The medical complications of cocaine abuse are being attacked by clinicians with increasing common occurrence The cardiovascular manifestations of cocaine abuse include chest pain.
The medical complications of cocaine abuse are being attacked by clinicians with increasing common occurrence The cardiovascular manifestations of cocaine abuse include chest pain, myocardial ischemia and infarction, congestive heart failure, arrhythmias, infective endocarditis, and aortic dissection. The pathogenesis of these cardiovascular complications has not been completely elucidated but may be related to a combination of the sympathomimetic and membrane anaesthetic purports of cocaine. We present these universals in a case discussion format.
[MVo.sub.2]=myocardial oxygen consumption
guide words: Cocaine abuse; congestive heart failure; dilated cardiomyopathy
Cocaine use can cause potentially life-threatening weights on the cardiovascular system.[1-3] The widespread abuse of this remedy during the last decade in the United States has serv as the impetus for intensive investigation into the mechanisms of cocaine cardiotoxicity. Despite the significant advances in our understanding of the actions of cocaine upon the cardiovascular system, the precise pathogenic basis of the cardiovascular complications associated with cocaine use remains undefined. The following is a report of a patient with chaste chronic dilated cardiomyopathy presumably caused by dint of the long-term use of freebase cocaine. This case will be under the orders of as the basis for a discussion of the forces of cocaine on the cardiovascular system
Case Report
A 56-year-old white man was admitted to the hospital with progressive dyspnea and pedal edema of 2 months' duration. Approximately 12 years before hospital admission, the patient began using cocaine intermittently, interspersed with periods of daily use. He initially used cocaine through nasal insufflation followed by smoking freebase cocaine in amounts varying between 025 g and 2 g Six years prior to admission, he was hospitalized with anasarca and dyspnea, befitting to advanced biventricular congestive heart failure. A multiple gated acquisition scan demonstrated diffuse hypokinesis of the left ventricle with an ejection fraction of 25 percent He was treated with intravenous diuretics and missed 20 kg. He was discharged from the hospital and maintained in succession a regimen of digoxin, lasix, and an angiotensin-converting enzyme inhibitor. During the nearest 6 years, he remained clinically stable without symptoms of congestive heart failure and demonstrated sustained radiographic improvement (Fig 1 top and center) Although he abstained from mix with drugs use for about 1 year, he then began smoking freebase cocaine one time per week. One year prior to hospital admission, he began increasing the common occurrence and amount of cocaine he ingested. brace months before admission, he noted dyspnea upon exertion and subsequently pedal edema. The patient did not accord to intensification of his outpatient medical regimen and was hospitalized.
The patient had a history of exogenous obesity, a 60-pack-year history of cigarette smoking, a 2-year history of impressed sign 2 adult onset diabetes mellitus that was well controll with oral hypoglycemic agents, and a history of infrequent use of small amounts of alcohol. There was no history of chest pain, myocardial infarction, hypertension, hyperlipidemia, thyroid disease, latter viral illness, or family history of heart disease.
upon physical examination, he was in moderate respiratory distress befitting to congestive heart failure. The electrocardiogram revealed sinus tachycardia and a nonspecific intraventricular conduction deficiency Chest radiography demonstrated severe cardiomegaly with a cardiothoracic ratio of 063 a marked increase from earlier chest radiographs (Fig 1) A multiple gated acquisition scan revealed an ejection fraction of 18 percent Cardiac catheterization and coronary angiography revealed inexorable pulmonary arterial and venous hypertension with a pulmonary artery, constraining force of 60/30 mm Hg and a pulmonary capillary wedge crushing of 35 mm Hg, a markedly reduceed cardiac index of 1.4 L/min/[m.sup.2], peremptory diffuse left ventricular hypokinesia, and a 40 percent stenotic lesion of the left circumflex artery. The patient was treated with intravenous diuretics, vasodilators, and inotropic agents, and he thrown away 8 kg. He was discharged from the hospital with compensated congestive heart failure. The patient refused to set in a drug counseling program.
Regarding the clinical manifestations of cocaine abuse, the following apply:
1 Cocaine use consequence s in more emergency department visits by dint of substance abusers than any other illicit remedy (T/F)
2. Serious noncardiac complications of cocaine abuse include the following:
a. seizures
b cerebrovascular accidents
c noncardiogenic pulmonary edema
d abnormal carbon monoxide diffusing capacity
e intestinal ischemia
f rhabdomyolysis with acute renal failure
g all of the above
3 More than 90 percent of the patients who are evaluated for chest pain following cocaine use are ultimately institute to have myocardial ischemia or infarction. (T/F)
4 Cardiovascular complications of cocaine abuse include the following:
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