We evaluated (i) the cytotoxicity of CM [both low-osmolality (LOCM) and iso-osmolality (IOCM)], of iodine alone, and of an hyperosmolar solution (mannitol 8%) on human embryonic kidney (HEK 293), porcine proximal renal tubular (LLC-PK1), and canine Madin–Darby distal tubular renal (MDCK) cells; and (ii) the effectiveness of various antioxidant compounds [n-acetylcysteine (NAC), ascorbic acid and sodium bicarbonate] in preventing CM cytotoxicity. The cytotoxicity of CM was assessed at different time points, with different methods: cell viability, DNA laddering, flow cytometry, and caspase activation.

Both LOCM and IOCM produced a concentration- and time-dependent increase in cell death as assessed by the different methods. On the contrary, iodine alone and hyperosmolar solution did not induce any significant cytotoxic effect. There was not any significant difference in the cytotoxic effect between LOCM and IOCM. Furthermore, both LOCM and IOCM caused a marked increase in caspase-3 and -9 activities and poly(ADP-ribose) fragmentation, while no effect on caspase-8/-10 was observed, thus indicating that the CM activated apoptosis mainly through the intrinsic pathway. Both CM induced an increase in protein expression levels of pro-apoptotic members of the Bcl2 family (Bim and Bad). NAC and ascorbic acid but not sodium bicarbonate had a dose-dependent protective effect on renal cells after 3 h incubation with high dose (200 mg iodine/mL) of both LOCM and IOCM.

Both LOCM and IOCM induce a dose-dependent renal cell apoptosis. NAC and ascorbic acid but not sodium bicarbonate prevent this contrast-induced apoptosis.

Outcome of 218 foetuses having been diagnosed with TOF (n = 153) or PA-VSD (n = 65) was reviewed. Abnormal karyotyping, 22q11 deletion, and extracardiac anomalies were found, respectively, in 11, 18, and 46%. Pregnancy was terminated in 75 cases (34%), and in three cases foetuses died in utero. Presence or absence and confluence of PA branches were confirmed after birth or pregnancy termination in all but five (5%) cases. Main pulmonary trunk (MPA) was incorrectly described in 11 (10%) cases and major aorto-pulmonary collateral arteries in 16 (13%) cases. Among live born infants, 110 (88%) were operated and 92 (74%) underwent complete repair in the first year of life. Size of confluent PAs and presence of MPA were related to the probability of having a complete repair in the first year of life.

Foetal diagnosis of TOF and PA-VSD has a major impact on pregnancy outcome, as associated anomalies are frequently found. Pre-natally determined size of PA branches and presence of MPA are good predictors of complete repair in the first year of life.

Patients (n = 100) were recruited consecutively in the setting of a double-blind, randomized trial. Bivalirudin or UFH was administered during PCI. Blood was drawn immediately before PCI, following administration of bivalirudin or UFH directly after PCI, and 24 h after PCI. Adenosine diphosphate (ADP)-induced platelet aggregation was assessed with light transmission aggregometry (LTA) and multiple electrode aggregometry (MEA). Before PCI, ADP-induced platelet aggregation was similar in UFH and bivalirudin patients (P = 0.99 for LTA; P = 0.28 for MEA). Administration of bivalirudin during PCI resulted in significant additional suppression of platelet aggregation (P = 0.012 for LTA; P = 0.008 for MEA). Administration of UFH did not have a significant influence on platelet aggregation (P = 0.42 for LTA; P = 0.78 for MEA). Platelet aggregation was again similar in the two groups 24 h after PCI (P > 0.05 for LTA and MEA).

Bivalirudin, given during PCI in patients pretreated with 600 mg of clopidogrel, is in contrast to UFH associated with further inhibition of platelet aggregation.

