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Biomedical subjects

K Swedberg

Publications and source records attributed to K Swedberg.

At least 127 records · Page 7Linked to original sources
PubMed1993

Early electrocardiographic changes in acute myocardial infarction treated by streptokinase or alteplase: a randomized study with dynamic, multi-lead, electrocardiographic monitoring.

Patients with a patent coronary artery after reperfusion therapy show an increased rate of evolution of QRS changes and of resolution of S-T changes as compared to patients with a persistent occlusion. Dynamic vectorcardiography permits multi-lead monitoring of changes in QRS complex and S-T segment over time. We monitored 150 patients randomized to alteplase or streptokinase for 24 h after admission. Alteplase was associated with significantly more rapid evolution of electrocardiographic changes but also with an increased occurrence of recurrent S-T changes. This may indicate a higher rate of early reperfusion with alteplase but due to recurrent ischemia, an electrocardiographic catch-up is seen with similar extent of myocardial damage observed after 24 h of monitoring.

Aged↗
PubMed1993

The role of exercise testing in heart failure.

The objectives of exercise testing in congestive heart failure (CHF) may be summarized as follows: (a) detect impaired cardiac performance, (b) grade severity of cardiac failure and classify functional capability, and (c) assess effects of interventions. Several different methods are available to make these assessments, and we have to ask ourselves how well exercise testing achieves these objectives. It has to be kept in mind that the power generated by the exercising muscles is dependent on the oxygen delivery to the skeletal muscles. Oxygen uptake is the result of an integrated performance of the lungs, heart, and peripheral circulation. In patients, as well as in normal subjects, oxygen uptake is related to hemodynamic indices such as cardiac output, stroke volume, or exercise duration when a stepwise regulated maximal exercise protocol is used. However, there are major differences in the concept of a true maximum in normal subjects versus heart failure patients. Fit-normal subjects will achieve a real maximal oxygen uptake, whereas patients may stop testing before a maximum is reached because of symptoms such as dyspnea or leg fatigue. Therefore, it is better if the actual oxygen uptake can be measured. "Peak" rather than true maximal oxygen uptake has been suggested for the classification of the severity of heart failure. Peripheral factors modify the cardiac output through such factors as vascular resistance, organ function, and hormonal release. Maximal exercise will stress the cardiovascular system to a point where the weakest chain will impose a limiting effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Reduction in mortality by pharmacological therapy in congestive heart failure.

Mortality in congestive heart failure remains high. In analysis of heart failure in the perspective of pathophysiological mechanisms, some approaches to treatment to improve survival become particularly interesting. The concept of unloading myocardial performance by reducing systemic vascular resistance has received general acceptance. This approach was associated with improved survival with nitrates and hydralazine in the V-HeFT I study. Stimulation of the myocardium in excess of what is achieved by endogenous stimulation might be dangerous. Long-term therapy with positive inotropic agents, therefore, is not an appropriate approach at present. However, addition of beta-blockers may protect the myocardium from the intense endogenous sympathetic stimulation in congestive heart failure. There are favorable trends with this approach in several small trials. An ongoing trial in idiopathic dilated cardiomyopathy may help to clarify this question. Counteraction of neuroendocrine activation may also be obtained by the addition of an angiotensin converting enzyme inhibitor. The CONSENSUS I study demonstrated a clear improvement in survival among very compromised patients by addition of enalapril. A positive effect was significantly associated with the degree of neuroendocrine activation at baseline. Two recent large-scale trials have emphasized the importance of adding an angiotensin converting enzyme inhibitor to other treatments in patients with mild to moderate symptoms and left ventricular dysfunction. These trials also support the importance of myocardial protection from neuroendocrine stimulation with symptomatic or asymptomatic myocardial failure. Antiarrhythmic agents have not been documented to improve survival. On the contrary, class I agents are deleterious in some patients with left ventricular dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1992

Effects of the early administration of enalapril on mortality in patients with acute myocardial infarction. Results of the Cooperative New Scandinavian Enalapril Survival Study II (CONSENSUS II)

