Vasospasm

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Vasospasm
Specialty Cardiology, neurosurgery

Vasospasm refers to a condition in which an arterial spasm leads to vasoconstriction. This can lead to tissue ischemia (insufficient blood flow) and tissue death (necrosis).

Contents

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's angina.

Cerebral vasospasm may arise in the context of subarachnoid hemorrhage as symptomatic vasospasm (or delayed cerebral ischemia), where it is a major contributor to post-operative stroke and mortality. Vasospasm typically appears 4 to 10 days after subarachnoid hemorrhage, however the relationship between radiological arterial spasm (seen on angiography) and clinical neurological deterioration is nuanced and uncertain. [1]

Pathophysiology

Normally endothelial cells release prostacyclin and nitric oxide (NO) which induce relaxation of the smooth muscle cells, and reduce aggregation of platelets. [2] 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.

In atherosclerosis, a dysfunctional endothelium is observed on 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. [3] [4] [5]

Complications

Vasospasm can occur in a wide variety of peripheral vascular beds under poorly understood mechanisms. Prinzmetal angina, Buerger's disease, contrast mediated selective renal vasospasm, hypercoagulability and cryoglobulinemia likely represent just a few of the known pieces of this puzzling phenomena. Ischemia in the heart due to prolonged coronary vasospasm can lead to angina, myocardial infarction and even death. Vasospasm in the hands and fingers due to prolonged exposure to vibration (30 – 300 Hz)[ failed verification ][ dubious – discuss ] and triggered by cold can lead to Hand-arm vibration syndrome in which feeling and manual dexterity are lost. [6]

Angiography

In angiography, vascular access through femoral and axillary arteries are preferred because they are less prone to vasospasm. Meanwhile, brachial artery is more prone to vasospasm during instrumental access. [7]

Hypothermia Rewarming

In a case study in 2000, following surgery for head trauma, a patient developed mild hypothermia, a typical defense mechanism the brain uses to protect itself after injury. After the hypothermia rewarming period, the patient died from increased intracranial pressure and anisocoria. A sample of the cerebrospinal fluid and autopsy results indicated cerebral vasospasm. [8]

Treatment

The occurrence of vasospasm 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, physical activity, and control for other risk factors including diabetes, obesity, and hypertension. Pharmacological therapies include hypolipidemic agents, thrombolytics and anticoagulants. Pharmacological options for reducing the severity and occurrence of ischemic episodes include the organic nitrates, which are rapidly metabolized to release nitric oxide in many tissues, [9] and are classified as having either long-acting (i.e. isosorbide dinitrate) or 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 vasospasm and ultimately ischemia include L-type calcium channel blockers (notably nimodipine, as well as verapamil, diltiazem, nifedipine) and beta-receptor antagonists (more commonly known as beta blockers or β-blockers) such as propranolol.

L-type calcium channel blockers can induce dilation of the coronary arteries while also decreasing the heart's demand for oxygen by reducing contractility, heart rate, and wall stress. The reduction of these latter three factors decreases the contractile force that the myocardium must exert in order to achieve the same level of cardiac output.

Beta-receptor antagonists do not cause vasodilation, but like L-type calcium channel blockers, they do reduce the heart's demand for oxygen. This reduction similarly results from a decrease in heart rate, afterload, and wall stress.

Adverse effects

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, reflex 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:

Contraindications

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

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.

See also

Related Research Articles

An antianginal is a drug used in the treatment of angina pectoris, a symptom of ischaemic heart disease.

<span class="mw-page-title-main">Coronary artery disease</span> Reduction of blood flow to the heart

Coronary artery disease (CAD), also called coronary heart disease (CHD), or ischemic heart disease (IHD), is a type of heart disease involving the reduction of blood flow to the cardiac muscle due to a build-up of atheromatous plaque in the arteries of the heart. It is the most common of the cardiovascular diseases. CAD can cause stable angina, unstable angina, myocardial ischemia, and myocardial infarction.

<span class="mw-page-title-main">Angina</span> Chest discomfort due to disorder of the heart muscles

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.

<span class="mw-page-title-main">Coronary circulation</span> Circulation of blood in the blood vessels of the heart muscle (myocardium)

Coronary circulation is the circulation of blood in the arteries and veins that supply the heart muscle (myocardium). Coronary arteries supply oxygenated blood to the heart muscle. Cardiac veins then drain away the blood after it has been deoxygenated. Because the rest of the body, and most especially the brain, needs a steady supply of oxygenated blood that is free of all but the slightest interruptions, the heart is required to function continuously. Therefore its circulation is of major importance not only to its own tissues but to the entire body and even the level of consciousness of the brain from moment to moment. Interruptions of coronary circulation quickly cause heart attacks, in which the heart muscle is damaged by oxygen starvation. Such interruptions are usually caused by coronary ischemia linked to coronary artery disease, and sometimes to embolism from other causes like obstruction in blood flow through vessels.

