Assessment of left ventricular volume by an ambulatory radionuclide monitoring system during head-up tilt in patients with unexplained syncope: relation to autonomic activity assessed by heart rate variability.

BACKGROUND: Decreased left ventricular volume during head-up tilt plays an important role in triggering syncope in patients with neurally mediated syncope. However, precise changes in left ventricular volume during head-up tilt have not been well investigated. This study was conducted to test the hypothesis that the decline in left ventricular volume during tilt could trigger ventricular mechanoreceptor activation. METHODS AND RESULTS: To investigate the mechanisms of tilt-induced syncope, we measured the temporal changes in left ventricular volume, ejection fraction, cardiac output, and heart rate variability indices during head-up tilt in 25 patients with syncope of undetermined etiology. Eleven patients had a cardioinhibitory response (CI group), 7 patients showed a vasodepressor response (VD group), and 7 patients demonstrated a negative response (NG group). Before syncope, ejection fraction increased most in the CI group, the left ventricular end-diastolic volume declined most in the VD group (VD group, -11.0% +/- 3.3%; CI group, -2.8% +/- 4.8%; NG group, -3.4% +/- 2.2%; P <.005), and the high-frequency spectra increased most in the CI group (CI group, 25.0% +/- 21.0%; VD group, -4.1% +/- 11.7%; NG group, -5.3% +/- 12.7%; P <.01). The vasodepressor response was dependent on left ventricular volume, whereas the cardioinhibitory response was related to the vagal activity reflected by high-frequency spectra. CONCLUSIONS: The precise evaluation of left ventricular volume by an ambulatory radionuclide monitoring system combined with a heart rate variability analysis is considered useful for clarifying the pathophysiology of neurally mediated syncope.

Different mechanisms of isoproterenol-induced and nitroglycerin-induced syncope during head-up tilt in patients with unexplained syncope: important role of epinephrine in nitroglycerin-induced syncope.

INTRODUCTION: A reduction in left ventricular volume and an increase in epinephrine levels have been reported in tilt-induced neurally mediated syncope. To compare the mechanisms of isoproterenol-induced and nitroglycerin-induced syncope during head-up tilt and to investigate the role of catecholamines, the temporal changes in plasma levels of norepinephrine and epinephrine and in left ventricular volume were measured. METHODS AND RESULTS: The first study population consisted of 90 patients with syncope of unknown etiology and 12 control subjects. The second study population consisted of 43 patients with unexplained syncope. In the first study, head-up tilt (80 degree angle) was conducted for 40 minutes, and norepinephrine and epinephrine levels were measured. In the second study, all patients were randomly allocated to either isoproterenol test (20 patients) or nitroglycerin test (23 patients) for 20-minute head-up tilt. Isoproterenol infusion was given at a rate of 1 to 3 microg/min. Intravenous infusion of nitroglycerin was started at 250 microg/hour with increasing dosages up to 1,500 microg/hour. Norepinephrine and epinephrine were measured in peripheral venous blood. Left ventricular volumes were measured by echocardiography with patients in the supine position and during head-up tilt every 1 minute. End-diastolic volume and end-systolic volume were calculated. In the first study, 61 patients demonstrated a positive response and 29 patients demonstrated a negative response. Plasma norepinephrine changes during head-up tilt were not significantly different, whereas epinephrine levels were significantly higher in the positive patients than in the negative and control subjects (148 +/- 118 pg/mL vs 66 +/- 31 pg/mL and 55 +/- 27 pg/mL). Thirteen of the 20 patients given isoproterenol and 15 of the 23 patients given nitroglycerin showed a positive head-up tilt (65.0% vs 65.2%; P = NS). During isoproterenol and nitroglycerin infusion head-up tilt, epinephrine in the positive group determined by the nitroglycerin test was significantly higher than that in the other three groups (103 +/- 38 pg/mL vs 60 +/- 33 pg/mL, 31 +/- 21 pg/mL, and 50 +/- 52 pg/mL). In contrast, end-systolic volume was significantly smaller in the positive group than in the other three groups based on findings of the isoproterenol test. CONCLUSION: The findings suggest that nitroglycerin triggers head-up tilt-induced syncope by increasing epinephrine levels, whereas isoproterenol induces syncope by decreasing left ventricular volume.

Endothelial dysfunction and decreased exercise tolerance in interferon-alpha therapy in chronic hepatitis C: relation between exercise hyperemia and endothelial function.

