These side effects may go away during treatment as your body adjusts to the medicine. Also, your health care professional may be able to tell you about ways to prevent or reduce some of these side effects. Check with your health care professional if any of the following side effects continue or are bothersome or if you have any questions about them:.
Other side effects not listed may also occur in some patients. If you notice any other effects, check with your healthcare professional. Call your doctor for medical advice about side effects. There is a problem with information submitted for this request.
Sign up for free, and stay up-to-date on research advancements, health tips and current health topics, like COVID, plus expert advice on managing your health. Long-term use can lead to drug tolerance, meaning a person needs more of the drug to get similar euphoric effects.
Opium use can also lead to physical dependence and addiction. Withdrawal symptoms can occur if long-term use is reduced or stopped. Signs of use include nausea, confusion and constipation. On This Page. Use of any drug always carries some risk. If you take a large amount of opium, you could overdose. Taking multiple depressant drugs, like opium with alcohol or benzodiazepines, can significantly increase the chances of overdose.
Taking opium with stimulants, like cocaine or speed, send opposite signals to your body, which can strain the heart. Mixing opium and stimulants may also mask the effects of each other, which can increase the risk of overdose. Giving up opium after using it for a long time is challenging because the body must get used to functioning without it. Withdrawing from opium is similar to withdrawing from other opioid drugs. Withdrawal symptoms usually start six to 24 hours after the last dose and can last around seven to ten days.
These symptoms are described as flu-like, and can include:. Opium is illegal in Australia. Federal and state laws provide penalties for possessing, using, cultivating or selling opium, or driving under its influence. If your use of opium is affecting your health, family, relationships, work, school, financial or other life situations, you can find help and support.
Not sure what you are looking for? Atherosclerosis depends on the immune response [ 59 ]. Some studies on substance use disorder consider opium as an immunosuppressive factor [ 59 ] and reveal an increase in inflammatory mediators such as C-reactive protein CRP , interleukin, and interleukin-1 receptor antagonist in opium users. Thus, aggravation of inflammation increases atheroma formation in dependent patients [ 40 ].
The level of interleukin-1 receptor antagonist was higher in the dependent cases, but opium did not have a significant effect on the plasma level of interleukin-6 [ 59 ].
Thirty-five dependent smokers were compared to 35 non-dependent smokers in another study, which revealed that the level of factor VII was significantly higher in addicted cases [ 60 ]. Opium consumption may have undesirable effects on lipid metabolism [ 61 , 62 ]. Some clinical studies have shown that opium may affect the levels of total cholesterol, TG, LDL cholesterol, and HDL cholesterol [ 17 , 32 , 63 , 64 , 65 ].
Oxidative stress plays a critical role in the pathogenesis of atherosclerosis. It has been advocated that morphine and heroin decrease the total antioxidant capacity irrespective of cigarette smoking. Therefore, elevated oxidative stress may involve in atherosclerosis in opium users [ 40 ]. Increased homocysteine is one of the factors that can result in the advancement of atherosclerosis and the development of CADs. It has been demonstrated that opium use disorder is strongly related to increased homocysteine, and consequently, the elevated risk of developing CADs [ 66 ].
Increased plasma fibrinogen is also considered as an independent risk factor for CADs and can increase the risk of thrombosis. Some studies have reported that plasma fibrinogen is significantly higher in opium-addicted patients [ 67 , 68 , 69 ]. PAI-1 inhibits the formation of plasmin through inhibitory effects on plasminogen activator and consequently prevents the clotting cascade in the arteries. Adiponectin has anti-diabetic and anti-atherogenic effects, and when decreased, it promotes the risk of developing metabolic disorders such as insulin resistance and cardiovascular diseases CVDs in patients with opium use disorder.
The relationship between adipokinase and opium use disorder can indirectly play a role in the development of atherosclerosis. One case-control study demonstrated that the serum level of adiponectin was significantly lower in patients with opium use disorder [ 71 ].
