Sverre E Kjeldsen

Oslo University Hospital, Kristiania (historical), Oslo, Norway

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Publications (702)3403.62 Total impact

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    ABSTRACT: Aims: Recent hypertension guidelines recommend that also in high cardiovascular (CV) risk, hypertensive patients blood pressure (BP) is lowered to <140/90 mmHg as no evidence is available supporting the lower target of <130/80 mmHg recommended in previous guidelines. Whether this represents the optimal treatment strategy is debated, however. Methods and results: The high CV risk hypertensive patients of the Valsartan Antihypertensive Long-term use Evaluation (VALUE) trial were divided into subgroups according to (i) the percentage of on-treatment visits in which BP was reduced to <140/90 or <130/80 mmHg or (ii) the mean systolic or diastolic BP (SBP/DBP) values achieved during the entire treatment period or up to the occurrence of an event. A progressive increase from <25 to ≥75% of the visits in which BP was <140/90 mmHg was accompanied by a significant, progressive marked decrease in the covariate adjusted risk of CV morbidity and mortality, cause specific CV events (myocardial infarction, heart failure, and stroke), and all-cause mortality. Except for a persistent progressive decrease in stroke, no significant trend to a risk decrease occurred for a similar progressive increment of the proportion of visits with BP <130/80 mmHg. Increasing the proportion of visits with a BP <140/90 mmHg (but not <130/80 mmHg) was accompanied by a decreased risk of events also when differences in baseline risk were adjusted using a propensity score. Finally, compared with patients remaining at a mean on-treatment SBP ≥140 or DBP ≥90 mmHg, the risk of all events was markedly reduced when on-treatment mean SBP was lowered to a mean SBP of 130-139 mmHg or a mean DBP of 80-89 mmHg, whereas at on-treatment mean SBP <130 mmHg or DBP <80 mmHg, an additional risk reduction was found for stroke but for any other type of event, the risk of which remained similar or only slightly greater than that seen at the higher BP target. Conclusions: In the high CV risk, hypertensives of the VALUE trial reducing BP consistently to <140/90 mmHg had marked beneficial effects both when data were calculated as proportion of visits at BP target or as on-treatment mean BP. Reducing BP to <130/80 mmHg led only to some possible further benefit on stroke, whereas the risk of other outcomes remained substantially similar to or slightly greater than that seen at the higher target. Thus, aggressive BP reductions when CV risk is high may not offer substantial advantages, except perhaps in patients or conditions in which stroke risk is particularly common.
    European Heart Journal 11/2015; DOI:10.1093/eurheartj/ehv633 · 15.20 Impact Factor
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    ABSTRACT: Previous studies have debated the notion that low blood pressure (BP) during treatment, particularly diastolic (DBP), is associated with increased risk of cardiovascular disease. We evaluated the impact of low BP on cardiovascular outcomes in a high-risk population of 15,244 hypertensive patients, almost half of whom had a history of coronary artery disease (CAD). In the prospective Valsartan Antihypertensive Long-term Use Evaluation (VALUE) trial, patients were randomized to valsartan or amlodipine regimens and followed for 4.2 years (mean) with no difference in the primary cardiovascular endpoint. A Cox proportional hazards model was used to evaluate the relationship between average on-treatment BP and clinical outcomes. The relationship between BP and cardiovascular events was adjusted for age, gender and body mass index, and baseline qualifying risk factors and diseases (smoking, high total cholesterol, diabetes mellitus, proteinuria, CAD, previous stroke and left ventricular hypertrophy). DBP ≥ 90 mmHg, compared with < 90 mmHg, was associated with increased incidence of the primary cardiovascular endpoint (all cardiac events); however, DBP < 70 mmHg, compared with ≥ 70 mmHg, was not associated with increased incidence after covariate adjustment (no J-shaped curve). Similar results were observed for death, myocardial infarction (MI), heart failure and stroke, considered separately. Nadir for MI was at DBP of 76 mmHg and for stroke 60 mmHg. The ratio of MI to stroke increased with lower DBP. In CAD patients the MI to stroke ratio was more pronounced than in patients without CAD but there was no significant J-curve in either group. Systolic BP ≥ 150 but not < 130 mmHg, compared with 130-149 mmHg, similarly was associated with increased risk for primary outcome. In conclusion, patients in BP strata ≥ 150/90 mmHg, but not patients in BP strata < 130/70 mmHg, were at increased risk for adverse outcomes in this hypertensive, high-risk population. Although benefit in preventing MI in relation to preventing stroke levels off for the lowest BPs, these data provide no support for a J-curve in the treatment of high-risk hypertensive patients . The increase in the ratio of MI to stroke with lower DBP indicates target organ heterogeneity in that the optimal on-treatment DBP for cerebroprotection is below that for cardioprotection.
