Myocardial protection during transient coronary artery occlusion in man: beneficial effects of regional beta-adrenergic blockade

The goal of this study was to verify whether myocardial protection could be achieved via the intracoronary administration of propranolol in patients undergoing percutaneous transluminal coronary angioplasty (PTCA). Accordingly, 21 patients undergoing PTCA were randomly assigned to receive either intracoronary placebo (group A, n = 10) or intracoronary propranolol (group B, n = 11). Three balloon inflations (i.e., coronary artery occlusions) were performed in each patient. Inflations I and II (maximum duration 60 sec) served as control occlusions. Inflation III (maximum duration 120 sec) was performed either after intracoronary administration of saline (2 ml) or propranolol (1.1 +/- 0.2 mg). The following electrocardiographic index of myocardial ischemic injury were measured: (1) time to development of ST segment elevation equal to 0.1 mV and (2) magnitude of ST segment elevation after 60 sec of coronary artery occlusion. Both indexes did not differ significantly between the groups during inflations I and II. In group A the time to development of ST segment elevation of 0.1 mV remained unchanged between the second and third occlusions (25 +/- 5 and 26 +/- 4 sec during inflations II and III, respectively). In group B subselective injection of propranolol into the affected coronary artery significantly prolonged the time to ST segment elevation of 0.1 mV from 19 +/- 4 sec (inflation II) to 53 +/- 9 sec (inflation III; p less than .001). Administration of placebo did not change the magnitude of ST segment elevation 60 sec after coronary artery occlusion between the second and third occlusion in group A (0.16 +/- 0.02 and 0.18 +/- 0.03 mV, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

Value of the intracoronary electrocardiogram to monitor myocardial ischemia during percutaneous transluminal coronary angioplasty

To enhance detection of ischemia during percutaneous transluminal coronary angioplasty (PTCA), unipolar intracoronary electrocardiograms (ECGs) were recorded during PTCA in 25 patients from the tips of guidewires positioned distal to stenoses being dilated. Surface electrocardiographic leads chosen to reflect likely areas of reversible ischemia during PTCA were recorded simultaneously. In 21 of 29 stenoses dilated (72%), ST segment elevation and/or T wave peaking in intracoronary ECG appeared during balloon inflation and disappeared after deflation, accompanied by transient angina on 19 occasions. Two patients had transient ST segment elevation in intracoronary ECGs during PTCA without associated angina. ST changes in the surface ECG during PTCA were seen on only nine occasions (31%), always accompanied by ST segment elevation in the intracoronary ECG that appeared earlier and was of much greater magnitude. Five patients with prior myocardial infarction and aneurysm formation had fixed ST segment elevation in the intracoronary ECG unrelated to balloon inflation. Myocardial ischemia during PTCA can be detected easily with intracoronary ECGs and with greater sensitivity than that of the surface ECG. Furthermore, intracoronary ECGs may help to clarify the nature of chest pain during balloon inflation or during suspected complications.     

The value of the intracoronary electrogram for the early detection of myocardial ischaemia during coronary angioplasty.

The clinical value of intracoronary electrography for the detection of myocardia ischaemia was assessed during coronary angioplasty and compared to a standard technique of surface ECG monitoring. In 73 patients undergoing single lesion angioplasty, an intracoronary electrogram and four representative surface ECG leads were obtained. During angioplasty of the left anterior descending artery leads, I, V3, V5, V6 were recorded. For the circumflex artery leads I, aVL, aVF, V6, and for the right coronary artery leads II, III, aVF, V6 were monitored. Eight patients were excluded due to transient intraventricular conduction disturbances during balloon inflation; 65 patients remained for further analysis. Out of a total of 154 balloon inflations (35 in the circumflex, 71 in the left anterior descending and 48 in the right coronary artery), the percentage that produced a greater than or equal to 1 mm ST segment elevation, the time to the appearance of a greater than or equal to 1 mm ST segment elevation and the maximal ST segment elevation were recorded. During inflations in the circumflex artery, the respective values of these three parameters were 20%, 22.6 +/- 11.5 s and 0.37 +/- 0.80 mm in V6, the most sensitive surface lead, versus 70% (P less than 0.001), 14.4 +/- 9.6 s (P less than 0.01) and 5.82 +/- 6.35 mm (P less than 0.0001) on the intracoronary electrogram.(ABSTRACT TRUNCATED AT 250 WORDS)     

Myocardial protection during percutaneous transluminal coronary angioplasty: effects of trimetazidine.

