Apical two- and four-chamber views (A2C and A4C) and real-time 3D datasets (Toshiba Artida 4D System) obtained in 43 patients with a wide range of LV size and function were analysed to measure LV end-systolic and end-diastolic volumes (ESV and EDV) using 2D and 3D-STE techniques. Short-axis CMR images (Siemens 1.5T scanner) acquired on the same day were analysed to obtain ESV and EDV reference values using the method of disks approximation. Reproducibility of both STE techniques was assessed using repeated measurements. While 2D-STE correlated well with CMR (r: 0.72–0.88), it underestimated LV volumes with relatively large biases (10–30 mL) and wide limits of agreement (SD: 36–51 mL), with A2C-derived measurements being worse than A4C values. The 3D-STE measurements showed higher correlation with CMR (0.87–0.92), and importantly smaller biases (1–16 mL) and narrower limits of agreement (SD: 28–37 mL). In addition, 3D-STE showed lower inter- and intra-observer variability (11–14% and 12–13%), than 2D-STE (16–17% and 12–16%, respectively).

This is the first study to validate the new 3D-STE technique for LV volume measurements and demonstrate its superior accuracy and reproducibility over previously used 2D-STE technique.

Perioperative ECGs, creatinine kinase MB fraction, and cardiac troponin I (cTnI) were assessed in 545 primary CABG patients. None of the ECG criteria for myocardial injury predicted mortality or HLOS. However, post-operative day (POD) 1 cTnI levels independently predicted 5-year mortality (hazard ratio = 1.42; 95% CI 1.14–1.76 for each 10 µg/L increase; P = 0.009), while adjusting for baseline demographic characteristics and perioperative risk factors. Moreover, cTnI was the only biomarker that significantly improved the prediction of 5-year mortality estimated by the logistic Euroscore (P = 0.02). Furthermore, the predictive value of cTnI for 5-year mortality was replicated in a separately collected cohort of 1031 CABG patients using cardiac troponin T.

Electrocardiogram diagnosis of post-operative myocardial injury after CABG does not independently predict an increased risk of 5-year mortality or HLOS. Conversely, cTnI is independently associated with an increased risk of mortality and prolonged HLOS.

The T111I variant was genotyped in case–control studies of CHD nested within the Diet, Cancer, and Health study with 998 cases, Nurses’ Health Study with 241 cases, and Health Professionals Follow-up Study with 262 cases. The minor allele frequency in the combined pool of controls was 0.29. The T111I variant was not associated with HDL-C or any other lipid and lipoprotein measures. Compared with wildtype homozygotes, the pooled estimate for risk of CHD was 0.95 (0.85–1.06) per T111I allele.

Our analysis among healthy Caucasian men and women from three independent studies does not support an association between the T111I variant and HDL-C, other plasma lipids, or risk of CHD.

In 454 patients undergoing PCI, acetylcholine (10^–6 to 10^–4 M) was infused in a coronary segment without significant CAD. Changes in coronary diameter were measured and an intravascular ultrasound examination (IVUS) was performed. On top of statin therapy, patients were randomized in a double-blind fashion to placebo or nifedipine GITS 30–60 mg/day and followed for 18–24 months.

Blood pressure was lower on nifedipine than on placebo by 5.8/2.1 mmHg (P < 0.001) as was total and LDL cholesterol (4.8 mg/dL; P = 0.495), while HDL was higher (3.6 mg/dL; P = 0.026). In the most constricting segment, nifedipine reduced vasoconstriction to acetylcholine (14.0% vs. placebo 7.7%; P < 0.0088). The percentage change in plaque volume with nifedipine and placebo, respectively, was 1.0 and 1.9%, ns.

The ENCORE II trial demonstrates in a multi-centre setting that calcium channel blockade with nifedipine for up to 2 years improves coronary endothelial function on top of statin treatment, but did not show an effect of nifedipine on plaque volume.

The CAPTIM study included 840 patients managed in a pre-hospital setting within 6 h of an acute ST-segment elevation myocardial infarction. Patients were randomized to either a primary angioplasty (n = 421) or a pre-hospital fibrinolysis (rt-PA) with immediate transfer to a centre with interventional facilities (n = 419). Long-term follow-up was obtained in blinded fashion from 795 patients (94.6%). Using an intent-to-treat analysis, all-cause mortality at 5 years was 9.7% in the pre-hospital fibrinolysis group when compared with 12.6% in the primary angioplasty group [HR 0.75 (95% CI, 0.50–1.14); P = 0.18]. For patients included within 2 h, 5 year mortality was 5.8% in the pre-hospital fibrinolysis group when compared with 11.1% in the primary angioplasty group [HR 0.50 (95% CI, 0.25–0.97); P = 0.04], whereas it was, respectively, 14.5 and 14.4% in patients included after 2 h [HR 1.02, (95% CI 0.59–1.75), P = 0.92].

