Development and validation of a clinical index to predict survival after cardiac resynchronisation therapy.

OBJECTIVE: To develop and validate a prognostic risk index of cardiovascular mortality after cardiac resynchronisation therapy (CRT). DESIGN: Prospective cohort study. SETTING: District general hospital. PATIENTS: 148 patients with heart failure (mean age 66.7 (SD 10.4) years), New York Heart Association class III or IV, LVEF <35%) who underwent CRT. INTERVENTIONS: CRT device implantation. MAIN OUTCOME MEASURES: Value of a composite index in predicting cardiovascular mortality, validated internally by bootstrapping. The predictive value of the index was compared to factors that are known to predict mortality in patients with heart failure. RESULTS: All patients underwent assessment of 16 prognostic risk factors, including cardiovascular magnetic resonance (CMR) measures of myocardial scarring (gadolinium-hyperenhancement) and dyssynchrony, before implantation. Clinical events were assessed after a median follow-up of 913 (interquartile range 967) days. At follow-up, 37/148 (25%) of patients died from cardiovascular causes. In Cox proportional hazards analyses, (DSC) Dyssynchrony, posterolateral Scar location (both p<0.0001) and Creatinine (p = 0.0046) emerged as independent predictors of cardiovascular mortality. The DSC index, derived from these variables combined, emerged as a powerful predictor of cardiovascular mortality. Compared to patients with a DSC <3, cardiovascular mortality in patients in the intermediate DSC index (3-5; HR: 11.1 (95% confidence interval (CI) 3.00 to 41.1), p = 0.0003) and high DSC index (> or =5; HR: 30.5 (95% CI 9.15 to 101.8), p<0.0001) were higher. Bootstrap validation confirmed excellent calibration and internal validity of the prediction model. CONCLUSION: The DSC index, derived from a standard CMR scan and plasma creatinine before implantation, is a powerful predictor of cardiovascular mortality after CRT.

Long-term effects of cardiac resynchronisation therapy in patients with atrial fibrillation.

OBJECTIVE: To compare the effects of cardiac resynchronisation therapy (CRT) in patients with heart failure (HF) in either atrial fibrillation (AF) or sinus rhythm (SR). DESIGN: Prospective observational study. PATIENTS: 295 consecutive patients with HF (permanent AF in 66, paroxysmal AF in 20, SR in 209; New York Heart Association (NYHA) class III or IV; left ventricular ejection fraction (LVEF) or=120 ms). INTERVENTIONS: All patients underwent CRT without atrioventricular junction ablation. MAIN OUTCOME MEASURES: The primary end point was the composite of cardiovascular death or unplanned hospitalisation for major cardiovascular events. Secondary end points included the composite of cardiovascular death or hospitalisation for worsening HF. Cardiovascular mortality, total mortality and changes in NYHA class, 6-minute walking distance, quality of life (Minnesota Living with Heart Failure questionnaire) and echocardiographic variables were also considered. RESULTS: Over a follow-up period of up to 6.8 years, no differences emerged between patients in AF or SR in any of the mortality or morbidity end points. The AF and SR groups derived similar improvements in mean NYHA class (-1.3 vs -1.2), 6-minute walking distance (92.3 vs 78.4 m) and quality of life scores (-25.2 vs -18.7) (all p<0.001). In both the AF and the SR groups, reductions were seen in left ventricular end-systolic (-25.9 vs -34.5 ml, both p<0.001) and end-diastolic (-20.2 ml, p = 0.001 vs 26.2 ml, p<0.001) volumes and improvements in LVEF (4.69% vs 7.86%, both p<0.001). CONCLUSIONS: Cardiac resynchronisation therapy leads to similar prognostic and symptomatic benefits in patients in AF and SR, even without atrioventricular junction ablation. Echocardiographic improvements are also comparable.

Effect of posterolateral left ventricular scar on mortality and morbidity following cardiac resynchronization therapy.

OBJECTIVES: To determine the effect of a posterolateral (PL) left ventricular scar on mortality and morbidity following cardiac resynchronization therapy (CRT). METHODS: Sixty-two patients with heart failure (age 67.3 +/- 9.6 yrs [mean +/- SD], 45 males, New York Heart Association class [NYHA] class III or IV, left ventricular ejection fraction [LVEF]= 35%, left bundle branch block, QRS > or = 120 ms) underwent late gadolinium enhancement cardiovascular magnetic resonance (LGE-CMR) for scar imaging. Patients were followed up for 741 (75-1602) days (mean [range]). RESULTS: The presence of a PL scar emerged as an independent predictor of the composite endpoint of cardiovascular death or hospitalization for worsening heart failure (HR: 3.06 [1.63, 7.7, P < 0.0001]) as well as the endpoint of cardiovascular death (HR: 2.63 [1.39, 6.65], P = 0.0016). A transmural PL scar was the strongest predictor of these endpoints (both P < 0.0001). The symptomatic responder rate (improvement by > or =1 NYHA classes or > or =25% in 6-min walking distance) was 83% in the group with non-PL scars, but only 47% in the group with transmural PL scars (P < 0.0001). Pacing over the scar was associated with a higher mortality and morbidity than pacing outside the scar (all P < 0.05). CONCLUSIONS: A PL scar is associated with a worse clinical outcome following CRT, particularly if it is transmural. Pacing scarred left ventricular myocardium carries a greater risk of mortality and morbidity than pacing nonscarred myocardium.

Late left ventricular lead displacement and treatment with a new endovenous active fixation lead.

Left ventricular (LV) lead displacement is an early complication of biventricular pacemakers and leads to loss of capture, diaphragmatic pacing, and symptomatic deterioration, requiring a revision procedure. We report a case of late LV lead displacement following a coughing fit and treatment with a lead with a new principle of active fixation.

Activated protein C resistance, factor V Leiden and peripheral vascular disease.

Activated protein C resistance caused by factor V Leiden is an important thrombophilia disorder which predisposes to venous thromboembolism. Some studies also suggest a role in the pathogenesis of arterial thrombosis and atherosclerosis. The authors have investigated the prevalence of activated protein C resistance and factor V Leiden in a series of 45 patients with peripheral vascular disease. Twelve patients were receiving warfarin. The activated protein C resistance ratios were significantly lower in the group of 33 non-warfarinized patients with peripheral vascular disease (median 2.82 (range 1.36-3.83)) compared with 33 age- and sex-matched controls (median 2.97 range 2.24-4.11); P<0.005; Wilcoxon rank sum). Eight patients (24%) had activated protein C resistance (ratio <2.2). The prevalence of factor V Leiden in patients with peripheral vascular disease was 17.8% (8/45). This is significantly increased compared with the local population and UK published frequency of 3.5% for this genotype. The presence of factor V Leiden did not affect the late outcome of arterial reconstructive surgery in terms of graft patency (P=0.5, Fisher's Exact test).