Trimetazidine (TMZ) has recently been shown to improve anginal symptoms without altering haemodynamic variables. A randomized, double-blind, placebo-controlled study was conducted in 20 patients to study the effects of TMZ on the severity of myocardial ischaemia during PTCA of the left anterior descending coronary artery. Five minutes after a first successful dilatation (D0), a control balloon inflation (D1) was performed until onset of ischaemic signs on both the intracoronary (i.c.) and precordial ECG. Two minutes later, patients received either TMZ 6 mg or placebo i.c. Another inflation (D2) was performed 5 min after D1. No differences were found between the two groups regarding responses in heart rate, systemic and i.c. pressures during the study. TMZ decreased the maximum ST-segment shift at D2 compared with D1 (0.8 +/- 0.1 vs 1.4 +/- 0.3 mV, P = 0.023) and delayed its onset (46 +/- 4 vs 36 +/- 5 s, P = 0.024). TMZ also decreased maximum T-wave changes (1.06 +/- 0.24 vs 2.19 +/- 0.3 mV, P = 0.001), and significantly reduced the area under the curve (mv s-1) of the i.c. ST-segment and T-wave changes during balloon inflation (P = 0.042 and P = 0.009 respectively). The placebo had no effect on these parameters. These results support the hypothesis that trimetazidine has a direct anti-ischaemic effect on human myocardial cells.     

Coronary vasodilation by nitrates is not mediated by the prostaglandin system: a quantitative cineangiographic study

The possible role of prostaglandins in mediating large coronary artery vasodilation by nitrates was investigated by quantitative magnification coronary angiography. The effects of aspirin (1 g systemically and 100 mg intracoronary) in preventing large coronary artery vasodilation induced by intracoronary isosorbide dinitrate was investigated in 16 patients. Of these, 5 received 0.3 mg (Group 1A) and 11 received 3 mg (Group 1B) intracoronary isosorbide dinitrate, before and 15 minutes after aspirin. Relative to control, 0.3 mg isosorbide dinitrate induced a 19 +/- 9% (mean +/- SD) (p less than 0.01) and 19.5 +/- 11% (p less than 0.01) increase in coronary diameter before and after aspirin, respectively (p = NS). Changes after 3 mg isosorbide were 23 +/- 12% (p less than 0.01) and 26.5 +/- 14% (p less than 0.01), respectively, before and after aspirin (p = NS). In 10 additional patients (Group 2), the effect of the same dose of aspirin on rest coronary artery tone was assessed: changes relative to control were 0.9 +/- 5.5% (p = NS) minutes after aspirin. The intracoronary administration of 3 mg isosorbide dinitrate produced a 24.7 +/- 11% increase in coronary diameter (p = NS versus pre- and postaspirin isosorbide in Group 1B). Urinary 6-ketoprostaglandin-F1 alpha values in urine samples collected in the 8 hours before and the 8 hours after the study in five patients in Group 1B and five patients of Group 2, revealed a 36 +/- 14% (mean +/- SD) reduction in excretion of prostacyclin (p less than 0.01). These data rule out a role for prostaglandins both in mediating dilation of large coronary arteries by nitrates and in affecting their vascular tone at rest.     