    Blood pressure 10/2015; DOI:10.3109/08037051.2015.1106750 · 1.81 Impact Factor
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    ABSTRACT: Background: In the BEtter control of BP in hypertensive pAtients monitored Using the HOTMAN sYstem study, we investigated whether utilizing noninvasive monitoring of hemodynamic parameters combined with a drug selection algorithm (integrated hemodynamic management - IHM) compared with conventional drug selection may improve uncontrolled hypertension in European Hypertension Excellence centers. Method: Uncontrolled (office SBP >140 mmHg and ambulatory daytime SBP >135 mmHg while taking ≥2 antihypertensive drugs) essential hypertensive patients were referred to five European Hypertension Excellence centers and, if eligible, were randomized to IHM-guided (n = 83) vs. conventional (control, n = 84) treatment adjustment in an investigator-initiated multicenter prospective randomized parallel groups controlled study. Results: The average number of antihypertensive drugs increased from 3.1 to 4.1 in both groups and differed only in a rise of the use of diuretics in the IHM groups (from 13 to 31%). Daytime SBP, defined as the primary endpoint, decreased markedly and to the same extent from baseline to 6 months in IHM (-15.8 ± 14.8 mmHg) and control (-15.4 ± 14.5 mmHg) groups (P = 0.87), with a similar behavior of office SBP (no between group differences, P = 0.18). Average number of adverse events was significantly lower in IHM than in controls (P = 0.008) but of the more general type and not necessarily related to drug treatment. Conclusion: Thus, noninvasive hemodynamic monitoring associated with a drug selection algorithm induced similar reductions in ambulatory daytime and office SBP compared with conventional drug selection in uncontrolled hypertensive patients referred to European Hypertension Excellence centers.Clinical Trial Registration - URL: Unique identifier: NCT01482364.
    Journal of Hypertension 10/2015; DOI:10.1097/HJH.0000000000000749 · 4.72 Impact Factor
  • Sverre E Kjeldsen · Suzanne Oparil · Krzysztof Narkiewicz · Thomas Hedner ·

    Blood pressure 10/2015; 25(1):1-3. DOI:10.3109/08037051.2016.1096564 · 1.81 Impact Factor
  • Sverre E. Kjeldsen · Eivind Berge ·

    Journal of Hypertension 10/2015; 33(10):2020-2021. DOI:10.1097/HJH.0000000000000689 · 4.72 Impact Factor
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    ABSTRACT: Background: Assessment of antihypertensive treatment is normally based on the mean value of a number of blood pressure (BP) measurements. However, it is uncertain whether high in-treatment visit-to-visit BP variability may be harmful in hypertensive patients with left ventricular hypertrophy (LVH). Methods: In 8505 patients randomized to losartan vs. atenolol-based treatment in the LIFE study, we tested whether BP variability assessed as SD and range for BP6-24months measured at 6, 12, 18 and 24 months of treatment was associated with target organ damage (TOD) defined by LVH on ECG and urine albumin/creatinine ratio at 24 months, and predicted the composite endpoint (CEP) of cardiovascular death, nonfatal myocardial infarction (MI) or stroke occurring after 24 months (CEP = 630 events). Results: In multiple regression models adjusted for mean BP6-24months and treatment allocation, neither high BP6-24months SD nor wide range were related to TOD at 24 months, except for a weak association between Sokolow-Lyon voltage and DBP6-24months SD and range (both β = 0.04, P < 0.01). Independently of mean BP6-24months, treatment allocation, TOD and baseline characteristics in Cox regression models, CEP after 24 months was associated with DBP6-24months SD [hazard ratio per 1 mmHg increase1.04, 95% confidence interval (95% CI) 1.01-1.06, P = 0.005], range (hazard ratio 1.02, 95% CI 1.01-1.03, P = 0.004), SBP6-24months SD (hazard ratio 1.01, 95% CI 0.99-1.02, P = 0.07) and range (hazard ratio 1.006, 95% CI 1.001-1.01, P = 0.04). Adjusted for the same factors, stroke was associated with DBP6-24months SD (hazard ratio 1.06, 95% CI 1.02-1.10, P = 0.001), range (hazard ratio 1.03, 95% CI 1.01-1.04, P = 0.001), SBP6-24months SD (hazard ratio 1.02, 95% CI 1.002-1.04, P = 0.04) and range (hazard ratio 1.008, 95% CI 1.001-1.02, P = 0.05), but MI was not. Conclusion: In LIFE patients, higher in-treatment BP6-24months variability was independently of mean BP6-24months associated with later CEP and stroke, but not with MI or TOD after 24 months.
