[Hyperthyroidism, eosinophilia, and fever in a 64-year-old patient]. / Hyperthyreose, Eosinophilie und Fieber bei einem 64-jährigen Patienten.

We report on a male patient suffering from loss of weight, fatigue, fever, eosinophilia, and hyperthyreoidism. The echocardiogram revealed a left atrial mass originating from the posterior mitral leaflet. In combination with the constitutional symptoms a left atrial myxoma was diagnosed. The tumor was surgically removed. Postoperatively therapy with corticosteroids and thiamazole was stopped. During follow-up, eosinophilia and hyperthyreodism could no longer be detected.

[The Ross procedure (pulmonary autograft) as an alternative for aortic valve replacement]. / Die Ross-Operation (pulmonaler Autograft) als alternativer Aortenklappenersatz.

BACKGROUND AND OBJECTIVE: The Ross procedure (pulmonary autograft) has since the 1980s attracted growing interest as an alternative to the widely practised insertion of a prosthetic aortic valve. The 12-year experience of a consecutive series from one centre are reported here. PATIENTS AND METHODS: Between February 1990 and January 2002 a Ross procedure, predominantly with the subcoronary technique, was performed in 244 consecutive patients with aortic valve disease (244 men, 54 women, mean age 46 +/- 13.5 years). Annual follow-up clinical examinations (mean postoperative period 32.9 +/- 29.5 months in 99 % of the cohort) were performed. RESULTS: Perioperative mortality was 0.8 % (n=2), and there were two late deaths unrelated to the aortic valve disease. Seven patients had to be re-operated for failure of the homograft (n=4) or autograft (n=4). According to clinical criteria, 99 % of the followed-up patients were in New York Heart Association (NYHA) functional class I or II, only two patients, with pulmonary comorbidity, were in class III. Echocardiography demonstrated autografts with nearly normal transvalvular gradient (mean maximal pressure gradient 6.5 +/- 3.3 mmHg), while nine patients had second-degree aortic regurgitation. The mean maximal gradient across the homograft valve in the pulmonary position was 12.0 +/- 6.9 mmHg, while ten patients had second-degree and one had third-degree pulmonary regurgitation. CONCLUSION: The technically demanding Ross procedure produced excellent clinical and hemodynamic mid-term results. It is thus an appealing alternative to the widely used replacement by a prosthetic valve. Definitive assessment awaits further long-term follow-up.

Decellularized pulmonary homograft (SynerGraft) for reconstruction of the right ventricular outflow tract: first clinical experience.

INTRODUCTION: Cryopreserved homograft valve conduits have been used to reconstruct the right and left ventricular outflow tract. Long-term studies have shown homograft degeneration and calcification, and it has been postulated that immunological mediated phenomena in a manner similar to that seen in chronic rejection may contribute to the degeneration process. The development of a decellularized, non-glutaraldehyde-fixed valve conduit creates a non-immunogenic connective tissue matrix for autologous recellularization by host cells. The aim of the study was to characterize the clinical and hemodynamic pattern in human implants of the novel decellularized pulmonary homografts (SynerGraft). METHODS: Reconstruction of the right ventricular outflow tract was performed in 17 patients: 15 patients with aortic valve disease and the Ross procedure, and two patients with redo procedures following Fallot tetralogy and severe pulmonary regurgitation. Patients with the Ross procedure with standard cryopreserved homografts as neopulmonic conduits served as controls. Within the follow-up over six months morphological and hemodynamic parameters were characterized by echocardiography: maximal and mean pressure gradient across the right and left ventricular outflow tract, their effective orifice areas, determination of neopulmonic and neoaortic regurgitation. RESULTS: One patient died six weeks following surgical treatment due to non-valve related end-stage cardiopulmonary failure; all patients were free of valve-related complications during the follow-up period. The matched Ross patients showed a gradual but significant increase of both the maximal and mean pressure gradient across the right ventricular outflow tract (Delta P max 5.5+/-2.5 to 11.4+/-6.4 mmHg, p=0.002; Delta P mean 3.0+/-1.3 to 6.2+/-3.9 mmHg, p=0.003), whereas in the SynerGraft group increase of pressure gradients were measurable but did not reach statistical significance (Delta P max 7.1+/-3.7 to 10.1+/-3.9 mmHg, p=0.11; Delta P mean 3.6+/-1.6 to 5.5+/-2.3 mmHg, p=0.12). The pulmonary effective orifice areas decreased in the control group from 1.74+/-0.33 to 1.18+/-0.36 cm(2)/m(2) (p=0.001). Within the SynerGraft group time dependent reduction of the orifice area was significantly less (1.51+/-0.37 to 1.25+/-0.26 cm(2)/m(2); p=0.08). CONCLUSION: Up to six months after implantation reconstruction of the right ventricular outflow tract with decellularized homografts was safe, stable, and the morphological and hemodynamic features are promising.

