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- Johannsson, Gudmundur, 1960, et al.
(författare)
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Long-term cardiovascular effects of growth hormone treatment in GH-deficient adults. Preliminary data in a small group of patients.
- 1996
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Ingår i: Clinical endocrinology. - 0300-0664. ; 45:3, s. 305-14
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Tidskriftsartikel (refereegranskat)abstract
- The long-term cardiovascular effects of GH administration in adults are of major clinical importance, given the increasing use of such treatment. We have evaluated long-term cardiovascular effects of recombinant human GH (rhGH) substitution in GH deficient men.S.c. rhGH 0.5 U/kg/week or placebo was administered in a 6-month double-blind, cross-over study, followed (after a year without substitution) by a 42-month period of open GH substitution.We evaluated 7 GH-deficient men serially and compared the results with 21 men matched in terms of age and height.Investigations included exercise tests and Doppler-echocardiography to determine exercise capacity and cardiovascular performance.Heart rate and systolic blood pressure at rest increased with GH substitution to the level of the controls, as did diastolic blood pressure after an initial reduction. Age-adjusted exercise capacity increased during the study and we found no evidence of ischaemic heart disease on exercise ECG. Stroke volume increased with GH substitution, thereby normalizing the initially reduced cardiac index. There was no significant change in left atrial or ventricular internal dimensions, systolic function as measured by fractional shortening, or diastolic function as measured by isovolumic relaxation time and left ventricular filling (A/E ratio). However, a lower atrial emptying index than that seen among controls might indicate some diastolic disturbance and there was a definite increase in left ventricular wall thickness compared with controls (to 25.1 +/- 1.5 vs 19.7 +/- 0.4 mm, P < 0.001).We found that GH substitution in GH-deficient adults had a beneficial effect on physical performance and cardiac output. The concomitant increase in left ventricular mass index might be an effect of an excessive substitution dose.
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| 3. |
- Andersson, Bert, 1952, et al.
(författare)
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An echocardiographic evaluation of patients with idiopathic heart failure.
- 1995
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Ingår i: Chest. - 0012-3692. ; 107:3, s. 680-9
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Tidskriftsartikel (refereegranskat)abstract
- The primary myocardial disease idiopathic dilated cardiomyopathy (IDCM) is not clearly defined in the literature. The description is both morphologic and etiologic. We examined consecutive patients with congestive heart failure (CHF) of unknown cause to identify possible cases of IDCM and to give a detailed description of echocardiographic data and possible diastolic dysfunction in this group. The hospital records of patients aged 16 to 65 years hospitalized due to CHF or IDCM during a 6-year period (N = 2,711) were evaluated in a defined region of western Sweden. Twenty-two percent (584/2,711) of these records contained no plausible cause of CHF or IDCM, and among patients being alive, obvious cause was lacking in 411 of 1,516 (27%). These 411 patients were offered a diagnostic investigation, including echocardiography, and they were compared with a randomly selected control group (n = 103) from the general population. Of 411 patients, 293 accepted investigation. From the control group, we defined the reference level for left ventricular (LV) dilatation to be > 32 mm/m2, and reduced ejection fraction according to Teichholz formula to be < 50%. Applying these borderlines, we identified LV dilatation and systolic dysfunction to be present in 30%, either dilatation or systolic dysfunction in 36%, and neither in 34%. In patients without any signs of systolic dysfunction 44% (26/59) showed signs of diastolic dysfunction. In a multivariate analysis, LV dimension was not independently correlated to disease, although LV dimension was univariately correlated to ejection fraction (EF) (r = -0.59; p < 0.0001). However, EF (p < 0.0001), left atrial dimension (p < 0.0001), and the first third filling fraction (p < 0.0001) were the constellation of parameters that most accurately separated patients from controls. By using these three parameters, a positive and negative predictive accuracy of 98% and 61%, respectively, was achieved. Thus, in a consecutive group of patients with idiopathic CHF recruited from a nonselected group of hospitalized patients with CHF, all grades of ventricular function were found. In this group, 30% were identified as having IDCM. We give reference values for the diagnosis of idiopathic IDCM and a simple tool to identify patients with systolic and diastolic dysfunction.
