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Background. Embolism is a dreaded complication of infective endocarditis (IE). Currently, antimicrobial therapy is the only medical intervention proven to decrease the risk of embolism associated with IE. We hypothesized that, because platelet aggregation is operative in the pathogenesis of vegetation formation, embolism associated with IE should occur less frequently among patients who have received prior, continuous daily antiplatelet therapy for noninfectious reasons. Methods. We studied a retrospective cohort of adult patients with a diagnosis of IE who presented to the Mayo Clinic (Rochester, MN) during 1980-1998. The cohort was divided into 2 groups on the basis of whether they had received continuous daily antiplatelet therapy for at least 6 months prior to the time of hospitalization for IE. Antiplatelet therapy included aspirin, dipyridamole, clopidogrel, ticlopidine, or any of combination of these agents. The primary end point was a symptomatic embolic event that occurred prior to or during hospitalization. Multivariable logistic regression was used to assess the impact of continuous daily antiplatelet therapy on risk of symptomatic emboli associated with IE. Results. One hundred forty-seven (24.5%) of 600 patients experienced a symptomatic embolic event; the most common embolic manifestation was stroke (in 48.2% of patients). Embolic events occurred significantly less often among those who had received prior, continuous daily antiplatelet therapy (12.0% of patients who had received therapy vs. 27.8% patients who had not receive therapy; P < .001). After adjustment for several covariates known to influence both risk of embolism and propensity for antiplatelet use, the adjusted odds ratio for a symptomatic embolic event was 0.36 (95% confidence interval, 0.19-0.68; P = .002) for patients receiving continuous daily antiplatelet therapy. Conclusions. The risk of symptomatic emboli associated with IE was reduced in patients who received continuous daily antiplatelet therapy before onset of IE. [ABSTRACT FROM AUTHOR]

Background: While echocardiography is used most frequently to assess right ventricular (RV) function in clinical practice, echocardiography is limited in its ability to provide an accurate measure of RV ejection fraction (RVEF). Hence, quantitative estimation of RV function has proven difficult in clinical practice. Objective: We sought to determine which commonly used echocardiographic measures of RV function were most accurate in comparison with an MRI-derived estimate of RVEF. Methods: We analyzed RV function in 36 patients who had cardiac MRI studies and echocardiograms within a 24 hour period. 2D parameters of RV function—right ventricular fractional area change (RVFAC), tricuspid annular motion (TAM), and transverse fractional shortening (TFS) were obtained from the four-chamber view. RV volumes and EFs were derived from volumetric reconstruction based on endocardial tracing of the RV chamber from the short axis images. Echocardiographic assessment of RV function was correlated with MRI findings. Results: RVFAC measured by echocardiography correlated best with MRI-derived RVEF (r = 0.80, P < 0.001). Neither TAM (r = 0.17; P = 0.30) nor TFC (r = 0.12; p< 0.38) were significantly correlated with RVEF. Conclusions: RVFAC is the best of commonly utilized echocardiographic 2D measure of RV function and correlated best with MRI-derived RV ejection fraction. Condensed Abstract: While echocardiography is used most frequently to assess RV function in clinical practice, echocardiography is limited in its ability to provide an accurate measure of RV ejection fraction (RVEF). Using cardiac MRI, RV fractional area change (RVFAC), determined either by MRI or echocardiography, was found to correlate best with MRI-derived RVEF. [ABSTRACT FROM AUTHOR]

