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BACKGROUND The present study was designed to evaluate the efficiency of a newly developed troponin T enzyme immunoassay for the detection of acute myocardial infarction. METHODS AND RESULTS The study comprised 388 patients admitted with chest pain and suspected myocardial infarction and 101 patients with skeletal muscle damage and additional suspected myocardial cell damage. Troponin T was elevated to more than twice the analytical sensitivity of the assay (0.5 microgram/l) in all patients with non-Q wave (range, 1.2-5 micrograms/l) and Q wave infarction (range, 3-220 micrograms/l). Troponin T appeared in serum as early as 3 hours after onset of pain in 50% of the patients and remained elevated in all patients for more than 130 hours, revealing release kinetics of both free cytosolic and structurally bound molecules. The diagnostic efficiency of troponin T was superior to that of creatine kinase-MB (98% versus 97%) and remained at 98% until 5.5 days after admission, if patients with unstable angina were excluded from analysis. In the 79 patients with unstable angina, troponin T was elevated (range, 0.55-3.1 micrograms/l) in at least one blood sample from each of 37 patients (56%). Circulating troponin T was correlated to the presence of reversible ST segment or T wave changes on the electrocardiogram (p less than 0.005) and to the frequency of in-hospital complications. In the 101 patients with skeletal muscle damage and suspected additional cardiac muscle damage, troponin T was the most useful test; its efficiency was 89% or 94% (depending on the discriminator value used) as compared with 63% for creatine kinase-MB. CONCLUSIONS Thus, the data of the study indicate that the newly developed troponin T test improves the efficiency of serodiagnostic tools for the detection of myocardial cell necrosis as compared with conventionally used cardiac enzymes.

Forty eight patients with bilateral isolated non-stenotic coronary artery ectasia or aneurysm without associated cardiac defects ("dilated coronaropathy") were identified in consecutive diagnostic cardiac catheterizations between 1986-6/1994 (angiographic incidence 0.44%). Ectasia was defined as a luminal dilatation of the 1.5-2-fold, aneurysm of more than double the normal limits. In 16 patients a myocardial infarction (5 non-q-infarctions/11 q-wave-infarctions) was the indication for coronary angiography, a thrombotic occlusion of the infarct vessel was documented in 8/16 patients. In patients without myocardial infarction (study group) an evaluation of exercise-induced myocardial ischemia was performed by means of a coronary sinus lactate study, treadmill ergometry and Thallium-201-scintigraphy. A corresponding coronary insufficiency was objective in all tests in the study group. An exercise-induced myocardial ischemia was found in 21/31 in the coronary sinus study, 19/29 in the treadmill ergometry and 13/26 patients in the scintigraphy; significant differences were found in comparison to the results of a control group of patients without heart disease (n = 29, p0.001). After administration of 0.8 mg nitroglycerin (NTG) a further significant deterioration of myocardial ischemia was measured in the 21 patients with pathologic lactate metabolism developing a frank cardiac lactate production (p0.03). The extent of myocardial ischemia in the coronary sinus study was significantly correlated to the coronary diameters of the proximal and middle segments of the Ramus interventricularis anterior and the middle segment of the Ramus circumflexus (r = 0.87, p0.02). A differentiation between ectasia and aneurysm therefore seems to be of functional relevance. Angiographic stigmata of an impaired coronary blood flow such as a segmental to and from movement and a local deposition of dye were found significantly more often with increasing coronary diameters (p0.04). "Dilated coronaropathy" is an entity of non-stenotic, ischemic coronary artery disease. NTG was of no therapeutic benefit or led to an aggravation of the exercise-induced myocardial ischemia. Because of this potential adverse effect the administration of NTG should be avoided in "dilated coronaropathy".

