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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cocaine is an extremely addictive agent which can produce stimulation of the sympathetic nervous system due to the inhibition of catecholamine reuptake at the synaptic junction. Probability of a patient presenting to the operating theatre with acute cocaine intoxication is increasingly likely. The physiological effects of even chronic cocaine abuse on various organ systems have an impact on anesthetic management. A preoperative review of major organ systems is essential. Nitroglycerin has been used in the management of hypertension associated with coronary vasoconstriction. Controversy exists regarding management of ventricular dysrhythmias and asystole. The use of epinephrine to treat asystole is controversial in the presence of a state of excess catecholamines induced by cocaine. General anesthesia may include barbiturates, nitrous oxide, and opioids, but inhalational agents must be used with caution due to their myocardial depressant effects. Regional anesthesia may be a good choice if coagulopathies and hypovolemia are corrected.
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PMID:The cocaine-using patient: perioperative concerns. 1583 Jul 66

A 34-year-old man was admitted in a coma after a nightlong abuse of cocaine and alcohol, whereupon he fell and convulsed at home. There was a fracture of the nose, hyperpyrexia, tachycardia and hypertension. Dry mouth and mydriasis were suggestive of anticholinergic poisoning. Physostigmine 3 mg were slowly administered intravenously, followed by complete neurological recovery and normalisation of the body temperature. There was no brain damage. Cocaine and atropine were found in the patient's urine. Several users of cocaine in various European countries have recently developed a central anticholinergic syndrome due to adulteration of cocaine with atropine. In the presence of indications for such an intoxication, physostigmine is the antidote of first choice.
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PMID:[Physostigmine for the immediate treatment of a patient with the central anticholinergic syndrome induced by cocaine cut with atropine]. 1610 18

Alcohol and stimulant abuse represents a major cause of cerebrovascular and cardiovascular disease in young adults. Although mild-to-moderate alcohol consumption has been linked to a decreased risk for stroke and CVD, excessive use is associated with an increased risk for intracranial hemorrhage and cardiomyopathy. Cocaine represents the single largest,cause of medical complications related to illegal drug use. Cocaine has been associated with cerebral infarction, intracranial hemorrhage, myocardial infarction, cardiomyopathy, and cardiac arrhythmias. Abuse of amphetamines is associated with complications similar to those of cocaine. The complications associated with stimulant abuse are thought to be primarily mediated through excess catecholamines, resulting in acute arterial hypertension, vasospasm, thrombosis, and accelerated atherosclerosis. Because many complications of alcohol and stimulant abuse are preventable and reversible, it is important to screen for these in patients with cerebrovascular and cardiovascular disease.
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PMID:Cerebrovascular and cardiovascular complications of alcohol and sympathomimetic drug abuse. 1622 66

Cocaine is one of the most commonly used illicit drugs. Acute renal failure is an emergent complication in patients with acute cocaine intoxication. It is well known that rhabdomyolysis and vasoconstriction can be important pathogenetic mechanisms resulting in acute renal failure in these patients. Clinically, although cocaine abuse is associated with elevated blood pressure, persistent accelerated hypertension reaching levels diagnostic of malignant hypertension is uncommon. Cocaine-induced malignant hypertension associated with morphologic features of thrombotic macroangiopathy has been rarely mentioned in the literature. We report 2 cases of cocaine abuse-associated malignant hypertension with renal failure. Kidney biopsies revealed thrombotic microangiopathy with fibrinoid necrosis of arterioles and glomerular tufts. Cocaine-mediated endothelial injury and platelet activation may play important pathogenetic roles in cocaine abusers who develop acute renal failure and malignant hypertension.
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PMID:Thrombotic microangiopathy in cocaine abuse-associated malignant hypertension: report of 2 cases with review of the literature. 1808 41

Epidemiological studies have shown a clear association of adverse intrauterine environment and an increased risk of cardiovascular diseases and hypertension in adult life. The present study tested the hypothesis that prenatal cocaine exposure causes reprogramming of vascular reactivity, leading to an increased risk of hypertension in adult offspring. Pregnant rats received cocaine (30 mg kg(-1) day(-1)) or saline from days 15 to 21 of gestational age, and experiments were conducted in 3-month-old offspring. Cocaine had no effect on the baseline blood pressure but significantly increased norepinephrine-stimulated blood pressure and decreased the baroreflex sensitivity in male but not female offspring. The cocaine treatment significantly increased norepinephrine-induced contractions in pressurized resistance-sized mesenteric arteries but not in aortas, which was primarily because of a loss of endothelial NO synthase-mediated inhibition and an enhanced Ca(2+) sensitivity in mesenteric arteries. In addition, the cocaine treatment significantly attenuated the endothelium-dependent relaxation in mesenteric arteries in male but not female offspring. Endothelial NO synthase protein levels in aortas but not mesenteric arteries were significantly increased in the cocaine-treated animals. However, cocaine significantly decreased phosphorylation levels of endothelial NO synthase in both aortas and mesenteric arteries. The results suggest that prenatal cocaine exposure programs vascular contractility via changes in endothelial NO synthase-regulated Ca(2+) sensitivity of myofilaments in the sex- and tissue-dependent manners in resistance arteries leading to an increased risk of hypertension in male offspring.
Hypertension 2009 Jun
PMID:Prenatal cocaine exposure differentially causes vascular dysfunction in adult offspring. 1938 Jun 15

