Supraventricular arrhythmias late after orthotopic cardiac transplantation: electrocardiographic and electrophysiological characterization and radiofrequency ablation.

AIMS: Cardiac transplantation (CTX) is an effective treatment for end-stage heart disease. Cardiac arrhythmias are increasingly recognized and associated with significant morbidity and mortality. We aim to describe the clinical and electrophysiological characteristics of patients with atrial arrhythmias occurring late after CTX. METHODS AND RESULTS: Sixteen patients with prior CTX who presented with late atrial arrhythmias for electrophysiological studies (EPS) were identified at two cardiac transplant centres. Among 859 patients, 16 (mean age 52 ± 14 years, 11 of 16 were men) patients underwent EPS for atrial arrhythmias presenting 8.6 ± 5.7 years following CTX. Among 16 patients, 14 underwent cardiac alone and 2 included lung transplantation. There were no cases of cardiac rejection. Arrhythmias were due to counterclockwise cavotricuspid-dependent atrial flutter (AFL) in 10 of 16, atrial tachycardia (AT) in 6 (1 patient had AFL and AT), and 1 due to atrioventricular nodal re-entrant tachycardia. Recipient-donor atrial electrical connection was seen in two of six AT and in no cases of AFL. In two cases, a focal AT was mapped to the remnant atrium conducting 2 : 1 or at variable block to the donor atrium. In four cases a focal/micro re-entrant AT originated within the vicinity of the interatrial suture scar. All cases were successfully ablated with radiofrequency energy; however, one case of AFL required a repeat ablation. Patients remained free of arrhythmia at 34 ± 15 months post-ablation. CONCLUSION: Typical AFL and AT are the most frequent supraventricular arrhythmias occurring late following CTX. Focal ATs may originate in low-voltage or border zones immediately adjacent to the atrio-atrial anastomosis. Radiofrequency ablation is an effective treatment strategy with high long-term success.

The impact of the right ventricular lead position on response to cardiac resynchronization therapy.

INTRODUCTION: Left ventricular (LV) lead placement to the latest contracting area (concordant LV lead) is associated with better response to cardiac resynchronization therapy (CRT) compared to a discordant LV lead. However, the effect of the right ventricular (RV) lead site on CRT response is unclear. We investigated the relationship of the RV and LV lead positions on CRT response. METHODS: In 131 CRT patients, the LV lead was positioned preferentially in a lateral or posterolateral vein and the RV lead to either the RV septum (RVS, n = 55) or RV apex (RVA, n = 76). The latest site of contraction was determined with two-dimensional speckle tracking radial strain imaging and patients had a concordant LV lead position if pacing the latest segment, and discordant if not. Response was defined as ≥15% reduction in LV end systolic volume (LVESV) at 6-month follow-up. RESULTS: There were no significant differences in mean reduction of LVESV at follow-up (RVS vs RVA: -23.3 ± 16% vs 22.1 ± 18%, P = 0.70) or rate of responders (58.2% vs 57.9%, P = 0.97) between the two groups. In patients with a concordant LV lead (n = 71), the response rate was significantly higher than those with a discordant lead (76.1% vs 36.7%, P < 0.001). There were no differences in outcomes in patients with a concordant or discordant LV lead according to the RV lead location. CONCLUSION: The extent of LV reverse remodeling following CRT is not related to the RV lead position, but is significantly higher in patients with a concordant LV lead.

Combined dyssynchrony and scar imaging with cardiac magnetic resonance imaging predicts clinical response and long-term prognosis following cardiac resynchronization therapy.

