Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atherosclerosis increases cardiovascular risk and the possibility of developing acute myocardial infarction (AMI) or stroke. Patients infected with human immunodeficiency virus (HIV) often present morphological and metabolic alterations (hypercholesterolemia, hypertriglyceridemia, insulin resistance, diabetes) that can increase vascular risk. The frequent coexistence of classic risk factors (atherogenic diet, smoking, physical inactivity, cocaine abuse), the progressive increase in mean age of HIV-1 infected patients, and the polymedication they receive make it difficult to estimate the direct effect that new therapies may have on cardiovascular risk. Retrospective clinical studies with diverse designs in large cohorts offer contradictory results for cardiovascular risk in the HIV-infected population. Longer observational periods are needed and the effect of other classic risk factors needs to be controlled, in order to establish the possible detrimental effect the new therapies may have on cardiovascular risk in this population.
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PMID:[Cardiovascular risk in patients with chronic HIV-1 infection: a controversy with therapeutic, clinical and prognostic implications]. 1475 7

Stroke in young adults has been related to mechanisms different to those found in older individuals. Cardiogenic embolism, arteritis, atherosclerosis, fibromuscular dysplasia, pregnancy-related angiopathy, migrainous stroke, anaemia, antiphospholipid syndrome, arterial dissection, the consumption of toxic substances and head trauma have been described. We present a young man with a case history of tobacco and cocaine abuse who suffered a mild head trauma, with normal neurological examination, and a computed tomography scan image of a right anterior cerebral infarction. Serum biochemistry showed no alterations according to the diagnosis protocol for stroke in young patients. Various mechanisms have been involved, such as vasospasm, increasing arterial pressure and embolism. Considering the cocaine abuse and the mild head trauma, in our patient vasospasm was thought to be the mechanism involved in the cerebral infarction, which proved a challenge to diagnose in the emergency room.
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PMID:Stroke in young patients: a diagnostic challenge in the emergency room. 1516 83

Cocaine abuse is known to induce many adverse cardiovascular effects, including hypertension, atherosclerosis, and aortic dissection. A major physiological event leading to these pathophysiological actions of cocaine could be apoptosis. This study was designed to investigate if primary cultured rat aortic vascular smooth muscle cells (VSMCs) can undergo apoptosis when treated with cocaine. After treatment with cocaine (10(-6) to 10(-4) M), morphological analysis of aortic VSMCs using confocal fluoresence microscopy showed that the percentage of apoptotic aortic VSMCs increased after cocaine (10(-6) to 10(-4) M) treatment for 12, 24, and 48 h. These results demonstrate that aortic VSMCs can undergo rapid apoptosis in response to cocaine in a concentration-dependent manner. Cocaine-induced apoptosis may thus play a major role in cocaine abuse-induced aortic dissection, atherosclerosis, and hypertension.
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PMID:Cocaine induces apoptosis in primary cultured rat aortic vascular smooth muscle cells: possible relationship to aortic dissection, atherosclerosis, and hypertension. 1537 Nov 67

Chronic cocaine abuse is known to cause endothelial dysfunction and atherosclerosis. The present study investigated the effect of binge cocaine treatment, a model for chronic cocaine abuse, on the blood flow responses to the adrenergic agonists norepinephrine, phenylephrine and isoproterenol, the endothelium-dependent vasodilator acetylcholine, and the endothelium independent vasodilator sodium nitroprusside (SNP) in the hindlimb vascular bed of male Sprague Dawley rats. Rats received either single binge or double binge treatment. Each binge treatment consisted of three doses of cocaine (30 mg kg(-1) i.p.) for 3 days. For double binge treatment, there was a 4 day recovery period between the binges. At the end of the treatment the rats were anesthetized and agonists were administered into the right hindlimb circulation through a catheter in the left iliac artery and blood flow responses were measured with a flow probe around the right iliac artery. Rats receiving double cocaine binges showed a significant decrease in the magnitude and duration of the blood flow response to norepinephrine and a decrease in the duration of the blood flow response to phenylephrine, isoproterenol and acetylcholine when compared with saline controls. The blood flow response to SNP was not changed. Total plasma nitrate-nitrite levels were significantly reduced and big endothelin levels were significantly increased in rats receiving double cocaine binges. This study demonstrates that binge cocaine treatment can alter endothelial function, while not changing smooth muscle function, and impairs the adrenergic pathway.
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PMID:Effect of binge cocaine treatment on hindlimb vascular function. 1609 79

