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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

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

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

As opposed to iatrogenic coronary dissection, spontaneous dissection is an extremely rare clinical condition. Typically seen in a single coronary vessel of peripartum women presenting with acute coronary syndrome, there are isolated case reports of men presenting multivessel involvement for this life-threatening condition. We describe a 54-year-old male with a history of diabetes, hypertension and methamphetamine abuse who presented to the emergency after a brief, witnessed cardiac arrest. Admission ECG revealed sinus tachycardia with inferior Q waves. He was found to have frequent runs of non-sustained ventricular tachycardia and minimal troponin-T elevation. His 2-D echocardiogram showed apical akinesis with an ejection fraction of 50%. Cardiac catheterization revealed a patent left main artery with a spontaneous dissection involving the mid to distal LAD artery, as well as large first diagonal branch with proximal dissection. His dominant RCA also showed long spontaneous dissection extending from proximal to distal vessel, along with distal focal 90% atherosclerotic lesion. Ramus intermedius and left circumflex vessels were free of disease. The patient underwent a 2-vessel coronary artery bypass grafting (CABG) with excellent outcome. Although cocaine abuse has been known to be associated with spontaneous dissection, this is the first reported case of a methamphetamine user presenting with multivessel coronary dissection.
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PMID:Spontaneous multivessel coronary artery dissection. 2004 5

Two young patients, a 23-year-old man and a 30-year-old woman, without any risk factors for coronary artery disease, apart from the woman being a smoker, were admitted to our hospital because of acute myocardial infarction (MI) due to spontaneous dissection of a coronary artery (SDCA). The first patient developed acute chest pain while playing soccer. The second patient had unspecific chest pain in the preceding four weeks and was admitted after successful resuscitation with ventricular fibrillation. Both patients were treated with primary percutaneous coronary intervention. SDCA is a rare cause of MI and sudden cardiac death with an indistinguishable presentation due to plaque rupture. The majority of cases occur in young women. It is associated with various pathophysiological mechanisms and can manifest during pregnancy, in the postpartum period, in collagen diseases, cocaine abuse, severe hypertension, smoking, oral contraceptives, heavy exercise, or vasospasm. Treatment, pharmacological or with revascularization, is based on the severity of the dissection. Patients who survive the acute phase have good long-term prognoses.
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PMID:[Coronary artery dissection in young adults]. 2085 7

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

Cocaine-induced cardiovascular disorders such as hypertension, thrombosis, myocardial dysfunction, cardiac dysrhythmias and endocarditis have received widespread attention in the context of cocaine abuse. The number of sudden deaths from cardiac causes, including myocardial infarction, ventricular tachyarrhythmia or aortic dissection, is also increasing. This manuscript will highlight the recent employment of study about cocaine cardiotoxicity and oxidative stress. Evidence has revealed that cardiac oxidative stress is a prominent early event of cocaine administration, which severely compromises the cardiac antioxidant cellular system and causes cardiac antioxidant cellular system injuries. Oxidative damage such as peroxidation of membrane phospholipids and depletion of nonenzymatic antioxidants such as glutathione have been found in the myocardium of chronic cocaine-treated animals and in patients. The data indicate that cocaine administration compromised the heart's antioxidant defense system. About the mechanisms involved in the cellular damage, the evidence that cocaine causes apoptosis in the heart comes from in vivo study. In animals model after short-term and long term-cocaine administration, the investigators demonstrates the role of Reactive Oxygen Species as a trigger of cardiac injury induced by cocaine. Cocaine also increased infiltration of inflammatory cells in the heart, and apoptotic cells were predominantly found near inflammatory cells. The role of oxidative stress in cocaine-induced apoptosis in the heart is wide studied and documented.
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PMID:Role of oxidative stress in cocaine-induced cardiotoxicity and cocaine-related death. 2285 62