Purpose: While both first-pass perfusion and late gadolinium enhancement by cardiovascular magnetic resonance (CMR) can assess coronary microvascular status in acute myocardial infarction (AMI), there are only limited data on their respective diagnostic utility. We aim to evaluate: the utility of first-pass perfusion and late gadolinium enhancement imaging in the detection and quantification of microvascular dysfunction after reperfused acute myocardial infarction, using TIMI frame count (TIMI FC) as the reference standard of microvascular assessment; and their relationship with infarct size and ventricular function. Methods: First-pass perfusion and late gadolinium enhancement imaging were performed in 25 consecutive AMI patients (84% men, age 58 ± 10) within 72 h of successful reperfusion. We assessed the myocardial extent of microvascular dysfunction using the size of the perfusion defect on first-pass perfusion (PD%) and the hypoenhanced core region within late gadolinium enhancement (MDEcore%). PD%, MDEcore%, and TIMI FC were analyzed independently of each other and with blinding to clinical data. We adjusted PD% and MDEcore% to the myocardial mass subtended by the infarct-related artery according to the 16-segment model. Results: Median infarct size involved 13.9% (interquartile range: 8.5 to 22.2%) of the left ventricle and median left ventricular ejection fraction was 52% (interquartile range: 43 to 61%). PD% demonstrated evidence of microvascular dysfunction more frequently (84% vs. 36% of patients, p < 0.002) and involved a larger myocardial extent (23.5 ± 17.5% vs. 3.5 ± 7.7%, p < 0.001) compared to MDEcore%. PD% had strong correlations with TIMI FC (Spearman ρ = 0.62, p < 0.001) and infarct size (ρ = 0.64, p < 0.001), and a moderate correlation with LVEF (ρ = -0.39, p = 0.055). MDEcore% also correlated with TIMI FC (ρ = 0.54, p = 0.005) and infarct size (ρ = 0.52, p < 0.01) but not with LVEF (p = NS). Conclusions: PD% appeared to provide a stronger noninvasive assessment of the microvascular function than MDEcore% and correlated well with prognostic markers such as left ventricular ejection fraction and infarct size. Future studies should consider quantitative analyses of both first-pass perfusion and late gadolinium enhancement imaging in the evaluation of novel therapies targeted to the microvasculature of the infarct-related artery. [ABSTRACT FROM AUTHOR]

Heart failure (HF) is a clinical syndrome that occurs when the ability of the heart to meet the requirements of the body fails. Myocardial infarction (MI) is a common antecedent event that predisposes a patient to HF. Loss of cardiac function following MI occurs in the context of myocyte death and ventricular remodeling. The clinical significance of HF following MI is underscored by the fact that among MI survivors, the risk of death is markedly elevated in those who develop HF compared with those who do not. Various modifying factors associated with the development of HF following MI have been identified. Use of multimodality therapy with improved clinical outcomes for HF has increased the need to specifically identify the failing heart at an earlier stage. The ability to identify heart failure early in its pathogenesis will enable finer risk stratification following MI. This article reviews various risk predictors for the development of HF following MI. [ABSTRACT FROM AUTHOR]

Cardiac remodelling is the expression of molecular, cellular and interstitial changes in response to cardiac injury, manifesting as adverse alterations in the size, shape and function of the ventricle. Several clinical studies have documented significant elevations in the levels of renin, angiotensin II (Ang II) and aldosterone attending acute myocardial infarction and/or congestive heart failure. Similar to catecholamines, markedly elevated activity of the renin-angiotensin-aldosterone system (RAAS) is associated with poor prognosis. The effects of Ang II upon cardiac tissue are related to two primary receptors, Ang II type 1 (AT 1) and Ang II type 2 (AT2). The AT1-receptor appears to mediate many of the deleterious effects of chronic RAAS activity, while the AT2-receptor is increasingly shown to have potential cardioprotective effects. Attenuating the deleterious effects of sustained Ang II stimulation can be achieved by direct inhibition of angiotensin-converting enzyme (ACE) and/or direct antagonism of AT receptors. ACE inhibition reduces left ventricular (LV) volumes, retards the progression of LV dilatation and hypertrophy and increases systolic function in systolic dysfunction. By blocking at the receptor level, Ang II receptor blockers (ARBs) provide an alternative and more direct approach to inhibiting the effects of Ang II; however, data relating to their effects upon ventricular remodelling, whether used in isolation or in combination with ACE inhibitors (ACE-Is), are less convincing. Data arising from several recent clinical trials suggest that simultaneous use of ACE-Is and ARBs maybe of more benefit in attenuating ventricular remodelling than either agent alone. [ABSTRACT FROM PUBLISHER]

A letter to the editor is presented highlighting the described association between gadolinium-containing contrast agents and nephrogenic systemic fibrosis.