Cocaine is a powerful stimulant that gives users a temporary sense of euphoria, mental alertness, talkativeness, and a decreased need for food and sleep. Cocaine intoxication is the most frequent cause of drug-related death reported by medical examiners in the US, and these events are most often related to the cardiovascular manifestations of the drug. Once playing a vital role in medicine as a local anesthetic, decades of research have established that cocaine has the ability to cause irreversible structural damage to the heart, greatly accelerate cardiovascular disease, and initiate sudden cardiac death. Although pathologic findings are often reported in the literature, few images are available to support these findings, and reviews of cocaine cardiopathology are rare. We describe the major pathologic findings linked to cocaine abuse in earlier research, their underlying mechanisms, and the treatment approaches currently being used in this patient population. A MEDLINE search was conducted to identify all English language articles from January 2000 to June 2008 with the subject headings and key words 'cocaine', 'heart', 'toxicity', and 'cardiotoxicity'. Epidemiologic, laboratory, and clinical studies on the pathology, pathophysiology, and pharmacology of the effects of cocaine on the heart were reviewed, along with relevant treatment options. Reference lists were used to identify earlier studies on these topics, and related articles from Google Scholar were also included. There is an established connection between cocaine use and myocardial infarction (MI), arrhythmia, heart failure, and sudden cardiac death. Numerous mechanisms have been postulated to explain how cocaine contributes to these conditions. Among these, cocaine may lead to MI by causing coronary artery vasoconstriction and accelerated atherosclerosis, and by initiating thrombus formation. Cocaine has also been shown to block K+ channels, increase L-type Ca2+ channel current, and inhibit Na+ influx during depolarization, all possible causes for arrhythmia. Additionally, cocaine use has been associated with left ventricular hypertrophy, myocarditis, and dilated cardiomyopathy, which can lead to heart failure if drug use is continued. Certain diagnostic tools, including ECG and serial cardiac markers, are not as accurate in identifying MI in cocaine users experiencing chest pain. As a result, clinicians should be suspicious of cocaine use in their differential diagnosis of chest pain, especially in the younger male population, and proceed more cautiously when use is suspected. Treatment for cocaine-related cardiovascular disease is in many ways similar to treatment for traditional cardiovascular disease. However use of beta-receptor antagonists and class Ia and III anti-arrhythmics is strongly discouraged if the patient is likely to continue cocaine use, because of documented adverse effects. The medical community is in urgent need of a pharmacologic adjunct to cocaine-dependence treatment that can deter relapse and reduce the risks associated with cardiovascular disease in these patients.
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PMID:Cocaine cardiotoxicity: a review of the pathophysiology, pathology, and treatment options. 1946 23

Cocaine, a crystalline tropane alkaloid which is obtained from the leaves of the coca plant, acts a powerfully addictive stimulant that directly targets the central nervous system. The effects of the drug appear almost immediately after a single dose (intravenous, intranasal, or inhaled), and disappear within a few minutes or hours. Although the free commercialization of the drug is illicit and severely penalized in virtually all countries, its use remains widespread in many social, cultural, and personal settings. There is a variety of well-recognized side effects of cocaine abuse, which involve virtually every organ system. There is also emerging evidence, however, that cocaine abuse might trigger a variety of cardiac disorders, ranging from arrhythmias to acute myocardial infarction (AMI), heart failure and even sudden cardiac death, especially in relatively young male patients (e.g., those in the mid-1930s), in those who concomitantly use tobacco and alcohol, in those having experienced a trauma or a car accident and lack traditional risk factors for atherosclerosis. Since the use of cocaine may influence the treatment strategies of patients being evaluated for possible acute coronary syndrome (ACS) as well as the prognosis of an AMI, it might be advisable to introduce cocaine screening in patients admitted with chest pain at the emergence department, especially in high-risk patients (i.e., young males with concurrent use of tobacco or alcohol, suffering from a recent accident and with no traditional atherosclerotic risk factors), or in those who are unresponsive and unreliable. This strategy might be helpful to adopt the best therapeutic approach for reducing the risks associated with cardiovascular disease in these patients, and also to deter relapse.
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PMID:Cocaine in acute myocardial infarction. 2085 18

