(1) Background: The exact mechanism underlying hand strength reduction (HSR) after coronary angiography with transradial access (TRA) or transulnar access (TUA) remains unknown. (2) Methods: This study aimed to assess the impact of using a larger or smaller forearm artery access on the incidence of HSR at 30-day follow-up. This was a prospective randomized trial including patients referred for elective coronary angiography or percutaneous coronary intervention. Based on the pre-procedural ultrasound examination, the larger artery was identified. Patients were randomized to larger radial artery (RA) or ulnar artery (UA) or a group with smaller RA/UA. The primary endpoint was the incidence of HSR, while the secondary endpoint was the incidence of subjective HSR, paresthesia, and any hand pain. (3) Results: We enrolled 200 patients (107 men and 93 women; mean age 68 ± 8 years) between 2017 and 2018. Due to crossover between TRA and TUA, there were 57% (n = 115) patients in larger RA/UA and 43% (n = 85) patients in smaller RA/UA. HSR occurred in 29% (n = 33) patients in larger RA/UA and 47% (n = 40) patients in smaller RA/UA (p = 0.008). Subjective HSR was observed in 10% (n = 12) patients in larger RA/UA and 21% (n = 18) patients in smaller RA/UA (p = 0.03). Finally, paresthesia was noted in 7% (n = 8) patients in larger RA/UA and 22% (n = 15) in smaller RA/UA (p = 002). Independent factors of HSR were larger RA/UA (OR 0.45; 95% CI, 0.24–0.82; p < 0.01) and the use of TRA (OR 1.87; 95% CI, 1.01–34; p < 0.05). (4) Conclusions: The use of a larger artery as vascular access was associated with a lower incidence of HSR at 30-day follow-up.
(1) Background: We aimed to assess the impact of the selection of a larger radial or ulnar artery on the efficacy of access and vascular complications, based on preprocedural ultrasonographic examination. (2) Methods: This prospective, randomized trial included patients undergoing coronary angiography (CAG) or percutaneous coronary intervention (PCI). Patients were randomized into either a larger ulnar artery (UA) or radial artery (RA) group or smaller UA/RA group. The primary endpoint was successful CAG/PCI without crossover to another artery. The secondary endpoints were incidences of radial or ulnar artery occlusion (RAO/UAO) at the 24 h and 30 day follow-up. (3) Results: Between 2017 and 2018, 200 patients (107 men, mean age 68 ± 8 years) were enrolled. The success of CAG/PCI via the access site was 98% and 83% (p < 0.001) in the larger UA/RA group and smaller UA/RA group, respectively. The independent factor for CAG/PCI success was the larger artery (OR 9.8, 95%CI 2.11–45.5; p < 0.005). The larger UA/RA was superior, with RAO/UAO at 24 h: OR 0.07, 95%CI 0.09–0.61; p < 0.016; and RAO/UAO at 30 days: OR 0.25, 95%CI 0.05–0.12; p < 0.001. (4) Conclusions: Larger artery access was shown to be more efficient and safer than recessive forearm artery access.
Recently, associations between the biomarker galectin-3 and numerous pathological processes involved in heart failure (HF) and right ventricular (RV) function have been observed. We aimed to assess the long-term prognostic ability of galectin-3 and RV function parameters for all-cause mortality in HF patients treated with cardiac resynchronization therapy (CRT). We prospectively studied 63 symptomatic HF patients with a left ventricular (LV) ejection fraction (EF) ≤ 35%. The median serum galectin-3 concentration was 13.4 ng/mL (IQR 11.05, 17.15). A detailed assessment of LV and RV geometry and function was performed with echocardiography. CRT defibrillator implantation was achieved in all patients without major complications. The follow-up lasted 5 years. In the multivariable Cox regression model, independent predictors for all-cause mortality were log baseline galectin-3 and baseline RV function expressed as tricuspid annular plane systolic excursion with HR 2.96 (p = 0.037) and HR 0.88 (p = 0.023), respectively. Analysis of subgroups defined by galectin-3 concentration and CRT response showed that patients with high baseline galectin-3 concentrations and a lack of response to CRT had a significantly lower probability of survival. In our patient cohort, the baseline galectin-3 concentration and RV function were independent predictors of long-term all-cause mortality in HFrEF patients following CRT implantation.
In patients with an implanted pacemaker, an increase of pacing threshold is one of the most dangerous complications, which may lead to syncope, cardiac arrest, or death in pacemaker-dependent patients. The increase of pacing threshold may be caused by electrolyte disturbances, acid-base disorders, hyperglycaemia, or hypothyroidism. In some cases it may also occur due to ischaemia or myocardial infarction in the area near the tip of the electrode. However, it is uncommon because pacing leads are usually implanted in the apex of the right ventricle where ischaemia is relatively rare. We present an illustrative case of an 84-year-old man with a dual-chamber pacemaker implanted due to complete atrioventricular block 10 years ago, hypertension, diabetes mellitus, chronic kidney disease, and hyperlipidaemia, without previous history of coronary artery disease, who was admitted to our hospital after sudden cardiac arrest due to ineffective pacing with no escape rhythm (Fig. 1). Interrogation of the pacemaker was performed and an increase of pacing threshold to 7.5 V at 1.0 ms was found. The chest radiograph and transthoracic echocardiography showed no pacing lead dislocation. Blood tests showed hyperglycaemia (330 mg/dL) and mild metabolic acidosis (pH 7.2). The level of serum troponin T increased, but without growth typical for myocardial infarction. After compensation of metabolic disorders (pH 7.45, glycaemia 171 mg/dL) a decrease in the pacing threshold was observed to 1.25 V at 1.0 ms, but it still remained elevated in comparison to the baseline parameters obtained at the last scheduled visit (1.0 V at 0.4 ms). Transthoracic echocardiography showed regional wall motion abnormalities near the tip of the ventricular pacing lead (Fig. 2). Next, coronary angiography was performed and showed significant stenosis of the left anterior descending artery with TIMI-2 flow (Fig. 3), requiring angioplasty and stent implantation with the final TIMI-3 effect. After percutaneous coronary intervention, an interrogation of the pacemaker was performed and a decrease in the pacing threshold was found 1.0 V at 1.0 ms (the trend of pacing threshold is shown in Fig. 4). This case report shows that metabolic disturbances and ischaemia may elevate the pacing threshold to very high values and should be considered as a possible and treatable cause of ineffective pacing.
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