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| 4. |
- Andersson, Bert, 1952, et al.
(författare)
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Angiotensin-II type 1 receptor gene polymorphism and long-term survival in patients with idiopathic congestive heart failure.
- 1999
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Ingår i: European journal of heart failure. - 1388-9842. ; 1:4, s. 363-9
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Tidskriftsartikel (refereegranskat)abstract
- It has been suggested that a genetic polymorphism in the angiotensin II type 1 receptor gene (ATRG) and the ACE gene DD genotype might have a synergistic influence on the risk of developing cardiovascular disease.To study the possible interaction between polymorphisms in the ACE gene and the ATRG, regarding survival and left ventricular function.Polymorphism of the two genes was studied in a population-based cohort of 194 patients with idiopathic heart failure, recruited from the western part of Sweden 1985-1988. The patients were investigated by echocardiography. The survival status was checked during the 7-year follow-up period.Although there was no statistically significant additive risk of the ATRG polymorphism, patients carrying the ACE gene DD genotype in combination with a C allele of the ATRG tended to have a poorer prognosis. DD +AA, OR 1.24 (95% CI 0.67-2.32, P = 0.49); DD +AC, OR 1.64 (95% CI 0.95-2.83, P = 0.08); DD + CC, OR 3.54 95% CI 0.78-16.1, P = 0.10); DD +AC/CC, OR 1.84 (95% CI 1.10-3.08, P = 0.02). Patients with the DD +AC/CC genotypes tended to have lower ejection fraction and increased left ventricular mass.There was a trend toward a worse prognosis in patients with the combination of a C-allele in the ATRG and the ACE gene DD genotype, suggesting an interaction of these two genetic polymorphisms on disease severity.
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| 6. |
- Andersson, Bert, 1952, et al.
(författare)
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Changes in early and late diastolic filling patterns induced by long-term adrenergic beta-blockade in patients with idiopathic dilated cardiomyopathy.
- 1996
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Ingår i: Circulation. - 0009-7322. ; 94:4, s. 673-82
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Tidskriftsartikel (refereegranskat)abstract
- beta-Blockers have been used in patients with idiopathic dilated cardiomyopathy to improve cardiac performance and theoretically would be beneficial to diastolic function. However, there are few reports on changes in diastolic function during chronic pharmacological treatment of congestive heart failure.The present study was a substudy in the international Metoprolol in Dilated Cardiomyopathy Trial. Transmitral Doppler echocardiography was used to evaluate diastolic function in 77 patients randomly assigned to placebo (n = 37) or metoprolol (n = 40). The patients were treated for 12 months. Changes in Doppler flow variables in the metoprolol group implied a less restrictive filling pattern, expressed as an increase in E-wave deceleration time (placebo, 185 +/- 126 to 181 +/- 64 ms; metoprolol, 152 +/- 63 to 216 +/- 78 ms; P = .01, placebo versus metoprolol). Maximal increase in deceleration time had occurred by 3 months, whereas systolic recovery was achieved gradually and maximal effect was seen by 12 months of treatment. Although deceleration time was correlated to heart rate at baseline, changes in deceleration time were not significantly correlated to changes in heart rate during treatment.During the first 3 months of treatment, maximal effects on diastolic variables were reached, whereas the most prominent effect on systolic function was seen late in the study. It is suggested that effects on diastolic filling account for subsequent later myocardial systolic recovery. The E-wave deceleration time, which in recent studies has been shown to be a powerful predictor of survival, was significantly improved in the metoprolol-treated patients.
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| 7. |
- Andersson, Bert, 1952, et al.
(författare)
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Exercise hemodynamics and myocardial metabolism during long-term beta-adrenergic blockade in severe heart failure.