Demographic and pre-operative clinical data were obtained retrospectively through case-note review. All operations were performed by a single surgeon. Actuarial freedom from ≥2+ AR (aortic regurgitation), elevated trans-valvular gradient (TVG) (≥25 mmHg) and ascending aortic dilatation (≥4.0 cm) were assessed using Kaplan–Meier curves and multivariable Cox proportional hazards regression. A propensity analysis was carried out using a non-parsimonius logistic regression model for implantation with SC vs. RR. Between 1 January 1991 and 1 January 2001, 215 patients underwent AVR with a homograft. The SC technique was used in 131 (61%) patients and 84 (39%) patients underwent RR. Technique was not an independent predictor for ≥2+ AR (adjusted hazard ratio 1.9; 95% CI 0.56–6.16, P = 0.31), elevated TVG (adjusted hazard ratio; 0.99; 95% CI 0.15–6.71, P = 0.99) or ascending aortic dilatation (adjusted hazard ratio 2.01; 95% CI 0.50–8.25, P = 0.33). One and 5 year actuarial freedom from ≥2+ AR (log-rank – P = 0.09) and ascending aortic dilatation (log-rank – P = 0.88) were not significantly different between groups.

The incidence of SVD and ascending aortic dilatation is not affected by the method of implantation of the aortic homograft. All homografts are prone to SVD which is responsible for a progressive increase in the prevalence of these changes over time.

Myocardial infarction was created by coronary ligation and immediately after reperfusion, autologous bone-marrow-derived MSCs were transplanted into the hearts of Chinese swine that were pretreated with or without Ator. Six weeks after transplantation, as evaluated by SPECT and MRI all the animals with Ator showed improved cardiac perfusion and contractility when compared with untreated. Increased survival and differentiation of implanted MSCs and decreased infarct area were observed in the Ator-treated, MSC-implanted animals. In the absence of Ator, MSC transplantation only achieved a modest improvement in perfusion and morphology. The combined treatment with Ator and MSCs significantly inhibited cardiac cell apoptosis, reduced oxidative stress, and suppressed expression of the inflammatory cytokines in the post-infarct myocardium.

Ator treatment may protect the myocardium undergoing acute infarction and reperfusion by creating a better environment for the survival and differentiation of implanted MSCs. The benefit of the Ator/stem cell combined therapy may result from the statin-mediated inhibition of apoptosis, oxidative stress, and inflammation in the infarcted myocardium.

At baseline, transthoracic echocardiography was performed with two-dimensional and Doppler imaging following a standardized protocol. Echo measurements including left ventricular (LV) dimensions and aortic root dimensions were obtained according to the ASE recommendations. MAC was identified by bright echoes at the base of the mitral leaflets or annulus on 2D imaging, and aortic valve calcification by visualization of bright echoes on the aortic valve leaflets. The degree of calcification was semi-quantitated from absent to severe. The study population included 219 patients (57 ± 14 years; 129 males), divided into two pre-specified categories; bicuspid (n = 133) and tricuspid (n = 86) aortic valves. Baseline LV dimensions, aortic valve haemodynamics, and cholesterol profiles were similar between the two groups at baseline. Individuals with tricuspid aortic valves were older, more hypertensive, with higher degrees of MAC and AV calcification (P < 0.001). The higher degree of MAC persisted in patients with tricuspid AV after adjustment for age and systolic blood pressure (P = 0.004).

In patients with asymptomatic mild to moderate AS, MAC is more prevalent in those individuals with tricuspid AV, independent of age, and systolic blood pressure. Whether the degree of MAC may be a surrogate for atherosclerosis, and predict the subset of patients who will respond to statin therapy in preventing the progression of AS, remains to be determined.

Fourteen patients with ischaemic cardiomyopathy who underwent SkM injection were compared with 28 non-randomized control patients matched for age, sex, location, and extent of myocardial infarction. Contrast echocardiography and tissue Doppler imaging (TDI) was performed to compare global and regional LV function. At 4-year follow-up, three patients (21%) had died in the treated group and 11 patients (39%) in the control group (P = 0.8). In the survivors, LV ejection fraction (EF) was 35 ± 10% and 37 ± 9% in the SkM group and 36 ± 8% and 36 ± 6% in the controls at baseline and 4 years follow-up, respectively (P = 0.96 between groups at follow-up). TDI-derived systolic velocity in the injected sites was 5.4 ± 1.8 cm/s in the SkM group when compared with 5.1 ± 1.6 cm/s in corresponding sites in the control group (P = 0.47). None of the secondary endpoints showed a difference between the groups. However, in the patients fitted with an internal cardioverter defibrillator, more arrhythmias leading to interventions occurred in the treated group than in the control group, 87% and 13%, respectively (P = 0.015).

