BackgroundVentricular arrhythmia is a leading cause of cardiac death among patients with post‐infarction left ventricular aneurysm (PI‐LVA). The effect of coronary revascularization in PI‐LVA patients with ventricular tachyarrhythmia remains unknown. This study aims to investigate the impact of revascularization therapy on clinical outcomes in these patients.MethodsA total of 238 PI‐LVA patients were enrolled, and 59 patients were presented with sustained ventricular tachycardia (VT) or ventricular fibrillation (VF). Patients were classified into 4 groups by treatment strategies (medical or revascularization) and the presence of VT/VF: group 1 (n = 57): VT/VF− and revascularization−; group 2 (n = 122): VT/VF− and revascularization+; group 3 (n = 34): VT/VF+ and revascularization+; and group 4 (n = 25): VT/VF+ and revascularization‐. The clinical outcomes were compared, and the primary endpoint was cardiac death or heart transplantation.ResultsPatients were followed up for 45 ± 16 months, and 41 patients (17.2%) reached the primary endpoint. Kaplan–Meier analysis showed that in VT/VF− patients, revascularization associated with higher cardiac survival compared with medical therapy (log‐rank p = .002), but in VT/VF+ patients, revascularization did not predict better cardiac outcome (log‐rank p = .901). Cox regression analysis revealed PET‐EF (HR 4.41, 95% CI: 1.72–11.36, p = .002) and moderate/severe mitral regurgitation (HR 2.32, 95% CI: 1.02–5.30, p = .046) as independent predictors of adverse cardiac outcome in patients with VT/VF.ConclusionPI‐LVA patients with VT/VF are at high risk of adverse cardiac outcome, and coronary revascularization does not mitigate this risk, although revascularization was associated with higher cardiac survival in PI‐LVA patients without VT/VF. 相似文献
Magnetic resonance imaging (MRI) at 3.0 T is becoming more common, but there is a lack of sufficient evidence on the safety of a 3.0 T scan in patients with pacemakers. This study aimed to investigate the safety and practical concerns of 3.0 T scans for patients with MR-conditional pacemakers.
Methods
Twenty consecutive patients were enrolled. A standardized protocol was developed by cardiologists, pacemaker engineers, and radiologists. Pacemaker interrogation was performed immediately before and after the scan. Scan-related adverse events were documented, and imaging quality was graded as level 1 to 4 by radiologists.
Results
Twenty-three MRI scans of different body regions (brain?=?13, lumbar spine?=?4, cervical spine?=?2, and heart?=?4) were performed, and the average time of a scan was 25?±?11 min. No significant changes in sensing amplitude (atrial 3.1?±?1.1 mV vs. 2.9?±?1.2 mV, P?=?0.71; ventricular 9.3?±?3.5 mV vs. 10.2?±?3.4 mV, P?=?0.46), lead impedances (atrial 647?±?146 Ω vs. 627?±?151 Ω, P?=?0.7; ventricular: 780?±?247 Ω vs.711?±?226 Ω, P?=?0.36), or pacing threshold (atrial 0.6?±?0.2 V/0.4 ms vs. 0.6?±?0.2 V/0.4 ms, P?=?0.71; ventricular 0.7?±?0.3 V/0.4 ms vs. 0.7?±?0.2 V/0.4 ms, P?=?0.85) were observed pre- and postscan. No adverse events were detected. Image quality review showed grade 1 quality in 16 patients and grade 2 quality in 4 patients with artifacts of pulse generators and leads in cardiac MRI scan and no impact on diagnostic value.
Conclusion
Our initial data indicated that 3.0 T scanning might be feasible under a standardized protocol with good diagnostic imaging quality irrespective of body region in patients with MR-conditional pacemakers.
The role of lipoprotein (a) [Lp(a)] in coronary artery diseases (CAD) with special clinical background such as type 2 diabetes mellitus (T2DM) has not been fully determined. The aim of the present study was to investigate the relation of Lp(a) to type 2 diabetic patients with or without CAD.
