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Biomedical subjects

L Erhardt

Publications and source records attributed to L Erhardt.

At least 37 records · Page 2Linked to original sources
PubMed1998

[Heart failure after myocardial infarction: diagnosis, treatment, prevention. Echocardiography should be a routine procedure in myocardial infarction].

Post-infarction prognosis is considerably impaired if left ventricular systolic dysfunction and/or symptomatic heart failure develops. As the symptoms of left ventricular dysfunction are often subtle or completely lacking, such patients can be identified only by objective evaluation of left ventricular function. However, as symptoms of heart failure may develop despite normal left ventricular function, objective evaluation of left ventricular function is also important in symptomatic patients, since prognosis is especially poor in the presence of systolic dysfunction. As echocardiography is the most suitable and accessible method in the context, also allowing assessment of cardiac dimensions and valvular function, its extended use in post-infarction patients is imperative. Left ventricular dysfunction should be prevented by adequate measures to limit the extent of infarction and prevent its recurrence. To improve prognosis, the use of ACE (angiotensin converting enzyme) inhibitors should be considered whenever left ventricular dysfunction is present, irrespective of symptomatology. Treatment with amiodarone has recently been shown to reduce mortality among patients with post-infarction heart failure, and should also be considered in such cases, especially if there is a need of antiarrhythmic therapy. Although beta-receptor blockers have well-documented beneficial effects in myocardial infarction, their effect on patients with latent or overt heart failure has not been specifically studied. The use of angiotensin II antagonists in patients with post-infarction heart failure or left ventricular dysfunction is currently under investigation.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

Exercise training in heart failure improves quality of life and exercise capacity.

AIMS: Benefit from exercise training in heart failure has mainly been shown in men with ischaemic disease. We aimed to examine the effects of exercise training in heart failure patients < or = 75 years old of both sexes and with various aetiology. METHODS AND RESULTS: Fifty-four patients with stable mild-to-moderate heart failure were randomized to exercise or control, and 49 completed the study (49% > or = 65 years; 29% women; 24% non-ischaemic aetiology; training, n = 22; controls, n = 27). The exercise programme consisted of bicycle training at 80% of maximal intensity over a period of 4 months. Improvements vs controls were found regarding maximal exercise capacity (6 +/- 12 vs -4 +/- 12% [mean +/- SD], P < 0.01) and global quality-of-life (2 [1] vs 0 [1] units [median ¿inter-quartile range¿], P < 0.01), but not regarding maximal oxygen consumption or the dyspnoea-fatigue index. All of these four variables significantly improved in men with ischaemic aetiology compared with controls (n = 11). However, none of these variables improved in women with ischaemic aetiology (n = 5), or in patients with non-ischaemic aetiology (n = 6). The training response was independent of age, left ventricular systolic function, and maximal oxygen consumption. No training-related adverse effects were reported. CONCLUSION: Supervised exercise training was safe and beneficial in heart failure patients < or = 75 years, especially in men with ischaemic aetiology. The effects of exercise training in women and patients with non-ischaemic aetiology should be further examined.

Activities of Daily Living↗
PubMed1998

Failure of thrombolytic therapy in patients with myocardial infarction is associated with high plasma levels of factor VII antigen.

Thrombolytic therapy in acute myocardial infarction fails to re-establish coronary blood flow in a significant number of patients. One reason for this may be haemostatic imbalance. We investigated whether coagulation factor VII antigen (FVIIag), fibrinogen and protein C were related to reperfusion. Plasma from 45 patients was drawn before treatment and reperfusion assessed by means of continuous, on-line, vector-ECG analysis. Among the 17 patients with no reperfusion, FVIIag levels were significantly higher than among the 28 with signs of reperfusion (560 vs. 410 microg/l median, p = 0.006). Protein C levels where higher in the group with successful reperfusion (1.10 vs. 1.01 U/ml median, p = 0.03), whereas no difference was seen in fibrinogen levels. The findings were not influenced by plasma-triglycerides, body-mass index, age or time between onset of chest pain and thrombolytic therapy. The results suggest that FVII is of importance for the formation as well as resolution of coronary clots.

Adult↗
PubMed1997

Left ventricular atrioventricular plane displacement: an echocardiographic technique for rapid assessment of prognosis in heart failure.