Percutaneous intramyocardial SkM injection in ischaemic cardiomyopathy has no sustained positive effect on resting global or regional LV function, respectively, at 4-year follow-up. Moreover, the procedure may induce a higher risk of developing serious arrhythmias, but larger patient series are required before more precise characterization of the safety and efficacy profile of the procedure is possible.

In 292 case and 316 control families, maternal peri-conception medicine use and low dietary intake of nicotinamide (≤13.8 mg/day) were independently associated with CHD risk [odds ratio (95% confidence interval) 1.6 (1.1–2.3) and 1.5 (1.03–2.3), respectively]. No significant association was found for the NNMT AG/AA genotype in mothers [0.9 (0.7–1.3)], fathers [1.1 (0.8–1.6)], or children [1.1 (0.8–1.6)]. However, the combination of peri-conception medicine use, low dietary nicotinamide intake, and the NNMT AG/AA genotype in mothers or children showed risk of 2.7 (1.02–8.1) and 8.8 (2.4–32.5), respectively.

Children carrying the NNMT A allele face additional CHD risk in combination with peri-conception exposure to medicines and/or a low dietary nicotinamide intake. These findings provide a first set of data against which future studies with larger sample sizes can be compared with.

Open-trial randomized 1028 patients with stable angina to group A (‘non-selective’—clopidogrel 600 mg >6 h before CAG; n = 513) or group B (‘selective’—clopidogrel 600 mg in the cath-lab after CAG, only in case of PCI; n = 515). Combined primary endpoint was death/periprocedural myocardial infarction (MI)/stroke/re-intervention within 7 days. Secondary endpoints were troponin elevation and bleeding complications. Primary endpoint occurred in 0.8% group A patients vs. 1% group B (P = 0.749; 90% CI for the percentage difference –1.2–0.8). Periprocedural troponin elevation (>3x ULN) was detected in 2.6% group A vs. 3.3% group B (P = 0.475; 90% CI –2.5–1.0). Bleeding complications occurred in 3.5% group A patients vs. 1.4% group B (P = 0.025). After adjustment for covariates and factors that may influence the bleeding risk, patients in group A were shown to have more likely bleeding complications when compared with group B (OR = 3.03; 95% CI 1.14–8.10; P = 0.027).

High (600 mg) loading dose of clopidogrel before elective CAG increased the risk of minor bleeding complications, while the benefit on periprocedural infarction was not significant. Clopidogrel can be given safely in the catheterization laboratory between CAG and PCI in chronic stable angina patients.

Thirty-nine patients were randomized to simvastatin 80 mg daily (S80; n = 20) or ezetimibe 10 mg and simvastatin 10 mg daily (E10/S10; n = 19) for 6 weeks, aiming at similar cholesterol reduction. Endothelial function, evaluated by brachial artery flow-mediated vasodilatation (FMD) and the effect of endothelin receptor blockade, serum lipids, and inflammatory markers were evaluated at baseline and follow-up. At follow-up, low-density lipoprotein cholesterol decreased from 3.1 (2.8–3.4) (median and quartiles) to 1.5 mmol/L (1.4–1.7) and from 3.0 (2.5–3.4) to 1.3 mmol/L (1.1–1.8), in the S80 and E10/S10 groups, respectively. In the entire study group, FMD increased from 4.3% (3.4–6.1) at baseline to 5.5% (3.4–6.6) at follow-up, while C-reactive protein decreased from 3.1 (1.7–7.6) to 2.3 mg/L (0.9–6.5). The changes in FMD and C-reactive protein from baseline to follow-up were not significantly different between patients on S80 and E10/S10 groups. Endothelin blockade enhanced endothelium-dependent vasodilatation both at baseline and follow-up.

Lipid lowering is more important than pleiotropic effects of statins for improvement in endothelial function and inflammatory markers in patients with dysglycaemia and CAD.

