European Heart Journal - recent issues

CardioPulse Articles

Wed, 01 Sep 2010 00:09:09 PDT

Atrial fibrillation and mortality: the impact of antithrombotic therapy

Lane, D. A., Lip, G. Y. H. — Wed, 01 Sep 2010 00:09:09 PDT

Enoxaparin and fibrinolysis: ExTRACTing prognosis from bleeding complications

Sinnaeve, P., Van de Werf, F. — Wed, 01 Sep 2010 00:09:09 PDT

Pulmonary arterial hypertension: from the kingdom of the near-dead to multiple clinical trial meta-analyses

Galie, N., Palazzini, M., Manes, A. — Wed, 01 Sep 2010 00:09:09 PDT

C-reactive protein is a mediator of cardiovascular disease

Wed, 01 Sep 2010 00:09:09 PDT

C-reactive protein is postulated to embody an index that can reflect cardiovascular risk and can be used to independently predict major cardiovascular events and mortality. On the other hand, credible experimental data have become available that demonstrate the abundant presence of C-reactive protein in atherosclerotic lesions and, moreover, identify C-reactive protein as an initiator of several pathogenic pathways that can cause atherogenic changes. Consequently, there has been a paradigm shift in which C-reactive protein is no longer regarded as merely an indicator of cardiovascular risk, but increasingly considered a direct partaker in the pathogenesis of atherosclerotic cardiovascular disease. These data underscore the need to explore risk-reducing interventions that selectively inhibit C-reactive protein activity as a novel strategy to prevent clinical manifestations of atherosclerosis.

C-reactive protein is a bystander of cardiovascular disease

Anand, S. S., Yusuf, S. — Wed, 01 Sep 2010 00:09:09 PDT

A large number of studies have evaluated the association of hs-C-reactive protein with atherosclerosis and coronary heart disease (CHD) in mechanistic, genetic, population-based studies, as well as clinical trials. This paper reviews the collective evidence to determine if hs-C-reactive protein is part of the causal pathway of atherosclerosis and CHD or whether it is a bystander.

A moving heart

Moonen, M. L., Davin, L., Lancellotti, P., Pierard, L. A. — Wed, 01 Sep 2010 00:09:09 PDT

One-year outcomes after a strategy using enoxaparin vs. unfractionated heparin in patients undergoing fibrinolysis for ST-segment elevation myocardial infarction: 1-year results of the ExTRACT-TIMI 25 Trial

Wed, 01 Sep 2010 00:09:09 PDT

\nAims\n

To determine the impact of a strategy using enoxaparin for up to 8 days compared with unfractionated heparin (UFH) for 48 h as an adjunct to fibrinolysis for ST-segment elevation myocardial infarction (STEMI) on 1-year clinical outcomes.

\n\nMethods and results\n

Follow-up at 1 year (n = 20 275) was conducted by telephone in the ExTRACT-TIMI 25 trial to ascertain the endpoints of death, MI, and disabling stroke. The primary endpoint of death or non-fatal MI occurred in 1614 (15.8%) and 1732 (17.0%) of patients allocated to enoxaparin and UFH, respectively [hazard ratio (HR) 0.92, 95% confidence interval (CI) 0.86–0.98, P = 0.01]. The enoxaparin strategy significantly reduced non-fatal MI at 1 year (5.7 vs. 6.8%, HR 0.82, 95% CI 0.73–0.92, P < 0.001). The risks of death (10.5 vs. 10.6%, HR 0.98, 95% CI 0.91–1.07) and disabling stroke (1.1 vs. 1.2%, HR 0.97, 95% CI 0.75–1.26) were not reduced. The composite of death, MI, or disabling stroke favoured enoxaparin (HR 0.91, 95% CI 0.85–0.98, P = 0.007).

\n\nConclusion\n

Compared with UFH for 48 h, a strategy using enoxaparin as an adjunct to fibrinolysis resulted in a sustained reduction in death or MI at 1 year with no additional benefit after 30 days. Mortality was not reduced at 1 year with the enoxaparin strategy.

The study was registered at ClinicalTrials.gov, NCT00077792.

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Relations between bleeding and outcomes in patients with ST-elevation myocardial infarction in the ExTRACT-TIMI 25 trial

Wed, 01 Sep 2010 00:09:10 PDT

\nAims\n

To evaluate the association of bleeding with mortality in ST-elevation myocardial infarction (STEMI).

\n\nMethods and results\n

We studied 20 323 patients with STEMI receiving fibrinolytic therapy and an antithrombin in ExTRACT-TIMI 25. Relationships between in-hospital bleeding, patient characteristics, treatments, and in-hospital cardiovascular complications with mortality were evaluated using Cox models. Likelihood ratios estimated each variable's model contribution. High 30-day mortality after major bleeding (n = 309, 37.6% mortality) was driven by the poor prognosis of intracranial haemorrhage (ICH; n = 143, 65.4% mortality, model contribution 7.8%). The adjusted hazard ratios (HRs) for 30-day death for any major bleeding and for ICH were 2.9 [2.4–3.6] and 10.3 [8.2–12.8], respectively. Neither non-ICH major nor minor bleeding was associated with 30-day death after adjustment. Cardiogenic shock (HR 13.5, 61% contribution) and age (HR 1.6/decade, 17% contribution) were most strongly correlated with 30-day death. Among 30-day survivors, age (HR 1.6/decade, contribution 43%) and heart rate (HR 1.2 per 10 b.p.m., contribution 18%) were most strongly associated with mortality between Days 31 and 365.

\n\nConclusion\n

Cardiogenic shock, age, and ICH were important independent correlates of 30-day and 1-year mortality in STEMI patients receiving fibrinolytic therapy. In-hospital non-ICH major and minor bleeding were not independently associated with increased mortality at 30 days or 1 year.

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Clinicopathological profiles of progressive heart failure in hypertrophic cardiomyopathy

Wed, 01 Sep 2010 00:09:10 PDT

\nAims\n

Hypertrophic cardiomyopathy (HCM) is an important cause of heart failure-related disability over a wide range of ages. Profiles of severe progressive heart failure symptoms and death, or heart transplantation deserve more complete definition within large patient cohorts.

\n\nMethods and results\n

Clinical and morphological features of heart failure were assessed in 293 consecutive HCM patients over a median follow-up of 6 (inter-quartile range 2–11) years. Gross and histopathological features were analysed in 12 patients for whom the heart was available for inspection. Of the 293 patients, 50 (17%) developed severe progressive heart failure, including 18 who died or were transplanted. Three profiles of heart failure were identified predominantly associated with: (i) end-stage systolic dysfunction (ejection fraction <50%) (15; 30%); (ii) left ventricular (LV) outflow obstruction at rest (11; 22%); and (iii) non-obstructive with preserved systolic function (24; 48%). Overall, atrial fibrillation (AF) contributed to heart failure in 32 patients (64%) among the three profiles. Compared with other patients, those non-obstructive with preserved systolic function had earlier onset of heart failure symptoms mainly due to diastolic dysfunction, and the most accelerated progression to advanced heart failure and adverse outcome (P = 0.04). Thrombi were identified in the left atrial appendage of five gross heart specimens all belonging to patients with AF, including three of which were unrecognized clinically and had previously embolized. Extensive myocardial scarring with LV remodelling was evident in all end-stage patients; no or only focal scars were present in other patients.

\n\nConclusion\n

Profiles of advanced heart failure in HCM are due to diverse pathophysiological mechanisms, including LV outflow obstruction and diastolic or global systolic ventricular dysfunction. Atrial fibrillation proved to be the most common disease variable associated with progressive heart failure. Recognition of the heterogeneous pathophysiology of heart failure in HCM is relevant, given the targeted management strategies necessary in this disease.

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Predictors of pregnancy complications in women with congenital heart disease

Wed, 01 Sep 2010 00:09:10 PDT

\nAims\n

Data regarding pregnancy outcome in women with congenital heart disease (CHD) are limited.