BACKGROUND: We previously reported that reversible endothelial dysfunction is caused by interferon-alpha therapy (IFN) in patients with chronic hepatitis C. In experimental studies, limb blood flow during exercise is reported to be dependent on endothelium-derived nitric oxide. HYPOTHESIS: The purpose of this study was to confirm the effect of IFN on endothelial function and to investigate whether exercise hyperemia is dependent on endothelial function in humans. METHODS: We performed symptom-limited exercise treadmill testing and measured flow-mediated vasodilation (FMD, endothelium-dependent vasodilation) and sublingual glyceryl-trinitrate-induced dilation (GTN-D, 0.3 mg, endothelium-independent vasodilation) in the brachial artery by using high-resolution ultrasound in 10 patients with chronic active hepatitis C (age 53 +/- 11 years, 2 men, 8 women) before and immediately after administration of recombinant interferon 2b (10 million U/day) for 4 weeks. RESULTS: There were no significant abnormal findings in any patients in routine studies of 24-h ambulatory electrocardiogram monitoring, two-dimensional echocardiography, and exercise treadmill testing both before and after treatment. Leg fatigue and exhaustion were the reasons for termination of exercise treadmill testing in each patient. Pressure rate product was calculated at rest and peak exercise. Interferon-alpha therapy significantly (p<0.05) decreased FMD (6.8 +/- 3.1 vs. 1.9 +/- 2.6%), exercise treadmill testing tolerance time (437 +/- 89 vs. 395 +/- 62 s) and peak pressure rate product (283 +/- 41 vs. 241 +/- 47 mmHg x beats/min x 10(-2)), but not GTN-D (13.4 +/- 5.4 vs. 17.0 +/- 5.5%). The change of FMD due to IFN significantly and highly correlated with exercise treadmill testing tolerance time (r = 0.86, p<0.001), but not with change of peak pressure rate product, suggesting that FMD is more closely related to the condition of the peripheral circulation than is cardiac performance. CONCLUSION: These results suggest that IFN in patients with chronic hepatitis C impairs endothelial function and exercise tolerance, and that endothelial function might be at least partly involved in exercise hyperemia in humans.

Coronary remodeling of proximal and distal stenotic atherosclerotic plaques within the same artery by intravascular ultrasound study.

The aim of this intravascular ultrasound study was to compare the type and the degree of vessel remodeling in proximal and distal de novo lesions within the same coronary artery in patients with stable angina pectoris. Seventy-six de novo coronary artery lesions in 38 coronary arteries of 38 patients were imaged by intravascular ultrasound. The vessel area (VA) within the external elastic lamina and the lumen area (LA) were measured, and the wall area (VA-LA) was calculated at the lesion site, and the proximal and distal reference sites. The VA ratio was defined as (lesion VA/average of the proximal and distal reference VAs) to represent the degree of vessel remodeling. The proximal coronary segments showed compensatory enlargement more often (68% vs 29%, p < 0.01) than the distal segments, and the VA ratio at the lesion site was significantly larger (1.1 +/- 0.3 vs 1.0 +/- 0.2, p <0 .01) in proximal segments than in distal segments. The type of coronary remodeling was discordant in 61% and concordant in only 39% of coronary arteries between the proximal and distal segments. The type of coronary remodeling of proximal and distal coronary lesions was inhomogeneous, even within the same vessel. Proximal coronary segments showed more prominent compensatory enlargement than distal segments, which have a similar degree of luminal narrowings.

Significance of circulatory epinephrine levels in exercise-induced neurally mediated syncope.