Hemodynamic evaluation of isosorbide dinitrate in alcoholic cirrhosis. Pharmacokinetic-hemodynamic interactions

Isosorbide dinitrate, a long-acting organic nitrate, has been shown to decrease portal pressure in the experimental animal and humans. We conducted a double-blind randomized hemodynamic evaluation of the effects of placebo and 10 mg and 20 mg isosorbide dinitrate in stable individuals with alcoholic cirrhosis. Baseline values for all three groups were similar. Isosorbide dinitrate resulted in a peak reduction of the hepatic venous gradient of 24.7% +/- 3.0%, with significantly decreased values 4 h after the administration of the 20-mg dose. A reduction of arterial pressure and cardiac index (peak decrease of 25.7% +/- 1.5%) was well tolerated by 13 of 15 patients. Changes in mean arterial pressure were not predictive of modifications in the hepatic vein wedge pressure. There was no relation between the area under the plasma isosorbide dinitrate concentration curve and hemodynamic changes. Levels of isosorbide-5-mononitrate, a vasoactive metabolite, were detectable for an 8-h period. Isosorbide dinitrate significantly reduced portal pressure in stable cirrhotics, in association with systemic hemodynamic changes. Thus, titration of isosorbide dinitrate is required to maximize hemodynamic benefits in individual patients. As the decrease in portal pressure is more predictable than the effect of previously tested pharmacologic agents, isosorbide dinitrate should be evaluated for its efficacy in the management of portal hypertension.     

Intracoronary electrocardiogram during coronary angioplasty.

This prospective study examines the data derived from the intracoronary electrocardiogram (ECG) (derived from the coronary guide wire) compared with that from four standard surface leads (I, II, III, and V2) in documenting myocardial ischemia during coronary angioplasty. Intracoronary and surface ECGs were simultaneously recorded in 300 consecutive patients (mean age 59 +/- 10; range 33 to 80 years; 246 males [82%] during coronary angioplasty in 368 lesions (167 left anterior descending [46%], 85 left circumflex [23%], 107 right coronary arteries [29%], and nine bypass grafts [2%]), before balloon inflation, at 1 minute of inflation, and at the end of the procedure. ST segment changes (greater than 0.1 mV) were observed in the intracoronary ECG in 306 lesions (83%) (151 left anterior descending [88%], 75 left circumflex [89%], and 80 right coronary arteries [73%]) versus in 245 lesions (67%) in the surface ECG (126 left anterior descending [73%], 43 left circumflex [47%], and 76 right coronary arteries [70%]; [p less than 0.0001]). The mean ST segment shift was 0.5 +/- 0.4 mV in intracoronary and 0.1 +/- 0.2 mV in standard leads (p less than 0.0001). ST elevation was seen in 97% of cases with intracoronary ECG changes versus in 83% with surface ECG changes. The remainder had ST depression. A total of 48 lesions (13%) did not produce ECG changes and 62 (16%) had silent ischemia. In 75 lesions (21%), ECG changes were seen only in the intracoronary ECG, compared with 14 lesions (4%) with changes only in the surface ECG (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Optimal ECG monitoring during percutaneous transluminal coronary angioplasty of the left anterior descending artery

During percutaneous transluminal coronary angioplasty (PTCA) frontal ECG leads are routinely monitored. The detection of ST segment deviation during the procedure is important for decisions regarding guiding catheter seating and the timing of balloon inflation and deflation. ST segment deviation appears on intracoronary electrograms in the absence of changes on the surface ECG in many patients, while the reverse is true in some individuals. When a precordial lead is employed, V5 or V6 is most commonly selected. The surface ECG leads most sensitive for monitoring ischemia during left anterior descending angioplasty are not known. In nine lead surface ECGs recorded during balloon inflation, a small degree of ST segment elevation occurred in leads I, aVL, and V5. Lead V2 demonstrated an increase in ST displacement from 0.0 ± 0.03 mV to 0.29 ± 0.25 mV during coronary occlusion (p<0.01). We conclude that if V5 or V6 is used as a single precordial lead, surface ECG alterations are easily overlooked. During left anterior descending occlusion the most sensitive surface lead is V2. Optimal ECG monitoring during PTCA in some cases should involve surface lead V2 or the intracoronary lead.     

