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The purpose of this study was to validate existing 12-lead electrocardiographic (ECG) ST-segment elevation myocardial infarction (STEMI) criteria in the diagnosis of acute myocardial infarction (AMI) and the application of similar ST-segment depression (STEMI-equivalent) criteria with contrast-enhanced cardiac magnetic resonance imaging (ceMRI) as the diagnostic gold standard.The admission ECG is the cornerstone in the diagnosis of AMI, and ceMRI is a new diagnostic gold standard that can be used to validate existing and novel 12-lead ECG criteria.One hundred fifty-one consecutive patients with their first hospital admission for chest pain underwent ceMRI. The 116 patients without ECG confounding factors were included in this study, and AMI was confirmed in 58 (50%). The admission ECG was evaluated on the basis of the lead distribution of ST-segment deviation according to current American College of Cardiology/European Society of Cardiology (ACC/ESC) guidelines.A sensitivity of 50% and specificity of 97% for AMI were achieved with the currently applied ST-segment elevation criteria. Consideration of ST-segment depression in addition to elevation increased sensitivity for detection of AMI from 50% to 84% (p0.0001) but only decreased specificity from 97% to 93% (p = 0.50). There were no significant differences in AMI location or size between patients meeting the 12-lead ACC/ESC ST-segment elevation criteria and those only meeting the ST-segment depression criteria.In patients admitted to hospital with possible AMI, the consideration of both ST-segment elevation and depression in the standard 12 lead-ECG recording significantly increases the sensitivity for the detection of AMI with only a slight decrease in the specificity.

Right ventricular systolic dysfunction (RVSD) at baseline (pre-treatment) predicts early death in patients with pulmonary hypertension (PH). However, RVSD can only be detected reliably by prohibitively invasive or expensive techniques. N-terminal B-type natriuretic peptide concentration ([NT-proBNP]) correlates with RV function in PH; however, an [NT-proBNP] threshold that indicates RVSD in individual patients has not previously been determined. Twenty-five patients with PH (pulmonary arterial hypertension (n = 19) or chronic thromboembolic PH (n = 6)) underwent cardiovascular magnetic resonance (CMR) imaging and NT-proBNP measurement at baseline. [NT-proBNP] was correlated against RV dimensions and ejection fraction (RVEF) measured directly by CMR imaging. The ability of NT-proBNP to detect RVSD (defined as a CMR-derived RVEF >2 SDS below control values) was tested and predictors of [NT-proBNP] identified. [NT-proBNP] correlated negatively with RVEF. RVSD was present in nine out of 25 patients. An [NT-proBNP] threshold of 1,685 pg.mL(-1) was sensitive (100%) and specific (94%) in detecting RVSD. RVEF and RV mass index independently predicted [NT-proBNP]. In pulmonary hypertension, a baseline N-terminal B-type natriuretic peptide concentration of >1,685 ng.L(-1) suggests right ventricular systolic dysfunction, and thus an increased risk of early death. N-terminal B-type natriuretic peptide could prove useful as an objective, noninvasive means of identifying patients with pulmonary hypertension who have right ventricular systolic dysfunction at presentation.

Objective: To compare the effect of the dual endothelin A/B receptor antagonist enrasentan with enalapril on left ventricular (LV) remodelling. Methods: Multicentre, randomised, double blind, parallel group study of 72 asymptomatic patients with LV dysfunction. Patients received enrasentan (60–90 mg/day) or enalapril (10–20 mg/day). The primary end point was the change in LV end diastolic volume index (EDVI) after six months’ treatment. Results: LV EDVI increased with enrasentan but decreased with enalapril (3.9 (1.8) v −3.4 (1.4) ml/m 2 , p = 0.001). Enrasentan increased resting cardiac index compared with enalapril (0.11 (0.07) v −0.10 (0.07) l/m 2 , p = 0.04), as well as LV mass index (0.67 (1.6) v −3.6 (1.6) g/m 2 , p = 0.04). Other variables were comparable between groups. Enalapril lowered brain natriuretic peptide more than enrasentan (–19.3 (9.4) v –5.8 (6.9) pg/ml, p = 0.005). Noradrenaline (norepinephrine) (p = 0.02) increased more with enrasentan than with enalapril. Enrasentan was associated with more serious adverse events compared with enalapril (six (16.7%) patients v one (2.8%), p = 0.02); the rate of progression of heart failure did not differ. Conclusion: In asymptomatic patients with LV dysfunction, LV EDVI increased over six months with enrasentan compared with enalapril treatment, with adverse neurohormonal effects. This suggests that enrasentan at a dose of 60–90 mg/day over six months causes adverse ventricular remodelling despite an increase in the resting cardiac index.

