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Biomedical subjects

K Thygesen

Publications and source records attributed to K Thygesen.

At least 55 records · Page 3Linked to original sources
PubMed1993

Effects of captopril on ischemia and dysfunction of the left ventricle after myocardial infarction.

BACKGROUND: Treatment with angiotensin converting enzyme inhibitors has been shown to be beneficial in patients with heart failure and myocardial infarction. Experimental studies have shown beneficial effects on the ischemic myocardium. METHODS AND RESULTS: The effects of captopril were evaluated in 64 patients with left ventricular dysfunction after myocardial infarction. The patients were randomized at day 7 to either placebo or captopril (50 mg daily) in a double-blind parallel study over a period of 6 months. The patients were followed up by means of ambulatory ECG monitoring, bicycle ergometer testing, and echocardiographic examination. The duration of ST segment depression detected during ambulatory ECG monitoring was lower in the captopril group (87 minutes) than in the placebo group (638 minutes) (p < 0.001), and the number of patients in the captopril group with exercise-induced ST segment depression (p < 0.01) was lower at the completion of the study. The working capacity increased during the study period from 540 +/- 47 seconds to 738 +/- 41 seconds (p < 0.01) in the captopril group and was higher than that in the placebo group (530 +/- 43 seconds, p < 0.01) at the end of the study. Furthermore, a significant dilation of the left ventricular end-diastolic and end-systolic volumes was observed in the placebo group (p < 0.05); this was prevented in the captopril group where, in addition, a reduction in end-systolic volume was observed (p < 0.05). CONCLUSIONS: Captopril has a favorable effect on the dysfunctioning myocardium after myocardial infarction inasmuch as the ischemic burden is reduced, the working capacity is increased, dilation of the left ventricle is prevented, and systolic function is improved.

Captopril↗
PubMed1992

Effects of captopril on left ventricular systolic and diastolic function after acute myocardial infarction.

The left ventricle progressively dilates in some patients after acute myocardial infarction (AMI). Both systolic and diastolic left ventricular (LV) dysfunction can be of significance in the development of heart failure. Captopril has been shown to prevent dilatation, but the effect on LV diastolic function is unknown. In a placebo-controlled double-blind parallel study, 58 AMI patients with heart failure or low ejection fraction, or both, were consecutively randomized at day 7 to either placebo or captopril (25 mg twice daily). No differences were present between the groups at baseline. Fifty-three patients completed the 6-month study period. Both LV diastolic and systolic volume indexes increased significantly in the placebo group (17 and 14%, respectively); in the captopril group there was no change in LV diastolic volume index, but a 13% reduction in LV systolic volume index. Ejection fraction increased significantly in the captopril group. The peak flow velocities of the early and atrial filling phases were measured, and the ratio between the velocities was calculated. A significant reduction was observed during the study period in early peak flow velocity (65 to 52 cm/s) and in the ratio between early and atrial peak flow velocity (1.3 to 0.8) in the placebo group (p less than 0.05), but no significant changes occurred in the captopril group. No correlation was found between dilatation of the left ventricle and reduction in early peak flow velocity or the ratio between early and atrial peak flow velocity. In conclusion, captopril prevented LV dilatation, improved ejection fraction and prevented LV diastolic dysfunction in AMI patients with early signs of LV systolic dysfunction.

Aged↗
PubMed1992

Risk stratification in suspected acute myocardial infarction based on a sensitive immunoassay for serum creatine kinase isoenzyme MB. A 2.5-year follow-up study in 156 consecutive patients.

This prospective study was an evolution of a new sensitive creatine kinase (CK) isoenzyme MB immunoassay in 156 patients, admitted consecutively to the coronary care unit, suspected of having acute myocardial infarction (MI), with regard to clinical applicability and clinical outcome. 42% of the patients had MI based on WHO criteria. The remaining 91 patients could be divided into a group with ischemic heart disease (IHD) without MI being present (n = 65) and a group with non-IHD (n = 26). In the former, a subgrouping based on changing CK MB levels (n = 24) or stable CK MB levels (n = 41) as compared to the non-IHD group could be performed. These patients were not diagnosed using the routine diagnostic procedures. Follow-up was carried out for 30 months (median 22). The prognosis as evaluated by cardiac death was significantly better for patients with stable CK MB levels than for those with changing CK MB levels, inasmuch as the cumulative probability not to suffer cardiac death was 95 +/- 3 and 66 +/- 10% after 2.5 years, respectively (p less than 0.003). It was 52 +/- 6% for the patients with MI, similar to patients with changing CK MB levels (p = 0.15). We conclude that this new CK MB assay can detect a subgroup of patients with IHD, which is not diagnosed using routine diagnostic procedures, with a poor clinical outcome.

Adult↗
PubMed1991

Gradation of unstable angina based on a sensitive immunoassay for serum creatine kinase MB.

