Efficacy of scleral-fixated 3-looped haptics intraocular lens implantation for surgical management of microspherophakia.

AIM: To evaluate the safety and efficacy of scleral-fixated 3-looped haptics intraocular lens (IOL) implantation for surgical management of microspherophakia. METHODS: A retrospective case series include 10 microspherophakic patients (15 eyes) who underwent lens removal plus a modified surgical treatment of scleral-fixated 3-looped haptics IOL implantation. The primary outcomes involved visual acuity, intraocular pressure (IOP). Secondary outcomes were spherical equivalent (SE), anterior chamber depth (ACD), corneal endothelial cell density and postoperative complications. RESULTS: After a postoperative follow-up of 17.60±15.44mo, improved visual outcomes can be observed. The uncorrected distance visual acuity (UCVA) logMAR improved from 1.54±0.59 preoperatively to 0.51±0.35 postoperatively (P=0.001), and best corrected visual acuity (BCVA) logMAR improved from 0.97±0.91 preoperatively to 0.24±0.23 postoperatively (P=0.003). Moreover, the SE decreased from -9.58±7.47D preoperatively to -0.65±2.21 D postoperatively (P<0.001). In terms of safety profile, the average IOP decreased from 21.10±12.94 mm Hg preoperatively to 14.03±3.57 mm Hg postoperatively (P=0.044), and the previously elevated IOP of three eyes decreased to the normal range. The ACD increased from 2.25±1.45 mm preoperatively to 3.35±0.39 mm postoperatively (P=0.017). The density of corneal endothelial cells did not change significantly after surgery (P=0.140). The posterior chamber IOLs were well centered and no severe complications were found. CONCLUSION: Lens removal plus the modified surgical treatment of scleral-fixated 3-looped haptics IOL implantation can help in improvement of visual acuity, which can be regarded as a relative safe method for the surgical management of microspherophakia.

Alterations in the transmural gradient of ventricular repolarization with different pacing sites in normal and heart failure canines.

Alterations of the transmural gradient of repolarization may contribute to the increase of transmural dispersion of repolarization and ventricular arrhythmias. The transmural gradient of repolarization may play an important role in sudden death associated with left ventricular epicardial pacing. To investigate the changes of transmural gradient dispersion of ventricular repolarization with different pacing sites in heart failure (HF) canines, 8 mongrel dogs were randomized into healthy group and HF group (n = 4). We mapped the monophasic action potential duration (MAPD) in the subendocardial, subepicardial and mid-myocardial layers of the left ventricle (LV) in canines of healthy and HF groups during right atrium (RA) pacing, right ventricular apical endocardial (RVEndo) pacing, left ventricular lateral epicardial (LVEpi) pacing and biventricular (Biv) pacing respectively. The results showed that in the healthy group, the MAPDs were significantly different among the three layers during RA pacing (all P < 0.05). The MAPD was longer in the mid-myocardial layer compared with those in the subepicardial and subendocardial layers during RVEndo, LVEpi or Biv pacing (P < 0.05). However, there was no significant difference in MAPD between the subendocardial and subepicardial layers during RVEndo, LVEpi or Biv pacing (P > 0.05). In the HF group, the MAPDs in all three layers were prolonged compared with those in the same locations in the healthy group (all P < 0.05). However, there were no differences in MAPD among the three layers during RA, RVEndo, LVEpi or Biv pacing (all P > 0.05). By MAP recording with our new mapping electrode, we found a transmural MAPD gradient among the three layers of the LV during RA pacing and the gradient between the subendocardial and subepicardial layers vanished during RVEndo, LVEpi or Biv pacing in healthy dogs. In contrast, there was no transmural MAPD gradient during RA, RVEndo, LVEpi or Biv pacing in HF dogs. These results are helpful to understand the mechanism of ventricular arrhythmias in patients with HF.

Myocardial ischemic changes of electrocardiogram in intracerebral hemorrhage: A case report and review of literature.

BACKGROUND: Cardiac injury may occur after acute pathology of central nervous system (CNS) without any evidence of primary cardiac diseases. The resulting structural and/or functional changes are called cerebrocardiac syndrome (CCS). The great majority of studies have been performed in patients with subarachnoid hemorrhage (SAH), while CCS data after intracerebral hemorrhage (ICH) are rare. It may cause diagnostic and therapeutic pitfalls for the clinician due to a lack of specific clinical manifestations and diagnostic methods. Understanding the underlying pathophysiological and molecular mechanism(s) following cerebrovascular incidents will help to implement prevention and treatment strategies to improve the prognosis. CASE SUMMARY: A 37-year-old man with a history of hypertension presented to our department on an emergency basis because of a sudden dizziness and left limb weakness. Cerebral computed tomography (CT) suggested ICH in the occipital and parietal lobes, and the chosen emergency treatment was hematoma evacuation. Left ventricular (LV) dysfunction occurred after the next 48 h and the electrocardiogram (ECG) showed non-ST elevation myocardial infarction. CCS was suspected first in the context of ICH due to the negative result of the coronary CT angiogram. CONCLUSION: Misinterpretation of ischemic-like ECGs may lead to unnecessary or hazardous interventions and cause undue delay of rehabilitation after stroke. Our objective is to highlight the clinical implications of CCS and we hope the differential diagnoses will be considered in patients with acute CNS diseases.