BACKGROUND AND HYPOTHESIS: Previous research has failed to document temporal changes in epinephrine levels in patients with neurally mediated syncope associated with exercise. The purpose of this study was to investigate the role of circulatory catecholamines in exercise-induced neurally mediated syncope, specifically focusing on epinephrine levels. METHODS: The present study deals with temporal changes of circulatory catecholamine levels during head-up tilt tests (40 min, 80 degree tilt) in 62 patients with syncope of unknown origin, 7 of whom had syncope associated with exercise (exercise-induced group, 19+/-3 years). Data were compared with 10 control subjects (control group, 45+/-23 years). Of the 55 patients with syncope not associated with exercise, 32 tested positive for the head-up tilt tests (positive group, 31+/-16 years) and 23 patients tested negative (negative group, 46+/-19 years). Blood samples for circulatory catecholamine assay were obtained from the antecubital vein in the baseline supine position 2 min after the tilt started, every 10 min during tilt, and at the time of the onset of symptoms or the end of tilt. Levels of norepinephrine and epinephrine were determined using the high-pressure liquid chromatography (HPLC) method (pg/ml). RESULTS: Plasma norepinephrine levels among the four groups were similar at the supine position and during tilt testing. In contrast, patients in the exercise-induced group had significantly higher maximum epinephrine levels during head-up tilt testing than the other three groups (288+/-191 vs. 148+/-117, 66+/-31, and 54+/-27 pg/ml, respectively, p < 0.05). Patients in the positive group had higher maximum epinephrine levels than those in the negative group (p <0.05). Also, patients in the exercise-induced group and those in the positive group had a significantly shorter tilt-testing time than patients in the negative and control groups. CONCLUSIONS: A marked increase of epinephrine was observed during head-up tilt testing in patients with neurally mediated syncope associated with exercise. The present findings further accelerate the identification of the role of epinephrine in the mechanisms behind neurally mediated syncope associated with exercise.

The repeatability of left ventricular volume assessment by a new ambulatory radionuclide monitoring system during head-up tilt.

The precise measurement of changes in left ventricular volume is important to elucidate the mechanisms of neurally mediated syncope. This study was conducted to determine whether or not a brand-new ambulatory radionuclide monitoring system (C-VEST system) can be clinically used to easily and precisely measure left ventricular volume and function in tilt testing. To assess the repeatability of the C-VEST system, 12 healthy volunteers (mean age 24+/-4 years old) underwent 20 minute head-up tilt testing and we measured the temporal changes in left ventricular volume and ejection fraction twice a day (first and second studies). To investigate the changes in the C-VEST measurements and the detector position in the first and second studies, tilt testing was performed with an 80-degree passive tilt, which is the same as the standard procedure used in diagnosing neurally mediated syncope. The coefficient of repeatability for both the C-VEST and detector position was well within the clinical range (coefficient of repeatability in left ventricular volume ranged from 1.7 to 2.8; coefficient of repeatability in the detector position ranged from 2.3 to 3.1). Precise evaluation of the left ventricular volume can be achieved by an ambulatory radionuclide monitoring system in tilt testing.

Endothelial function and peripheral vasomotion in the brachial artery in neurally mediated syncope.

BACKGROUND: Paradoxical peripheral vasodilation is one of the suspected mechanisms of neurally mediated syncope. Parasympathetic stimulation following sympathetic activation during orthostatic stress mainly contributes to this vasodilation. HYPOTHESIS: Since endothelial function modulates peripheral vascular tone, this study aimed to determine whether endothelial function and inappropriate peripheral vasomotion has a significant role in the pathogenesis of neurally mediated syncope. METHODS: To investigate whether endothelial function is augmented or whether abnormal peripheral vasomotion exits, flow-mediated dilation (FMD, endothelium-dependent vasodilation) and sublingual glyceryl trinitrate-induced dilation (0.3 mg, GTN-D, endothelium-independent vasodilation) were measured in the brachial artery in 16 patients with neurally mediated syncope, aged 33 +/- 10 years, by using high-resolution ultrasound. All patients underwent positive head-up tilt testing. These measures were compared with those in 16 control subjects matched with the patients by age, gender, and coronary risk factors. For FMD, percent diameter changes were obtained from baseline to hyperemic conditions (1 min after 5 min occlusion of the forearm artery). There were five smokers in both the patient and the control groups, but there was no structural heart disease in either group. RESULTS: Baseline brachial artery diameters were comparable (3.8 +/- 0.6 vs. 3.8 +/- 0.7 mm, NS). Flow-mediated dilation in patients with neurally mediated syncope had a normal value of 9.8 +/- 5.0% despite the inclusion of five smokers. Flow-mediated dilation and GTN-D in patients with neurally mediated syncope were significantly greater than those in controls (9.0 +/- 5.0 vs. 3.0 +/- 3.5%, p<0.05; 18.4 +/- 5.5 vs. 14.1 +/- 4.4%, p<0.05). CONCLUSIONS: Augmented endothelial function and/or abnormal peripheral vasomotion in peripheral arteries are important in patients with neurally mediated syncope in selected populations.

