anzctr.org.au Identifier: ACTRN12612001120864; slctr.lk Identifier: SLCTR/2015/020.

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 )

BackgroundMelioidosis is an infection caused by a facultative intracellular Gram-negative bacterium, Burkholderia pseudomallei. It can present as septicemia, localized infection with/without septicemia, asymptomatic infections, ulcers, pneumonia, visceral abscesses, neurological infection, musculoskeletal infections and can involve any organ.Case presentationA 56 year old Sri Lankan diabetic female presented with fever, chills and rigors for 2 weeks. She also had malaise and loss of appetite, but no other features. On examination, she was febrile (temperature was 101.4 0 F) and rest of the examination was unremarkable. Her blood culture was positive for Burkholderia pseudomallei and she was started on IV antibiotics, on day 3. During her 2nd week of hospital stay, she developed right sided low back pain with buttock pain, right hip joint pain and restricted hip joint movements suggestive of right sacroiliitis. CE CT and MRI scans confirmed the diagnosis of right iliopsoas abscesses and right sacroiliitis.Incision and drainage was performed and a pigtail catheter was left in place for continuous drainage of abscesses. Her intensive phase was initiated with IV ceftazidime 2 g every 6 h for 12 days, then changed over to IV meropenem 2 g every 8 h together with oral co-trimoxazole. 2 weeks later, oral co-trimoxazole was replaced by oral doxycycline for another 6 weeks (due to transient pancytopaenia). She made a complete and uneventful recovery with oral co-trimoxazole for another 6 months, in her eradication phase.We report this case to show the importance in early diagnosis of melioidosis, and to consider it in the differential diagnosis of multiple abscesses and to emphasize the importance in suspecting melioidosis as a causative agent in infective sacroiliitis.DiscussionMelioidosis can have 2 major presentations; acute infection (symptoms lasting less than 2 months) and chronic infection (symptoms lasting more than 2 months). Musculoskeletal melioidosis is a well-recognized manifestation of the disease, which can manifest as soft tissue abscesses, septic arthritis, spondylitis, sacroiliitis and osteomyelitis.Management of melioidosis consists of 2 phases. The intensive phase and the eradication phase. These are aimed at the importance of rapidly treating the septicemia, the need of eradication of the persistent disease and the prevention of recurrent infections or relapses. The intensive phase consists of minimum 10–14 days of IV antibiotics: IV ceftazidime or IV carbapenem (meropenem/ imipenem). Eradication phase should be followed by 3–6 months of oral co-trimoxazole alone or in combination with oral doxycycline/ oral amoxiciliin-clavulanic acid.

Background Inflammation in myocardial infarction has a complex immunogenic origin and is suspected to be closely involved in its aetio-pathogenesis as well as outcome. In this study the objective was to further elucidate the clinical correlations of inflammation using clinical parameters and basic inflammatory markers and how it correlates with patient risk parameters, imaging findings and outcome. Methods An observational descriptive cross sectional study was carried out at the Institute of Cardiology, National Hospital of Sri Lanka, where consenting patients presenting for further management of ST- elevation myocardial infarction were recruited. Venous blood samples were collected on admission to assess C-reactive protein levels and on a timed manner to asses Troponin I levels as well as on subsequent days to performs whole blood analysis. Patients underwent 6 hourly axillary temperature assessment. All patients underwent 2D transthoracic echocardiographic analysis via biplane Simpson’s method to ascertain ejection fraction as well. Results Eighty eight subjects were recruited into the study. Fever was noted in 20.5% ( n = 18). Fever was usually intermittent and seen commonly between day 1 and 3 post-acute myocardial infarction. Haematological abnormalities indicative of inflammation were also observed as whole blood analysis demonstrated predominant leukocytosis and elevated C-reactive protein levels. Significant correlation was noted between presence of leukocytosis ( P = 0.033) and fever as well as with the presence of diabetes mellitus ( P = 0.005). Development of acute heart failure also showed significant correlation with leukocytosis ( P = 0.002). Correlation was also observed between LV dysfunction and elevated C-reactive protein and Troponin I levels with P values of P = 0.023 and P = 0.011 ( P < 0.05) respectively. Conclusions Inflammation is appreciated following acute myocardial infarction. Biochemical evidence of inflammation is commonly seen. Clinical manifestation as fever however is seen less often. Patient factors correlate poorly with inflammation but diabetes mellitus may have a contributory role. Whole blood analysis derangement is a simple test that correlates well with inflammation as well as presence of fever and development of heart failure. Inflammation also correlated with left ventricular dysfunction and may thus have an impact on clinical morbidity and mortality. Delineating associates of inflammation will hopefully help improve therapy of myocardial infarction.

Contrast-induced encephalopathy is a rare idiosyncratic reaction to contrast material. A 56-year-old woman with hypertension developed a hemiparesis with confusion and disorientation 3 hours after routine coronary angiography. The procedure had been prolonged, and during it she had received 130 mL of iopromide contrast. A metabolic screen was negative, and cerebral angiography and MR scan of brain were normal. She recovered completely by day 5. Contrast-induced encephalopathy should be considered in patients developing focal neurological deficits following coronary angiography. Patients requiring investigations to exclude acute stroke in this setting should not receive additional intravenous or intra-arterial contrast, although MR with gadolinium appears safe. Better awareness of this complication should avoid potentially harmful interventions such as thrombolysis.