| 51. |
- Höijer, Carl Johan, et al.
(författare)
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Improved cardiac function and quality of life following upgrade to dual chamber pacing after long-term ventricular stimulation.
- 2002
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Ingår i: European Heart Journal. - : Oxford University Press (OUP). - 1522-9645 .- 0195-668X. ; 23:6, s. 490-497
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Tidskriftsartikel (refereegranskat)abstract
- Aims Many patients with sinus node disease or atrioventricular block have previously received pacemakers with only ventricular stimulation (VVI or VVIR). This study aimed to investigate whether quality of life and cardiac function were affected by an upgrade to dual chamber pacing (DDDR or DDIR) following long-term ventricular stimulation. Methods After implantation of an atrial lead and a DDDR pulse generator, a randomized, double-blind crossover study was performed in 19 patients, previously treated with ventricular pacing for a median time of 6center dot8 years. Patients were randomized to 8 weeks with either VVIR or DDDR/DDIR pacing; after this time, the other mode was programmed for 8 weeks. At the end of each period, the patients' quality of life was evaluated and echocardiography was performed together with Holter monitoring and blood samples for brain natriuretic peptide. Results Sixteen of the patients preferred DDDR and two VVIR pacing (P=0center dot001); one was undecided. Seven patients demanded an early crossover while paced in the VVIR mode, vs none in the DDDR mode (P=0center dot008). Quality of life was higher in the DDDR mode in 11 of 17 modalities, reaching statistical significance for dyspnoea (P<0center dot05) and general activity (P<0center dot05). Echocardiography showed significantly larger left ventricular end-diastolic dimensions in the DDDR mode (P=0center dot01), whereas end-systolic dimensions did not differ. Left ventricular systolic function was significantly superior in the DDDR mode (mean aortic velocity--time integral: P<0center dot001) and left atrial diameter was significantly smaller in the DDDR mode (P=0center dot01). The plasma level of brain natriuretic peptide was significantly lower in DDDR mode (P=0center dot002). Conclusion An upgrade to dual chamber rate adaptive pacing results in significantly improved quality of life and cardiac function as compared to continued VVIR stimulation and should thus be considered in patients with ventricular pacemakers who have not developed permanent atrial fibrillation or flutter.
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| 52. |
- Jander, Nikolaus, et al.
(författare)
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Indexing aortic valve area by body surface area increases the prevalence of severe aortic stenosis
- 2014
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Ingår i: Heart. - : BMJ. - 1355-6037 .- 1468-201X. ; 100:1, s. 28-33
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Tidskriftsartikel (refereegranskat)abstract
- Background To account for differences in body size in patients with aortic stenosis, aortic valve area (AVA) is divided by body surface area (BSA) to calculate indexed AVA (AVA(index)). Cut-off values for severe stenosis are <1.0cm(2) for AVA and <0.6cm(2)/m(2) for AVA(index). Objective To investigate the influence of indexation on the prevalence of severe aortic stenosis and on the predictive accuracy regarding clinical outcome. Methods Echocardiographic and anthropometric data from a retrospective cohort of 2843 patients with aortic stenosis (jet velocity >2.5m/s) and from 1525 patients prospectively followed in the simvastatin and ezetimibe in aortic stenosis (SEAS) trial were analysed. Results The prevalence of severe stenosis increased with the AVA(index) criterion compared to AVA from 71% to 80% in the retrospective cohort, and from 29% to 44% in SEAS (both p<0.001). Overall, the predictive accuracy for aortic valve events was virtually identical for AVA and AVA(index) in the SEAS population (mean follow-up of 46months; area under the receiver operating characteristic curve: 0.67 (95% CI 0.64 to 0.70) vs 0.68 (CI 0.65 to 0.71) (NS). However, 213 patients additionally categorised as severe by AVA(index) experienced significantly less valve related events than those fulfilling only the AVA criterion (p<0.001). Conclusions Indexing AVA by BSA (AVA(index)) significantly increases the prevalence of patients with criteria for severe stenosis by including patients with a milder degree of the disease without improving the predictive accuracy for aortic valve related events.
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| 53. |
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| 54. |
- Jander, Nikolaus, et al.
