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L Erhardt

Publications and source records attributed to L Erhardt.

At least 19 recordsLinked to original sources
PubMed2003

Levosimendan: a new dual-action drug in the treatment of acute heart failure.

Levosimendan is a new agent for the treatment of acute heart failure. Levosimendan acts via complementary mechanisms; it enhances contractility by sensitising cardiac myofilaments to calcium and dilates blood vessels by opening ATP-dependent potassium channels. In contrast to traditional inotropes (beta-agonists or phosphodiesterase inhibitors), levosimendan does not raise myocyte calcium levels and is therefore less likely to elicit arrhythmias or to impair diastolic relaxation. The clinical efficacy of levosimendan is supported by four key clinical studies, including more than 900 patients hospitalised for cardiac decompensation due to acutely worsened chronic heart failure or to heart failure following myocardial infarction. When given as short-term therapy, levosimendan enhances cardiac output, reduces systemic vascular resistance and lowers pulmonary capillary wedge pressure. At 31 days post-treatment, mortality rates were halved in decompensated chronic heart failure patients who received levosimendan, compared with those on dobutamine--an advantage sustained at 180 days. Similar survival gains were observed among acute failure patients treated with levosimendan following myocardial infarction. With its substantial haemodynamic and survival benefits, levosimendan is well suited to be part of routine management for patients with acutely decompensated heart failure.

Acute Disease↗
PubMed2002

Public perceptions of cardiovascular risk in five European countries: the react survey.

Little is known of the attitudes and behaviours of the general public with regard to their general and personal risk factors for coronary heart disease (CHD), particularly in relation to cholesterol. This study attempted to determine patient perceptions of general population and personal risks regarding cardiovascular disease. Face-to-face interviews were conducted with 5104 members of the public in five countries (France, Germany, Italy, Sweden and the UK). Main results showed only 45% of the public correctly identified CHD as the leading cause of death in their country, and only 51% were aware that high cholesterol increases CHD risk. The presence of cardiovascular disease or risk factors in respondents did not appear to alter perceptions of risk compared with the public who had no existing disease. Of the different nationalities interviewed, the Swedes and the Germans appeared to be most aware of CHD risk factors. Awareness and knowledge of LDL-C and HDL-C were very poor in all countries except Italy Half of the general public (50%) reported they had never discussed their cholesterol levels with a physician and only 33% knew what their target level was. Despite this, the most common source of information on CHD and cholesterol was the physician (60%). Only 9% of the total sample reported that they were currently taking medication for high cholesterol, compared with 20% for hypertension. In summary the general public in several European countries has major lack of awareness of the risks of CHD. This gap in knowledge is particularly marked over the risks of high cholesterol. Significant public health education is required.

Adult↗
PubMed2001

[Quality assurance of secondary prevention of coronary artery disease. Ongoing project offers possibilities for improved treatment].

Regional programs for secondary prevention of coronary artery disease have been under development for nearly a decade in Sweden. To achieve maximum adherence these programs were created in close collaboration between hospital and primary care physicians. The programs are local applications of national guidelines and aim to support compliance among both patients and physicians. In January 1998 the Swedish Society of Cardiology and the Swedish Association of General Practice launched a program for quality control and quality assurance of these initiatives. So far, 51 of 79 districts have joined the program. Patients' diaries used for risk factor registration contain 7 report cards on the management of risk factors and medication. These cards are sent to a central registry upon release from the hospital, after 3-6 months, and annually for 5 years. Results from the first year point to differences between the various districts with respect to compliance with both local programs and European guidelines. Overall, results are promising and indicate that this program is successful and leads to improved management of patients with coronary artery disease.

Coronary Disease↗
PubMed2001

Association of outpatient utilisation of non-steroidal anti-inflammatory drugs and hospitalised heart failure in the entire Swedish population.

