Asymptomatic myocardial ischemia before and after surgical revascularization in patients with multivessel occlusive coronary disease

INTRODUCTION: The objective of this study was to examine the occurrence of asymptomatic myocardial ischemia prior to and after myocardial revascularization in patients with multivessel occlusive coronary disease. Asymptomatic ischemia can be described as real ischemia without anginal pain or other ischemic symptoms in patients with coronary disease or coronary artery spasm. Our study examined silent ischemia after myocardial revascularization. Early detection of silent ischemia is important for prevention of cardiac incidents. MATERIAL AND METHODS: We have examined patients with multivessel coronary disease with occurrence of continued preoperative silent ischemia. All patients have undergone ECG examination, exercise stress test and Holter-monitoring prior to and after myocardial revascularization. RESULTS: The investigation comprised 27 patients and their average age was 54.5 years. All patients with silent ischemia had a multivessel occlusive coronary disease and have undergone myocardial revascularization managed with triple or quadruple aortocoronary bypass surgery. Exercise stress test was performed postoperatively in elder patients, as well as ECG and Holter-monitoring. Silent ischemia was established in 21.6% of patients, while in 87.5% untreated diabetes mellitus was diagnosed. Silent ischemia most often occurred in the early morning hours and it was frequently associated with heart rhythm disturbances (VES) whereas these rhythm disturbances depended on the length of the ischemic episode. Intermittent 2nd degree atrioventricular block was found in one patient. CONCLUSION: Silent myocardial ischemia occurred in 21% of patients after myocardial revascularization. It is most often detected in the early morning hours and is associated with ventricular rhythm disorders. Silent ischemia is easily detected by simple examination procedures providing adequate therapy and prevention of cardiac incidents.     

Anti-ischemic and anti-anginal effects of thoracic epidural anesthesia versus those of conventional medical therapy in the treatment of severe refractory unstable angina pectoris

BACKGROUND: Cardiac sympathetic blockade by thoracic epidural anesthesia (TEA) dilates stenotic coronary arteries and has been used to control pain in patients with unstable angina. The aim of the present study was to evaluate the potential anti-ischemic effects of cardiac sympathetic blockade by TEA in severe, refractory, unstable angina. METHODS AND RESULTS: Forty patients with unstable angina refractory to standard anti-anginal therapy were randomized to receive either continuous epidural infusion of bupivacaine (TEA, Th1 to Th5) or to standard anti-anginal therapy including beta-blockers, calcium antagonists, aspirin, heparin, and nitroglycerin infusion (control group). The primary end points were number of anginal attacks and severity of myocardial ischemia assessed by 48-hour ambulatory Holter monitoring. The incidence of myocardial ischemia was lower in the TEA group (22% versus 61%; P<.05). The number of ischemic episodes per patient was 1.0+/-0.6 in the TEA group and 3.6+/-0.9 in the control group (P<.05). The episode duration per patient was 4.1+/-2.5 minutes and 19.7+/-6.2 minutes in the TEA and the control groups, respectively (P<.05). The mean area-under-the-ST-time-curve was 6.8+/-4.3 and 32.2+/-14.3 (mm-min) in the TEA and the control groups, respectively (P<.05). Fifteen anginal attacks were recorded in the control group and one attack in the TEA group (0.83+/-0.21 versus 0.06+/-0.06/patient, respectively, P<.01). CONCLUSIONS: The anti-ischemic and anti-anginal effects of continuous TEA are superior to those of conventional therapy in the treatment of refractory unstable angina.     

Results of dobutamine stress echocardiography in patients with syndrome X

This study describes the results of Dobutamine stress echocardiography in 10 patients with Syndrome X. The diagnosis of Syndrome X was made on the basis of the presence of exertional angina, positive exercise stress test, negative ergonovine stress test and normal coronary arteries at angiography. All patients underwent Dobutamine stress echocardiography after interruption of any antianginal therapy. Dobutamine was infused starting with a dose of 5 mcg/kg/min over 3 minutes with incremental steps of 5 mcg/kg/min every 3 minutes up to a maximal dose of 40 mcg/kg/min. Two-dimensional echocardiography and 12-lead electrocardiography was monitored during the infusion of the drug. Nine patients received the maximal dose while one patient prematurely stopped the test for the occurrence of side effects. None of the ten patients developed segmental left ventricular wall motion abnormalities indicative of myocardial ischemia; ST-segment depression diagnostic for ischemia developed in 30% of patients; angina was elicited in one of these patients and in two additional patients. A hyperkinetic response to Dobutamine infusion involving all the segments of the left ventricle was observed both in patients with and without chest pain or electrocardiographic changes. In patients with Syndrome X Dobutamine induces a hyperkinetic left ventricular response indicative of normal contractile reserve despite the presence in some cases of angina and electrocardiographic signs of ischemia.     

