Amelioration of ischemia during angioplasty of the left anterior descending coronary artery with an autoperfusion catheter

A new autoperfusion balloon angioplasty catheter with sideholes proximal and distal to the balloon--facilitating distal blood flow during inflation--was compared with standard angioplasty catheters in a prospective, randomized study with blinded data analysis. Hemodynamic and electrocardiographic markers of ischemia after 1 minute of standard or autoperfusion catheter inflations were compared with ischemia after control inflation with standard balloons. In the patient group randomized to standard balloon inflation only, ST-segment elevation after control inflation with a standard balloon catheter was 0.37 +/- 0.04 mV; ST-segment elevation after final balloon inflation with a standard catheter was unchanged at 0.35 +/- 0.04 mV (difference not significant). In the group randomized to the autoperfusion catheter, control inflation with a standard catheter resulted in 0.48 +/- 0.1 mV ST elevation; final inflation with the autoperfusion catheter demonstrated 0.16 +/- 0.09 mV ST elevation (p less than 0.005). Autoperfusion catheter inflation was continued for 2 minutes without change in electrocardiographic findings: ST segments remained at 0.08 +/- 0.03 mV, unchanged from 0.07 +/- 0.03 mV before angioplasty (difference not significant). Thus, while coronary angioplasty performed with standard catheters resulted in marked ST-segment elevation, in patients undergoing angioplasty with the autoperfusion catheter, ischemia was generally not seen, despite sustained balloon inflation for 2 minutes.     

Effect of the calcium antagonist nisoldipine on coronary circulation and myocardial ischemia in temporary coronary occlusion

Sixteen patients undergoing PTCA of a significant lesion of the left anterior descending coronary artery received either 0.3 mg nisoldipine or placebo intravenously. Immediately before and during balloon inflation the following parameters were measured: aortic pressure, post-stenotic pressure, coronary occlusion pressure, diastolic pulmonary artery pressure, coronary sinus flow (thermodilution), and intracoronary ECG. After placebo there were no statistically significant changes. Nisoldipine led to a decrease in aortic pressure from 109 +/- 12 to 93 +/- 11 mm Hg (p less than 0.05) before, and from 103 +/- 14 to 92 +/- 8 mm Hg (NS) during balloon inflation. In contrast, coronary occlusion pressure remained unchanged. Heart rate increased from 80 +/- 13 to 96 +/- 16/min before (p less than 0.05), and from 87 +/- 18 to 97 +/- 17/min during balloon inflation (NS). Coronary sinus flow was increased from 95 +/- 16 to 116 +/- 13 ml/min before balloon inflation (p less than 0.01), and from 70 +/- 25 to 86 +/- 26 ml/min during balloon inflation (NS). ST-segment depression or elevation, severity of angina pectoris, and the diastolic pulmonary artery pressure remained unchanged. Thus, 0.3 mg nisoldipine led to a peripheral vasodilatation. While the aortic pressure decreased, coronary occlusion pressure remained unaffected. This could be explained by a marked dilatation of collateral vessels due to nisoldipine. However, myocardial ischemia remained unaffected as a result of the constant coronary occlusion pressure.     

Analysis of the signal-averaged P-wave duration in patients with percutaneous coronary angioplasty-induced myocardial ischemia.