    Journal of Hypertension 09/2015; DOI:10.1097/HJH.0000000000000739 · 4.72 Impact Factor
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    ABSTRACT: The blood pressure (BP)-lowering effect of renal sympathetic nervous denervation (RDN) in resistant hypertension (rHT) shows large variation among studies. We meta-analyzed summary statistics of randomized clinical trials on RDN in rHT. For continuous outcomes, we assessed heterogeneity by Cochran's Q test and used random-effect models weighted for the inverse of the variance. We assessed safety by assessing the risk of major adverse events from stratified contingency tables. Of 5652 patients screened in seven trials, 985 (17.4%) qualified and were randomized to control (n = 397) or RDN with SYMPLICITY(™) catheters (n = 588). Follow-up was 6 months. In both control and RDN patients, antihypertensive treatment was continued or optimized. At enrolment, age averaged 58.1 years, systolic/diastolic office and 24 h BP 168.5/93.3 mmHg and 151.8/86.1 mmHg, respectively, and estimated glomerular filtration rate (eGFR) 79.3 ml/min/1.73 m². For BP outcomes, there was heterogeneity among trials. Pooled effects (control minus RDN) were -4.9/-3.5 mmHg (95% confidence interval, -20.9 to 11.1/-8.9 to 1.9) for office BP, -2.8/-1.5 mmHg (-6.5 to 0.8/-3.3 to 0.4) for 24 h BP and 0.81 ml/min/1.73 m² (-1.69 to 3.30) for eGFR. Removing one trial at a time produced confirmatory results. Adverse events occurred in 7.4% and 9.9% of control and RDN patients, respectively (p = 0.24). In selected rHT patients maintained on antihypertensive drugs, RDN with the SYMPLICITY systems does not significantly decrease BP but is safe. Future trials with next-generation catheters should aim at identifying responders in patients with evidence of sympathetic nervous overactivity.
    Blood pressure 07/2015; 24(5):1-12. DOI:10.3109/08037051.2015.1058595 · 1.81 Impact Factor
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    ABSTRACT: Low insulin sensitivity is closely related to both cardiovascular diseases and diabetes development. Still, correlates of insulin sensitivity have mainly been examined in cross-sectional studies. As far as we are aware, the longitudinal stability of insulin sensitivity in young men is largely unknown. We aimed for the first time to examine both the stability (tracking) and longitudinal predictors of future insulin sensitivity in healthy young men with and without a family history of diabetes or hypertension. We performed a 17-year follow-up study of a cohort of 100 healthy young men. Cardiovascular risk markers, including insulin sensitivity measured by the gold standard method - hyperinsulinaemic isoglycaemic glucose clamp - were examined both at baseline and at follow-up. Baseline insulin sensitivity showed no significant correlation with insulin sensitivity at follow-up, whereas all other measured cardiovascular risk markers had significant correlation (tracking coefficients 0.4-0.7). In multiple regression analyses, family history of hypertension and baseline triglycerides remained the negative predictors of future insulin sensitivity. This was driven by the strong correlations in men with family history of diabetes. Our data suggest that clamp-derived insulin sensitivity is not a stable feature in young men, and that family history of hypertension and baseline triglycerides were associated with future insulin sensitivity, especially in men with a family history of diabetes, and irrespective of blood pressure status 17 years earlier. These findings provide further insight into the development of insulin sensitivity and related diseases.