The traditional assumption has been that there is a close relationship between the electrical and anatomical axes of the heart. The aim of this study was to test the hypothesis that there is a correlation between the electrical and anatomical axes of the heart, in both the frontal and transverse planes, in healthy subjects.Ninety-four healthy volunteers (48 men, 46 women; age 21-82 years) were studied by cardiac magnetic resonance and 12-lead electrocardiogram. The anatomical axis was determined by cardiac magnetic resonance and projected onto the frontal and transverse orthogonal planes for comparison with the electrical axis in the corresponding planes.The electrical and anatomical axes were in the same range in the frontal plane (mean +/- SD, +39 degrees +/- 31 degrees and +38 degrees +/- 10 degrees), but in different ranges in the transverse plane (mean +/- SD, -30 degrees +/- 18 degrees and +46 degrees +/- 7 degrees). The partial correlation coefficients between electrical and anatomical axes were r = 0.30 (P.01) and r = 0.14 (P = NS) in the frontal and transverse planes, respectively. Age was more strongly correlated to electrical axis than to anatomical axis in the frontal plane.There is only a weak correlation between electrical and anatomical axes in the frontal plane and no correlation in the transverse plane. The change of electrical axis with increased age is not explained only by change in the anatomical axis. The results suggest that there is no simple relationship between the electrical and anatomical axes of the heart.

Background: It has previously been shown that magnetic resonance imaging (MRI) can be used to accurately determine left ventricular (LV) long-axis orientation in healthy individuals. However, the inter- and intra-observer variability in patients with acute coronary syndrome (ACS) and chronic heart failure (CHF) has not been explored. Furthermore, the changes in LV long-axis orientation because of respiration and during the cardiac cycle remain to be determined. Methods: LV long-axis orientation was determined by MRI in the frontal and transverse planes in 44 subjects with no cardiac disease, 20 ACS patients and 13 CHF patients. Changes in LV long-axis orientation because of respiration were assessed in a subset of 25 subjects. Changes during the cardiac cycle were assessed in six subjects from each subject group. Reproducibility was assessed by a re-examination of 17 subjects after 28 days. Results: The inter- and intra-observer variability for LV long-axis orientation was low for all subject groups. The difference between the baseline and the 28 days examinations was -1.4 +/- 5.9 degrees and -0.8 +/- 4.4 degrees in the frontal and transverse planes, respectively. No significant change in LV long-axis orientation was found between end-expiration and end-inspiration (frontal plane, P = 0.63 and transverse plane, P = 0.42; n = 25). No significant difference in change of the LV long-axis orientation during the cardiac cycle was found between the subject groups (frontal plane, chi-square 1.8, P = 0.40 and transverse plane, chi-square 5.7, P = 0.06). Conclusions: There is a low inter-and intra-observer variability and a high reproducibility for determining LV long-axis orientation in patients with no cardiac disease as well as in patients with ACS or CHF. There is no significant change in LV long-axis orientation due to respiration, and only small changes during the cardiac cycle in these groups. (Less)

The relation between matrix metalloproteinase-1 promoter genotype and remodeling was studied in 42 patients after their first acute myocardial infarctions. Patients possessing 2 GG alleles were at increased risk for remodeling compared with homozygotes for the G allele and heterozygotes possessing 1 G and 1 GG allele.

Arterial stiffness has a strong relationship with cardiovascular disease. Pulse wave velocity (PWV) is increasingly used as a measure of arterial stiffness. The calculation of PWV requires accurate measurement of blood flow velocity and aortic length. Using magnetic resonance imaging (MRI), we are able to accurately acquire blood flow velocity and to virtually measure the aortic length inside the central aorta. Manual measurement of aorta length is inaccurate and subjective. In this study, we set out to develop a method which automatically locates the thoracic aorta and measures aortic length, allowing noninvasive measurement of PWV derived from the aortic flow. Our method is novel, efficient and robust. This offers a reliable and convenient tool for PWV measurement allowing detailed non invasive assessment of cardiovascular risk.

Aims To determine the presence and extent of delayed contrast enhancement (DCE) in patients with pulmonary hypertension (PHT) using contrast enhanced-cardiovascular magnetic resonance imaging (ce-CMR). Methods and results Twenty-five patients with PHT underwent ce-CMR and right heart catheterization. Right ventricular (RV) and left ventricular (LV) volumes, ejection fraction, mass, and DCE mass were determined with ce-CMR. Mean pulmonary artery pressure (mean PAP) averaged 43 (12) mmHg and cardiac output 4.3 (1.2) L/min. DCE was demonstrated in 23 out of 25 patients. DCE was confined to the RV insertion points (RVIPs) in seven patients and extended into the interventricular septum (IVS) in the remaining 16 patients. In these 16 patients, septal contrast enhancement was associated with IVS bowing. The extent of contrast enhancement correlated positively with RV end-diastolic volume/body surface area, RV mass, mean PAP, and pulmonary vascular resistance and correlated inversely with RV ejection fraction. Conclusion DCE was present within the RVIPs and IVS of most patients with PHT studied. Extent of DCE correlated with RV function and pulmonary haemodynamics. DCE was associated with IVS bowing and may provide a novel marker for occult septal abnormalities directly relating to the haemodynamic stress experienced by these patients.