In men, low testosterone level can cause CADs and increase the risk of cardiovascular-related mortality. The level of plasma testosterone is lower in those with opium use disorder.
Similarly, low level of estrogen and reduction of estrogen in the pre-menopause period have been reported in addicted females, which can cause CADs [ 40 ]. Opium increases the level of prolactin in the blood. Prolactin can induce smooth muscle cells growth through a mechanism that depends on protein kinase C and may also play a role in the hyperplasia of muscle cells of the arteries and lead to atherosclerosis [ 40 ]. Similar to type 2 diabetic patients, people with opium use disorder show insulin resistance and an increase in the insulin level of the blood.
Insulin resistance results in the atherosclerosis of coronary arteries and the advancement of coronary plaques [ 40 ]. The presence of impurities such as lead in opium can be a factor causing adverse effects on the cardiovascular system. Lead has been reported to be present in opium samples, and blood lead level has been shown to be high in those with opium use disorder [ 72 , 73 , 74 ]. Some studies have indicated a relationship between blood lead concentration, hypertension, and development of atherosclerosis [ 75 ].
Opium is a CNS suppressant and can decrease physical activity in addicted individuals, which increases the risk of CVDs [ 40 ]. In a study, depression, reduction of physical activity, and obesity were all reported in addicted patients [ 76 ].
Also, some studies showed that opium users followed treatment and nutrition advice and performed cardiovascular activities less than others [ 3 , 51 ].
One study investigating the effects of long-term use of opioids on the extent of CADs showed that the coronary arteries clogged less severely in opioid dependents [ 19 ]. In a cross-sectional study conducted on patients who were candidates for coronary artery bypass grafting [CABG], opium users and non-users , fewer coronary arteries were involved in opium users, and there was no relationship between the number of involved coronary arteries and stenosis and long-term opium use [ 1 ].
Some studies reflect that opioids can reduce inflammation and CADs [ 19 , 40 ]. It has been stated that long-term opium use reduces atherosclerosis directly and protects against ischemic and infarction damages [ 19 ].
As there are more than 40 different alkaloids in opium, more research is required to better understand the effect of opium on the inflammatory response. Several other studies have shown that opium increases serum antioxidant capacity [ 77 ]. Several studies have demonstrated a remarkable hypocholesterolemia pattern in patients with substance use [ 79 ]. All of the issues mentioned above mandate the necessity of more in-depth research on this subject.
Some studies deem the effects of opium on the development of atherosclerosis to be insignificant. A study on candidates for coronary angiography showed that opium users had a higher chance of acute CADs, although this relationship was not statistically significant [ 20 ]. In a study of patients with CADs, it was revealed that smoking and recent myocardial infarction MI were more common in patients with opium use disorder, and hyperlipidemia and diabetes were more common in patients without opium use disorder.
The results showed that there was no statistically significant difference in the number of involved coronary arteries between the two groups of people with and without opium use disorder [ 21 ]. A study on CAD patients showed that the number of involved coronary arteries was similar between these two groups [ 22 ].
Rezvani , in a cross-sectional study on 81 patients suffering from IHD, showed that orally consumed OR: 0. Oral consumption of opium was a protective factor against stroke but not against IHD [ 23 ]. In a study of patients undergoing CABG, it was demonstrated that patients with a positive history of opium use 82 people were similar to non-users people regarding the number of the involved arteries [ 24 ].
Shahryari conducted an experimental study on male hamsters to investigate the influence of daily opium use on lipid profile and aortic atherosclerosis in one month. The results showed that the levels of LDL and TG were significantly higher, and HDL level was significantly lower in opium dependent hamsters than the control group. In addition, histopathologic changes in the heart i.
Myocardial infarction occurs due to a block in the blood flow to a part of the myocardium. There are different risk factors for this condition, and some believe that endorphin and endogenous opioids play an important role in the development of MI, while others point to their protective or ineffective role in the development of MI. Roohafza et al. In a case-control study, MI patients in the coronary care unit were compared with heart-healthy patients admitted to other wards. Another nested case-control study conducted among 11, patients suffering from MI showed that using opioids increased the risk of MI up to 1.