OBJECTIVE: Individual-based studies on restricted geographical settings have suggested that non-steroidal anti-inflammatory drugs (NSAIDs) may precipitate congestive heart failure. As NSAID use is very extensive, it might increase the occurrence of symptomatic heart failure in the general population. Therefore, in order to study the impact of NSAID utilisation (prescribed and over the counter) on hospitalised heart failure in an entire country (Sweden), we performed an ecological analysis, a design appropriate for studying large geographical areas. METHODS: We employed weighted (population size) ecological linear regression to study the association between outpatient utilisation of NSAIDs during 1989-1993 and hospitalised heart failure in 1993 in 283 of Sweden's 288 municipalities. Data were adjusted for age and gender proportions, socio-economic factors, latitude and utilisation of cardiovascular drugs, aspirin, low-dose aspirin and paracetamol. RESULTS: The unadjusted relative risk of hospitalised heart failure for each increase of one standard deviation of NSAID utilisation (5.8 defined daily doses/1000 inhabitants/day) was 1.23 [95% confidence interval (CI) 1.18, 1.27]. After adjustments, the relative risk was 1.08 (95% CI 1.04, 1.12); the corresponding values if aspirin (non-low-dose) was included as an NSAID were 1.26 (95% CI 1.23, 1.28) and 1.07 (95% CI 1.04, 1.10). There was no such adjusted association with the utilisation of paracetamol-0.95 (95% CI 0.92, 0.98). CONCLUSION: The NSAID--heart failure association already established by individual-based studies on restricted geographical settings was corroborated in the present ecological study based on the whole population of an entire country (Sweden). Efforts should be made to promote a rational use of NSAIDs in the general population.

Adult↗
PubMed2001

Effects on quality of life, symptoms and daily activity 6 months after termination of an exercise training programme in heart failure patients.

BACKGROUND: Exercise training in heart failure patients improves exercise capacity, physical function, and quality-of-life. Prior studies indicate a rapid loss of these effects following termination of the training. We wanted to assess any sustained post-training effects on patients global assessment of change in quality-of-life (PGACQoL) and physical function. METHODS: Fifty-four stable heart failure patients were randomised to exercise or control. The 4-month exercise programme consisted of bicycle training at 80% of maximal intensity three times/week, and 49 patients completed the active study period. At 10 months (6 months post training) 37 patients were assessed regarding PGACQoL, habitual physical activity, and dyspnea-fatigue-index. RESULTS: Both post-training patients (n=17) and controls (n=20) deteriorated PGACQoL during the 6-month extended follow-up, although insignificantly. However, post-training patients improved PGACQoL slightly but significantly from baseline to 10 months (P=0.006), differing significantly (P=0.023) from controls who were unchanged. Regarding dyspnea-fatigue-index, post-training patients were largely unchanged and controls deteriorated insignificantly, during the extended follow-up as well as from baseline to 10 months. Both groups decreased physical activity insignificantly during the extended follow-up, and from baseline to 10 months post-training patients tended to decrease whereas controls significantly (P=0.007) decreased physical activity. CONCLUSION: There was no important sustained benefit 6 months after termination of an exercise training programme in heart failure patients. A small, probably clinically insignificant sustained improvement in PGACQoL was seen in post-training patients. Controls significantly decreased the habitual physical activity over 10 months and post-training patients showed a similar trend. Exercise training obviously has to be continuing to result in sustained benefit.

Activities of Daily Living↗
PubMed2001

Practical recommendations for the use of ACE inhibitors, beta-blockers and spironolactone in heart failure: putting guidelines into practice.

Surveys of prescribing in both hospitals and primary care have shown delays in translating improved survival data from clinical trials into clinical practice thereby denying patients the benefits of proven treatments, such as the angiotensin converting enzyme inhibitors. This may be due to unfamiliarity with clinical guidelines and concerns about adverse events. Recent trials have shown that substantial improvements in survival are associated with spironolactone and beta-blocker therapy. In order to accelerate the uptake of these treatments, and to ensure that all eligible patients should receive the most appropriate medications, a clear and concise set of clinical recommendations has been prepared by a group of clinicians with practical expertise in the management of heart failure. The objective of these recommendations is to provide practical guidance for non-specialists in order to support the implementation of evidenced-based therapy for heart failure. These practical recommendations are meant to supplement rather than replace existing guidelines.

Adrenergic beta-Antagonists↗
PubMed2000

Inhibition of the sodium-hydrogen exchanger with cariporide to prevent myocardial infarction in high-risk ischemic situations. Main results of the GUARDIAN trial. Guard during ischemia against necrosis (GUARDIAN) Investigators.