    Journal of Hypertension 06/2015; 33(9). DOI:10.1097/HJH.0000000000000632 · 4.72 Impact Factor
  • Peter M Okin · Sverre E Kjeldsen · Richard B Devereux ·
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    ABSTRACT: Hypertensive patients with electrocardiographic left ventricular hypertrophy are at increased risk of all-cause and cardiovascular death. Lowering blood pressure (BP) after stroke reduces the risk of recurrent stroke, but recent data suggest that lower systolic BP (SBP) measured 5 years after stroke is associated with increased mortality. Whether lower SBP is associated with increased short-term mortality after stroke in hypertensive patients is unclear. All-cause and cardiovascular mortality were examined in relation to average on-treatment SBP after stroke in 541 hypertensive patients with electrocardiographic left ventricular hypertrophy randomly assigned to losartan- or atenolol-based treatment who had new strokes during follow-up. Patients with on-treatment SBP<144 mm Hg (lowest tertile) and SBP>157 (highest tertile) were compared with patients with average SBP between 144 and 157. During 2.02±1.65 years mean follow-up after incident stroke, 170 patients (31.4%) died, 135 (25.0%) from cardiovascular causes. In multivariate Cox analyses, adjusting for significant univariate predictors of mortality, compared with average SBP between 144 and 157, an average SBP<144 was a significant predictor of all-cause (hazard ratio, 1.81; 95% confidence interval, 1.20-2.73) and cardiovascular mortality (hazard ratio, 1.60; 95% confidence interval, 1.02-2.54), whereas patients who had an average SBP>157 had no significant increased risk of death. Lower achieved SBP (<144 mm Hg) is associated with a significantly increased risk of cardiovascular and all-cause mortality after initial stroke in hypertensive patients during short-term follow-up. Further study is required to determine ideal SBP goals after stroke. URL: Unique identifier: NCT00338260. © 2015 American Heart Association, Inc.
    Stroke 06/2015; 46(8). DOI:10.1161/STROKEAHA.115.009592 · 5.72 Impact Factor
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    ABSTRACT: : There is a well-established association between hypertension and atrial fibrillation (AF); indeed, even upper normal systolic blood pressures (SBP) are long-term predictors of incident AF. These findings suggest that more aggressive BP control may reduce the risk of new AF. However, whether lower achieved SBP is associated with a lower incidence of AF remains unclear. The risk of new-onset AF was examined in relation to last in-treatment SBP before AF diagnosis or last in-study measurement in the absence of new AF in 8831 hypertensive patients with ECG left ventricular hypertrophy with no history of AF, in sinus rhythm on their baseline ECG, randomly assigned to losartan- or atenolol-based treatment. Patients with in-treatment SBP ≤130 mm Hg (lowest quintile at last measurement) and SBP between 131 and 141 mm Hg were compared with patients with in-treatment SBP ≥142 mm Hg (median SBP at last measurement). During follow-up of 4.6±1.1 years, new-onset AF was diagnosed in 701 patients (7.9%). In multivariate Cox analyses, compared with in-treatment SBP ≥142 mm Hg, in-treatment SBP ≤130 mm Hg entered as a time-varying covariate was associated with a 40% lower risk (95% confidence interval, 18%-55%) and in-treatment SBP of 131 to 141 mm Hg with a 24% lower risk (95% confidence interval, 7%-38%) of new AF. Thus, achieved SBP ≤130 mm Hg is associated with a lower risk of new-onset AF in hypertensive patients with ECG left ventricular hypertrophy. Further study is needed to determine whether targeting hypertensive patients without AF to lower SBP goals can reduce the burden of new AF in this high-risk population. URL: Unique identifier: NCT00338260. © 2015 American Heart Association, Inc.