Combined effects of nitrates on the coronary and peripheral circulation in exercise-induced ischemia

We compared the effects of isosorbide dinitrate (ISDN) administered by intracoronary and intravenous routes in 10 patients with severe coronary artery disease, stable effort angina, and very low exercise tolerance. Supine bicycle ergometer exercise was performed under four conditions: 1) control, 2) after intracoronary administration of 0.4 mg ISDN, 3) 1 hour later (control 2), and 4) after administration of intravenous 4 mg ISDN. At rest, intracoronary ISDN caused no significant hemodynamic effects, whereas intravenous infusion of ISDN resulted in a decline in left ventricular (LV) systolic pressure (-20 +/- 5 mm Hg), LV end-diastolic volume (-27 +/- 3%), and LV end-systolic volume (-30 +/- 4%). After intracoronary infusion of ISDN, ST segment depression and the increase in LV end-diastolic pressure and LV end-systolic volume induced by exercise were significantly less abnormal than during control (0.20 +/- 0.09 vs. 0.14 +/- 0.08 mV, 36 +/- 7 vs. 24 +/- 8 mm Hg, and 91 +/- 40% vs. 40 +/- 29%, respectively). When exercise was performed after intravenous infusion of ISDN, the above-mentioned parameters were significantly improved even further: ST segment depression to 0.05 +/- 0.07 mV, end-diastolic pressure to 14 +/- 7 mm Hg, and LV end-systolic volume to 5 +/- 11% (all p less than 0.01 compared with intracoronary ISDN). Thus, in patients with severe coronary artery disease, it is suggested that intracoronary nitrates increase coronary blood supply during effort-induced ischemia, based on significant improvements in the indirect measures of ST segment depression, LV end-diastolic pressure, and LV volume.(ABSTRACT TRUNCATED AT 250 WORDS)     

Concomitant calcium antagonist plus isosorbide dinitrate therapy for markedly active variant angina

The present study was performed to assess the efficacy of concomitant calcium antagonist/isosorbide dinitrate therapy in patients with frequent episodes of variant angina and to compare such combination therapy with isosorbide dinitrate alone. We enrolled nine such patients (six men and three women, aged 47 ± 9 [mean ± standard deviation] years) in a long-term comparison of (1) oral isosorbide dinitrate (117 ± 63 mg per day) alone, (2) verapamil (453 ± 75 mg per day) + isosorbide dinitrate (given in the same dose as stated above), and (3) nifedipine (71 ± 14 mg per day) + isosorbide dinitrate (also given in the same dose as stated), each administered for 2 months. During isosorbide dinitrate therapy, these nine patients averaged 23.7 ± 37.3 chest pains per week, consumed 24.4 ± 47.4 sublingual nitroglycerin tablets per week, and demonstrated 46.5 ± 43.2 episodes per week of transient ST segment deviations on calibrated two-channel Holter monitoring. During therapy with verapamil/isosorbide dinitrate and nifedipine/isosorbide dinitrate, the frequency of angina and ST segment deviations was dramatically reduced (verapamil/isosorbide dinitrate, 3.9 ± 3.6 chest pains per week and 3.5 ± 2.6 ST segment deviations per week, p < 0.05; nifedipine/isosorbide dinitrate, 3.1 ± 4.0 chest pains per week and 5.5 ± 6.6 ST segment deviations per week, p < 0.05). In all respects, verapamil/isosorbide dinitrate and nifedipine/isosorbide dinitrate were similar to one another. Thus, in patients with very frequent episodes of variant angina, a calcium antagonist/isosorbide dinitrate combination is much more effective than isosorbide dinitrate alone in reducing the frequency of angina and ischemic ECG alterations.     