BACKGROUND: The transmembrane sodium/hydrogen exchanger maintains myocardial cell pH integrity during myocardial ischemia but paradoxically may precipitate cell necrosis. The development of cariporide, a potent and specific inhibitor of the exchanger, prompted this investigation of the potential of the drug to prevent myocardial cell necrosis. METHODS AND RESULTS: A total of 11 590 patients with unstable angina or non-ST-elevation myocardial infarction (MI) or undergoing high-risk percutaneous or surgical revascularization were randomized to receive placebo or 1 of 3 doses of cariporide for the period of risk. The trial failed to document benefit of cariporide over placebo on the primary end point of death or MI assessed after 36 days. Doses of 20 and 80 mg every 8 hours had no effect, whereas a dose of 120 mg was associated with a 10% risk reduction (98% CI 5.5% to 23.4%, P=0.12). With this dose, benefit was limited to patients undergoing bypass surgery (risk reduction 25%, 95% CI 3.1% to 41.5%, P=0.03) and was maintained after 6 months. No effect was seen on mortality. The rate of Q-wave MI was reduced by 32% across all entry diagnostic groups (2.6% versus 1.8%, P=0.03), but the rate of non-Q-wave MI was reduced only in patients undergoing surgery (7.1% versus 3.8%, P=0.005). There were no increases in clinically serious adverse events. CONCLUSIONS: No significant benefit of cariporide could be demonstrated across a wide range of clinical situations of risk. The trial documented safety of the drug and suggested that a high degree of inhibition of the exchanger could prevent cell necrosis in settings of ischemia-reperfusion.

Aged↗
PubMed2000

A reply.

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Journal Article↗
PubMed2000

Are we treating to target?

The identification of a number of independent risk factors for coronary heart disease (CHD) led to the development of guidelines for the prevention of CHD in an attempt to target these risk factors and reduce the rates of CHD-related morbidity and mortality. Surveys conducted of physician's clinical practice patterns indicate, however, that the recommendations made in the guidelines are often not implemented and the predefined goals of therapy for patients are not achieved. Possible reasons for this apparent shortfall in preventive care include a lack of physician awareness of evidenced-based guidelines, an insufficient focus towards preventive care in health care systems, and patient non-compliance with lifestyle changes and medication. To ensure an optimal outcome, specialists, primary care physicians and the patient need to provide an integrated approach to the management of CHD. The first step is to achieve universal understanding and implementation of the guidelines. Not only do guidelines promote interventions of proven benefit, but when followed they also improve consistency of care. Nurse-led shared-care programs, which individualize care based on a comprehensive assessment of CHD risk factors, are of proven benefit and offer continuity between the hospital and a patients return to the community. Patients themselves also have a role to play in the management of their disease by adhering to lifestyle changes and medication.

Coronary Disease↗
PubMed1999

Changes in levels of factor VII and protein S after acute myocardial infarction: effects of low-dose warfarin.

Persistent coagulation activity after an acute myocardial infarction may increase the risk of reinfarction. We prospectively investigated the effects on plasma coagulation of a low, fixed dose of warfarin in combination with aspirin after myocardial infarction. We also evaluated the influence of coagulation activity on clinical outcome. Plasma samples from 97 patients, randomised to 1.25 mg of warfarin daily in combination with 75 mg of aspirin or aspirin alone were drawn 4 days, 1 month, and 6 months after myocardial infarction. Patients receiving warfarin had a greater reduction in factor VII coagulation activity (FVII:C) after 6 months: 0.18 vs. 0.06 U/mL,(95% CI, 0.02-0.22), whereas no differences were seen in levels of protein C, protein S, or prothrombin fragment 1+2. In the acute phase, the level of free protein S was lower than after 6 months in both groups: 25.6 vs. 28.8% (95% CI, 4.19--2.35). Cardiovascular mortality, reinfarction, and stroke were evaluated after 4 years (median). In a survival analysis, every 0.1 U/mL increase in the level of FVII:C1 month after myocardial infarction was associated with an 15% increase in risk of cardiovascular events (95% C1, 1.01-1.30). Warfarin at 1.25 mg daily reduces FVII:C but not systemic thrombin generation measured as prothrombin fragment 1 +2. Low levels of the anticoagulant protein S may contribute to a procoagulant state.

Adult↗
PubMed1999

Left atrioventricular plane displacement at rest is reduced in relation to severity of coronary artery disease irrespective of prior myocardial infarction.