\n\nMethods and results\n

In 1802 women with CHD, 1302 completed pregnancies were observed. Independent predictors of cardiac, obstetric, and neonatal complications were calculated using logistic regression. The most prevalent cardiac complications during pregnancy were arrhythmias (4.7%) and heart failure (1.6%). Factors independently associated with maternal cardiac complications were the presence of cyanotic heart disease (corrected/uncorrected) (P < 0.0001), the use of cardiac medication before pregnancy (P < 0.0001), and left heart obstruction (P < 0.0001). New characteristics were mechanical valve replacement (P = 0.0014), and systemic (P = 0.04) or pulmonary atrioventricular valve regurgitation related with the underlying (moderately) complex CHD (P = 0.03). A new risk score for cardiac complications is proposed. The most prevalent obstetric complications were hypertensive complications (12.2%). No correlation of maternal characteristics with adverse obstetric outcome was found. The most prevalent neonatal complications were premature birth (12%), small for gestational age (14%), and mortality (4%). Cyanotic heart disease (corrected/uncorrected) (P = 0.0003), mechanical valve replacement (P = 0.03), maternal smoking (P = 0.007), multiple gestation (P = 0.0014), and the use of cardiac medication (P = 0.0009) correlated with adverse neonatal outcome.

\n\nConclusion\n

In our tertiary CHD cohort, cardiac, obstetric, and neonatal complications were frequently encountered, and (new) correlations of maternal baseline data with adverse outcome are reported. A new risk score for adverse cardiac complications is proposed, although prospective validation remains necessary.

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Mortality predictors and effects of antithrombotic therapies in atrial fibrillation: insights from ACTIVE-W

Wed, 01 Sep 2010 00:09:10 PDT

\nAims\n

To assess the risk of death after the occurrence of different types of non-fatal events in patients with atrial fibrillation (AF). Antithrombotic therapies in AF have primarily focused on stroke prevention and bleeding. However, strokes and bleeds differ in severity, and the level of severity may differently impact mortality.

\n\nMethods and results\n

We analysed the risk of subsequent mortality after the occurrence of non-fatal vascular and bleeding events in the Atrial Fibrillation Clopidogrel Trial with Irbesartan for Prevention of Vascular Events (ACTIVE)-W trial. In the 3371 patients randomized to vitamin K antagonists and the 3335 patients randomized to clopidogrel plus aspirin in ACTIVE-W, the hazard ratio (HR) and 95% confidence intervals (95% CIs) for subsequent death associated with the occurrence of non-fatal stroke was 5.58 (95% CI 3.84–8.10, P < 0.0001). Both ischaemic (HR 5.29, 95% CI 3.53–7.93, P < 0.0001) and haemorrhagic strokes (HR 7.38, 95% CI 2.74–19.9, P < 0.0001) increased mortality, but transient ischaemic attacks did not. Disabling strokes (Rankin's score ≥3) increased mortality (HR 9.54; 95% CI 6.42–14.2, P< 0.0001), but non-disabling strokes did not. Severe bleeding increased mortality (HR 3.35, 95% CI 2.12–5.27, P < 0.0001), but major bleeding that was not severe according to the study definitions did not.

\n\nConclusion\n

Non-fatal strokes increased mortality in ACTIVE-W, but non-disabling strokes did not. Among major bleeding events, only those also classified as severe increased mortality. Future research should emphasize the prevention of disabling strokes and severe bleeds and place less emphasis on non-disabling stroke or major bleeds that are not severe.

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Cleft bicuspid aortic valve: the Achilles' heel of echocardiography?

Piccoli, G., Slavich, G., Gianfagna, P., Gasparini, D. — Wed, 01 Sep 2010 00:09:10 PDT

Simplifying cardiovascular risk estimation using resting heart rate

Wed, 01 Sep 2010 00:09:11 PDT

\nAims\n

Elevated resting heart rate (RHR) is a known, independent cardiovascular (CV) risk factor, but is not included in risk estimation systems, including Systematic COronary Risk Evaluation (SCORE). We aimed to derive risk estimation systems including RHR as an extra variable and assess the value of this addition.

\n\nMethods and results\n

The National FINRISK study (including 14 997 men and 15 861 women) was used to derive two formulas for estimation of 10 year risk of CV disease (CVD) mortality. The first formula contained current SCORE variables—total cholesterol, systolic blood pressure, smoking, age and gender. Inclusion of RHR resulted in only minor improvements in discrimination, based on both area under receiver operating characteristic curve (AUROC, men: 0.840 from 0.838, P = 0.5038; women: 0.87 from 0.865, P = 0.0522) and net reclassification index (NRI). The second, simplified formula contained only, age, smoking, gender, and body mass index. Addition of RHR to this simplified formula resulted in a statistically significant and meaningful improvement in AUROC (men: 0.819 from 0.812, P = 0.037; women: 0.862 from 0.827, P = 0.023) and NRI (0.05). Calibration also improved. A simple chart for estimating 10 year risk of fatal CVD including RHR is presented.

\n\nConclusion\n

Addition of RHR to formulas already containing lipid and blood pressure measures does not appreciably improve risk estimation. However, inclusion of RHR in simple systems, which can potentially enhance cost-effectiveness and accessibility of risk estimation, is useful.

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Cardiac pheochromocytoma

Cheng, Z., Zhang, S., Fang, Q. — Wed, 01 Sep 2010 00:09:11 PDT

Instantaneous coronary collateral function during supine bicycle exercise

Wed, 01 Sep 2010 00:09:11 PDT

\nAims\n

The instantaneous response of the collateral circulation to isometric physical exercise in patients with non-occlusive coronary artery disease (CAD) is not known.

\n\nMethods and results\n

Thirty patients (age 59 ± 9 years) undergoing percutaneous coronary intervention because of stable CAD were included in the study. Collateral function was determined before and during the last minute of a 6 min protocol of supine bicycle exercise during radial artery access coronary angiography. Collateral flow index (CFI, no unit) was determined as the ratio of mean distal coronary occlusive to mean aortic pressure both subtracted by central venous pressure. To avoid confounding due to recruitment of coronary collaterals by repetitive balloon occlusions, patients were randomly assigned to a group ‘rest first’ with CFI measurement during rest followed by CFI during exercise, and to a group ‘exercise first’ with antecedent CFI measurement during exercise before CFI at rest. Simultaneously, coronary collateral conductance (occlusive myocardial blood flow per aorto-coronary pressure drop) was determined by myocardial contrast echocardiography in the last 10 consecutive patients. Overall, CFI increased from 0.168 ± 0.118 at rest to 0.262 ± 0.166 during exercise (P = 0.0002). The exercise-induced change in CFI did not differ statistically in the two study groups. Exercise-induced CFI reserve (CFI during exercise divided by CFI at rest) was 2.2 ± 1.8. Overall, rest to peak bicycle exercise change of coronary collateral conductance was from 0.010 ± 0.010 to 1.109 ± 0.139 mL/min/100 mmHg (P < 0.0001); the respective change was similar in both groups.

\n\nConclusion\n

In patients with non-occlusive CAD, collateral flow instantaneously doubles during supine bicycle exercise as compared with the resting state.

ClinicalTrials.gov Identifier: NCT00947050.

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Early routine percutaneous coronary intervention after fibrinolysis vs. standard therapy in ST-segment elevation myocardial infarction: a meta-analysis

Wed, 01 Sep 2010 00:09:11 PDT

\nAims\n

Multiple trials in patients with ST-segment elevation myocardial infarction (STEMI) compared early routine percutaneous coronary intervention (PCI) after successful fibrinolysis vs. standard therapy limiting PCI only to patients without evidence of reperfusion (rescue PCI). These trials suggest that all patients receiving fibrinolysis should receive mechanical revascularization within 24 h from initial hospitalization. However, individual trials could not demonstrate a significant reduction in ‘hard’ endpoints such as death and reinfarction. We performed a meta-analysis of randomized controlled trials to define the benefits of early PCI after fibrinolysis over standard therapy on clinical and safety endpoints in STEMI.