AIMS: Cardiac resynchronization therapy (CRT) is advocated in advanced heart failure; however, patient selection remains challenging. We examined the utility of multi-sequential cardiac magnetic resonance imaging (CMR) in predicting outcome after CRT. METHODS AND RESULTS: We performed multi-sequential CMR on 40 subjects with cardiomyopathy and advanced heart failure, despite optimized medical therapy. All patients had been recommended for CRT according to accepted clinical guidelines. Patients were defined by CMR as likely responders if they had significant mechanical dyssynchrony (> or =65 ms delay between septal and posterolateral wall contraction on cine imaging), and no transmural scarring of the anteroseptal or posterolateral wall on delayed contrast-enhanced imaging. Clinical composite score was recorded at baseline and 6 months post-CRT. Long-term follow-up (transplant-free survival) was 497 +/- 55 days post-CRT. A clinical response was achieved in 19/26 (73%) of the CMR-predicted responders and 2/12 (17%) of the CMR-predicted non-responders (P < 0.01, chi(2)). The sensitivity of CMR for prediction of clinical response to CRT was 90%, with a specificity of 59%. Transplant-free survival post-CRT was achieved in 88% of the CMR-predicted responders and 58% of the CMR-predicted non-responders (P < 0.05, Kaplan-Meier survival analysis). CONCLUSION: Multi-sequential CMR identifies patients with severe cardiomyopathy who will respond to CRT with a favourable long-term prognosis.

Mortality and target haemoglobin concentrations in anaemic patients with chronic kidney disease treated with erythropoietin: a meta-analysis.

BACKGROUND: Recombinant human erythropoietin is commonly used for treatment of anaemia. Our aim was to determine whether targeting different haemoglobin concentrations with such treatment is associated with altered all-cause mortality and cardiovascular events in patients with anaemia caused by chronic kidney disease. METHODS: We did a meta-analysis of randomised controlled clinical trials that were identified in medical databases and trial registration websites. Trials were eligible for inclusion if they assessed the effects of targeting different haemoglobin concentrations in patients with anaemia caused by chronic disease who were randomly assigned to treatment with recombinant human erythropoietin, recruited at least 100 patients, and had a minimum follow-up of 12 weeks. FINDINGS: We analysed nine randomised controlled trials that enrolled 5143 patients. There was a significantly higher risk of all-cause mortality (risk ratio 1.17, 95% CI 1.01-1.35; p=0.031) and arteriovenous access thrombosis (1.34, 1.16-1.54; p=0.0001) in the higher haemoglobin target group than in the lower haemoglobin target group in the fixed effects model without heterogeneity between studies. There was a significantly higher risk of poorly controlled blood pressure (1.27, 1.08-1.50; p=0.004) in the higher haemoglobin target group than in the lower target haemoglobin group with the fixed effects model; however, this was not significant in the random effects model (1.31, 0.97-1.78; p=0.075). The incidence of myocardial infarction was much the same in the two groups. INTERPRETATION: To target higher haemoglobin concentrations when treating patients with anaemia caused by chronic kidney disease with recombinant human erythropoietin puts such patients at increased risk of death. Current guidelines do not include an upper limit for the target haemoglobin concentration; such an upper limit should be considered in future recommendations.

Cardiac resynchronisation therapy: pacemaker versus internal cardioverter-defibrillator in patients with impaired left ventricular function.

OBJECTIVE: Studies have shown beneficial effects of cardiac resynchronisation therapy (CRT) on mortality among patients with heart failure. However the incremental benefits in survival from CRT with a defibrillator (CRT-D) are unclear. The choice of appropriate device remains unanswered. METHOD: This is a single-centre observational study in a tertiary cardiac centre. Patients (n=500) implanted with a CRT device with pacing alone (CRT-P) (n=354) and CRT-D (n=146) were followed for at least 2 years (mean 29 months, SD 14 months). The primary end point was all-cause mortality. RESULTS: A total of 116 deaths (23.2%) were recorded: 88 (24.8%) and 28 (19.2%), in the CRT-P and CRT-D groups, respectively. At 1 year there was a trend favouring CRT-D (HR 0.54, 95% CI 0.27 to 1.07, p=0.08) but this was attenuated by the 2nd year and became insignificant at the end of follow-up (HR 0.76, 95% CI 0.50 to 1.170, p=0.21). There was no survival benefit from having an internal cardioverter-defibrillator if patients were deemed non-responders to CRT. 27% of the CRT-P patients with ischaemic cardiomyopathy met indications for potential internal cardioverter-defibrillator implantation for primary prevention. These were older patients with poorer baseline function in comparison with CRT-D patients with devices for primary prevention. Once these differences were adjusted for, there was no difference in outcome between the groups. CONCLUSIONS: CRT-D did not offer additional survival advantage over CRT-P at longer-term follow-up, as the clinical benefit of a defibrillator attenuated with time. Further work is needed to define which subset of patients benefit from CRT-D.