Simultaneous thrombosis of multiple epicardial coronary arteries is an uncommon clinical finding in ST-segment elevation myocardial infarction (STEMI). We describe a 44 year-old male present with STEMI who was found to have simultaneously occluded two epicardial arteries. There is many clinical states that can lead to multiple thrombosis i.e. essential trombocytosis, hiperhomocysteinaemia, depletion of antitrombin III, cocaine abuse etc. In this particular case L-arginin supplementation and association with thrombosis or atherosclerosis progression is discussed.
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PMID:[Acute myocardial infarction with simultaneous occlusions of two coronary arteries in a 44 year-old man]. 2357 85

: 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

Myocardial infarction (MI) due to coronary atherosclerosis in young adults is uncommon; rare causes such as cocaine abuse, arterial dissection, and thromboembolism should be considered. A 21-year-old football player, and otherwise healthy African American man, developed chest pain during exercise while bench-pressing 400 lbs. Acute MI was diagnosed based on physical examination, electrocardiography findings, and elevated cardiac enzymes. Coronary arteriography showed a thrombus occluding the proximal left anterior descending artery (LAD). Aggressive antiplatelet therapy with aspirin, clopidogrel, and eptifibatide was pursued, in addition to standard post-MI care. This led to the successful resolution of symptoms and dissolution of the thrombus, demonstrated by repeat coronary arteriography. Five months later, he presented with similar symptoms during exercise after lifting heavy weights, and was found to have another acute MI. Coronary arteriography again showed a thrombus occluding the LAD. No evidence of coronary artery dissection or vasospasm was found. Only mild atherosclerotic plaque burden was observed on both occasions by intravascular ultrasound. A bare metal stent was placed at the site as it was thought this site had acted as a nidus for small plaque rupture and thrombus formation. Elevated serum factor VIII activity at 205% (reference range 60%-140%) was found, a rare cause of hypercoagulability. Further workup revealed a patent foramen ovale during a Valsalva maneuver by transesophageal echocardiography. Both events occurred during weight lifting, which can transiently increase right heart pressure in a similar way to the Valsalva maneuver. In light of all the findings, we concluded that an exercise-related increase in factor VIII activity led to coronary arterial thrombosis in the presence of a small ruptured plaque. Alternatively, venous clots may have traversed the patent foramen ovale and occluded the LAD. In addition to continuing aggressive risk factor modification, anticoagulation therapy with warfarin was initiated with close follow-up.
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PMID:Recurrent myocardial infarctions in a young football player secondary to thrombophilia, associated with elevated factor VIII activity. 2538 85

Isolated spontaneous renal artery dissection (RAD) without known trauma is rare, and its etiology has not been determined. However, notable risk factors including hypertension, strenuous exercise, connective tissue disorders, atherosclerosis, extracorporeal shock wave lithotripsy, and cocaine abuse have been reported. To the best of our knowledge, isolated RAD caused by lumbar vertebra osteophytes in patients with degenerative lumbar scoliosis has not been reported in the literature. In this article, we present a case of RAD caused by lumbar vertebra osteophyte in a patient with degenerative scoliosis and discuss the management of the disease.
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PMID:Renal Artery Dissection in a Patient With Degenerative Scoliosis: A Rare Complication Caused by Lumbar Vertebra Osteophyte. 2949 58


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