Antiischemic effect of intracoronary diltiazem on myocardial ischemia during PTCA

Summary To evaluate the effect of intracoronary diltiazem on myocardial ischemia during percutaneous transluminal coronary angioplasty (PTCA), 38 patients were randomly assigned to receive inactive placebo (n = 19; group C) or a low dose (1 mg,n = 10; group D1), or a high dose (2 or 3mg,n = 9; group D2) of diltiazem in a double-blind manner. The agent was administered directly into the coronary artery via a balloon catheter following a control balloon inflation. Chest pain score (maximum, 10) and the magnitude of ischemic ST elevation on standard and intracoronary electrocardiograms (ECGs) during a balloon inflation were assessed in the control and posttreatment periods. After the administration of diltiazem, the chest pain score was significantly decreased in group D1 (control: 5.1 ± 3.6, posttreatment: 3.8 ± 3.1,P < 0.01) and group D2 (3.4 ± 2.5 vs 2.5 ± 2.0,P < 0.01), but not in group C (4.1 ± 3.1 vs 3.7 ± 3.3, difference not significant). The magnitude of ST elevation relative to the control on standard and intracoronary ECGs was significantly smaller in groups D1 and D2 than in group C (standard ECG; D1: 51.8 ± 10.6% of control, D2: 41.6 ± 28.7% vs C: 93.3 ± 15.6% and intracoronary ECG; D1: 47.1 ± 11.7% of control, D2: 27.5 ± 26.9% vs C: 94.6 ± 29.3%, allP < 0.01). Although systolic blood pressure decreased slightly in groups D1 and D2, there was no significant correlation between the change in ST elevation and the change in the rate-pressure product. Pretreatment with a small dose of intracoronary diltiazem attenuated myocardial ischemia during PTCA and this pretreatment may enable us to perform balloon inflation for a longer period.     

Nitrates in myocardial infarction: influence on infarct size, reperfusion, and ventricular remodelling.

OBJECTIVE--To assess the possible benefits of intravenous isosorbide dinitrate in acute myocardial infarction and oral isosorbide mononitrate in subacute myocardial infarction. METHODS--316 patients presenting with acute myocardial infarction were entered into double blind placebo controlled clinical trials assessing infarct size by enzyme release, ventricular size and function by echocardiography, reperfusion by continuous 12 lead ST segment monitoring and late potentials by high resolution electrocardiography. RESULTS--301 patients, of whom 292 (97%) received thrombolytic treatment, were randomised on admission to intravenous isosorbide dinitrate or placebo. Overall, there was no significant effect of treatment on infarct size, ST segment resolution, ventricular remodelling, or late potentials at day 3. A trend was observed towards a reduction in infarct size in patients with non-Q wave infarction treated with isosorbide dinitrate. Heterogeneity of nitrate effect was observed in relation to the degree of ST segment elevation on presentation with a clear benefit of isosorbide dinitrate in patients with moderate ST segment elevation (472 U/l v 704 U/l, P = 0.003) and a trend towards a deleterious effect in patients with marked ST segment elevation (1152 U/l v 1058 U/l, P = 0.2). ST segment re-elevation was more common among patients receiving nitrate treatment than in those assigned to placebo (29 v 16, P < 0.05). Some 160 patients underwent a further randomisation to sustained release isosorbide mononitrate or placebo on day 3. Echocardiographic volumes after 6 weeks of treatment were similar in the two groups. CONCLUSIONS--No benefit was observed with administration of nitrates in the treatment groups as a whole for either acute or subacute infarction. There was, however, evidence of heterogeneity of effect in the different subgroups of acute infarction, and the possibility that nitrates may have differing actions in different groups of patients should be considered.     

Comparison of electrocardiogram and intrathoracic electrogram signals for detection of ischemic ST segment changes during normal sinus and ventricular paced rhythms