Long-term outcomes (>2 years) of atrial fibrillation ablation using a multi-electrode ablation catheter in patients with paroxysmal atrial fibrillation.

PURPOSE: Catheter ablation for paroxysmal atrial fibrillation (PAF) is an effective treatment. Favourable outcomes at 6-12 months post-ablation have been reported using the multi-electrode catheter 'pulmonary vein ablation catheter (PVAC)' but little is known about longer term outcomes. There are also limited data on quality of life (QoL) post-atrial fibrillation (AF) ablation beyond 2 years of follow-up. METHODS: Two hundred three consecutive patients (77 % male, mean age 57.7 ± 11 years) who had a PAF ablation were included. Patients underwent conventional pulmonary vein isolation (PVI) (n = 128) or PVAC ablation (n = 75). Patients' symptoms were scored at baseline, at clinic follow-up and on questionnaire follow-up using the validated Canadian Cardiovascular Society Severity of AF (CCS-SAF) scale. The 'AF Effect on QualiTy of life' (AFEQT) questionnaire was used on questionnaire follow-up. RESULTS: Mean questionnaire follow-up was 854 ± 176 days with 74 % response rate. The majority of patients (91.6 % overall) were highly symptomatic at baseline with CCS-SAF class 3 or 4 symptoms. CCS-SAF class on follow-up questionnaire decreased significantly from baseline for both groups (mean 1.69 ± 1.7 for PVAC and 1.45 ± 1.5 for PVI, p = 0.001 and p < 0.001, respectively) with no difference between groups (p = 0.52) and the majority being class 0 or 1 (59.9 % overall). Mean AFEQT questionnaire scores were similar between both groups (78.1 ± 25 vs. 82 ± 23, p = 0.35). Total procedure time was significantly shorter in the PVAC group (135 ± 54 vs. 178 ± 43 min, p < 0.001). CONCLUSION: There was a comparable and significant improvement in QoL post-ablation in patients who underwent ablation using PVAC catheter and conventional techniques.

Utility of cardiac magnetic resonance imaging, echocardiography and electrocardiography for the prediction of clinical response and long-term survival following cardiac resynchronisation therapy.

Cardiac resynchronisation therapy (CRT) can reduce symptoms, hospitalisations, and mortality in patients with severe left ventricular (LV) systolic dysfunction and electro-mechanical dyssynchrony. Unfortunately, approximately 30 % of eligible patients fail to respond to CRT. This study prospectively compared electrocardiography (ECG), echocardiography, and cardiac magnetic resonance (CMR) imaging for the prediction of response to CRT. We performed ECG, echocardiography and CMR on 46 patients prior to planned CRT implantation. Patients were divided into predicted responder and non-responder groups using previously described criteria for each modality. Changes in indicators of CRT response were recorded 6 months post-implantation, and later for transplant-free survival. Less dyspnoea, lower levels of N-terminal pro-brain natriuretic peptide, more LV reverse remodelling, and longer transplant-free survival were observed in predicted responders compared to predicted non-responders using each of the three modalities (p < 0.05 for each comparison). Additionally, for patients with QRS duration <150 ms and/or non-left bundle branch block (non-LBBB) QRS morphology, CMR predicted both clinical response and improved longer term transplant-free survival (80 % transplant-free survival in predicted responders vs. 20 % in predicted non-responders, p = 0.04). ECG and cardiac imaging techniques predict improvements in markers of response following CRT with similar accuracy. However, for CRT candidates with shorter, non-LBBB QRS complexes, a subgroup known to derive less benefit from CRT, CMR may predict those who are more likely to gain both symptomatic and survival benefits.