    Hypertension 06/2015; 66(2). DOI:10.1161/HYPERTENSIONAHA.115.05728 · 6.48 Impact Factor
  • Article: PP.26.28
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    ABSTRACT: Objective: Treatment resistant hypertension is a challenge for the physician and represents a substantial cardiovascular risk for patients. While many patients are referred to specialists for resistant hypertension, the true resistant subjects are hard to find. We aimed to report the reasons for noneligibility in the Oslo Renal Denervation (RDN)Study following directly observed therapy (DOT) of antihypertensive drugs prior to ambulatory blood pressure monitoring (ABPM). Design and method: Patients with apparent resistant hypertension (n = 83), supposed to fulfill the inclusion/exclusion criteria, which were similar, but not identical with the SYMPLICITY HTN-2 criteria, were referred for renal denervation. All patients went through a throrough clinical and laboratory work-up including screening for renovascular hypertension, renal disease, primary hyperaldosteronism, Cushing's syndrome and pheochromocytoma. Nonadherence to antihypertensive drugs and white coat hypertension were controlled for by directly observed therapy followed by ABPM. Results: The proportion of patients being noneligible for renal denervation according to our inclusion/exclusion criteria was 69.9 %. The main reasons for noneligibility were normalization of blood pressure following witnessed intake of antihypertensive drugs (DOT) (43.0 %). Those with high office blood pressure in our clinic, but without prior ABPM from their referring physician, who had normal ABPM after DOT, were labeled white coat hypertensives. However, the possibility of nonadherence even among these subjects cannot be ruled out. Copyright
    Journal of Hypertension 06/2015; 33:e365. DOI:10.1097/01.hjh.0000468511.04394.f9 · 4.72 Impact Factor
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    ABSTRACT: A hypertensive response to exercise at moderate workload is associated with future risk of coronary heart disease (CHD) and mortality. Yet there is still no consensus regarding the cut-off value for an inappropriate increase in exercise systolic blood pressure. We have previously shown that exercise blood pressure at 100W workload (SBP100W) > 200 mmHg is associated with increased risk of CHD and mortality. We now aimed to investigate the possible association between SBP100W >/= 190mmHg and risk of CHD over up to 28 years follow-up. Of the 1999 apparently healthy, middle-aged men who underwent thorough medical examination and laboratory testing, including a symptom-limited bicycle ergometer test, during 1972-1975, 1392 men were still healthy at survey 2 seven years later and completed a workload of 100 W at both surveys. Systolic blood pressure was measured near completion of the 100W stage (SBP100W). By comparing subjects having SBP100W >/=190 mmHg at baseline, follow-up or both(n=365) with subjects having SBP100W < 190 mmHg at both surveys (n = 1027), we estimated the risk of CHD (angina pectoris, non-fatal myocardial infarction and death from coronary heart disease). The combined endpoint of CHD occurred in 452 of the 1392 men; 243 events among the 365 men with SBP100W >/= 190 mmHg. When adjusting for survey 1 smoking status, age, systolic blood pressure at rest, total cholesterol and family history of coronary heart disease, there was a 1.38-fold (CI 1.11-1.71, p < 0.005) increased risk of CHD. When further adjusting for physical fitness, SBP100W >/=190mmHg was associated with a 1.35-fold (1.08-1.65) increased risk of CHD. Our findings indicate that a systolic blood pressure of 190 mmHg or more at moderate workload is associated with future risk of CHD among apparently healthy middle-aged men.(Figure is included in full-text article.).