To assess the impact of angioplasty-induced myocardial ischemia on the duration of the surface P wave, patients undergoing elective angioplasty of isolated lesion in the left anterior descending, circumflex or right coronary arteries were monitored with a 3-channel electrocardiographic Holter system. The leads used were modified bipolar chest leads V5, aVF and V2 (CM-V5, CS-aVF and CM-V2). After echocardiographic signal-averaging, the earliest onset and the latest offset of the P wave were identified in all of the above time-aligned signal-averaged leads, and the composite maximal P duration was measured under 10 x magnification. The maximal ST-segment shift during balloon inflation was also measured in all of the above leads at 60 ms after the J point. In the study group comprising 47 patients, the mean signal-averaged P-wave duration was 125.0 +/- 16 ms at baseline versus 130.0 +/- 15 ms during balloon inflation, p less than 0.005. In the left anterior descending coronary artery group (n = 23), the mean signal-averaged P-wave duration was 122.4 +/- 17 ms and 131.3 +/- 16 ms during balloon inflation, p less than 0.005). In the group with a right coronary artery lesion (n = 18), the values were 127.3 +/- 14 ms and 128.4 +/- 13 ms respectively (p = not significant). Significant increases in the P-wave duration were found to occur in groups both with (n = 34) and without (n = 13) ST-segment shift greater than or equal to 1 mm (both p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical, hemodynamic, electrocardiographic and mechanical events during nonocclusive, coronary atherectomy and comparison with balloon angioplasty.

The periprocedural events and myocardial function during nonocclusive coronary atherectomy by Rotablator or transluminal extraction catheter (TEC) may differ from events during balloon angioplasty. This may have important clinical consequences and needs to be defined further. Therefore, 17 patients undergoing Rotablator and 18 undergoing TEC atherectomy were assessed by clinical, hemodynamic and electrocardiographic monitoring and simultaneous transesophageal echocardiography. The findings were compared with similar parameters during subsequent balloon angioplasty performed in 16 of 17 patients undergoing Rotablator and 14 of 18 undergoing TEC atherectomy. Chest pain occurred more frequently during balloon inflation than during either atherectomy (p less than 0.02), whereas ST-segment and T-wave electrocardiographic changes were equally frequent. Transient second- or third-degree atrioventricular block occurred in 6 patients during Rotablator but in none during TEC atherectomy or balloon inflation (p less than 0.01 for each). Hemodynamic parameters and global left ventricular function remained unchanged during atherectomy. Regional myocardial function in the distribution of the target coronary artery, assessed by a wall motion score, was not affected during Rotablator, but deteriorated slightly during TEC atherectomy and more significantly during balloon inflation (score from 0.3 +/- 0.5 to 1.0 +/- 0.7 during TEC and 2.0 +/- 0.6 during balloon inflation, p less than 0.005 for both). Thus, chest pain is infrequent, whereas hemodynamics and global left ventricular function are preserved during Rotablator and TEC atherectomy. Transient atrioventricular block during Rotablator and regional myocardial dysfunction during TEC atherectomy may occur without significant consequences. These data suggest that these techniques may be preferable to balloon angioplasty for preserving intraprocedural left ventricular function.     

Usefulness of intracoronary isosorbide dinitrate in alleviating myocardial ischaemia during coronary balloon angioplasty.

The effect of intracoronary isosorbide dinitrate on provoked myocardial ischaemia during percutaneous transluminal coronary angioplasty (PTCA) was studied in 60 patients who had at least 1 mm electrocardiographic (ECG) ST segment deviation during a 70 s control balloon inflation period. Isosorbide dinitrate (dose 1 mg, 2 mg or 3 mg) or placebo (saline) was administered by slow intracoronary injection, and the ST segment changes recorded again during an identical dilatation period 2-4 min later. Following injection of isosorbide dinitrate, the severity of ST segment deviation decreased (1 mg -31 +/- 30%, P = 0.03; 2 mg -51 +/- 35%, P = 0.0001; 3 mg -36 +/- 32%, P = 0.002) during coronary balloon inflation, and the time until onset of 1 mm ST deviation was prolonged (1 mg +79 +/- 137%, P = 0.06; 2 mg +85 +/- 87%, P = 0.02; 3 mg +78 +/- 109%, P = 0.02). With the 3 mg dose, the time to maximum ECG change increased (+37 +/- 87%, P = 0.02). In the placebo group, there was a small decrease in the severity of ST segment deviation in patients receiving placebo (-23 +/- 32%, P = 0.03), but no change in the time to its onset or in the time to maximum ST deviation. Isosorbide dinitrate did not alter heart rate, systolic arterial pressure or the rate-pressure product at maximum ST segment change, implying that when isosorbide was administered by direct intracoronary injection, a direct cardiac effect was responsible for the major anti-ischaemic effect of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)     