\n\nMethods and results\n

We identified seven eligible trials, enrolling a total of 2961 patients. No difference was found in the incidence of death at 30 days between the two strategies. Early PCI after successful fibrinolysis reduced the rate of reinfarction (OR: 0.55, 95% CI: 0.36–0.82; P = 0.003), the combined endpoint death/reinfarction (OR: 0.65, 95% CI: 0.49–0.88; P = 0.004) and recurrent ischaemia (OR: 0.25, 95% CI: 0.13–0.49; P < 0.001) at 30-day follow-up. These advantages were achieved without a significant increase in major bleeding (OR: 0.93, 96% CI: 0.67–1.34; P = 0.70) or stroke (OR: 0.63, 95% CI: 0.31–1.26; P = 0.21). The benefits of a routine invasive strategy over standard therapy were maintained at 6–12 months, with persistent significant reduction in the endpoints reinfarction (OR: 0.64, 95% CI: 0.40–0.98; P = 0.01) and combined death/reinfarction (OR: 0.71, 95% CI: 0.52–0.97; P = 0.03).

\n\nConclusion\n

Early routine PCI after fibrinolysis in STEMI patients significantly reduced reinfarction and recurrent ischaemia at 1month, with no significant increase in adverse bleeding events compared to standard therapy. Benefits of early PCI persist at 6–12 month follow-up.

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A method for standardized computed tomography angiography-based measurement of aortic valvar structures

Wed, 01 Sep 2010 00:09:11 PDT

\nAims\n

Reliable assessment of the aortic valvar apparatus (AVAp) is essential as it may facilitate consistent outcomes with percutaneous aortic valvar therapies. The commonly referenced aortic annulus is problematic since this measurement does not correspond to any actual anatomic structure. We aim to describe a reliable method of measuring relevant structures of the AVAp based on widely available computed tomography analyses.

\n\nMethods and results\n

Retrospective analysis of computed tomograms of 75 patients with severe aortic stenosis (45 females, age 81.2 ± 7.8 years). Curved multiplaner reconstruction technique was used to measure average diameters of the ‘Aortic Leaflets Basal Attachment Plane’ (ALBAP), sinuses of Valsalva (SV), sinutubular junction (STJ), ascending aorta (AA), and distance from coronary arteries to the base of the cusps. Angulation between the AA and the left ventricle (LV) was measured in one plane that included the LV inflow long axis and the maximum visualization of the aortic root. Inter-rater reliability and absolute agreement among three raters were evaluated. Intra-class correlation coefficients for ALBAP, SV, STJ, and AA diameters were 0.90, 0.99, 0.95, and 0.94, respectively (P < 0.001) with 95% limits of agreement of the observed differences falling in the less than 1 mm range. Intra-class correlation coefficients were 0.82 for the angle and 0.61 and 0.78 for distances to the right and left coronary arteries (P < 0.001).

\n\nConclusion\n

This method showed a high degree of inter-rater reliability and absolute agreement for AVAp diameters. Agreement was lower for AA–LV angle and distance to coronary artery measurements, emphasizing the need for software improvements and standardized image acquisition protocols.

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The fate of bioresorbable struts located at a side branch ostium: serial three-dimensional optical coherence tomography assessment

Okamura, T., Serruys, P. W., Regar, E. — Wed, 01 Sep 2010 00:09:11 PDT

CardioPulse Articles

Sat, 14 Aug 2010 00:08:36 PDT

Happy birthday European Heart Journal: in 30 years, from Cinderella to centre stage

Sat, 14 Aug 2010 00:08:36 PDT

Vasovagal syncope, sympathetic mechanisms and prognosis: the shape of things to come

Grassi, G. — Sat, 14 Aug 2010 00:08:36 PDT

Pneumopericardium

Lucarelli, K., Troisi, F., Langialonga, T. — Sat, 14 Aug 2010 00:08:36 PDT

Experience with revascularization procedures does matter: low volume means worse outcome

Wijns, W., Kolh, P. H. — Sat, 14 Aug 2010 00:08:36 PDT

Hepatocellular carcinoma presenting as right heart failure

Nayar, V., Singh, B., Pugh, P. J. — Sat, 14 Aug 2010 00:08:36 PDT

Degenerative mitral valve regurgitation: best practice revolution

Adams, D. H., Rosenhek, R., Falk, V. — Sat, 14 Aug 2010 00:08:36 PDT

Degenerative mitral valve disease often leads to leaflet prolapse due to chordal elongation or rupture, and resulting in mitral valve regurgitation. Guideline referral for surgical intervention centres primarily on symptoms and ventricular dysfunction. The recommended treatment for degenerative mitral valve disease is mitral valve reconstruction, as opposed to valve replacement with a bioprosthetic or mechanical valve, because valve repair is associated with improved event free survival. Recent studies have documented a significant number of patients are not referred in a timely fashion according to established guidelines, and when they are subjected to surgery, an alarming number of patients continue to undergo mitral valve replacement. The debate around appropriate timing of intervention for asymptomatic severe mitral valve regurgitation has put additional emphasis on targeted surgeon referral and the need to ensure a very high rate of mitral valve repair, particularly in the non-elderly population. Current clinical practice remains suboptimal for many patients, and this review explores the need for a ‘best practice revolution’ in the field of degenerative mitral valve regurgitation.

Secondary prevention through cardiac rehabilitation: physical activity counselling and exercise training: Key components of the position paper from the Cardiac Rehabilitation Section of the European Association of Cardiovascular Prevention and Rehabilitation

Sat, 14 Aug 2010 00:08:36 PDT

Cardiac patients after an acute event and/or with chronic heart disease deserve special attention to restore their quality of life and to maintain or improve functional capacity. They require counselling to avoid recurrence through a combination of adherence to a medication plan and adoption of a healthy lifestyle. These secondary prevention targets are included in the overall goal of cardiac rehabilitation (CR). Cardiac rehabilitation can be viewed as the clinical application of preventive care by means of a professional multi-disciplinary integrated approach for comprehensive risk reduction and global long-term care of cardiac patients. The CR approach is delivered in tandem with a flexible follow-up strategy and easy access to a specialized team. To promote implementation of cardiac prevention and rehabilitation, the CR Section of the EACPR (European Association of Cardiovascular Prevention and Rehabilitation) has recently completed a Position Paper, entitled ‘Secondary prevention through cardiac rehabilitation: A condition-oriented approach’. Components of multidisciplinary CR for seven clinical presentations have been addressed. Components include patient assessment, physical activity counselling, exercise training, diet/nutritional counselling, weight control management, lipid management, blood pressure monitoring, smoking cessation, and psychosocial management. Cardiac rehabilitation services are by definition multi-factorial and comprehensive, with physical activity counselling and exercise training as central components in all rehabilitation and preventive interventions. Many of the risk factor improvements occurring in CR can be mediated through exercise training programmes. This call-for-action paper presents the key components of a CR programme: physical activity counselling and exercise training. It summarizes current evidence-based best practice for the wide range of patient presentations of interest to the general cardiology community.

Arterial and aortic valve calcification inversely correlates with osteoporotic bone remodelling: a role for inflammation

Sat, 14 Aug 2010 00:08:36 PDT

\nAims\n

Westernized countries face a growing burden of cardiovascular calcification and osteoporosis. Despite its vast clinical significance, the precise nature of this reciprocal relationship remains obscure. We hypothesize that cardiovascular calcification progresses with inflammation and inversely correlates with bone tissue mineral density (TMD).

