BACKGROUND Guidelines recommend nonstatin lipid-lowering agents in patients at very high risk for major adverse cardiovascular events (MACE) if low-density lipoprotein cholesterol (LDL-C) remains ≥70 mg/dL on maximum tolerated statin treatment. It is uncertain if this approach benefits patients with LDL-C near 70 mg/dL. Lipoprotein(a) levels may influence residual risk. OBJECTIVES In a post hoc analysis of the ODYSSEY Outcomes (Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab) trial, the authors evaluated the benefit of adding the proprotein subtilisin/kexin type 9 inhibitor alirocumab to optimized statin treatment in patients with LDL-C levels near 70 mg/dL. Effects were evaluated according to concurrent lipoprotein(a) levels. METHODS ODYSSEY Outcomes compared alirocumab with placebo in 18,924 patients with recent acute coronary syndromes receiving optimized statin treatment. In 4,351 patients (23.0%), screening or randomization LDL-C was <70 mg/dL (median 69.4 mg/dL; interquartile range: 64.3–74.0 mg/dL); in 14,573 patients (77.0%), both determinations were ≥70 mg/dL (median 94.0 mg/dL; interquartile range: 83.2–111.0 mg/dL). RESULTS In the lower LDL-C subgroup, MACE rates were 4.2 and 3.1 per 100 patient-years among placebo-treated patients with baseline lipoprotein(a) greater than or less than or equal to the median (13.7 mg/dL). Corresponding adjusted treatment hazard ratios were 0.68 (95% confidence interval [Cl]: 0.52–0.90) and 1.11 (95% Cl: 0.83–1.49), with treatment-lipoprotein(a) interaction on MACE ( P interaction = 0.017). In the higher LDL-C subgroup, MACE rates were 4.7 and 3.8 per 100 patient-years among placebo-treated patients with lipoprotein(a) >13.7 mg/dL or ≤13.7 mg/dL; corresponding adjusted treatment hazard ratios were 0.82 (95% Cl: 0.72–0.92) and 0.89 (95% Cl: 0.75–1.06), with P interaction = 0.43. CONCLUSIONS In patients with recent acute coronary syndromes and LDL-C near 70 mg/dL on optimized statin therapy, proprotein subtilisin/kexin type 9 inhibition provides incremental clinical benefit only when lipoprotein(a) concentration is at least mildly elevated. (ODYSSEY Outcomes: Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab; NCT01663402 )

Percutaneous coronary revascularisation [PCR] improves angina and health related quality of life [HRQOL] compared to standard medical therapy. It is unknown whether PCR has the same benefits for patients with a history of CABG. Over a period of 5 years, we assessed HRQOL of patients undergoing PCR using Part 1 of the Nottingham Health Profile [NHP] at baseline 3, 12 and 24 months. We compared HRQOL after PCR in 255 patients with CABG to 2680 without. There were more males [81.1% v 69.6% p=0.002] and older patients [mean age 60.1 years v. 58.0 p=0.03] in CABG group.Perceived HRQOL improved at 24 months for pain, energy and emotional reaction but the improvement was less in the CABG group. However, mean NHP scores at 24 months for those with CABG had returned to baseline levels for sleep [34.9] and for physical function was worse than at baseline [22.0 vs 30.7]. This relationship persisted after adjustment for male sex, history of previous MI and coronary stent usage. Patients with previous CABG had less improvement in HRQOL after PCR. Further work is needed to assess the benefits and cost effectiveness of PCR in these patients.

a b s t r a c tBacterial endocarditis gives rise to a variety of complications due to local tissue damage, immunological phenomena, and embolic phenomena. Only a small number of cases of coronary embolization have been reported in infective endocarditis patients. This is a case of subacute bacterial endocarditis in a postpartum mother complicated by fatal left and right coronary artery embolization. A 32-year-old postpartum mother with a history of rheumatic heart disease presented with a history of fever, shortness of breath, and bilateral ankle edema for 1-week duration. On admission, the patient was alert, febrile with a pulse rate of 90 beats/min, blood pressure 105/70 mmHg, and her lungs were clear. Transthoracic echocardiography revealed vegetations attached to both mitral and aortic valves. She was started on intravenous antibiotics. Her fever was settled and during the following 2 weeks she was clinically improving with settling inflammatory markers. On the 20th day of the illness, the patient developed sudden onset of chest pain, dyspnea with sinus bradycardia, and later developed pulseless electric activity. She expired despite intense cardiopulmonary resuscitation. Postmortem revealed multiple vegetations in both mitral and aortic valves and complete occlusion of both left and right coronary ostia by embolized vegetative materials.

Thrombocytopenia, both at baseline and acquired throughout admission is associated with poor clinical outcomes in patients with coronary artery disease. It is not known whether severe thrombocytopenia in patients receiving glycoprotein IIb/IIIa inhibitors (GPI) carries the same risk as thrombocytopenia from other aetiologies. We identified 50 consecutive patients referred for percutaneous coronary intervention (PCI) who developed severe thrombocytopenia (<50  × 10(9) cells/l) and followed their clinical course to 30 days. Two groups were compared: (1) severe thrombocytopenia following GPI usage and (2) severe thrombocytopenia without exposure to GPI. Baseline platelet counts were higher in GPI group (201 ± 62 vs. 112 ± 83  × 10(9) cells/l, p < 0.05). Patients in GPI group had more profound thrombocytopenia yet quicker recovery of platelet counts. The GPI group received fewer blood product transfusions (red cells: 0.1 ± 0.4 vs. 1.3 ± 2.0, p < 0.05, platelets: 0.22 ± 0.6 vs. 1.1 ± 1.7, p < 0.05) and had lower event rates for the primary end point of 30-day mortality (3.7% vs. 42.1%, p < 0.05), and for major bleeding (0% vs. 15.8%, p < 0.05). In conclusion, GPI associated severe thrombocytopenia follows a distinct clinical course when compared to severe thrombocytopenia due to other aetiologies. Our results suggest that patients who develop severe thrombocytopenia following GPI therapy may be managed conservatively with careful monitoring.

We found a decline in compliance to NICE guidelines on GPI usage during PCI. This was likely influenced by contemporary trials demonstrating little or no benefit of GPI in patients undergoing elective PCI who are adequately pretreated with clopidogrel. Our findings suggest the need for a mechanism whereby regular updates to guidelines can be disseminated following new trial evidence.