A total of 118 patients with AF (74 paroxysmal AF, 44 persistent AF) underwent transthoracic echocardiography with Doppler-derived SR examinations before and after ablation as well as during 3 months of follow-up (FU). Peak SR and strain (S) were measured at each left atrium (LA) segment (septal, lateral, anterior, inferior) during systole (LAs) and at early (LAe) and late diastole (LAa). Clinical and echocardiographic parameters of patients with maintained sinus rhythm during FU were compared with those with recurrent AF and controls (n = 25 patients). Of 118 patients 82 (69%) showed stable sinus rhythm during FU. Atrial myocardial properties after catheter ablation differed significantly in patients with paroxysmal AF (SR-LAs 2.5 s^–1, S-LAs 30%, SR-LAa –2.2 s^–1) from patients with persistent AF (SR-LAs 2.3 s^–1, S-LAs 25%, SR-LAa –1.9 s^–1) and controls (SR-LAs 4.1 s^–1, S-LAs 88%, SR-LAa –2.9 s^–1) (P = 0.011). Best individual predictors of sinus rhythm maintenance were cut-off values of >2.25 s^–1 for septal and inferior SR-LAs and of >19.5% for inferior S-LAs (P < 0.001). LA deformation properties increased in patients with maintained sinus rhythm during FU in contrast to patients with recurrent AF (P = 0.001).

SR imaging enables the quantitative assessment of the LA function and can be considered as a potential marker of atrial reverse remodelling. Patients with higher atrial S and SR after catheter ablation appear to have a greater likelihood of maintenance of sinus rhythm. This may have further implications for the anticoagulation regime and the risk of cardioembolic complications.

Immunoassays against calponin (acidic, basic, and neutral isoforms) were developed and the levels were compared in a convenience sample of 59 patients with radiographically proven AD [34 males, age 59 ± 15 (SD) years] vs. 158 patients suspected of having AD at presentation (116 males, age 63 ± 15 years) but whose final diagnosis was not AD. Basic calponin, which is the most specific and abundant in smooth muscle, and acidic calponin, respectively, showed greater than two-fold and three-fold elevations in patients with acute AD. Diagnostic performance as determined by receiver-operating characteristics curve analysis showed that both acidic and basic calponin have the potential to detect AD in the first 24 h [respective areas under the curve (AUCs) 0.63 and 0.58], with superior performance of basic calponin (when compared with acidic) in the initial 6 h (respective AUCs 0.63 and 0.67).

Circulating calponin levels were elevated in acute AD compared with controls. These biomarkers have the potential for use as an early diagnostic biomarker for acute AD.

In 108 apparently healthy male marathon runners aged ≥50 years, with ≥5 marathon competitions during the previous three years, the running history, Framingham risk score (FRS), CAC, and presence of myocardial late gadolinium enhancement (LGE) were measured. Control groups were matched by age (8:1) and FRS (2:1) from the Heinz Nixdorf Recall Study. The FRS in marathon runners was lower than in age-matched controls (7 vs. 11%, P < 0.0001). However, the CAC distribution was similar in marathon runners and age-matched controls (median CAC: 36 vs. 38, P = 0.36) and higher in marathon runners than in FRS-matched controls (median CAC: 36 vs. 12, P = 0.02). CAC percentile values and number of marathons independently predicted the presence of LGE (prevalence = 12%) (P = 0.02 for both). During follow-up after 21.3 ± 2.8 months, four runners with CAC ≥ 100 experienced coronary events. Event-free survival was inversely related to CAC burden (P = 0.018).

Conventional cardiovascular risk stratification underestimates the CAC burden in presumably healthy marathon runners. As CAC burden and frequent marathon running seem to correlate with subclinical myocardial damage, an increased awareness of a potentially higher than anticipated coronary risk is warranted.

A total of 142 patients (53 men, 89 women; mean ± SD age, 49.3 ± 11.7 years) with early CAD simultaneously underwent intravascular ultrasonography and coronary endothelial function assessment. Atheroma burden in the left main and proximal left anterior descending (LAD) arteries was significantly greater in men than women (median, 23.0% vs. 14.1%, P = 0.002; median, 40.1% vs. 29.3%, P = 0.001, respectively). Atheroma eccentricity in the proximal LAD artery was significantly higher in men than women (median, 0.89 vs. 0.80, P = 0.04). The length of the coronary segments with endothelial dysfunction was significantly longer in men than women (median, 39.2 vs. 11.1 mm, P = 0.002). In contrast, maximal coronary flow reserve was significantly lower in women than men (2.80 vs. 3.30, P < 0.001). Sex was an independent predictor of atheroma burden in the left main and proximal LAD arteries (both P < 0.05) by multivariate analysis.