A new anti-fibrotic drug attenuates cardiac remodeling and systolic dysfunction following experimental myocardial infarction.

BACKGROUND: Pathological deposition of extracellular matrix in the non-infarct zone (NIZ) of the ventricle post myocardial infarction (MI) is a key contributor to cardiac remodeling and heart failure. FT011, a novel antifibrotic compound, was evaluated for its efficacy in neonatal cardiac fibroblasts (NCF) and in an experimental MI model. METHODS AND RESULTS: Collagen synthesis in NCF was determined by (3)H-proline incorporation following stimulation with TGF-ß or angiotensin II (Ang II). FT011 inhibited collagen synthesis to both agents in a dose dependent manner. In vivo, Sprague Dawley rats underwent left anterior descending coronary artery ligation or sham surgery and were randomized one week later to receive either FT011 (200mg/kg/day) or vehicle for a further 4 weeks. Echocardiography and cardiac catheterization were performed, and tissues were collected for histological analysis of collagen, myocyte hypertrophy, interstitial macrophage accumulation and Smad2 phosphorylation. mRNA expression of collagens I and III and TGF-ß was measured using in situ hybridization and RT-PCR, respectively. FT011 treatment was associated with improved cardiac function (increased ejection fraction, fraction shortening and preload recruitable stroke work) and myocardial remodeling (reduced left ventricular diameter and volume at both end diastolic and systolic) compared with vehicle treatment. FT011 significantly reduced collagen matrix deposition, myocyte hypertrophy and interstitial macrophage infiltration, and mRNA expression of collagens I and III in NIZ compared with vehicle treatment. CONCLUSION: Anti-fibrotic therapy with FT011 in MI rats attenuated fibrosis and preserved systolic function.

Targeted left ventricular lead placement to guide cardiac resynchronization therapy: the TARGET study: a randomized, controlled trial.

OBJECTIVES: This study sought to assess the impact of targeted left ventricular (LV) lead placement on outcomes of cardiac resynchronization therapy (CRT). BACKGROUND: Placement of the LV lead to the latest sites of contraction and away from the scar confers the best response to CRT. We conducted a randomized, controlled trial to compare a targeted approach to LV lead placement with usual care. METHODS: A total of 220 patients scheduled for CRT underwent baseline echocardiographic speckle-tracking 2-dimensional radial strain imaging and were then randomized 1:1 into 2 groups. In group 1 (TARGET [Targeted Left Ventricular Lead Placement to Guide Cardiac Resynchronization Therapy]), the LV lead was positioned at the latest site of peak contraction with an amplitude of >10% to signify freedom from scar. In group 2 (control) patients underwent standard unguided CRT. Patients were classified by the relationship of the LV lead to the optimal site as concordant (at optimal site), adjacent (within 1 segment), or remote (≥2 segments away). The primary endpoint was a ≥15% reduction in LV end-systolic volume at 6 months. Secondary endpoints were clinical response (≥1 improvement in New York Heart Association functional class), all-cause mortality, and combined all-cause mortality and heart failure-related hospitalization. RESULTS: The groups were balanced at randomization. In the TARGET group, there was a greater proportion of responders at 6 months (70% vs. 55%, p = 0.031), giving an absolute difference in the primary endpoint of 15% (95% confidence interval: 2% to 28%). Compared with controls, TARGET patients had a higher clinical response (83% vs. 65%, p = 0.003) and lower rates of the combined endpoint (log-rank test, p = 0.031). CONCLUSIONS: Compared with standard CRT treatment, the use of speckle-tracking echocardiography to the target LV lead placement yields significantly improved response and clinical status and lower rates of combined death and heart failure-related hospitalization. (Targeted Left Ventricular Lead Placement to Guide Cardiac Resynchronization Therapy [TARGET] study); ISRCTN19717943).