Clinical validation of intravascular ultrasound imaging for assessment of coronary stenosis severity: comparison with stress myocardial perfusion imaging.

OBJECTIVES: To validate intravascular ultrasound (IVUS) measurements for differentiating functionally significant from nonsignificant coronary stenosis. BACKGROUND: To date, there are no validated criteria for the definition of a flow-limiting coronary artery stenosis by IVUS. METHODS: Preinterventional IVUS imaging (30-MHz imaging catheter) of 70 de novo coronary lesions was performed. The lesion lumen area and three IVUS-derived stenosis indixes comparing lesion lumen area with the lesion external elastic lamina (EEL) area, the mean reference lumen area and the mean reference EEL area were compared with the results of stress myocardial perfusion imaging. RESULTS: The lesion lumen area and three IVUS-derived stenosis indexes showed sensitivities and specificities ranging between 80% and 90% using stress myocardial perfusion imaging as the gold standard. The lesion lumen area < or =4 mm2 is a simple and highly accurate criterion for significant coronary narrowing. CONCLUSIONS: Quantitative IVUS indices can be reliably used for identifying significant epicardial coronary artery stenoses.

Use of head-up tilt testing to determine a possible cause of unexpected cardiac asystole during epidural anesthesia.

Head-up tilt testing is widely used in the diagnosis of syncope of unknown origin. In this report, head-up tilt testing elucidated the etiology of cardiac asystole of unexpected and sudden onset during orthopedic surgery under epidural anesthesia in a 30-year-old woman. Conventional diagnostic approaches were ineffective. Venous pooling in the lower legs as a result of vasodilation and subsequent vagotony due to epidural anesthesia, a condition mimicking orthostatic stress, is proposed as the mechanism of asystole. Follow-up examinations over 16 months revealed no further syncope and a good clinical course. Head-up tilt testing was useful in determining etiology in this case.

Autonomic responses to orthostatic stress in head-up tilt testing: relationship to test-induced prolonged asystole.

BACKGROUND: Prolonged asystole is sometimes an extreme manifestation of neurally mediated syncope. HYPOTHESIS: To investigate the mechanism of head-up tilt testing-induced prolonged (life-threatening) cardiac asystole, we measured temporal changes in frequency domain heart rate variability indices in 25 patients with syncope of undetermined etiology. METHODS: Head-up tilt testing (80 degrees) was performed in 25 patients for up to 40 min or until asystole or syncope occurred. Three patients (Group 1; 37 +/- 13 years, 1 man 2 women) had an episode of prolonged cardiac asystole (> or = 10 s) during testing, necessitating cardiopulmonary resuscitation. Syncope, but no asystole, was induced in 10 patients (Group 2; 48 +/- 31 years, 6 men, 4 women), and 12 patients (Group 3; 55 +/- 20 years, 5 men, 7 women) failed to show asystole or syncope during testing. Power spectra of low (0.04-0.15 Hz) and high (0.15-0.40 Hz) frequency, and total (0.01-1.00 Hz) frequency spectra were measured in consecutive 2 min segments throughout the test. RESULTS: Maximally changed values in heart rate, systolic blood pressure, and heart rate variability indices during testing were compared among the three groups (maximally changed values did not include the values during tilt-induced symptoms). High frequency spectra in Groups 2 and 3, but not in Group 1, decreased during the test. High frequency spectra, low frequency spectra, and total spectra in Group 1 were significantly higher than those in Groups 2 and 3 during testing. In Group 1 patients, findings at test-induced asystole were consistent with exaggerated sympathetic and concurrent persistent parasympathetic activity. CONCLUSION: Unusual autonomic responses to orthostatic stress can cause prolonged asystole, and this autonomic nerve dysregulation may relate to asystolic episodes associated with cardiovascular collapse.

Angioscopic coronary macromorphology after thrombolysis in acute myocardial infarction.

In addition to a disruption of yellow plaque, vasospasm may also play a role in thrombotic occlusions of coronary arteries in small cases of infarction. Macroscopic vascular injury and thrombus seemed to be unnecessary for vasospasm culminating in myocardial infarction.

Angioscopy in variant angina: coronary artery spasm and intimal injury.