Protection of regional mechanics and mitochondrial oxidative phosphorylation by amlodipine in transiently ischemic myocardium

The effects of amlodipine (0.3 mg/kg administered intravenously, n = 5) and placebo (n = 5) on recovery of myocardial function and respiration of isolated mitochondria were examined in "stunned" myocardium of normotensive pentobarbital-anesthetized dogs. Measures of myocardial wall motion, using sonomicrometers, and tissue blood flow, by radioactive microspheres, were obtained at baseline, 15 minutes after administration of amlodipine or placebo, after 10 minutes of left circumflex artery ligation and at 60 minutes of reperfusion. Mean aortic pressure decreased from 115 +/- 6 to 101 +/- 5 mm Hg after administration of amlodipine and remained decreased throughout the experiment. Heart rate was not significantly affected at any time. Both groups showed similar degrees of ischemia: elevation of ST segment to 4.7 +/- 1.4 vs 6.2 +/- 1.9 mV; reduction of ischemic zone shortening fraction to 0.6 +/- 1.9 vs -3.4 +/- 2.7%; and reduction of epicardial and endocardial blood flows (epicardial = 40 +/- 13 vs 43 +/- 13 ml/100 g/min; endocardial = 7 +/- 4 vs 13 +/- 6 ml/100 g/min [values for amlodipine vs placebo]). Mitochondrial state 3 rate of respiration and respiratory control index indicative of rate of adenosine triphosphate synthesis and membrane integrity in myocardial samples taken after 10 minutes of ischemia were significantly reduced in the placebo but not in the amlodipine group. Myocardial function showed significantly greater improvement in amlodipine vs placebo at 60 minutes of reperfusion as indicated by shortening fraction (17.7 +/- -1.4 vs 5.8 +/- -3.5%, amlodipine vs placebo), which may have been related to increased myocardial blood flow and decreased blood pressure during reperfusion. Thus, amlodipine pretreatment prevented mitochondrial dysfunction during ischemia and accelerated recovery of both myocardial mechanical function and blood flow when compared with placebo.     

Prolongation of the QTc interval is seen uniformly during early transmural ischemia.

OBJECTIVES: In order to more clearly understand the electrocardiographic manifestations of early transmural ischemia, we studied electrocardiograms (ECGs) in patients undergoing balloon angioplasty. BACKGROUND: Decisions regarding reperfusion strategies in patients with acute myocardial infarction rely largely on the presence of ST-segment elevation (STE) in the ECG, consequently with significant limitations. Studies of the "ischemic cascade" show that ST-segment changes occur well after the onset of wall motion abnormalities. METHODS: We prospectively analyzed ECGs obtained at 20-s intervals in 74 patients undergoing elective balloon angioplasty. The ECGs were analyzed using 3 methodologies. In 74 patients, the ST-segment, the T-wave, and the QT-interval were analyzed using the MUSE (General Electric HC, Menomonee Falls, Wisconsin) automated system (MUSE). Fifty patients were also analyzed using the Interval Editor automated system (IE; General Electric HC). In 20 patients, measurements were made manually. RESULTS: Transmural ischemia prolonged the QTc interval (using the Bazett's formula) in 100% of patients. In all 74 patients analyzed with MUSE, QTc interval prolonged from 423 +/- 25 ms to 455 +/- 34 ms (p < 0.001). In the 50 patients analyzed with IE, QTc interval prolonged in 50 of 50 (100%) patients (from 424 +/- 27 ms to 458 +/- 33 ms [p < 0.001]). Mean time to maximal QTc interval prolongation, changes in T-wave polarity, > or =1 mm STE, and ST-segment depression (STD) were 22, 24, 29, and 35 s, respectively. Although QTc interval prolonged in 100% of patients, T-wave changes, STE, and STD (> or =1 mm) occurred in 7%, 15%, and 7%, respectively. CONCLUSIONS: The QTc interval prolongs in 100% of patients with early transmural ischemia. When compared with clinically accepted indexes of transmural ischemia (i.e., STD and STE [> or =1 mm]) it is the earliest ECG abnormality.     