\n\nMethods and results\n

Arterial, valvular, and bone metabolism were visualized using near-infrared fluorescence (NIRF) molecular imaging agents, targeting macrophages and osteogenesis. We detected significant arterial and aortic valve calcification in apoE^–/– mice with or without chronic renal disease (CRD, 30 weeks old; n = 28), correlating with the severity of atherosclerosis. We demonstrated decreases in osteogenic activity in the femurs of apoE^–/– mice when compared with WT mice, which was further reduced with CRD. Three-dimensional micro-computed tomography imaging of the cortical and cancellous regions of femurs quantified structural remodelling and reductions in TMD in apoE^–/– and CRD apoE^–/– mice. We established significant correlations between arterial and valvular calcification and loss of TMD (R² = 0.67 and 0.71, respectively). Finally, we performed macrophage-targeted molecular imaging to explore a link between inflammation and osteoporosis in vivo. Although macrophage burden, visualized as uptake of NIRF-conjugated iron nanoparticles, was directly related to the degree of arterial and valvular inflammation and calcification, the same method inversely correlated inflammation with TMD (R² = 0.73; 0.83; 0.75, respectively).

\n\nConclusion\n

This study provides direct in vivo evidence that in arteries and aortic valves, macrophage burden and calcification associate with each other, whereas inflammation inversely correlates with bone mineralization. Thus, understanding inflammatory signalling mechanisms may offer insight into selective abrogation of divergent calcific phenomena.

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The relation between volume and outcome of coronary interventions: a systematic review and meta-analysis

Post, P. N., Kuijpers, M., Ebels, T., Zijlstra, F. — Sat, 14 Aug 2010 00:08:36 PDT

\nAims\n

Although various studies reported better outcomes in centres performing a high volume of procedures of coronary artery bypass grafting (CABG) or percutaneous coronary interventions (PCIs), it is unclear how strong this relation is and whether it pertains to today's practice.

\n\nMethods and results\n

Medline, Embase, and conference reports were searched for studies reporting the effect of high volume of CABG or PCI on in-hospital mortality, adjusted for differences in case-mix. Of 140 potentially relevant papers, 15 were included, 2 of which reported data on both CABG and PCI. Meta-analysis of 10 studies on PCI, comprising 1 322 342 patients in 1746 hospitals, indicated an odds ratio (OR) of in-hospital mortality for patients treated in a high-volume hospital of 0.87 (95% confidence interval (CI) 0.83–0.91) compared to those treated in a low-volume hospital. The 7 CABG studies taken together, comprising 1 470 990 patients in 2040 hospitals, also revealed a significant effect of high volume (OR 0.85; CI 0.79–0.92). A differential effect for specific cut-off points could not be identified. Meta-regression did not show notable changes in the effect size over the years.

\n\nConclusions\n

Patients undergoing CABG or PCI in a high-volume hospital exhibit lower in-hospital mortality than those treated at low-volume hospitals. Our meta-analysis does not support the view that this relation has attenuated over time.

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Patients with acute coronary syndromes and elevated levels of natriuretic peptides: the results of the AVANT GARDE-TIMI 43 Trial

Sat, 14 Aug 2010 00:08:36 PDT

\nAims\n

Elevated natriuretic peptides (NPs) are associated with an increased cardiovascular risk following acute coronary syndromes (ACSs). However, the therapeutic implications are still undefined. We hypothesized that early inhibition of renin–angiotensin–aldosterone system (RAAS) in patients with preserved left ventricular function but elevated NPs but following ACS would reduce haemodynamic stress as reflected by a greater reduction NP compared with placebo.

\n\nMethods and results\n

AVANT GARDE-TIMI 43 trial, a multinational, double-blind trial, randomized 1101 patients stabilized after ACS without clinical evidence of heart failure or left ventricular function ≤40% but with an increased level of NP 3–10 days after admission to aliskiren, valsartan, their combination, and placebo. The primary endpoint was the change in NT-proBNP from baseline to Week 8. NT-proBNP declined significantly in each treatment arm, including placebo, by Week 8, though there were no differences in the reduction between treatment strategies (42% in placebo, 44% in aliskiren, 39% in valsartan, and 36% in combination arm). Although several subgroups had higher baseline levels of NP and greater reductions over the study period, there were no differences among treatment groups in any subgroup. There were no differences in clinical outcomes but there were more adverse events, including serious events and adverse events leading to early study drug discontinuation, in patients treated with active therapy.

\n\nConclusion\n

In this study of a high-risk population with elevated levels of NPs but relatively preserved systolic function and no evidence of heart failure following ACS, there was no evidence for a benefit of early initiation of inhibition of RAAS with valsartan, aliskiren, or their combination compared with placebo with respect to a reduction in NP over 8 weeks of therapy. Moreover, adverse events were reported more frequently in patients assigned to active therapy.

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Time course of global left ventricular strain after acute myocardial infarction

Sat, 14 Aug 2010 00:08:36 PDT

\nAims\n

The purpose of the present study was to assess the evolution of left ventricular (LV) function after acute myocardial infarction (AMI) using global longitudinal peak systolic strain (GLPSS) during 1 year follow-up. In addition, patients were divided in groups with early, late, or no improvement of LV function and predictors of recovery of LV function were established.

\n\nMethods and results\n

A total of 341 patients with AMI were evaluated. Two-dimensional echocardiography was performed at baseline, 3, 6, and 12 months. At baseline, LV function was assessed with traditional parameters and GLPSS. Global longitudinal peak systolic strain was re-assessed at 3, 6, and 12 months. Improvement of LV function was based on GLPSS and was observed in 72% of the patients. No differences were observed between patients with early and late improvement. The left anterior descending coronary artery as culprit vessel, peak cardiac troponin T level, diastolic function, and baseline GLPSS were identified as independent predictors of recovery of LV function.

\n\nConclusion\n

Improvement of LV systolic function occurred in the majority of patients during follow-up. Global longitudinal peak systolic strain, left anterior descending coronary artery as culprit vessel, peak cardiac troponin T level, and diastolic function were independent predictors of recovery of LV function. Quantification of GLPSS may be of important value for the prediction of recovery of LV function in patients after AMI.

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Comparison of sirolimus-eluting and bare metal stent for treatment of patients with total coronary occlusions: results of the GISSOC II-GISE multicentre randomized trial

Sat, 14 Aug 2010 00:08:36 PDT

\nAims\n

Percutaneous coronary intervention with bare metal stent (BMS) in chronic total coronary occlusions (CTOs) is associated with a higher rate of angiographic restenosis and reocclusion than that observed in subtotal stenoses. Preliminary reports have suggested a better performance of drug-eluting stents in CTO. In this multicentre, randomized trial, we compared the mid-term angiographic and clinical outcome of sirolimus-eluting stent (SES) or BMS implantation after successful recanalization of CTO.

\n\nMethods and results\n

Patients with CTO older than 1 month, after successful recanalization, were randomized to implantation of SES (78 patients) or BMS (74 patients) in 13 Italian centres. Clopidogrel therapy was prescribed for 6 months. The primary endpoint was in-segment minimal luminal diameter (MLD) at 8-month follow-up. Secondary clinical endpoints included death, myocardial infarction (MI), target lesion revascularization (TLR), and target vessel revascularization (TVR) at 24 months. Patients treated with SES showed, at in-segment analysis, a larger MLD (1.98 ± 0.57 vs. 0.98 ± 0.80 mm, P < 0.001), a lower late luminal loss (–0.06 ± 0.49 vs. 1.11 ± 0.79 mm, P < 0.001), and lower restenosis (9.8 vs. 67.7%, P < 0.001) and reocclusion (0 vs. 17%, P = 0.001) rates. At 24-month follow-up, patients in the SES group experienced fewer major adverse cardiac events (50.0 vs. 17.6%, P < 0.001) mainly due to a lower rate of both TLR (44.9 vs. 8.1%, P < 0.001) and TVR (44.9 vs. 14.9%, P < 0.001).

\n\nConclusion\n

In CTO, SES is markedly superior to BMS in terms of restenosis and reocclusion rate, and incidence of repeat revascularization at 24 months.

Clinicaltrials.gov identifier: NCT00220558

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Early and late outcome of treated patients referred for syncope to emergency department: the EGSYS 2 follow-up study

Sat, 14 Aug 2010 00:08:36 PDT

\nAims\n

We evaluated the early (1 month) and late (2 years) death rate and syncopal relapses of patients referred for syncope to 11 general hospitals emergency departments. Patients were enrolled in the Evaluation of Guidelines in SYncope Study 2 (EGSYS 2) study. The guidelines of the European Society of Cardiology were strictly followed in the management of patients.