BACKGROUND: Long-term administration of angiotensin-converting--enzyme (ACE) inhibitors has been shown to improve survival in patients with symptomatic left ventricular failure and to attenuate left ventricular dilatation in patients with myocardial infarction. We studied whether mortality could be reduced during the 6 months after an acute myocardial infarction with use of the ACE inhibitor enalapril. METHODS: At 103 Scandinavian centers patients with acute myocardial infarctions and blood pressure above 100/60 mm Hg were randomly assigned to treatment with either enalapril or placebo, in addition to conventional therapy. Therapy was initiated with an intravenous infusion of enalapril (enalaprilat) within 24 hours after the onset of chest pain, followed by administration of oral enalapril. RESULTS: Of the 6090 patients enrolled, 3046 were assigned to placebo and 3044 to enalapril. The life-table mortality rates in the two groups at one and six months were not significantly different (6.3 and 10.2 percent in the placebo group vs. 7.2 and 11.0 percent in the enalapril group, P = 0.26). The relative risk of death in the enalapril group was 1.10 (95 percent confidence interval, 0.93 to 1.29). Death due to progressive heart failure occurred in 104 patients (3.4 percent) in the placebo group and 132 (4.3 percent) in the enalapril group (P = 0.06). Therapy had to be changed because of worsening heart failure in 30 percent of the placebo group and 27 percent of the enalapril group (P less than 0.006). Early hypotension (systolic pressure less than 90 mm Hg or diastolic pressure less than 50 mm Hg) occurred in 12 percent of the enalapril group and 3 percent of the placebo group (P less than 0.001). CONCLUSIONS: Enalapril therapy started within 24 hours of the onset of acute myocardial infarction does not improve survival during the 180 days after infarction.

Administration, Oral↗
PubMed1992

Renal function in severe congestive heart failure during treatment with enalapril (the Cooperative North Scandinavian Enalapril Survival Study [CONSENSUS] Trial).

The effect on renal function of long-term treatment with either enalapril (n = 123) or placebo (n = 120) in addition to conventional therapy was studied in a randomized trial in patients with severe congestive heart failure (New York Heart Association functional class IV; the Cooperative North Scandinavian Enalapril Survival Study). Enalapril was administered in a dose of 2.5 to 40 mg/day. The analysis was restricted to the first 6 months of treatment. There was an average initial increase of 10 to 15% (10 to 20 mumol/liter) irrespective of baseline serum creatinine within the first 3 weeks of enalapril treatment, whereafter mean serum creatinine remained on a similar level during the first 6 months. Enalapril was well-tolerated by most patients, and serum creatinine was reduced in 24%. Serum creatinine increased by greater than 100% in 13 patients (11%) in the enalapril group (mainly as a consequence of intercurrent disease or severe hypotension, and usually transiently) and in 4 (3%) in the placebo group. The maximal increase in serum creatinine in the enalapril group was inversely correlated to the diastolic blood pressure (p = 0.008) at baseline and to the mean diastolic and systolic blood pressures measured at the time of the maximal increase in serum creatinine (p = 0.0001). According to multivariate regression analysis, the maximal increase in serum creatinine was also slightly influenced by the dose of furosemide taken. The development of hypotension emerged as the strongest factor explaining an abnormal increase in serum creatinine.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Effects of enalapril on long-term mortality in severe congestive heart failure. CONSENSUS Trial Group.

All surviving patients in a double-blind study comparing the effects of enalapril and placebo on survival in severe congestive heart failure were recommended to be treated with active drug after stopping the trial. Two-year follow-up from the end of the blinded trial demonstrated that among 77 survivors of 127 patients originally allocated to the group with enalapril, 38 were still alive. Of 126 patients allocated to the group with placebo 58 survived the blinded study, and after 2-year follow-up 26 were still alive. Thus, the difference between the original treatment groups remained, despite that treatment with enalapril was made available to all surviving patients and that those in the group with enalapril were sicker at baseline than those in the group with placebo. If enalapril was prescribed, the mortality was 47% compared with 75% if it was not. Life-table analysis suggests a marked carry-over effect of treatment in the group with enalapril that lasted for up to 15 months before mortality rates became comparable in the 2 treatment groups. This strongly suggests that enalapril confers structural protection to the failing myocardium.

Adult↗
PubMed1992

The effect of treatment on survival in congestive heart failure.