The autoperfusion balloon angioplasty catheter limits myocardial ischemia and necrosis during prolonged balloon inflation

A new balloon angioplasty catheter with multiple proximal and distal side holes has previously been shown to allow significant protection from ischemia during a 3 min balloon inflation in a coronary artery. Because of the potential benefits of very long periods of inflation, 21 anesthetized thoracotomized dogs were randomized to left circumflex coronary artery occlusion with either a standard or an autoperfusion balloon catheter for 90 min. Nine dogs sustained ventricular fibrillation before completing the study, eight after standard balloon inflation and one after autoperfusion balloon inflation (p = 0.04). ST segment elevation was 0.45 +/- 0.13 mV after 15 min of standard balloon inflation versus -0.03 +/- 0.03 mV after autoperfusion balloon inflation (p less than 0.001). Regional myocardial blood flow was 0.02 +/- 0.01 ml/min per g after 30 min of standard balloon inflation compared with 0.78 +/- 0.23 ml/min per g in the group subjected to autoperfusion balloon inflation (p = 0.01). The area of necrosis/area at risk in the standard catheter group was 40.4 +/- 19.3% versus 1.2 +/- 1.2% for the autoperfusion catheter group (p = 0.01). Thus, the autoperfusion catheter preserves blood flow and limits myocardial ischemia and necrosis despite 90 min of balloon inflation.     

Body surface potential mapping improves detection of ST segment alteration during percutaneous coronary intervention

BACKGROUND: The 12-lead electrocardiogram underestimates ST segment alteration in acute coronary syndromes compared with multi-lead body surface mapping. We assessed whether 80-lead mapping would improve detection of ST alteration during percutaneous coronary intervention. METHODS: Simultaneous maps and 12-lead electrocardiograms were recorded pre-procedure, during balloon inflation and post-procedure from patients undergoing elective intervention to native coronary arteries. Recordings were obtained from 39 inflations (19 patients). All arteries were successfully stented. RESULTS: Mean 'lead specific' ST alteration (the difference in ST elevation/depression between pre-procedure and inflation recordings in the lead showing maximal ST alteration) was greater on the map than on electrocardiogram, both for ST elevation (0.16+/-0.02 vs. 0.06+/-0.01 mV; p<0.001) and ST depression (0.11+/-0.017 vs. -0.03+/-0.006 mV; p<0.001). During first inflations (n=19), mean lead specific ST elevation and depression on map were greater than on electrocardiogram (0.20+/-0.034 vs. 0.07+/-0.015 mV; p<0.001 and 0.11+/-0.029 vs. 0.03+/-0.009 mV; p=0.001, respectively). Mapping detected greater summated ST elevation and depression during inflation than electrocardiogram (0.04+/-0.005 vs. 0.021+/-0.003 mV; p<0.001 and 0.026+/-0.004 vs. 0.011+/-0.002 mV; p<0.001, respectively). Qualitative analysis of maps and electrocardiograms showed that 21/39 (53.8%) maps recorded during inflation met criteria for myocardial ischaemia compared with 7/39 (17.9%) electrocardiograms (p<0.001). CONCLUSION: Body surface mapping compared with the 12-lead electrocardiogram improves detection of myocardial ischaemia during intervention.     

Ethanol abolishes ischemic preconditioning in humans.

