- 7%). These data suggest that during the stress of pacing blood flow to collateralized and noncollateralized myocardium is improved in the presence of ETA receptor blockade.

Variant Angina Pectoris Due to Coronary Artery Spasm

CHEST Journal ◽  
1975 ◽  
Vol 67 (6) ◽  
pp. 727-729 ◽  
Author(s):  
Dariush Owlia ◽  
Ravindra Prabhu ◽  
John A. Pierce ◽  
Peter V. Stoughton ◽  
Kanakaiahnavara R. Shankar ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Angina Pectoris ◽  
Coronary Artery Spasm ◽  
Variant Angina ◽  
Variant Angina Pectoris

scholarly journals Perioperative coronary artery spasm leading to myocardial ischaemia after vein graft surgery.

Heart ◽  
1983 ◽  
Vol 49 (3) ◽  
pp. 280-283 ◽  
Author(s):  
B Zingone ◽  
A Salvi ◽  
B Branchini
Keyword(s):  
Coronary Artery ◽  
Myocardial Ischaemia ◽  
Vein Graft ◽  
Coronary Artery Spasm

scholarly journals Coronary artery spasm induced by intracoronary administration of acetylcholine in a patient with variant angina.

1986 ◽  
Vol 75 (12) ◽  
pp. 1730-1734
Author(s):  
Kunihisa MIWA ◽  
Fumio MATSUYAMA ◽  
Masahiro GOTO ◽  
Akira HARA ◽  
Toru NAKAMURA
Keyword(s):  
Coronary Artery ◽  
Coronary Artery Spasm ◽  
Variant Angina ◽  
Intracoronary Administration

scholarly journals Recurrent Coronary Artery Spasm Induced by Vasopressors During Two Operations in the Same Patient Under General Anesthesia

2018 ◽  
Vol 65 (1) ◽  
pp. 44-49 ◽  
Author(s):  
Naotaka Kishimoto ◽  
Munenori Kato ◽  
Yasunori Nakanishi ◽  
Akari Hasegawa ◽  
Yoshihiro Momota
Keyword(s):  
Computed Tomography ◽  
Coronary Artery ◽  
General Anesthesia ◽  
Computed Tomography Angiography ◽  
Coronary Artery Spasm ◽  
Variant Angina ◽  
St Segment Elevation ◽  
Know How ◽  
St Segment

Variant angina is caused by coronary artery spasm (CAS) with ST-segment elevation. We herein report a case of recurrent CAS during 2 operations in the same patient. An 80-year-old woman was scheduled to undergo tracheostomy, submandibular dissection, left partial maxillectomy, and coronoidectomy. We administered ephedrine and phenylephrine to manage hypotension during general anesthesia. Immediately after the administration of these drugs, the ST segment elevated. We decided to cease the operation and transport the patient to the department of cardiology. Computed tomography angiography revealed pneumomediastinum. The cardiologists considered that the electrocardiography findings had changed secondary to pneumomediastinum. About 6 weeks later, a second operation was scheduled. We administered ephedrine and phenylephrine to manage hypotension during general anesthesia. Immediately after the administration of these drugs, ST-segment elevation occurred. We discontinued use of these drugs, and the ST-segment elevation did not recur. We considered that the cause of the ST-segment elevation was vasopressor-induced CAS because the vasopressors were administered immediately before the occurrence of CAS. Vasopressors such as ephedrine or phenylephrine are frequently used to manage hypotension during general anesthesia. Therefore, anesthesiologists should consider the occurrence of CAS before using vasopressors and know how to manage CAS well.

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