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PURPOSE: Nicotine replacement therapy has become a popular therapy for smokers attempting to stop smoking. Unfortunately, some subjects continue to smoke while receiving it. Since nicotine is believed to be the primary constituent of cigarette smoke responsible for its acute adverse effects on myocardial oxygen supply and demand, concomitant nicotine replacement therapy and smoking theoretically could provoke a marked decrease in myocardial oxygen supply and increase in demand. This study was performed to assess the effects of cigarette smoking with and without concomitant intranasal nicotine spray on: (a) myocardial oxygen demand, (b) coronary arterial dimensions, and (c) the development of acute cardiovascular tolerance. PATIENTS AND METHODS: In 19 smokers referred for cardiac catheterization for the evaluation of chest pain, we assessed the effects of cigarette smoking with and without concomitant intranasal nicotine spray on. (a) heart rate-systolic arterial pressure product lan estimate of myocardial oxygen demand), (b) coronary arterial dimensions (measured with computer-assisted quantitative arteriography), and (c) the development of acute cardiovascular tolerance. RESULTS: Smoking a first cigarette increased rate pressure product (P

Background: Cocaine and ethanol are often abused concomitantly, and this combination may be more lethal than either substance alone. Although previous studies showed that cocaine causes coronary arterial vasoconstriction, the combined effect of cocaine and ethanol on the coronary vasculature in humans is unknown. Thus, we assessed the effects of intranasal cocaine, intravenous ethanol, or a cocaine-ethanol combination on heart rate, systemic arterial pressure, and coronary arterial dimensions in humans. Methods: Thirty-four subjects with chest pain (27 men and seven women, aged 34 to 67 years) who were referred for catheterization received one of the following pharmacologic interventions: (1) intranasal (2 mL) and intravenous (5 mL/kg) saline (n = 8 [group A]); (2) intranasal cocaine (2 mg/kg) and intravenous saline (5 mL/kg) (n = 9 [group B]); (3) intranasal saline (2 mL) and intravenous 10% ethanol (5 mL/kg) (n = 9 [group C]); or (4) intranasal cocaine (2 mg/kg) and intravenous 10% ethanol (5 mL/kg) (n = 8 [group D]). Heart rate, systemic arterial pressure, left coronary arterial dimensions (by computer-assisted quantitative angiography), as well as blood cocaine, ethanol, and cocaine metabolite concentrations were measured before and 30, 60, and 90 minutes after initiation of the intravenous infusions. Results: No hemodynamic or angiographic changes were observed in the group A (saline) subjects. In the group B (cocaine) subjects, the heart rate--systolic arterial pressure product increased by 5% and 10% at 30 and 90 minutes, respectively, and coronary arterial diameter decreased by 14% at these times. In the group C (ethanol) subjects, no hemodynamic changes were noted, but coronary arterial diameters increased by 12%, 11%, and 12% at 30, 60, and 90 minutes, respectively. In the group D (cocaine-ethanol) patients, rate-pressure product increased by 17%, 10%, and 16%, and coronary arterial diameters increased by 7%, 12%, and 13%, at 30, 60, and 90 minutes, respectively. Conclusion: The combination of intranasal cocaine and intravenous ethanol causes an increase in the determinants of myocardial oxygen demand. However, it also causes a concomitant increase in epicardial coronary arterial diameter. (Arch Intern Med. 1995;155:1186-1191)

In patients with acute myocardial infarction, percutaneous transluminal coronary angioplasty (PTCA) may be used (1) to restore antegrade flow in the infarct artery (so called 'primary' PTCA) instead of thrombolytic therapy, (2) to establish antegrade coronary flow after unsuccessful thrombolytic therapy (so called 'rescue' or 'salvage' PTCA), and (3) to reduce the residual infarct artery stenosis after successful thrombolysis. This review examines the prospective, randomized studies that have addressed the use of PTCA for each of these purposes. In selected circumstances, PTCA is a reasonable alternative to thrombolytic therapy in patients with evolving or recent Q-wave myocardial infarction. In those patients with acute myocardial infarction complicated by cardiogenic shock, PTCA may be the preferred treatment. After thrombolytic therapy, the use of PTCA in the absence of spontaneous or provocable ischemia offers no benefit with regard to left ventricular function or survival. in this circumstance, its use is associated with an excessive risk of bleeding, transfusions, and emergent coronary artery bypass surgery when performed within hours of infarction.