Calcium channel blockers (CCB), calcium channel antagonists or calcium antagonists are a group of medications that disrupt the movement of calcium through calcium channels. Calcium channel blockers are used as antihypertensive drugs, i.e., as medications to decrease blood pressure in patients with hypertension. CCBs are particularly effective against large vessel stiffness, one of the common causes of elevated systolic blood pressure in elderly patients. Calcium channel blockers are also frequently used to alter heart rate, to prevent peripheral and cerebral vasospasm, and to reduce chest pain caused by angina pectoris.

<span class="mw-page-title-main">Vasodilation</span> Widening of blood vessels

Vasodilation, also known as vasorelaxation, is the widening of blood vessels. It results from relaxation of smooth muscle cells within the vessel walls, in particular in the large veins, large arteries, and smaller arterioles. Blood vessel walls are composed of endothelial tissue and a basal membrane lining the lumen of the vessel, concentric smooth muscle layers on top of endothelial tissue, and an adventitia over the smooth muscle layers. Relaxation of the smooth muscle layer allows the blood vessel to dilate, as it is held in a semi-constricted state by sympathetic nervous system activity. Vasodilation is the opposite of vasoconstriction, which is the narrowing of blood vessels.

<span class="mw-page-title-main">Ischemia</span> Restriction in blood supply to tissues

Ischemia or ischaemia is a restriction in blood supply to any tissue, muscle group, or organ of the body, causing a shortage of oxygen that is needed for cellular metabolism. Ischemia is generally caused by problems with blood vessels, with resultant damage to or dysfunction of tissue i.e. hypoxia and microvascular dysfunction. It also implies local hypoxia in a part of a body resulting from constriction.

<span class="mw-page-title-main">Infarction</span> Tissue death due to inadequate blood supply

Infarction is tissue death (necrosis) due to inadequate blood supply to the affected area. It may be caused by artery blockages, rupture, mechanical compression, or vasoconstriction. The resulting lesion is referred to as an infarct (from the Latin infarctus, "stuffed into").

Microvascular angina (MVA), previously known as cardiac syndrome X, also known as coronary microvascular dysfunction(CMD) or microvascular coronary disease is a type of angina (chest pain) with signs associated with decreased blood flow to heart tissue but with normal coronary arteries.

<span class="mw-page-title-main">Haemodynamic response</span>

In haemodynamics, the body must respond to physical activities, external temperature, and other factors by homeostatically adjusting its blood flow to deliver nutrients such as oxygen and glucose to stressed tissues and allow them to function. Haemodynamic response (HR) allows the rapid delivery of blood to active neuronal tissues. The brain consumes large amounts of energy but does not have a reservoir of stored energy substrates. Since higher processes in the brain occur almost constantly, cerebral blood flow is essential for the maintenance of neurons, astrocytes, and other cells of the brain. This coupling between neuronal activity and blood flow is also referred to as neurovascular coupling.

<span class="mw-page-title-main">Variant angina</span> Cardiac chest pain at any time, not just periods of exertion

Variant angina, also known as Prinzmetal angina,vasospastic angina, angina inversa, coronary vessel spasm, or coronary artery vasospasm, is a syndrome typically consisting of angina. Variant angina differs from stable angina in that it commonly occurs in individuals who are at rest or even asleep, whereas stable angina is generally triggered by exertion or intense exercise. Variant angina is caused by vasospasm, a narrowing of the coronary arteries due to contraction of the heart's smooth muscle tissue in the vessel walls. In comparison, stable angina is caused by the permanent occlusion of these vessels by atherosclerosis, which is the buildup of fatty plaque and hardening of the arteries.

<span class="mw-page-title-main">Nicorandil</span> Chemical compound

Nicorandil is a vasodilator drug used to treat angina.

Coronary vasospasm refers to when a coronary artery suddenly undergoes either complete or sub-total temporary occlusion.

Fasudil (INN) is a potent Rho-kinase inhibitor and vasodilator. Since it was discovered, it has been used for the treatment of cerebral vasospasm, which is often due to subarachnoid hemorrhage, as well as to improve the cognitive decline seen in stroke patients. It has been found to be effective for the treatment of pulmonary hypertension. It has been demonstrated that fasudil could improve memory in normal mice, identifying the drug as a possible treatment for age-related or neurodegenerative memory loss.

<span class="mw-page-title-main">Nitrovasodilator</span> Drug that causes vasodilation by releasing nitric oxide

A nitrovasodilator is a pharmaceutical agent that causes vasodilation by donation of nitric oxide (NO), and is mostly used for the treatment and prevention of angina pectoris.