Silent myocardial ischemia in Kawasaki disease: evaluation of percutaneous transluminal coronary angioplasty by dobutamine stress testing

BACKGROUND: Myocardial ischemia and myocardial infarction are the most serious complications of coronary artery lesions in children with Kawasaki disease (KD). Therefore, early detection and treatment of myocardial ischemia in patients with KD is essential. We studied the effectiveness of percutaneous transluminal coronary angioplasty (PTCA) in patients with silent myocardial ischemia detected by dobutamine stress 99mTc myocardial scintigraphy (TMS), body surface mapping (BMS), and signal-averaged ECG late potentials (ELP). METHODS AND RESULTS: Eight of 76 asymptomatic patients with a coronary stenosis >25% and a positive dobutamine stress test were considered to have silent myocardial ischemia. All eight patients had >95% stenoses demonstrated by coronary angiography (CAG) just before PTCA. After PTCA, CAG showed that all of the coronary artery stenoses had been reduced to <50%. Additionally, intravascular ultrasonography (IVUS) performed in five patients before and after PTCA demonstrated adequate dilation of the coronary stenosis after PTCA. All eight patients underwent dobutamine stress TMS, BMS, and ELP 2 to 3 months after PTCA, which demonstrated no regions of myocardial ischemia. Approximately 6 months later, CAG was performed in all eight patients, and only one patient had developed restenosis. CONCLUSIONS: PTCA effectively dilates stenotic coronary arteries in children with KD. Moreover, dobutamine stress TMS, BMS, and ELP are useful for detecting silent myocardial ischemia and estimating the effectiveness of PTCA. Furthermore, IVUS is useful for evaluating the severity of coronary artery lesions before and after PTCA in patients with KD.     

Cardiotoxicity of 5-fluorouracil in combination with folinic acid in patients with gastrointestinal cancer

BACKGROUND: Cardiotoxicity related to the widely used cytotoxic compound 5-fluorouracil (5-FU) is rare compared with the frequency observed with the use of anthracyclines. More effective protocols incorporating active biomodulatory compounds like folinic acid (FA) or combination chemotherapy change type and severity of toxicity as well. The objective of the current study was to assess cardiotoxicity of the combination 5-FU and folinic acid. METHODS: The authors' multicenter experience with 390 patients treated for advanced gastrointestinal cancer with intermediate-dose folinic acid and 5-FU was reviewed. RESULTS: The overall risk of cardiotoxicity was 3%, which is not significantly higher than that reported with 5-FU alone. Eight of 53 patients with a history of cardiac disease reported cardiac symptoms (15.1%), compared with 5 of 337 patients (1.5%) with a no history of cardiac disease. Median time to symptoms was 3 days (range, 2-6). Nine patients had symptoms resembling myocardial ischemia, one patient died due to assumed myocardial infarction related closely to fluorouracil treatment, four patients had supraventricular arrhythmia, and one patient had congestive heart failure. A history of cardiac disease was the only risk factor associated with cardiotoxicity. Relapses were frequent on reinstitution of therapy despite cardiac symptoms in the preceding cycle. Therapeutically or prophylactically administered nitrates had no significant effect. CONCLUSION: Physicians should be aware of the cardiotoxic properties of active fluorouracil treatment. The combination of 5-FU and leucovorin does not differ from single-agent therapy in frequency or type of cardiotoxicity. Close monitoring of patients is mandatory, especially for those patients at high risk for cardiac side effects. Treatment should be discontinued if coronary symptoms develop, because neither effective treatment nor prophylaxis exists for such symptoms.     