Studies in pigs and dogs show that intimal injury is related to coronary artery spasm; it is not known whether intimal injury is related to coronary artery spasm in human beings. We examined intima at the site of coronary artery spasm by percutaneous transluminal coronary angioscopy in 10 of 13 consecutive patients with variant angina. Coronary artery spasms occurred spontaneously or were induced by intracoronary acetylcholine (10-100 micrograms). Angioscopy showed intimal injuries (haemorrhage, flap, thrombus, or ulcer) in 4 of the 10. We suggest that intimal injury is related to coronary artery spasm in human beings.

Angioscopy, coronary thrombi and acute coronary syndromes.

Coronary angioscopy is a new diagnostic imaging technique in which optic fibres are used to directly observe the intracoronary lumen. Angioscopy provides a full colour, high resolution, three-dimensional image of the intracoronary artery surface morphology. Studies using angioscopy revealed that the frequency of coronary thrombi in patients with acute coronary syndromes was higher than previous studies, based on arteriography, had reported. Arteriographic recognition of thrombus in unstable angina was from 1.3% to 52%. On the other hand, thrombi were observed in 88% by angioscopy in patients with rest angina in our study. Whereas ordinary arteriography provides only two-dimensional black and white images, angioscopy can distinguish between a thrombus and a plaque, even if the clot is very small. In a study of 17 unstable angina and 22 myocardial infarction patients, the frequencies of coronary thrombi in the two groups were essentially the same. Grayish-white thrombi were observed in most of the unstable angina patients but in none of the infarction patients. On the other hand, red or mixed red and white thrombi were observed in all infarction patients but in only a few unstable angina patients. This difference may account for the contrasting results of thrombolytic therapy.

The effectiveness of coronary angioscopy in detecting intraluminal pathologic changes.

We have evaluated the feasibility of percutaneous transluminal coronary angioscopy for detecting intraluminal pathological changes as a diagnostic tool, and investigated the pathogenesis of two acute coronary disorders, acute myocardial infarction and unstable angina. Twelve patients with an acute coronary disorder and 20 patients who underwent percutaneous transluminal coronary angioplasty were selected for this comparison between the diagnostic accuracy of angioscopy and arteriography. One hundred and thirty patients were investigated by angioscopy as follows in order to investigate the pathogenesis of their acute coronary disorders: 22 within 8 h of onset acute myocardial infarction; 28 from one day to 2 months since onset recent myocardial infarction; 37 with an old myocardial infarction; 26 with unstable angina; and 23 with stable angina. Our results have indicated thrombi were detected more frequently by angioscopy than by arteriography (p less than 0.01). Also, thrombi, intimal irregularities, and xanthomatous atheromas were observed more frequently in patients with acute myocardial infarction, recent myocardial infarction, and unstable angina. It is concluded that coronary angioscopy is a much more sensitive method for detecting intraluminal changes, and that a thrombus overlying a rupture in the lining of plaque plays a major role in an acute coronary disorders, and that the fragile, lipid-rich gruel atheroma may precede its rupture.

A serial observation of coronary thrombi in vivo by a new percutaneous transluminal coronary angioscope.

This study was undertaken to observe coronary thrombus formation serially from an antegrade perspective by means of a new thin flexible angioscope that has an inflatable balloon at the distal tip and an angulation mechanism. To test its capabilities, thrombi were induced in the left anterior descending coronary artery of 11 dogs by copper coils, and the thrombi were then observed through this angioscope, which had been introduced into the coronary artery by a guide catheter. Five minutes after insertion of the copper coil, fibrin-like material and white components of the thrombi were seen massing around the copper coil. Then, thin, mixed thrombotic white and red components formed around the copper coil. At fifteen minutes after the copper coil insertion, the thrombi grew in size. Ten minutes later, the thrombi finally obstructed the coronary lumen in most dogs. The red and white appearance of these thrombi was confirmed macroscopically, and the microscopic findings of these occluding thrombi revealed a fibrinous network with platelet aggregates and blood cell coagulation. Though ordinary angiography cannot reveal the precise features of the various coronary thrombi, this new angioscope was able to discern them from the antegrade perspective. The capabilities of this angioscope, which enabled these findings, should prove helpful in evaluating the stages of human coronary thrombosis. Of additional benefit, this angioscope can be used clinically for cardiac catheterization.

Painless myocardial ischemia in elderly patients compared with middle-aged patients and its relation to treadmill testing and coronary hemodynamics.

