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

Cocaine abuse may lead to serious cardiac complications, including myocardial ischemia and infarction, myocarditis, cardiomyopathy and arrhythmias. With concomitant use of alcohol and cocaine, cocaethylene is produced by hepatic transformation. Cocaethylene is now thought to be primarily responsible for the deaths that occur among cocaine abusers. Treatment of cardiovascular complications focuses on cocaine-induced ischemia, hypertension and arrhythmias. The use of thrombolytic agents in myocardial infarction remains controversial. Concurrent detoxification with bromocriptine and norepinephrine is recommended.
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PMID:Cardiovascular complications of cocaine abuse. 846 3

Cocaine abuse is widespread, and its use by the parturient has potential significant adverse effects in both the mother and the newborn. This study was undertaken in gravid ewes to determine the effects of treatment of cocaine-induced hypertension with hydralazine (Apresoline) on the maternal and fetal cardiovascular systems, catecholamine response, blood gas and acid-base status, and uterine blood flow (UBF). Twenty-one experiments were performed in 15 chronically instrumented ewes near term gestation. After a 30-min control period, cocaine was given intravenously to all ewes for 55 min to induce and maintain increased maternal mean arterial pressure (MMAP) and reduced UBF. The sheep were randomly assigned to receive either cocaine alone (n = 11, control group) or hydralazine (n = 10, treatment group), starting 15 min after the cocaine administration. Both drugs were discontinued 55 min after the start of the cocaine administration, followed by a 35-min recovery period. In the control group, cocaine administration resulted in a 31 +/- 13% (SD) increase in MMAP (P less than 0.05) and a 26 +/- 21% reduction in UBF (P less than 0.05). In the treatment group, the initial cocaine administration resulted in a similar increase in MMAP and decrease in UBF. Hydralazine therapy restored MMAP toward baseline after 20 min of administration, but UBF remained reduced (37 +/- 17%) throughout therapy (P less than 0.05) and recovery (18 +/- 13%) (P less than 0.05). The maternal heart rate increased maximally by 121 +/- 33% (P less than 0.05) after the administration of hydralazine, compared with a 14 +/- 21% increase (P less than 0.05) in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hydralazine does not restore uterine blood flow during cocaine-induced hypertension in the pregnant ewe. 155 Feb 83

Cardiovascular complications are among the most common and dangerous complications of cocaine abuse, ranging from episodic arrhythmias to myocardial infarction, strokes, cardiomyopathy, and sudden death. The central nervous system-mediated action of cocaine triggers an increase in circulating catecholamines, resulting in arterial vasoconstriction, increase in myocardial oxygen demand, myocardial ischemia, tachycardia, and other arrhythmias. The peripheral cardiovascular action of cocaine involves the inhibition of reuptake of catecholamines at adrenergic nerve terminals, with local release of epinephrine, direct stimulation and vasospasm of the coronary arteries, coronary intimal hyperplasia, inhibition of baroreceptors, interference with the electrical conduction through the myocardium, and direct myocardial toxicity. The cardiovascular complications of cocaine include cardiac dysrhythmias and hypertension, acute myocardial infarction, myocarditis, infectious endocarditis, ventricular dysfunction, dilated cardiomyopathy, hypotensive shock, and cerebral strokes. Cocaine-related vascular changes in the pregnant woman and fetus have been related to an increased incidence of abortion, abruptio placentae, and congenital anomalies of the fetus.
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PMID:Cardiovascular complications of cocaine abuse. 158 6