PURPOSE: As cocaine abuse has become widespread, catastrophic cocaine-associated cardiovascular events have been noted with increasing frequency. Although these incidents are thought to be caused by drug-induced vasoconstriction and/or arterial thrombosis, the influence of cocaine on the plasma constituents involved in endogenous thrombosis and thrombolysis has not been characterized. PATIENTS AND METHODS: In 22 patients (8 men, 14 women, ages 32 to 62 years) undergoing cardiac catheterization, blood samples were procured before and 15 minutes after the administration intranasal saline (n = 8, controls) or cocaine, 2 mg/kg (n = 14), and the plasma concentrations of fibrinogen, plasminogen, and lipoprotein(a), as well as tissue plasminogen activator activity and plasminogen activator inhibitor (PAI-1) activity, were measured. RESULTS: No variable changed with the use of intranasal saline, whereas the use of cocaine resulted in an increase in PAI-I activity (0.48 + 0.06 (mean + SD] nmol\L at baseline, 0.53 + 0.05 nmol/L after cocaine, P = 0.011). CONCLUSION: Intranasal cocaine administration is associated with an increase in plasma PAI-1 activity. This may be important in recreational users of cocaine who experience vascular thrombosis.

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 [+ or -] 0.7 versus 1.5 [+ or -] 1.0 [mean + or -] 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). Eight-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 [+ or -] 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.

Cocaine use has been associated with a number of cardiovascular complications, including angina pectoris, myocardial infarction and sudden cardiac death.[1-4] Previous studies in humans have shown that cocaine causes epicardial coronary vasoconstriction, which is mediated, at least in part, by [alpha]-adrenergic stimulation.[5-10] Studies in experimental animals have suggested that cocaine may also cause vasoconstriction by altering calcium transport in vascular smooth muscle,[11] and this can be attenuated by calcium channel blockade. The present study was performed to assess the effect of verapamil, a calcium antagonist, on cocaine-induced coronary vaso-constriction in humans.

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 [is less than or equal to]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 [+ or -] 19 [mean [+ or -] SD] vs 59 [+ or -] 15 ml/[m.sup.2], p 0.50. (Am J Cardiol 1994;73:65-69)

The hydrogen inhalation technique is easily performed and exquisitely sensitive for detecting intracardiac left-to-right shunting. Previous studies of this technique relied heavily on data from infants and children, and the distinction between 'normal' and 'abnormal' was imprecise and somewhat arbitrary. The present study was done to assess the results of hydrogen inhalation in adults with and without intracardiac left-to-right shunting. In 45 adult subjects (15 men, 30 women, aged 18 to 72 years) (18 without and 27 with intracardiac left-to-right shunting), the elapsed time from hydrogen inhalation to its appearance in the pulmonary artery was measured. The 18 patients without shunting had an appearance time of 12 [+ or -] 3 (mean [+ or -] SD) seconds, and it was [greater than or equal to]9 seconds in all. In contrast, the 27 subjects with shunting had an appearance time of 1.5 [+ or -] 0.7 second, with only 1 of 27 being [greater than or equal to]3 seconds. There was no relation between the magnitude of left-to-right shunting and the hydrogen appearance time. Thus, the hydrogen inhalation technique easily and reliably separates adult subjects with and without intracardiac left-to-right shunting, with no overlap between the 2 groups.

In survivors of acute myocardial infarction (AMI), the restoration of anterograde flow in the infarct artery, even if accomplished beyond the time for myocardial salvage, may reduce the frequency of subsequent arrhythmic events and sudden death. Twelve subjects (8 men and 4 women, aged 39 to 69 years) with a first AMI, signal-averaged electrocardiographic late potentials, and an occluded infarct artery were prospectively identified. Seven (group I) had successful coronary angioplasty 6 to 15 days after AMI, and 5 (group II) were managed conservatively. Follow-up signal-averaged electrocardiography was performed 3 to 7 months later. From baseline to follow-up, the 7 group I subjects had a significant change in QRS duration (117 [+ or -] 13 [mean + SD] to 102 [+ or -] 10 ms), root-mean-square voltage (10.4 [+ or -] 4.7 to 31.0 [+ or -] 7.6 [Micro]V), and low-amplitude signal duration (47.5 [+ or -] 8.5 to 32.4 [+ or -] 5.2 ms) (p [less than or equal to]0.05 for all 3 variables). No group I patient had a late potential at follow-up. In contrast, the 5 group II patients showed no change in QRS duration or low-amplitude signal duration from baseline to follow-up, and all 5 had a late potential at follow-up. At follow-up, the root-mean-square voltage was significantly greater and the low-amplitude signal and QRS durations significantly less in group I than in group II (p (Am J Cardiol 1992;70:1515-1519)