The 5-year follow-up is consistent with the 30-day outcomes of the trial, showing similar mortality for primary percutaneous coronary intervention and a policy of pre-hospital lysis followed by transfer to an interventional center. In addition, for patients treated within 2 h of symptom onset, 5-year mortality was lower with pre-hospital lysis.

All hearts were exposed to 30 min regional ischaemia followed by 120-(isolated hearts) or 180-(in situ hearts) min reperfusion. BAY-58 (1–50 nM) infused for 60 min starting 5 min before reperfusion significantly reduced infarction from 33.0 ± 3.2% in control isolated rabbit hearts to 9.5–12.7% (P < 0.05). In a more clinically relevant in situ rabbit model, infarct size was similarly reduced with a loading dose of 53.6 µg/kg followed by a 60 min infusion of 1.25 µg/kg/min (41.1 ± 3.1% infarction in control hearts to 16.0 ± 4.4% in treated hearts, P < 0.05). BAY-58 similarly decreased infarction in the isolated rat heart, and protection was abolished by co-treatment with a protein kinase G (PKG) antagonist, or a mitochondrial K_ATP channel antagonist. Conversely, N-nitro-L-arginine-methyl-ester-hydrochloride, a NO-synthase inhibitor, failed to block BAY-58's ability to decrease infarction, consistent with the latter's putative NO-independent activation of PKG. Finally, BAY-58 increased myocardial cGMP content in reperfused hearts while cAMP was unchanged.

When applied at reperfusion, BAY-58 is an effective cardioprotective agent with a mechanism similar to that of ischaemic pre-conditioning and, hence, should be a candidate for treatment of acute myocardial infarction in man.

Personal exposures to PM₁₀, PM_2.5, and PM_0.25 was measured over 24 h in 39 patients (36 males, 3 females; mean age 60.3 years) with prior myocardial infarction (>6 months). Simultaneously, a 24 h ECG was recorded and then analysed for HRV and ventricular arrhythmias. Breath condensate and blood samples also were collected at the end of monitoring to measure several indexes of inflammation. Negative correlation was found between HRV and exposure to PM_0.25 in a group of patients not taking β-blockers. More severe ventricular arrhythmias were observed at the highest concentrations of PM₁₀ and PM_2.5. Indexes of inflammation in either breath condensate or blood did not correlate with PM exposures.

Our study shows that exposure to ultrafine particles is associated with autonomic dysregulation in selected patients with myocardial infarction. More severe arrhythmias occur at the highest exposures to larger particles. Nevertheless, the underlying mechanisms remain hypothetical because inflammation may be evoked by PM or be related to the disease itself.

Since 1996, all patients with ischaemic heart disease, receiving ICD therapy for secondary prevention of sudden death, were included in the current study. Patients were evaluated at implantation and during long-term follow-up. A total of 456 patients were included in the analysis and followed for 54 ± 35 months. During follow-up, 100 (22%) patients died and ICD therapy was noted in 216 (47%) patients, of which 138 (30%) for fast, potentially life-threatening ventricular arrhythmia. Multivariate analysis revealed a history of atrial fibrillation or flutter (AF), ventricular tachycardia as presenting arrhythmia, and wide QRS and poor left ventricular ejection fraction as independent predictors of life-threatening ventricular arrhythmias. The strongest predictor was AF with a hazard ratio of 2.1 (95% confidence interval 1.3–3.2). On the basis of the available clinical data, it was not possible to identify a group which exhibited no risk on recurrence of potentially life-threatening ventricular arrhythmias.

Ischaemic secondary prevention ICD recipients exhibit a high recurrence rate of potentially life-threatening ventricular arrhythmias. Factors that increase risk can be identified but, even with these factors, it was not possible to distinguish a recurrence-free group.

Prevalence and depth of coronary artery bridges (CBs) were assessed in 255 hearts, including 115 with HCM (median age 29, range 5–90; 75% male), and 140 controls. Coronary artery bridges were more common in HCM (47/115; 41%) than in patients who died of a variety of non-HCM-related causes (21/100; 21%; P = 0.002), or in patients with congenital aortic stenosis and left ventricular (LV) hypertrophy (5/40; 12%; P = 0.001). Among the HCM hearts, CBs were present in 33 of 77 patients (43%) with sudden death, in 10 of 27 (37%) with heart failure death (or heart transplantation), and in 4 of 11 (36%) with other modes of death (P = 0.826). Deeply embedded CBs (≥2 mm) occurred with similar frequency in HCM patients with sudden (21 of 77; 27%) or heart failure death (5 of 27; 13%; P = 0.191). In sudden death patients, the presence of CB was unrelated to gender (33% in women and 45% in men, P = 0.406) and age (41% <18 years vs. 44% ≥18 years; P = 0.827).

