Aims:The aim of this study was to assess the stroke rate after transcatheter mitral valve repair (TMVR) with the MitraClip, comparing it with surgical mitral valve repair (SMVR) and optimal medical treatment (OMT). Methods and results:In December 2018, we systematically searched PubMed, Embase and Cochrane Controlled Register of Trials for studies comparing TMVR with SMVR and/or OMT for the treatment of severe mitral regurgitation. Random-effects and cumulative meta-analysis was performed. Ten studies were included (seven of TMVR versus SMVR and three of TMVR versus OMT), providing a total of 1,881 patients and 61 pooled strokes (16 in TMVR versus SMVR and 45 in TMVR versus OMT). There was no difference in stroke incidence between TMVR and SMVR (pooled OR 0.49 [0.17, 1.42], p=0.19). However, there was a trend towards a lower stroke risk in TMVR. For TMVR versus OMT, no difference in stroke rate was identified (pooled OR 1.09 [0.60, 1.97], p=0.79). Post-procedure de novo atrial fibrillation was more frequent in SMVR when compared with TMVR.Conclusions: Despite both a low number of pooled stroke events and the failure to reach the pre-specified statistical significance, there was a trend for a lower post-procedure stroke rate in TMVR when compared with SMVR and a similar one between TMVR and OMT alone.

Alport syndrome (AS) is caused by pathogenic mutations in the genes encoding α3, α4 or α5 chains of collagen IV (COL4A3/COL4A4/COL4A5), resulting in hematuria, chronic renal failure (CRF), sensorineural hearing loss (SNHL) and ocular abnormalities. Mutations in the X-linked COL4A5 gene have been identified in 85% of the families (XLAS). In this study, 22 of 60 probands (37%) of unrelated Portuguese families, with clinical diagnosis of AS and no evidence of autosomal inheritance, had pathogenic COL4A5 mutations detected by Sanger sequencing and/or multiplex-ligation probe amplification, of which 12 (57%) are novel. Males had more severe and earlier renal and extrarenal complications, but microscopic hematuria was a constant finding irrespective of gender. Nonsense and splice site mutations, as well as small and large deletions, were associated with younger age of onset of SNHL in males, and with higher risk of CRF and SNHL in females. Pathogenic COL4A3 or COL4A4 mutations were subsequently identified in more than half of the families without a pathogenic mutation in COL4A5. The lower than expected prevalence of XLAS in Portuguese families warrants the use of next-generation sequencing for simultaneous COL4A3/COL4A4/COL4A5 analysis, as first-tier approach to the genetic diagnosis of collagen type IV-related nephropathies.

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Due to concerns regarding neurohormonal activation and fluid retention, adrenergic alpha‐1 receptor antagonists (A1Bs) are generally avoided in the setting of heart disease, namely, symptomatic heart failure (HF) with reduced ejection fraction (HFrEF). However, this contraindication is mainly supported by ancient studies, having recently been challenged by newer ones. We aim to perform a comprehensive meta‐analysis aimed at ascertaining the extent to which A1Bs might influence cardiovascular (CV) outcomes. We systematically searched PubMed, Cochrane Central Register of Controlled Trials and Web of Science for both prospective and retrospective studies, published until 1 December 2020, addressing the impact of A1Bs on both clinical outcomes—namely, acute heart failure (AHF), acute coronary syndrome (ACS), CV and all‐cause mortality—and on CV surrogate measures, specifically left ventricular ejection fraction (LVEF) and exercise tolerance, by means of exercise duration. Both randomized controlled trials (RCTs) and studies including only HF patients were further investigated separately. Study‐specific odds ratios (ORs) and mean differences (MDs) were pooled using traditional meta‐analytic techniques, under a random‐effects model. A record was registered in PROSPERO database, with the code number CRD42020181804. Fifteen RCTs, three non‐randomized prospective and two retrospective studies, encompassing 32 851, 19 287, and 71 600 patients, respectively, were deemed eligible; 62 256 patients were allocated to A1B, on the basis of multiple clinical indications: chronic HF itself [14 studies, with 72 558 patients, including seven studies with 850 HFrEF or HF with mildly reduced ejection fraction (HFmrEF) patients], arterial hypertension (four studies, with 44 184 patients) and low urinary tract symptoms (two studies, with 6996 patients). There were 25 998 AHF events, 1325 ACS episodes, 955 CV deaths and 33 567 all‐cause deaths. When considering only RCTs, A1Bs were, indeed, found to increase AHF risk (OR 1.78, [1.46, 2.16] 95% CI, P < 0.00001, i2 2%), although displaying no significant effect on neither ACS nor CV or all‐cause mortality rates (OR 1.02, [0.91, 1.15] 95% CI, i2 0%; OR 0.95, [0.47, 1.91] 95% CI, i2 17%; OR 1.1, [0.84, 1.43] 95% CI, i2 17%, respectively). Besides, when only HF patients were evaluated, A1Bs revealed themselves neutral towards not only ACS, CV, and all‐cause mortality events (OR 0.49, [0.1, 2.47] 95% CI, i2 0%; OR 0.7, [0.21, 2.31] 95% CI, i2 21%; OR 1.09, [0.53, 2.23] 95% CI, i2 17%, respectively), but also AHF (OR 1.13, [0.66, 1.92] 95% CI, i2 0%). As for HFrEF and HFmrEF, A1Bs were found to exert a similarly inconsequential effect on AHF rates (OR 1.01, [0.5–2.05] 95% CI, i2 6%). Likewise, LVEF was not significantly influenced by A1Bs (MD 1.66, [−2.18, 5.50] 95% CI, i2 58%). Most strikingly, exercise tolerance was higher in those under this drug class (MD 139.16, [65.52, 212.8] 95% CI, P < 0.001, i2 26%). A1Bs do not seem to exert a negative influence on the prognosis of HF—and even...

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