INTRODUCTION: The aim of this study was to compare surface ECGs with electrograms (EGM) that are available from implanted devices for the ability to detect ischemic ST segment changes during normal sinus (NS) and ventricular paced (VP) rhythms. METHODS AND RESULTS: ECG leads I, II, and V2, right atrial ring to left pectoral patch (representing the can of the device), right ventricular ring to left pectoral patch, and right atrial ring to right ventricular ring EGM were recorded continuously during percutaneous transluminal coronary angioplasty. One balloon inflation (> or = 60 sec) was analyzed from each of 22 NS and 22 VP subjects. The parameter AST was defined as the maximum absolute ST segment deviation (from isoelectric) during the first 60 seconds of inflation, measured relative to the baseline (preinflation) ST segment deviation. For EGM, a normalized deltaST was defined as the AST divided by the ratio of QRS amplitudes of EGM to ECG. During NS, the deltaST for EGM (0.43 mV) was significantly larger than that of ECG (0.09 mV, P = 0.0001) but the normalized deltaST for EGM (0.11 mV) was comparable to that of ECG (0.09 mV, P = 0.45). During VP, the AST for EGM (1.08 mV) was significantly larger than that of ECG (0.17 mV, P = 0.0001), but the normalized AST for EGM (0.11 mV) was significantly smaller than that of ECG (0.17 mV, P = 0.02). CONCLUSION: During both NS and VP, ischemic ST segment changes were significantly larger in EGM than in ECG. Much of this difference appears to be related to larger amplitudes of EGM signals. (J     

Evaluation using serial exercise tests of verapamil alone and combined with isosorbide dinitrate in exertional angina

The response to verapamil alone and combined with isosorbide dinitrate in a group of 12 patients with severe ischemic heart disease and stable effort angina was assessed by means of serial treadmill testing. The study was randomized, of a square latin design and double-blind. The tested drugs and dosages were 120 mg of verapamil, 120 mg of verapamil plus 20 mg of isosorbide dinitrate and placebo. Patients were serially tested (Bruce protocol) over three consecutive days at 8-9-12 and 16 hours. A significative improvement was observed in several ischemic parameters both with verapamil alone and combined with isosorbide dinitrate, but this improvement was remarkably enhanced with the combination of drugs. The mean exercise time to produce angina improved from 268 +/- 18 sec (basal) to 379 +/- 19 sec (verapamil plus isosorbide dinitrate) and the time for 1 mm ST segment depression from 163 +/- 22 sec (basal) to 257 +/- 19 sec (verapamil plus isosorbide dinitrate) when measured at the last daily test (8 hours after drug administration). It is concluded that both verapamil alone and combined with isosorbide dinitrate at the chosen doses are clinically efficient, significantly improving the ischemic parameters. The combination of verapamil and isosorbide dinitrate resulted in a remarkably better improvement in this group of patients with stable effort angina.     

Reactivity of eccentric and concentric coronary stenoses in patients with chronic stable angina

Dynamic coronary stenoses may be the cause of a variable angina threshold and rest angina in patients with chronic stable angina. It has been suggested that eccentric but not concentric coronary artery stenoses have the potential for dynamic changes of caliber in response to vasoactive stimuli. The vasomotor response of eccentric (asymmetric narrowing) and concentric (symmetric narrowing) coronary stenoses to ergonovine (20 micrograms intracoronary or 300 micrograms intravenous) and isosorbide dinitrate (1 mg intracoronary) was studied in 51 patients with chronic stable angina. Diameter of reference segments (angiographically normal segments proximal to the stenoses) and that of eccentric (n = 30) and concentric (n = 35) coronary stenoses that ranged from 50% to 90% luminal diameter reduction were measured by computerized quantitative angiography before and after ergonovine and isosorbide dinitrate. Ergonovine reduced stenosis diameter (by greater than or equal to 10%) in 80% of eccentric stenoses and 42% of concentric stenoses (p less than 0.05). Mean (+/- SEM) diameter reduction with ergonovine was 19 +/- 3% and 9.5 +/- 2% for eccentric and concentric stenoses, respectively (p less than 0.05). Isosorbide dinitrate increased coronary diameter (by greater than or equal to 10%) in 70% of eccentric and 43% of concentric stenoses (p less than 0.05). Mean diameter of eccentric stenoses increased from 1.15 +/- 0.05 to 1.35 +/- 0.06 mm after nitrate (18.6 +/- 2.5%), whereas diameter of concentric stenoses increased from 1.05 +/- 0.05 to 1.14 +/- 0.05 mm (10 +/- 2.5%) (p less than 0.05). Average dilation of reference segments with administration of isosorbide dinitrate and constriction with ergonovine were not significantly different in patients with concentric and eccentric stenoses.(ABSTRACT TRUNCATED AT 250 WORDS)     

Intracoronary electrocardiogram and angina pectoris during percutaneous coronary interventions as an assessment of myocardial viability: comparison with low-dose dobutamine echocardiography.

