Trapped free radicals and electrons in organic glasses.

Free radicals, hydrogen atoms, and electrons produced in rigid organic glasses at sufficiently low temperatures have lifetimes of minutes to years. They can be studied by their electron spin resonance spectra and, in the case of electrons, by their optical spectra, recombination luminescence, and electrical conductivity. The decay kinetics of these reaction intermediates serve to distinguish those trapped as geminate pairs or in spurs of high concentration from those formed with random distributions. Electron spin resonance studies of relaxation times and of the spectra of radical pairs provide further evidence on geometrical distributions. The decay rates of radicals combining with reactive geminate partners are dependent on the size and shape of the radical, the temperature, and the nature of the matrix. Decay is much slower in deuterated matrices than in protiated matrices. The factors that control the physical trapping of electrons in organic glasses are under intensive investigation. There is evidence that many electrons trapped relatively weakly during irradiations at 4 degrees K deepen their traps by orientation of dipoles when the matrix is warmed; that most electrons are trapped in the field of the geminate positive ion; that in some matrices the traps have a bound excited state to which the electron can be promoted without detrapping; and that trapped electrons can tunnel to solute molecules with a higher electron affinity than the trap depth.

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.

Spontaneous alterations in coronary blood flow velocity before and after coronary angioplasty in patients with severe angina.

Cyclic coronary artery flow variations with a spontaneous decline in coronary blood flow to very low levels have been documented in stenosed canine coronary arteries with endothelial injury. These flow variations are associated with transient platelet aggregation and dislodgment and the release of selected mediators, including thromboxane A2 and serotonin. However, cyclic or spontaneous flow variations have not been demonstrated in stenosed coronary arteries in humans. In this study, the hypothesis was tested that spontaneous coronary blood flow velocity variations occur in some patients with stenosed coronary arteries before or after coronary artery angioplasty. Thus, 13 patients with severe and limiting angina underwent intracoronary pulsed Doppler velocimetry of their dilated artery immediately before and after percutaneous transluminal coronary angioplasty, whereas 9 control patients underwent velocimetry of an angiographically normal coronary artery. A 3F catheter with a 20 MHz Doppler crystal was positioned to achieve a maximal stable signal, and the flow velocity signal was recorded continuously for 20 min. Spontaneous flow velocity variations (greater than or equal to 38% change in Doppler frequency shift with wide morphologic changes) were present in 3 of the 13 patients tested. Spontaneous flow velocity variations occurred before angioplasty in one patient, after angioplasty in another and both before and after angioplasty in a third. In addition, 2 of the 13 patients, 1 with spontaneous coronary artery flow velocity variations before angioplasty, had frank vasospasm in an adjacent area just distal to the area of coronary dilation immediately after balloon inflation. These data establish that spontaneous coronary artery flow velocity variations occur in some patients with severe and limiting angina before and after coronary angioplasty. These variations may be related to platelet aggregation or coronary vasoconstriction, or both, at sites of endothelial injury resulting from plaque fissuring or ulceration and endothelial and medial injury occurring during coronary angioplasty.

Intravascular ultrasound imaging of saphenous vein grafts in vitro: comparison with histologic and quantitative angiographic findings.

The ubiquity of coronary artery disease and the resultant widespread use of saphenous veins for coronary artery bypass surgery has stimulated considerable interest in the morphologic and pathophysiologic alterations these vessels undergo after implantation. This study was undertaken to determine the ability of intravascular ultrasound to identify and characterize abnormalities in saphenous vein grafts. Ten saphenous vein grafts excised at autopsy and nine saphenous vein segments harvested during coronary artery bypass surgery were examined with intravascular ultrasound imaging, quantitative coronary angiographic techniques and histologic analysis. Intravascular ultrasound lumen measurements were strongly correlated with quantitative coronary arteriographic measurements (r 0.91, SEE 0.5 mm). Wall thickness was significantly greater in the vein grafts after long-term implantation than in the freshly harvested veins (average thickness 1.4 +/- 0.5 vs. 0.7 +/- 0.2 mm, p less than 0.007); this finding correlated histologically with vein wall fibrosis. There was good correlation between ultrasound imaging and histologic analysis, with the ability to distinguish among normal intima, intimal hyperplasia, vein wall fibrosis and atheromatous plaque. Thus, this preliminary study demonstrates the ability of intravascular ultrasound to provide real-time cross-sectional images of saphenous veins and morphologic characterization of their walls. This modality may have important clinical applications, including the ability to detect serial changes in vein graft intimal hyperplasia and atherosclerosis.

