血管攣縮、血管れん縮

関: angiospasm、vasospasm

WordNet

a painful and involuntary muscular contraction (同)cramp, muscle_spasm
(pathology) sudden constriction of a hollow organ (as a blood vessel)
of or relating to or having vessels that conduct and circulate fluids; "vascular constriction"; "a vascular bundle"

PrepTutorEJDIC

(筋肉などの)けいれん / (感情・活動などの)発作《+『of』+『名』》
(血液・樹液などを運ぶ)管の,導管の,血管の
鉱泉,温泉 / 温泉場

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/02/10 12:44:33」(JST)

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[Wiki en表示]

Vasospasm refers to a condition in which a blood vessel's spasm leads to vasoconstriction. This can lead to tissue ischemia and tissue death (necrosis). Cerebral vasospasm may arise in the context of subarachnoid hemorrhage. Symptomatic vasospasm or delayed cerebral ischemia is a major contributor to post-operative stroke and death especially after aneurysmal subarachnoid hemorrhage. Vasospasm typically appears 4 to 10 days after subarachnoid hemorrhage.

Along with physical resistance, vasospasm is a main cause of ischemia. Like physical resistance, vasospasms can occur due to atherosclerosis. Vasospasm is the major cause of prinzmetal angina.

General pathophysiology of vasospasms[edit]

Normally endothelial cells release prostacyclin and nitric oxide (NO) which induce relaxation of the smooth muscle cells, and reduce aggregation of platelets. Aggregating platelets stimulate ADP to act on endothelial cells and help them induce relaxation of the smooth muscle cells. However, aggregating platelets also stimulate thromboxane A2 and serotonin which can induce contraction of the smooth muscle cells. In general, the relaxations outweighs the contractions.

During atherosclerosis a dysfunctional endothelium is observed during examination. It does not stimulate as much prostacyclin and NO to induce relaxation on smooth muscle cells. Also there is not as much inhibition of aggregation of platelets. In this case, the greater aggregation of platelets produce ADP, serotonin, and thromboxane A2. However the serotonin and the thromboxane A2 cause more contraction of the smooth muscle cells and as a result contractions outweigh the relaxations.

Complications[edit]

Ischemia in the heart due to coronary vasospasm can lead to angina, myocardial infarction and even death.

Treatment[edit]

The occurrence of vasospams can be reduced by preventing the occurrence of atherosclerosis. This can be done in several ways, the most important being lifestyle modifications — decreasing low-density lipoprotein (LDL), quitting smoking. Pharmacological therapies include hypolipidemic agents, thrombolytics and anticoagulants. Pharmacological options for reducing the severity and occurrence of ischemic episodes include the organic nitrates classified as having long acting (i.e. isosorbide dinitrate) and short acting (i.e. nitroglycerin) durations of action.

These drugs work by increasing nitric oxide levels in the blood and inducing coronary vasodilation which will allow for more coronary blood flow due to a decreased coronary resistance, allowing for increased oxygen supply to the vital organs (myocardium). The nitric oxide increase in the blood resulting from these drugs also causes dilation of systemic veins which in turn causes a reduction in venous return, ventricular work load and ventricular radius. All of these reductions contribute to the decrease in ventricular wall stress which is significant because this causes the demand of oxygen to decrease. In general organic nitrates decrease oxygen demand and increase oxygen supply. It is this favourable change to the body that can decrease the severity of ischemic symptoms, particularly angina.

Other medications used to reduce the occurrence and severity of vasospams and ultimately ischemia include L-type calcium channel blockers (i.e. verapamil, diltiazem, nifedipine), nimodipine and Beta-receptor antagonists also known as beta blockers or β-blockers (i.e. propranolol).

Beta-receptor antagonists do not cause vasodilation but they do decrease the heart's demand for oxygen. This decrease is caused by a reduction in heart rate, afterload and wall stress, leading to less contraction force needed by the myocardium. B-antagonists also increase coronary blood flow since they reduce heart rate.

L-type calcium channel blockers induce coronary dilation as well as decrease the heart's demand for oxygen by reducing contractility, heart rate, and wall stress.

Adverse effects[edit]

Like most pharmacological therapeutic options, there are risks that should be considered. For these drugs in particular, vasodilation can be associated with some adverse effects which might include orthostatic hypotension, tachycardia, headaches and palpitations. Tolerance may also develop over time due compensatory response of the body, as well as depletion of -SH groups of glutathione which are essential for the metabolism of the drugs to their active forms.

Potential side effects:

Verapamil: hypotension, bradycardia, constipation
Diltiazem: hypotension, bradycardia
Nifedipine: hypotension
Propranolol: asystole, asthma attacks

Contraindications[edit]

Organic nitrates should not be taken with PDE5 inhibitors (i.e. sildenafil) since both NO and PDE5 inhibitors increase cyclic GMP levels and the sum of their pharmacodynamic effects will greatly exceed the optimal therapeutic levels. What you could see upon taking both medications at the same time, as caused by the much higher induction of relaxation of smooth muscle cells, include a severe drop in blood pressure.