In this morphological analysis of more than 250 hearts, CBs are a frequent component of phenotypically expressed HCM, and more common than in other disorders with or without LV hypertrophy. Although no systematic association with HCM-related sudden death is evident, our findings do not exclude the possibility that CB could contribute to increased risk in some individual patients, potentially impacting management decision-making on a case-by-case basis.

The study included 15 patients. Tako-tsubo cardiomyopathy was diagnosed by coronary angiography and ventriculography. Cardiac MRI was performed within 24 h of admission. Endomyocardial biopsies were taken during the acute phase and after recovery. The content of fibrosis was determined by immunohistochemical staining of collagen-1. In the acute phase, cardiac MRI revealed LGE in five patients. This was completely reversed at follow-up [14, inter-quartile range (IQR) 11–14.5 days]. All patients showed a significant increase of collagen-1 compared with control tissue. Moreover, the amount of collagen-1 was significantly higher in LGE positive patients (LGE positive: 18.84, IQR 13.82–19.75 AU/µm²; LGE negative: 7.57, IQR 5.41–9.19 AU/µm², P = 0.001). The presence of LGE was not associated with poorer left ventricular function.

The presence of LGE cannot rule out tako-tsubo cardiomyopathy. Instead it defines a special subgroup of patients with a disproportionate increase of extracellular matrix.

We measured left heart dimensions of 25 healthy twin pairs with a 1.5T MR scanner, analysed with the mass©, Medis Software. We performed heritability analysis and tests for genetic influences shared between cardiac structures. We found that CMR-based heritability estimates (h² = 84%) substantially exceeded estimates based on echocardiography. We also found significant genetic influence on papillary muscle mass (h² = 82%). Bivariate analysis of papillary and LV muscle mass revealed significant genetic influences shared by both phenotypes (genetic correlation 0.59) and suggested an additional genetic component specific to papillary muscle. We observed correlations between body mass index, surface area, and systolic blood pressure with cardiac dimensions, even in this small study. Environmental influences were relevant as well, indicating reciprocal influences on papillary vs. LV muscle mass.

Cardiovascular magnetic resonance, even with few subjects, allows a genetic assessment of cardiac structures that cannot be attained with echocardiography. Hitherto fore unappreciated relationships can be uncovered by this method.

We screened the promoter region of human calmodulin III gene (CALM3) and identified a new –34T>A polymorphism with a T-allele frequency of 0.70. The distribution of CALM3 genotypes differed in 180 unrelated FHC patients carrying a known FHC mutation compared with 134 controls, with higher TT-genotype frequency (0.73 vs. 0.51) and lower frequencies of AT- (0.24 vs. 0.37) and AA genotypes (0.03 vs. 0.11; P = 0.0005). To study whether the –34T>A polymorphism could play a modifier role, patients’ relatives including both affected and healthy carriers were added. Affected carriers had a 0.56 times higher odds of carrying a T allele than healthy carriers (P = 0.053). We then investigated whether the –34T>A polymorphism affects the promoter activity using luciferase reporter vectors containing either CALM3-T or CALM3-A promoters. The activity of CALM3-T was lower than CALM3-A in HEK293 cells (1.00 ± 0.19 vs. 2.31 ± 0.13, P = 0.00001) and in cardiomyocytes (0.96 ± 0.10 vs. 1.33 ± 0.08, P = 0.00727).

These data suggest that the –34T>A CALM3 polymorphism is a modifier gene for FHC, potentially by affecting expression level of CALM3 and therefore Ca²⁺-handling and development of hypertrophy.

PREAMI included 1252 post-AMI patients (age 73 ± 6 years, LV ejection fraction 59.1 ± 7.7%) receiving optimal therapy after AMI, randomized to perindopril 8 mg/day (n = 631) or placebo (n = 621); n = 896 had complete echo-Doppler data. Outcome measures were clinical [death, heart failure (HF)] and standard echo-Doppler parameters. Pre-discharge LV end-diastolic volume (LVEDV) was similar: 81.1 ± 23.1 (perindopril) and 79.6 ± 22.7 mL (placebo). At 6 months and 1 year, LVEDV remained unchanged with perindopril (81.2 ± 24.4 and 81.8 ± 26.8 mL, respectively), but increased with placebo (83.0 ± 25.3 and 83.6 ± 25.7 mL, respectively, both P < 0.001 vs. baseline). Perindopril reduced cardiac sphericity vs. placebo (P = 0.015 at 6 months; P = 0.020 at 1 year). Classification regression tree analysis showed treatment as the most important predictor of remodelling. Multiple pre-discharge echocardiographic variables predicted the death/HF endpoint, independently of treatment (P ≤ 0.05).

Remodelling occurs in post-AMI in elderly patients with normal LV function. Echo-Doppler variables at baseline have prognostic implications. Treatment with perindopril reduces progressive LV remodelling that can occur even in the case of small infarct size.