OBJECTIVE: To assess the prognostic value of atrioventricular plane displacement in heart failure patients. DESIGN: Patients were followed prospectively for one year after atrioventricular plane displacement determination. SETTING: Malmö University Hospital, with a primary catchment area of 250,000 inhabitants. PATIENTS: 181 patients with a clinical diagnosis of heart failure; age 75.7 (SD 5.2) years, duration of heart failure 2.7 (5.7) years; 100 men, 81 women. MAIN OUTCOME MEASURES: Mortality in relation to atrioventricular plane displacement. RESULTS: Total mortality was 22.7% (41/181), and was highly significantly (P = 0.001) related to atrioventricular plane displacement. Mortality within prospectively defined categories of displacement was: > or = 10.0 mm, 0% (0/19); 8.2 to 9.9 mm, 10.3% (3/29); 6.4 to 8.1 mm, 19.4% (12/62); and < 6.4 mm, 36.6% (26/71). The groups were similar in age, sex, angiotensin converting enzyme inhibitor and beta blocker treatment, and cause and duration of heart failure. CONCLUSIONS: Mortality in heart failure is strongly related to atrioventricular plane displacement.

Aged↗
PubMed1997

Cost effectiveness in the treatment of heart failure with ramipril. A Swedish substudy of the AIRE study. Acute Infarction Ramipril Efficacy.

We estimated the cost effectiveness of adding the ACE inhibitor ramipril to conventional treatment in patients with heart failure after acute myocardial infarction. These estimates were based on the Acute Infarction Ramipril Efficacy (AIRE) study and on complementary Swedish healthcare resource use data for a subset of patients. The average follow-up period was 15 months (minimum 6 months, maximum 3.8 years). The perspective of the analysis was that of the county councils (third-party payers), and we focused on the cost of drugs and hospitalisation. The marginal cost effectiveness of the treatment was estimated over 3 treatment periods: 1, 2 and 3.8 years. The cost-effectiveness ratios varied between SEK14,148 and SEK33,033 per life-year gained ($US1 = SEK7.70. Pounds 1 = SEK12.40) for the 3 treatment periods. Adding ramipril to conventional treatment for heart failure after acute myocardial infarction is therefore cost effective, and compares favourably with the cost effectiveness of other common medical therapies in the cardiovascular field.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

Effect of ramipril on morbidity and mode of death among survivors of acute myocardial infarction with clinical evidence of heart failure. A report from the AIRE Study Investigators.

BACKGROUND: The importance of the effects of ACE inhibitors on sudden death, progressive heart failure and recurrent infarction to the reduction in overall mortality in heart failure and after myocardial infarction is disputed. METHODS: The AIRE study randomized 2006 patients with clinical or radiological evidence of heart failure within 2-9 days of a myocardial infarction to receive ramipiril 5 mg b.d. or matching placebo. Outcomes were assessed independently by members of an end-points committee blinded to treatment allocation. RESULTS: Fewer patients developed severe resistant heart failure as their first validated end-point on rampril, despite the greater number of at-risk survivors, compared to placebo (n = 143 vs 178; risk reduction 23%; CI 5 to 39%; P = 0.017). Ramipril did not alter the rate of reinfarction or stroke. Irrespective of treatment allocation 182 (46%) patients developed resistant heart failure prior to death. A validated acute or remote myocardial reinfarction occurred in 76 (19%) patients prior to death and chest pain occurred in 90 (23%) patients around the time of death suggesting an ischaemic element to these deaths Eighty deaths occurred on the index admission, 167 during re-admission and 145 out-of-hospital. Sudden death accounted for 54% of all deaths and 93% of out-of-hospital deaths. Ramipril reduced the risk of sudden death by 30% (95% CI: 8-47%; P = 0.011). However, overall, 45% of those patients who died suddenly had severe or worsening heart failure prior to their death. Only 39% of sudden deaths were considered to be due to arrhythmias. Ramipril reduced the risk of death from circulatory failure by 18%, but this did not reach statistical significance (95% CI; 41 to -14%; P = 0.237). The magnitude of the effects on sudden death and death due to circulatory failure were not significantly different. However, 38% of the reduction in overall mortality was from the subgroup with sudden death who had developed prior severe resistant heart failure (placebo n = 35, ramipril n = 15), again emphasizing the marked benefit in preventing failure. Ramipril did not selectively alter the proportion of in- to out-of-hospital deaths. CONCLUSION: Ramipril reduces mortality and progression to resistant heart failure among patients with evidence of heart failure early after myocardial infarction. Retarding the progression of heart failure appears to be a major factor contributing to the reduction in mortality both by reducing circulatory failure and by reducing sudden death.