Bartolucci et al. They showed that users had a significantly higher risk of ST-elevation and infarction in the anterior wall [ 29 ].
Another study demonstrated that creatinine phosphokinase, lactate dehydrogenase, and CKmb enzymes were higher in patients with opium use disorder and acute MI [ 30 ]. An experimental study evaluated the effects of inhaled opium on rabbits and showed that using opium increased the level of troponin-I and exacerbated electrocardiographic ECG changes. It was also revealed that long-term use of opium raised the frequency of ST elevation. Exposure to opium reduced myocardium degeneration after the induction of ischemia but increased tissue congestion and hemorrhage [ 31 ].
The high prevalence of ischemic changes in ECG ST-T changes in the ECG and increased heart enzymes in patients with opium use disorder can be related to the relieving effects of opium on chest pain and the high prevalence of silent MI in these patients [ 1 ].
Also, the relationship between opium use and MI can be a result of opium effects on the development of coronary atherosclerosis. A study among patients suffering from acute MI people with opium use disorder and without opium use disorder revealed that the emergence of MI in the anterior wall was significantly less common in opium users. The emergence of posterior wall infarction was similar between the two groups [ 32 ].
The results of a retrospective study investigating the information of men undergoing percutaneous coronary intervention PCI from the data bank of Tehran Heart Center showed that the ratio of involvement of the left anterior descending artery was higher in non-users.
However, the reference vessel diameter and lesion length were not different between the two groups [ 33 ]. Another experimental study on the rabbit heart showed that morphine reduced cardiomyocyte apoptosis through the activation of delta-opioid receptors [ 34 ]. Research on the mouse heart showed that kappa opioid receptors in the heart caused enlargement in the infarction area, while delta-opioid receptors had protective effects [ 35 ].
Activation of delta-opioid receptors prior to ischemia reduced the infarct area in several animal models, including rats [ 80 ], rabbits [ 81 ], and pigs [ 82 ]. Recent data has also shown that opioid peptides are involved in a phenomenon called preconditioning, which protects the heart from the damages of long-term ischemia by temporary ischemia or hypoxia and reduces the size of the infarct area. Shultz et al. Also, the results of another study on MI patients showed that the number of extensive infarctions was twice in people with opium use disorder, but this difference was statistically insignificant [ 37 ].
Another study on males diagnosed with acute MI also confirmed that there were no differences between those with and without opium use disorder in terms of location of the MI, angiography findings, and the level of troponin-I [ 38 ]. Overall, the majority of the studies pinpoint opium as a risk factor for MI. This substance can hide MI symptoms through its pain-relieving properties,and consequently, delay treatment and cause lesion progression [ 40 ]. Premature ventricular contractions PVCs and ventricular tachycardia VT are significantly more common in opium-addicted individuals [ 41 ].
The results of a cross-sectional study on patients suffering from MI revealed that ventricular arrhythmias such as PVCs, VT, and ventricular fibrillation VF were significantly more prevalent in patients with opium use disorder [ 37 ]. Another study on addicted and non-addicted CAD patients showed that complications after cardiac arrhythmia surgery were significantly higher in opium users [ 21 ]. In patients with opium and ephedrone use, sinus tachycardia, ventricular extrasystole, and supraventricular extrasystole were diagnosed in 4.
Another cross-sectional study showed that The combined effect of opium use and hypercholesterolemia was investigated on fatal heart arrhythmia in an experimental study on rabbits, which showed that long-term use of opium increased the atherogenic index of plasma.
For a short period, QT interval increased significantly in the hypercholesterolemic group, but the index was similar in the two groups in the long run [ 43 ]. The results of another study showed that morphine and pentazocine had arrhythmogenic effects on the pig heart [ 44 ].