Soluble L-selectin and neutrophil derived oxidative stress after pacing induced myocardial ischemia in chronic stable coronary artery disease.

We studied the effect of atrial pacing induced myocardial ischemia on levels of soluble L-selectin (sL-selectin) and generation of neutrophil derived reactive oxygen species (ROS) in 10 patients with coronary artery disease (CAD) and stable angina and in six individuals without CAD. Myocardial ischemia was measured metabolically by lactate sampling from the coronary sinus (CS) and arterial blood at each pacing step. Before each pacing step, at peak pacing and shortly after cessation, plasma concentrations of sL-selectin and generation of ROS using the chemiluminescence method were measured in CS and femoral artery blood. Baseline sL-selectin levels in CS samples were significantly lower in the CAD compared to the control group (547 +/- 80 vs 836 +/- 82 ng/mL, P = 0.03). At peak pacing, nine of ten patients with CAD developed myocardial ischemia (lactate extraction ratio at rest 28% +/- 7%, at peak pacing -16% +/- 6%). In these patients, luminol-enhanced chemiluminescence (CL, 0.88 +/- 0.45 vs 1.9 +/- 0.9 cpm x 10(5), P = 0.09) and levels of sL-selectin (547 +/- 80 vs 764 +/- 86 ng/mL, P = 0.03) from naive neutrophils increased significantly in CS blood suggesting a potent in vivo activation of neutrophils. In control patients, incremental pacing caused neither myocardial ischemia nor a significant change of chemiluminescence or of sL-selectin levels. In conclusion, myocardial ischemia induced by pacing tachycardia is able to activate neutrophils in patients with chronic stable coronary artery disease leading to increased generation of ROS and shedding of L-selectin into the coronary circulation.

Exercise-induced myocardial ischemia in isolated coronary artery ectasias and aneurysms ("dilated coronopathy").

OBJECTIVES: The purpose of our study was to evaluate the clinical significance of isolated coronary artery ectasias or aneurysms (CEA). BACKGROUND: It has been postulated that altered coronary blood flow in CEA predisposes patients to the development of myocardial ischemia (CI) and infarction. METHODS: Sixty-seven patients with bilateral nonobstructive CEA without associated cardiac defects ("dilated coronaropathy") were derived from 16,341 cardiac catheterizations between 1986 and 1997. Ectasias were defined as luminal dilation of 1.5- to 2.0-fold, aneurysms of >2.0-fold of normal limits. Eleven of 25 patients presented with myocardial infarction due to an occlusion of the infarct vessel. In 42 patients without infarction (study group), exercise-induced CI was investigated. RESULTS: A corresponding CI was documented in 32 of 42 patients in a coronary sinus lactate study (reduced lactate extraction 5.6 +/- 4.1%) and in 29 of 40 patients in an ergometry (0.25 +/- 0.06 mV ST depressions). The results differed significantly from a control group of 29 patients without heart disease (p < 0.001). Nitroglycerin (0.8 mg) provoked a further significant deterioration of CI in the 32 of 42 developing a frank cardiac lactate production (-2.6 +/- 6.8%, p < 0.001). The metabolic extent of CI was significantly correlated to the coronary diameters of the proximal and middle segments of left anterior descending artery and the middle segment of left circumflex artery (r = 0.87, p < 0.001). Stigmata of an impaired coronary blood flow such as delayed antegrade filling, segmental backflow phenomenon and local deposition of dye were found significantly more often with increasing coronary diameters (p < 0.04). CONCLUSIONS: "Dilated coronaropathy" is an entity of nonobstructive, ischemic coronary artery disease. Nitroglycerin is of no therapeutic benefit but leads to an aggravation of exercise-induced CI.