- 1991
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Ingår i: Journal of the American College of Cardiology. - 0735-1097 .- 1558-3597. ; 18:4, s. 1059-66
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Tidskriftsartikel (refereegranskat)abstract
- Hemodynamics and myocardial metabolism at rest and during exercise were investigated in 21 patients with heart failure. The patients were evaluated before and after long-term treatment (14 +/- 7 months) with the beta-adrenergic blocking agent metoprolol. Clinical improvement with increased functional capacity occurred during treatment. Maximal work load increased by 25% (104 to 130 W; p less than 0.001). Hemodynamic data showed an increased cardiac index (3.8 to 4.6 liters/min per m2; p less than 0.02) during exercise. Pulmonary capillary wedge pressure decreased at rest (20 to 13 mm Hg; p less than 0.01) and during exercise (32 to 28 mm Hg; p = NS). Stroke volume index (30 to 39 g.m/m2; p less than 0.006) and stroke work index (28 to 46 g.m/m2; p less than 0.006) increased during exercise and long-term metoprolol treatment. The arterial norepinephrine concentration decreased at rest (3.72 to 2.19 nmol/liter; p less than 0.02) but not during exercise (13.2 to 11.1 nmol/liter; p = NS). The arterial-coronary sinus norepinephrine difference suggested a decrease in myocardial spillover during metoprolol treatment (-0.28 to -0.13 nmol/liter; p = NS at rest and -1.13 to -0.27 nmol/liter; p less than 0.05 during exercise). Coronary sinus blood flow was unchanged during treatment. Four patients produced myocardial lactate before the study, but none produced lactate after beta-blockade (p less than 0.05). There was no obvious improvement in a subgroup of patients with ischemic cardiomyopathy. In summary, there were signs of increased myocardial work load without higher metabolic costs after treatment with metoprolol.
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| 8. |
- Andersson, Bert, 1952, et al.
(författare)
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Heart rate dependency of cardiac performance in heart failure patients treated with metoprolol.
- 1999
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Ingår i: European heart journal. - 0195-668X. ; 20:8, s. 575-83
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Tidskriftsartikel (refereegranskat)abstract
- To investigate whether a low heart rate is necessary to maintain improvement in myocardial function after long-term treatment with a beta-blocker in patients with heart failure.Forty-eight patients with congestive heart failure were investigated: 30 patients with dilated cardiomyopathy participating in a placebo-controlled trial (15 on placebo, 15 on metoprolol), and 18 patients treated by metoprolol in an open protocol. Investigations of spontaneous heart rate and of matched paced heart rates were performed at baseline and after 3, 6 and 12 months of follow-up by radionuclide angiography. There were significant signs of improvement in systolic indices of the spontaneous heart rate in the metoprolol-treated group (peak ejection rate: 0.98 to 1.32 end-diastolic volume.s-1, P = 0.015) as compared to placebo (1.14 to 1.19 end-diastolic volume.s-1, not significant). Similar effects were observed during the matched paced heart rate (peak ejection rate: metoprolol 0.91 to 1.38 end-diastolic volume.s-1, P = 0.037; placebo 1.22 to 1.12 end-diastolic volume.s-1, not significant). No effects were observed in the early peak filling rate. Left ventricular volumes decreased during metoprolol treatment, both for the spontaneous heart rate and during matched pacing.These data imply that beta-blocker treatment improves the force-frequency relationship of myocardial performance. A lower heart rate is not necessary to maintain cardiac function on a short-term basis, once myocardial recovery has occurred.
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| 9. |
- Andersson, Bert, 1952, et al.
(författare)
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Idiopathic dilated cardiomyopathy among Swedish patients with congestive heart failure.