OBJECTIVES: This study sought to assess the effect of acute alcohol intake on ischemic preconditioning (IPC) in humans using the clinical model of 2 sequential balloon inflations during a percutaneous coronary intervention (PCI). BACKGROUND: Ischemic preconditioning is the most potent form of endogenous myocardial protection from irreversible ischemic injury. Experimental observations suggest that acute ethanol administration might abolish IPC. METHODS: We studied 30 consecutive patients (22 men, mean age 65 years) undergoing elective coronary angioplasty who were randomized to receive an oral dose of 40 g ethylic alcohol (administered as 149 ml of Gordon's Gin) or 149 ml of water 30 min before PCI. Intracoronary electrocardiogram was continuously monitored to assess the greatest ST-segment elevation or depression from baseline. RESULTS: In placebo-treated patients, the change of ST-segment shift during the second inflation was significantly smaller than that during the first inflation (19.3 +/- 9.1 vs. 15.7 +/- 8.7, p = 0.005). In contrast, in gin-treated patients, the change of ST-segment shift during the second inflation was significantly greater than that during the first inflation (18.7 +/- 7.2 vs. 22 +/- 10, p = 0.03). The group-inflation interaction for ST-segment changes was highly significant (p < 0.001). CONCLUSIONS: This randomized, prospective study in humans shows that administration of a moderate dose of ethanol abolishes IPC occurring during sequential episodes of myocardial ischemia and is associated with worsening ischemia. Based on our study, intake of moderate to high doses of alcoholic beverages should be avoided in patients at high risk of acute myocardial infarction.     

Nicorandil, a potent cardioprotective agent, reduces QT dispersion during coronary angioplasty

BACKGROUND: Previous studies have found that ST-segment elevation and QT dispersion are smaller in second coronary occlusions than in first occlusions, a trend that suggests ischemic preconditioning. It has not been established whether nicorandil reduces ST-segment elevation and QT dispersion during coronary angioplasty. METHODS AND RESULTS: Thirty patients with stable angina undergoing coronary angioplasty in the proximal left anterior descending artery were randomly assigned to one of two groups, receiving either 5 mg oral nicorandil 3 times daily (n = 15) or placebo (n = 15). In the control patients, the total ST-segment elevation decreased from 14 +/- 3 mm during the first inflation to 7 +/- 2 mm during the second inflation (P < .01). In contrast, in the nicorandil-treated patients, the total ST-segment elevation during the second inflation was roughly equivalent to that during the first inflation (8 +/- 3 mm vs 8 +/- 3 mm, P = not significant). After the first reperfusion, a significantly smaller increase in QT dispersion was observed in the nicorandil-treated patients than in the control patients (43 +/- 15 ms vs 54 +/- 15 ms, P < .001). However, after the second reperfusion, QT dispersion was similar for the two groups (32 +/- 15 ms vs 34 +/- 13 ms, P = not significant). CONCLUSIONS: Nicorandil may precondition the myocardium and may prevent the occurrence of ventricular arrhythmias after coronary reperfusion by suppressing the increase in QT dispersion.     

Preservation of distal coronary perfusion during prolonged balloon inflation with an autoperfusion angioplasty catheter

A newly designed balloon coronary angioplasty catheter that allows passive antegrade blood flow during balloon inflation (autoperfusion catheter) was compared with a standard balloon coronary angioplasty catheter. In a randomized sequence, inflations were performed for 3 min in the left circumflex coronary artery of 12 dogs with the standard catheter followed by the autoperfusion catheter or vice versa. During inflation with the standard catheter, the ST segment of standard limb lead II increased from -0.02 +/- 0.03 mV to 0.39 +/- 0.08 mV (p less than .001), whereas during inflation with the autoperfusion catheter the ST segment did not change (-0.03 +/- 0.03 vs -0.01 +/- 0.04 mV; p = NS). Regional myocardial blood flow measured by the radioactive microsphere technique in the posterior subepicardium and subendocardium was 0.12 +/- 0.03 and 0.08 +/- 0.03 ml/min/g, respectively, with the standard catheter as compared with 0.57 +/- 0.08 and 0.61 +/- 0.14 ml/min/g with the autoperfusion catheter (both p less than .01 compared with the standard catheter). Thus, unlike the standard catheter, the autoperfusion catheter allows for inflations up to 3 min in duration without producing deleterious changes in the ST segment or severe reductions in regional myocardial blood flow.     

