D. Brent Glamann

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

BACKGROUND In humans, the use of cocaine and cigarette smoking each increase the hearts 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.

Recurrent Coronary Vasoconstriction Caused by Intranasal Cocaine: Possible Role for Metabolites

OBJECTIVE To define the temporal characteristics of cocaine-induced coronary vasoconstriction in humans and to assess the relation between cocaine-induced coronary vasoconstriction and the blood concentration of cocaine and its main metabolites. DESIGN Randomized, double-blind, controlled clinical trial. SETTING Cardiac catheterization laboratory of a large teaching hospital. PATIENTS Eighteen patients (16 men and 2 women, 37 to 65 years of age) having catheterization for evaluation of chest pain. MEASUREMENTS At catheterization, patients received intranasal saline (8 patients) or cocaine, 2 mg/kg body weight (10 patients). Cineangiographic examination of the left coronary artery and quantitation of the blood concentration of cocaine and its metabolites were done before (baseline) and 30, 60, and 90 minutes after administration of intranasal saline or cocaine. RESULTS In response to cocaine, proximal coronary arterial diameter decreased from 2.4 +/- 1.6 mm (mean +/- SD) at baseline to 2.0 +/- 1.4 mm at 30 minutes (P less than 0.05). This change corresponded temporally to the peak blood concentration of cocaine. At 60 minutes, the cocaine concentration decreased and coronary artery diameter returned to baseline (2.3 +/- 1.6 mm) (P greater than 0.05 compared with baseline). At 90 minutes, all patients had recurrent vasoconstriction (1.9 +/- 1.4 mm, P less than 0.05) despite a further decrease in the blood cocaine concentration. This vasoconstriction corresponded temporally with an increasing blood concentration of cocaines main metabolites, benzoylecgonine and ethyl methyl ecgonine. No changes were observed in the control group. CONCLUSION Intranasal cocaine causes recurrent coronary vasoconstriction, which may be due to its metabolites.

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.

Gonococcal Endocarditis: Twenty-Five Year Experience

Gonococcal endocarditis is a devastating albeit rare complication of disseminated gonorrhea. It virtually disappeared as a disease entity with the advent of antibiotic therapy. Recently, it has reappeared with surprisingly high frequency for unclear reasons. Since 1983, the authors have observed six episodes of this disease in five patients, the largest series reported to date. It is predominantly a disease of young people without underlying valvular heart disease. Characteristic clinical features include a high frequency of congestive heart failure and nephritis and a proclivity for aortic valve involvement, commonly with associated ring abscess, and large vegetations. Genitourinary symptoms, arthralgias, and rash are uncommon. Previously undescribed features include involvement of all four valves simultaneously, recurrence on an aortic valve prosthesis, and a high frequency of terminal complement deficiencies. Precipitous hemodynamic deterioration despite appropriate therapy is not uncommon, and overall mortality rate remains an alarming 19%.

Electrophysiologic effects of intranasal cocaine

Abstract In conclusion, intranasal cocaine, 2 mg/kg, induced no change in electrocardiographic intervals or a variety of electrophysiologic variables.

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.

Effects of intravenous ethanol on diameter of epicardial coronary arteries

T here is controversy concerning the effects of ethanol on the coronary vasculature. In animals, ethanol causes inte;lse coronary arterial vasoconstriction.‘,2 In contrast, in man, intracoronary ethanol increases coronary blood flow without changing epicardial coronary arterial dimensions, presumably by dilating the small resistance vessels.3 Because of these conflicting results, we performed this study to assess the influence of intravenous ethanol on heart rate, systemic arterial pressure, and epicardial coronary arterial dimensions in humans. . . . We studied 16 patients (13 men and 3 women, aged 37 to 67 years) undergoing cardiac catheterization for the evaluation of chest pain. The protocol was approved by the Human Subjects Review Committee of the University of Texas Southwestern Medical Center, and all patients gave written, informed consent. No subject had a previous or ongoing problem with alcohol abuse. Antianginal medications were discontinued for >12 hours before the study; no patient smoked for >3 hours before study. All patients were studied in the fasting state after premeditation with oral diazepam 5 to 10 mg. An 8Fr sheath was inserted percutaneously in the femoral artery, through which a Judkins catheter was advanced to the ostium of the left coronary artery. Systemic arterial pressure was measured through the catheter, and heart rate was determined electrocardiographically. The heart rate-systolic arterial pressure product was used as an estimate of myocardial oxygen demand.4 An initial cineangiogram was performed to exclude narrowing of the left main coronary artery. Provided that

Use of the left ventricular peak systolic pressure/end-systolic volume ratio to predict symptomatic improvement with valve replacement in patients with aortic regurgitation and enlarged end-systolic volume

OBJECTIVES This study was designed to assess the left ventricular peak systolic pressure/end-systolic volume (PSP/ESV) ratio in predicting symptomatic improvement with valve replacement in patients with aortic regurgitation and enlarged left ventricular volume. BACKGROUND Patients with aortic regurgitation and a left ventricular end-systolic volume < or = 60 ml/m2 show symptomatic improvement with valve replacement, whereas the response of those with an enlarged end-systolic volume > 60 ml/m2 is mixed. Most benefit, but some do not. Valve replacement appears to help those whose end-systolic volume is enlarged because of excessive left ventricular afterload but appears to have little or no effect in those whose end-systolic volume is enlarged because of depressed left ventricular contractility. METHODS We studied 27 patients (21 men and 6 women aged 18 to 72 years) with moderate or severe aortic regurgitation, no other cardiovascular abnormalities and left ventricular end-systolic volume > 60 ml/m2. In this group we assessed the ability of preoperative variables routinely measured at cardiac catheterization to predict symptomatic improvement with valve replacement. RESULTS Of the 27 subjects, 1 (4%) died 51 days postoperatively. Six months postoperatively, symptoms had lessened in 17 patients (63%), were unchanged in 8 (29%) and had worsened in 1 (4%). By multivariate analysis, the PSP/ESV ratio was the strongest predictor of both functional class 6 months postoperatively (p = 0.026) and change in functional class from before operation to 6 months postoperatively (p = 0.033). By 6 months after valve replacement, all patients with a ratio > or = 1.72 mm Hg/ml per m2 were in functional class I or II; in contrast, of those with a ratio < 1.72 mm Hg/ml per m2, 31% were in functional class III, and 1 (8%) had died. CONCLUSIONS The PSP/ESV ratio may help to predict which patients with aortic regurgitation and enlarged left ventricular end-systolic volume will have symptomatic improvement with valve replacement.