- 1995
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Ingår i: European heart journal. - 0195-668X. ; 16:1, s. 53-60
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Tidskriftsartikel (refereegranskat)abstract
- Idiopathic dilated cardiomyopathy (IDCM) is an exclusion diagnosis. Although it is a prognostically important entity and a common indication for cardiac transplantation, the incidence and age distribution of idiopathic IDCM in a well-defined population today is unknown. The present study intended to estimate the proportion of IDCM among congestive heart failure (CHF) patients, and to evaluate its prognostic implications. The records of all 16-65-year-old patients hospitalized for CHF or IDCM during a 6-year period (n = 2711) were evaluated in a defined region of Western Sweden (1.05 million inhabitants 16-65 years of age). Twenty-two percent (584/2711) of these records contained no plausible cause of CHF or IDCM, and among living patients an obvious aetiology was lacking in 27% (411/1516). These 411 patients were subsequently offered a diagnostic investigation including echocardiography, and were compared to a randomly selected healthy control group (n = 103). Of 411 patients, 293 accepted the investigation and 286 had acceptable echocardiographic recordings, indicating left ventricular dilatation and systolic dysfunction in 30%. From the hospital records, 170 patients were identified as new cases of IDCM during the 6-year period. Adding another 34 cases revealed by our diagnostic procedures yielded an age-gender standardized incidence rate of 29.2 cases per 10(6) persons/year. The incidence of IDCM increased considerably with age, although in younger patients its relative contribution to heart failure was greater. The incidence of IDCM was higher in the urban compared to the rural parts of the region 21 vs 32/10(6); P = 0.013). The estimated prevalence was 131/10(6).(ABSTRACT TRUNCATED AT 250 WORDS)
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| 10. |
- Andersson, Bert, 1952, et al.
(författare)
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Improved exercise hemodynamic status in dilated cardiomyopathy after beta-adrenergic blockade treatment.
- 1994
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Ingår i: Journal of the American College of Cardiology. - 0735-1097. ; 23:6, s. 1397-404
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Tidskriftsartikel (refereegranskat)abstract
- This study was performed to investigate exercise hemodynamic status in a double-blind, placebo-controlled trial and was a substudy in the Metoprolol in Dilated Cardiomyopathy Trial.Previous open studies have shown beneficial effects on exercise hemodynamic status after beta-adrenergic blocking agent therapy in patients with congestive heart failure.The study included 41 patients with idiopathic dilated cardiomyopathy with ejection fraction < 0.40 (metoprolol, 20 patients; placebo, 21 patients) whose hemodynamic status was investigated at rest and during supine submaximal exercise, at baseline and after 6 and 12 months of treatment. Myocardial metabolism was evaluated in a subset of 19 patients.Metoprolol-treated patients responded favorably, as expressed by improved exercise cardiac index ([mean +/- SD] placebo 4.8 +/- 1.6 to 4.7 +/- 1.8 liters/min per m2, metoprolol 4.3 +/- 1.1 to 5.4 +/- 1.9 liters/min per m2, p = 0.0001) and stroke work index (placebo 44 +/- 20 to 41 +/- 27 g.m/m2, metoprolol 35 +/- 16 to 58 +/- 28 g.m/m2, p < 0.0001). Exercise systolic arterial pressure increased (placebo 161 +/- 25 to 151 +/- 23 mm Hg, metoprolol 155 +/- 29 to 165 +/- 37 mm Hg, p = 0.0003) as well as exercise oxygen consumption index (placebo 463 +/- 194 to 474 +/- 232 ml/min per m2, metoprolol 406 +/- 272 to 507 +/- 298 ml/min per m2, p = 0.045). There was a significant increase in exercise duration in the metoprolol group (63 +/- 38 s) compared with the placebo group (-24 +/- 42 s) (p = 0.01). Net myocardial lactate extraction increased in the metoprolol group, suggesting less myocardial ischemia (placebo 17 +/- 22 to 9.5 +/- 6.4 mmol/min, metoprolol -32 +/- 100 to 42 +/- 45 mmol/min, p = 0.03). Peripheral levels of norepinephrine tended to decrease at rest and during exercise, whereas myocardial net spillover was unchanged.Metoprolol improved hemodynamic status in patients with dilated cardiomyopathy at rest and had a more pronounced effect during exercise. These positive effects were achieved along with improved or stable myocardial metabolic data.
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