Effects of cocaine on anterior pituitary and gonadal hormones.

Acute and chronic cocaine administration has been reported to change endocrine and neurochemical functions in animals and human drug abusers. This study examined the effects of acute cocaine administration on anterior pituitary and gonadal hormones in male human volunteers without a history of drug abuse. Using a double-blind, randomized study design, luteinizing hormone, follicle-stimulating hormone (FSH), prolactin and testosterone levels were measured in 12 healthy men before and after intranasal administration of 2 mg/kg cocaine or placebo. Each subject was studied twice, serving as his own control. Compared to placebo, both luteinizing hormone, and, to a lesser degree, follicle-stimulating hormone levels increased significantly after cocaine, reaching a peak value 60 min after the administration of the study drug. This pattern is consistent with a possible cocaine induced rise in gonadotropin-releasing hormone and subsequent rise in luteinizing hormone and follicle-stimulating hormone due to stimulation of gonadotroph cells in the pituitary gland. Neither cocaine nor placebo induced a change in testosterone levels. Prolactin levels showed a decrease from base line after both placebo and cocaine administration, with a significantly more pronounced decrease after cocaine. This likely reflects the combination of the physiologic diurnal variation in prolactin secretion and an added inhibitory effect on prolactin due to cocaine. These findings show that the acute administration of cocaine significantly alters anterior pituitary hormonal release patterns.

Effects of in vivo cocaine administration on human platelet aggregation.

To evaluate whether cocaine administration to human volunteers in vivo increases platelet aggregation, 12 healthy male volunteers were studied twice in a prospective, double-blinded fashion. There was a decrease in aggregation following cocaine exposure compared to placebo, which was most prominent at high doses of adenosine diphosphate.

Utilization of the coronary balloon-expandable coil stent without anticoagulation or intravascular ultrasound.

BACKGROUND: The balloon-expandable coil stent has been proved effective in the management of acute and threatened closure after coronary balloon angioplasty and has been shown to reduce restenosis in patients with suboptimal results after coronary balloon angioplasty. Coronary artery stenting has been limited by the occurrence of stent thrombosis and comorbidity related to anticoagulation. This study was undertaken to determine whether anticoagulation may be removed from poststenting protocols, thus reducing comorbidity without increasing stent thrombosis. METHODS AND RESULTS: Between September 1994 and May 1995, 369 patients received balloon-expandable coil stents in native coronary arteries at our institution. Of these patients, 216 were selected for a protocol of aspirin and ticlopidine (for 1 month) without anticoagulation. Eligibility for this protocol followed satisfaction of certain procedural and angiographic criteria. These criteria included adequate coverage of intimal dissections, absence of residual filling defects, and normal (TIMI grade 3) flow in the stented vessel after high-pressure balloon inflations. Intravascular ultrasound was not used to guide stent deployment. The stenting procedure was planned in 37% of patients and unplanned in 63% of patients, including 25 (12%) for acute or threatened closure. During the 30-day follow-up period, stent thrombosis occurred in 2 patients (0.9%), there was 1 death (0.5%), and 2 patients (0.9%) underwent coronary bypass surgery. Vascular access-site complications occurred in 4 patients (1.9%), and bleeding that required blood transfusion occurred in 4 patients (1.9%). CONCLUSIONS: Patients who receive the coronary balloon-expandable coil stent with optimal angiographic results without intravascular ultrasound guidance can be managed safely with a combination of aspirin and ticlopidine without anticoagulation.

Gastro-oesophageal reflux and adverse respiratory events in children under anaesthesia.

The incidence of gastro-oesophageal reflux in children undergoing general anaesthesia has not previously been studied. One-hundred-and-twenty children (ASA Class 1-2) were studied intraoperatively using continuous oesophageal pH monitoring. The incidence of reflux was 2.5% (3 of 120). None of these three patients had an adverse respiratory event. There was no correlation between reflux and adverse respiratory events. Thirteen patients had minor respiratory events without evidence of acid reflux. Gastro-oesophageal reflux does occur in healthy paediatric patients having minor surgery, but was not a significant cause of the adverse respiratory events that occurred in our study.

Effects of cocaine on cortisol secretion in humans.

The effects of acute cocaine administration on the pituitary adrenal axis in humans without a history of drug abuse are unknown. The authors studied 12 male volunteers twice in a double-blinded, placebo-controlled, randomized fashion. After intranasal administration of 2 mg/kg cocaine, cortisol levels were significantly higher than after placebo administration. The authors concluded that acute administration of cocaine to humans increases cortisol secretion.

Coronary anatomy and prognosis of young, asymptomatic survivors of myocardial infarction.

PURPOSE: To assess the coronary anatomy and prognosis of young, asymptomatic survivors of myocardial infarction. PATIENTS AND METHODS: The records of all 5,316 patients who underwent cardiac catheterization at Parkland Memorial Hospital from July 1978 to December 1992 were reviewed to identify those patients 40 years old and younger who were catheterized within 60 days of a first myocardial infarction. Of 129 such patients, 48 had no indication for catheterization other than age (group I), and 81 were catheterized for spontaneous or provocable ischemia (group II). Extent of coronary artery disease and long-term follow-up were examined to ascertain the utility of cardiac catheterization in the asymptomatic patients. RESULTS: The 2 groups were similar with respect to clinical variables. The asymptomatic survivors of infarction (group I) had fewer diseased coronary arteries than did those with post-infarction ischemia (group II) (1.0 +/- 0.7 versus 1.5 +/- 1.0 [mean +/- SD] diseased coronary arteries, respectively; P = 0.002) and were less likely to have left-main or 3-vessel coronary artery disease (4% versus 20%, respectively; P = 0.027). Eighty-three percent of the group I patients had one diseased coronary artery, or less, and no patient underwent angioplasty or coronary bypass grafting on the basis of catheterization. After 71 +/- 44 months of follow-up, only 5 (10%) had died of a coronary-related event. CONCLUSIONS: Asymptomatic survivors of myocardial infarction who are 40 years of age or less rarely have left-main or 3-vessel coronary artery disease, and their long-term prognosis with conservative therapy is good. Routine catheterization in these patients is not warranted and should be reserved for those who manifest spontaneous or provocable post-infarction ischemia.