Hemodynamic effects of intranasal cocaine in humans.

Intranasal cocaine, 2 to 3 mg/kg body weight, is a commonly used local anesthetic for rhinolaryngologic procedures, and many persons who abuse it ingest a similar amount. Previous studies in humans showed that this dose of cocaine causes coronary vasoconstriction, and studies in animals showed that larger amounts given intravenously diminish myocardial performance. This study assessed the hemodynamic effects of intranasal cocaine, 2 mg/kg, in humans. In 15 patients (8 men and 7 women, aged 30 to 70 years) referred for cardiac catheterization, heart rate, systemic arterial pressure, cardiac index, pulmonary capillary wedge and pulmonary artery pressures and left ventricular pressure and its first derivative (dP/dt) were measured before and 15, 30 and 45 min after intranasal administration of saline solution (n = 5) or cocaine, 2 mg/kg (n = 10). No variable changed with saline solution. In those given cocaine, there was an increase in heart rate (17 +/- 16%, mean +/- SD), mean systemic arterial pressure (8 +/- 7%), cardiac index (18 +/- 18%) and positive and negative dP/dt (18 +/- 20% and 15 +/- 22%, respectively) (p less than 0.05 for all). Thus, intranasal cocaine in a dose similar to that used medicinally or "recreationally" does not exert a deleterious influence on intracardiac pressures and left ventricular performance.

Cocaine-induced alterations in prostaglandin production in rabbit aorta.

To determine if alterations in endothelial prostaglandin production occur after long-term cocaine use, 26 New Zealand White rabbits were randomized to a low fat diet with (n = 12) or without (n = 14) daily intravenous cocaine (2 mg/kg body weight). Rabbits were killed at 6 or 12 weeks. Segments of aorta were examined in blinded manner for histologic changes. Additional slices were incubated in oxygenated Krebs buffer and release of 6-keto-prostaglandin F1 alpha, thromboxane B2 and prostaglandin E2 was assayed by radioimmunoassay. Minimal intimal histologic changes were seen in the aorta of three cocaine-treated rabbits. At 12 weeks 6-keto-prostaglandin F1 alpha was increased in the cocaine group (p = 0.063) as compared with levels in the control group. When rabbits killed at 6 and 12 weeks were considered together, increases in thromboxane B2 (p = 0.044) and a trend to increased prostaglandin E2 (p = 0.083) were seen in the cocaine group. The ratio of thromboxane B2 to 6-keto-prostaglandin F1 alpha was increased in the cocaine group compared with that in the control group (p less than 0.02). These data suggest that an increase in prostaglandin production occurs in the vascular endothelium of rabbits ingesting cocaine before gross histologic changes are evident. In addition, thromboxane B2 increases disproportionately with respect to 6-keto-prostaglandin F1 alpha, suggesting that a milieu for thrombosis may exist in users of cocaine.

Influence of cocaine, ethanol, or their combination on epicardial coronary arterial dimensions in humans.

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.

Influence of labetalol on cocaine-induced coronary vasoconstriction in humans.

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% +/- 10% (mean +/- standard deviation) decrease in coronary arterial area in 32. Subsequently, no variable changed after saline administration. Although labetalol reduced mean arterial pressure (117 +/- 14 mm Hg after cocaine, 110 +/- 11 mm Hg after labetalol; p < 0.05), it induced no change in the coronary arterial area (3.47 +/- 1.37 mm2 after cocaine, 3.37 +/- 1.32 mm2 after labetalol; p = NS). CONCLUSION: Labetalol reverses the cocaine-induced rise in mean arterial pressure, but does not alleviate cocaine-induced coronary vasoconstriction.

Coronary angioplasty in the patient with acute myocardial infarction.

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.

Influence of intranasal cocaine on plasma constituents associated with endogenous thrombosis and thrombolysis.

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 of 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-1 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.

Intranasal nicotine spray does not augment the adverse effects of cigarette smoking on myocardial oxygen demand or coronary arterial dimensions.