<span class="mw-page-title-main">Coronary ischemia</span> Medical condition

Coronary ischemia, myocardial ischemia, or cardiac ischemia, is a medical term for abnormally reduced blood flow in the coronary circulation through the coronary arteries. Coronary ischemia is linked to heart disease, and heart attacks. Coronary arteries deliver oxygen-rich blood to the heart muscle. Reduced blood flow to the heart associated with coronary ischemia can result in inadequate oxygen supply to the heart muscle. When oxygen supply to the heart is unable to keep up with oxygen demand from the muscle, the result is the characteristic symptoms of coronary ischemia, the most common of which is chest pain. Chest pain due to coronary ischemia commonly radiates to the arm or neck. Certain individuals such as women, diabetics, and the elderly may present with more varied symptoms. If blood flow through the coronary arteries is stopped completely, cardiac muscle cells may die, known as a myocardial infarction, or heart attack.

<span class="mw-page-title-main">Cocaine intoxication</span> Medical condition

Cocaine intoxication refers to the subjective, desired and adverse effects of cocaine on the mind and behavior of users. Both self-induced and involuntary cocaine intoxication have medical and legal implications.

Cerebral vasospasm is the prolonged, intense vasoconstriction of the larger conducting arteries in the subarachnoid space which is initially surrounded by a clot.

Kounis syndrome is defined as acute coronary syndrome caused by an allergic reaction or a strong immune reaction to a drug or other substance. It is a rare syndrome with authentic cases reported in 130 males and 45 females, as reviewed in 2017; however, the disorder is suspected of being commonly overlooked and therefore much more prevalent. Mast cell activation and release of inflammatory cytokines as well as other inflammatory agents from the reaction leads to spasm of the arteries leading to the heart muscle or a plaque breaking free and blocking one or more of those arteries.

Adrenergic neurone blockers, commonly known as adrenergic antagonists, are a group of drugs that inhibit the sympathetic nervous system by blocking the activity of adrenergic neurones. They prevent the action or release of catecholamines such as norepinephrine and epinephrine. They are located throughout the body, causing various physiological reactions including bronchodilation, accelerated heartbeat, and vasoconstriction. They work by inhibiting the synthesis, release, or reuptake of the neurotransmitters or by antagonising the receptors on postsynaptic neurones. Their medical uses, mechanisms of action, adverse effects, and contraindications depend on the specific types of adrenergic blockers used, including alpha 1, alpha 2, beta 1, and beta 2.

References

  1. ↑ Whittle, Caed; Hollingworth, Milo A.; Dulhanty, Louise; Patel, Hiren C. (2023-12-01). "What are the predictors of delayed cerebral ischaemia (DCI) after aneurysmal subarachnoid haemorrhage? An up-to-date systematic review". Acta Neurochirurgica. 165 (12): 3643–3650. doi:10.1007/s00701-023-05864-4. ISSN   0942-0940.
  2. ↑ Yakubu, MA; Shibata, M; Leffler, CW (1994). "Subarachnoid Hematoma Attenuates Vasodilation and Potentiates Vasoconstriction Induced by Vasoactive Agents in Newborn Pigs". Pediatric Research. 36 (5): 589–594. doi: 10.1203/00006450-199411000-00009 . PMID   7877876. S2CID   22708777.
  3. ↑ Yakubu, MA; Leffler, CW (September 1999). "Regulation of ET-1 biosynthesis in cerebral microvascular endothelial cells by vasoactive agents and PKC". American Journal of Physiology. Cell Physiology. 276 (2): C300–C305. doi:10.1152/ajpcell.1999.276.2.C300. PMID   9950756.
  4. ↑ Yakubu, MA; Shibata, M; Leffler, CW (September 1995). "Hematoma-induced enhanced cerebral vasoconstrictions to leukotriene C4 and endothelin-1 in piglets: role of prostanoids". Pediatric Research. 38 (1): 119–123. doi: 10.1203/00006450-199507000-00021 . PMID   7478789. S2CID   23885828.
  5. ↑ Yakubu, MA; Shibata, M; Leffler, CW (1994). "Subarachnoid Hematoma Attenuates Vasodilation and Potentiates Vasoconstriction Induced by Vasoactive Agents in Newborn Pigs". Pediatric Research. 36 (5): 589–594. doi: 10.1203/00006450-199411000-00009 . PMID   7877876. S2CID   22708777.
  6. ↑ "Hand-Arm Vibration Syndrome (HAVS)". www.vibrosense.eu. 2019-01-15. Archived from the original on 2019-01-16. Retrieved 2019-01-15.
  7. ↑ Lindbom, Åke (June 1957). "Arterial spasm caused by puncture and catheterization". Acta Radiologica. 47 (6): 449–460. doi: 10.3109/00016925709170919 . ISSN   0001-6926. PMID   13444055.
  8. ↑ Jimbo, H; Dohi, K; Nakamura, Y; Izumiyama, H; Ikeda, Y; Matsumoto, K; Kushima, M; Takaki, A (2000). "Fatal severe vasospasm due to rewarming following hypothermia--case report". Neurologia Medico-chirurgica. 40 (9): 463–6. doi: 10.2176/nmc.40.463 . PMID   11021078.
  9. ↑ "Organic Nitrates". 2018-04-27. PMID   31643263 . Retrieved 2023-03-27.
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