Cocaine abuse is a significant problem among pregnant women. The present study tested the hypothesis that prenatal cocaine exposure impairs myogenic reactivity of coronary arteries in adult offspring. Pregnant rats received cocaine (30 mg kg(-1) day(-1)) or saline from days 15 to 21 of gestational age, and experiments were conducted in 3-month-old offspring. In pressurized coronary septal arteries, the diameter and vessel wall intracellular Ca2+ concentrations were measured simultaneously in the same tissue as a function of intraluminal pressure. Cocaine did not affect KCl-induced contractions of coronary arteries in either males or females but decreased the distensibility in male vessels. In male offspring, cocaine treatment resulted in a significant decrease in pressure-dependent myogenic contractions. Inhibition of eNOS with NG-nitro-L-arginine did not alter the myogenic response in either saline control or cocaine-treated animals. In females, cocaine caused a significant increase in pressure-dependent myogenic contractions. NG-nitro-L-arginine did not affect the myogenic response in the control animals but blocked the cocaine-mediated effect. In both males and females, the pressure-induced increases in vessel wall Ca2+ concentrations were not significantly different between cocaine and saline groups. The ratio of changes in the diameter to Ca2+ concentrations in the pressurized arteries was significantly less in male but greater in female offspring after cocaine treatment. The results suggest that prenatal cocaine exposure causes reprogramming of coronary myogenic tone via changes in the Ca2+ sensitivity in a sex-dependent manner, leading to an increased risk of dysfunction of coronary autoregulation in adult offspring.
Hypertension 2009 Nov
PMID:Prenatal cocaine exposure causes sex-dependent impairment in the myogenic reactivity of coronary arteries in adult offspring. 1970 3

Aortic dissection is a rare, potentially catastrophic vascular emergency. Early recognition of the clinical manifestations, rapid confirmation using imaging modalities, urgent administration of appropriate medication and expedient selection of definitive long-term therapy are key to preserving life and reducing morbidity. In recent years it has become increasingly clear that there is a relation between cocaine and aortic dissection. Cocaine serves as both a predisposing factor to aortic dissection due to its effect on aortic connective tissue and as a precipitating factor due to its propensity to produce abrupt and severe hypertension. While similarities exist in the clinical features and diagnostic methods between cocaine-related aortic dissection and aortic dissection unrelated to cocaine use, there are important differences in management between these two syndromes which are rooted in the pharmacology and physiology of cocaine. An understanding of these differences is key to effective early and long-term management of cocaine-related aortic dissection.
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PMID:Cocaine and aortic dissection. 2023 7

Cocaine use is associated with ischemic stroke through unique mechanisms, including reversible vasospasm, drug-induced arteritis, enhanced platelet aggregation, cardioembolism, and hypertensive surges. To date, no study has described disability in patients with cocaine-related ischemic stroke. The present study compared risk factors, comorbidities, complications, laboratory findings, medications, and outcomes in patients with cocaine-related (n = 41) and non-cocaine-related (n = 221) ischemic stroke (n = 147) and transient ischemic attack (n = 115) in 3 academic hospitals. The patients with cocaine-related stroke were younger (mean age, 51.9 years vs 59.1 years; P = .0008) and more likely to be smokers (95% vs 62.9%; P < .004). The prevalence of arrhythmias was significantly higher in the patients with cocaine-related stroke, and that of diabetes was significantly higher in those with non-cocaine-related strokes. The prevalence of hypertension and lipid profiles were similar in the 2 groups; however, those with cocaine-related stroke were less likely to receive statins. Antiplatelet use was similar in the 2 groups. Survivors of both groups had similar modified Rankin scores and lengths of hospital stay. In the older urban population, smoking and cocaine use may coexist with other cerebrovascular risk factors, and cocaine-related strokes have similar morbidities and mortality as non-cocaine-related strokes. Moreover, because the patients with cocaine-related stroke is younger, they have an earlier morbidity. New strategies for effective stroke prevention interventions are needed in this subgroup.
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PMID:Clinical profiles, complications, and disability in cocaine-related ischemic stroke. 2081 50

In arterial dissection, blood may enter the arterial wall through an intimal tear, splitting the arterial wall and activating the coagulation cascade at the site of endothelial damage. Dissection of extracranial and intracranial vessels may lead to ischemic stroke through thromboembolic or hemodynamic mechanisms. Major blunt trauma or rapid acceleration-deceleration may cause dissection, but in patients with inherent arterial wall weakness, dissection can occur spontaneously or as a result of minor neck movement. Cocaine use has been associated with dissection of the aortic arch and coronary and renal arteries through cocaine-mediated hypertension. Recent preclinical studies have suggested, however, that cocaine may cause apoptosis of cells in the vascular wall. In this article, we postulate that cocaine may cause apoptosis of vascular endothelial and/or smooth muscle cells, thus weakening the vascular wall and resulting in a dissection-prone state. We review the literature and propose a biological basis for vasculopathy, vascular dissection, and ischemic stroke in the setting of cocaine use. Further research studies on vascular cells, as well as focused analysis of human pathological material, will be important in providing evidence for or against our hypotheses.
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PMID:Cocaine mediated apoptosis of vascular cells as a mechanism for carotid artery dissection leading to ischemic stroke. 2154 66

Aortic dissection is a potentially fatal but rare disease characterized by an aortic intimal tear with blood passing into the media creating a false lumen and with resultant high mortality depending on the location of dissection if not aggressively treated. Cocaine users are known to have a higher incidence of aortic dissection. We report here aortic dissection in a patient with cocaine abuse which did not respond to traditional medication regimes used currently in this setting. Worth mentioning is the use of an alpha-2 receptor selective agonist named Dexmedetomidine as a treatment modality to control hypertension in this patient, which is approved only for sedation of intubated and mechanically ventilated patients in the intensive care settings and for sedation during invasive procedures. This paper illustrates the practical beneficial role of Dexmedetomidine in controling blood pressure in the settings of cocaine-induced sympathetic surge when other treatment modalities fail.
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PMID:Dexmedetomidine use in the setting of cocaine-induced hypertensive emergency and aortic dissection: a novel indication. 2196 Oct 11


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