[Cardiac endothelin release into the coronary sinus in myocardial ischemia and coronary endothelial injury]. / Untersuchungen zur kardialen Endothelin-Freisetzung in den Koronarsinus bei Myokardischämie und koronarem Endotheltrauma.

UNLABELLED: Endothelin has both vasoconstrictor and mitogenic properties and might, therefore, play a role in the pathogenesis of acute coronary syndromes and coronary atherosclerosis. The aim of the study was to characterize the mechanisms and kinetics of cardiac endothelin-1 (ET-1) release following a local endothelial injury during PTCA (group A) and after sustained myocardial ischemia (group B). Additionally, the precision of agreement between measurements in coronary sinus and peripheral venous samples should be analyzed. In group A, elective PTCA was performed in 20 patients with stable angina pectoris and a > 70% type A stenosis. Simultaneous determinations of ET-1 from coronary venous and peripheral venous blood were done before balloon inflation and during the several hours following the last dilatation procedure. A coronary sinus study with high rate atrial pacing was performed in 20 group B patients with coronary multivessel disease. ET-1 was determined from coronary sinus and peripheral venous blood samples prior to stimulation and during several hours after cessation of pacing. Control groups were provided for both groups. The control group consisted of 10 patients with coronary angiography without PTCA for group A and 10 patients with angiographic normal coronary arteries for group B.PTCA induced an instantaneous increase of coronary sinus ET levels from 4.1 +/- 1.1 pg/ml to 13.7 +/- 2.3 pg/ml (peripheral venous 7.9 +/- 2.5 pg/ml), which was more pronounced if the target vessel was the left anterior descending artery. This peak was followed by a gradual decrease of ET-1 to the limit of normal within 6 hours. The concentrations of ET, furthermore, remained higher in the coronary sinus compared with the peripheral vein indicating a persisting cardiac release of ET. In group B, incremental atrial pacing resulted in myocardial ischemia, and a significant increase in ET-1 from 4.6 +/- 0.6 pg/ml to 13.1 +/- 2.8 pg/ml was detected in the coronary sinus samples. A persistent cardiac release of ET-1, as reflected by sustained elevated coronary sinus concentrations, was observed for up to one hour after cessation of pacing. The analysis of measurement agreement between coronary venous and peripheral venous samples revealed considerable variations of the differences between the two sampling sites indicating wide limits of agreement. Despite a significant positive correlation, our date reflecting a remarkable lack of agreement. CONCLUSIONS: 1) An enhanced release of ET-1 following PTCA is mainly due to the localized endothelial injury, and the ET-1 levels remain elevated for up to hours after the mechanical stimulus. 2) A short-lasting myocardial ischemia is associated with a significant ET-1 increase. 3) For refined evaluations of release kinetics of cardiac ET-1, blood sampling from the coronary sinus seems to be essential.

Acquired thromboatheromatous coarctation of the aorta: acquired coarctation of the aorta.

BACKGROUND: Atheromatosis of the thoracic aorta and aortic arch is a well established source of systemic embolism. Acquired atheromatous coarctation of the aortic arch is a rare finding and not well documentated so far. CASE REPORT AND FINDINGS: Two patients presenting with intermittent claudication of the lower extremities were identified as having thromboatheromatous coarctation of the aortic arch as visualized by magnetic resonance tomography, fast CT scan, transesophageal echocardiography, cardiac catheterization and aortography. All findings including invasive hemodynamics resembled congenital coarctation of the aorta. One patient was treated surgically, while the other refused surgery and received long-term anticoagulation. CONCLUSION: Atheromatosis of the thoracic aorta and aortic arch not only cause systemic embolism, but may lead to the clinical and hemodynamic picture of coarctation of the aortic arch.