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 (an 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 < 0.001) and decreased coronary arterial dimensions (P < 0.0001). Subsequently, neither variable was altered by intranasal nicotine spray or a second cigarette. Despite a substantial increase in serum nicotine concentration with nicotine spray and smoking, acute cardiovascular tolerance appears to develop. CONCLUSIONS: Cigarette smoking causes an increase in myocardial oxygen demand and concomitant coronary arterial vasoconstriction. However, further increases in the serum nicotine concentration do not cause a greater increase in demand or decrease in coronary arterial dimensions. These data suggest that humans acutely develop tolerance to an increasing nicotine concentration, thereby helping to explain the apparent lack of a potential synergistic adverse effect associated with continued smoking during nicotine replacement therapy.

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.

Hydrogen inhalation for detecting intracardiac left-to-right shunting in adults.

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 +/- 3 (mean +/- SD) seconds, and it was > or = 9 seconds in all. In contrast, the 27 subjects with shunting had an appearance time of 1.5 +/- 0.7 second, with only 1 of 27 being > or = 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.

Markedly increased periprocedure mortality of cardiac catheterization in patients with severe narrowing of the left main coronary artery.

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 catheterization, 5 occurred 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 +/- 8 vs 58 +/- 12 years), and had more severe LMCAD (92 +/- 10% vs 72 +/- 16%) and a lower cardiac index (1.9 +/- 0.4 vs 2.6 +/- 0.7 liters/min/m2) (p < 0.05 for all 3 variables). Thus, even in the 1980s and early 1990s, patients with LMCAD have a high pericatheterization mortality, especially those who are older and have severe LMCAD.

Influence of collateral filling of the occluded infarct-related coronary artery on prognosis after acute myocardial infarction.

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 subjects (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 +/- 28 (mean +/- 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.

Effects of the intracoronary infusion of cocaine on coronary arterial dimensions and blood flow in humans.

This study was done to assess the influence of large concentrations of cocaine (infused into the left coronary artery) on coronary arterial dimensions and blood flow in humans. In 20 subjects undergoing cardiac catheterization, incrementally increasing doses of (1) saline solution (n = 10, controls) or (2) cocaine hydrochloride (n = 10) were infused into the left coronary artery, and the effects on heart rate, systemic arterial pressure, coronary sinus blood flow, and coronary arterial dimensions were measured. Saline solution induced no change in any variable. With the infusion of cocaine, there was an incremental increase in its concentration in the systemic (femoral arterial) and coronary (coronary sinus) circulations (maximal concentrations, 0.14 +/- 0.06 [mean+/-SD] and 3.50 +/- 0.70 mg/L, respectively). At the maximal cocaine infusion rate, heart rate and diastolic arterial pressure increased slightly, but coronary sinus blood flow and the dimensions of nondiseased and diseased coronary arterial segments did not change. Thus, intracoronary infusion of cocaine in an amount sufficient to achieve a high concentration in the coronary circulation does not induce epicardial coronary arterial vasoconstriction or alter blood flow.

Quantitation of cardiac output with velocity-encoded, phase-difference magnetic resonance imaging.

Velocity-encoded, phase-difference magnetic resonance imaging (MRI) previously has been used to measure flow in the aorta, as well as in the pulmonary, carotid, and renal arteries, but these measurements have not been validated against currently accepted invasive techniques. To determine the accuracy of velocity-encoded, phase-difference MRI measurements of cardiac output, 23 subjects (11 men and 12 women, aged 15 to 72 years) underwent velocity-encoded, phase-difference MRI measurements of cardiac output in the proximal aorta, followed immediately by cardiac catheterization, with measurement of cardiac output by the Fick principle and by thermodilution. For MRI, Fick, and thermodilution measurements, stroke volume was calculated by dividing cardiac output by heart rate. The magnetic resonance images were acquired in 1 to 3 minutes. For all patients, the agreement between measurements of stroke volume was 3 +/- 9 ml for MRI and Fick, -3 +/- 11 ml for MRI and thermodilution, and 0 +/- 8 ml for MRI and the average of Fick and thermodilution. Compared with standard invasive measurements, velocity-encoded, phase-difference MRI can accurately and rapidly determine cardiac output.