The EVEREST trial randomized 4133 patients hospitalized for worsening HF and low ejection fraction (≤40%) to tolvaptan, a vasopressin antagonist, or placebo. Following discharge, BW was assessed at 1, 4, and 8 weeks, and every 8 weeks thereafter. A time-dependent Cox proportional Hazard model explored the relationship between change in BW at 60, 120, and 180 days from discharge and the risks of HF hospitalization, cardiovascular (CV) hospitalization, and all-cause mortality. For subjects re-hospitalized for heart failure at 60, 120, and 180 days after discharge, mean BW increase prior to the event was 1.96, 2.07, and 1.97 kg, respectively, compared with 0.74, 0.90, and 1.04 kg in patients without re-hospitalization (P < 0.001 all groups). A similar pattern was observed with CV hospitalization. However, increases in BW were not predictive of all-cause mortality.

Increases in BW after hospitalization for worsening HF was predictive of repeat hospitalization events, but not mortality in the post-discharge period.

Ninety-eight patients (14 females, 84 males, mean age: 57.7 years) with MI reperfused with percutaneous coronary intervention (PCI) were studied within the first week (1W) and at 4 months (4M) after the event. T2-weighted MRI was used to differentiate between haemorrhagic (i.e. hypointense core) and non-haemorrhagic infarcts (i.e. hyperintense core). Microvascular obstruction and infarct size were determined on contrast-enhanced MRI, whereas cine MRI was used to quantify LV volumes, mass, and function. Twenty-four patients (25%) presented with a haemorrhagic MI. In the acute phase, the presence of myocardial haemorrhage was related to larger infarct size and infarct transmurality, lower LV ejection fraction, and lower systolic wall thickening in the infarcted myocardium (all P-values <0.001). At 4M, a significant improvement in LV ejection fraction in patients with non-haemorrhagic MI was seen (baseline: 49.3 ± 7.9% vs. 4M: 52.9 ± 8.1%; P < 0.01). Left ventricular ejection fraction did, however, not improve in patients with haemorrhagic MI (baseline: 42.8 ± 6.5% vs. 4M: 41.9 ± 8.5%; P = 0.68). Multivariate analysis showed myocardial haemorrhage to be an independent predictor of adverse LV remodelling at 4M (defined as an increase in LV end-systolic volume). This pattern was independent of the initial infarct size.

Myocardial haemorrhage, the presence of which can easily be detected with T2-weighted MRI, is a frequent complication after successful myocardial reperfusion and an independent predictor of adverse LV remodelling regardless of the initial infarct size.

Of the 14 703 patients with heart failure (HF), left ventricular systolic dysfunction, or both enrolled in VALIANT, 1026 (7%) had prior CABG. Prior CABG patients were older [mean age (SD): 67 (10) vs. 65 (12) years; P < 0.0001], had more comorbidity, and more frequent non-Q wave MI (66 vs. 30%; P < 0.0001). At hospital presentation, prior CABG patients received less aspirin (82 vs. 90%; P < 0.0001) and thrombolysis (21 vs. 36%; P < 0.0001), but had a similar rate of primary percutaneous coronary intervention (14 vs. 15%; P = 0.2). Prior CABG patients were more likely to experience the composite outcome of cardiovascular death, MI, HF, resuscitated cardiac arrest, or stroke; 3 year Kaplan–Meier rate, 64 vs. 39% (adjusted hazard ratio 1.29, 95% confidence interval 1.17–1.43; P < 0.0001).

Patients with prior CABG had a worse clinical profile and experienced more fatal and non-fatal outcomes. Greater recognition is necessary for these high-risk patients including optimization of evidence-based secondary preventive therapy.

A multivariable Cox regression model was developed relating 13 independent baseline predictors to 1-year mortality for 13 819 patients with moderate and high-risk ACS enrolled in the Acute Catheterization and Urgent Intervention Triage strategy trial. After adjustment for baseline predictors, Cox models with major bleeding and recurrent MI as time-updated covariates estimated the effect of these events on mortality hazard over time. Within 30 days of randomization, 705 patients (5.1%) had an MI, 645 (4.7%) had a major bleed; 524 (3.8%) died within a year. The occurrence of an MI was associated with a hazard ratio of 3.1 compared with patients not yet having an MI, after adjustment for baseline predictors. However, MI within 30 days markedly increased the mortality risk for the first 2 days after the event (adjusted hazard ratio of 17.6), but this risk declined rapidly post-infarct (hazard ratio of 1.4 beyond 1 month after the MI event). In contrast, major bleeding had a prolonged association with mortality risk (hazard ratio of 3.5) which remained fairly steady over time throughout 1 year.

