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E Giannitsis

Publications and source records attributed to E Giannitsis.

36 records · Page 2Linked to original sources
PubMed2000

Relationship of cardiac troponin T and procoagulant activity in unstable angina.

OBJECTIVE: The present study sought to determine the incidence of increased procoagulant activity in patients with unstable angina (UAP), and to evaluate the relationship between cardiac troponin T (cTnT) and molecular markers of hemostatic activation. Method. We studied 44 patients with UAP further classified by plasma cTnT levels. All patients received an antithrombotic therapy consisting of therapeutic doses of unfractionated heparin and acetylsalicylic acid. Quantitative levels of cTnT and plasma concentrations of fibrin monomers (FM), prothrombin fragments F1+2, thrombin antithrombin III complexes (TAT), plasminogen and alpha2-antiplasmin were sampled serially within the first 48 h. RESULTS: Increased plasma concentrations of FM were detected in 45.5% of patients and were more frequently present among those with cTnT concentrations > or =0.1 ng/ml (13 of 18 vs 7 of 26 patients, p = 0.003). In these patients, mean plasma concentrations of FM were significantly higher than in patients with cTnT <0.1 ng/ml (7.93 +/- 2.3 vs 3.12 +/- 0.6 microg/ml, p = 0.02). There was a close relationship between plasma levels of cTnT and FM (r = 0.74, p <0.004), prothrombin fragments F1+2 (r = 0.71, p = 0.046) and a trend to significance was noted for TAT (r = 0.42, p = 0.055). No significant correlation was observed with markers of the fibrinolytic system (plasminogen and alpha2-anti-plasmin). Plasma levels of cTnT > or =0.1 ng/ml identified a concomitant increase of hemostatic markers with a sensitivity, specificity and positive predictive value of 65, 79, and 72% for FM, 63, 76, and 67% for prothrombin fragments F1+2, and 58, 66, and 39% for TAT, respectively. CONCLUSIONS: In patients with UAP, cTnT identifies patients with increased procoagulant activity and is closely related to plasma levels of molecular markers of hemostatic activation. Therefore, cTnT alone or in combination with one of these markers may be helpful to identify patients requiring more potent antithrombin or antiplatelet therapy.

Aged↗
PubMed1999

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.

Aged↗
PubMed1999

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.

Antithrombin III↗
PubMed1999

[Cardiac endothelin release into the coronary sinus in myocardial ischemia and coronary endothelial injury].

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.

Aged↗
PubMed1999

Strategies for clinical assessment of patients with suspected acute coronary syndromes.

Clinical assessment of patients with acute coronary syndromes is routinely employed for risk stratification and selection of treatment strategies. Both, patients risk and treatment options vary in unstable angina, non-Q-wave infarction and massive Q-wave infarction. Clinical symptoms and admission ECG are the key elements in the daily work-up of chest pain patients. However, absent or nonconclusive ECG changes, even in patients with confirmed acute myocardial infarction, and high variability of clinical symptoms, particularly in elderly patients, limit their diagnostic value and their precision for risk stratification of acute coronary syndromes. Additional diagnostic testing such as 24 hours Holter ECG depicting prolonged episodes of ST-segment depression, and radio-nuclide tomography using Tc-Sestamibi improves accuracy of risk assessment. However, in clinical practise these techniques are not readily available. Troponins, particularly cardiac specific troponin T, are paramount for risk stratification of acute coronary syndromes, either alone, or in combination with admission ECG or a predischarge exercise stress test. Stratifying individuals into high, intermediate, and low risk for death and subsequent cardiac events may aid to improve outcomes by tailored use of a more aggressive therapy in these subjects.

Acute Disease↗
PubMed1998

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.

Aged↗
PubMed1998

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.

Aged↗
PubMed1998

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.

Aged↗
PubMed1998

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.

Aged↗
PubMed1998

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.

Cardiac Pacing, Artificial↗
PubMed1997

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.

Adult↗
PubMed1997

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.

Cardiac Pacing, Artificial↗
PubMed1997

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.

Coronary Angiography↗
PubMed1997

Apical hypertrophic cardiomyopathy of the Japanese type coexistent with a coronary muscle bridge. A case report and review.

We describe the case of a 21-year-old Italian male who presented with giant negative T-waves and left ventricular hypertrophy on the electrocardiogram suggestive of apical hypertrophic cardiomyopathy. Clinically, he suffered from new onset of exertional angina, dyspnea and palpitations during soccer playing or heavy exercise beginning one week before admission. Echocardiography and cardiac catheterization conformed the rare combination of a nonobstructive apical hypertrophic cardiomyopathy of the "Japanese" type coexistent with an extensive muscular bridge involving almost the entire anterior interventricular branch of the left coronary artery. Although the patient complained of exertional angina pectoris, absence of objective evidence of myocardial ischemia by means of treadmill stress test, exercise thallium scan, dobutamine stress echocardiography as well as atrial pacing stress emphasized the benign nature of this complex anomaly.

