Cerebral microbleed distribution following cardiac surgery can mimic cerebral amyloid angiopathy.

BACKGROUND AND AIMS: Having anecdotally noted a high frequency of lobar-restricted cerebral microbleeds (CMBs) mimicking cerebral amyloid angiopathy (CAA) in patients with previous cardiac surgery (especially valve replacement) presenting to our transient ischaemic attack (TIA) clinic, we set out to objectively determine the frequency and distribution of microbleeds in this population. METHODS: We performed a retrospective comparative cohort study in consecutive patients presenting to two TIA clinics with either: (1) previous coronary artery bypass grafting (CABG) (n=41); (2) previous valve replacement (n=41) or (3) probable CAA (n=41), as per the Modified Boston Criteria, without prior cardiac surgery. Microbleed number and distribution was determined and compared. RESULTS: At least one lobar-restricted microbleed was found in the majority of cardiac surgery patients (65%) and 32/82 (39%) met diagnostic criteria for CAA. Valve replacement patients had a higher microbleed prevalence (90 vs 51%, p<0.01) and lobar-restricted microbleed count (2.6±2.7 vs 1.0±1.4, p<0.01) than post-CABG patients; lobar-restricted microbleed count in both groups was substantially less than in CAA patients (15.5±20.4, p<0.01). In postcardiac surgery patients, subcortical white matter (SWM) microbleeds were proportionally more frequent compared with CAA patients. Receiver operator curve analysis of a 'location-based' ratio (calculated as SWM/SWM+strictly-cortical CMBs), revealed an optimal ratio of 0.45 in distinguishing cardiac surgery-associated microbleeds from CAA (sensitivity 0.56, specificity 0.93, area under the curve 0.71). CONCLUSION: Lobar-restricted microbleeds are common in patients with past cardiac surgery, however a higher proportion of these CMBs involve the SWM than in patients with CAA

Quantifying the Shift Toward Transcatheter Aortic Valve Replacement in Low-Risk Patients: A Meta-Analysis.

BACKGROUND: In recent years, use of transcatheter aortic valve replacement has expanded to include patients at intermediate- and low-risk cohorts. We sought to determine disease prevalence and treatment distribution including transcatheter aortic valve replacement eligibility in low-risk patients across 37 advanced economies. METHODS AND RESULTS: Four systematic searches were conducted across MEDLINE, EMBASE, and the Cochrane database for studies evaluating disease prevalence, severity, decision making, and survival in patients with aortic stenosis. Estimates of disease prevalence and treatment eligibility were calculated using stochastic simulation and population data for the 37 countries comprising the International Monetary Fund's advanced economies index. Fifty-six studies comprising 42 965 patients were included across 5 domains: prevalence, severity, symptom status, treatment modality, and outcome. The pooled prevalence in the general population aged 60 to 74 years and >75 years was 2.8% (95% confidence interval [CI], 1.4%-4.1%) and 13.1% (95% CI, 8.2%-17.9%), respectively-corresponding to an estimated 16.1 million (95% CI, 12.2-20.3) people in 37 advanced economies. Of these, an estimated 3.2 million (95% CI, 2.2-4.4) patients have severe aortic stenosis with 1.9 million (95% CI, 1.3-2.6) eligible for surgical aortic valve replacement. There are ≈485 230 (95% CI, 284 550-66 7350) high-risk/inoperable patients, 152 690 (95% CI, 73 410-263 000) intermediate-risk patients, and 378 890 (95% CI, 205 130-610 210) low-risk patients eligible for transcatheter aortic valve replacement. CONCLUSIONS: With a prevalence of 4.5%, an estimated 16.1 million people aged ≥60 years across 37 advanced economies have aortic stenosis. Of these, there are ≈1.9 million patients eligible for surgical aortic valve replacement and 1.0 million patients eligible for transcatheter aortic valve replacement.British Heart Foundation Translational Award TG/15/4/31891 (Drs De Sciscio, Brubert, and Moggridge) and British Heart Foundation Special Project Grant SP/15/5/31548 (Drs Serrani, Stasiak, and Moggridge)

Hydralazine does not ameliorate nitric oxide resistance in chronic heart failure

Purpose: The A-HeFT trial demonstrated incremental survival with hydralazine/isosorbide dinitrate combination in African–American patients with chronic heart failure (CHF). It has been suggested that hydralazine might enhance nitric oxide (NO)—mediated effects of organic nitrates by decreasing superoxide (O2−) formation, one of the factors inducing NO resistance. We evaluated whether hydralazine therapy potentiates nitrate-induced vasodilation and inhibition of platelet aggregation by ameliorating NO resistance. Methods: Patients (n  = 14) with NYHA class II-III CHF were studied in a randomised, double-blind, placebo-controlled, crossover study of the effects of hydralazine therapy (25 mg b.d., for 1 week) on physiological responsiveness to glyceryl trinitrate (GTN). Vascular response to GTN was assessed via applanation tonometry, as change in augmentation index (AIx) over time. Platelet responsiveness to GTN and sodium nitroprusside (SNP) was determined, as inhibition of ADP-induced platelet aggregation. O2− release was evaluated during aggregation via lucigenin-derived chemiluminescence. Results: Platelet responsiveness to the NO donors GTN and SNP was impaired, denoting the presence of severe NO resistance. Hydralazine therapy decreased systolic blood pressure by 6.8 ± 10.5 (S.D.) mmHg (p = 0.02), and caused a reduction in AIx by 15 ± 24% (p = 0.03). However, there were no significant changes in platelet aggregability and associated O2− release, or in platelet or vascular responses to NO donor. Conclusion: The results of the present study do not support the assumption that hydralazine could be viewed as a “NO enhancer”; there is no evidence of attenuation of NO resistance by hydralazine treatment.Yuliy Y. Chirkov, Michele De Sciscio, Aaron L. Sverdlov, Sue Leslie, Peter R. Sage and John D. Horowit