\n\nMethods and results\n

Out of the 465 patients enrolled in the EGSYS 2 study, 398 (86%) underwent a complete follow-up. We excluded 18 patients with non-syncopal attacks. Among the remaining 380 patients, death of any cause occurred in 35 (9.2%). The mean follow-up was 614 ± 73 days. Six deaths (17% of total) occurred during the first month of follow-up. Patients who died were older, had a higher incidence of structural heart disease and/or abnormal ECG, had injuries related to syncope and higher EGSYS score. Syncope recurred in 63 (16.5%) patients. Syncopal relapses occurred in only one patient during the first month of follow-up. The incidence of syncopal recurrences was unrelated to the mechanism of syncope. No clinical differences were found between patients with or without syncopal recurrence and in patients with EGSYS score < or ≥3.

\n\nConclusion\n

A peak of cardiovascular mortality but not of syncopal recurrences was observed in patients attending to the emergency department for syncope within the first month. Late unfavourable outcomes were caused by associated cardiovascular diseases rather than by the mechanism of syncope. The causes of syncope did not determine the recurrence rate.

\n\n

Persistence of muscle sympathetic nerve activity during vasovagal syncope

Vaddadi, G., Esler, M. D., Dawood, T., Lambert, E. — Sat, 14 Aug 2010 00:08:36 PDT

\nAims\n

To determine whether sympathetic nerve firing to skeletal muscle vasculature is withdrawn during vasovagal syncope (VVS) precipitated by passive graded head-up tilt (HUT) table testing.

\n\nMethods and results\n

We performed passive graded HUT table testing in 18 patients with a history of recurrent postural VVS whom we evaluated during the syncopal event. All patients developed typical VVS during testing. Blood pressure was measured continuously via intra-brachial arterial line. Muscle sympathetic nerve activity (MSNA) was measured using an electrode in the peroneal nerve. Passive graded HUT was then applied. No pharmacological agents were used to provoke syncope. The recording site was maintained through the syncopal event in 10 of 18 patients and we were able to demonstrate persistence of MSNA during syncope in 9. The predominant haemodynamic pattern of syncope in this cohort was mixed—hypotension and bradycardia, with heart rate not falling <40 b.p.m. (n = 10).

\n\nConclusion\n

Our data challenge the established view that the final trigger for human orthostatic vasovagal reactions is sympathetic nervous system inhibition. Efferent sympathetic nerve traffic to the skeletal muscle vasculature was nearly always maintained through the faint. This finding supports an alternative viewpoint, that vasodilator mechanisms underlie the blood pressure fall in VVS.

\n\n

Coronary artery fistula in infancy

Wilmes, C., Lehn, M., Sreeram, N. — Sat, 14 Aug 2010 00:08:36 PDT

Association between short-term exposure to ultrafine particles and hospital admissions for stroke in Copenhagen, Denmark

Sat, 14 Aug 2010 00:08:36 PDT

\nAims\n

The relevance of ultrafine particles (UFPs, particles <0.1 µm diameter), the smallest fraction of ambient particulate matter, on stroke morbidity has not been documented. We studied the effects of short-term changes in exposure to these particles on stroke, separately for ischaemic and haemorrhagic strokes, mild and severe strokes, and ischaemic strokes with (likely embolic) and without (likely thrombotic) atrial fibrillation (AF).

\n\nMethods and results\n

We used a time-stratified case-crossover design to study the association between short-term exposure to UFPs, particulate matter <10 µm in diameter (PM₁₀), nitrogen oxides (NO_x) and carbon monoxide (CO) (measured at single background station) and hospital admissions for stroke in Copenhagen (2003–2006). Of 7485 stroke admissions, 6798 were ischaemic and 687 haemorrhagic, 3485 mild, and 2248 severe. Of the ischaemic stroke cases, 1204 had AF and 5273 did not. We found significant positive association with exposure to UFPs, NO_x and CO, and ischaemic strokes, and UFPs and NO_x and mild strokes, 4 days before admission. The strongest associations were with UFPs. Exposure to UFPs lead to a 21% increase in hospital admissions (per interquartile range of 5-day averages; 95% confidence interval 4–41%) for mild ischaemic stroke of without AF (likely thrombotic origin).

\n\nConclusion\n

Our results indicate possible effects of traffic-related air pollution, mainly UFPs, on hospital admissions for ischaemic stroke, especially for mild ischaemic stroke of likely thrombotic origin (without AF). These are novel findings regarding the relevance of UFPs and the heterogeneous effect of air pollution on the severity and origin of stroke, and need confirmation by other data.

\n\n

Is carotid intima media thickness useful for individual prediction of cardiovascular risk? Ten-year results from the Carotid Atherosclerosis Progression Study (CAPS)

Lorenz, M. W., Schaefer, C., Steinmetz, H., Sitzer, M. — Sat, 14 Aug 2010 00:08:36 PDT

\nAims\n

Carotid intima media thickness (cIMT) is an intermediate phenotype of early atherosclerosis that independently predicts vascular events. It is often suggested that cIMT be used as a screening tool to select subjects with an elevated event risk. Whether cIMT adds information to traditional risk models has so far received little investigation.

\n\nMethods and results\n

The 10-year follow-up of 4904 subjects from the Carotid Atherosclerosis Progression Study (CAPS) without pre-existing vascular disease included cardiovascular events and total mortality. Using Cox models and reclassification statistics, we investigated the usefulness of cIMT in individual risk prediction beyond the Framingham and the SCORE models, using risk strata of 0–5, 5–10, 10–20, and ≥20% over 10 years. Carotid intima media thickness was significantly and independently predictive for cardiovascular events. Compared with a model using the Framingham risk factors, a second model that included the common carotid-IMT led to the reclassification of 357 subjects (8.1%). In 107 subjects (30.0%), this reclassification was correct as confirmed with the actual outcome over 10 years. Net reclassification improvement was –1.41% (P = NS); integrated discrimination improvement was 0.04% (P = NS). More subjects were shifted to lower than to higher risk categories by the inclusion of cIMT. Analyses including other endpoint definitions, other carotid segments, and the SCORE risk model for baseline prediction did not result in consistently better risk prediction with cIMT.

\n\nConclusion\n

Despite cIMT being predictive for cardiovascular endpoints, it did not consistently improve the risk classification of individuals. Carotid intima media thickness may not be useful for the risk stratification of individuals in the general population.

\n\n

Recombinant apolipoprotein A-I Milano rapidly reverses aortic valve stenosis and decreases leaflet inflammation in an experimental rabbit model

Sat, 14 Aug 2010 00:08:36 PDT

\nAims\n

Aortic stenosis (AS) is associated with significant morbidity and mortality. Recombinant apolipoprotein A-I Milano (rApoA-I_M) induces atherosclerotic plaque regression. The aims of this study were to determine the effects of rApoA-I_M on experimental aortic valve degeneration and its mechanisms of action.

\n\nMethods and results\n

New Zealand White rabbits (n = 20) were fed an atherogenic diet for 9 months and then randomized to either placebo or rApoA-I_M. Echocardiography was used to assess the effect of the treatments on AS. Porcine aortic valve myofibroblasts (PAVMF) treated with oxidized low-density lipoprotein served to define the effects of rApoA-I_M on the expression of monocyte chemoattractant protein-1 (MCP-1), nuclear factor (NF)-B, and alkaline phosphatase (AP). Recombinant apolipoprotein A-I Milano increased aortic valve area (AVA) by 32% (0.25 ± 0.05 to 0.34 ± 0.07 cm², P < 0.01); whereas AVA remained unchanged in the placebo group (0.24 ± 0.05 to 0.26 ± 0.04 cm², P = 0.58). Histopathological examination of aortic valves in the rApoA-I_M animals showed significantly less leaflet thickening, inflammation, and calcification vs. the placebo group. In vitro, rApoA-I_M significantly inhibited MCP-1, AP, and NF-B and decreased intracellular cholesterol content in PAVMF.