Adult↗
PubMed1996

Continuous vectorcardiographic changes in relation to scintigraphic signs of reperfusion in patients with acute myocardial infarction receiving thrombolytic therapy.

OBJECTIVES: Changes in the electrical activity of the heart reflecting the infarct process can be recorded by continuous vector-ECG, a method which is now clinically available for cardiac supervision. Shifts of the ST-segment and QRS-vector reflect ischaemia and necrosis of the myocardium. Continuous vector-ECG changes were evaluated against myocardial scintigraphy in 18 patients with acute myocardial infarction treated with streptokinase in order to study the impact of improved myocardial perfusion. DESIGN: Myocardial perfusion was analysed with 99Tcm-Sestamibi (Cardiolite, DuPont Scandinavia AB, Kista, Sweden) single photon emission computerized tomography (SPECT). Registrations were performed before and after thrombolysis in order to estimate the amount of myocardium with impaired perfusion initially (threatened myocardium) and the degree of perfusion improvement in this myocardial area. X, Y, Z vectors were registered continuously by Frank leads (Ortivus Medical, Täby, Sweden). QRS-vector difference, and the time to plateau phase and the ST-vector magnitude were used as a measurement of ischaemia and size of the myocardial infarction. RESULTS: In seven out of 11 patients treated within 3 h of onset of symptoms, an improvement in myocardial perfusion in the initially hypoperfused areas was achieved in contrast to none of the seven patients treated > 3 h after onset of pain (P < 0.05). In the whole patient material, there was a negative correlation between the time to plateau level for the QRS-vector and the improvement in myocardial perfusion (r = -0.53, P < 0.05). Among patients treated within 3 h, there was a negative correlation between the plateau level for the QRS-vector magnitude compared to the improvement in myocardial perfusion (r = -0.61, P < 0.05) and a negative correlation between the plateau level and the myocardial perfusion level after therapy (r = -0.69, P < 0.05). In these patients, there were also negative correlations between the maximal ST-vector magnitude and the myocardial perfusion both before and after thrombolysis (r = -0.81, P < 0.05 and r = -61, P < 0.05, respectively). CONCLUSION: Patients with marked improvement in myocardial perfusion indicating successful thrombolysis reach their plateau levels of the QRS-change faster and have lower total QRS-vector differences than patients without successful thrombolysis as reflected by myocardial scintigraphy. Patients with a high ST-vector magnitude have low perfusion levels both before and after therapy indicating a pronounced ischaemic damage of the myocardium. Thus, VCG-changes reflect impairment in myocardial perfusion during acute myocardial infarction.

Aged↗
PubMed1996

Prevalence of factor V gene mutation amongst myocardial infarction patients and healthy controls is higher in Sweden than in other countries.

OBJECTIVE: Haemostatic imbalance may be an aetiological factor in the development of acute coronary syndromes. Inherited resistance to activated protein C (APC) is a common disorder associated with hypercoagulability and lifelong risk of venous thrombosis. APC resistance is due to a single mutation in the gene coding for coagulation factor V (FV:Q506). To test the importance of the FV:Q506 mutation in premature myocardial infarction (MI), its prevalence was investigated in Swedish patients with MI before the age of 50 years. DESIGN, SETTING AND SUBJECTS: In a retrospective case-control study, the FV:Q506 mutation was investigated in 101 survivors of MI (79 men, 22 women) and in 101 healthy sex- and age-matched controls. MAIN OUTCOME MEASURE: The prevalence of FV:Q506 mutation. RESULTS: The FV:Q506 mutation was found in 18% of patients versus 11% of controls (P = 0.16). The mutation was significantly more frequent amongst male patients than amongst controls (23 vs. 10%; P = 0.03), the calculated odds ratio being 2.6 (95% CI, 1.1-6.4). CONCLUSION: The high prevalence of the FV:Q506 mutation found amongst Swedish MI patients, especially amongst men, is noteworthy, and calls for further studies on the outcome of MI in APC-resistant patients. The prevalence of the FV:Q506 mutation in controls is higher than figures reported from other countries, suggesting that at least 10% of the Swedish population are carriers of a congenital prothrombotic disorder.

