Various comorbidities represent risk factors for severe coronavirus disease 2019 (COVID‐19). The impact of smoking on COVID‐19 severity has been previously reported in several meta‐analyses limited by small sample sizes and poor methodology. We aimed to rigorously and definitively quantify the effects of smoking on COVID‐19 severity. MEDLINE, Embase, CENTRAL, and Web of Science were searched between 1 December 2019 and 2 June 2020. Studies reporting smoking status of hospitalized patients with different severities of disease and/or at least one clinical endpoint of interest (disease progression, intensive care unit admission, need for mechanical ventilation, and mortality) were included. Data were pooled using a random‐effects model. This study was registered on PROSPERO: CRD42020180920. We analyzed 47 eligible studies reporting on 32 849 hospitalized COVID‐19 patients, with 8417 (25.6%) reporting a smoking history, comprising 1501 current smokers, 5676 former smokers, and 1240 unspecified smokers. Current smokers had an increased risk of severe COVID‐19 (risk ratios [RR]: 1.80; 95% confidence interval [CI]: 1.14‐2.85; P = .012), and severe or critical COVID‐19 (RR: 1.98; CI: 1.16‐3.38; P = .012). Patients with a smoking history had a significantly increased risk of severe COVID‐19 (RR: 1.31; CI: 1.12‐1.54; P = .001), severe or critical COVID‐19 (RR: 1.35; CI: 1.19‐1.53; P < .0001), in‐hospital mortality (RR: 1.26; CI: 1.20‐1.32; P < .0001), disease progression (RR: 2.18; CI: 1.06‐4.49; P = .035), and need for mechanical ventilation (RR: 1.20; CI: 1.01‐1.42; P = .043). Patients with any smoking history are vulnerable to severe COVID‐19 and worse in‐hospital outcomes. In the absence of current targeted therapies, preventative, and supportive strategies to reduce morbidity and mortality in current and former smokers are crucial.

Background: Despite the initial evidence supporting the utility of intravascular imaging to guide percutaneous coronary intervention (PCI), adoption remains low. Recent new trial data have become available. An updated study‐level meta‐analysis comparing intravascular imaging to angiography to guide PCI was performed. This study aimed to evaluate the clinical outcomes of intravascular imaging–guided PCI compared with angiography‐guided PCI. Methods and Results: A random‐effects meta‐analysis was performed on the basis of the intention‐to‐treat principle. The primary outcomes were major adverse cardiac events, cardiac death, and all‐cause death. Mixed‐effects meta‐regression was performed to investigate the impact of complex PCI on the primary outcomes. A total of 16 trials with 7814 patients were included. The weighted mean follow‐up duration was 28.8 months. Intravascular imaging led to a lower risk of major adverse cardiac events (relative risk [RR], 0.67 [95% CI, 0.55–0.82]; P <0.001), cardiac death (RR, 0.49 [95% CI, 0.34–0.71]; P <0.001), stent thrombosis (RR, 0.63 [95% CI, 0.40–0.99]; P =0.046), target‐lesion revascularization (RR, 0.67 [95% CI, 0.49–0.91]; P =0.01), and target‐vessel revascularization (RR, 0.60 [95% CI, 0.45–0.80]; P <0.001). In complex lesion subsets, the point estimate for imaging‐guided PCI compared with angiography‐guided PCI for all‐cause death was a RR of 0.75 (95% CI, 0.55–1.02; P =0.07). Conclusions: In patients undergoing PCI, intravascular imaging is associated with reductions in major adverse cardiac events, cardiac death, stent thrombosis, target‐lesion revascularization, and target‐vessel revascularization. The magnitude of benefit is large and consistent across all included studies. There may also be benefits in all‐cause death, particularly in complex lesion subsets. These results support the use of intravascular imaging as standard of care and updates of clinical guidelines.

The effect of atrial fibrillation catheter ablation on cardiovascular outcomes in heart failure is an important outstanding research question. We undertook a meta-analysis of randomized controlled trials comparing ablation to medical therapy in patients with AF and heart failure. We systematically identified all trials comparing catheter ablation to medical therapy in patients with heart failure and atrial fibrillation. The pre-specified primary endpoint was all-cause mortality in trials with at least 2 years of follow-up. The secondary endpoint was heart failure hospitalization. Sensitivity analyses were performed for trials with any follow-up and trials deemed at low risk of bias. Eight trials (1390 patients) were included. Seven hundred and seven patients were randomized to catheter ablation and 683 to medical therapy. In the primary analysis (three trials, n = 977), catheter ablation reduced mortality compared with medical therapy [relative risk (RR): 0.61, 95% confidence interval (CI): 0.44 to 0.84, P = 0.003]. Catheter ablation also reduced heart failure hospitalizations compared with medical therapy (RR: 0.60, 95% CI: 0.49–0.74, P < 0.001). The effect on stroke was not statistically significant (RR: 0.62, 95% CI: 0.28–1.37, P = 0.237). There was low heterogeneity between studies. Sensitivity analyses were consistent with the primary analyses. In patients with atrial fibrillation and heart failure, catheter ablation reduces mortality and the occurrence of heart failure hospitalizations.

Background: Maternal cardiovascular risk factors have been associated with adverse maternal and fetal outcomes. Given the difficulty in establishing causal relationships using epidemiological data, we applied Mendelian randomization to explore the role of cardiovascular risk factors on risk of developing preeclampsia or eclampsia, and low fetal birthweight. Methods: Uncorrelated single-nucleotide polymorphisms associated systolic blood pressure (SBP), body mass index, type 2 diabetes, LDL (low-density lipoprotein) with cholesterol, smoking, urinary albumin-to-creatinine ratio, and estimated glomerular filtration rate at genome-wide significance in studies of 298 957 to 1 201 909 European ancestry participants were selected as instrumental variables. A 2-sample Mendelian randomization study was performed with primary outcome of preeclampsia or eclampsia (PET). Risk factors associated with PET were further investigated for their association with low birthweight. Results: Higher genetically predicted SBP was associated increased risk of PET (odds ratio [OR] per 1-SD SBP increase 1.90 [95% CI=1.45–2.49]; P =3.23×10 ⁻⁶ ) and reduced birthweight (OR=0.83 [95% CI=0.79–0.86]; P =3.96×10 ⁻¹⁸ ), and this was not mediated by PET. Body mass index and type 2 diabetes were also associated with PET (respectively, OR per 1-SD body mass index increase =1.67 [95% CI=1.44–1.94]; P =7.45×10 ⁻¹² ; and OR per logOR increase type 2 diabetes =1.11 [95% CI=1.04–1.19]; P =1.19×10 ⁻³ ), but not with reduced birthweight. Conclusions: Our results provide evidence for causal effects of SBP, body mass index, and type 2 diabetes on PET and identify that SBP is associated with reduced birthweight independently of PET. The results provide insight into the pathophysiological basis of PET and identify hypertension as a potentially modifiable risk factor amenable to therapeutic intervention.