Thallium-201 myocardial scintigraphy in patients with normal coronary arteries and normal left ventriculogram - comparison with hemodynamics, metabolic and morphologic findings (author's transl)

36 consecutive patients with chest pain and/or severe ventricular dysrhythmias, but normal coronary arteries and normal left ventriculogram, underwent thallium-201 myocardial imaging at rest and during exercise. The myocardial scintigram was abnormal in 27 patients (group A) and normal in only 9 patients patients (group B). To answer the question, whether the scintigram was false positive or a correct expression of a myocardial disorder not detectable with angiocardiographic methods, we compared the scintigraphic results with the findings of resting and exercise ECG (n = 36), mean pulmonary artery pressure during exercise (n = 27), myocardial lactate extraction during highrate atrial pacing (n = 14) and light- and electronmicropic examination of right ventricular endomyocardial biopsies (n = 14). The resting ECG was abnormal in 7 of 27 patients of group A and 1 of 9 patients of group B, the exercise ECG in 20 of 27 patients of group A and 1 of 9 patient B. An abnormally elevated exercise pulmonary artery pressure was measured in 10 of 21 patients of group A and 1 of 6 patients of group B. High rate atrial pacing induced an abnormal myocardial lactate extraction in 3 of 13 patients of group A, but not in the single investigated patient of group B. All 12 examined patients of group A and 1 of 2 patients of group B had abnormal biopsy findings. The high incidence of abnormal findings in group A compared to the rare incidence in group B suggests, that the abnormal myocardial scintigrams in patients with chest pain and normal coronary arteries is likely not false positive but reflects a myocardial disorder not being recognized on angiography.     

Embolization in the treatment of aneurysmal bone cysts

The successful stent placement for treatment of recurrent vasospastic angina in a patient with nonstenotic coronary arteries is described. Use of the Palmaz-Schatz stent resulted in successful vasodilation that completely prevented anginal attacks. This procedure represents an alternative treatment for patients with vasospastic angina refractory to aggressive medical therapy.     

Pseudoaneurysm of femoral artery after catheterisation: treatment by a mechanical compression device guided by colour Doppler ultrasound

A 28-year-old woman presented to the emergency department for evaluation of acute chest pain. She lacked risk factors for coronary artery disease and her initial electrocardiogram (ECG) was nondiagnostic. Within 45 minutes of presentation she developed nausea, vomiting, restrosternal chest pain, and ECG changes compatible with an acute inferoposterior myocardial infarction. Emergent cardiac catheterization revealed three-vessel coronary artery ectasia and two-vessel occlusion. She underwent emergency coronary artery bypass grafting. Her myocardial ischemia was believed to have been induced by methergine, which she had been taking over the preceding 3 days. The etiology and pathophysiology of coronary artery ectasia, as well as the cardiovascular effects of methergine and a related drug, ergotamine, are discussed.     

Refractory angina pectoris in end-stage coronary artery disease: evolving therapeutic concepts

Refractory angina pectoris in coronary artery disease is defined as the persistence of severe anginal symptoms despite maximal conventional antianginal combination therapy. Further, the option to use an invasive revascularization procedure such as percutaneous coronary balloon angioplasty or aortocoronary bypass grafting must be excluded on the basis of a recent coronary angiogram. This coronary syndrome, which represents end-stage coronary artery disease, is characterized by severe coronary insufficiency but only moderately impaired left ventricular function. Almost all patients demonstrated severe coronary triple-vessel disease with diffuse coronary atherosclerosis, had had one or more myocardial infarctions, and had undergone aortocoronary bypass grafting (70% of cases). We present three new approaches with antiischemic properties: long-term intermittent urokinase therapy, transcutaneous and spinal cord electrical nerve stimulation, and transmyocardial laser revascularization.     

Esophageal dysfunction in syndrome X

Syndrome X is defined as anginal chest pain accompanied by objective signs of ischemia on exercise testing or myocardial scintigraphy, but with angiographically "normal" coronary arteries. The etiology of this enticing syndrome is still not known. Besides myocardial ischemia, esophageal dysfunction and visceral hypersensitivity may play a role in the development of pain. The purpose of this study was to study esophageal function and visceral sensitivity in patients with syndrome X. Twenty consecutive patients with the diagnosis of syndrome X were investigated with esophageal manometry and a 24-hour pH recording. Visceral esophageal sensitivity was explored by balloon distention of the distal esophagus, as well as by instillation of acid. Twelve patients (67% of the 18 evaluated) had some abnormality on 24-hour pH monitoring; 2 had abnormal global acid exposure time (pH <4) and 7 had symptoms coincidental with episodes of pH <4. Seven patients (35%) had esophageal dysmotility including 5 with the "nutcracker" esophagus. Esophageal hypersensitivity to acid (n = 9) or distention (n = 13) was seen in 14 of the 20 patients. Eleven patients received acid suppressive therapy that resulted in amelioration of chest pain in 8 (73%). Thus, results suggest that esophageal hypersensitivity rather than gross functional abnormality is an important factor for the development of chest pain in patients with syndrome X, and that acid in the context of a hypersensitive esophagus is the main culprit. Acid suppression may ameliorate pain in a substantial proportion of patients.     