Adult↗
PubMed1996

Accelerated ST-segment reduction after thrombolytic therapy with recombinant tissue plasminogen activator (rtPA) compared to urokinase.

Effects of therapy with urokinase (UK) and with recombinant tissue plasminogen activator (rtPA) were compared in patients with acute myocardial infarction (AMI). To achieve homogenous therapeutic conditions the comparison was restricted to patients having their first AMI and to cases of clinically successful thrombolytic therapy (defined by non-invasive criteria, such as a 50% decrease in elevated ST-segment in the worst load of a 12 lead ECG within 300 min after onset of thrombolytic therapy, complete pain resolution during thrombolytic therapy, and later confirmed by angiography 10 days after AMI). Effects of UK and rtPA on continuous multilead ST-segment analysis and cardiac proteins (creatine kinase and its isoenzyme CK-MB, aspartate transaminase and hydroxybutyrate dehydrogenase) were analyzed during 24 hours following onset of therapy. Continuous ST analysis showed a faster resolution of the elevated ST-segments after thrombolytic therapy with rtPA than with UK(p < 0.01). Accelerated idioventricular rhythms (p < 0.05) occurred sooner following rtPA than UK treatment. The wash-out of creatine kinase was increased (p < 0.01) after rtPA. Although both drugs induced comparable, angiographically controlled reperfusion, the results suggest that the process of reperfusion was accelerated during thrombolysis with rtPA compared to UK. Thrombolytic therapy of AMI with rtPA may hence improve myocardial salvage.

Adult↗
PubMed1995

[Noninvasive diagnosis of coronary heart disease with cardiokymography: use of signal averaging technique].

Regional wall motion abnormality is the best indicator for coronary ischemia. Myocardial wall motion is registrated by cardiokymography (CKG), a mechanocardiographic method. Because of the high incidence of artefacts, echocardiography and nuclear imaging technique have been preferred. Computer-assisted signal averaging CKG improves practicability and allows measurements during exercise testing. Exercise testing was performed in 54 patients with suspected ischemic heart disease without mitral or aortic valve dysfunction, myocardial infarction or prior cardiac surgery. The results of simultaneously recorded ECG and CKG were compared with coronary angiographic results. CKG sensitivity and specificity were higher than that of ECG (76 and 80% vs 71 and 52%). If diagnosis was based on pathological or nonpathological results of both CKG and ECG, sensitivity and negative predictive value increased to 87 and 83%, respectively. Sensitivity reached 93% when only one pathological result was required. CKG combined with signal-averaging techniques has advanced to become a specific and sensitive tool in the non-invasive diagnostic approach to ischemic heart disease.

Adult↗
PubMedDate not supplied

Risk stratification and therapeutic decision making in patients with acute coronary syndrome--the role of cardiac troponin T.

Patients with chest pain represent an inhomogeneous group with greatly varying severity of coronary artery disease and cardiac risk. The proper selection of different treatment strategies in these patients requires reliable risk assessment. Patients with definitive myocardial infarction: in patients with ST-segment elevation on ECG, a positive troponin T (cTnT) on admission identifies a group of patients having a threefold higher mortality rate than patients with a negative cTnT test. The differences in risk based on cTnT are found for patients treated with thrombolytic as well as mechanical recanalization therapy. These differences in mortality based on admission cTnT may be explained by more severe coronary artery disease, worse left ventricular function, and less efficient microvascular reperfusion in the cTnT-positive patients. Patients with rest angina: in patients with angina at rest, a positive cTnT value on admission identifies a subgroup having a threefold higher cardiac event rate than cTnT-negative patients. The cTnT-positive patients seem to benefit from treatment with low molecular weight heparin and fibrinogen receptor antagonists, while cTnT-negative patients do not. The differences in risk and response to therapy may be due to more severe coronary artery disease, more critical coronary artery stenoses, and a higher rate of intracoronary thrombus formation in the cTnT-positive versus negative patients. Low risk chest pain patients: in low risk chest pain patients, (i.e. no rest angina, no ECG-changes) cTnT-positive patients on admission have a twofold higher cardiac event rate than cTnT-negative patients. The proper treatment strategy for the low risk cTnT-positive patients remains to be determined. Troponin T versus troponin 1: many of the findings on cTnT also relate to troponin I. However, there is a high interassay variability of troponin I assays, which has to be taken into consideration.

Angina Pectoris↗