A newly developed, highly sensitive immunoassay for creatine kinase MB isoenzyme was evaluated in 68 patients with or without different types of ischaemic heart disease. Patients were classified on the basis of clinical criteria in four groups: no ischaemic heart disease, stable angina, unstable angina, and acute myocardial infarction. Enzyme concentration in patients with stable angina was the same (even during exercise) as seen in the patients without ischaemic heart disease. Patients with unstable angina, however, could be divided into two groups. One group showed clear evidence of severe myocardial ischaemia by serial changes and higher mean values of creatine kinase MB up to 40 hours after the onset of symptoms, whereas in the remainder values were stable and resembled those seen in the patients without ischaemic heart disease. The changes in concentration correlated with signs of repetitive ischaemic episodes deduced from continuous ST segment monitoring during the first 24 hours after admission. These findings indicate that patients with unstable angina are a heterogenous group. In some, severe and prolonged ischaemia can be detected by a serological assay with high sensitivity.

Angina Pectoris↗
PubMed1990

Effects of glutamate on exercise tolerance and circulating substrate levels in stable angina pectoris.

The effects of glutamate on exercise tolerance, ischemic threshold and venous substrate concentrations were studied in 20 patients with stable angina pectoris and positive stress tests. Each patient underwent 4 upright bicycle exercise tests on consecutive days. The first and fourth tests were performed without medication while the second and third tests were preceded by a low and high bolus dose of monosodium glutamate, either 0.8 and 1.5 mg/kg body weight intravenously (10 patients) or 40 and 80 mg/kg orally (10 patients). Comparison of the first and fourth tests revealed good reproducibility of electrocardiographic, hemodynamic and metabolic data. Glutamate increased exercise duration (p less than 0.05) in a dose-related way when given intravenously (59 +/- 14 and 153 +/- 14 seconds) and when given orally (53 +/- 21 and 90 +/- 23 seconds; all data are mean +/- standard error of the mean). It also delayed the onset of ST-segment depression (p less than 0.05) by 73 +/- 19, 120 +/- 23, 62 +/- 27 and 80 +/- 30 seconds, respectively. Hemodynamics were not changed by glutamate at rest or at comparable workloads, but at onset of ST-segment depression the heart rate-blood pressure product was increased (p less than 0.05). Glutamate administration induced dose-related 1.5- to 10-fold elevations in plasma glutamate, 15 to 50% decreases in plasma free fatty acids (p less than 0.05) and 5 to 30% increases in plasma alanine contents. Circulating levels of glucose, lactate, citrate and albumin were not modified by glutamate.(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine↗
PubMed1990

Flecainide acetate in atrial flutter and fibrillation. The arrhythmogenic effects.

The arrhythmogenic effects of flecainide in atrial fibrillation and flutter were assessed in a consecutive material of 100 patients without severe heart failure (NYHA class I or II). Severe arrhythmogenic events occurred in 9% (4-16%) of the patients: within the first 5 days of treatment in seven patients, and in two patients after 60 and 240 days of flecainide treatment. Patients with proarrhythmic events tended to be older and to have a longer QRS duration. Following flecainide therapy conversion to sinus rhythm was achieved in 21 of 43 patients (49%) with atrial fibrillation and in 10 of 29 (34%) with atrial flutter. It is concluded that flecainide, although an effective antiarrhythmic drug, has potential proarrhythmic effects and therefore cautious use of this drug is mandatory.

Aged↗
PubMed1989

[Enzyme diagnosis of acute myocardial infarction].

During the past decade, determinations of enzyme concentrations in the blood in patients admitted with suspected acute myocardial infarction has been of increasing significance not only for early elucidation but also for establishing the correct diagnosis. This is partly the result of methods which can demonstrate the presence of myocardium-related isoenzymes and also because of the physiological basis for the release of enzymes and their metabolism bas been elucidated. In the present report, guidelines for clinical employment of enzyme investigations in acute myocardial infarction are presented. By means of blood sampling twice or thrice within a time interval af approximately 8-24 hours after the presumed time of infarction and determination of a limited number of enzymes in these samples, it is possible to exclude or confirm the presence of an infarct with high probability.

Humans↗
PubMed1986

Altered plasma concentrations of glutamate, alanine and citrate in the early phase of acute myocardial infarction in man.

Plasma levels of glutamate, alanine, free fatty acids (FFA), citrate, glucose, insulin, lactate, creatine kinase and aspartate aminotransferase were determined frequently during the first 2-48 h after onset of chest pain in 10 patients who developed acute myocardial infarction (AMI) and in 8 who did not (non-AMI). An initial decrease in plasma glutamate and increase in alanine was found in AMI compared to non-AMI patients. The AMI group showed early, moderate rises of plasma FFA and citrate concentrations, positively related to the initial ST-segment elevation and to the enzymatic estimated infarct size. The AMI patients were continuously hyperglycaemic, but their relative insulin response i.e. plasma glucose/insulin ratio was identical to that of non-AMI patients. Lactate values did not differ between the two groups. Via participation in the malate-aspartate shuttle and by shunting pyruvate to alanine instead of lactate, glutamate is of importance for maintaining myocardial glucose utilization. Our finding of initial low plasma glutamate concentrations after onset of myocardial infarction suggests insufficient glutamate supply to the ischaemic myocardium. On basis of this and animal experiments, an external supply of glutamate might be a 'metabolic' treatment of AMI, alternative or additional to glucose-insulin-potassium infusion in order to promote myocardial glucose oxidation.