Influence of metoprolol on heart rate variability in survivors of remote myocardial infarction.

We assessed the influence of metoprolol on heart rate variability in survivors of remote myocardial infarction. In 43 survivors of myocardial infarction 12 to 18 months previously (26 men and 17 women, aged 38 to 69 years), two 24-hour ambulatory electrocardiograms were recorded 2 weeks apart. In patients in group A (n=28), who had taken metoprolol for the previous year, the drug was discontinued for 2 weeks, after which the first recording was done. The second recording was done 2 weeks after metoprolol was resumed. In patients in group B (n=15), who had not taken metoprolol for the previous year, it continued to be withheld, and two 24-hour recordings were done 2 weeks apart. In group A, metoprolol increased the time domain variables indicative of enhanced vagal tone; root-mean-square successive difference in normal RR (NN) intervals was 20 +/- 11 ms (mean +/- SD) without and 24 +/- 9 ms with metoprolol (p<0.05), and the proportion of NN that differ by >50 ms (pNN50%) was 3.6 +/- 6.0 without and 5.5 +/- 6.0 with metoprolol (p<0.05). In the frequency domain, the logarithms of the 24-hour very low frequency and the 24-hour high-frequency power (reflecting parasympathetic activity) were increased (5.12 +/- 1.03 and 4.48 +/- 1.51, respectively, without metoprolol; 5.32 +/- 0.99 and 4.83 +/- 1.24, respectively, with metoprolol, p <0.05 for both). Thus, in survivors of remote myocardial infarction, metoprolol enhances parasympathetic cardiac activity in the time and frequency domain measures of heart rate variability.

Incidence and treatment of elastic recoil occurring in the 15 minutes following successful percutaneous transluminal coronary angioplasty.

This study was performed (1) to assess the incidence and magnitude of elastic recoil occurring within 15 minutes of successful coronary angioplasty, and (2) to determine the effect of subsequent additional balloon inflations on coronary luminal diameter in patients displaying substantial recoil. The coronary angiograms of 50 consecutive patients who underwent a successful percutaneous transluminal coronary angioplasty were analyzed using computer-assisted quantitative analysis. The patients were divided into 2 groups based on the magnitude of early elastic recoil following angioplasty: those with < or = 10% (group I, n = 30) and those with > 10% (group II, n = 20) loss of minimal luminal diameter as assessed by comparing the angiogram obtained immediately after successful angioplasty with that obtained 15 minutes later. The 2 groups were similar in clinical, angiographic, and procedural characteristics. Of the 20 group II subjects, 18 (90%) underwent repeat balloon dilatations, and 2 patients (10%) had no further intervention. After additional balloon inflations were performed in these 18 patients, 16 (90%) had a final result with < 10% loss of minimal luminal diameter 15 minutes later. In conclusion, elastic recoil 15 minutes after apparently successful percutaneous transluminal coronary angioplasty is frequent, occurring in approximately 40% of patients, and is attenuated in 90% of subjects with additional balloon inflations. The resultant larger lumen diameter may exert a salutary effect on long-term outcome.

Utility of the 12-lead electrocardiogram in identifying underlying coronary artery disease in patients with depressed left ventricular systolic function.

We assessed the utility of the 12-lead electrocardiogram (ECG) in identifying severe coronary artery disease (CAD) in patients with depressed left ventricular (LV) systolic function. In 336 patients referred for cardiac catheterization with LV ejection fractions < 0.50, we compared the 12-lead ECG of those with and without CAD by multivariate analysis. The sensitivities, specificities, and positive and negative predictive values of all dichotomous electrocardiographic variables for identifying the presence of severe CAD were determined. In comparison to subjects with CAD, those without disease were more likely to exhibit left-axis deviation (p = 0.01), left bundle branch block (p < 0.001), or LV hypertrophy (p < 0.001), and less likely to exhibit pathologic inferior Q waves (p < 0.001). The presence of anterior or any Q waves was similar between the groups. The presence of any diagnostic Q wave had a positive predictive value of 92%, sensitivity of 57%, and specificity of 80% for identifying severe CAD. In patients with LV systolic dysfunction, the 12-lead ECG is insensitive and nonspecific for identifying those with concomitant severe CAD.