2 The procedure
2.1.1 Angina pectoris is chest discomfort, often described as pressure or pain, typically occurring on exertion. It is caused by inadequate delivery of oxygen to the heart muscle, usually because of coronary artery disease. Refractory angina is a severe angina form that cannot be controlled by normal medical or surgical treatment.
2.1.2 Angina treatment depends on symptoms, medical history and angiography findings. Treatments include anti-anginal medication and revascularisation interventions (percutaneous coronary intervention or coronary artery bypass surgery). For patients with refractory angina, these treatments have either failed or are not clinically suitable.
2.2.1 Transmyocardial laser revascularisation for refractory angina pectoris is carried out with the patient under general anaesthesia. Ischaemic areas are selected for treatment using echocardiography or myocardial perfusion scan and coronary angiography before surgery. A left thoracotomy is performed and the pericardium opened. A laser device is then used to create a number of channels in the myocardium. Transoesophageal echocardiography confirms complete passage across the myocardial wall by the laser.
2.2.2 A number of different types of laser can be used for this procedure.
Sections 2.3 and 2.4 describe efficacy and safety outcomes which were available in the published literature and which the Committee considered as part of the evidence about this procedure. For more detailed information on the evidence, see the overview.
2.3.1 A meta-analysis of ten randomised controlled trials (RCTs) (total 1359 patients) found no difference in 12-month mortality between TMLR-treated patients and controls (treated either medically or with coronary artery bypass grafting [CABG]) (odds ratio [OR] 0.89; 95% confidence interval [CI] 0.5 to 1.8). Nor was there any difference in mortality when studies comparing TMLR plus CABG against CABG alone were excluded (OR 0.8; 95% CI 0.5 to 1.2).
2.3.2 An RCT of 100 patients treated either with TMLR or medically reported that myocardial contractility (assessed with stress echocardiography or single photon emission computed tomography [SPECT]; lower value indicating worse function) was significantly lower in TMLR-treated patients (1.49 ± 0.44) than those treated medically (1.56 ± 0.47) at 12-month follow-up (p < 0.05). Six other RCTs found no significant difference in myocardial perfusion (examined with stress testing or perfusion scanning) in TMLR-treated patients, compared with patients treated medically. A meta-analysis of four RCTs (total 323 patients) reported greater mean improvement (from baseline) in total exercise time in TMLR-treated patients compared with those treated medically at 6-month follow-up (pooled mean difference 120.1 seconds; 95% CI 4.5 to 235.7).
2.3.3 A meta-analysis of three studies (total 135 patients) reported an improvement from baseline in angina score (measured using four-point scales) in TMLR-treated patients compared with those treated medically, with a reduction in mean difference in angina score between TMLR and non-TMLR treatment groups of –1.8 (95% CI –2.4 to –1.1) at 6-month follow-up and –1.0 (95% CI –1.7 to –0.3) at 12-month follow-up.
2.3.4 Five RCTs measured quality of life with different instruments. One RCT showed no significant difference between TMLR-treated patients and patients treated with thoracic sympathectomy, while the other four RCTs found significant improvements in quality of life for TMLR-treated patients compared with those treated medically (significance not stated). None of the studies had blinded patients to their treatment.
2.3.5 Specialist Advisers listed key efficacy outcomes as angina severity reduction, exercise capacity improvement, reduced medicine use and increased quality of life.
2.4.1 A meta-analysis of ten RCTs indicated no difference in postoperative mortality between TMLR-treated patients and controls treated medically or with CABG (pooled OR 0.78; 95% CI 0.34 to 1.7). However, when two trials comparing TMLR plus CABG against CABG alone were excluded, postoperative mortality was greater in TMLR-treated patients than controls (OR 0.35; 95% CI 0.13 to 0.93).
2.4.2 In seven RCTs the subsequent myocardial infarction rate was higher in TMLR-treated patients than in controls (6% [41/633] compared with 2% [11/651]; follow-up period 12 months; significance not stated).
2.4.3 An RCT of 100 patients reported that postoperative heart failure occurred more frequently in TMLR-treated patients (34% [17/50]) than in medically treated patients (0% [0/50]) (significance not stated). An RCT of 182 patients reported that thromboembolic events occurred more frequently in TMLR-treated patients (10% [9/92]) than those treated medically (3% [3/90]) (significance and follow-up not stated).
2.4.4 A case series of 169 TMLR-treated patients reported that 14% (23/169) developed acute non-inflammatory pericarditis following the procedure (sequelae not reported). In a case series of 20 TMLR-treated patients, acute mitral regurgitation was reported in 5% (1/20). An international multicentre case series of 932 patients reported cardiac tamponade in < 1% (5/932) of patients.
2.4.5 A retrospective non-randomised controlled trial of 255 patients reported that neurological complications occurred more frequently after TMLR plus CABG (3% [1/36]) than after CABG alone (1% [3/219]) (significance and follow-up not stated).
2.4.6 Specialist Advisers stated that adverse events reported in the literature included death, myocardial infarction, heart failure, arrhythmias, and wound and other infections.
2.5.1 The Committee noted that some studies showed improvements in symptoms and quality of life, but considered that these were likely to be placebo responses in the light of evidence that showed no objective benefits.
2.5.2 The Committee considered evidence on TMLR alone for refractory angina pectoris, and also on TMLR performed concomitantly with CABG.