Aged↗
PubMed1986

Prognosis in treated hypertension.

The aim of this study has been to demonstrate to what extent antihypertensive treatment reduces the survival gap between hypertensives and the general population. In 673 outpatients treated for arterial hypertension, the 10-year survival has been assessed by actuarial methods and compared with expected survival of a matched background population computed from the life tables of the Danish population. In primary hypertension WHO stage I, survival did not differ from that of the background population, a congruence which of course may be a mere chance but excludes any major difference. However, when severe organ involvement was present, as in WHO stage III and renal hypertension, treatment did not eliminate the survival gap. The survival rate did not differ between sexes or between patients with high and low body mass, but decreased with increasing age. Myocardial infarction was the most frequent single cause of death, whereas stroke accounted for less than 10% of all fatalities.

Adolescent↗
PubMed1986

Creatine kinase and creatine kinase B-subunit in stable and unstable angina pectoris.

Repetitive ischaemic episodes may have a cumulative effect leading to irreversible myocardial cell damage with enzyme release. Using plasma creatine kinase (CK) and creatine kinase B-subunit (CK-B) concentrations this theory has been tested in forty-eight patients admitted with acute chest pain, but without ECG signs of acute myocardial infarction (AMI). The patients were classified into four groups: Fourteen patients with non-ischaemic heart disease (non-IHD), seventeen with stable angina pectoris (SAP), ten with unstable angina pectoris (UAP), and seven patients who developed AMI during the study period. The enzyme variation in non-IHD delineates the background noise, and the increased variability in AMI indicates the full scale of the enzyme signals in cases of irreversible cell damage. Patients with SAP have the same enzyme signal as the background noise in respect of both CK and CK-B. However, in UAP the signal of CK-B equals the background noise, whereas the CK signal is separated from the latter. The reason may be that the signal to noise ratio of CK-B is poor and the analytical sensitivity low. Therefore, the behaviour of CK-B in this study does not support the above theory although our findings for CK indicate that the consequence of repeated ischaemic attacks is slight enzyme release.

Angina Pectoris↗
PubMed1983

Limitation of enzymatic models for predicting myocardial infarct size.

The possibility of predicting myocardial infarct size from early enzyme measurements was studied using a physiological two compartment distribution model. Based on this the time dependent appearance function in plasma was calculated for creatine kinase, aspartate aminotransferase, and lactate dehydrogenase in 29 patients suffering from acute myocardial infarction. On average, the appearance function of the three enzymes started four hours after the onset of symptoms, and the maximum was reached after 12 hours for creatine kinase, 13 hours for aspartate aminotransferase, and 22 hours for lactate dehydrogenase. The cumulated appearance function was used as an acceptable estimate of infarct size. The prediction of infarct size from defined points of the appearance function curve for each of the three enzymes was attempted according to a set schedule during the first 25 hours after the onset of myocardial infarction. The prediction using creatine kinase was superior to the other enzymes. Even so, a reliable prediction could only be established at the very earliest from nine hours and this is too late, as irreversible loss of myocardium occurs rapidly after the onset of symptoms. This, together with the fact that other models have unacceptable variability of the prediction, lead to the conclusion that enzymatic predictive models are of no practical value in clinical intervention studies to reduce infarct size.

Adult↗
PubMed1981

Praecordial ECG mapping in acute anterior myocardial infarction. The evolution of ST segment and Q and R waves.

Praecordial ECG mapping (42 leads) was carried out in 16 patients with anterior myocardial infarction, admitted up to 3 hours after the onset of symptoms. The mappings were performed according to a set time schedule throughout the acute phase and one year after the infarction. For each ECG map the number of leads with ST elevation greater than or equal to 1.5 mm (NST) and the sum of these (epsilon ST) were calculated. In addition, the sum of Q amplitudes (epsilon Q) and R amplitudes (epsilon R) were determined. On average, the initial epsilon ST elevation decreased from 2 to 8 hours. A secondary increase, occurring in 14 patients, was maximal during days 2-5. Based on the appearance function of creatine kinase in plasma and the QRS alterations, it is suggested that this re-elevation of the St segment was due to infarct extension (5 pats.) or expansion (9 pats.). The course of the average NST was similar to epsilon ST. epsilon Q began to develop at 3 hours, the maximum deflection being reached after about 24 hours (range 8-45). epsilon R was falling at 2 hours; the maximum rate of decrease occurred, on average, within the first 24 hours (range 12-54). One year after the infarction, both epsilon Q and epsilon R had the same level as at 8 hours. The ST elevation at 4 hours was related to the development of Q and R waves within 24 hours, but only a weak or no correlation was found. Thus, there was very little value in predicting the development of QR changes from the ST elevation at 4 hours.

Adult↗