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)     

ECG evidence of limited myocardial infarction following coronary occlusion treated by early intravenous rt-PA infusion

Serial 12-lead surface electrocardiograms (ECGs) were analysed in 110 patients with first evolving myocardial infarction entered in a double-blind placebo-controlled trial of intravenous rt-PA within 2.5 h (mean 1.9 +/- 0.5 (SD)) of pain onset. ECG analysis was performed by two 'blinded' analysts. QRS scoring (by the modified Selvester method) was used as an index of myocardial necrosis. Patient results were analysed according to infarct location. There was no difference between the two treatment groups in ST-segment elevation or QRS score at entry or up to 24 h after symptom onset. However from 24 h, QRS score was lower in patients with anterior infarction given rt-PA than in those given placebo: 5.4 +/- 2.8 vs 7.7 +/- 4.1 (P = 0.02) at 48 h; 4.7 +/- 3.2 vs 8.0 +/- 4.0 (P = 0.01) at 4-10 days; and 4.6 +/- 3.9 vs 7.5 +/- 3.9 (P = 0.01) at 21 days. For patients with inferior infarction, rt-PA treatment also resulted in a lower QRS score although this was not significantly different from the score of the placebo group (P = 0.07). Comparison of QRS scores with ejection fraction measured from the contrast ventriculogram taken at 21 days showed a moderate correlation (r = 0.46) in patients with anterior infarction but a poor correlation in patients with inferior infarction. These ECG results indicate that in evolving anterior myocardial infarction, there is limitation of infarct size from early rt-PA infusion.     

Effects of K(ATP) channel blockade by glibenclamide on the warm-up phenomenon.

AIMS: The increased tolerance to myocardial ischaemia observed during the second of two sequential exercise tests, i.e. the warm-up phenomenon, has been proposed as a clinical model of ischaemic preconditioning. As ATP-sensitive K+ channels appear to be a mediator of ischaemic preconditioning in both experimental and clinical studies, the aim of this study was to investigate the role of K(ATP) channels in the warm-up phenomenon. METHODS AND RESULTS: Twenty-six patients with coronary artery disease were randomized to receive 10 mg oral glibenclamide, a selective ATP-sensitive K+ channel blocker, or placebo. Sixty minutes after glibenclamide or placebo administration, patients were given an infusion of 10% dextrose (8 ml x min(-1)) to correct glucose plasma levels or, respectively, an infusion of saline at the same infusion rate. Thirty minutes after the beginning of the infusions, both patient groups underwent two consecutive treadmill exercise tests, with a recovery period of 15 min to re-establish baseline conditions. Before exercise tests, blood glucose levels were similar in placebo and glibenclamide groups (96 +/- 10 vs 105 +/- 22 mg x 100 ml(-1), P=ns). After placebo administration, rate-pressure product at 1.5 mm ST-segment depression significantly increased during the second exercise test compared to the first (220 +/- 41 vs 186 +/- 29 beats x min(-1) x mmHg x 10(2), P<0.01), but it did not change after glibenclamide (191 +/- 34 vs 187 +/- 42 beats x min(-1) x mmHg x 10(2), P=ns), with a significant drug-test interaction (P=0.0091, at two-way ANOVA). CONCLUSIONS: Glibenclamide, at a dose previously shown to abolish ischaemic preconditioning during coronary angioplasty, prevents the increase of ischaemic threshold observed during the second of two sequential exercise tests. These findings confirm that ischaemic preconditioning plays a key role in the warm-up phenomenon and that in this setting is, at least partially, mediated by activation of ATP-sensitive K+ channels.     

Outcome after prolonged balloon inflations of greater than 20 minutes for initially unsuccessful percutaneous transluminal coronary angioplasty.