Predictive value of prominent pulmonary arterial wedge V waves in assessing the presence and severity of mitral regurgitation.

Indwelling pulmonary arterial catheters are often used to monitor and to guide therapy in critically ill patients. The magnitude of the V wave recorded from the pulmonary arterial wedge (PAW) position is sometimes used to assess the presence and severity of mitral regurgitation (MR). The present study was performed to assess the relation (or lack thereof) between a "prominent" PAW V wave and qualitative and quantitative estimates of MR. In 903 subjects (445 men and 458 women, aged 49 +/- 13 [mean +/- SD] years) referred for cardiac catheterization, an oximetrically confirmed PAW pressure was recorded with a large-lumen stiff catheter, and a left ventriculogram was recorded. In 646 of these subjects (328 men and 318 women, aged 50 +/- 13 years), forward cardiac output was measured by the Fick principle, and a regurgitant fraction was calculated. Prominent PAW V waves--as defined in several ways--were insensitive and had poor positive predictive value in identifying moderate or severe MR. At the same time, the absence of prominent PAW V waves was relatively specific for the absence of moderate or severe MR, and the negative predictive value of small V waves was very good. Thus, the prominence of a PAW V wave cannot be used to assess the presence or severity of MR.

Coronary-artery vasoconstriction induced by cocaine, cigarette smoking, or both.

BACKGROUND: In humans, the use of cocaine and cigarette smoking each increase the heart's metabolic need for oxygen but may also decrease the supply of oxygen. As cocaine abuse has proliferated, cocaine-associated chest pain, myocardial infarction, and sudden death have occurred, especially among smokers. We assessed the influence of intranasal cocaine and cigarette smoking, alone and together, on myocardial oxygen demand and coronary arterial dimensions in subjects with and subjects without coronary atherosclerosis. METHODS: In 42 smokers (28 men and 14 women; age, 34 to 79 years; 36 with angiographically demonstrable coronary artery disease), we measured the product of the heart rate and systolic arterial pressure (rate-pressure product) and coronary arterial diameters before and after intranasal cocaine at a dose of 2 mg per kilogram of body weight (n = 6), one cigarette (n = 12), or intranasal cocaine at a dose of 2 mg per kilogram followed by one cigarette (n = 24). RESULTS: No patient had chest pain or ischemic electrocardiographic changes after cocaine use or smoking. The mean (+/- SE) rate-pressure product increased by 11 +/- 2 percent after cocaine use (n = 30, P < 0.001), by 12 +/- 4 percent after one cigarette (n = 12, P = 0.021), and by 45 +/- 5 percent after both cocaine use and smoking (n = 24, P < 0.001). As compared with base-line measurements, the diameters of nondiseased coronary arterial segments decreased on average by 7 +/- 1 percent after cocaine use (P < 0.001), by 7 +/- 1 percent after smoking (P < 0.001), and by 6 +/- 2 percent after cocaine use and smoking (P < 0.001). The diameters of diseased segments decreased by 9 +/- 2 percent after cocaine use (n = 18, P < 0.001), by 5 +/- 5 percent after smoking (n = 12, P = 0.322), and by 19 +/- 4 percent after cocaine use and smoking (n = 12, P < 0.001). The increase in the rate-pressure product and the decrease in the diameters of diseased segments caused by cocaine use and smoking together were greater (P < 0.001 and P = 0.037, respectively) than the changes caused by either alone. CONCLUSIONS: The deleterious effects of cocaine on myocardial oxygen supply and demand are exacerbated by concomitant cigarette smoking. This combination substantially increases the metabolic requirement of the heart for oxygen but simultaneously decreases the diameter of diseased coronary arterial segments.

Frequency, cause and effect on operative outcome of depressed left ventricular ejection fraction in mitral stenosis.

To assess the incidence, pathophysiology and influence on operative outcome of a depressed left ventricular (LV) ejection fraction (EF) in patients with mitral stenosis (MS), demographic, hemodynamic and cineangiographic data on 72 patients (16 men, 56 women, aged 19 to 75 years) with isolated MS were reviewed. Of the 45 who had mitral commissurotomy or replacement, operative course and functional class before and after surgery were assessed. Of the 72 patients, 21 (29%) had an LVEF < or = 0.50. These 21 were similar to the 51 with an LVEF > 0.50 in age, gender, heart rate, intracardiac pressures, transvalvular gradient and valve area, but they had larger LV end-diastolic (79 +/- 19 [mean +/- SD] vs 59 +/- 15 ml/m2, p < 0.001) and end-systolic volumes (46 +/- 13 vs 23 +/- 8 ml/m2, p < 0.0001). Of the 45 subjects undergoing surgery, operative outcome was similar in the 14 with a depressed and the 31 with a normal LVEF. Thus, about 1/3 of patients with isolated MS have a depressed LVEF. Compared with those with MS and a normal LVEF, these subjects have hemodynamic derangements of similar severity, but they have larger LV end-diastolic and end-systolic volumes, suggesting that impaired LV contractile function or excessive afterload (rather than diastolic underfilling), or both, is the cause of a low LVEF. Those with an LVEF < or = 0.50 who undergo valve surgery have a similar operative outcome as those with an LVEF > 0.50.