\n\nConclusion\n

Recombinant apolipoprotein A-I Milano treatment reverses AS in this experimental rabbit model. The beneficial effects seem to be mediated by enhanced cholesterol removal and by reduced inflammation and calcification.

\n\n

Cardiac remodelling as a result of pre-term birth: implications for future cardiovascular disease

Bensley, J. G., Stacy, V. K., De Matteo, R., Harding, R., Black, M. J. — Sat, 14 Aug 2010 00:08:36 PDT

\nAims\n

Pre-term birth affects 10–12% of live births and occurs when the myocardium is still developing; therefore, the final structure of the myocardium could be altered. We hypothesized that, in response to pre-term birth, structural remodelling occurs within the myocardium which enables the immature heart muscle to adapt to the haemodynamic transition at birth but results in persistent alterations in its structure. Our objective was to determine how pre-term birth alters the final structure of the myocardium.

\n\nMethods and results\n

Using sheep, pre-term birth was induced at 0.9 of term; hearts were examined at 9 weeks after term-equivalent age, when cardiomyocyte proliferation and maturation have ceased. In pre-term lambs, we found that cardiomyocytes of both ventricles and the interventricular septum were hypertrophied. Cardiomyocyte maturation in pre-term lambs was altered in that there was a greater proportion of mononucleated, polyploid (4n) cardiomyocytes in both ventricles compared with controls; importantly, induction of polyploidy is associated with irreversible stress-related changes in DNA. We also found a six- to seven-fold increase in collagen deposition, usually accompanied by lymphocytic infiltration.

\n\nConclusion\n

We conclude that pre-term birth leads to remodelling of the myocardium that alters its final structure. This may programme for long-term cardiac vulnerability.

\n\n

CardioPulse Articles * ESC Heart Failure Association Congress, 29 May to 1 June 2010, Berlin * Climbing the academic ladder in cardiology: Norway * Cardiologists need a PhD for a University Hospital academic and clinical career in Norway * Cardiovascular medicine in South Africa: interplay of personalities and politics? * The evolution of cardiopulmonary resuscitation * Book review * Core topics in transoesophageal echocardiography

Sun, 01 Aug 2010 00:07:59 PDT

Central haemodynamics and clinical outcomes: going beyond brachial blood pressure?

Williams, B., Lacy, P. S. — Sun, 01 Aug 2010 00:07:59 PDT

256- and 320-row coronary CTA: is more better?

West, A. M., Beller, G. A. — Sun, 01 Aug 2010 00:07:59 PDT

Changing patterns in epidemiological profiles and prevention strategies in infective endocarditis: from teeth to healthcare-related infection

Thuny, F., Avierinos, J.-F., Habib, G. — Sun, 01 Aug 2010 00:07:59 PDT

Shock in acute myocardial infarction: the Cape Horn for trials?

Thiele, H., Allam, B., Chatellier, G., Schuler, G., Lafont, A. — Sun, 01 Aug 2010 00:07:59 PDT

Despite therapeutic improvements, cardiogenic shock (CS) remains the most common cause of death in patients with acute myocardial infarction (AMI). In addition to percutaneous coronary intervention, inotropes, fluids, adjunctive medication, intra-aortic balloon counterpulsation, and also assist devices are widely used for treatment. However, currently, there is only limited evidence for any of the above treatments. This review will therefore outline the underlying causes, pathophysiology, and treatment of CS complicating AMI with major focus on interventional techniques and advancement of new therapeutical arsenals, both pharmacological and mechanical.

Highly sensitive troponin T assay in normotensive patients with acute pulmonary embolism

Sun, 01 Aug 2010 00:07:59 PDT

\nAims\n

To assess the role of cardiac troponin T (cTnT) levels on admission using a new, highly sensitive assay (hsTnT) in the risk assessment of normotensive patients with acute pulmonary embolism (PE).

\n\nMethods and results\n

We prospectively studied 156 consecutive normotensive patients with confirmed PE. The prognostic value of hsTnT at baseline was compared with the conventional cTnT troponin assay and with N-terminal pro-brain natriuretic peptide concentrations. Long-term follow-up was available for 153 patients (98.1%). Highly sensitive troponin T values ranged from 0.001 to 357.2 pg/mL [median 27.2 (25th–75th percentile 9.4–69.4) pg/mL]. Overall, 100 patients (64%) had hsTnT ≥14 pg/mL. Baseline hsTnT was higher in patients with an adverse 30-day outcome (≥1: death, need for catecholamines, endotracheal intubation, or cardiopulmonary resuscitation) compared with an uncomplicated course [71.7 (35.5–117.9) vs. 26.4 (9.2–68.2) pg/mL; P = 0.027]. The cut-off value of 14 pg/mL showed an excellent prognostic sensitivity and negative predictive value (both 100%). In comparison, as many as 50% of the patients with an adverse early outcome would have been misclassified as low risk by cTnT (cut-off 0.03 ng/mL). Logistic regression indicated a two-fold increase in the risk of an adverse outcome for each increase of hsTnT by 1SD of the natural logarithm (P = 0.037). Patients with elevated hsTnT levels had a reduced probability of long-term survival (P = 0.029 by log-rank); by Cox's regression analysis, hsTnT was the only laboratory biomarker predicting an elevated risk of death over the long term.

\n\nConclusion\n

Highly sensitive troponin T assays may be capable of improving risk stratification of non-high-risk PE.

\n\n

aVR ST elevation: an important but neglected sign in ST elevation acute myocardial infarction

Sun, 01 Aug 2010 00:08:00 PDT

\nAim\n

This study evaluated the prognostic implications of aVR ST elevation during ST elevation acute myocardial infarction (AMI).

\n\nMethods and results\n

The Hirulog and Early Reperfusion/Occlusion-2 study randomized 17 073 patients with acute ST elevation AMI within 6 h of symptom onset to receive either bivalirudin or heparin, in addition to streptokinase and aspirin. The treatments had no effect on the primary endpoint of 30-day mortality. Electrocardiographic recordings were performed at randomization and at 60 min after commencing streptokinase. aVR ST elevation ≥1 mm was associated with higher 30-day mortality in 15 315 patients with normal intraventricular conduction regardless of AMI location (14.7% vs. 11.2% for anterior AMI, P = 0.0045 and 16.0% vs. 6.4% for inferior AMI, P < 0.0001). After adjusting for summed ST elevation and ST depression in other leads, associations with higher mortality were found with aVR ST elevation of ≥1.5 mm for anterior [odds ratio 1.69 (95% CI 1.16 to 2.45)] and of ≥1 mm for inferior AMI [odds ratio 2.41 (95% CI 1.76 to 3.30)]. There was a significant interaction between aVR ST elevation and infarct location. Thirty-day mortality was similar with anterior and inferior AMI when aVR ST elevation was present (11.5% vs. 13.2%, respectively, P = 0.51 with 1 mm and 23.5% vs. 22.5% respectively, P = 0.84 with ≥ 1.5 mm ST elevation). After fibrinolytic therapy, resolution of ST elevation in aVR to <1 mm was associated with lower mortality, while new ST elevation ≥1 mm was associated with higher mortality.

\n\nConclusion\n

aVR ST elevation is an important adverse prognostic sign in AMI.

\n\n

Genetic determinants of treatment benefit of the angiotensin-converting enzyme-inhibitor perindopril in patients with stable coronary artery disease

Sun, 01 Aug 2010 00:08:00 PDT

\nAims\n

The efficacy of angiotensin-converting enzyme (ACE)-inhibitors in stable coronary artery disease (CAD) may be increased by targeting the therapy to those patients most likely to benefit. However, these patients cannot be identified by clinical characteristics. We developed a genetic profile to predict the treatment benefit of ACE-inhibitors exist and to optimize therapy with ACE-inhibitors.