Prothrombin fragments F1+2, thrombin-antithrombin III complexes, fibrin monomers and fibrinogen in patients with coronary atherosclerosis.

We determined the plasma levels of prothrombin fragment F1+2, thrombin-antithrombin III complexes (TAT), fibrin monomers (FM), D-dimers (DD) and fibrinogen in 57 patients with angiographically verified graded coronary artery disease (CAD) free of concomitant peripheral atherosclerosis, cerebrovascular disease or diabetes mellitus and a group of 21 apparently healthy controls. Blood was collected from the antecubital vein through atraumatic venipuncture prior to the angiographic procedure. Plasma levels of hemostatic markers were related to the presence and graded severity of CAD. The levels of prothrombin fragment F1+2 (1.74+/-0.11 vs. 1.0+/-0.07 nmol/l, P<0.001), FM (41.6+/-5.5 vs. 7.42+/-3.05 nmol/l, P<0.001), TAT (15.6+/-2.7 vs. 2.96+/-0.32 microg/l, P<0.001) and fibrinogen (3.64+/-1.3 vs. 3.08+/-0.33 g/l, P<0.01) were significantly higher in patients with CAD compared to controls, while there was no difference regarding the fibrinolytic system represented by DD (441.6+/-58.9 vs. 337.4+/-42.05 microg/l, n.s.). Within the CAD group, patients with extensive coronary atherosclerosis (> or =2 vessel disease) had significantly higher values for prothrombin fragment F1+2 (1.89 vs. 1.57 nmol/l, P = 0.04), FM (50.7 vs. 29.8 nmol/l, P = 0.03), and a trend to significance was noted for fibrinogen (3.9 vs. 3.3 g/l, P = 0.07) suggesting that blood coagulability was related to the severity of the disease and that hemostatic markers of thrombin activity represent a useful tool to identify patients with a latent hypercoagulable state with a higher susceptibility to sustain coronary thrombosis.

[Atherosclerosis of the aorta as a source of arterial embolisms]. / Die Atherosklerose der Aorta als Quelle arterieller Embolien.

Aortic atherosclerosis has early been recognized as a potential source of embolism. The histological finding of cholesterol clefts in small end-arteries characterized the entity of cholesterol embolism. The clinical picture was extremely variable and the diagnosis was frequently established post-mortem or by means of invasive although insensitive procedures including biopsy and angiography. Therefore, cholesterol embolism was thought to be rare. With the routine use of transesophageal echocardiography for the diagnostic workup of arterial embolism, aortic atherosclerosis was shown to be the source of otherwise unexplainable embolism. Cross-sectional studies demonstrated an independent association between prominent plaques of more than 4 to 5 mm of thickness or plaques with mobile components in the aortic arch. In follow-up studies, the risk of embolic events in patients with this kind of lesions exceeded 10% per patient-year. The results of pathological studies were consistent with these findings showing that ulcerated complex plaques carry an independent risk for embolic events. Apart from spontaneous embolism, atherosclerosis of the proximal aorta was shown to be a cause of embolic complications during cardiac surgery and catheterization procedures which involve the aorta. Medical treatment for the prevention of embolism in atherosclerotic disease of the aorta has not been studied systematically. In a variant form of aortic atherosclerosis consisting of mobile pedunculated thrombi inserting on relatively small plaques, anticoagulant therapy has proved to be useful in small numbers of patients. Recurrent embolic events could be prevented and regression of the thrombotic masses has been observed.

Cardiac release and kinetics of endothelin after uncomplicated percutaneous transluminal coronary angioplasty.