Effect of increased free fatty acids on myocardial oxygen extraction and angina threshold during atrial pacing

To evaluate whether elevated arterial free fatty acids (FFA) increase myocardial oxygen demand and ischemia, 15 fasting patients with coronary artery disease underwent a standardized atrial pacing test before (PTI) and during (PT2) heparin infusion. The patients were monitored for clinical and electrocardiographic (ECG) manifestations of ischemia. Myocardial extraction of lactate, inorganic phosphate, oxygen and FFA was measured before and during each PT. The control arterial FFA was 0.65 +/- 0.03 micromole/ml and rose to 1.83 +/- 0.16 micromole/ml during heparin influsion. Myocardial oxygen extraction at rest and during PT was not affected by the increase in arterial FFA. Seven patients asymptomatic during PT1 did not develop ischaemic manifestations during PT2. In eight patients with angina during both PTs, increased arterial FFA concentration did not modify the severity of anginal pain, the amount of ST-segment depression and the myocardial balance of lactate or inorganic phosphate. Elevation of arterial FFA by heparin neither increased myocardial oxygen extraction at rest or during pacing nor accentuated ischemic manifestations during PT.     

Spectrum of coronary arterial spasm. Clinical, angiographic and myocardial metabolic experience in 29 cases

A relationship of coronary arterial spasm to variant angina pectoris, subendocardial ischemia, major ventricular arrhythmias and myocardial infarction has been demonstrated. In 29 patients, spasm was angiographically observed in normal-appearing coronary arteries (7 patients) as well as superimposed on various degrees of coronary atherosclerotic obstruction (22 patients). All patients experienced an atypical anginal syndrome;16 patients also experienced typical exertional angina. Coronary spasm appeared to be a major contributory factor in eight occurrences of myocardial infarction and in 11 incidents of ventricular tachycardia, ventricular fibrillation and heart block. Coronary spasm in the 29 cases was distributed in the following fashion: left main trunk, 6 cases; right main trunk, 12 cases; proximal left anterior descending artery, 13 cases; proximal circumflex artery, 1 case; distal left anterior descending artery, 1 case; and distal circumflex artery, 2 cases. In 5 cases coronary spasm was noted at multiple sites.     

Left main coronary artery compression during primary pulmonary hypertension

Primary pulmonary hypertension (PPH) is often associated with angina-like chest pain, the mechanism of which is controversial. A 37-year-old woman with severe PPH and angina had transient ischemic ECG changes and reversible anterior perfusion defect on 201thallium scintigraphy. Coronary angiography revealed severe stenosis of the left main coronary artery (LMCA) and otherwise normal vessels. After heart-lung transplantation, examination of the explanted heart showed normal coronary arteries. Compression of the LMCA by the dilated pulmonary artery trunk was responsible for myocardial ischemia. This mechanism should be considered in patients with PPH and angina and might contribute to the high sudden death rate.     

The electrocardiogram during physical stress and Holter monitoring in the detection of asymptomatic myocardial infarct