    Journal of Hypertension 06/2015; 33 Suppl 1 - ESH 2015 Abstract Book:e28. DOI:10.1097/01.hjh.0000467422.11441.b2 · 4.72 Impact Factor
  • Article: PP.20.40
    E. Prestgaard · I. Grundvold · S.E. Kjeldsen · J. Bodegard · E. Berge ·
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    ABSTRACT: Objective: The incidence and determinants of stroke in healthy, middle-aged people are not well known. We report results from long-term follow-up in the Oslo Ischaemia Study. Copyright
    Journal of Hypertension 06/2015; 33:e318. DOI:10.1097/01.hjh.0000468352.59133.a6 · 4.72 Impact Factor
  • Article: 3D.01
    M Mehlum · K Liestøl · S Julius · S E Kjeldsen · T.A. Hua · P M Rothwell · G Mancia · G Parati · M.A. Weber · E Berge ·
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    ABSTRACT: High blood pressure variability has been associated with an increased risk of cardiovascular events. We aimed to assess if increased visit-to-visit variability in systolic blood pressure increases the risk of stroke or cardiac events (fatal/non-fatal coronary or heart failure events) in the VALUE population. The VALUE trial was a randomised-controlled, double-masked investigation of valsartan versus amlodipine in patients 50 years or older with hypertension and high risk of cardiovascular events. Mean follow-up time was 4.2 years. We calculated the standard deviation (SD) of mean systolic blood pressure from visits from 6 months onward, excluding patients with less than 2 visits, or stroke or cardiac events during the first 6 months. In the pooled treatment arms, we grouped SD in quintiles and compared the risk of stroke or cardiac events in the highest and the lowest quintile, using a Cox regression model, adjusting for a number of prognostic variables, including randomised treatment and mean BP from 6 months onwards. Of 14.146 patients included, 1278 (9.0%) experienced a cardiac event and 473 (3.3%) experienced a stroke. Compared to patients with the lowest variability, those in the highest quintile had an increased risk of stroke or cardiac events (HR 1.4, 95% CI 1.0-1.8, p = 0.045 and HR 1.9, 95% CI 1.6-2.3, p < 0.0001, respectively, Figure). Visit-to-visit systolic BP variability predicts stroke and cardiac events in high risk hypertensive patients receiving valsartan or amlodipine, and independent of mean BP. Systolic blood pressure variability was a stronger predictor of cardiac events than of stroke.(Figure is included in full-text article.).
    Journal of Hypertension 06/2015; 33 Suppl 1 - ESH 2015 Abstract Book:e40. DOI:10.1097/01.hjh.0000467454.55397.ea · 4.72 Impact Factor
  • Article: 8B.01
    F Fadl Elmula · Y Jin · A.C. Larstorp · A Persu · S E Kjeldsen · J A Staessen ·
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    ABSTRACT: Renal sympathetic denervation (RDN) has been and is still proposed as a new treatment modality in patients with treatment resistant hypertension (TRH), a condition defined as persistent blood pressure (BP) elevation despite prescription of at least 3 antihypertensive drugs, including a diuretic. However, the randomized controlled evidence that RDN effectively lowers BP is scarce and contradictory. This study investigated the current effectiveness of RDN for TRH. We performed a systematic review and meta-analysis of the randomized controlled trials (RCT) that reported office and ambulatory systolic BP in RDN and control (sham control or drug adjustment) groups at 6 months of follow-up in patients with TRH. Pooled effect sizes were derived, using a random-effects model. The literature search identified five RCTs with 867 randomized patients. In the pooled analysis, RDN was not associated with a significant decrease, either in office systolic BP (weighted mean difference (WMD): - 4.21 mmHg, 95% confidence interval: -17.12 to 8.69, p = 0.52), or in 24-h ambulatory systolic BP (WMD: -1.94 mmHg, 95% confidence interval: -6.05 to 2.17 mmHg, p = 0.36) compared to control at 6-months of follow-up.(Figure is included in full-text article.) CONCLUSIONS:: In patients with TRH, the overall BP lowering effect of RDN is not superior to control. Accordingly, RDN should not be considered as a treatment modality of RHT in clinical practice. Future research should identify the characteristics of patients who might respond to RDN, effective ablation dose and measure that could confirm that RDN do occur.