After accounting for baseline predictors of mortality, major bleeds and MI have similar overall strength of association with mortality in the first year after ACS. MI is correlated with a dramatic increase in short-term risk, whereas major bleeding correlates with a more prolonged mortality risk.

Fifty-six patients (mean age 55 ± 9 years, 38 men) with chronic ischaemic left ventricular (LV) dysfunction underwent two-dimensional echocardiography and contrast-enhanced magnetic resonance imaging (ceMRI). The extent of myocardial infarction was determined as relative amount of hyperenhancement by ceMRI in a 16-segment LV model (0%, no infarction; 1–50%, non-transmural infarction; 51–100%, transmural infarction). On the basis of two-dimensional echocardiographic parasternal short-axis views peak systolic circumferential strain was determined for the total wall thickness and for each of three myocardial layers (endocardial, mid-myocardial, and epicardial) using an automatic frame-by-frame tracking system of acoustic echocardiographic markers (EchoPAC, GE Ultrasound). In non-transmural infarction impairment of circumferential strain was greater in the endocardial than the epicardial layer, relative reduction compared with control segments, 45% vs. 28% (P < 0.001), respectively. In transmural infarction additional impairment of circumferential strain was greater in the epicardial than the endocardial layer, relative reduction compared with non-transmural infarction 29% vs. 7% (P < 0.001), respectively. Endocardial layer circumferential strain allowed distinction of non-transmural vs. no infarction with higher accuracy than total wall thickness strain [area under the curve (AUC) 0.842 vs. 0.774, respectively, P = 0.001]. Epicardial layer circumferential strain allowed distinction of transmural from non-transmural infarction with higher accuracy than total wall thickness strain (AUC 0.819 vs. 0.762, respectively, P = 0.005).

Non-transmural infarction results in greater functional impairment of the endocardial than of the epicardial myocardial layer. In transmural infarction both layers are affected similarly compared with controls. A layer-specific analysis of myocardial deformation allows accurate discrimination between different transmurality categories of myocardial infarction.

A total of 47 patients with either stable angina or unstable angina, or silent myocardial ischaemia, based on a de novo coronary stenosis that could be covered by a single 18 mm stent in a native coronary artery with a diameter between 3.0 and 3.5 mm were enrolled at three sites. The primary endpoint was in-stent late loss at 4 months. The secondary endpoints include %volume obstruction of the stents assessed by intravascular ultrasound (IVUS) at 4 months and major adverse cardiac events (MACE) at 6 months. Forty-seven patients were enrolled. Procedural success was achieved in 97.9%. At 4-month follow-up, in-stent late loss was 0.99 ± 0.46 mm, whereas in-stent %volume obstruction in IVUS was 34.8 ± 15.8%. At 6 months, there were no deaths, but 2 patients suffered from a myocardial infarction and 11 patients required ischaemia-driven repeat revascularization. The composite MACE rate was 23.4%.

This tacrolimus-eluting stent failed to prevent neointimal hyperplasia, despite the theoretical advantages of the tacrolimus, which has less inhibitory effects on endothelial cells than smooth muscle cells.

Estimated glomerular filtration rate (eGFR), plasma amino terminal pro-brain natriuretic peptide (NT-proBNP), and radionuclide ventriculography were obtained in 1063 patients with MI between 24–96 h of symptom onset. Mortality and HF were documented over follow-up of 9.3 years. Estimated GFR, NT-proBNP, and left ventricular ejection fraction (LVEF) each independently predicted 10 year mortality. Reduced eGFR (below 60 mL/min/1.73 m²) combined with increased NT-proBNP (above 1000 pg/mL) was associated with higher mortality rate compared with preserved eGFR together with lower NT-proBNP (60 vs. 14%, P < 0.001). Similar results for mortality were identified for eGFR combined with LVEF (dichotomized about 50%) (58 vs. 17%, P < 0.001). Corresponding analysis combining eGFR and NT-proBNP to predict HF yielded rates of 34 and 7% for high- and low-risk groups, respectively (P < 0.001). Similar risk stratification for HF was observed when combining eGFR with LVEF (35 vs. 7%, P < 0.001).

Ten year rates of mortality and HF are 5–10 times higher when lower eGFR is present together with increased NT-proBNP or depressed LVEF.

Diet was measured using food-frequency questionnaires. Men were followed for HF through Swedish inpatient and cause-of-death registers from 1 January 1998 to 31 December 2004. We used proportional hazards models adjusted for age and other covariates to estimate hazard ratios (HR). Compared with no consumption, men who ate fatty fish once per week had an HR of 0.88 (95% CI 0.68–1.13). Hazard ratios for consumption two times per week and ≥3 times per week were 0.99 and 0.97, respectively. Hazard ratios across quintiles of marine omega-3 were 1, 0.94 (95% CI 0.74–1.20), 0.67 (95% CI 0.50–0.90), 0.89 (95% CI 0.68–1.16), 1.00 (95% CI 0.77–1.29).