To examine the effects of [BETA]-adrenergic blockade on neurohormonal activation in patients with congestive heart failure, 15 men had assessments of hemodynamics and supine peripheral renin and norepinephrine levels before and after 3 months of oral therapy with bucindolol, a nonselective [beta] antagonist. At baseline, plasma renin activity did not correlate with any hemodynamic parameter. However, norepinephrine levels had a weak correlation with left ventricular end-diastolic pressure (r = 0.74, p, Congestive heart failure (CHF) is a condition resulting from the inability of the heart to pump sufficient blood to the body. There are numerous neuroendocrine alterations that occur in CHF, some of which represent the body's attempt to compensate for the insufficient blood supply. However, in some cases, these neuroendocrine changes can actually work against normalizing the imbalance. To investigate the effects of one therapeutic strategy, the administration of beta blockers (agents that inhibit the actions of norepinephrine in causing the constriction of blood vessels) on the elevated neuroendocrine levels seen in CHF, 15 men with CHF were studied before and during three months of oral administration of the nonselective (acting on all blood vessels) beta blocker bucindolol. Prior to drug treatment, elevated renin activity (an enzyme involved in the synthesis of angiotensin, a hormone causing elevated blood pressure) was not correlated with any index of cardiovascular function; norepinephrine levels, on the other hand, did show a correlation with several of these indices. During treatment, renin levels decreased, while norepinephrine levels were unchanged. Heart rate decreased in spite of the lack of alteration in norepinephrine levels, suggesting that bucindolol was, in fact, blocking the receptors. In individual patients, neither changes in renin nor norepinephrine levels predicted improvement in cardiovascular status. These results are consistent with the interpretation that beta blockade by bucindolol reduces neurohormonal activation in CHF. (Consumer Summary produced by Reliance Medical Information, Inc.)

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 [+ or -] 13 [mean [+ or -] 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 [+ or -] 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. (Am J Cardiol 1994;73:S68-570)

PURPOSE: Although labetalol is sometimes given to patients with cocaine-associated chest pain, its influence on cocaine-induced coronary vasoconstriction is unknown. PATIENTS AND METHODS: In 15 patients (7 men, 8 women, aged 40 to 79 years) undergoing catheterization for chest pain, heart rate, mean arterial pressure, and coronary arterial area (by computer-assisted quantitative angiography) were measured (1) at baseline, (2) 15 minutes after intranasal cocaine, 2 mg/kg, then (3) 5 minutes after intravenous saline (n = 6) or labetalol, 0.25 mg/kg (n = 9). RESULTS: Of 40 coronary arterial segments analyzed, cocaine induced a 13% [+ or -] 10% (mean [+ or -] standard deviation) decrease in coronary arterial area in 32. Subsequently, no variable changed after saline administration. Although labetalol reduced mean arterial pressure (117 [+ or -] 14 mm Hg after cocaine, 110 [+ or -] 11 mm Hg after labetalol; p < 0.05), it induced no change in the coronary arterial area (3.47 [+ or -] 1.37 [mm.sup.2] after cocaine, 3.37 [+ or -] 1.32 [mm.sup.2] after labetalol; p = NS). CONCLUSION: Labetalol reverses the cocaine-induced rise in mean arterial pressure, but does not alleviate cocaine-induced coronary vasoconstriction.

In early reports, coronary arteriography in patients with left main (LM) coronary artery disease (CAD) had a substantial risk, but recent reports suggest that arteriography in these subjects is now associated with a low mortality. The present study was performed to examine the periprocedure mortality in patients with LMCAD undergoing catheterization, to compare the periprocedure mortality in these patients with that in subjects with less CAD and to identify the variables associated with pericatheterization mortality in this patient cohort. Of 4,009 patients undergoing elective coronary arteriography from 1978 to 1992, 176 had LMCAD. Of the 10 deaths during or within 24 hours of cathetezation, 5 occured in these 176 subjects. This periprocedure mortality of 2.8% in patients with LMCAD was >20 times that of those without LMCAD (0.13%). In comparison with the 171 patients with LMCAD who survived, the 5 who died were older (67[+ or -]8 vs 58[+ or -]12 years), and had more severe LMCAD (92[+ or -]10% vs 72 :E 16%) and a lower cardiac index (1.9[+ or -]0.4 vs 2.6[+ or -]0.7 liters/min/[m.sup.2]) (p (Am J Cardiol 1992;70:1388-1390)

Previous studies showed that long-term morbidity and mortality after acute myocardial infarction (AMI) are influenced by the presence or absence of anterograde flow in the infarct artery. In comparison with patients with anterograde flow, those whose infarct artery remains occluded are more likely to have unstable angina, recurrent AMI, congestive heart failure and sudden death. This study was performed to assess the influence of collateral filling of the infarct artery on long-term morbidity and mortality in surviving patients of initial AMI in whom the infarct artery was occluded. Over a 12.5-year period, 146 subject (108 men and 38 women, aged 25 to 76 years) with AMI, no anterograde flow in the infarct artery, and no disease of other coronary arteries were medically treated and followed for 42 [+ or -] 28 (mean [+ or -] standard deviation) months. Of these subjects, 120 had angiographic evidence of collateral filling of the infarct artery (group I), whereas the remaining 26 did not (group II). The groups were similar in age, sex, cardioactive medications, left ventricular performance and infarct artery. They were also similar in incidence of unstable angina (19% of group I, 31% of group II; p = not significant [NS]), recurrent AMI (12% of group I, 8% of group II; p = NS), congestive heart failure (16% of group I, 12% of group II; p = NS) and cardiac death (16% of group I, 19% of group II; p = NS). Thus, angiographic evidence of collateral filling of the infarct artery in surviving patients of AMI exerts no demonstrable influence (beneficial or detrimental) on long-term morbidity or mortality.