    Journal of Hypertension 06/2015; 33 Suppl 1 - ESH 2015 Abstract Book:e107. DOI:10.1097/01.hjh.0000467637.16752.63 · 4.72 Impact Factor
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    European Heart Journal 05/2015; 36(33). DOI:10.1093/eurheartj/ehv192 · 15.20 Impact Factor
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    ABSTRACT: The Symplicity HTN-1 and 2 studies proposed renal denervation (RDN) as an effective and safe approach to treat patients with resistant hypertension, and were followed by an unprecedented wave of enthusiasm. The announcement that Symplicity HTN-3 failed to meet its primary efficacy endpoint put an abrupt stop to these overoptimistic expectations. The use of a sound methodology was enough to see the typical 25-30mmHg systolic blood pressure decrease observed after RDN melt down to <3mmHg. RDN certainly deserves further investigation but is not ready for wide clinical application. For the time being, physicians should focus on improvement of drug adherence and skilful drug treatment adjustment, which allow reaching blood pressure target in the large majority of hypertensive patients. Copyright © 2015. Published by Elsevier Ltd.
    Current Opinion in Pharmacology 04/2015; 21. DOI:10.1016/j.coph.2014.12.013 · 4.60 Impact Factor
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    ABSTRACT: Approximately 10-20% of the general population have masked hypertension. However, how best to identify affected individuals is uncertain, and what predicts future masked hypertension is largely unknown. This study aimed to identify longitudinal predictors of masked hypertension. A long-term follow-up study of 100 healthy young men who had normal (n = 28) or high (n = 72) screening blood pressure (BP) at the compulsory military draft was carried out. They were examined in a detailed and highly standardized way for cardiovascular risk markers at baseline and at follow-up after a mean of 17.4 years. At follow-up, 40% had masked hypertension. Participants with high screening BP had a 4.8 times higher likelihood of having masked hypertension at follow-up compared to men with low screening BP (odds ratio 4.8, 95% confidence interval 1.7-13.5, p = 0.003). Furthermore, only 25% of the men with masked hypertension had high normal office BP at follow-up, and the remaining 75% would, according to guidelines, not be recommended ambulatory BP measurements, and thus go undiagnosed. Our data suggest that high screening BP at a young age is an important predictor of future masked hypertension in young men, and that BP measurement according to guidelines is insufficient to uncover masked hypertension.
    Blood pressure 04/2015; 24(3):1-8. DOI:10.3109/21695717.2015.1030889 · 1.81 Impact Factor
  • Sverre E Kjeldsen · Fadl Elmula M Fadl Elmula · Alexandre Persu ·

    Journal of the American College of Cardiology 04/2015; 65(13):1322-3. DOI:10.1016/j.jacc.2015.01.038 · 16.50 Impact Factor
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    ABSTRACT: Digoxin is widely used for rate control of atrial fibrillation. However, recent studies have reported conflicting results on the association of digoxin with mortality when used in patients with atrial fibrillation. Moreover, the relationship of digoxin use to mortality in hypertensive patients with atrial fibrillation has not been examined. All-cause mortality was examined in relation to in-treatment digoxin use in 937 hypertensive patients with ECG left ventricular hypertrophy in atrial fibrillation at baseline (n = 134) or who developed atrial fibrillation during follow-up (n = 803), randomly assigned to losartan or atenolol-based treatment, in post-hoc analysis of a substudy of the Losartan Intervention For Endpoint Reduction in hypertension (LIFE) trial. During 4.7 ± 1.1 years of mean follow-up, 167 patients died (17.8%) and 372 (39.7%) were treated with digoxin. In univariate Cox analyses, in-treatment digoxin use, entered as a time-varying covariate, was associated with a 61% higher risk of dying (hazard ratio 1.61, 95% confidence interval 1.18-2.19, P = 0.003). After adjusting for other univariate predictors of death in this population, including age, diabetes, history of ischemic heart disease, stroke, or heart failure, baseline Cornell product, QRS duration, heart rate, serum glucose, creatinine and high-density lipoprotein cholesterol, and a propensity score for digoxin use entered as standard covariates, and for in-treatment heart rate, pulse pressure, and Sokolow-Lyon voltage treated as time-varying covariates, digoxin use was no longer a significant predictor of mortality (hazard ratio 1.04, 95% confidence interval 0.73-1.48, P = 0.839). In hypertensive patients with ECG left ventricular hypertrophy with existing or new atrial fibrillation, digoxin use is not associated with a significantly increased risk of all-cause mortality after adjusting for other independent predictors of death and for the factors associated with the propensity to use digoxin in this population. These findings suggest that factors other than digoxin use may account for the increased mortality found with digoxin use in some studies. .