(författare)
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Outcome of Patients With Low-Gradient "Severe" Aortic Stenosis and Preserved Ejection Fraction
- 2011
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Ingår i: Circulation. - 1524-4539 .- 0009-7322. ; 123:8, s. 887-895
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Tidskriftsartikel (refereegranskat)abstract
- Background-Retrospective studies have suggested that patients with a low transvalvular gradient in the presence of an aortic valve area <1.0 cm(2) and normal ejection fraction may represent a subgroup with an advanced stage of aortic valve disease, reduced stroke volume, and poor prognosis requiring early surgery. We therefore evaluated the outcome of patients with low-gradient "severe" stenosis (defined as aortic valve area < 1.0 cm(2) and mean gradient <= 40 mm Hg) in the prospective Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) study. Methods and Results-Outcome in patients with low-gradient "severe" aortic stenosis was compared with outcome in patients with moderate stenosis (aortic valve area 1.0 to 1.5 cm(2); mean gradient 25 to 40 mm Hg). The primary end point of aortic valve events included death from cardiovascular causes, aortic valve replacement, and heart failure due to aortic stenosis. Secondary end points were major cardiovascular events and cardiovascular death. In 1525 asymptomatic patients (mean age, 67 +/- 10 years; ejection fraction, >= 55%), baseline echocardiography revealed low-gradient severe stenosis in 435 patients (29%) and moderate stenosis in 184 (12%). Left ventricular mass was lower in patients with low-gradient severe stenosis than in those with moderate stenosis (182 +/- 64 versus 212 +/- 68 g; P < 0.01). During 46 months of follow-up, aortic valve events occurred in 48.5% versus 44.6%, respectively (P=0.37; major cardiovascular events, 50.9% versus 48.5%, P=0.58; cardiovascular death, 7.8% versus 4.9%, P=0.19). Low-gradient severe stenosis patients with reduced stroke volume index (<= 35 mL/m(2); n=223) had aortic valve events comparable to those in patients with normal stroke volume index (46.2% versus 50.9%; P=0.53). Conclusions-Patients with low-gradient "severe" aortic stenosis and normal ejection fraction have an outcome similar to that in patients with moderate stenosis. (Circulation. 2011;123:887-895.)
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| 55. |
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| 56. |
- Kennedy, Linn, et al.
(författare)
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Impact of neurohormonal blockade on association between body mass index and mortality.
- 2007
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Ingår i: International Journal of Cardiology. - : Elsevier BV. - 0167-5273. ; 119, s. 33-40
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Tidskriftsartikel (refereegranskat)abstract
- The prognostic impact of body mass index ( BMI) in patients following acute myocardial infarction ( AMI) may be altered by neurohormonal blockade. Methods: The impact of neurohormonal blockade on the association between BMI and mortality was examined in 5548 patients following AMI ( CONSENSUS II), 50% receiving enalapril and 7% beta- blockade, and in 4367 patients with coronary artery disease ( CAD) ( 4S), 79% with prior AMI, 12% receiving ACEi and 67% beta- blockade. Median follow- up was 0.4 and 5.2 years, respectively. Patients were categorized into 4 BMI groups: Underweight, b22.00; normal- weight, 22.00 - 24.99; overweight, 25.00 - 29.99; obese, = 30.00 kg/ m(2). Multivariable analysis adjusted for demographics, patient history, physical examination, biochemistry and medication. Results: CONSENSUS II: Overall, adjusted mortality ( n= 301) risk was similar across BMI groups. Comparing overweight with normalweight patients, the hazard ratios ( HRs) for mortality differed significantly ( P= 0.028) between patients randomized to placebo ( HR 1.41) and enalapril ( HR 0.75). 4S: Overall, adjusted mortality ( n= 421) risk was similar for normal- weight, overweight and obese patients. In a time- dependent analysis for drug use, comparing obese with normal- weight patients, the HRs for mortality differed significantly ( P= 0.047) between patients without ( HR 1.86) and those with ( HR 0.97) neurohormonal blockade. Conclusion: In patients after AMI or with CAD, high BMI was associated with increased mortality risk among patients not receiving neurohormonal blockade, but with decreased or neutral mortality risk among those receiving neurohormonal blockade. Tests for interaction indicate that neurohormonal blockade may attenuate the relationship between high BMI and increased mortality risk. Neurohormonal blockade may thus partly explain the so- called obesity paradox. (C) 2006 Elsevier Ireland Ltd. All rights reserved.
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| 57. |
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| 58. |
- Kennedy, Linn, et al.