OBJECTIVE: To examine whether left atrioventricular plane displacement (AVPD) at rest was related to severity of coronary atherosclerosis. DESIGN AND PATIENTS: Global and regional left AVPD was evaluated by echocardiography in 159 consecutive patients with significant stenoses at coronary angiography and in 15 age-matched healthy controls. The setting was the University hospital with a primary catchment area of 250,000 inhabitants. RESULTS: Mean AVPD in controls, patients with one-, two-, and three-vessel disease was 13.5+/-1.1, 12.4+/-1.5, 11.3+/-2.2 and 10.9+/-2.1 mm, respectively (P<0.0001). Similar significant differences were found both in those with (n=69) and without (n=90) a diagnosis of prior myocardial infarction. Regional AVPD did not correspond to the localization of infarction or coronary atherosclerosis. CONCLUSION: Irrespective of a diagnosis of prior myocardial infarction, left AVPD was related to the degree and extent of coronary artery disease. It was significantly decreased compared to controls in patients with one-vessel disease, and was further decreased with increasing extent of coronary atherosclerosis. Determination of regional left AVPD could not be used to identify regions perfused by stenotic coronary arteries or regions affected by prior myocardial infarction.

Aged↗
PubMed1999

Left atrioventricular plane displacement is related to both systolic and diastolic left ventricular performance in patients with chronic heart failure.

AIMS: Left atrioventricular plane displacement is proposed to reflect left ventricular systolic function and is strongly related to prognosis in patients with heart failure. Left atrioventricular plane displacement is a different measure of left ventricular function compared to ejection fraction, and the factors influencing left atrioventricular plane displacement are insufficiently characterized. We wanted to assess any relationship between left atrioventricular plane displacement and left ventricular diastolic performance. METHODS AND RESULTS: Left ventricular diastolic filling, left atrioventricular plane displacement, and fractional shortening were assessed by echocardiography/Doppler in 54 patients with chronic heart failure (age 64 +/- 7 years). Left atrioventricular plane displacement correlated significantly with Doppler variables of left ventricular filling, in particular the inverse logarithm of early transmitral flow deceleration time; log-1 Edt (r = -0.61, P < 0.0001, n = 54). Left atrioventricular plane displacement also correlated with fractional shortening (r = 0.49, P < 0.001, n = 50). However, fractional shortening did not correlate with any Doppler variable. Log-1 Edt, fractional shortening, age, heart rate, left ventricular and atrial size, and degree of mitral regurgitation were included in a multiple regression analysis. Only log-1 Edt (P = 0.001) and fractional shortening (P = 0.03) correlated independently with left atrioventricular plane displacement. Among patients with similar fractional shortening, those with more compromised diastolic performance had lower left atrioventricular plane displacement. CONCLUSION: Left atrioventricular plane displacement was related to both systolic and diastolic left ventricular performance, which may explain some of the discrepancies between left atrioventricular plane displacement and ejection fraction.

Aged↗
PubMed1999

ACE inhibition with ramipril improves left ventricular function at rest and post exercise in patients with stable ischaemic heart disease and preserved left ventricular systolic function.

AIMS: To assess the effects of 6 months intervention with +ramipril on resting and post exercise left ventricular function in patients with stable ischaemic heart disease and preserved left ventricular systolic function. METHODS AND RESULTS: Patients (n=98, age 65+/-9 years, 37% women) were randomized to double-blind treatment with ramipril 5 mg. day(-1)(n=32), ramipril 1.25 mg. day(-1)(n=34), or placebo (n=32). Resting and post maximum exercise echocardiography/Doppler examinations were performed at baseline and after 6 months. Changes over 6 months in resting transmitral E-wave deceleration time (Edt) and Edt adjusted for heart rate (Edt/RR) differed between the ramipril 5 mg, ramipril 1.25 mg, and placebo groups: Edt 24+/-82, -1+/-69, and -29+/-64 ms, respectively, P=0. 012; Edt/RR 30+/-105, 2+/-61, and -28+/-69 ms, respectively, P=0.015. Changes in the difference between resting and post exercise Edt/RR also varied between groups: -53+/-137, -28+/-118, and 35+/-101 ms, respectively, P=0.029. No differences in E/A indices were noted. Resting atrioventricular plane displacement improved in the combined ramipril groups vs the placebo group: 0.2+/-0.8 vs -0.2+/-1.3 mm, P<0.05.Conclusion Six months ramipril treatment in patients with stable ischaemic heart disease and preserved left ventricular systolic function improved resting left ventricular function and reduced the exercise induced diastolic filling abnormalities usually seen in these patients.

Aged↗