Relation of peripheral collagen markers to death and hospitalization in patients with heart failure and preserved ejection fraction: results of the I-PRESERVE collagen substudy.

BACKGROUND: Heart failure with preserved ejection fraction (HFPEF) is a common and increasing public health problem. Myocardial fibrosis is a key pathological feature of HFPEF. Peripheral collagen markers may reflect this excess fibrosis; however, the relation of these markers to prognosis in patients with HFPEF has not as yet been determined. METHODS AND RESULTS: This substudy of the Irbesartan in Heart Failure With Preserved Systolic Function (I-PRESERVE) trial measured plasma levels of procollagen type I amino-terminal peptide, procollagen type III amino-terminal peptide, and osteopontin in 334 patients with HFPEF. Measurements were performed at baseline and 6 months after randomization to placebo or irbesartan 300 mg/day. The relation of baseline collagen markers to the I-PRESERVE primary end point (all-cause death and hospitalization for prespecified cardiovascular causes) was evaluated by single and multivariable analysis. Similar evaluations were performed for all-cause death alone as well as heart failure events (death or hospitalization because of heart failure). Increased plasma levels of collagen markers at baseline were associated with increased frequency of the study primary end point for all collagen markers. For each 10-µg/L increase in procollagen type I amino-terminal peptide, the hazard ratio (HR) for the primary end point was 1.09 (95% CI, 1.052 to 1.13; P<0.0001); for each 10-µg/L increase in procollagen type III amino-terminal peptide procollagen type I amino-terminal peptide, the HR was 2.47 (95% CI, 0.97 to 6.33; P=0.059); and for each 10-nmol/L increase in osteopontin, the HR was 1.084 (95% CI, 1.026 to 1.15; P=0.004). No variable remained significant as an independent predictor when introduced into a multivariable model. Both treatment groups tended to reduce collagen markers, with the reduction significantly greater for placebo versus irbesartan for procollagen type III amino-terminal peptide only (P=0.0185). CONCLUSIONS: Increased peripheral collagen turnover markers were not independently associated with increased mortality and cardiovascular hospitalization in an HFPEF population on multivariable analysis but were associated on single-variable analysis. These findings provide some support to the hypothesis that pathological fibrosis in the heart, and possibly the peripheral vasculature, may be contributory to adverse clinical outcomes in patients with HFPEF. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00095238.

Diagnostic characteristics of clozapine-induced myocarditis identified by an analysis of 38 cases and 47 controls.

OBJECTIVE: To analyze cases of clozapine-induced myocarditis for clinical and diagnostic trends. METHOD: A case definition was developed by a multidisciplinary group using reports of myocarditis with clozapine submitted to the Australian Therapeutic Goods Administration. The definition uses for diagnosis either histology or the combination of new signs of cardiac dysfunction combined with a cardiac-specific diagnostic parameter occurring within 45 days of starting clozapine. Potential cases of clozapine-related myocarditis occurring between January 1993 and September 2008 and a comparative group of long-term clozapine users were documented from the patients' medical records. RESULTS: Thirty-eight of 59 reviewed cases met the case definition. Three patients died, and the diagnosis for these was confirmed on cardiac histology. Nearly all of the remaining patients had persistent tachycardia and elevated troponin level. The time to onset was 14-22 days in all except 2 patients. Of the patients who survived, 66% (23 cases) had eosinophilia occurring 0-7 days (mean, 4.0) after the peak in troponin. C-reactive protein (CRP) level was elevated to above 100 mg/L (952 nmol/L) in 79% (23 cases), and some had elevated levels of CRP when troponin level was still normal. None of the control group (47 patients) met the case definition. CONCLUSIONS: Eosinophil counts should not be relied on for diagnosis of clozapine-related myocarditis, but elevated CRP may be an early indicator of developing myocarditis. Patients starting clozapine should be actively monitored for myocarditis during the first 4 weeks, with extra care taken during week 3.