INTRODUCTION: In patients with myocardial infarction acute myocardial ischaemia could be manifested by characteristic ischaemic symptoms or noncharacteristic symptoms such as cardiac insufficiency or heart rhythm disturbances. Sometimes myocardial ischaemia is not followed by any symptom. This condition is known as asymptomatic myocardial ischaemia. Asymptomatic myocardial ischaemia usually could be detected by treadmill exercise tolerance test or 24-hour Holter ECG monitoring. PATIENTS AND METHODS: We analyzed a group of 58 patients suffering from myocardial infarction with ST segment depression during the treadmill exercise tolerance test. All patients were on Holter 24-hour ECG monitoring. As a criterion of myocardial ischaemia during Holter monitoring ST segment depression of 1 mm and more, lasting 1 minute and more, and 0.08" of J point was accepted. RESULTS: During the treadmill exercise tolerance test segment depression was not followed by any symptom in 18 (31%) patients. There were no differences in the number of patients with hypertension in the group with symptoms and the group without symptoms. Diabetes mellitus was more frequent in the group with asymptomatic myocardial ischaemia. The average values of maximum ST segment depression and heart rates during treadmill tests were not statistically significant in both groups (with and without symptoms). During daily activities myocardial ischaemia was found in 30 (51%) patients by a 24-hour Holter ECG monitoring. We observed 198 episodes of myocardial ischaemia of which 138 (69.1%) were asymtomatic. The amplitude of ST segment depression and duration of these changes were significantly greater in the group with symptomatic episodes than in the group with asymptomatic episodes of myocardial ischaemia. DISCUSSION: Asymptomatic myocardial ischaemia is an often appearance in patients with myocardial ischaemia. Almost in 25% of persons in whom sudden death occurred obstructive changes in coronary arteries during the autopsy were found. Asymptomatic myocardial ischaemia could be found even an a "completely healthy person" without any complaints. Asymptomatic myocardial ischaemia is usually detected in a "completely healthy person" by casual diagnosis, in patients with stable and non stable angina pectoris, in patients with stenosis of the coronary arteries proved by angiography, and in patients after myocardial infarction. Some authors considered that treadmill exercise tolerance testing is less reliable to discover asymptomatic myocardial ischaemia comparing to the continuous 24-hour Holter ECG monitoring. It is know that in patients with diabetes mellitus neuropathy precedes the onset of symptomatic myocardial ischaemia. Asymptomatic myocardial ischaemia has the same predictive value for prognosis of the disease as symptomatic myocardial ischaemia. In some patients "anginal alarm system" is defective, and perception and conduction of pain sensations are disturbed. CONCLUSION: 1. In 31% of patients who suffered from myocardial infarction with ST segment depression during the treadmill testing asymptomatic myocardial ischaemia was found. 2. By Holter monitoring ischaemia ST segment depression during the exertion is observed in 52% of patients. Most of ischaemic episodes were asymptomatic. 3. The amplitude of ST segment depression is significantly greater and duration of depression is significantly longer in symptomatic episodes of myocardial ischaemia comparing to asymptomatic myocardial ischaemia obtained by Holter ECG monitoring.     

New approaches to resolving diagnostic problems in patients with angina pectoris

Several new noninvasive techniques are now available to evaluate the patient with chest pain to determine if myocardial ischemia is present. Continuous ambulatory ECG monitoring can detect myocardial ischemia in some patients who have normal ECG responses to graded exercise tests. Defects in myocardial perfusion can be visualized by radionuclide imaging at rest and after exercise. Also, abnormal left ventricular wall motion due to myocardial ischemia can be detected by gated blood pool scanning at the same time. Other techniques can olso be valuable in evaluating wall motion. Standard M-mode echocardiography can detect anteroseptal and posteroinferior wall motion abnormalities with remarkable anatomic detail, and newer echo techniques are promising for delineating the motion of other parts of the left ventricle. Finally, abnormal contractile areas can be assessed by videotracking the fluoroscopic cardiac silhouette and by a new noninvasive technique, the displacement cardiograph, which does not involve radiation exposure. Although none of these tests are both highly sensitive and highly specific for myocardial ischemia, their combined application in a symptomatic patient may provide considerable useful information which will help to determine who should be subjected to the risk and expense of coronary arteriography.     