\n\nMethods and results\n

In 8907 stable CAD patients participating in the randomized placebo-controlled EUROPA-trial, we analysed 12 candidate genes within the pharmacodynamic pathway of ACE-inhibitors, using 52 haplotype-tagging-single nucleotide polymorphisms (SNPs). The primary outcome was the reduction in cardiovascular mortality, non-fatal myocardial infarction, and resuscitated cardiac arrest during 4.2 years of follow-up. Multivariate Cox regression was performed with multiple testing corrections using permutation analysis. Three polymorphisms, located in the angiotensin-II type I receptor and bradykinin type I receptor genes, were significantly associated with the treatment benefit of perindopril after multivariate adjustment for confounders and correction for multiple testing. A pharmacogenetic score, combining these three SNPs, demonstrated a stepwise reduction of risk in the placebo group and a stepwise decrease in treatment benefit of perindopril with an increasing scores (interaction P < 0.0001). A pronounced treatment benefit was observed in a subgroup of 73.5% of the patients [hazard ratio (HR) 0.67; 95% confidence interval (CI) 0.56–0.79], whereas no benefit was apparent in the remaining 26.5% (HR 1.26; 95% CI 0.97–1.67) with a trend towards a harmful effect. In 1051 patients with cerebrovascular disease from the PROGRESS-trial, treated with perindopril or placebo, an interaction effect of similar direction and magnitude, although not statistically significant, was observed.

\n\nConclusion\n

The current study is the first to identify genetic determinants of treatment benefit of ACE-inhibitor therapy. We developed a genetic profile which predicts the treatment benefit of ACE-inhibitors and which could be used to optimize therapy.

\n\n

Prediction of cardiovascular events and all-cause mortality with central haemodynamics: a systematic review and meta-analysis

Sun, 01 Aug 2010 00:08:00 PDT

\nAims\n

To calculate robust quantitative estimates on the predictive value of central pressures and derived central haemodynamic indices for cardiovascular (CV) outcomes and all-cause mortality by meta-analysis of longitudinal studies.

\n\nMethods and results\n

We meta-analysed 11 longitudinal studies that had employed measures of central haemodynamics and had followed 5648 subjects for a mean follow-up of 45 months. The age- and risk-factor-adjusted pooled relative risk (RR) of total CV events was 1.088 (95% CI 1.040–1.139) for a 10 mmHg increase of central systolic pressure, 1.137 (95% CI 1.063–1.215) for a 10 mmHg increase of central pulse pressure (PP), and 1.318 (95% CI 1.093–1.588) for a 10% absolute increase of central augmentation index (AIx). Furthermore, we found that a 10% increase of central AIx was associated with a RR of 1.384 (95% CI 1.192–1.606) for all-cause mortality. When compared with brachial PP, central PP was associated with marginally but not significantly higher RR of clinical events (P = 0.057).

\n\nConclusion\n

Central haemodynamic indexes are independent predictors of future CV events and all-cause mortality. Augmentation index predicts clinical events independently of peripheral pressures, while central PP has a marginally but not significantly (P = 0.057) better predictive ability when compared with peripheral PP.

\n\n

Iron deficiency: an ominous sign in patients with systolic chronic heart failure

Sun, 01 Aug 2010 00:08:00 PDT

\nAims\n

Beyond erythropoiesis, iron is involved in numerous biological processes crucial for maintenance of homeostasis. Patients with chronic heart failure (CHF) are prone to develop iron deficiency (ID), and iron supplementation improves their functional status and quality of life. We sought to examine the relationship between ID and survival in patients with systolic CHF.

\n\nMethods and results\n

In a prospective observational study, we evaluated 546 patients with stable systolic CHF [age: 55 ± 11 (mean ± standard deviation) years, males: 88%, left ventricular ejection fraction: 26 ± 7%, New York Heart Association (NYHA) class (I/II/III/IV): 57/221/226/42]. Iron deficiency was defined as: ferritin <100 µg/L, or 100–300 µg/L with transferrin saturation <20%. The prevalence of ID was 37 ± 4% [±95% confidence intervals (CI)] in the entire CHF population (32 ± 4 vs. 57 ± 10%—in subjects without vs. with anaemia defined as haemoglobin level <12 g/dL in women and <13 g/dL in men, P < 0.001). In a multiple logistic model, ID was more prevalent in women, those in the advanced NYHA class, with higher plasma N-terminal pro-type B natriuretic peptide and higher serum high-sensitivity C-reactive protein (all P < 0.05). At the end of follow-up (mean duration: 731 ± 350 days), there were 153 (28%) deaths and 30 (6%) heart transplantations (HTX). In multivariable models, ID (but not anaemia) was related to an increased risk of death or HTX (adjusted hazard ratio 1.58, 95% CI 1.14–2.17, P < 0.01).

\n\nConclusion\n

In patients with systolic CHF, ID is common and constitutes a strong, independent predictor of unfavourable outcome. Iron supplementation may be considered as a therapeutic approach in these patients to improve prognosis.

\n\n

Age-dependent values of N-terminal pro-B-type natriuretic peptide are superior to a single cut-point for ruling out suspected systolic dysfunction in primary care

Sun, 01 Aug 2010 00:08:00 PDT

\nAims\n

The study evaluated the use of age-related decision limits for N-terminal pro-B-type natriuretic peptide (NT-proBNP), for ruling out suspected systolic dysfunction in symptomatic patients in primary care, compared with the present standards.

\n\nMethods and results\n

Data were obtained from 5508 patients from 10 studies in the UK, New Zealand, Europe, and USA. All have had NT-proBNP analysis and echocardiography. The median age was 62 years (range 18–100 years) with a prevalence of reduced left ventricular systolic function (left ventricular ejection fraction ≤40%) of 18%. In a receiver operating characteristic curve analysis, overall area under the curve (AUC) was 0.89. When looking at different age groups, AUC was highest (0.95) for <50 years, intermediate (0.90) for 50–75 years, and lowest (0.82) for >75 years. Using optimized decision limits, sensitivity, specificity, and negative predictive values (NPVs) were: <50 years (50 ng/L): 99.2, 57.2, and 99.7%; 50–75 years (75 ng/L): 95.9, 51.0, and 96.8%; and >75 years (250 ng/L): 87.9, 53.7, and 92.4%, respectively. Using only a single decision value (125 ng/L for all ages) gave sensitivities of 89.1, 91.9, and 94.3%; specificities of 84.0, 69.1, and 29.3% and NPVs of 97.7, 97.6, and 93.4%. A decision value of 400 ng/L for all ages gave much lower sensitivities.

\n\nConclusion\n

In a large population of patients in primary care, the use of age-stratified NT-proBNP decision limits considerably improves performance over current standards, with an excellent NPV for exclusion of reduced left ventricular systolic function.

\n\n

Small black holes in optical frequency domain imaging matches intravascular neoangiogenesis formation in histology

Vorpahl, M., Nakano, M., Virmani, R. — Sun, 01 Aug 2010 00:08:00 PDT

Health care exposure and age in infective endocarditis: results of a contemporary population-based profile of 1536 patients in Australia

Sy, R. W., Kritharides, L. — Sun, 01 Aug 2010 00:08:00 PDT

\nAims\n

Institutional-based studies of infective endocarditis (IE) are limited by referral bias. Longitudinal population-based data were used to overcome such bias to provide a contemporary profile of IE and specifically investigate the importance of health care-associated IE and age.

\n\nMethods and results\n

Between 2000 and 2006, 1536 consecutive adult admissions with IE were identified in the Australian state of New South Wales using a state-wide database. The annual incidence was 4.7 per 100 000 (95% CI 4.4–4.9) being highest in patients aged between 80 and 84 years. The most frequent causative organism was Staphylococcus aureus (32%). Surgery was performed in 20% and the 6-month mortality was 18%. During the study period, the median age of patients increased from 61 to 65 years (P = 0.02), but microbiology, surgery, and mortality rates remained stable. Health care-associated IE was identified in 30% and was associated with older age, diabetes, renal impairment, heart failure, and infection with methicillin-resistant Staphylococcus aureus and enterococcus. Even after adjustment for these differences, recent health care exposure was an independent predictor of mortality (hazard ratio 1.62, 95% CI 1.34–1.96).