This prospective cross-sectional study include 100 consecutive patients (56 males, 44 females, 29 to 86 (mean = 67.5 +/- 12.2) years) with ventricular inhibited demand pacemakers 0.1 to 94.7 (mean 23.3 +/- 25.4) months after pacemaker implantation. Fifty-two patients were free of symptoms, whereas 48 patients were still complaining of syncope, dizziness, or palpitations. After history, physical examination, and 12-lead standard ECG all patients underwent 24-h Holter monitoring. A computer-aided analysis of spontaneous arrhythmias was done first. In a second run computed-aided analysis of transient pacemaker dysfunctions was performed with a specially designed pacemaker module. There were no significant differences between asymptomatic and symptomatic patients with regard to the incidence of transient pacemaker dysfunctions, with regard to defined types of pacemaker dysfunctions, spontaneous ventricular arrhythmias, and with regard to supraventricular tachycardias. A significant difference between asymptomatic and symptomatic patients was found, however, regarding the Lown classification of ventricular arrhythmias, because asymptomatic patients showed class 0 and I/II arrhythmias more frequently (p0.025). In the 100 patients a total of 6609 pacemaker dysfunctions were observed, 5104 failures to sense and 1505 inappropriate inhibitions. Most patients showed up to 240 pacemaker dysfunctions per 24 h. There were no failures to capture. Different types of pacemaker dysfunctions were found with different clinical implications. Due to the Holter findings in nine patients pacemakers were reprogrammed or replaced. After pacemaker implantation the number of patients with severe symptoms significantly decreased compared to the number of patients before pacemaker implantation. Nonetheless, there was a number of patients still complaining of symptoms after pacemaker implantation. In only a few patients did pacemaker implantation worsen symptoms . Our data show that with use of long-term ECG transient pacemaker dysfunctions and spontaneous arrhythmias are more frequent than patients' history and common standard techniques in the pacemaker clinic may suggest Holter monitoring, therefore, is a useful diagnostic tool, not only in symptomatic, but also in asymptomatic pacemaker patients. It allows to obtain a reliable survey of the real amount of transient pacemaker dysfunctions in the individual patient, which is the base for further therapeutic decisions.

The purpose of the study was to evaluate alterations of the hemostatic system and the effect of anticoagulant therapy in nonvalvular atrial fibrillation. A set of molecular hematologic markers was measured prospectively in 69 patients with atrial fibrillation and 28 age-matched patients in sinus rhythm. Significantly elevated levels of thrombin-antithrombin III complex (8.5 +/- 1.6 vs. 2.5 +/- 0.3 micrograms/l; p0.001), fibrin monomers (27.1 +/- 3.2 vs. 13.4 +/- 3.7 nM; p0.001), D-dimers (788 +/- 76 vs. 405 +/- 46 micrograms/l; p0.005), and tissue-type plasminogen activator (9.6 +/- 0.5 vs. 7.2 +/- 0.5 micrograms/l; p0.05) were observed in patients with atrial fibrillation compared to those in sinus rhythm. In a subgroup of patients in whom anticoagulant therapy with oral coumadin or standard intravenous heparin was established after the initial study, hemostatic activation decreased significantly. In conclusion, molecular hematologic markers indicate a hypercoagulable state in atrial fibrillation which may characterized a group of patients at elevated risk of thromboembolic disease.

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.

The importance of the pacemaker follow-up clinic has markedly increased in the face of the currently available multiprogrammable pacemakers. In contrast to the common standard techniques in assessing pacemaker dysfunctions, Holter monitoring allows the detection of transient pace-maker dysfunctions during a long period of time. Especially computer-aided analysis provides a considerable progress, because different pacemaker dysfunctions can be detected during prolonged time periods, and--in contrast to visual analysis--a reliable survey of the real extent of transient pacemaker dysfunctions in the individual patient is assessed. The reliability of computer-aided analysis by a specially designed module was prospectively investigated in 100 consecutive patients with permanent ventricular inhibited demand pacemakers. It could be demonstrated that the positive predictive accuracy of this analysis was limited to 60.2% in detecting failures to sense and 63.2% in detecting inappropriate inhibitions, respectively. All detected failures to capture were false positive events. The positive predictive accuracy, therefore, was not calculated for this category of event. The overall positive predictive accuracy was 59.9%. In contrast, the sensitivity of computer-aided analysis was remarkably high. Possible causes of false positive and false negative findings are described. The reliability of pacemaker pulse detection was also investigated. Out of 100 analyzed Holter recordings five showed a temporary total loss of pacemaker pulses. Loss of single pacemaker pulses was found in 30 patients. False positive pacemaker pulses were seen in three patients. These results show that visual control and validation by an experienced physician are mandatory.(ABSTRACT TRUNCATED AT 250 WORDS)

We report on a 44-year-old male with primary cardiac angiosarcoma who died 11 months after onset of nonspecific symptoms (thoracic pain and general fatigue) of intracerebral metastases. A right atrial tumor mass and a pericardial effusion could be demonstrated by transthoracic and transesophageal echocardiography. Cardiac angiography showed a right atrial hemangioma, fed by the right coronary artery. In a review of 108 cases of primary cardiac angiosarcoma we summarize clinical features, diagnostic means, therapeutic approaches and life expectancy of this rare disease.