Correlation between clinical course and quantitative analysis of the ischemia related artery in patients with unstable angina pectoris, refractory to medical treatment. Results of two randomized trials. The European Cooperative Study Group

Patients with unstable angina, refractory to intensive medical therapy, are at high risk for developing thrombotic complications, such as recurrent ischemia, myocardial infarction and coronary occlusion during coronary angioplasty. As both platelet aggregation and/or thrombus formation play an important role in this ongoing ischemic process, a monoclonal platelet GPIIb/IIIa receptor antibody (c7E3) or thrombolytic therapy (alteplase) might be able to modify the clinical course and underlying coronary lesion morphology. To evaluate whether alteplase or c7E3 could influence the incidence of complications, we randomized 36 and 60 patients, respectively to alteplase or placebo, or c7E3 or placebo. All patients exhibited dynamic ECG changes and recurrent pain attacks, despite maximal tolerated medical therapy. Patients were randomized in both studies after initial angiography had demonstrated a culprit lesion amenable for angioplasty. After study drug infusion quantitative angiography was repeated and angioplasty performed. Recurrent ischemia during study drug infusion occurred in 5, 6, 9 and 16 patients from the alteplase, placebo, c7E3 and placebo group, respectively. Major events defined as death, myocardial infarction or urgent intervention occurred in 7, 3, 1 and 7 patients, respectively. Two patients died: one in the alteplase group and one in the placebo group from the c7E3 study. The first patient due to retroperitoneal hemorrhage, the second as a result of recurrent infarction. Qualitative angiography showed resolution of clots in the c7E3 group only, while the same group of patients showed in 20% an improvement in TIMI flow grade, without deterioration in any patient from this group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute von Willebrand factor secretion from the endothelium in vivo: assessment through plasma propeptide (vWf:AgII) Levels

STUDY OBJECTIVES: Patients with coronary heart disease (CHD) and obstructive sleep apnea may have an increased cardiac risk due to nocturnal myocardial ischemia triggered by apnea-associated oxygen desaturation. Sleep structure in patients with obstructive sleep apnea is fragmented by activation of the central nervous system (CNS) (arousal) due to obstructive apneas. Nocturnal myocardial ischemia may lead to activation of the CNS as well. PATIENTS: Fourteen patients with obstructive sleep apnea and CHD disease and seven patients suffering from obstructive sleep apnea without CHD were studied. Overnight sleep studies and simultaneous six-lead ECG recordings were performed. In addition, sleep studies and ECG recordings were performed with administration of a sustained-release nitrate in these patients in a double-blinded crossover design. RESULTS: Analysis of three nights' recordings revealed 144 episodes of nocturnal myocardial ischemia in six subjects. Five patients had underlying CHD and one patient exhibited diffuse wall defects of the coronary arteries; also, 85.4% of ischemic episodes were concomitant with apneas and oxygen desaturation > 3%, and 77.8% of ischemic episodes occurred during rapid eye movement (REM) sleep, although total amount of REM sleep was only 18% of total sleep time. Mean oxygen saturation was significantly lower (p < 0.05) during apnea-associated ischemic episodes than during nonapnea-associated ischemia (77.3% vs 93.1%). Nitrate administration did not reduce ischemic episodes. Sleep architecture (macrostructure) exhibited a reduction in sleep stages non-REM 3 and 4 and REM sleep. Comparing the microstructure of sleep (arousals) within episodes with and without ischemia but similar criteria like sleep stage, apnea activity, and oxygen saturation, we found significantly more (p < 0.01) and severe (p < 0.001) arousals during periods with myocardial ischemia than during control episodes. In addition, microstructure of sleep was disturbed by myocardial ischemia itself in absence of apneas. CONCLUSION: It is concluded that patients with CHD and obstructive sleep apnea are endangered by apnea-associated ischemia and that these ischemic episodes lead to activation of the CNS and additional fragmentation of sleep. Patients with nocturnal ischemia should be screened for underlying sleep apnea even if nitrate therapy fails.     

Soluble P-selectin is released into the coronary circulation after coronary spasm

BACKGROUND: The glycoprotein P-selectin is an adhesion molecule involved in the property change of leukocytes at the initiation of the inflammatory process. The purpose of the present study was to determine whether acute myocardial ischemia induced by coronary spasm causes an acute inflammatory response in the coronary circulation. METHODS AND RESULTS: We examined plasma soluble P-selectin levels in the coronary sinus and the aortic root simultaneously in 16 patients with coronary spastic angina before and after left coronary artery spasm induced by intracoronary injection of acetylcholine and in 15 patients with stable exertional angina before and after acute myocardial ischemia induced by rapid atrial pacing. Ten control patients with chest pain but normal coronary arteries and no coronary spasm also received intracoronary acetylcholine. Plasma soluble P-selectin levels were increased significantly in the coronary sinus (32.8 +/- 3.6 to 52.8 +/- 5.9 ng/mL, P < .001) and in the aortic root (34.6 +/- 3.7 to 41.9 +/- 4.4 ng/mL, P < .05) after the attacks in the coronary spastic angina group but remained unchanged in the stable exertional angina group after the attacks and in the control group after the administration of acetylcholine. Furthermore, the coronary sinus-arterial difference of soluble P-selectin increased significantly after the attacks in the coronary spastic angina group (-1.8 +/- 2.2 to 10.9 +/- 2.7 ng/mL, P < .001). CONCLUSIONS: Our data indicate that soluble P-selectin is released into the coronary circulation after coronary artery spasm. We conclude that coronary artery spasm may induce the leukocyte adhesion in the coronary circulation and may lead to myocardial damage.     