Prolonged balloon inflation with or without autoperfusion techniques is a common initial approach to major dissection or abrupt occlusion after percutaneous transluminal coronary angioplasty (PTCA). To assess such a strategy in the setting of unsuccessful angioplasty, 40 patients who underwent prolonged balloon inflations of greater than 20 minutes between January and July of 1991 after initially unsuccessful angioplasty were studied. These patients (median age 59 years) underwent PTCA for progressive or unstable angina (16[40%]), symptomatic or asymptomatic residual stenosis after myocardial infarction (10[25%]), acute myocardial infarction (3[8%]), stable angina (3[8%]), reinfarction (2[5%]), and other indications (6[15%]). The significant stenoses were primarily in the proximal and midportions of the right coronary (53%), left anterior descending (30%) and left circumflex (17%) coronary arteries. Before prolonged balloon inflation, the longest single inflation was 11 +/- 6 minutes and the total time of all inflations was 17 +/- 8 minutes (mean +/- standard deviation). Stenosis was reduced from 91 +/- 9 to 68 +/- 16% before prolonged inflation. After prolonged balloon inflation of 30 +/- 9 minutes, the residual stenosis was 47 +/- 21% (p = 0.0001 vs value before prolonged inflation). Furthermore, improvements in the appearance of filling defects or dissections, or both, occurred in 19 patients (48%). Procedural success was obtained in 32 of 40 patients (80%). Coronary bypass grafting was performed in 8 patients (20%): 4 after unsuccessful PTCA (3 emergently) and 4 electively after initially successful PTCA. Although 5 patients had creatine kinase-MB elevations greater than 20 IU/liter after the procedure, only 1 sustained a Q-wave myocardial infarction. There were no deaths in the hospital.(ABSTRACT TRUNCATED AT 250 WORDS)     

Reactive hyperemia following coronary balloon angioplasty, but not dipyridamole-induced hyperemia, predicts resolution of exercise-induced ST-segment depression

OBJECTIVES: To characterize delayed restoration of coronary blood flow following successful percutaneous transluminal coronary angioplasty (PTCA). BACKGROUND: Delayed restoration of coronary blood flow following successful PTCA is common and likely the result of multiple factors. Temporary myocardial ischemia and dipyridamole administration both result in increased coronary blood flow, but by different mechanisms. The relationship between these phenomena and exercise-induced ST-segment depression after PTCA was investigated to determine if any correlation existed. METHODS: Forty consecutive patients with single-vessel coronary artery disease underwent treadmill exercise testing before and after PTCA. The percentage change in coronary blood flow before and after 90 s balloon inflation was assessed. After a new steady state had been reached, dipyridamole was infused and changes in coronary blood flow were again determined. The relationship between changes in coronary blood flow and the presence of ST-segment depression during exercise testing after PTCA was determined. RESULTS: Peak coronary blood flow induced by reactive hyperemia was significantly greater than that in the steady state after balloon inflation (48.5+/-38.8 compared with 15.1+/-13.2 ml/min, P<0.0001). Dipyridamole administration also resulted in significant increases in coronary blood flow (15.1+/-13.2 ml/min compared with 31.0+/-24.9 ml/min, P<0.0001). ST-segment depression after PTCA was significantly less than before (0.10+/-0.07 mV compared with 0.19+/-0.08 mV, P<0.001). Further, reactive hyperemia, but not dipyridamole-induced hyperemia, correlated with attenuation of exercise-induced ST-segment depression after PTCA (r=0.62, P<0.0001). CONCLUSIONS: Reactive hyperemia following temporary coronary occlusion recreates local conditions associated with delayed resolution of myocardial ischemia following successful PTCA. Further, this phenomenon appears to be distinct from changes in coronary blood flow induced by dipyridamole.     

Buccal nitroglycerin decreases ischemic pain during coronary angioplasty: a double-blind, randomized, placebo-controlled study.