This study was designed to assess the release kinetics of endothelin after percutaneous transluminal coronary angioplasty (PTCA) and to prove the coronary endothelium as the source of the endothelin release. Twenty-seven patients with single-vessel coronary artery disease underwent PTCA. Endothelin, troponin T, myoglobin, and creatine phosphokinase paired blood samples were withdrawn from the coronary sinus and a peripheral vein before the balloon maneuver and at 1, 5, 10, 30, 45 minute(s), and at 1, 2, 3, 6, 12, and 24 hour(s) after the last balloon maneuver. Myocardial ischemia was monitored by means of cardiac lactate metabolism and 12-lead electrocardiogram. Thirteen patients who underwent a diagnostic cardiac catheterization served as a control group. In the left coronary artery, PTCA (n = 19) endothelin concentrations increased from 4.1 pg/ml as a common mean baseline level before intervention to 13.9 +/- 2.6 pg/ml (mean +/- SD) in the coronary sinus and 7.9 +/- 2.2 pg/ml (mean +/- SD) in the peripheral vein at 1 minute after the intervention (p <0.001). The levels remained elevated for 3 hours with higher coronary sinus than peripheral venous concentrations due to persistent cardiac endothelin release. PTCA of the right coronary artery (n = 8) also led to an instantaneous endothelin increase from a mean concentration of 4.4 before intervention to 8.3 pg/ml after intervention with identical coronary sinus and peripheral venous levels (p <0.001). Endothelin levels gradually decreased to normal within 6 hours. No patient developed a measurable myocardial ischemia or a myocardial infarction. In the control group all parameters remained unchanged. Uncomplicated PTCA was followed by a significant cardiac endothelin release that seems to indicate endothelial injury and not myocardial ischemia.

An optimized AV delay algorithm for patients with intermittent atrioventricular conduction.

Detection and promotion of an intermittent atrioventricular (AV) conduction is the objective of an AV delay hysteresis algorithm in dual chamber pacemaker (DDD) pacing. The AV delay following an atrial event is automatically extended by a programmable interval (AV hysteresis interval) if the previous cycle showed spontaneous AV conduction, i.e., a ventricular event was detected within the previous AV delay. An automatic search mode scans for spontaneous ventricular events during the hysteresis interval: a single AV delay extension (equal to the programmed AV delay hysteresis) will occur after a successive, programmable number of AV cycles with ventricular pacing. If a spontaneous AV conduction is present, the AV delay will remain extended by the hysteresis interval. Our first results in 17 patients with intermittent AV block disclosed a satisfactorily working algorithm with effective reduction of ventricular stimuli. In relation to the underlying conduction disturbance and pacemaker settings, the majority of our patients showed a reduction of ventricular pacing events up to 90% without any adverse hemodynamic or electrophysiological changes. Based on clinical (promotion of a physiological activation and contraction sequence) and technical (reduction of power consumption) advantages, the AV hysteresis principle could be of incremental value for future dual chamber pacing in patients with intermittent complete heart block.

Topographic pattern of advanced atherosclerotic lesions in carotid arteries.

Ulcers in extracranial carotid arteries are a known source of cerebral embolism. However, there are no data available on the prevalence of ulcerations located at the origin of these vessels in the aortic arch. Therefore, in this pathological study the topographic distribution of ulcerated lesions were determined in these arteries. One hundred and one consecutively autopsied patients composed the study group. Ulcerated plaques were sought for in both carotid arteries, from their origin in the arch up to the carotid canal, and also in the aortic arch and ascending aorta. The two anatomical sites mostly affected by atherosclerosis were the region of the carotid sinus and the orifices of cervical arteries in the aortic arch. More than one third of all ulcers were at the orifices of cervical arteries in the arch. Interestingly, ulcers at the orifice of the left common carotid artery in the arch were accompanied with other ulcers located elsewhere in the remaining segments of the left carotid system, whereas ulcerations at the orifice of brachiocephalic trunk were not accompanied with other concomitant lesions in the right carotid system. Furthermore, there was no symmetric distribution of ulcerated plaques in both carotid systems.

Myocardial ischemia in generalized coronary artery-left ventricular microfistulae.