The aims of this study were to evaluate the diagnostic value of intracoronary electrocardiogram (ECG) and presence of angina pectoris during percutaneous coronary interventions in the prediction of myocardial viability assessed by low-dose dobutamine echocardiography (LDDE). Seventy-one patients (60 men; mean age, 54 +/- 11 years) with recent Q-wave MI and angiographically documented regional wall motion abnormality in the presence of a significant (>/= 70%) nonocclusive stenosis of the infarct-related vessel who were referred for angioplasty were prospectively included in the study. The intracoronary ECG was recorded using coronary angioplasty guidewire. Significant ST segment elevation was defined as a new or worsening ST segment elevation of >/= 0.1 mV at 80 msec after the J-point. Angina pectoris was noted as present or absent during balloon inflation. All patients underwent LDDE for viability assessment. Significant ST segment elevation in the intracoronary ECG and chest pain were observed in 56 (78.9%) and 49 (69%) of the 71 patients. Viability was present on LDDE in 52 (92.9%) of 56 patients with and 3 (20%) of 15 without ST segment elevation. Viability was detected in 45 (91.8%) of 49 patients with and 10 (45.4%) of 22 without angina pectoris during balloon occlusion. The sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of ST segment elevation for viability were 94.5%, 75%, 92.9%, 80%, and 90.1%, respectively. The sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of angina pectoris for viability were 81.8%, 75%, 91.8%, 54.5%, and 80.3%, respectively. The present study demonstrated that a simple assessment of ST segment elevation in the intracoronary ECG or angina pectoris during coronary angioplasty can be used to assess myocardial viability identified by LDDE in patients with previous MI.     

Effects of isosorbide dinitrate on exercise capacity in cardiac patients--relationship between oxygen uptake responses and hemodynamic effects

Acute effects of oral isosorbide dinitrate on exercise capacity were evaluated in 14 patients with chronic heart disease measuring the anaerobic threshold and left ventricular function during exercise. A symptom-limited exercise test was performed on a bicycle ergometer with work rates increased by 1W every 6 seconds. Left ventricular function was continuously monitored with a computerized cadmium telluride detector following the intravenous injection of technetium-labeled red blood cells. Thirty minutes after the control exercise test, patients were given isosorbide dinitrate, 5 mg orally. The second exercise test was performed 30 min later. Isosorbide dinitrate improved the anaerobic threshold from 715.4 +/- 172.9 to 774.9 +/- 173.5 ml/min (p less than 0.01) and ejection fraction at peak exercise from 36.7 +/- 11.6 to 39.9 +/- 12.3% (p less than 0.05). However, there was no significant change in maximum work rate or peak oxygen uptake. Those patients for whom isosorbide dinitrate resulted in a 10% or greater improvement in the anaerobic threshold had both higher pre-treatment ejection fractions and greater increases in peak exercise ejection fraction following isosorbide dinitrate. Measurements of the anaerobic threshold and left ventricular function during exercise may be useful in the evaluation of the efficacy of vasodilators in cardiac patients.     

