NHS England-funded CT fractional flow reserve in the era of the ISCHEMIA trial.

BACKGROUND: The National Institute for Health and Care Excellence (NICE) 2016 guidelines (CG95) recommend patients with new stable chest pain be investigated with computed tomography coronary angiography (CTCA). An updated guideline (MTG32) recommended using CT fractional flow reserve (CTFFR) as a gatekeeper to invasive coronary angiography (ICA) for patients with coronary stenosis on CTCA. Subsequently, NHS England negotiated a UK-wide contract with HeartFlow, the provider of CTFFR. We describe our experience with CTFFR and consider the impact of the recent ISCHEMIA trial on these guidelines. METHODS: We prospectively collected ICA and revascularisation data on all patients undergoing CTFFR from January 2019 to March 2020. RESULTS: One-hundred and twenty-five of 140 patients completed CTFFR analysis. Eighty-one patients had CTCA stenosis >50%. Thirty-six had positive CTFFR; 29 underwent ICA with 22 (75.9%) revascularised. Forty-five had negative CTFFR; 14 underwent ICA and four (28.6%) were revascularised. The average cost of investigation per patient (PP) was £971.95. Had these patients undergone ICA directly with no functional test after CTCA, the average cost would be £932.51 PP. CONCLUSION: Our revascularisation rates suggest that CTFFR can potentially be a gatekeeper to ICA but does not necessarily yield cost savings.

Absence of Myocardial Fibrosis Predicts Favorable Long-Term Survival in New-Onset Heart Failure.

BACKGROUND: Myocardial fibrosis, identified by late gadolinium enhancement cardiovascular magnetic resonance, predicts outcomes in chronic heart failure (HF). Its prognostic significance in new-onset HF and reduced left ventricular ejection fraction (LVEF) is unclear. We investigated whether the pattern and extent of fibrosis predict survival in new-onset HF and reduced LVEF of initially uncertain pathogenesis. METHODS AND RESULTS: Of 120 consecutive patients with new-onset (<6 months) HF and reduced LVEF, 31 (26%) had infarct fibrosis, 25 (21%) had midwall fibrosis, and 64 (53%) had no fibrosis. During median follow-up of 8.9 years, 33 (28%) patients died. Patients with infarct fibrosis (hazard ratios [HR], 3.32; 95% CI, 1.46-7.58; P=0.004) or midwall fibrosis (HR, 2.99; 95% CI, 1.24-7.19; P=0.014) were more likely to die compared with those without fibrosis. On multivariable analysis, the pattern and extent of fibrosis were both associated with all-cause mortality (by fibrosis pattern: infarct: HR, 2.60; 95% CI, 1.08-6.27; P=0.033; midwall: HR, 2.64; 95% CI, 1.08-6.47; P=0.034; by fibrosis extent per 1%: HR, 1.07; 95% CI, 1.03-1.12; P<0.001). Fibrosis pattern also predicted composites of cardiovascular mortality or aborted sudden cardiac death (infarct: HR, 3.45; 95% CI, 1.20-9.90; P=0.022; midwall: HR, 6.59; 95% CI, 2.26-19.22; P<0.001), and all-cause mortality, HF hospitalization, or aborted sudden cardiac death (infarct: HR, 2.69; 95% CI, 1.26-5.76; P=0.011; midwall fibrosis: HR, 2.97; 95% CI, 1.37-6.45; P=0.006). Addition of fibrosis pattern to LVEF improved risk prediction for all-cause mortality (LVEF versus LVEF+fibrosis C statistic: 0.66 versus 0.71; P=0.033). Importantly, the absence of fibrosis heralded a favorable prognosis with an 85% survival rate over the duration of follow-up. CONCLUSIONS: The pattern and extent of myocardial fibrosis predict adverse outcomes in new-onset HF and reduced LVEF. In contrast, the absence of fibrosis portends a durable warranty period with a low incidence of adverse events. These findings support a role for late gadolinium enhancement cardiovascular magnetic resonance in the early risk stratification of patients with HF of uncertain pathogenesis.

Role of late gadolinium enhancement cardiovascular magnetic resonance in the risk stratification of hypertrophic cardiomyopathy.