    Journal of Hypertension 03/2015; 33(7). DOI:10.1097/HJH.0000000000000559 · 4.72 Impact Factor

Publication Stats

39k Citations
3,403.62 Total Impact Points


  • 1986-2015
    • Oslo University Hospital
      • Department of Cardiology
      Kristiania (historical), Oslo, Norway
    • Universitetet i Tromsø
      Tromsø, Troms, Norway
  • 1984-2015
    • University of Oslo
      • • Department of Cardiology
      • • Department of General Internal Medicine
      • • Department of Obstetrics and Gynaecology (OBSTGYN)
      • • Division of Medicine
      Kristiania (historical), Oslo, Norway
  • 2013
    • University of Leuven
      • Department of Cardiovascular Sciences
      Louvain, Flanders, Belgium
  • 1989-2012
    • University of Michigan
      • • Division of Cardiovascular Medicine
      • • Department of Internal Medicine
      Ann Arbor, Michigan, United States
  • 2006-2011
    • Weill Cornell Medical College
      • Division of Cardiology
      New York, New York, United States
    • Medical University of Gdansk
      • Department of Hypertension and Diabetes
      Danzig, Pomeranian Voivodeship, Poland
    • Malmö University
      Malmö, Skåne, Sweden
    • University of Glasgow
      Glasgow, Scotland, United Kingdom
  • 2010
    • University of Massachusetts Medical School
      • Department of Medicine
      Worcester, Massachusetts, United States
  • 2006-2009
    • Concordia University–Ann Arbor
      Ann Arbor, Michigan, United States
  • 2007
    • Imperial College London
      • International Centre for Circulatory Health
      London, ENG, United Kingdom
    • Semmelweis University
      Budapeŝto, Budapest, Hungary
  • 2005-2007
    • Umeå University
      • Department of Public Health and Clinical Medicine
      Umeå, Västerbotten, Sweden
    • Università degli Studi di Milano-Bicocca
      • Department of Statistics and Quantitative Methods
      Milano, Lombardy, Italy
    • University of Naples Federico II
      Napoli, Campania, Italy
    • Royal College of Surgeons in Ireland
      Dublin, Leinster, Ireland
  • 2001-2007
    • University of Milan
      Milano, Lombardy, Italy
    • Cornell University
      • Department of Medicine
      Ithaca, NY, United States
  • 2002-2006
    • University of Helsinki
      • Department of Oral Medicine
      Helsinki, Uusimaa, Finland
    • Steno Diabetes Center
      Gjentofte, Capital Region, Denmark
    • Copenhagen University Hospital
      København, Capital Region, Denmark
    • Frederiksberg Hospital
      Фредериксберг, Capital Region, Denmark
  • 2003
    • University of Alabama at Birmingham
      Birmingham, Alabama, United States
  • 2000-2003
    • Glostrup Hospital
      • Department of Clinical Physiology and Nuclear Medicine
      Glostrup, Capital Region, Denmark
  • 1997
    • Akershus universitetssykehus
      Kristiania (historical), Oslo, Norway
  • 1996
    • Norsk Treteknisk Institutt
      Kristiania (historical), Oslo County, Norway
  • 1988
    • Hospital Bærum
      Drammen, Buskerud, Norway