A case report demonstrated atrial flutter in an infant whose mother was addicted to cocaine and opiates. The infant was born to a year-old mother through cesarean section due to fetal tachycardia in the 36th week of gestation and weighted 3.
It had atrioventricular tachycardia, and ultimately, an atrial flutter developed [ 45 ]. The initial pathophysiology of arrhythmia is related to dysfunction in the conduction system. Opioid receptors in the ventricles and atria may play an essential role in the development of different arrhythmias [ 87 , 88 ] by increasing heart rate and causing changes in heart rhythm [ 89 , 90 ].
Based on evidence, kappa opioid receptors can be involved in the development of an arrhythmic response. Coles et al. They demonstrated that neither pentazocine nor morphine had protective effects on the heart, and the pro-arrhythmic effects of these medications were removed through blockage of the k receptors [ 44 ]. Several studies suggest that the potential arrhythmogenic activities of opioids at small doses occur through the activation of kappa opioid receptors, and their anti-arrhythmic actions at larger doses occur due to direct interaction with heart cell membranes [ 92 ].
Opioid peptides have also been advocated to stimulate the autonomic nervous system and raise heart rate and systolic blood pressure, which may cause arrhythmia per se [ 87 ]. Endogenous opioids, together with the sympathetic and parasympathetic systems in the brain stem, control the cardiovascular function.
The postganglionic fibers innervating the rabbit heart have been shown to contain opioid and cannabinoid receptors, through the inhibition of which, neurogenic tachycardia ensues [ 93 ]. A cross-sectional study on patients with acute MI showed that patients with and without opium use disorder did not have any difference in the development of arrhythmia [ 47 ]. It was previously shown that patients with a history of opium use had a significantly lower EF compared to those who did not use opium, although the functional class was similar between the two groups [ 24 ].
A study of diabetic CAD patients showed that EF was significantly lower in opium users with a statistically similar functional class [ 22 ]. In addition, two other studies conducted on patients undergoing CABG showed that EF was significantly lower in opium users [ 21 , 48 ].
In , 65 patients who used opium and ephedrone were investigated by h Holter monitor, ECG, and echocardiography. Although none of the patients had heart failure and cardiac muscle contractions were normal, echocardiography showed abnormal changes in the left ventricle including ventricular enlargement, reduced EF, and systolic shortening of myocardial fibers which were indicators of a decline in the compensatory mechanisms of the myocardium in substance users [ 42 ].
In another study conducted on patients undergoing coronary artery grafting surgery, 50 opium users and 50 non-users were compared regarding EF before the surgery. Left ventricular end-diastolic pressure was also higher in addicted patients [ 49 ]. Garg reported a case of poisoning due to the consumption of raw opium resulting in severe depression in a year-old female who did not have any relevant medical history.
Opium contains 80 different alkaloids, such as morphine and codeine. It has also been demonstrated that increased contractile response due to the stimulation of rat cardiac beta-adrenergic receptors is reversed through delta receptor agonism [ 95 ].
A study on two groups of diabetic patients undergoing angiography showed that EF was similar between opium users and non-users [ 12 ]. EF and Killip class were similar between addicted and non-addicted patients in studies on and MI patients [ 32 , 47 ].
Another study evaluating 53 patients with CAD and 33 patients with normal angiography concluded that EF was similar between patients with and without opium use disorder [ 16 ]. The results of two other descriptive studies on and male patients undergoing CABG also showed that the functional class and EF before the surgery and six months after that were similar between case and control groups [ 3 , 51 ].
Evaluations performed on CABG candidates opium users and non-users showed that there was no relationship between the duration of opium use and EF before and after surgery [ 1 ].
Davoodi et al. Sharafi et al. Similar results were withdrawn from other studies, all confirming that EF, the emergence of heart failure after MI, and Killip class were similar between opium dependent and non-dependent patients [ 23 , 39 , 52 , 53 , 54 ].
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