Men have greater atheroma burden, more eccentric atheroma, and more diffuse epicardial endothelial dysfunction than women. These results suggest that men have more severe structural and functional abnormalities in epicardial coronary arteries than women, even in patients with early atherosclerosis, which may result in the higher incidence rates of CAD and ST-segment myocardial infarction in men than women.

Data from emergency room resuscitation records were collected throughout the year from all hospitals in the West of Ireland and recorded according to pre-specified criteria. Hospital records of survivors were analysed. Simultaneously, autopsy reports from all pathology laboratories in the region were systematically reviewed and cases of SCD identified. Cardiac arrest associated with non-cardiac pathology was excluded. The population base was 414 277. There were 212 recorded cases of out-of-hospital SCD; 160 (75.5%) were male and the mean age was 63.3 years. The incidence rate was 51.2/100 000/year. The most common aetiology was coronary artery disease (161 cases; 75.9%). The majority of cases occurred in the home (152, 71.7%). Thirteen (6.1%) patients survived to admission of whom eight (3.8%) were alive at discharge. All survivors had ventricular fibrillation as the presenting rhythm.

The burden of SCD in the West of Ireland is considerable. The vast majority of cases occur in the home. Survival rates in this rural population cohort remain low.

Patients with a body mass index ≥30 or >27 kg/m² with treated/untreated hypertension, dyslipidaemia, or both, were randomized to double-blind treatment with placebo, rimonabant 5 or 20 mg once daily plus a calorie-restricted diet for 2 years. Weight loss from baseline to 2 years in the intention-to-treat population was significantly greater with rimonabant 20 mg (mean ± SD: –5.5 ± 7.7 kg; P < 0.001) and 5 mg (–2.9 ± 6.5 kg; P = 0.002) than placebo (–1.2 ± 6.8 kg). Rimonabant 20 mg produced significantly greater improvements than placebo in waist circumference, high-density lipoprotein cholesterol, triglycerides, fasting glucose and insulin levels, insulin resistance, and metabolic syndrome prevalence. Rimonabant 20 mg produced clinically meaningful improvements in all Impact of Weight on Quality of Life-Lite questionnaire domain scores at 2 years. Rimonabant was generally well tolerated and rates of adverse events, including depressed mood disorders and disturbances were similar to placebo during year 2. Proportions of patients with clinically significant depression (Hospital Anxiety and Depression Scale score >11) were similar in all treatment groups.

Rimonabant 20 mg over 2 years promoted clinically relevant and durable weight loss and improvements in cardiometabolic risk factors.

In 2190 FH patients, we genotyped six RAAS polymorphisms and five adrenalin/noradrenalin polymorphisms. For each patient, we calculated two gene-load scores by counting the number of risk genotypes within each pathway. Four of the six RAAS polymorphisms and none of the polymorphisms in the adrenalin/noradrenalin system were significantly associated with CHD (P < 0.05). The RAAS gene-load score was significantly associated with CHD (P_{linear trend} < 0.001): in patients with a gene-load score of 5 or 6, the CHD risk was 2.3 times as high as in patients with a score of 0 or 1. The gene-load score of the adrenalin/noradrenalin system was not associated with CHD.

Genetic variation in the RAAS contributes gene-dose dependently to CHD risk in patients with FH, whereas genetic variation in the adrenalin/noradrenalin system is not associated with CHD.

We analysed outcomes in the Candesartan in Heart failure—Assessment of Reduction in Mortality and morbidity (CHARM) programme which randomized 7599 patients with symptomatic HF and a broad range of EF. The prevalence of diabetes was 28.3% in patients with preserved EF (>40%) and 28.5% in those with low EF (≤40%). Diabetes was associated with a greater relative risk of CV death or HF hospitalization in patients with preserved EF [hazard ratio (HR) 2.0 (1.70–2.36)] than in patients with low EF [HR 1.60 (1.44–1.77); interaction test P = 0.0009]. For all-cause mortality, the risk conferred by diabetes was similar in both low and preserved EF groups. The effect of candesartan in reducing CV morbidity and mortality outcomes was not modified by having diabetes at baseline (P = 0.09 test for interaction).

Diabetes was an independent predictor of CV morbidity and mortality in patients with HF, regardless of EF. The relative risk of CV death or HF hospitalization conferred by diabetes was significantly greater in patients with preserved when compared with those with low EF HF.

