RESUMO
BACKGROUND@#Coronary atherosclerotic plaque could go through rapid progression and induce adverse cardiac events. This study aimed to evaluate the impacts of smoking status on clinical outcomes of coronary non-target lesions.@*METHODS@#Consecutive patients with coronary heart disease who underwent two serial coronary angiographies were included. All coronary non-target lesions were recorded at first coronary angiography and analyzed using quantitative coronary angiography at both procedures. Patients were grouped into non-smokers, quitters, and smokers according to their smoking status. Clinical outcomes including rapid lesion progression, lesion re-vascularization, and myocardial infarction were recorded at second coronary angiography. Multivariable Cox regression analysis was used to investigate the association between smoking status and clinical outcomes.@*RESULTS@#A total of 1255 patients and 1670 lesions were included. Smokers were younger and more likely to be male compared with non-smokers. Increase in percent diameter stenosis was significantly lower (2.7 [0.6, 7.1] % vs. 3.5 [0.9, 8.9]%) and 3.4 [1.1, 7.7]%, P = 0.020) in quitters than those in smokers and non-smokers. Quitters tended to have a decreased incidence of rapid lesions progression (15.8% [76/482] vs. 21.6% [74/342] and 20.6% [89/431], P = 0.062), lesion re-vascularization (13.1% [63/482] vs. 15.5% [53/432] and 15.5% [67/431], P = 0.448), lesion-related myocardial infarction (0.8% [4/482] vs. 2.6% [9/342] and 1.4% [6/431], P = 0.110) and all-cause myocardial infarction (1.9% [9/482] vs. 4.1% [14/342] and 2.3% [10/431], P = 0.128) compared with smokers and non-smokers. In multivariable analysis, smoking status was not an independent predictor for rapid lesion progression, lesion re-vascularization, and lesion-related myocardial infarction except that a higher risk of all-cause myocardial infarction was observed in smokers than non-smokers (hazards ratio: 3.00, 95% confidence interval: 1.04-8.62, P = 0.042).@*CONCLUSION@#Smoking cessation mitigates the increase in percent diameter stenosis of coronary non-target lesions, meanwhile, smokers are associated with increased risk for all-cause myocardial infarction compared with non-smokers.
RESUMO
Objectives: To study serum level of M2-muscarinic receptor autoantibody (M2-AAb) in hypertrophic cardiomyopathy (HCM) patients with its relationship to relevant clinical parameters. Methods: Our research included in 2 groups: HCM group, 133 patients and they were divided into 3 subgroups:Obstructive hypertrophic cardiomyopathy (HOCM) subgroup, 72, Latent obstructive hypertrophic cardiomyopathy (LHOCM) subgroup, 22 and Non-obstructive hypertrophic cardiomyopathy (NOCM) subgroup, 39; since there was no obstruction of left ventricular outflow tract (LVOT) in LHOCM and NOCM patients at resting, LHOCM and NOCM patients were combined as LHOCM+NOCM subgroup, 61 in comparison with HOCM subgroup. And Control group, 40 subjects had no organic heart disease and autoimmune diseases which were confirmed by 12 lead ECG, transthoracic echocardiography and routine hematological tests, they were not using β-blockers, glucocorticoids and immune-suppressants. Serum levels of M2-AAb were examined by ELISA, the relationship between M2-AAb and relevant clinical parameters were studied. Results: Compared with Control group, HCM group had increased serum level of M2-AAb [22.91 (17.21, 29.64) ng/ml] vs (17.14±5.66) ng/ml, P<0.01; M2-AAb was similar among HOCM, LHOCM and NOCM subgroups; M2-AAb in female patients were higher than male, P=0.001. Further investigation presented that the patients with family history of sudden death had the higher M2-AAb, P<0.05; patients with atrial fibrillation (AF) or left atrial diameter (LAD)≥50 mm or moderate to severe mitral regurgitation (MR) had the higher M2-AAb than those without such problems, all P<0.05. In HCM group, log M2-AAb was positively related to resting LVOT gradient (r=0.178, P=0.040); in HOCM subgroup, log M2-AAb was marginal positively related to resting LVOT gradient (r=0.224, P=0.058). Conclusions: Serum M2-AAb was elevated in HCM patients; gender, family history of sudden death may affect M2-AAb level; patients combining AF or LAD≥50 mm or moderate-severe MR had the higher M2-AAb and it was related to resting LVOT gradient.