Troponin T is a unique cardiac antigen which is continuously released from infarcting myocardium. Its cardiospecificity as a marker protein might be particularly useful in assessing myocardial cell damage in patients undergoing cardiac surgery. Therefore, circulating troponin T was measured in serial blood samples from 56 patients undergoing cardiac surgery and in two control groups--22 patients undergoing minor orthopaedic surgery and 12 patients undergoing lung surgery by median sternotomy. In both control groups no troponin T could be detected, whereas activities of creatine kinase were raised in all 12 lung surgery controls and activities of the MB isoenzyme were raised in five of the 12 patients in the lung surgery group and in four of the 22 patients in the orthopaedic surgery group, respectively. All the patients undergoing coronary artery bypass grafting (n = 47) and cardiac surgery for other reasons (n = 9) had detectable concentrations of troponin T. Five patients had perioperative myocardial infarction detected as new Q waves and R wave reductions. In these five patients troponin T release persisted and serum concentrations (5.5-23 micrograms/l) reached a peak on the fourth postoperative day. In the 51 patients without perioperative myocardial infarction serum concentrations and the release kinetics of troponin T depended on the duration of cardiac arrest. In patients in whom aortic cross clamping was short troponin T increased slightly on the first postoperative days; in patients with longer periods of aortic cross clamping troponin T concentrations were higher and remained so beyond the fifth postoperative day. In patients with non-specific changes on the electrocardiogram troponin T concentrations were significantly higher on days 1 and 4 after operation than in patients with normal postoperative electrocardiograms(11.2 (5) and 4.5 (2.6) v 8.2 (3.4) and 2.9 (1.6) 1microg/l). Serum concentrations of troponin T showed some myocardial cell damage in every patient undergoing cardiac surgery. The persistent increases that were more common in patients with longer periods of cardiac arrest must have been caused by damage to the contractile apparatus. These results suggest that perioperative myocardial cell necrosis may be more common than indicated by changes of the QRS complex on the electrocardiogram.

In anesthetized rats under artificial respiration, intravenous infusion of nisoldipine (0.1 mg/kg x min) caused significant decreases in blood pressure, heart rate, cardiac output and peripheral resistance. The animals died 54.7 +/- 11.1 min after initiation of the infusion. The electrocardiogram showed sinus bradycardia, increasing AV blockade and displacement of the pacemaker into the AV node or the bundle of His. Survival time under nisoldipine infusion increased more than two-fold with simultaneous infusion of calcium gluconate, isoprenaline (isoproterenol) or dopamine. Norepinephrine (noradrenaline) had no significant effect on survival time; the latter decreased to 19.4 +/- 1.6 min by plasma volume expansion with polygeline. All antidotes prolonging survival time also normalized the cardiac output diminished after nisoldipine. Electrocardiographic changes were antagonized only by isoprenaline. Suitable antidotes for intoxication or over-dosage of nisoldipine are calcium salts as well as beta-sympathomimetic drugs; sheer volume substitution and peripheral vascular constriction should not be resorted to.

The value of persistent ST-T elevations in the standard 12-lead ECG for the diagnosis of left-ventricular aneurysm (VA) was retrospectively analysed for 200 patients (171 males and 29 females) who had sustained a myocardial infarction at least 12 weeks previously. 105 patients (group 1) had a left-ventricular aneurysm confirmed by ventriculography; in 95 patients (group 2) an aneurysm had been excluded by ventriculography. Persistent ST-T elevations were present in 98 patients of group 1 (sensitivity 93.3%) and in 26 of group 2 (specificity 72.6%). In the 26 patients without VA, ST-T elevations occurred in at most three leads, but in 60 with aneurysm in four to nine leads. In addition, the area under the ST-T elevations and its height 1 mm after onset of the elevation and its maximal height were measured. The sums of the values in the limb and chest leads were statistically significantly different between the two groups for all three parameters. These measurements thus contribute to a reliable differentiation between patients with and without VA. The results also emphasize the importance of the 12 standard leads in the diagnosis of VA.

The effectiveness of the calcium-antagonist Ro 11-1781 (Tiapamil) was investigated in 23 patients with extrasystoles of different origin using continuous ECG recordings. Two 24-hour ECG recordings were registered without antiarrhythmic medication, one of these as a placebo period, and 3 during oral application of 3 x 200 mg/day Ro 11-1781, if the state of the health of the patients allowed it. No positive effects of Ro 11-1781 in supraventricular and ventricular extrasystoles were demonstrable, supported by 8 premature terminations of the study. The missing antiarrhythmic effectiveness of Ro 11-1781 corresponds to Verapamil in oral application.