Cocaine abuse can cause cardiovascular damage leading to hypertension, myocardial ischaemia and infarction. This might be partly due to the effects of cocaine on the microcirculation about which little is known, although its effects on the macrovessels are well documented. Accordingly, we used in vivo videomicroscopy to study the vasoconstrictive effect of cocaine on arterioles of different diameter. They were classified into three orders (A2, A3, A4) according to their position in the microvascular network and their diameter. Since calcium antagonists have been reported to exert a protective effect against the cardiovascular disorders induced by cocaine, we tested the hypothesis that this protective action occurs in the microcirculation. We found that intra-arterial administration of the calcium antagonist Nitrendipine greatly inhibited the vasoconstriction induced by cocaine in all three arteriole orders. The degree of inhibition ranged from 44 to 56%. Combined administration of benzodiazepine and an angiotensin converting enzyme inhibitor has also been reported to protect rats against cocaine-induced hypertension and to increase survival rates after a toxic dose of cocaine. Since the mechanisms of this protection are not yet clear, we also studied the effect of the angiotensin converting enzyme inhibitor Enalaprilat on cocaine-induced vasoconstriction. Intra-arterial administration of Enalaprilat inhibited this vasoconstriction slightly but significantly in arteriole orders 2 and 3 by 27 and 24% respectively, but not in order 4. We concluded that Nitrendipine is a powerful inhibitor of cocaine-induced vasoconstriction in the microcirculation. The small but significant inhibition found with Enalaprilat for the larger arterioles suggests that the local angiotensin II level may affect the response to cocaine. However, since the Enalaprilat-induced inhibition was very limited, we conclude that mechanisms other than those occurring in the peripheral microcirculation account for the protection afforded by Enalaprilat against the harmful effects of cocaine.
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PMID:Microvascular effects of cocaine; interaction with nitrendipine and enalaprilat. 164 95

We performed serial umbilical artery Doppler flow velocimetry studies on 314 women and grouped them according to history of antepartum cocaine abuse, placental abruption with antepartum cocaine abuse, preterm labor with antepartum cocaine abuse, preterm labor without antepartum cocaine abuse, and controls without preterm labor or antepartum cocaine abuse. Analyses excluded twin gestation, diabetes, and hypertension. The overall incidence of deliveries at or before 36 weeks was 28% (31 of 112). Thirteen (12%) of the infants were small for gestational age (SGA) and 33 (29%) were low birth weight (LBW). Almost all subjects with a history of cocaine abuse had normal systolic-diastolic ratios (S/Ds). All patients with abruption had abnormal S/Ds, as did 14 of 64 subjects who had preterm labor and a history of cocaine abuse. No abnormal S/Ds were found in the women with preterm labor or in controls. Among cocaine-abusing women, there was a significant correlation between placental abruption and abnormal S/Ds (P less than .05) and between abnormal S/Ds and the incidence of preterm birth and SGA and LBW infants.
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PMID:Relationship between antepartum cocaine abuse, abnormal umbilical artery Doppler velocimetry, and placental abruption. 206 75

Toxic injury is one of the many ways by which the functional integrity of the heart may become compromised. Any of the subcellular elements may be the target of toxic injury, including all of the various membranes and organelles. Understanding the mechanisms underlying cardiotoxicity may lead to treatment of the toxicity or to its prevention. Doxorubicin and its analogs are very important cancer chemotherapeutic agents that can cause cardiotoxicity. Other agents which are cardiotoxic and which have profound public health implications include the alkaloid emetine in ipecac syrup, cocaine, and ethyl alcohol. The most important cardiotoxic mechanisms proposed for doxorubicin include oxidative stress with its resultant damage to myocardial elements, changes in calcium homeostasis, decreased ability to produce ATP, and systemic release of cardiotoxic humoral mediators from tissue mast cells. Each of the first 3 mechanisms can lead to each of the other 2, and the causal relationships between all of these mechanisms are not clear. New evidence suggests that doxorubicinol, one of the metabolites of doxorubicin may be the moiety responsible for cardiotoxicity. Several other potential mechanisms also have been proposed for doxorubicin. Emetine in ipecac syrup is the first aid treatment of choice for many acute toxic oral ingestions and the alkaloid, itself, is used to treat amebiasis. Cardiotoxicity occurs following chronic exposure, such as occurs therapeutically in amebiasis and with ipecac abuse by bulemics. A number of mechanisms are proposed for emetine cardiotoxicity, but the current mechanistic literature is quite scarce. Cocaine abuse recently has caught the public interest, in particular because of the drug-related sudden deaths of certain athletes. Cocaine can cause hypertension, arrhythmias, and reduced coronary blood flow, each of which can contribute to its lethality. However, it may be possible that cocaine sudden death episodes are more related to hyperthermia and convulsive seizures, rather than to cardiovascular toxicity. Chronic alcohol use leads to dilated cardiomyopathy and failure as part of the general physical degeneration that occurs with alcoholism. Several mechanisms are proposed for the cardiomyopathy, but only 2 things seem clear. The cardiotoxicity is due to an intrinsic effect of alcohol, rather than to malnutrition or co-toxicity, and abstinence is the only effective treatment for the cardiomyopathy. Recent articles indicate that very moderate use of alcohol may be beneficial and protect against cardiovascular-related morbidity. One explanation for these findings seems to be that the non-drinking groups, against whom the moderate drinking comparisons were made, were enriched in former drinkers with significant alcohol-related cardiovascular pathology.
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PMID:Toxic mechanisms of the heart: a review. 209 Dec 37