OBJECTIVE: Myocardial fibrosis identified by late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR) in patients with hypertrophic cardiomyopathy (HCM) is associated with adverse cardiovascular events, but its value as an independent risk factor for sudden cardiac death (SCD) is unknown. We investigated the role of LGE-CMR in the risk stratification of HCM. METHODS: We conducted a prospective cohort study in a tertiary referral centre. Consecutive patients with HCM (n=711, median age 56.3 years, IQR 46.7-66.6; 70.0% male) underwent LGE-CMR and were followed for a median 3.5 years. The primary end point was SCD or aborted SCD. RESULTS: Overall, 471 patients (66.2%) had myocardial fibrosis (median 5.9% of left ventricular mass, IQR: 2.2-13.3). Twenty-two (3.1%) reached the primary end point. The extent but not the presence of fibrosis was a significant univariable predictor of the primary end point (HR per 5% LGE: 1.24, 95% CI 1.06 to 1.45; p=0.007 and HR for LGE: 2.69, 95% CI 0.91 to 7.97; p=0.073, respectively). However, on multivariable analysis, only LV-EF remained statistically significant (HR: 0.92, 95% CI 0.89 to 0.95; p<0.001). For the secondary outcome of cardiovascular mortality/aborted SCD, the presence and the amount of fibrosis were significant predictors on univariable but not multivariable analysis after adjusting for LV-EF and non-sustained ventricular tachycardia. CONCLUSIONS: The amount of myocardial fibrosis was a strong univariable predictor of SCD risk. However, this effect was not maintained after adjusting for LV-EF. Further work is required to elucidate the interrelationship between fibrosis and traditional predictors of outcome in HCM.

Role of cardiovascular magnetic resonance as a gatekeeper to invasive coronary angiography in patients presenting with heart failure of unknown etiology.

BACKGROUND: In patients presenting with new-onset heart failure of uncertain etiology, the role of coronary angiography (CA) is unclear. Although conventionally performed to differentiate underlying coronary artery disease from dilated cardiomyopathy, CA is associated with a risk of complications and may not detect an ischemic cause resulting from arterial recanalization or an embolic episode. In this study, we assessed the diagnostic accuracy of a cardiovascular magnetic resonance (CMR) protocol incorporating late gadolinium enhancement (LGE) and magnetic resonance CA as a noninvasive gatekeeper to CA in determining the etiology of heart failure in this subset of patients. METHODS AND RESULTS: One hundred twenty consecutive patients underwent CMR and CA. The etiology was ascribed by a consensus panel that used the results of the CMR scans. Similarly, a separate consensus group ascribed an underlying cause by using the results of CA. The diagnostic accuracy of both strategies was compared against a gold-standard panel that made a definitive judgment by reviewing all clinical data. The study was powered to show noninferiority between the 2 techniques. The sensitivity of 100%, specificity of 96%, and diagnostic accuracy of 97% for LGE-CMR were equivalent to CA (sensitivity, 93%; specificity, 96%; and diagnostic accuracy, 95%). As a gatekeeper to CA, LGE-CMR was also found to be a cheaper diagnostic strategy in a decision tree model when United Kingdom-based costs were assumed. The economic merits of this model would change, depending on the relative costs of LGE-CMR and CA in any specific healthcare system. CONCLUSION: This study showed that LGE-CMR is a safe, clinically effective, and potentially economical gatekeeper to CA in patients presenting with heart failure of uncertain etiology.

Reversion and maintenance of sinus rhythm in patients with permanent atrial fibrillation by internal cardioversion followed by biatrial pacing.

Patients in atrialfibrillation (AF) who fail external cardioversion are usually regarded as in permanent AF. Internal cardioversion may revert many such patients into sinus rhythm (SR) but the majority relapse rapidly into AF. We investigated whether internal cardioversion followed by biatrial pacing is an effective to restore and subsequently maintain SR in patients with permanent AF. Patients in permanent AF underwent internal cardioversion that was followed by biatrial temporary pacing for 48 hours. Those who remained in SR received a permanent biatrial pacemaker programmed to a rate responsive mode with a lower rate 90 beats/min. Primary end point of the study included maintenance in SR 3 months after internal cardioversion. Sixteen patients (14 men, 57 +/- 11 years) were cardioverted. The median duration of AF was 24 months (quartiles, Q1 = 8.5 and Q3 = 102) and mean left atrium diameter was 48 +/- 04 mm. A permanent biatrial pacemaker was implanted in 11 patients. At a mean fallow-up of 15 months (range 4 to 24), 8 patients remained in SR for more than 3 months. AF was eliminated in 5 patients, while in two a second internal cardioversion on amiodarone was required. Antiarrhythmic therapy was used in half of our population and did not predict the long-term maintenance of SR. Following internal cardioversion with continuous biatrial pacing, 50% of patients with permanent AF were maintained for prolonged periods in SR. This is a new modality of treatment of permanent AF directed to the maintenance of SR that provides a further therapeutic option in end-stage AF.