In 18 out of 419 successive myocardial infarctions an increase in R-wave amplitude compared to the pre-infarction ecg had been observed. It concerned to leads III, aVF and II in posterior and inferior infarctions. The alteration of R-wave amplitude was accompanied by a dextroversion of electrical heart axis in the frontal plane. Direction of inscription of QRS loop changed in most cases. R-wave increase was demonstrated in the first ecg after the beginning of subjective symptoms and disappeared within few hours or days in general. Clinical course was rather serious in the cases described. As a pathophysiological mechanism of the phenomenon mentioned above either the influence of an injury potential upon ecg pattern or the presence of left posterior conduction defect is discussed.

In 27 patients presenting with angina pectoris at rest and normal serum creatine kinase (CK) activity, cardiac myosin light chains (CM-LC), myoglobin (MG), and CK-B isoenzyme were determined in 7 serial blood samples by radioimmunoassays. Measurable amounts of CM-LC were found in at least one serum sample in 13 patients. MG was found to be elevated in 9, and CK-B in 8 of these patients. In the 189 serum samples determined, CM-LC were found more frequently elevated (21.7%) than MG (13.2%, P less than 0.05) or CK-B (12.2%, P less than 0.05). Coronary angiograms were obtained in 21 of the 27 patients. Elevated marker protein concentrations were found only in patients with coronary artery stenosis greater than or equal to 70% of at least one coronary artery. The incidence of elevated serum concentrations of any of the 3 marker proteins determined was higher in patients with 3 vessel disease than in those with 1 or 2 vessel disease (33.9% vs 15.6%, P less than 0.05), and it was higher in patients with a history of previous myocardial infarction than in those without (34.5% vs 11.4%, P less than 0.001). The findings suggest that in a subgroup of patients with angina pectoris at rest but without evidence of acute myocardial infarction, ischaemic damage of small myocardial areas can be detected by serological assays of high sensitivity. Among the marker proteins studied, CM-LC were found the most sensitive.

The kinetics of cytosolic and structural marker protein release from myocardium were studied in 44 patients with acute myocardial infarction. After intracoronary infusion of streptokinase, there was early recanalization of the infarct-related artery in 8 patients and late recanalization in 18. In 18 patients the infarct-related artery remained occluded. Creatine kinase (CK) level peaked and normalized significantly earlier in patients with early reperfusion than in patients with late reperfusion, and in patients with late reperfusion earlier than in patients with permanent occlusion. Thus, the interval of absolute diagnostic sensitivity of CK depends on early infarct perfusion. In contrast, release of myosin light chains was not significantly changed by recanalization of the infarct-related artery compared with that in nonreperfused myocardial infarction. Thus, in patients with acute myocardial infarction, myosin light chains may be superior to CK as a diagnostic means and for estimation of infarct size.

To detect myocardial cell damage, serum samples of 42 consecutive patients with angina at rest were screened for cardiac myosin light chains, which were detected in 22 patients (52%). In 17 of these patients there was a persistent release of myosin light chains lasting until the 4th hospital day, whereas in 7 patients myosin light chains were only detectable during the initial 24 h after admission. The presence of myosin light chains correlated with signs of ischemia in the electrocardiogram (ECG) (p less than 0.05) and with the extent of coronary artery narrowing (p less than 0.05). Cardiac myosin light chains were elevated in serum only if there was a greater than or equal to 75% diameter narrowing in at least one major vessel. In all five patients who developed transmural myocardial infarction during the course of their hospital stay, myosin light chains were detectable greater than or equal to 28 h before the diagnosis of myocardial infarction could be established by ECG criteria and conventional serum enzymes. Thus the detection of circulating cardiac myosin light chains enables one to identify a subgroup of patients with angina at rest having more severe coronary artery disease with a worse outcome.