An increase in cocaine abuse by pregnant women has been associated with a range of maternal/fetal cardiovascular complications. Intracerebral hemorrhage has been reported as a cocaine-related complication, but has not previously been associated with pregnancy. We report a case of cocaine-associated intracerebral hemorrhage in the postpartum period which complicated the differential diagnosis and management of hypertension and seizures.
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PMID:Cocaine, pregnancy, and postpartum intracerebral hemorrhage. 249 50

Drug abuse has become a social and medical problem. Amphetamine and cocaine have a potent sympathicomimetic action, so they have important effects on the Central Nervous and Cardiovascular Systems. Their neurological complications are principally: psychic alterations, seizures and stroke (hemorrhagic and ischemic). The latter are the most important in the clinical practice. Their capacity to produce transit arterial hypertension and cerebral vascular constriction could be the physiopathological substrate of such alterations. Angiographic studies have shown lesions suggesting vasculopathy. In the last ten years cocaine abuse has become an authentic epidemic. We have reviewed its neurological complications, particularly the vascular ones--42 hemorrhagic and 24 ischemic--and the following conclusions were drawn: it should be considered as a risk factor in the younger age group; a short period of time between the last drug dose and the clinical picture is frequently seen; clinical features may appear with the first drug administration; no characteristic lesion in relation to the way of administration or consumption time was elicited.
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PMID:[Neurologic complications caused by use of cocaine, amphetamines and sympathomimetics]. 270 Feb 92

Since our initial report in 1984 of six patients with AMI temporally related to cocaine use, we have observed 19 additional patients in whom ischemic chest pain syndromes occurred shortly after intranasal or IV use of cocaine or after smoking the drug. Seventeen patients (89 percent) developed non-Q wave infarction and two had Q-wave infarction. One patient manifested angina with striking ST-segment elevation. None of the patients had diabetes or hypertension, and all but one were cigarette smokers. The serum cholesterol level was 162 +/- 7 mg/dl. Four of the five patients who consented to coronary angiographic studies displayed normal coronary arteries, and one showed proximal stenosis of the right coronary artery. The cold pressor test was performed in seven patients; none had angina or ECG changes induced by cold stimulation. We conclude that T-wave infarction is a common form of an acute cardiac event related to cocaine abuse, and its pathogenesis may involve that of the cocaine-induced coronary vasospasm.
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PMID:Acute non-Q wave cocaine-related myocardial infarction. 276 21

A retrospective study of 343 women who lacked prenatal care was conducted to ascertain the effect of recent cocaine abuse on birth weight and gestational age. All pregnant women admitted in labor to a large urban teaching hospital between January 1 and December 31, 1986 who had not received prenatal care were included. The charts of these women were evaluated to obtain information about medical and obstetric complications of pregnancy, labor and delivery, and birth weight and gestational age of the infant. Information about drug use was obtained by urine toxicology at the time of admission. Results of ordinary least-squares multiple regression analyses indicated cocaine abuse to be a significant predictor of low birth weight and early gestational age. No correlation was found between cocaine abuse and abruptio placentae or maternal hypertension.
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PMID:The effect of cocaine abuse on birth weight and gestational age. 340 50


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