Generalized (multiple) arterio-systemic fistulae are fistulae arising from all three major coronary arteries and drain into the left ventricle are rare and the clinical and hemodynamic sequelae are incompletely understood. This communication is based on the clinical and hemodynamic data of a series of patients (eight cases out of 7262 consecutive patients) incidentally identified at coronary angiography combined with data from cases previously reported in literature. The aim was to assess the role of generalized coronary artery fistulae as a non-atherosclerotic cause of myocardial ischemia by means of a coronary sinus lactate study. Coronary sinus lactate study demonstrated myocardial ischemia in 6/7 patients. Mean arterio-coronary venous lactate difference decreased from 0.31+/-0.18 mmol/l (lactate extraction ratio, LER, 29.4+/-13.9%) at rest to 0.04+/-0.13 mmol/l (LER -4.0+/-13.3%) at peak exercise. Five minutes after cessation of pacing, lactate difference increased to 0.22+/-0.21 mmol/l (LER -20.7+/- 13.2%). At peak pacing stress, 4/7 patients showed frank lactate production, and two patients presented with a reduced cardiac lactate extraction rate also indicating myocardial ischemia metabolically. In the present study, we demonstrated a possible role of a coronary steal mechanism due to microfistulae pathways in the pathogenesis of myocardial ischemia in patients with generalized coronary artery-left ventricular microfistulae.

Relation between QT dispersion and the extent of myocardial ischemia in patients with three-vessel coronary artery disease.

The aim of the study was to examine the relation between the extent of myocardial ischemia and changes in QT interval dispersion in patients with obstructive coronary artery disease and in patients with normal coronary arteries. QT interval dispersion reflects regional variations in ventricular repolarization and cardiac electrical instability. Previous studies showed QT interval dispersion changes during episodes of myocardial ischemia in patients with coronary artery disease, but no data on the relation between extent of myocardial ischemia and degree of QT interval dispersion changes are available. To assess the effects of myocardial ischemia on myocardial repolarization by analyzing the change in QT dispersion during incremental atrial pacing, we studied 33 patients (7 women and 26 men, mean age 60.1 +/- 5.1 years, 18 patients with normal coronary arteries, 15 patients with coronary 3-vessel disease). QT dispersion was measured at baseline, after each pacing period, within 30 seconds after cessation of pacing ("peak ischemic stress"), and at 1-minute intervals for up to 5 minutes. Paired blood samples for determination of serum lactate were withdrawn from the coronary sinus and radial artery to determine the cardiac lactate extraction ratio at each point of electrocardiographic registration. In patients with coronary artery disease, QT dispersion increased from a baseline value of 39 +/- 7 ms to a peak ischemic stress value of 63 +/- 10 ms (p <0.0001). Patients with normal coronary arteries showed almost unchanged values of QT dispersion (41 +/- 9 vs 42 +/- 7 ms). There was a significant relation between the pacing-induced change in QT dispersion and the induced change in myocardial lactate extraction ratio (r = 0.76, p <0.0001). The change in QT dispersion (baseline vs peak pacing stress) was related to the extent of the cardiac lactate extraction ratio (r = -0.79, p <0.0001). These data indicate that the severity or extent of induced myocardial ischemia was related to the degree of induced changes of the variability in the timing of the ventricular recovery pattern.

Neutrophil-derived oxidative stress after myocardial ischemia induced by incremental atrial pacing.

We studied the effect of atrial pacing-induced myocardial ischemia on the generation of oxygen free radicals (OFR) in 8 patients with verified coronary artery disease (CAD) and in a control group of 4 patients without coronary atherosclerosis. Myocardial ischemia was measured metabolically by simultaneous lactate sampling from coronary sinus (CS) and arterial blood. Generation of OFR from purified viable polymorphonuclear neutrophils (PMN) was assessed by means of the chemiluminescence (CL) method. At peak pacing, 7 of 8 patients with CAD exhibited transient myocardial ischemia (mean lactate extraction ratio at rest: 23.6 +/- 7.7 vs 5.21 +/- 5.1% at peak pacing, p = 0.012). In these patients, unstimulated PMN harvested from the CS depicted a significant increase of luminol-enhanced CL (from 1.06 +/- 0.54 to 2.15 +/- 1.28 cpm x 10(5), p = 0.012) after atrial pacing. There was no additional effect from further ex vivo stimulation with phorbol myristate acetate. This finding underscores the role of myocardial ischemia as a potent endogenous activator of PMN function and may have implications in the pathogenesis and progression of atherosclerosis.