In this population, moderate intake of fatty fish and marine omega-3 fatty acids was associated with lower rates of HF, though the association for fish intake was not statistically significant; higher intake was not associated with additional benefit.

Twenty-six patients with chronic ischaemic cardiomyopathy [ejection fraction (EF) 32 ± 6%, wall motion score index (WMSI) 2.45 ± 0.33] and viable myocardium (low-dose dobutamine echocardiography) were examined at baseline and ≥4 months after revascularization. Diastolic function was assessed by transmitral pulsed-wave Doppler and tissue Doppler imaging (TDI) at the mitral annulus.

At baseline, 62% of patients showed non-restrictive filling (non-RF) pattern, and 38% restrictive filling (RF) pattern. After revascularization, along with improvement in systolic function (EF 43 ± 10%, WMSI 1.78 ± 0.47, P = 0.0002 for both), diastolic filling improved in most patients, with only three patients still exhibiting RF pattern (P = 0.016); furthermore, E' velocity increased (32 ± 42%, P = 0.0028) and E/E' decreased (–19 ± 31%, P = 0.0378) compared with baseline. Left ventricular filling pressure also decreased, from 17.5 ± 6.8 to 13.1 ± 6.5 mmHg (P = 0.005). Improvement of diastolic function by TDI was related to the extent of viability at baseline (P = 0.0098) and to LV reverse remodelling after revascularization (P = 0.0092).

In patients with ischaemic cardiomyopathy, LV diastolic filling may largely improve after revascularization. Improvement of diastolic dysfunction is related to the amount of viable tissue and it may represent an additional advantage of revascularizing dyssinergic but viable myocardium.

One hundred and five patients with unexplained syncope who underwent HUT were included. Fifty-two had a positive test. Receptor genotype determinations were performed in patients and in 121 healthy subjects. Genotype (TT, CC, TC) was determined from DNA leucocytes. The distribution of the polymorphism showed significant (P < 0.0001) difference when the results of HUT were analysed. Fifty-two per cent of patients with a positive HUT had a CC genotype and 34.6% a TC genotype, whereas 13.2% of the patients with a negative HUT had a CC genotype and 71.7% a TC genotype. Patients with a CC genotype had a higher incidence of spontaneous syncopal episodes.

In patients with unexplained syncope, a significant association between high incidence of syncopal episodes, positive HUT, and the presence of the CC variant in the adenosine A_2A receptor gene was elicited.

Obese patients [n = 32, body mass index (BMI) 46.1 ± 5.9 kg/m²] underwent clinical examinations and blood sampling for measurement of glucose and lipid parameters as well as non-traditional cardiovascular risk markers, i.e. high-sensitivity C-reactive protein, plasminogen activator inhibitor-1 (PAI-1), soluble cellular adhesion molecules (CAM), MMP-2, MMP-9, CD40L, and Lp-PLA₂ before and after 1 year following laparoscopic adjustable gastric banding (LAGB), respectively. In patients undergoing LAGB, blood pressure (P < 0.0001) and blood glucose (P = 0.02) were significantly lowered by approximately 16% as well as triglyceride levels by approximately 29% (P = 0.002). In addition to a decrease of the inflammatory and pro-thrombotic marker PAI-1 (P = 0.001), CAMs, and MMP-9 (P = 0.004) were reduced, whereas no change was observed for plasma levels of MMP-2, sCD40L, and Lp-PLA₂ after LAGB, respectively. Individual changes in (ICAM-1) intercellular adhesion molecule-1 (ICAM-1) were related to changes in insulin (fasting insulin) before and after LAGB (r = 0.36 and r = 0.38; both P = 0.04). E-selectin correlated positively with changes in BMI (r = 0.38; P = 0.04 and r = 0.36; P = 0.05), while Lp-PLA₂ concentration was negatively correlated with BMI (r =–0.41; P = 0.02) after 1 year. Changes were comparable in both overweight diabetic and non-diabetic subjects.

LAGB not only induced weight loss but also an improvement in the subclinical pro-inflammatory state. However, concentrations of most of the non-traditional risk factors for plaque instability, i.e. MMP-9, sCD40L, and Lp-PLA₂ remained unchanged.

Four hundred subjects (mean age 79 ± 6 years) were studied. Left ventricular mass was measured echocardiographically in accordance with American Society of Echocardiography and normalized for body height to the 2.7 (LVMI). Global cognitive function was evaluated with the mini-mental state examination (MMSE) (maximum score 30). Dementia was defined as an MMSE score <21. Arterial stiffness was evaluated as carotid–femoral pulse wave velocity by Complior^®. Prevalence of hypertension was 70% and diabetes mellitus was diagnosed in 25%. No significant differences in traditional CV risk factors were observed across LVMI quartiles. Mini-mental state examination showed an inverse trend across LVMI quartiles (the higher the LVMI, the lower the MMSE, P for trend <0.05); systolic and diastolic BP levels were not different across LVMI quartiles. In multivariable logistic regression models, including age, sex, BP levels, and use of antihypertensive drugs as covariates, the highest LVMI was found to be independently associated with a two-fold higher likelihood of having dementia. The association persisted significant even after adjustment for arterial stiffness.

