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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".

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.

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.

A 20-year-old woman, admitted to an intensive care unit in ventricular fibrillation, had marked QT prolongation in the ECG after successful defibrillation. Family study revealed ECG signs of QT prolongation, as seen in the Romano-Ward syndrome, in four generations. Syncopal attacks only occurred in the third generation, affecting four siblings. In the described patient the intraventricular ECG revealed additional depolarizations (after-potentials) during and following repolarization (ST-T) in the surface ECG. The patient died later as a result of irreversible hypoxic cerebral damage. Invasive ECG studies in the mother also revealed after-potentials. In the patient, morbid-anatomical examination revealed, in addition to fibrosis and lipomatosis around the sinus and AV nodes, focal round-cell ganglionitis in both sympathetic trunks, but predominantly on the right. These infiltrations have not previously been described in this disease and could be of significance in the pathogenesis of the prolonged QT syndrome.

Noninvasive and invasive diagnostic procedures permit a differentiated insight into the hypertrophic cardiomyopathies. For a better understanding of the disease, classification according to morphologic and functional criteria was introduced. It has proven useful to subdivide hypertrophic obstructive cardiomyopathy into two types: idiopathic hypertrophic subaortic stenosis and midventricular obstruction; hypertrophic nonobstructive cardiomyopathies can be subdivided into two forms designated as asymmetrical septal hypertrophy and apical hypertrophy. Combined forms can also be recognized. With a high degree of accuracy, it is possible to differentiate between hypertrophic obstructive and hypertrophic nonobstructive cardiomyopathy by means of noninvasive procedures such as clinical examination, electrocardiography, mechanocardiography and, above all, echocardiography. Experience has shown that two-dimensional echocardiography, in particular, has assumed an especially important role, the value of which approaches that of cardiac catheterization. In this overview, emphasis is placed on the diagnostic peculiarities of idiopathic hypertrophic subaortic stenosis as well as the findings in midventricular obstruction and apical hypertrophy. In the past, only relatively little attention has been focused on the latter subgroups even though they can be diagnosed with a high degree of accuracy with noninvasive as well as invasive procedures.

The role of delayed potentials in ventricular arrhythmias occurring in connection with acute myocardial infarction has been of increasing interest in recent years. In order to obtain further information about delayed electrical activity, we studied a group of 51 patients in the acute phase of myocardial infarction, and intracardiac recordings were made using bipolar electrodes. In 31 of the 51 patients we recorded delayed potentials 150-200 ms after the beginning of QRS. 14 patients showed delayed electrical activity in diastole even after the T wave. The same potentials as those obtained by intracardiac recording techniques were also recorded from the body surface using a signal-averaging technique. In several cases we were able to show that these delayed potentials initiated premature ventricular beats. In 1 patient a sustained ventricular tachycardia induced by delayed potentials was recorded. We found that delayed potentials could be abolished by antiarrhythmic drugs. There thus appears to be an important relationship between delayed electrical activity and the occurrence of ventricular arrhythmias.

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.

A coronary artery-to-left ventricular fistula is a rare finding; to the best of our knowledge, a total of only 35 cases have been reported. Only 5 cases of a generalized arterio-systemic fistula with three vessel involvement have been reported in the literature. We describe another case involving all major coronary arteries. A review of the literature is presented and the data of the reported cases are analyzed. A 55 year old woman was examined because of recurrent chest pain which had persisted for 2 years. On physical examination, the only abnormal finding was a fourth heart sound. Exertional chest pain, a positive exercise stress test, and the results of a lactate extraction study suggested severe myocardial ischemia. Thallium myocardial scintigraphy showed no evidence of a perfusion defect. Cardiac catheterization revealed an irregular left ventricular endocardial pattern (Thebesian veins). Selective coronary angiography showed communicating fistulae of all three major coronary arteries with the left ventricular cavity. We assume that this vascular anomaly causes a coronary steal phenomenon and subsequent myocardial ischemia.

The left ventricular (LV) cineangiograms of ten patients with apical hypertrophy (AH, group I) as a form of hypertrophic nonobstructive cardiomyopathy (HNCM) were analyzed. The left ventricular ejection dynamics, the extent and pattern of left ventricular contraction were compared with eight patients with secondary myocardial hypertrophy due to arterial hypertension (group II) and eight normal subjects (group III). End-diastolic, end-systolic and stroke volumes were significantly lower in group I. The analysis of left ventricular ejection dynamics with frame-by-frame-analysis revealed the typical ejection pattern of hypertrophic nonobstructive cardiomyopathy: Left ventricular ejection was completed within two thirds of the systolic ejection period. This ejection pattern is of diagnostic value when compared with the dynamics in group II. Although the apical segment in group I shows a good fiber shortening, the overall contribution to systolic performance is low; systolic function in apical hypertrophy is maintained by a compensatory increase in regional wall motion of the basal and midzonal part of the left ventricular free wall. There is no striking difference between apical hypertrophy with and without giant negative T waves with respect to the ejection pattern. Within these subgroups, the only difference was the greater left ventricular mass in patients with giant T wave inversion. Thus, the ejection dynamics in apical hypertrophy is typical of hypertrophic nonobstructive cardiomyopathy. Global parameters of systolic left ventricular performance revealed supernormal values even though systolic function is impaired. Segmental analysis of ejection phase was most sensitive in establishing the diagnosis.

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.

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.

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.