Priming of neutrophils after elective percutaneous transluminal coronary angioplasty is unrelated to accompanying brief myocardial ischemia.

OBJECTIVE: The purpose of this study was to investigate the effect of brief myocardial ischemia and vascular trauma induced by elective percutaneous transluminal coronary angioplasty on in vivo 'priming' and activation of neutrophils. PATIENTS AND METHODS: We studied 16 patients undergoing elective coronary angioplasty for symptomatic coronary artery disease and a control group of seven patients undergoing diagnostic cardiac catheterization. Free radical production from purified neutrophils (Ficoll-Hypaque density gradient method) was measured indirectly by the chemiluminescence method. Myocardial ischemia during balloon inflation was assessed by serial lactate determinations from coronary sinus and arterial blood. The degree of transient angioplasty-related myocardial ischemia was related to the oxidative response of activated neutrophils. RESULTS: Mean (+/-S.E.M.) oxidative response, i.e. the lucigenin- and luminol-enhanced-chemiluminescence (counts per minute) of neutrophils sampled from the coronary sinus increased significantly after percutaneous transluminal coronary angioplasty (Lucigenin-chemiluminescence: pre-angioplasty 3.69+/-0.64x10(5) vs. post-angioplasty 7.08+/-1.2x10(5), P<0.01; Luminol-chemiluminescence: pre-angioplasty 2.81+/-0.67x10(6) vs. post-angioplasty 5.2+/-0.92x10(6), P<0.01). Twelve of 16 patients developed transient cardiac lactate production (mean coronary sinus lactate excess: +0.12 mmol/l) and three disclosed a lactate extraction ratio <10%, both suggestive of myocardial ischemia. However, there was no correlation between the cardiac lactate production and the increased oxidative response after coronary angioplasty (r2 (Lucigenin-chemiluminescence)=0.02, n.s.; r2 (Luminol-chemiluminescence)=0.06, n.s.). CONCLUSION: 'Priming' of neutrophils, as reflected by increased oxidative response, is likely to occur after coronary angioplasty, but not after the angiographic procedure itself. However, 'priming' seems to be unrelated to the transient brief period of myocardial ischemia and rather depends on an alternative mechanism.

Cardiac release and kinetics of endothelin after severe short-lasting myocardial ischemia.

OBJECTIVES: The aim of this study was to investigate the release kinetics of endothelin after induced short-lasting myocardial ischemia. BACKGROUND: Endothelin is an endothelium-derived vasoactive peptide. Unequivocal proof of its cardiac release in ischemic syndromes has not yet been demonstrated. METHODS: A coronary sinus study with atrial pacing was performed in 23 patients with coronary artery disease. Endothelin (ET), cardiac troponin-T (TnT), myoglobin (Mb) and creatine kinase (CK) samples were withdrawn from the coronary sinus and a peripheral vein before and 1, 5, 10, 30 and 45 min and 1, 2, 3 and 6 h after pacing. The appearance of angina pectoris, abnormal cardiac lactate metabolism and ST segment depression were further criteria for myocardial ischemia. RESULTS: In the study group, pacing stress induced severe ischemia (mean duration +/- SD 6.1 +/- 1.2 min), with a maximum of 0.34 +/- 0.12-mV ST segment depression in 21 of 23 patients and angina pectoris in 22 of 23. The maximal cardiac lactate production was 42.8 +/- 17.3% (p < 0.03). TnT and CK levels in the total group were normal; in 14 of 23 patients a transient elevation of Mb with a maximum after 3 h was detected (86.4 +/- 27.1 micrograms/liter, p < 0.03). The ET concentrations increased significantly (p < 0.001) in the coronary sinus (from 4.6 +/- 0.8 [baseline] to 12.9 +/- 2.7 pg/ml at 1 min after cessation of pacing) and the peripheral vein, respectively (from 4.7 +/- 0.7 [baseline] to 8.3 +/- 2.1 pg/ml at 1 min). ET further remained elevated for 1 h with persisting higher coronary sinus than peripheral venous concentrations, indicating cardiac ET release. In a control group of 18 patients without heart disease, all variables were unchanged. CONCLUSIONS: Short-lasting severe myocardial ischemia was associated with significant ET release of cardiac origin that lasted up to 1 h.