We compared painless ST-segment depression (1 mm greater than or equal to 80 ms and lasting greater than or equal to 60 s) in elderly patients with coronary artery disease (greater than or equal to 65 years, mean 67 years; n = 22) and that of middle-aged patients (less than 60 years, mean 54 years; n = 20) by Holter monitoring for 24 hours to determine the relationship between episodes of painless myocardial ischemia, findings of treadmill testing, and coronary hemodynamics. Coronary arteriographic findings (Gensini score) and ejection fraction (EF) did not differ between the two groups. Painless ST-segment depression was found to be 77% in the older age group versus 45% in the middle-aged group (p less than 0.05). However, treadmill exercise score, ST-segment depression, and ST-segment integral achieved did not differ significantly between the two groups. Within 2 weeks after the above testing, coronary hemodynamic study was performed. The increment of coronary sinus flow in the older age group was 1.4 +/- 0.3 versus 1.8 +/- 0.3 in the middle-aged group (p less than 0.05), and the change of lactate extraction ratio from the basal condition in the older age group was -50 +/- 40% versus -2 +/- 15% in the middle-aged group (p less than 0.05). We conclude that episodes of painless myocardial ischemia in elderly patients with aging may be associated with the impairment of the coronary vascular reserve and easier anaerobic myocardial metabolism by pacing stress despite similar findings of coronary artery disease and EF in both groups.

The effects of trapidil on left ventricular function and platelet aggregation in patients with coronary artery disease subjected to pacing.

The effects of the intravenous administration of 100 mg of trapidil on systolic and diastolic left ventricular functions and coronary sinus blood flow, as well as on myocardial lactate metabolism and platelet aggregation, were investigated before and after pacing in 12 patients with coronary artery disease. Pacing without administration of trapidil provoked angina in 6 of these patients. During rest, trapidil decreased the mean blood pressure by an average of 5 mmHg (from 112 +/- 15 to 107 +/- 8 mmHg, p less than 0.05) and the left ventricular end-diastolic pressure by an average of 4 mmHg (from 10 +/- 3 to 6 +/- 2 mmHg, p less than 0.05). Trapidil also caused both the max dp/dt and the coronary sinus blood flow to increase slightly, although it had no significant effect on diastolic function, myocardial lactate metabolism, or platelet aggregation. During the pacing that followed trapidil administration, chest pain was not provoked in the same 6 patients who had previously experienced chest pain on pacing. The extent of ST-segment depression also improved from -1.6 +/- 0.3 to -0.9 +/- 0.7 mm (p less than 0.05) and there was a significant suppression of the production of myocardial lactate. When pacing was terminated, trapidil caused a decrease in left ventricular systolic pressure from 173 to 156 mmHg (p less than 0.05), and also caused a decrease of the left ventricular end-diastolic pressure, from 16 +/- 4 to 8 +/- 2 mmHg (p less than 0.05). Trapidil had no significant effect on platelet aggregation activity with either a 1 microM or a 2 microM dose of ADP (adenosine diphosphate). However, the beta-TG level was suppressed, decreasing from 119 +/- 14 to 99 +/- 19 ng/ml in the arterial blood (p less than 0.1) and from 114 +/- 9 to 103 +/- 17 ng/ml (p less than 0.1) in the coronary sinus blood. Reductions in the preload and afterload by trapidil were of far greater magnitude than either its coronary dilatory or positive chronotropic effects in patients with coronary artery disease. Thus trapidil, a new antianginal agent appears to inhibit the production of platelet derived growth factors and may, therefore, protect the arteries from atherosclerosis as it promotes beneficial systemic hemodynamics in patients with depressed ventricular function.

How long can a coronary reperfusion catheter be placed in acute coronary occlusion following failed transluminal coronary angioplasty? A case report.

A coronary reperfusion catheter (CRC) is designed to preserve antegrade coronary flow when abrupt coronary closure occurs during percutaneous transluminal coronary angioplasty (PTCA). Insertion of the catheter to an occluded coronary artery for a few hours has been reported to be effective for myocardial salvage: however, it is unknown how long the catheter can be kept in place without causing extension of myocardial ischemia. The authors experienced a case in which the CRC was kept in place for twenty-four hours for anticoagulant therapy of an occluded coronary artery following failure of PTCA. This case suggests that adequate anticoagulant therapy can prolong the period during which a CRC can be kept in place if emergency coronary bypass surgery cannot be performed immediately after failure of coronary angioplasty.