Measurement of cerebral blood flow during cardiopulmonary bypass with near-infrared spectroscopy

OBJECTIVES: We sought to assess the incidence and clinical relevance of examination data to recurrent ischemia within an international randomized trial. BACKGROUND: Ischemic symptoms commonly recur after thrombolysis for acute myocardial infarction. METHODS: Patients (n = 40,848) were prospectively evaluated for recurrent angina and transient electrocardiographic (ECG) or hemodynamic changes. Five groups were developed: Group 1, patients with no signs or symptoms of recurrent ischemia; Group 2, patients with angina only; Group 3, patients with angina and ST segment changes; Group 4, patients with angina and hemodynamic abnormalities; and Group 5, patients with angina, ST segment changes and hemodynamic abnormalities. Baseline clinical and outcome variables were compared among the five groups. RESULTS: Group 1 comprised 32,717 patients, and Groups 2 to 5 comprised 20% of patients (4,488 in Group 2; 3,021 in Group 3; 337 in Group 4; and 285 in Group 5). Patients with recurrent ischemia were more often female, had more cardiovascular risk factors and less often received intravenous heparin. Significantly more extensive and more severe coronary disease, antianginal treatment, angioplasty and coronary bypass surgery were observed as a function of ischemic severity. The 30-day reinfarction rate was 1.6% in Group 1, 6.5% in Group 2, 21.7% in Group 3, 13.1% in Group 4 and 36.5% in Group 5 (p < 0.0001); in contrast, the 30-day mortality rate was significantly lower (p < 0.0001) in Groups 1, 2 and 3 (6.6%, 5.4% and 7.7%, respectively) than in Groups 4 and 5 (21.8% and 29.1%). CONCLUSIONS: Postinfarction angina greatly increases the risk of reinfarction, especially when accompanied by transient ECG changes. However, mortality is markedly increased only in the presence of concomitant hemodynamic abnormalities.     

Randomised comparison of subcutaneous heparin, intravenous heparin, and aspirin in unstable angina. Studio Epoorine Sottocutanea nell'Angina Instobile (SESAIR) Refrattorie Group

Intravenous heparin has been used in the control of myocardial ischaemia in patients with unstable angina. We set out to assess the efficacy of subcutaneous heparin in reducing myocardial ischaemia in patients with unstable angina. 343 of 399 patients with unstable angina were monitored for 24 h and 108 were refractory to conventional antianginal treatment and were entered into a randomised multicentre trial. 37 patients were assigned to heparin infusion (partial thromboplastin time 1.5-2 times baseline), 35 to subcutaneous heparin (adjusted dose with partial thromboplastin time 1.5-2 times baseline), and 36 to aspirin (325 mg daily). All had additional conventional antianginal therapy. After the run-in patients were monitored for 3 days. The primary endpoint was reduced myocardial ischaemia assessed by the number of anginal attacks, silent ischaemic episodes, and duration of ischaemia per day. At 1 week and 1 month we accounted for anginal attacks and other clinical events (myocardial infarction, revascularisation procedures, and death). Aspirin did not significantly affect the incidence of myocardial ischaemia. On the first 3 days, infused and subcutaneous heparin significantly decreased the frequency of angina (on average by 91% and 86%, respectively), episodes of silent ischaemia (by 56% and 46%), and the overall duration of ischaemia (66% and 61%) versus run-in day and aspirin (p < 0.001 for all variables). The favourable effects of heparin therapy remained evident during follow-up. Only minor bleeding complications occurred. Subcutaneous heparin is effective in the control of myocardial ischaemia in patients with unstable angina.