Hypertrophic cardiomyopathy (HCM) has various manifestations with respect to the localization of the hypertrophy. In this study we report clinical, electrocardiographic (ECG), echocardiographic (echo), and hemodynamic findings in midventricular obstruction (MO), an uncommon form of hypertrophic obstructive cardiomyopathy (HOCM) in 9 patients. The prevalence of systolic anterior motion of anterior mitral leaflet (SAM) in MO, an echocardiographic diagnostic hallmark in HOCM, was another purpose of this study. All patients had complete clinical, ECG, echo, and hemodynamic workup, including left ventricular (in 4 patients simultaneous biventricular, SBVA) and coronary angiograms. All patients had dyspnea and palpitations, chest pain, 2 had syncope. In the ECG, atrial fibrillation was present in 2, and left ventricular hypertrophy in 9 patients. Septal and left ventricular free wall thickening was significantly present in all patients in echo, and SAM in 1 patient. The intraventricular gradient (IVG) was 40-176 mmHg, in 1 case 40 mmHg by provocation, Brockenbrough was positive in all patients. Two patients had right ventricular IVG. A positive beta-blocking agent effect was present in 6 cases. The best localization of the obstruction was possible with SBVA and 2D-echo. We conclude that MO has all the signs of HOCM, but SAM in echocardiography is uncommon. SAM is occasionally present and is not a necessary factor to produce an intraventricular pressure gradient in HOCM, especially in MO. It seems that hypertrophic right ventricular obstruction is relatively common in MO (2 of 9 cases), and may have the same obstructive mechanism.

Rupture of the ventricular septum after acute transmural myocardial infarction occurred in four patients aged between 53 and 79 years. The rupture was verified by means of right-side cardiac catheterization. Only in two cases did two-dimensional echocardiography reveal the rupture; in both cases the rupture site located by echocardiography was confirmed at autopsy. In each of the four patients the left-to-right shunt could be identified by means of pulsed Doppler echocardiography which showed a turbulence in the right ventricle. Furthermore, the combination of two-dimensional echocardiography and Doppler echocardiography allowed a correct localization of the turbulent left-to-right flow in all cases. In view of these findings, the combination of Doppler echocardiography and two-dimensional echocardiography may be regarded as a suitable method for a readily available, non-invasive diagnosis of ventricular septum rupture in patients with acute myocardial infarction in an intensive care unit.

The influence of 3-(2-diethylaminoethyl)-4-methyl-7-(carbethoxy-methoxy)-2-oxo-1,2-chromene-hydr ochloride (carbocromen, Intensaïn) on A-V-conduction and refractory period was studied by means of His-bundle-electrography on 12 anaesthetized cats. Immediately after application of carbocromen 6 mg/kg the A-H-conduction time was increased. In contrast to this, 12 mg/kg carbocromen caused significant prolongation of H-v interval. This study shows that carbocromen has effects on intraventricular conduction.

After the loss of membrane integrity cardiospecific myosin light chains are released as a result of proteolytic degradation of the insoluble myosin pool. Thus, as with cytosolic enzymes, the measurement of the serum concentration changes of myosin light chains may allow a non-invasive estimation of infarct size. A two compartment model was used to describe the serum concentration changes of myosin light chains after a bolus injection into awake beagle dogs. The initial distribution volume was 7.4% of body weight, whereas the second compartment accounted for 4.7% of body weight. The fractional disappearance rate of 0.0092.min-1 resulted in a serum half life of myosin light chains of 75 min. In 30 patients with acute non-reperfused myocardial infarction a close correlation was found between the cumulative appearance of myosin light chains and their maximal serum concentration. In these patients the cumulative appearance of myosin light chains correlated with serum creatine kinase estimates of infarct size, with impairment of left ventricular ejection fraction, and with mortality during hospital admission. Thus the maximal serum concentration and the cumulative appearance of myosin light chains allow a non-invasive estimation of infarct size and may serve as a serological indicator of the patient's prognosis.

The case of acute purulent group B streptococcal myocarditis in a 29-year-old Turk is described, no similar case having previously been published. He fell ill suddenly with gastro-intestinal symptoms, high fever and pain in arms and legs. The ECG had low voltage in the limb leads and signs of a large acute myocardial infarct. The sedimentation rate was slightly raised, an initial leukopenia was followed by leukocytosis and high enzyme activity. He died in cardiogenic shock on the third day of illness. The post-mortem examination revealed acute purulent myocarditis, and numerous group B streptococci (Strept. agalactiae) were found in the myocardium.

Plasma levels of lidocaine were determined in either 10 patients following injection into the deltoid and lateral vastus muscle, respectively. We used an automatic injector containing 250 mg of lidocaine in a 10% solution. In the early phase after injection, plasma levels were higher, when the deltoid muscle had been chosen for administration. This was the same result as referred by other authors using normal injectors. Variance of single plasma values was smaller in the vastus group.