We measured baseline total- and HMW-adiponectin in 1051 patients aged 30–70 years with incident CHD and a prospective follow-up was conducted [median: 56.6 months (interquartile range: 53.2; 57.5)]. During this period, 95 patients (incidence: 22.3/1000 patient years) experienced a secondary cardiovascular disease (CVD) event. After adjustment by Cox proportional hazard models, neither total- nor HMW-adiponectin was associated with secondary CVD events. In contrast, LDL-cholesterol and markers of atherogenic dyslipidaemia were independently associated with secondary CVD events (relative risk per unit increase: LDL-cholesterol: 1.54; 95%CI 1.18–2.01; P = 0.001, triglycerides: 1.58; 95%CI 1.31–1.90; P < 0.0001 and HDL-cholesterol: 0.34; 95%CI 0.14–0.79; P = 0.01).

Measurement of total- and HMW-adiponectin may add no significant value to risk stratifications in patients with incident CHD. In contrast, approaching atherogenic dyslipidaemia may represent a promising target in secondary prevention programs for high-risk patients.

Data from 1285 consecutive patients implanted with CRT devices are presented: 1042 patients were in sinus rhythm (SR) and 243 (19%) in AF. Rate control in AF was achieved by either ablating the AVJ in 118 patients (AVJ-abl) or prescribing negative chronotropic drugs (AF-Drugs). Compared with SR, patients with AF were significantly older, more likely to be non-ischaemic, with higher ejection fraction, shorter QRS duration, and less often received ICD back-up. During a median follow-up of 34 months, 170/1042 patients in SR and 39/243 in AF died (mortality: 8.4 and 8.9 per 100 person-year, respectively). Adjusted hazard ratios were similar for all-cause and cardiac mortality [0.9 (0.57–1.42), P = 0.64 and 1.00 (0.60–1.66) P = 0.99, respectively]. Among AF patients, only 11/118 AVJ-abl patients died vs. 28/125 AF-Drugs patients (mortality: 4.3 and 15.2 per 100 person-year, respectively, P < 0.001). Adjusted hazard ratios of AVJ-abl vs. AF-Drugs was 0.26 [95% confidence interval (CI) 0.09–0.73, P = 0.010] for all-cause mortality, 0.31 (95% CI 0.10–0.99, P = 0.048) for cardiac mortality, and 0.15 (95% CI 0.03–0.70, P = 0.016) for HF mortality.

Patients with HF and AF treated with CRT have similar mortality compared with patients in SR. In AF, AVJ ablation in addition to CRT significantly improves overall survival compared with CRT alone, primarily by reducing HF death.

Fifty consecutive patients presenting with congestive heart failure (age: 58 ± 16 years) underwent simultaneous right heart catheterization and transthoracic echocardiography. Left ventricular (LV) volumes, mass, EF, meridional, and circumferential wall stress were measured in addition to haemodynamic measurements. 2-D speckle tracking was applied to measure longitudinal, radial, and circumferential strain and twist. Twist was reduced only in patients with systolic heart failure (SHF: 5 ± 2°, DHF: 13 ± 6°, control: 14 ± 5°, P < 0.001). Circumferential strain was not different between DHF (–15 ± 5%) and control groups (–20 ± 3%, P > 0.05), though it was significantly lower in patients with SHF (–7 ± 3%, P < 0.05). Importantly, longitudinal (DHF:–12%, SHF: –4%, control: –19%, P < 0.001) and radial (DHF: 28 ± 9%, SHF: 14 ± 8%, control: 47 ± 7%, P < 0.001) strains were significantly lower in both heart failure groups than in controls, and were depressed to a larger extent in SHF patients than in those with DHF (both P < 0.05).

LV longitudinal and radial strains are reduced, but circumferential deformation and twist are normal in DHF patients. On the other hand, in patients with SHF, longitudinal, radial, and circumferential deformation, and twist are all reduced. Multivariable regression analysis suggests that preserved LV twist and circumferential strain may contribute to normal EF in patients with DHF.