Congestive heart failure (CHF) is a disorder characterized by a variety of clinical, biochemical, electrophysiological, and hemodynamic abnormalities. During the past two decades, numerous drugs have been employed in the treatment of this complex syndrome, and many agents have been shown to improve symptoms and ventricular function in patients with CHF. Because CHF is associated with a high risk of death, treatment should be directed not only toward the relief of symptoms, but also toward a reduction in mortality. Many variables have been shown to be related to survival; taken individually, however, each is limited in its utility in predicting prognosis. In recent years, large-scale studies with large sample sizes have directly assessed the effects of treatment on mortality in CHF. Results from these trials indicate that vasodilators and angiotensin-converting enzyme (ACE) inhibitors may improve mortality in patients with symptoms of heart failure. Additional trials are now in progress to evaluate the effect of treatment on patients with asymptomatic left ventricular dysfunction.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1992

Dynamic changes of the QRS complex in unstable angina pectoris.

Despite intensive medical treatment to control chest pain, about one-third of patients with unstable angina have an unfavourable outcome within a period of 1 to 2 months. Holter monitoring can identify patients with silent myocardial ischaemia that are at a high risk of sustaining a major cardiovascular event. The present paper describes the use of dynamic, continuous, computerized on-line vectorcardiography for real-time monitoring of QRS-complex and ST-segment changes in patients with unstable coronary disease. In many patients a pattern of frequent repetitive episodes of QRS change was observed, with or without concomitant ST change. Whereas no patient had episodes of ST-vector change without also having episodes of significant QRS change, 15 patients had several episodes of QRS changes without any episode of significant ST change. The number of episodes of significant increase of the QRS vector difference correlated weakly but significantly with the number of episodes of significant ST-vector magnitude change (r = 0.34, p less than 0.05). The present study suggests that myocardial ischaemia will influence the QRS complex as well as the ST segment. The mechanism behind the QRS changes observed is not clear but episodes of QRS change without ST change or chest pain, may reflect sudden depressions of left ventricular function, as has been reported by others to occur in patients with coronary artery disease. Dynamic vectorcardiography offers the opportunity to monitor all parts of the QRST complex in real time.

Adult↗
PubMed1992

The predictive value of CKMB mass concentration in unstable angina pectoris: preliminary report.

Unstable angina pectoris is a common clinical problem, and the diagnosis is based on clinical symptoms. However, these symptoms cannot identify high-risk patients. Holter monitoring can identify patients at high risk, but analysis of a large number of patients is time- and resource-consuming, as is angiographic examination. We determined whether creatine kinase MB isoenzyme mass concentration could predict the prognosis for patients with unstable angina pectoris. A total of 101 consecutive patients were studied, and blood samples were collected three times a day for 48 h after admission. Patients with unstable angina and elevated CKMB (but still within the normal range) had a significantly higher risk of developing acute myocardial infarction or requiring revascularization during 6 months of follow-up than patients without elevated CKMB. We conclude that CKMB analysis is a valuable tool that may be of use in selecting high-risk patients with unstable angina pectoris. This finding needs to be confirmed by more extensive studies.

Aged↗
PubMed1991

Dynamic QRS-complex and ST-segment monitoring in acute myocardial infarction during recombinant tissue-type plasminogen activator therapy. The TEAHAT Study Group.

Changes of the QRS complex are the electrocardiographic expression of irreversible injury of the myocardium. In humans, the process of infarction occurs over several hours. A more rapid development of QRS changes has been reported in patients treated with thrombolytic agents. Patients with strongly suspected acute myocardial infarction (AMI) included in a placebo-controlled trial of 100 mg of recombinant tissue-type plasminogen activator (rt-PA) were monitored for 24 hours with continuous, on-line vectorcardiography. The magnitude of the QRS vector changes correlated with infarct size estimated by the maximal value of lactate dehydrogenase-1 (r = 0.69, p less than 0.001) as well as with left ventricular ejection fraction 30 days after randomization (r = 0.49, p less than 0.001). Treatment with intravenous rt-PA limited total QRS vector change but the QRS vector changes observed occurred more rapidly and reached a plateau 131 minutes earlier in patients treated with rt-PA than in those receiving placebo (p less than 0.01). A certain pattern of highly variable ST vector magnitude was identified and was associated with higher maximal lactate dehydrogenase-1 values (23 +/- 13 vs 14 +/- 10 mu kat/liter, p less than 0.001) and a tendency to higher 1-year mortality (24 vs 9%, p = 0.08) than in patients without this pattern. In patients with this pattern, rt-PA did not affect maximal lactate dehydrogenase-1, time to maximal creatine kinase and final magnitude of QRS vector change.