Nitroglycerin (NTG) has the potential to reduce myocardial ischemia during percutaneous transluminal coronary angioplasty (PTCA). Buccal administration of NTG offers practical advantages compared to intravenous or intracoronary administration. In a double-blind, randomized, placebo-controlled study, 100 patients were given 5 mg of buccal NTG or placebo during PTCA. A scoring system for ischemic pain during balloon inflation was defined as pain intensity (0 to 5) multiplied by duration of pain after balloon deflation (1 = 0 to 30 seconds, 2 = 30 to 60 seconds, 3 = 60 to 120 seconds, 4 = greater than 120 seconds but subsiding, and 5 = until next inflation). Fourteen patients were excluded: 12 for vagal reaction (eight NTG and four placebo; p greater than 0.05) requiring atropine, making buccal absorption unreliable, and two for inability to dilate. Eighteen patients (nine NTG and nine placebo) had no pain during balloon inflation. Sixty-eight patients (32 NTG and 36 placebo) had ischemic pain with a pain score (mean +/- SD) of 4.8 +/- 3.8 for the NTG group versus 7.1 +/- 4.8 for the placebo group (p = 0.03). We conclude that buccal NTG significantly decreases myocardial ischemia during PTCA.     

Comparison of the electrocardiographic changes induced by dipyridamole infusion and treadmill exercise in patients with coronary artery disease

To determine whether dipyridamole infusion can be used as an alternative method to physical exercise, 87 lead body surface mapping was performed to compare the distribution patterns of ST-segment depression after 0.568 mg/kg/4 min dipyridamole infusion (D) and after submaximal treadmill exercise (T) in 21 patients with coronary artery disease. Significant ST-segment depression (greater than or equal to 0.05 mV) was observed in 19 patients after D and in 18 after T. After D and T, each patient showed a similar distribution pattern of ST-segment depression. There were no significant differences in the number of leads which showed ST-segment depression (nST: D, 15.6 +/- 11.1 vs T, 15.2 +/- 10.8) and in the maximal value of ST-segment depression (STmax: D, -0.24 +/- 0.16 vs T, -0.20 +/- 0.13 mV). Good correlations were observed in nST (r = 0.84) and in STmax (r = 0.87) between D and T. The increase in mean pressure-rate product after T was 89%, while the increase after D was only 22%. Our results suggest that this pharmacologic test to induce myocardial ischemia may be useful in the evaluation of coronary artery disease in patients who are physically unable to perform adequate exercise.     

Ambulatory heart rate and ST-segment depression during painful and silent myocardial ischemia in chronic stable angina pectoris

The relation between heart rate and ischemic ST-segment depression was studied in 70 patients with documented obstructive coronary artery disease (CAD) and reproducible effort angina. Symptom-limited treadmill exercise testing was performed before and after a 2-week placebo period and 24-hour FM ambulatory electrocardiographic monitoring at the end of the placebo period. The means (+/- standard deviation) of the basal and placebo values for exercise time, heart rate and maximal ST-segment depression were: 6.4 +/- 2.6 minutes vs 6.9 +/- 2.8 minutes (difference not significant [NS]), 125 +/- 17 beats/min vs 125 +/- 19 beats/min (NS) and 2.3 +/- 0.8 mm vs 2.1 +/- 0.8 (NS), respectively. Ambulatory monitoring revealed 205 episodes of significant ST-segment depression (J + 80 ms; 49 episodes with more than 1 mm, 83 with more than 2 mm, 39 with more than 3 mm and 34 with more than 4 mm). Of all episodes of ST-segment depression, 130 (64%) were asymptomatic. The episodes lasted for 3 to 110 minutes. The maximal 24-hour ambulatory heart rate and ST-segment depression during ischemic episodes were expressed as a percentage of those seen during exercise-induced ischemia. When all ambulatory ischemic episodes (both symptomatic and asymptomatic) were compared with exercise-induced ischemic changes in the individual patient, there was little difference in heart rate (91 +/- 15% vs 90 +/- 18%, NS) but there was a greater magnitude of ST-segment depression (122 +/- 57% vs 104 +/- 52%, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)