Differences between beta-blockers in patients with chronic heart failure and chronic obstructive pulmonary disease: a randomized crossover trial.

OBJECTIVES: The purpose of this study was to determine the respiratory, hemodynamic, and clinical effects of switching between beta1-selective and nonselective beta-blockers in patients with chronic heart failure (CHF) and chronic obstructive pulmonary disease (COPD). BACKGROUND: Carvedilol, metoprolol succinate, and bisoprolol are established beta-blockers for treating CHF. Whether differences in beta-receptor specificities affect lung or vascular function in CHF patients, particularly those with coexistent COPD, remains incompletely characterized. METHODS: A randomized, open label, triple-crossover trial involving 51 subjects receiving optimal therapy for CHF was conducted in 2 Australian teaching hospitals. Subjects received each beta-blocker, dose-matched, for 6 weeks before resuming their original beta-blocker. Echocardiography, N-terminal pro-hormone brain natriuretic peptide, central augmented pressure from pulse waveform analysis, respiratory function testing, 6-min walk distance, and New York Heart Association (NYHA) functional class were assessed at each visit. RESULTS: Of 51 subjects with a mean age of 66 +/- 12 years, NYHA functional class I (n = 6), II (n = 29), or III (n = 16), and left ventricular ejection fraction mean of 37 +/- 10%, 35 had coexistent COPD. N-terminal pro-hormone brain natriuretic peptide was significantly lower with carvedilol than with metoprolol or bisoprolol (mean: carvedilol 1,001 [95% confidence interval (CI): 633 to 1,367] ng/l; metoprolol 1,371 [95% CI: 778 to 1,964] ng/l; bisoprolol 1,349 [95% CI: 782 to 1,916] ng/l; p < 0.01), and returned to baseline level on resumption of the initial beta-blocker. Central augmented pressure, a measure of pulsatile afterload, was lowest with carvedilol (carvedilol 9.9 [95% CI: 7.7 to 12.2] mm Hg; metoprolol 11.5 [95% CI: 9.3 to 13.8] mm Hg; bisoprolol 12.2 [95% CI: 9.6 to 14.7] mm Hg; p < 0.05). In subjects with COPD, forced expiratory volume in 1 s was lowest with carvedilol and highest with bisoprolol (carvedilol 1.85 [95% CI: 1.67 to 2.03] l/s; metoprolol 1.94 [95% CI: 1.73 to 2.14] l/s; bisoprolol 2.0 [95% CI: 1.79 to 2.22] l/s; p < 0.001). The NYHA functional class, 6-min walk distance, and left ventricular ejection fraction did not change. The beta-blocker switches were well tolerated. CONCLUSIONS: Switching between beta1-selective beta-blockers and the nonselective beta-blocker carvedilol is well tolerated but results in demonstrable changes in airway function, most marked in patients with COPD. Switching from beta1-selective beta-blockers to carvedilol causes short-term reduction of central augmented pressure and N-terminal pro-hormone brain natriuretic peptide. (Comparison of Nonselective and Beta1-Selective Beta-Blockers on Respiratory and Arterial Function and Cardiac Chamber Dynamics in Patients With Chronic Stable Congestive Cardiac Failure; Australian New Zealand Clinical Trials Registry, ACTRN12605000504617).

Effect of low-amplitude two-dimensional radial strain at left ventricular pacing sites on response to cardiac resynchronization therapy.