Using cardiac magnetic resonance (MR) imaging, a combination of late contrast enhanced MR (ceMR) and cinematographic (CINE) images, a myocardial viability score can be derived. At present this score is produced by visual evaluation of wall motion abnormalities in combination with presence or absence of late hyper enhancement (LE) on ceMR. We set out to develop and validate image processing techniques derived from stereo vision capable of reducing the observer dependence and improving accuracy in the diagnosis of viable myocardium.

Brain- and N-terminal pro brain natriuretic peptide (NT-proBNP) have been identified as promising markers for heart failure. However, previous studies have revealed that they may hold insufficient diagnostic power for implementation into clinical practice because of a significant overlap in the range of plasma levels between healthy subjects and subjects with heart failure. We hypothesized that imprecision of the reference method (ie, the echocardiographic evaluation of left ventricular [LV] function) may have affected results from those earlier studies. We therefore wanted to investigate the diagnostic potential of NT-proBNP with magnetic resonance imaging as the reference method for the cardiac measurements.Forty-eight patients with stable symptomatic heart failure in New York Heart Association functional classifications II to IV were examined once with blood samples and magnetic resonance imaging along with 20 age-matched and gender-matched healthy control subjects.NT-proBNP was associated with LV end-diastolic (r = 0.69; P.0001) and end-systolic (r = 0.73; P.0001) volume indices, LV mass index (r = 0.69; P.0001), and LV ejection fraction (r = -0.75; P.0001). Receiver operating characteristic curves were calculated for the ability of NT-proBNP to detect LV end-diastolic volume index (105 mL. m(-2)[cut-off]; sensitivity/specificity, 82%/87%), LV end-systolic volume index (35 mL. m(-2); sensitivity/specificity, 86%/86%), LV mass index (152 g. m(-2); sensitivity/specificity, 85%/86%), and LV ejection fraction (58%; sensitivity/specificity, 84%/85%) deviating more than 2 standard deviations from control values.NT-proBNP is a powerful marker for LV dimensions and systolic function in patients with heart failure and discriminates well between healthy subjects and subjects with impaired LV systolic function or increased LV dimensions.

A 35-year-old man attended the Emergency Room with his first episode of central chest pain. The pain began 8 h prior to presentation and the 12-lead ECG showed ST-segment elevation of >1 mm in leads II, III, and aVF ( Figure , lower panel). He was treated with thrombolysis and transferred to the Coronary Care Unit. Troponin I was 60.9 pg/mL (normal

Left ventricular (LV) remodeling after myocardial infarction (MI) has received much attention because of its severe impact on morbidity and mortality rates. However, the incidence and extent of LV remodeling in a modern infarct population who were offered antiremodeling treatment in compliance with daily clinical practice is unknown. The purpose of this study was to clarify this issue and to evaluate the predictive value of N-terminal pro brain natriuretic peptide (NT-proBNP).Forty-two patients with a first transmural MI were examined after 1 week, 1 month, 3 months, 6 months, and 1 year with blood samples and magnetic resonance imaging.In 12 patients (29%), LV end-diastolic volume index (LVEDVI) and LV end-systolic volume index (LVESVI) increased by 24% and 22% (P.0001; P =.01). In 12 patients (29%), LVEDVI and LVESVI decreased by 19% and 23% (P.0001; P =.0005), whereas the remaining 18 patients (43%) had stable conditions regarding these LV measures. LV ejection fraction at baseline was significantly reduced in all patient categories but was unchanged over time. Elevated NT-proBNP level at baseline was identified as an independent predictor of increase in LVEDVI during follow-up examination (P =.007). A baseline level of NT-proBNP115 pmol/L identified patients who later had LV dilatation develop with a sensitivity and specificity of 89% and 68% (area under curve = 0.77).In this 1-year follow-up study of patients with a first transmural MI, approximately 30% had significant increments develop in LVEDVI and LVESVI, and LV ejection fraction remained unchanged. Patients in whom LV dilatation developed could be identified early after the MI with elevated plasma levels of NT-proBNP.