Adult↗
PubMed1996

Effects of beta receptor antagonists on left ventricular function in patients with clinical evidence of heart failure after myocardial infarction. A double-blind comparison of metoprolol and xamoterol. Echocardiographic results from the Metoprolol and Xamoterol Infarction Study (MEXIS).

Two hundred and ten patients with clinical evidence of heart failure, developing after an acute myocardial infarction, were randomized to treatment with the beta 1-receptor antagonist metoprolol 50-100 mg b.i.d. (n = 106) or the beta 1-receptor partial agonist xamoterol 100-200 mg b.i.d. (n = 104). Left ventricular systolic and diastolic function were assessed with echocardiography and transmitral Doppler cardiography before and after 3 and 12 months of double-blind treatment. E-point septal separation and percent left ventricular fractional shortening were used as indices of systolic function. The ratio between peak early and late mitral diastolic flow (E/A ratio) and isovolumic relaxation time were used as indices of diastolic function. In the xamoterol group, there was a deterioration in E-point septal separation (P < 0.05). A difference between the treatment groups was present both at 3 months (E-point septal separation 11.4 vs 13.0 mm, P < 0.01, fractional shortening 27.1 vs 25.2%, P < 0.05) and 12 months (E-point septal separation 11.1 vs 13.2 mm. P < 0.005, fractional shortening 26.9 vs 25.0%, P < 0.05). E/A ratio increased in the metoprolol group (P < 0.05) but not in the xamoterol group. At 3 months there was a significant difference (0.85 vs 0.67, P < 0.005) between the groups but not at 12 months. In comparison with the beta 1-receptor antagonist metoprolol, the beta 1-receptor partial agonist xamoterol impaired left ventricular systolic function in patients with clinical evidence of heart failure after an acute myocardial infarction.

Adrenergic beta-Antagonists↗
PubMed1996

Mode of death in chronic heart failure. A request and proposition for more accurate classification.

The proportion of patients reported to die suddenly or from progressive circulatory failure is not consistent among studies of heart failure. Lack of an adequate or consistent classification of how patients die contributes to the current confusion over the mode of death in heart failure. Defining how patients with heart failure die could be important in developing strategies to reduce the continuing high mortality associated with this condition. We identified 27 studies that reported 50 or more deaths among patients with heart failure to ascertain how death was classified. Definitions of sudden death appeared heterogeneous and the majority of studies failed to publish or make reference to how circulatory failure was defined. A framework for the classification of the mode of death has been developed in which clear separation of the activity and place at the time of death, cause of death, mode of death, and events prior to death is made (ACME: Activity, Cause, Mode and Event). This mode of classifying death has been successfully piloted in two mortality studies; AIRE and NETWORK. Classifying mortality in this way will help identify pathways leading to death and hence suggest therapies and strategies to reduce mortality in patients with heart failure, a group of patients whose prognosis remains poor.

Adult↗
PubMed1996

ACE inhibitors before or after heart failure?

Heart failure is a progressive disease and once the process has started it continues with further deterioration of cardiac function or ends in sudden death. In many patients changes within the heart start to develop long before clinical symptoms occur. The left ventricle goes through a number of adaptions-remodelling-to compensate for increased pressure or volume load or subsequent myocardial infarction. Several of these compensatory changes have prognostic implications and indicate increased risk of clinical heart failure or cardiac events. Thus, increased left ventricular dimensions, volume and mass together with reduced systolic function are all markers of poor prognosis. Treatment with angiotensin-converting enzyme (ACE) inhibitors before the onset of clinical heart failure has been shown to improve prognosis. Identification of individuals at high risk is difficult since signs and symptoms of heart failure are often lacking. A strategy to find these patients must use objective methods to characterise the state of the left ventricle. It is likely that not only patients with significant reduction of systolic function but also other signs of impaired left ventricular dysfunction will benefit from treatment with ACE inhibitors. Only by preventive treatment may we be able to decrease the number of patients with new onset of clinical heart failure.

Angiotensin-Converting Enzyme Inhibitors↗