经皮冠状动脉腔内成形术中冠状动脉内心电图的应用研究

目的　探讨冠状动脉内心电图（ＩＣ－ＥＣＧ）在经皮冠状动脉腔内成形术（ＰＴＣＡ）术中的应用。方法对４４例冠心病病人的５１支冠状动脉行ＰＴＣＡ时记录ＩＣ－ＥＣＧ和体表ＥＣＧ,分析心绞痛组、心肌梗塞溶栓再通组、溶栓未通组ＩＣ－ＥＣＧ的缺血性心电图改变情况,并与体表监护导联ＥＣＧ相比较。结果９６．１％的血管行球囊扩张时ＩＣ－ＥＣＧ有缺血性改变;心绞痛组、心肌梗塞溶栓再通组及溶栓未通组的ＩＣ－ＥＣＧ的ＳＴ段上移程度有明显差别。结论ＩＣ－ＥＣＧ比体表ＥＣＧ在反映心肌缺血方面更敏感,ＰＴ－ＣＡ时ＩＣ－ＥＣＧ的ＳＴ段变化能一定程度地反映残余心肌的成活情况。     

Relationship between plasma oxidized low-density lipoprotein and the coronary vasomotor response to acetylcholine in patients with coronary artery disease

The present study examined the relation of plasma oxidized low-density lipoprotein (LDL) levels to plasma LDL cholesterol levels and the impairment of endothelium-dependent coronary vasorelaxation in patients with coronary artery disease (CAD). In the first study, the relationship between plasma levels of oxidized LDL and LDL cholesterol were investigated in 88 patients with CAD. In the second study, the changes in the diameter of the left anterior descending (LAD) and the left circumflex (LCX) coronary arteries were measured after intracoronary administration of acetylcholine (15 microg) and isosorbide dinitrate (2.5 mg) in 15 patients with CAD. Plasma oxidized LDL levels were determined with a sandwich enzyme-linked immunosorbent assay. Plasma oxidized LDL levels did not correlate with plasma LDL cholesterol levels (r=-0.03, p=NS). The % diameter changes (mean+/-SEM) in the LAD and LCX after intracoronary acetylcholine were -8.3+/-3.5% and -10+/-4.2%, respectively. The % diameter changes in the LAD and LCX after intracoronary isosorbide dinitrate were 23+/-4.8% and 23+/-5.1%, respectively. The % diameter changes in the LAD and LCX inversely correlated with plasma oxidized LDL levels after intracoronary acetylcholine (LAD: r=-0.55, p=0.03; LCX: r=-0.59, p=0.02), but were not after intracoronary isosorbide dinitrate. Plasma LDL cholesterol, triglyceride, and high-density lipoprotein cholesterol levels did not correlate with the coronary vasoreaction to acetylcholine. In conclusion, plasma oxidized LDL levels do not correlate with plasma LDL-cholesterol levels and are related to impairment of endothelium-dependent coronary vasodilation in patients with CAD.     

Effects of Amlodipine and Isosorbide Dinitrate on Exercise-Induced and Ambulatory Ischemia in Patients with Chronic Stable Angina Pectoris

This study was designed to compare once-daily administration of 5–10 mg amlodipine with two daily doses of 40 mg sustained-release isosorbide dinitrate in 59 patients with stable angina using a randomized, double-blind, crossover study design. Anginal episodes, nitroglycerin consumption, and possible adverse events were recorded in a diary. A maximal symptom-limited bicycle exercise test and 48-hour ambulatory ECG monitoring were performed at baseline and at the end of each 5-week period of therapy. Exercise time, time to angina, time to ST depression, and maximal ST depression were measured during exercise. During ambulatory monitoring, the number of ischemic episodes and the duration per hour of ST depression were assessed. Amlodipine significantly reduced anginal episodes (P < 0.001) when compared with isosorbide dinitrate. Furthermore, amlodipine prolonged time to ST depression (P < 0.001) and time to angina (P < 0.05) when compared with isosorbide dinitrate. The number and duration of ischemic episodes during ambulatory monitoring were significantly reduced with amlodipine when compared with baseline values (P < 0.05), whereas no differences were found between isosorbide dinitrate and baseline. Adverse events were reported more frequently with isosorbide dinitrate than with amlodipine (P < 0.02). Amlodipine appears to be more effective and tolerable than sustained-release isosorbide dinitrate as monotherapy for chronic stable angina. This revised version was published online in July 2006 with corrections to the Cover Date.