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Biomedical subjects

K W Diederich

Publications and source records attributed to K W Diederich.

At least 19 recordsLinked to original sources
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↗
PubMed1991

[Pacemaker syndrome with AV-synchronized stimulation of the heart].

Characteristic signs of the pacemaker syndrome occurred in a 69-year-old woman with intermittent 3 degrees atrioventricular (AV) block after implantation of a dual-chamber AV-synchronized pacemaker. Cannon beats due to inappropriate atrial timing were the main haemodynamic finding. Their development and size depended on the programmed AV interval and AV-synchronized mode of stimulation. Very long AV intervals in the DDD mode at a heart rate of 100/min caused very unpleasant palpitations and pulsations in the upper thorax. The symptoms due to the cannon beats were avoided by changing to a short AV interval. The clinical and haemodynamic events were thus the consequence of preserved sinus node function with subsequent atrial triggering.

Aged↗
PubMed1991

Intracellular compartmentation of cardiac troponin T and its release kinetics in patients with reperfused and nonreperfused myocardial infarction.

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)

Animals↗
PubMed1991

Non-invasive assessment of perioperative myocardial cell damage by circulating cardiac troponin T.

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.

Acute Disease↗
PubMed1991

Diagnostic efficiency of troponin T measurements in acute myocardial infarction.

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.

Adult↗
PubMed1990

[Chronic ventricular aneurysm. The sensitivity and specificity of persistent ST-T elevations 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.

Chronic Disease↗
PubMed1990

Expression of human beta-myosin heavy chain fragments in Escherichia coli; localization of actin interfaces on cardiac myosin.

A cDNA clone coding for an internal fragment of slow-cardiac beta-myosin heavy chain was isolated from a lambda gt10 human skeletal muscle library. Six overlapping cDNA subclones, which span myosin heavy chain subregions and presumably interact with actin, were derived from this clone, fused to a beta-galactosidase vector and expressed in Escherichia coli. Three of the subclones were obtained by PCR (polymerase chain reaction) which enables gene or cDNA fragments to be amplified independently of preexisting restriction sites. Initially, various experiments were carried out using a long MHC (myosin heavy chain) fusion protein containing the 50 kDa-20 kDa connecting region, the whole 20 kDa region and the short subfragment 2 region. This MHC fusion protein was chemically or proteolytically cleaved in the same conditions as the native myosin molecule. Whole and truncated forms of the MHC fusion protein were separated on polyacrylamide gels, electroblotted on nitrocellulose sheets and renatured. They were then assayed in overlay experiments with F-actin and/or myosin light chains in solution. Specific antibodies were used to detect interactions between heavy chain fragments and F-actin or light chains. We thus observed that one long heavy chain fragment synthesized by E. coli behaved like proteolytic or chemical MHC preparations made from native myosin molecules. Two chymotryptic fragments of the MHC fusion protein, which are soluble at low ionic strength, cosedimented with F-actin in solution. Our results demonstrate that, in actin overlay experiments with whole fusion proteins, interactions seem to be due to the heavy chain fragment, not to the bacterial component. All interactions were non ATP-sensitive. We further investigated the possible participation of the six recombinant MHC fragments in contributing to the actomyosin interfaces on the 50 kDa-20 kDa regions of the human cardiac beta-MHC. The present procedure, which enables the synthesis of any MHC fragment independent of any protease site, is a powerful new tool for studying structure-function relationships within the myosin molecule family.

Actins↗
PubMed1990

The complete sequence of the human beta-myosin heavy chain gene and a comparative analysis of its product.

We have isolated and sequenced the gene and the cDNA coding for the human cardiac beta-myosin heavy chain (designated MYH7). The gene is 22,883 bp long. The 1935 amino acids of this protein (Mr223,111) are encoded by 38 exons. The 5' untranslated region (86 bp) is split by two introns. The 3' untranslated region is 114 bp long. Three Alu repeats were identified within the gene and a fourth one in the 3' flanking intergenic region. The molecular organization of this gene reflects the conservative pattern with respect to size, coding ratio, and number or position of introns characteristic of vertebrate sarcomeric myosin heavy chain genes. The protein sequence of the human beta-heavy chain was compared with corresponding (homologous) sequences of rabbit, rat, and hamster as well as with the (heterologous) embryonic heavy chain sequences of rat, chicken, and man. The results show that protein subregions responsible for basic functions of myosin heavy chains (nucleotide binding and actin binding) are very similar in homologous and heterologous heavy chains. Regions that differ in their primary sequences in heterologous heavy chains appear to be highly conserved within mammalian beta-myosin heavy chains. Constant and variable subregions of heavy chains are discussed in terms of functional significance and evolutionary relatedness.

Amino Acid Sequence↗
PubMed1990

Studies of antidote therapy for nisoldipine intoxication in experimental animals.

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.

Animals↗
PubMed1989

Isolation and characterization of the complete human beta-myosin heavy chain gene.

The entire gene coding for the human beta-myosin heavy chain has been isolated from genomic EMBL3A phage libraries by chromosomal walking starting from clone gMHC-1, reported earlier (Appelhans and Vosberg 1983). gMHC-1 has been shown to carry coding information for the C-terminal two-thirds of beta-myosin heavy chain, which is expressed in cardiac muscle and in slow skeletal muscle fibers (Lichter et al. 1986). Three DNA clones were identified as overlapping with gMHC-1 by restriction mapping and DNA sequencing. They span a 30-kb region in the genome. About 22 kb extend from the initiation codon ATG to the poly(A) addition site. The clones include about 4 kb of 5' flanking sequences upstream of the promoter. Comparisons of beta- and alpha-myosin heavy chain sequences indicate that gene duplication of the cardiac myosin heavy chain isogenes preceded the mammalian species differentiation.

Animals↗
PubMed1988

[Acute myocardial infarct: myosin-light-chain liberation and ventricular function].

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.

Cardiac Output↗
PubMed1988

Circulating cardiac myosin light chains in patients with angina at rest: identification of a high risk subgroup.

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.

Adult↗
PubMed1988

Myosin light chains release in acute myocardial infarction: non-invasive estimation of infarct size.

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.

Adult↗
PubMed1988

Non-invasive assessment of infarct reperfusion: the predictive power of the time to peak value of myoglobin, CKMB, and CK in serum.

Intravenous thrombolytic therapy has become a routine therapeutic intervention in acute myocardial infarction. In order to evaluate its success in the general hospital community noninvasive methods are needed. Therefore, the effect of infarct reperfusion on the times to peak value of myoglobin, CKMB, and CK were studied in patients with acute myocardial infarction. Recanalization of the occluded coronary artery was achieved by intracoronary infusion of streptokinase in eight patients within 3.5 h, and in 18 patients more than 3.5h after onset of pain. In 10 patients, the coronary artery remained occluded, and in eight patients thrombolysis was not attempted. Analyzing the times to peak value of myoglobin, CKMB, and CK, the probability of correct classification of infarct reperfusion varied between 1 and 0.9, if recanalization was achieved within 3.5 h after onset of pain. The predictive power could be improved further by a combined analysis of the times to peak value of both myoglobin and CK. In cases where reperfusion was achieved more than 3.5 h after the onset of pain, the probability of correct classification of infarct reperfusion varied between 0.99 and 0.05. Among the marker proteins analyzed, myoglobin allowed the earliest and best discrimination between reperfusion or no reperfusion. Thus, by applying the time to peak value analysis, infarct reperfusion can only be predicted reliably if it is achieved early after onset of pain.

Clinical Enzyme Tests↗