In elderly subjects, LVMI is associated with a progressive cognitive decline. This association is independent of BP levels and/or large artery stiffness.

Retrospective analysis of foetal (n = 602) and neonatal ECHO databases (n = 1477) between 1998 and 2007. Clinical and imaging studies were reviewed for pathology due to or associated with premature closure of the duct. Twelve cases were identified. Eight (1.3%) were diagnosed pre-natally at a median gestational age of 29.0 weeks (range: 20.0–37.5 weeks). Four neonates (0.3%) with significant cyanosis and absence of the arterial duct were also included. The most common ECHO features were: excessive right ventricular (RV) hypertrophy (100%), more than expected tricuspid and pulmonary regurgitation (100% and 92%, respectively), and right atrial dilation (75%). Premature induction of delivery was advised for five patients. Neonatal therapy consisted of observation and oxygen administration (n = 7), ventilation with pulmonary vasodilators (n = 5), and one required extracorporeal membrane oxygenation. There were three deaths due to respiratory failure with severe pulmonary hypertension. During follow-up, two children required additional right heart procedures and one developed a non-compaction cardiomyopathy.

Foetal premature closure of the arterial duct causes stress at different foetal ages and many different levels of the right heart and pulmonary circulation, resulting in a wide range of secondary pathology. Disproportionate RV hypertrophy is the most common finding. Clinical outcomes range from mild symptomatology to lethal respiratory insufficiency.

Two hundred patients were randomized to intracoronary infusion of UNSEL (n = 80) or SEL (n = 80) BM cells or to the control (CTRL) group without BM cell treatment. Primary endpoint: change of LVEF and volumes measured by magnetic resonance imaging before and 6 months after the procedure. After 6 months, LVEF increased by 3% (P = 0.01) in patients treated with UNSEL, 3% in patients receiving SEL (P = 0.04) and remained unchanged in CTRL group (P = 0.73). There were no significant differences in absolute changes of LVEF between the groups. Absolute changes of left ventricular end-systolic volume and left ventricular end-diastolic volume were not significantly different in all groups. Significant increase of LVEF was observed only in patients treated with BM cells who had baseline LVEF < median (37%). Baseline LVEF < median and time from the onset of symptoms to primary percutaneous coronary intervention ≥ median were predictors of LVEF improvement in patients receiving BM cells. There were no differences in major cardiovascular event (death, re-infarction, stroke, target vessel revascularization) between groups.

In patients with AMI and impaired LVEF, treatment with BM cells does not lead to a significant improvement of LVEF or volumes. There was however a trend in favour of cell therapy in patients with most severely impaired LVEF and longer delay between the symptoms and revascularization.

Myocardial perfusion imaging (MPI) was performed acutely to assess area at risk (AAR) before angioplasty and repeated after 30 days to assess FIS (% of LV myocardium), salvage index (% non-infarcted AAR), and left ventricular ejection fraction (LVEF). Late presenters (n = 55) compared with early presenters (n = 341) had larger median FIS [14% (inter-quartile range 3–30) vs. 7% (2–18), P = 0.005], lower salvage index [53% (27–89) vs. 69% (45–91), P = 0.05], and lower LVEF [48% (44–58%) vs. 53% (47–59), P = 0.04]. However, FIS, salvage index, and LVEF correlated weakly with symptom duration (R²-values <0.10). In patients with TIMI-flow 0 (n = 247), late presenters had lower salvage index than early presenters [44% (23–73) vs. 57% (42–86), P = 0.03], but substantial salvage (>50% of AAR) was observed in 41% of late presenters despite total infarct-artery occlusion.

FIS is larger in late presenters (>12 h) than early presenters after primary angioplasty for STEMI. However, substantial myocardial salvage can be obtained beyond the 12 h limit, even when the infarct-related artery is totally occluded.