We report clinical outcomes in young (<70), elderly (70–80), and very elderly (>80 years) patients with high-risk NSTE-ACS enrolled in GRACE between 1999 and 2006. Six month data were available in 18 466 patients (27% elderly, 16% very elderly). Elderly and very elderly patients were less likely to receive evidence-based treatments at discharge and had a longer hospital stay (6 vs. 5 days). Angiography was performed more frequently in younger patients (67 vs. 33% in very elderly, 55% in elderly; P < 0.0001). Multiple logistic regression analysis confirmed the benefit of revascularization on the primary study endpoint (6-month stroke, death, myocardial infarction) in young [odds ratio (OR) 0.69, 95% confidence interval (CI) 0.56–0.86], elderly (0.60, 0.47–0.76), and very elderly (0.72, 0.54–0.95) patients. Revascularization was associated with reductions in 6-month mortality (OR 0.52, 95% CI 0.37–0.72 in young; 0.38, 0.26–0.54 in elderly; 0.68, 0.49–0.95 in very elderly). Stroke risk in hospital or at 6 months was not increased by revascularization.

Following presentation with high-risk NSTE-ACS, an evidence-based approach to management was noted less frequently with advancing patient age. Angiography, in particular, was less likely to be undertaken. Revascularization, however, when performed, was associated with significant benefits at 6 months, independent of age, and did not increase risk of stroke.

We determined the positive predictive value (PPV) of PEFA in relation to other risk factors for SCD and outcomes in 179 patients with HCM and no prior history of cardiac arrest. Patients were followed over a mean 4.3 years (range: 1.1–6.3 years). Thirteen patients had SCD-equivalent events: four of these patients died suddenly, three were resuscitated from ventricular fibrillation (VF), and six had implantable cardioverter-defibrillator (ICD) discharges in response to VF. PEFA identified nine of these patients and another 14 non-VF patients yielding a censored PPV of between 0.19 and 0.59 that was greater than the PPV that was the formal stopping point of the trial (0.18). Eighty per cent of patients were followed for 4 years or more. The PPV for the identification of SCD in this group was 0.38 (0.17–0.59). The use of two or more conventional markers to predict SCD identified five patients with SCD-equivalent events in the 4-year follow-up group and 42 other patients without events yielding a PPV of 0.106 (confidence limits 0.02–0.15).

PEFA identifies HCM patients at risk of SCD with greater accuracy than non-invasive techniques and may have an important role in determining indications for ICD prescription.

Ninety-three consecutive patients in sinus rhythm with dilated cardiomyopathy but without suspicion of coronary artery disease (CAD) were enrolled when admitted for angiography. Accuracy of CT to detect significant stenosis (>50% lumen narrowing) was compared with quantitative coronary angiography. IHF was defined as a significant stenosis on left main or proximal left anterior descending artery or two or more vessels. Forty-three out of 1395 segments (3%) were heavily calcified and excluded. CT correctly assessed 103 of 142 (73%) significant stenosis and identified 46 of 50 (92%) patients without and 42 of 43 (98%) patients with CAD, 60 of 62 (97%) patients without and 28 of 31 (90%) patients with IHF. Overall, accuracy, sensitivity, specificity, positive predictive value, and negative predictive value of CT for identifying CAD by segment was 96, 73, 99, 92, and 97%, respectively; by patient was 95, 98, 92, 91, and 98%, respectively; and for identifying IHF was 95, 90, 97, 93, and 95%, respectively.

Non-invasive 64-slice CT assessment of the extent of CAD may offer a valid alternative to angiography for the diagnosis of IHF.

Time to adverse outcomes (death, non-fatal myocardial infarction, or non-fatal-stroke) and predictive values of baseline and follow-up RHR were assessed in INternational VErapamil-SR/trandolapril STudy (INVEST) patients randomized to either a verapamil-SR (Ve) or atenolol (At)-based strategy. Higher baseline and follow-up RHR were associated with increased adverse outcome risks, with a linear relationship for baseline RHR and J-shaped relationship for follow-up RHR. Although follow-up RHR was independently associated with adverse outcomes, it added less excess risk than baseline conditions such as heart failure and diabetes. The At strategy reduced RHR more than Ve (at 24 months, 69.2 vs. 72.8 beats/min; P < 0.001), yet adverse outcomes were similar [Ve 9.67% (rate 35/1000 patient-years) vs. At 9.88% (rate 36/1000 patient-years, confidence interval 0.90–1.06, P = 0.62)]. For the same RHR, men had a higher risk than women.

Among CAD patients with hypertension, RHR predicts adverse outcomes, and on-treatment RHR is more predictive than baseline RHR. A Ve strategy is less effective than an At strategy for lowering RHR but has a similar effect on adverse outcomes.