\n\nConclusion\n

Contemporary IE contributes to health care-related infection, occurs in an increasingly elderly population, and remains a condition with unacceptably high mortality.

\n\n

Long-term response to calcium-channel blockers in non-idiopathic pulmonary arterial hypertension

Sun, 01 Aug 2010 00:08:00 PDT

\nAims\n

To assess the acute vasodilator response and long-term response to calcium-channel blockers (CCB) in pulmonary arterial hypertension (PAH) with associated conditions.

\n\nMethods and results\n

The response to acute vasodilator testing [>20% decrease in mean pulmonary artery pressure (mPAP) and total pulmonary resistance] was assessed in 663 consecutive PAH patients with connective tissue disease (CTD; n = 168), portal hypertension (PoPH; n = 153), anorexigen use (n = 127), human immunodeficiency virus infection (HIV; n = 124), congenital heart disease (CHD; n = 50), and pulmonary veno-occlusive disease or capillary haemangiomatosis (PVOD/PCH; n = 41). An acute vasodilator response was observed in 13.4% of PAH-anorexigen patients, 12.2% of PVOD/PCH, 10.1% of CTD, 1.6% of HIV, 1.3% of PoPH, and was absent in CHD. A long-term response to CCB (marked haemodynamic improvement at 3–4 months and New York Heart Association functional class I or II after 1 year) was reported in 9.4% of PAH-anorexigen patients but was rare in HIV, PoPH, CTD (1.6, 0.7, and 0.6%, respectively) and absent in PVOD/PCH. All patients with a long-term CCB response were alive after 5 years; two deaths not related to PAH occurred after this time. Recent criteria for acute response based on the fall in mPAP to <40 mmHg are more specific to detect long-term responders to CCB.

\n\nConclusion\n

A long-term CCB response was reported in patients with PAH associated with anorexigen use, but was rare in patients with PoPH or HIV and absent in PVOD/PCH, CHD, and the vast majority of CTD. The prognosis of long-term responders was favourable and related to the underlying cause of PAH.

\n\n

Diagnostic accuracy of 320-row multidetector computed tomography coronary angiography in the non-invasive evaluation of significant coronary artery disease

Sun, 01 Aug 2010 00:08:00 PDT

\nAims\n

Multidetector computed tomography coronary angiography (CTA) has emerged as a feasible imaging modality for non-invasive assessment of coronary artery disease (CAD). Recently, 320-row CTA systems were introduced, with 16 cm anatomical coverage, allowing image acquisition of the entire heart within a single heart beat. The aim of the present study was to assess the diagnostic accuracy of 320-row CTA in patients with known or suspected CAD.

\n\nMethods and results\n

A total of 64 patients (34 male, mean age 61 ± 16 years) underwent CTA and invasive coronary angiography. All CTA scans were evaluated for the presence of obstructive coronary stenosis by a blinded expert, and results were compared with quantitative coronary angiography. Four patients were excluded from initial analysis due to non-diagnostic image quality. Sensitivity, specificity, and positive and negative predictive values to detect ≥50% luminal narrowing on a patient basis were 100, 88, 92, and 100%, respectively. Moreover, sensitivity, specificity, and positive and negative predictive values to detect ≥70% luminal narrowing on a patient basis were 94, 95, 88, and 98%, respectively. With inclusion of non-diagnostic imaging studies, sensitivity, specificity, and positive and negative predictive values to detect ≥50% luminal narrowing on a patient basis were 100, 81, 88, and 100%, respectively.

\n\nConclusion\n

The current study shows that 320-row CTA allows accurate non-invasive assessment of significant CAD.

\n\n

The diagnostic accuracy of 256-row computed tomographic angiography compared with invasive coronary angiography in patients with suspected coronary artery disease

Sun, 01 Aug 2010 00:08:00 PDT

\nAims\n

To assess the diagnostic accuracy of 256-row computed tomographic angiography (CTA) in patients with suspected coronary artery disease (CAD). Non-invasive imaging of the coronary artery by CTA has increasingly been used in recent years. The accuracy of 256-row CTA has not yet been studied. We sought to assess the accuracy of 256-row CTA compared with invasive coronary angiography (ICA) in the diagnosis and assessment of CAD.

\n\nMethods and results\n

We prospectively evaluated 104 consecutive individuals who accepted CTA and then underwent ICA. The presence of stenosis ≥50% was considered obstructive. The diagnostic accuracy of CTA for detecting obstructive stenosis was compared with that of ICA. The area under the receiver-operating-characteristic curve (AUC) was used to evaluate the diagnostic accuracy of CTA relative to ICA. A total of 86 patients had obstructive CAD. The patient-based analysis of CTA for detecting stenosis ≥50% according to ICA revealed an AUC of 0.744 [95% confidence interval (CI), 0.572–0.916], with a sensitivity of 98.8%, a specificity of 50%, a positive predictive value (PPV) of 92.4%, and a negative predictive value (NPV) of 87.5%. The segment-based analysis revealed an AUC of 0.915 (95% CI, 0.847–0.982), with a sensitivity of 93.5%, a specificity of 95%, a PPV of 77.6%, and an NPV of 98.7%. The vessel-based analysis revealed an AUC of 0.887 (95% CI, 0.808–0.966), with a sensitivity of 94.3%, a specificity of 87.3%, a PPV of 82.7%, and an NPV of 95.9%.

\n\nConclusion\n

256-Row CTA is a highly sensitive test of CAD and has a high predictive value. 256-Row CTA may be a potential alternative to detect coronary artery stenosis and rule out CAD in suspected patients.

\n\n

Ventricular septal crypt in hypertrophic cardiomyopathy

Maron, B. J., Lindberg, J., Lesser, J. R. — Sun, 01 Aug 2010 00:08:00 PDT

Exercise acutely reverses dysfunction of circulating angiogenic cells in chronic heart failure

Sun, 01 Aug 2010 00:08:00 PDT

\nAims\n

Recruitment of endothelial progenitor cells (EPCs) and enhanced activity of circulating angiogenic cells (CACs) might explain the benefits of exercise training in reversing endothelial dysfunction in chronic heart failure (CHF) patients. We studied baseline EPC numbers and CAC function and the effect of a single exercise bout.

\n\nMethods and results\n

Forty-one CHF patients (mild, n = 22; severe, n = 19) and 13 healthy subjects were included. Migratory activity of CACs was evaluated in vitro and circulating CD34+ and CD34+/KDR+ (EPC) cells were quantified by flow cytometry before and after cardiopulmonary exercise testing (CPET). Circulating stromal cell-derived factor-1 (SDF-1) and vascular endothelial growth factor (VEGF) concentrations were measured.

Both CAC migration as well as CD34+ cell numbers were significantly reduced in CHF, whereas CD34+/KDR+ cells were not different from controls. Endothelial dysfunction was related to impaired CAC migration (r = 0.318, P = 0.023). Cardiopulmonary exercise testing improved CAC migration in severe (+52%, P < 0.005) and mild CHF (+31%, P < 0.005), restoring it to levels similar to controls. Following CPET, SDF-1 increased in healthy controls and mild CHF (P < 0.005). Vascular endothelial growth factor, CD34+, and CD34+/KDR+ cell numbers remained unchanged.

\n\nConclusion\n

The present findings reveal a potent stimulus of acute exercise to reverse CAC dysfunction in CHF patients with endothelial dysfunction.

\n\n

Vascular insights into the treatment of acute myocardial infarction by post-mortem in situ microcomputed tomography and histology

Ball, T. C., Foerst, J. R., Vorpahl, M. — Sun, 01 Aug 2010 00:08:00 PDT

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