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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 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.

In a previous study on the diagnostic efficiency of troponin T measurements in patients with suspected acute myocardial infarction (AMI), the authors found a high variability of troponin T serum concentration changes on day 1 in patients with AMI who underwent thrombolytic treatment. Therefore, the aims of the present study were to investigate the intracellular compartmentation of troponin T and to analyze the effects of AMI reperfusion on the appearance kinetics of cardiac troponin T in serum. Cardiac troponin T was measured with a newly developed bideterminant sandwich assay using cardiospecific, affinity-purified polyclonal antibodies and peroxidase-labeled monoclonal antibody. An unbound cytosolic troponin T pool was found in ultracentrifuged homogenates of myocardial tissue of different species ranging from 0.013 to 0.036 mg/g wet weight. The soluble troponin T molecule had electrophoretic properties identical to troponin T compartmented in the myofibrils. The clinical study group comprised 57 patients with AMI undergoing thrombolytic treatment. Blood flow to the infarct zone and point of time of reperfusion were tested by immediate and late angiography. The appearance of troponin T in serum on day 1 after the onset of AMI depended strongly on reperfusion and on duration of ischemia before reperfusion. Thus, in patients with early reperfused AMI, a marked peak in troponin T serum concentrations was found at 14 hours after the onset of pain. This early troponin T peak was absent in patients with AMI reperfusion occurring greater than 5.5 hours after the onset of pain and in patients with nonreperfused AMI. By contrast, the kinetics of troponin T release after the first day after AMI were unaffected by reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

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".

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.

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.

Infarct size can be estimated noninvasively by analysis of circulating CK-MB and/or cardiac myosin light chains. To investigate whether myosin light chains release is correlated with the impairment of left ventricular function in acute myocardial infarction, this marker protein was determined by liquid phase radioimmunoassay in serial blood samples of 25 patients. Likewise CK-MB was measured in the same blood samples. From the serum concentration changes the cumulative appearance was calculated as an estimate of infarct size. Left ventricular enddiastolic pressure, global and regional ejection fraction were measured immediately and 3 weeks after admission. Particularily during the chronic phase of myocardial infarction a close correlation was found between serological estimates of infarct size and impairment of left ventricular function. The cumulative appearance of myosin light chains was superior to CKMB in assessing the hemodynamic impact of myocardial infarction in the acute and chronic stage. Therefore, myosin light chains are an appropriate serological indicator for the hemodynamic significance of myocardial infarction during the acute and chronic stage and might allow an assessment of the patients' risk.

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.

The rare case of pericardial effusion with starting tamponade in post-myocardial infarction syndrome (Dressler's Syndrome) is described. Diagnosis and comment: The consequential steroid therapy improves the cardial situation dramatically. There is no echocardiographic differential diagnostic criteria, but in the case of the symptoms of Dressler's Syndrome (fever, pleuritis, pneumonia, serologic changes and pericarditis) allows the diagnosis of this pericardial disease. A latent period of several weeks to some months after myocardial infarction is possible.

The aging heart differs in several aspects from the heart in younger people: Cardiac muscle mass, systolic and diastolic wall stress increase, the velocity of electrical conduction decreases in different anatomical structures. Supraventricular and ventricular arrhythmias appear more frequently than in younger people. Heart rate and cardiac index tend to diminish, especially under work load. Work capacity is reduced. In the treatment of coronary heart disease drugs are preferred which lead to a reduction of preload. Nitrates and molsidomine are followed by calcium channel blockers and--afterwards--by beta-blockers. Bypass surgery is performed in elderly patients more often for therapeutical than for prognostic reasons, similarly in the case of valvular surgery. Typical tachyarrhythmias are treated only in case of hemodynamic relevance, whereas pacemaker therapy is not limited by greater age. The choice of the most suitable pacemaker model, however, has to be based upon the overall circumstances in each individual case. For the treatment of congestive heart failure, vasodilators, especially angiotensin-converting enzyme inhibitors, seem to be superior, in elderly patients, to diuretics and digitalis glycosides.

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.

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.

Infarct size can be estimated noninvasively by analysis of circulating CK-MB and/or cardiac myosin light chains. To investigate whether myosin light chains release is correlated with the impairment of left ventricular function in acute myocardial infarction, this marker protein was determined by liquid phase radioimmunoassay in serial blood samples of 25 patients. Likewise CK-MB was measured in the same blood samples. From the serum concentration changes the cumulative appearance was calculated as an estimate of infarct size. Left ventricular end diastolic pressure, global and regional ejection fraction were measured immediately and 3 weeks after admission. Particularly during the chronic phase of myocardial infarction a close correlation was found between serological estimates of infarct size and impairment of left ventricular function. The cumulative appearance of myosin light chains was superior to CKMB in assessing the hemodynamic impact of myocardial infarction in the acute and chronic stage. Therefore, myosin light chains are an appropriate serological indicator for the hemodynamic significance of myocardial infarction during the acute and chronic stage and might allow an assessment of the patients' risk.

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.

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.

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.

In a double blind study performed in cooperation with 69 emergency doctors and general practitioners in the catchment areas of the university and of the city hospital in Lübeck the action of intramuscular lidocaine on mortality and on the incidence of arrhythmias was investigated in patients with acute myocardial infarction aged less than 70 years. The mortality in the lidocaine group was significantly lower than in the placebo group. The incidence of ventricular arrhythmias up to 120 minutes after the lidocaine injection was also lower than in the placebo group. However, the only case of primary ventricular fibrillation was in the lidocaine group. As the difference in mortality between the two groups appeared at a time when an antifibrillatory action of lidocaine can no longer be assumed one must question whether the positively beneficial effect was real or whether the lower mortality was in fact due to primarily milder disease in the lidocaine group.