In this follow-up study we enrolled 17 patients (age 31 ± 22 years, 11 females) with a clinical diagnosis of NMS and two consecutive positive tilt tests. The head-up tilt test was repeated day after day: one session per day. All patients were instructed to continue a programme of daily standing training at home. Follow-up tilt testing was performed after a period of 6 weeks in 14 patients. ECG and finger arterial blood pressure (Portapres) were recorded during subsequent tilt testing. Left ventricular stroke volume (SV), cardiac output, and systemic vascular resistance were computed from the pressure pulsations (Modelflow). Spontaneous cardiac baroreflex sensitivity was estimated by cross-spectral analysis of heart rate (HR) and systolic blood pressure. In all patients, orthostatic tolerance was restored after 4.1 ± 0.9 tilt sessions, median 4. The follow-up tilt test was also negative in all patients. This was accompanied by a significant rise in systemic vascular resistance to compensate for a postural reduction in SV in the sustained head-up tilt position. No evidence could be provided of altered baroreflex control of HR after tilt training.

Tilt training restores orthostatic tolerance at least in part by increasing the amount of vasoconstriction that can ultimately be made available during sustained orthostatic stress. The increased vasoconstrictor reserve is preserved after 6 weeks of continued standing training at home.

Data were analysed of two right-heart catheterizations of 52 patients with pulmonary arterial hypertension and 10 with chronic-thromboembolic PH. The product of R and C (= stroke volume over pulse pressure) did not change during therapy (P = 0.320), implying an inverse relationship. Changes in cardiac index correlated significantly (P < 0.001) with changes in R (R² = 0.37), better with changes in C (R² = 0.66), and best with changes in both (R² = 0.74).

During therapy for PH, R and C remain inversely related. Therefore, changes in both R and C better explain changes in cardiac index than either of them alone. Not only resistance but also compliance plays a prominent role in PH especially in an early stage of the disease.

Sixty-six consecutive patients >70 years (83 ± 6 years) were referred for severe AS. Their mortality risk predicted by the logistic European System for Cardiac Operative Risk Evaluation and the Society of Thoracic Surgeons-Predicted Risk of Mortality scores were on average 20 ± 14% and 17 ± 7%, respectively. Thirty-nine patients (59%) were considered at high-risk for surgery or inoperable after multidisciplinary evaluation: 12 (31%) underwent a transfemoral aortic valve implantation and 27 were considered unsuitable and treated medically (n = 16) or with valvuloplasty (n = 7), or were re-directed towards surgery (n = 4). The 27 other patients underwent valve replacement. In-hospital mortality was 9% (6 of 66). There were three hospital deaths in patients treated percutaneously, two in those treated medically, and one after surgery. At 6 months, 10% (6 of 60) of the survivors died: two after valvuloplasty and four after medical treatment.

A large proportion of elderly patients referred for management of severe AS have a high-risk profile. The availability of percutaneous valvular interventions increases the number of those who are offered interventions.

In all, 88 of 311 men developed hypertension during the follow-up. A 1-SD increment in triglyceride concentrations was associated with a 1.6-fold [95% CI(confidence interval) 1.2–2.3] increased risk of developing hypertension, independently of features related to the metabolic syndrome. In separate multivariable models, the triglyceride content of high-density lipoprotein (HDL) cholesterol and apolipoprotein B concentrations were also associated with new-onset hypertension. In a stepwise backwards logistic regression model, concentrations of low-density lipoprotein (LDL) cholesterol [odds ratio (OR) 1.3, 95% CI 1.0–1.7 for a 1-SD change] and triglyceride content of HDL cholesterol (OR) 1.5, 95% CI 1.1–1.9) were positively associated with incident hypertension, whereas HDL concentrations (OR 0.7, 95% CI 0.5–0.9) seemed protective. In factor analyses, elevated triglyceride levels and related disturbances in lipid and cholesterol metabolism were associated with new-onset hypertension.

Dyslipidaemia characteristic of the metabolic syndrome predicts the development of hypertension during a 7-year follow-up of eastern Finnish men, independently of features related to insulin resistance. The recognition of dyslipidaemia and initiation of lifestyle treatment even in the absence of hypertension is likely to reduce the long-term burden of cardiovascular disease.