Methods and results
A total of 2040 consecutive patients with T2DM who received selective coronary angiography (CAG) due to angina-like chest pain were enrolled. The patients were subsequently divided into CAD and non-CAD groups according to the results of CAG. The severity of CAD was evaluated by the Gensini Score (GS), number of stenotic vessels, and history of myocardial infarction (MI). Data showed that Lp(a) levels were higher in the CAD group than in the non-CAD group (median: 15.00 mg/dL vs. 11.88 mg/dL, P = 0.025). The results from CAD subgroup analysis indicated that the patients with MI, multiple-vessel disease and high GS had higher Lp(a) levels compared with those in their matched subgroups (P < 0.05, respectively). After adjustment for confounders, Lp(a) levels were independently related to the presence and severity of CAD (CAD:OR = 1.564; MI:OR = 1.523; high GS:OR = 1.388; multiple-vessel disease:OR = 1.455; P < 0.05, respectively).
Conclusion
Elevated Lp(a) levels were independently associated with the presence and severity of CAD in patients with T2DM. More studies are necessary to confirm our findings. 相似文献
Premature ventricular complex (PVC) was mainly studied by 24-hour Holter in previous studies. However, the value of long-term Home Monitoring of PVC burden early after ICD implantation is unknown.
Methods
The data of 416 patients with ICD were analyzed. The percentage of days with frequent PVC (≥10/h) within 30th–90th days was calculated as the continuous frequent PVC (CfPVC) percentage. ROC curve of CfPVC percentages was plotted. Kaplan-Meier survival and Cox regression were used to assess the cumulative risks.
Results
Based on ROC curves, the cut-off value for the CfPVC percentage was 40%. According to Kaplan-Meier analysis and multivariate Cox regression analysis, CfPVC percentage ≥40% was an independent predictor of higher incidences of VAEs, appropriate ATP, appropriate shocks, and cardiac death.
Conclusion
A long-term continuous burden of frequent PVC with CfPVC percentage ≥40% can be a predictor of future VAEs, appropriate ATP, appropriate shocks and cardiac death in ICD recipients. 相似文献
The role of heme oxygenase-1 (HO-1) in the cardioprotection induced by delayed remote ischemic preconditioning (DRIPC) has not been investigated. Therefore, this study was designed to investigate whether HO-1 is involved in DRIPC-mediated cardioprotection in an isolated perfused rat heart model.
Materials and methods
Isolated rat hearts were subjected to 30 min ischemia followed by 60 min reperfusion. DRIPC (four cycles 5-min occlusion and 5-min reflow at the unilateral hind limb once per day for 1, 2, or 3 d before heart isolation, abbreviated as D1RIPC, D2RIPC, or D3RIPC respectively). Infarct size, myocardial troponin levels, and heart function were measured. The protein and messenger RNA levels of HO-1 were determined.
Results
DRIPC facilitated postischemic cardiac functional recovery and decreased cardiac enzyme release. The infarct size-limiting effect of DRIPC was more pronounced in the D3RIPC group (10.22 ± 2.57%) than the D1RIPC group (22.34 ± 4.02%, P < 0.001) or the D2RIPC group (14.60 ± 3.13%, P = 0.034). These effects in the D1RIPC group could be blocked by Zinc Protoporphyrin IX (ZnPP) (an HO-1 specific inhibitor). DRIPC-mediated cardioprotection was associated with enhanced HO-1 protein expression (D1RIPC, 0.11 ± 0.03; versus 0.15 ± 0.06 in the D2RIPC group, P = 0.06; versus 0.20 ± 0.04 in the D3RIPC group, P = 0.04) and messenger RNA levels of HO-1 expression.
Conclusions
Our findings suggest that HO-1 is involved in the cardioprotection induced by DRIPC, and that increase in the number of preconditioning stimuli may enhance cardioprotective effects accompanied with increased HO-1 level. 相似文献