Most pheochromocytomas are not suspected clinically while a high percentage of them are curable with surgery. We present the case of an adult cocaine-addicted male patient with an underlying pheochromocytoma and repeated myocardial infarctions. Computed tomography showed a left round adrenal mass, also high 24-hour urine levels of catecholamines and metanephrines were detected from urinalysis. The patient was given alpha and beta blockers, moreover a laparoscopic left adrenalectomy was performed. Cocaine can block the reuptake of noradrenaline, leading to increasing its concentration and consequently its effects as well, and induce local or diffuse coronary vasoconstriction in normal coronary artery segments per se, cocaine can also trigger pheochromocytoma crisis, and therefore, cardiac complications such as myocardial infarction due to these additive effects are intended to occur. For this reason, in the presence of typical clinical manifestations of pheochromocytoma, such as sustained or paroxysmal hypertension, headache, sweating, tachycardia and abdominal pain, probable association of this tumor in patients with cocaine abuse and associated cardiac complications must be ruled out.
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PMID:Acute myocardial infarction secondary to catecholamine release owing to cocaine abuse and pheochromocytoma crisis. 2385 20

: Cocaine is the most commonly used recreational drug among young adults with levels reaching epidemics proportions. This accelerated rate of use is due mainly to easy access and administration, reduced cost, and, importantly, underestimation of the drug risks. Cocaine, instead, is responsible of endothelial dysfunction and accelerated atherosclerosis with consequent organ damage. Cocaine abuse is not only associated with central necrotizing vasculitis, but it is also appeared to play a role in the development of peripheral vasoconstriction with symptoms similar to Buerger's disease. The current study reports a middle-aged man addicted to cocaine for 20 years. The patient presents several cardiovascular disease risk factors and manifestations, including diabetes mellitus and hypertension. Additionally, arteriography showed complete left posterior tibial artery obstruction with distal collateral vessels and severe leftfoot ischemia. For clinical worsening 1 month later, the patient underwent another arteriography. Although angioplasty of posterior tibial artery showed recovery of blood flow, immediately after treatment (selective percutaneous transluminal angioplasty of posterior tibial artery, dilation with balloon without stenting), a return to pretreatment blood flow 2 min later was observed. This transient change was mediated by severe vasospasm resulting in a complete re-obstruction of the vessel. The poor vascular manifestations are most probably due to cocaine-necrotizing vasculitis subsequent to endothelial dysfunction and accelerated atherosclerosis usually associated with cardiovascular risk factors. Therefore, treatments of young cocaine addicts presenting many cardiovascular risk factors and manifestations should always be carefully investigated and cautiously approached, especially in those with poor outcomes.
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PMID:Lower limb ischemia due to long-term abuse of cocaine. 2483 35

Cocaine is abused worldwide as a recreational drug. It is a potent activator of the sympathetic nervous system leading to intense vasoconstriction, endothelial dysfunction, oxidative stress, platelet activation and decrease in prostaglandins E2 and prostacyclin. Cocaine can lead to widespread systemic adverse effects such as stroke, myocardial infarction, arterial dissection, vascular thrombosis and rhabdomyolysis. In human and rat kidneys, cocaine has been associated with glomerular, tubular, vascular and interstitial injury. It is not uncommon to diagnose cocaine-related acute kidney injury (AKI), malignant hypertension and chronic kidney disease. Cocaine abuse can lead to AKI by rhabdomyolysis, vasculitis, infarction, thrombotic microangiopathy and malignant hypertension. It is reported that 50-60% of people who use both cocaine and heroin are at increased risk of HIV, hepatitis and additional risk factors that can cause kidney diseases. While acute interstitial nephritis (AIN) is a known cause of AKI, an association of AIN with cocaine is unusual and seldom reported. We describe a patient with diabetes mellitus, hypertension and chronic hepatitis C, who presented with AKI. Urine toxicology was positive for cocaine and a kidney biopsy was consistent with AIN. Illicit drugs such as cocaine or contaminants may have caused AIN in this case and should be considered in the differential diagnosis of causes of AKI in a patient with substance abuse. We review the many ways that cocaine adversely impacts on kidney function.
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PMID:Cocaine and kidney injury: a kaleidoscope of pathology. 2585 66


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