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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

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.

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.