Beta-receptor antagonists should be avoided in patients with reactive pulmonary disease to avoid asthma attacks. Also Beta-receptor antagonists should be avoided in patients with AV node dysfunction and/or patients on other medications which might cause bradycardia (i.e. calcium channel blockers). The potential for these contraindications and drug-drug interaction could lead to asystole and cardiac arrest.

Certain calcium channel blocker should be avoided with some beta-receptor blockers since they may cause severe bradycardia and other potential side effects.

Corrective Therapy[edit]

Since vasospasms can be caused by atherosclerosis and contribute to the severity of ischemia there are some surgical options which can restore circulation to these ischemic areas. Regarding coronary vasospasm, one surgical intervention, referred to as percutaneous coronary intervention or angioplasty, involves placing a stent at the site of stenosis in an artery and inflating the stent using a balloon catheter. Another surgical intervention is coronary artery bypass.

References[edit]

This information is a summary of a lecture given by a professor at Albany College of Pharmacy.

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English Journal

A predictive score of radial artery spasm in patients undergoing transradial percutaneous coronary intervention.

Giannopoulos G1, Raisakis K2, Synetos A3, Davlouros P4, Hahalis G4, Alexopoulos D4, Tousoulis D3, Lekakis J5, Stefanadis C6, Cleman MW7, Deftereos S8.
International journal of cardiology.Int J Cardiol.2015 Jun 1;188:76-80. doi: 10.1016/j.ijcard.2015.04.024. Epub 2015 Apr 4.
OBJECTIVE: Radial artery spasm may hinder completion of transradial angiography or PCI, leading to access site crossover, prolonged procedure times and complications. The aim of this study was to derive a radial artery spasm risk score in patients undergoing elective percutaneous coronary interventi
PMID 25889332

Recurrent Angina Due to Epicardial Coronary Artery Spasm After Successful Bioresorbable Vascular Scaffold Implantation.

Lindemann H1, Sechtem U, Ong P.
Circulation journal : official journal of the Japanese Circulation Society.Circ J.2015 May 7. [Epub ahead of print]
PMID 25947090

Potassium induced contraction of the internal thoracic artery in vitro is time related: the potential consequences in the analysis of the mechanism of the spasm after coronary artery bypass grafting and in the analysis of the results of in vitro studies.

Kleszczewski T1, Buzun L, Lisowska A, Modzelewska B.
Heart and vessels.Heart Vessels.2015 May 5. [Epub ahead of print]
The aim of the present study was to examine how, under in vitro conditions, the human left internal thoracic artery (LITA) reacts to contractile agonist:potassium chloride (KCL) as a function of time, as well as to examine whether a change in the LITA reactivity can correlate with the occurrence of
PMID 25939631

Japanese Journal

Structural and Functional Coronary Artery Abnormalities in Patients With Vasospastic Angina Pectoris

Ong Peter,Aziz Ahmed,Hansen Henrik Steen,Prescott Eva,Athanasiadis Anastasios,Sechtem Udo
Circulation Journal 79(7), 1431-1438, 2015
… Coronary spasm is involved in many clinical scenarios, such as stable angina, acute coronary syndrome, sudden cardiac death, non-ischemic cardiomyopathy, arrhythmia and syncope. … They share the common pathophysiological phenomenon of vascular smooth muscle hyperreactivity leading to spasm caused by various factors that may also overlap. …
NAID 130005083960

Structural and Functional Coronary Artery Abnormalities in Patients With Vasospastic Angina Pectoris

Ong Peter,Aziz Ahmed,Hansen Henrik Steen,Prescott Eva,Athanasiadis Anastasios,Sechtem Udo
Circulation Journal advpub(0), 2015
… Coronary spasm is involved in many clinical scenarios, such as stable angina, acute coronary syndrome, sudden cardiac death, non-ischemic cardiomyopathy, arrhythmia and syncope. … They share the common pathophysiological phenomenon of vascular smooth muscle hyperreactivity leading to spasm caused by various factors that may also overlap. …
NAID 130005078366

Recurrent Angina Due to Epicardial Coronary Artery Spasm After Successful Bioresorbable Vascular Scaffold Implantation

Lindemann Hannes,Sechtem Udo,Ong Peter
Circulation Journal advpub(0), 2015
NAID 130005068476

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★リンクテーブル★

リンク元	「血管痙攣」「血管攣縮」「vasospasm」「血管れん縮」「angiospasm」
拡張検索	「cerebrovascular spasm」
関連記事	「spasm」「vascular」