We analysed the relationship between haemoglobin (Hb) and outcome in 5010 patients with AMI complicated by heart failure in the OPTIMAAL study. In 3921 patients, follow-up Hb levels were available at 365 (±90) days. In a subgroup of 224 patients, iron-related haematinics were assessed at baseline and during follow-up. At baseline, mean Hb was 12.6 ± 1.3 g/dL in women and 13.7 ± 1.4 g/dL in men. Hb < 11.5 g/dL was found in 9.3% of patients (women: 18.2%, men: 5.8%). Lower haemoglobin at baseline was clearly associated with female gender and the presence of diabetes, higher age and Killip class, lower body mass index, systolic blood pressure, total cholesterol, and the absence of current smoking (all P < 0.05). Higher Hb [per one standard deviation (SD)] related to lower mortality [adjusted hazard ratios (HR) 0.88; 95% confidence interval (CI) 0.83–0.93], CHF hospitalizations [HR 0.85 (0.77–0.93)], and all-cause hospitalizations [HR 0.96 (0.92–0.99), all P < 0.05]. In patients without anaemia at baseline, the anaemia incidence after 1 year of follow-up was 10.1% in women and 10.0% in men. Of patients with anaemia at baseline, 65% did not have anaemia at 12 months and 46% did not have anaemia at any time during follow-up (median 3.0 years, inter-quartile range, Q1–Q3 = 2.7–3.3 years). At 12 months, an increase in Hb (per SD) was related to lower mortality [HR 0.73 (0.63–0.85; P < 0.0001)] independent of baseline Hb and other clinical characteristics.

In patients with complicated AMIs, anaemia on admission and/or reductions in haemoglobin during follow-up are independent risk factors for mortality and hospitalization. Studies are warranted to determine whether correcting anaemia after a complicated AMI improves outcome.

Two hundred patients (age 63 ± 10.4, males 75%) undergoing implantation of first-generation DES (Taxus or Cypher stents) were enrolled. We measured serum levels of ECP and total IgE by enzyme-linked immunosorbent assay and of C-reactive protein by high-sensitivity nephelometry prior to percutaneous coronary intervention. A clinical follow-up was planned 18 months after discharge. Major adverse cardiac events (MACEs), such as cardiac death, recurrent myocardial infarction, or clinically driven target lesion revascularization, were the endpoint of the study. Twenty-two patients (11%) had MACEs and showed higher serum levels of ECP compared with those without MACEs [30.5 (14.4–50) vs. 12.2 (4.4–31) µg/L, P = 0.004]. At simple Cox regression analysis, serum levels of ECP were a significant predictor of MACEs (hazard ratio 1.016, 95% confidence interval 1.003–1.03, P = 0.018).

This study shows for the first time an association between baseline ECP levels and the occurrence of MACEs in patients undergoing implantation of DES. Further studies are warranted to establish whether in this setting ECP is a risk marker or plays a contributory pathogenetic role.

This study comprised 83 consecutive patients with NSTEACS who underwent OCT and successful emergent primary stenting. On the basis of post-stent TIMI flow, patients were divided into two groups: no-reflow group (n = 14) and reflow group (n = 69). Thin-cap fibroatheroma (TCFA) was defined as a plaque presenting lipid content for >90°, and with thinnest part of the fibrous cap measuring <70 µm. Thin-cap fibroatheroma were more frequently observed in the no-reflow group than in the reflow group (50% vs. 16%, P = 0.005). The frequency of the no-reflow phenomenon increases according to the size of the lipid arc in the culprit plaque. Final TIMI blush grade also deteriorated according to the increase in the lipid arc. A multivariable logistic regression model revealed that lipid arc alone was an independent predictor of no-reflow (odds ratio 1.018; CI 1.004–1.033; P = 0.01).

Optical coherence tomography can predict no-reflow after percutaneous coronary intervention (PCI) in NSTEACS. The lipid contents of a culprit plaque may play a key role in damage to the microcirculation after PCI for NSTEACS. From our results, it is found that OCT is useful tool for stratifying risk for PCI for NSTEACS.

Endothelium-independent response to intracoronary nitroglycerin and adenosine and endothelium-dependent response to intracoronary acetylcholine (Ach) were assessed in 15 SRL- and 21 CyA- treated subjects with angiographically normal coronary arteries. Baseline mean blood pressure was lower in the SRL group (85.6 ± 10.3 vs. 105.2 ± 8.7 mmHg, P = 0.002). There was no difference between the groups in coronary flow reserve after adenosine administration in multivariable analysis (P = 0.34). Nitroglycerin administration resulted in increase in coronary artery diameter in the SRL compared with the CyA groups (2.79 ± 0.54 vs. 2.57 ± 0.61, P = 0.0036). In 13 SRL-treated subjects without evidence of cardiac allograft vasculopathy (CAV), Ach administration resulted in less epicardial vasoconstriction compared with CyA-treated subjects (2.7 ± 17.7 vs. –15.6 ± 17.2%, P = 0.005). Two SRL-treated subjects with three-dimensional intravascular ultrasound evidence of CAV developed coronary spasm in response to Ach 10^–4. Microvascular endothelial function did not differ between the groups.

Sirolimus immunosuppression is associated with less pronounced coronary epicardial endothelial dysfunction compared with CyA immunosuppression. Improvement of coronary vasomotor function with SRL may be an important mechanism for the prevention of CAV.