Impact of early accelerated dose tissue plasminogen activator on in-hospital patency of the infarcted vessel in patients with acute right ventricular infarction.

OBJECTIVE: To assess the efficacy of early accelerated dose tissue plasminogen activator on in-hospital patency of the infarct related artery in patients with inferior myocardial infarction with and without right ventricular involvement. DESIGN: Single centre prospective assessment before discharge of infarct related vessel patency after early thrombolysis. SETTING: Tertiary cardiac referral centre at a university hospital. PATIENTS AND METHODS: 90 consecutive unselected patients with acute myocardial infarction, of whom 35 (39%) had electro-cardiographic evidence of right ventricular involvement (ST segment elevation greater than 0.1 mV in right precordial lead V4R), were studied. All patients received accelerated dose tissue plasminogen activator 100 mg within six hours from the onset of symptoms and had control angiography before discharge. MAIN OUTCOME MEASURES: Infarct related coronary artery patency using the Thrombolysis in Myocardial Infarction (TIMI) grading system before discharge. Incidence of prolonged systemic hypotension, sinus bradycardia, complete atrioventricular block, and ventricular tachyarrhythmia during early hospitalisation. RESULTS: Despite aspirin and bolus heparinisation before thrombolysis and high dose heparinisation thereafter for at least 48 hours the infarct related artery was more likely to be occluded (TIMI 0 or 1 flow) in patients with right ventricular involvement than in those without (69 v 29%, P < 0.001), as shown by control angiography performed a mean of 12.8 days after thrombolysis. These findings may be explained, at least in part, by predominant involvement of the proximal right coronary artery (66 v 31%, P < 0.05) and a low cardiac output syndrome, being indirectly reflected by a high incidence of prolonged hypotension (26 v 7%, P = 0.02), bradycardia (34 v 14%, P = 0.03), and complete atrioventricular block (37 v 5%, P = 0.0001). CONCLUSION: Primary angioplasty should be considered as the treatment of choice in patients with acute inferior infarction with right ventricular involvement because of the high failure rate of thrombolysis.

Vascular events during follow-up in patients with aortic arch atherosclerosis.

BACKGROUND AND PURPOSE: An association between aortic arch atherosclerosis and vascular events has been demonstrated. However, few data exist regarding follow-up evaluation of this disease. METHODS: In this study, 183 patients with the diagnosis of aortic arch atherosclerosis were prospectively followed up. This diagnosis was made during an echocardiographic cross-sectional study. In 136 patients, raised plaques with thickness < 5 mm had been shown to exist, and in 47 patients complex plaques with thickness > or = 5 mm or plaques with mobile components had been demonstrated on the initial transesophageal echocardiography. RESULTS: During a mean follow-up period of 16 +/- 7 months, vascular events with a presumed embolic origin occurred in 15 patients. The incidence was 4.1 per 100 person-years in patients with raised plaques compared with 13.7 per 100 person-years in the group with complex plaques. The Kaplan-Meier survival analysis revealed a significantly higher rate of vascular events in patients who were found to have complex plaques (P < .01). In the Cox proportional hazards analysis, the finding of complex plaques (relative risk [RR], 4.3; 95% confidence interval [CI], 1.5 to 12.0; P = .006), coronary artery disease (RR, 4.0; 95% CI, 1.2 to 13.1; P = .02), and a history of previous embolism (RR, 4.0; 95% CI, 1.1 to 14.4; P = .03) were independent predictors of vascular events. CONCLUSIONS: Patients with the finding of protruding plaques or plaques with mobile components have a high risk of subsequent vascular events.