Double-Blind Method↗
PubMed1991

Buccal versus intravenous nitroglycerin in unstable angina pectoris.

The clinical syndrome of unstable angina includes patients with the first onset of angina, change in a previous stable pattern or the development of chest pain at rest. Administration of intravenous nitroglycerin is established therapy in unstable angina. Buccal nitroglycerin has been introduced as an alternative means of administering nitroglycerin, which provides relief of anginal pain within 2 to 3 min and a sustained effect for 3 to 5 h. Twenty-nine patients admitted to the coronary care unit due to unstable angina were randomized to receive treatment with nitroglycerin i.v. for 24 h or buccal nitroglycerin every 4 h. Therapy was titrated according to haemodynamic effects. The mean dose of buccal nitroglycerin was 4.42 mg versus 0.45 micrograms.kg-1.min-1 in the intravenous group. The efficacy of treatment was similar in the two groups. Buccal nitroglycerin appeared to cause fewer adverse effects, especially less haemodynamic intolerance and headache, although the differences were not significant. Repeated administration of buccal nitroglycerin appears to be a safe and well tolerated alternative to high-dose i.v. nitroglycerin treatment in unstable angina pectoris.

Administration, Buccal↗
PubMed1991

Dynamic QRS complex and ST segment vectorcardiographic monitoring can identify vessel patency in patients with acute myocardial infarction treated with reperfusion therapy.

Reperfusion therapy has lowered the mortality in patients suffering acute myocardial infarction. Failure to reperfuse is associated with significantly higher risk of short- and long-term mortality. Detection of reperfusion is thus important. In a prospective pilot study, we used continuous on-line computerized vectorcardiography to monitor 21 patients with acute myocardial infarction treated with reperfusion therapy to noninvasively detect coronary patency. By using trend analysis of QRS vector difference, we were able to correctly blindly identify 15 of 16 patients with a perfused infarct-related artery and four of six patients with a persistently occluded artery at an early angiogram. The present results are based on a limited number of patients, but suggest that QRS complex and ST segment monitoring with continuous on-line vectorcardiography has substantial potential for monitoring patients with acute myocardial infarction treated with reperfusion therapy.

Coronary Vessels↗
PubMed1991

Enalaprilat in acute myocardial infarction: tolerability and effects on the renin-angiotensin system.

We treated 48 patients with intravenous enalaprilat within 24 hours from the onset of acute myocardial infarction. Concomitant therapy included thrombolytic treatment (29), intravenous metoprolol (34), intravenous nitroglycerin (16) and intravenous furosemide (15). The first 40 patients included had systolic blood pressure at baseline greater than or equal to 110 mmHg. Intravenous bolus injections of 0.2-1.2 mg (mean 1.0 mg) enalaprilat in one hour were given to 20 patients and an intravenous infusion of 1 mg over two hours was administered to another 20 patients, as well as to a separate group of 8 patients with systolic blood pressure between 100-109 mmHg at baseline. The infusion was stopped in five cases when the systolic blood pressure fell below 100 and 90 mmHg, respectively, in the two infusion groups. No hypotensive reactions were symptomatic. Blood pressure decreased from a mean of 134/82, 131/79 and 106/72 mmHg to a minimum of 117/71, 118/73 and 97/63 mmHg, respectively, in the three groups. Almost complete suppression of plasma angiotensin converting enzyme activity was achieved within 30 minutes. No significant changes were found in plasma levels of angiotensin II, renin activity or atrial natriuretic peptide between baseline and 24 hours. Treatment was continued with oral enalapril 2.5-10 mg/day, which was generally well tolerated. We conclude that intravenous and oral enalapril added to conventional therapy in the early phase of acute myocardial infarction is well tolerated in selected patients, but should be carefully titrated.

Aged↗