(författare)
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Weight-change as a prognostic marker in 12 550 patients following acute myocardial infarction or with stable coronary artery disease.
- 2006
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Ingår i: European Heart Journal. - : Oxford University Press (OUP). - 1522-9645 .- 0195-668X. ; 27, s. 2755-2762
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Tidskriftsartikel (refereegranskat)abstract
- Aims To examine the prognostic importance of weight-change in patients with coronary artery disease (CAD), especially following acute myocardial infarction (AMI). Methods and results In 4360 AMI patients (OPTIMAAL trial) without baseline oedema, we assessed 3-month weight-change, baseline body mass index (BMI), demographics, patient history, medication, physical examination, and biochemical analyses. Weight-change was defined as change >+/- 0.1 kg/baseline BMI-unit. Patients were accordingly categorized into three groups; weight-loss, weight-stability, and weight-gain. Our findings were validated in 4012 AMI patients (CONSENSUS II trial) and 4178 stable CAD patients (79% with prior AMI, 4S trial). Median follow-up was 2.7 years, 3 months, and 4.4 years, respectively. In OPTIMAAL, 3-month weight-loss (vs. weight-stability) independently predicted increased all-cause death [n=471; hazard ratio (HR) 1.26; 95% CI 1.01-1.56; P=0.039] and cardiac death (n=299, HR 1.33, 95% CI 1.02-1.73, P=0.034). Weight-gain yielded risk similar to weight-stability (HR 1.07, P=0.592 and 0.97, P=0.866, respectively). In CONSENSUS II, 3-month weight-loss independently predicted increased mortality (HR 3.87, P=0.008). Weight-gain yielded risk similar to weight-stability (HR 1.11, P=0.860). In 4S, 1-year weight-loss independently predicted increased mortality (HR 1.44, P=0.004). Weight-gain conferred risk similar to weight-stability (HR 1.05, P=0.735). Conclusion In patients following AMI or with stable CAD, weight-loss but not weight-gain was independently associated with increased mortality risk.
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| 59. |
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| 60. |
- Krum, Henry, et al.
(författare)
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Effect on Mode of Death of Heart Failure Treatment Started with Bisoprolol Followed by Enalapril, Compared to the Opposite Order: Results of the Randomized CIBIS III Trial
- 2011
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Ingår i: Cardiovascular Therapeutics. - : Wiley. - 1755-5914. ; 29:2, s. 89-98
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Tidskriftsartikel (refereegranskat)abstract
- P>Background: Mode of death in chronic heart failure (CHF) may be of relevance to choice of therapy for this condition. Sudden death is particularly common in patients with early and/or mild/moderate CHF. beta-Blockade may provide better protection against sudden death than ACE inhibition (ACEI) in this setting. Methods: We randomized 1010 patients with mild or moderate, stable CHF and left ventricular ejection fraction < 35%, without ACEI, beta-blocker or angiotensin-receptor-blocker therapy, to either bisoprolol (n = 505) or enalapril (n = 505) for 6 months, followed by their combination for 6-24 months. The two strategies were blindly compared regarding adjudicated mode of death, including sudden death and progressive pump failure death. Results: During the monotherapy phase, 8 of 23 deaths in the bisoprolol-first group were sudden, compared to 16 of 32 in the enalapril-first group: hazard ratio (HR) for sudden death 0.50; 95% confidence interval (CI) 0.21-1.16; P = 0.107. At 1 year, 16 of 42 versus 29 of 60 deaths were sudden: HR 0.54; 95% CI 0.29-1.00; P = 0.049. At study end, 29 of 65 versus 34 of 73 deaths were sudden: HR 0.84; 95% CI 0.51-1.38; P = 0.487. Comparable figures for pump failure death were: monotherapy, 7 of 23 deaths versus 2 of 32: HR 3.43; 95% CI 0.71-16.53; P = 0.124, at 1 year, 13 of 42 versus 5 of 60: HR 2.57; 95% CI 0.92-7.20; P = 0.073, at study end, 17 of 65 versus 7 of 73: HR 2.39; 95% CI 0.99-5.75; P = 0.053. There were no significant between-group differences in any other fatal events. Conclusion: Initiating therapy with bisoprolol compared to enalapril decreased the risk of sudden death during the first year in this mild systolic CHF cohort. This was somewhat offset by an increase in pump failure deaths in the bisoprolol-first cohort.
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