BACKGROUND: Left ventricular (LV) lead placement to areas of scar has detrimental effects on response to cardiac resynchronization therapy (CRT). Speckle-tracking radial two-dimensional strain offers assessment of the extent of regional myocardial deformation. The aim of this study was to assess the impact of LV lead placement at areas of low-amplitude strain on CRT response. METHODS: The optimal cutoff of radial strain amplitude at the LV pacing site associated with an unfavorable CRT response was determined in a derivation group (n = 65) and then tested in a second consecutive validation group (n = 75) of patients with heart failure. Patients had concordant LV leads if placed at the most delayed site, and dyssynchrony was defined as anteroseptal to posterior delay ≥ 130 msec. CRT response was defined as a ≥15% reduction in LV end-systolic volume at 6 months. RESULTS: In the derivation group, a derived cutoff for radial strain amplitude of <9.8% defined low-amplitude segments (LAS) and had a high specificity but low sensitivity for predicting LV reverse remodeling, suggesting a strong negative predictive value. In the validation group, compared with patients without LAS at the LV pacing site, in patients with LAS (n = 16), CRT response was significantly lower (62.7% vs 31.3%, P < .05). By multivariate analysis, LV lead concordance and the absence of an LAS at the LV pacing site but not dyssynchrony were significantly related to CRT response. CONCLUSION: LV lead placement over segments with two-dimensional radial strain amplitudes <9.8% is associated with poor outcomes of CRT.

Predicting coronary artery bypass graft surgery in acute coronary syndromes.

AIMS: To identify features predictive of hospital coronary artery bypass graft (CABG) surgery in patients with acute coronary syndromes (ACSs). METHODS AND RESULTS: Data from 17,434 patients enrolled in an observational study were analysed. Patients in private hospitals were more likely to undergo CABG than those in public hospitals (10.3% vs. 6.9%, P<0.01); CABG was more frequent in the USA than in Europe (11.9 % vs 3.5%, P<0.01). Clinical features independently predictive of CABG on multivariable analysis included no previous CABG, male sex, history of angina, hypertension, hyperlipidaemia, or diabetes, no history of atrial fibrillation or congestive heart failure, ST depression in multiple territories, and absence of ST elevation. These factors were assigned a score to quantify the likelihood of CABG (c-statistic 0.69). This score was predictive regardless of ACS subgroup (c-statistic 0.65-0.71) and remained predictive across institutions regardless of the frequency with which CABG was performed. The score was of greatest clinical utility among hospitals performing CABG in >10% of their ACS patients. CONCLUSIONS: Identifying ACS patients likely to undergo CABG using clinical features alone remains difficult. In hospitals with higher rates of surgical revascularisation, a subgroup of patients with an approximate 30% likelihood of CABG can be identified. Therapy in these patients can be tailored to minimise bleeding risk without compromising outcomes.

Atrial and ventricular echocardiographic correlates of the extent of pulmonary embolism in the elderly.

BACKGROUND: Acute pulmonary thromboembolism (PTE) can be associated with right ventricular (RV) dysfunction. The relative importance of individual echocardiographic parameters, including those suggesting interdependence between right and left heart chambers, in predicting thromboembolic burden in elderly patients with acute PTE is unknown. METHODS: We retrospectively studied the transthoracic echocardiograms of 63 elderly patients (age 71 +/- 16 years) with acute PTE, and assessed which individual echocardiographic parameters identified more than 30% pulmonary artery obstruction on the basis of quantitative ventilation/perfusion pulmonary scintigraphy. RESULTS: RV hypokinesis (visual grade 0-3, P = .02), and the quantitative parameters RV end-systolic area (P = .005) and RV ejection area (P = .01) were associated with more extensive pulmonary artery obstruction. Although right atrial end-systolic area and RV end-diastolic area did not correlate with extent of PTE, the ratio of RV:left ventricular end-diastolic area (P = .003), and ratio of right:left atrial end-systolic area (P = .004), were strongly associated with the extent of pulmonary artery obstruction. These transthoracic echocardiographic parameters were independent of clinical variables such as prior chronic lung disease, congestive cardiac failure, or prior PTE. CONCLUSION: RV systolic dysfunction, RV end-systolic dilatation, right:left atrial end-systolic area ratio, and RV:left ventricular end-diastolic area ratio correlate with extent of PTE in the elderly.