BACKGROUND: It is known that there is a pronounced circardian periodicity for the time of onset of acute myocardial infarction(AMI), with prominent increase in incidence of onset in the morning hours. However, the characteristic circardian variability in AMI is blunted in patients receiving beta-blockers or aspirin therapy before their presentation with AMI. These findings are attributed to the increase in platelet aggregability, blood coagulability, and plasma catecholamine that change coronary tone and myocardial oxygen demand. We hypothesize that, in addition to above physiologic and biochemical parameters, morphologic patterns of the coronary artery lesions are related to the development of circardian variation in AMI. METHOD: Subjects were 160 patients with AMI(male 92, female 68, mean age 56.9 +/-10.5 years old). Patients were classified by the time of onset of typical chest pain(AMI) by 6-hour interval from mid-night. Circardian variability of onset of AMI was compared with clinical findings and coronary angiographic findings. RESULTS: Incidence of onset of AMI was most frequent in the morning hours(6AM-noon,42.5%). There was no difference in degree of stenosis, lesion length, incidence of intraluminal thrombus, among 3 subgroups of AMI according to time of attack. Morning hour group had more frequent ulceration of coronary lesion than that of other groups(22.4% vs. 5.4%, p<0.01), and less frequent calcified lesion than that of other groups(3.0% vs 5.4%, p<0.05). Normal or minimal coronary artery lesion, that is Iess than 25% stenosis, was more frequent in the morning hour group comparing to that of other groups(11.9% vs. 9.78%). Eccentric stenosis(15.7% vs, 11,1%) and diffuse irregular lesion(25.5% vs. 16.7%) tended to be more frequent in the morning hour group. There were no differences in sex, age, incidence of hypertension, cigarette smoking, diabetes, degree of alcohol ingestion, ejection fraction, maximal CK value, preinfarction angina duration, past history of MI, and in incidence of arrhythmia. CONCLUSIONS: There were more ulcerative coronary atherosclerotic lesions, but fewer calcified coronary lesions in the morning group than in afternoon and night group. These findings indicate that morphology of coronary artery lesions may play a role in causing circardian variation in AMI.
Angina, Unstable ; Arrhythmias, Cardiac ; Aspirin ; Blood Platelets ; Constriction, Pathologic ; Coronary Vessels* ; Eating ; Female ; Humans ; Hypertension ; Incidence ; Myocardial Infarction* ; Oxygen ; Periodicity ; Plasma ; Smoking ; Thorax ; Thrombosis ; Ulcer

BACKGROUND: It is known that there is a pronounced circardian periodicity for the time of onset of acute myocardial infarction(AMI), with prominent increase in incidence of onset in the morning hours. However, the characteristic circardian variability in AMI is blunted in patients receiving beta-blockers or aspirin therapy before their presentation with AMI. These findings are attributed to the increase in platelet aggregability, blood coagulability, and plasma catecholamine that change coronary tone and myocardial oxygen demand. We hypothesize that, in addition to above physiologic and biochemical parameters, morphologic patterns of the coronary artery lesions are related to the development of circardian variation in AMI. METHOD: Subjects were 160 patients with AMI(male 92, female 68, mean age 56.9 +/-10.5 years old). Patients were classified by the time of onset of typical chest pain(AMI) by 6-hour interval from mid-night. Circardian variability of onset of AMI was compared with clinical findings and coronary angiographic findings. RESULTS: Incidence of onset of AMI was most frequent in the morning hours(6AM-noon,42.5%). There was no difference in degree of stenosis, lesion length, incidence of intraluminal thrombus, among 3 subgroups of AMI according to time of attack. Morning hour group had more frequent ulceration of coronary lesion than that of other groups(22.4% vs. 5.4%, p<0.01), and less frequent calcified lesion than that of other groups(3.0% vs 5.4%, p<0.05). Normal or minimal coronary artery lesion, that is Iess than 25% stenosis, was more frequent in the morning hour group comparing to that of other groups(11.9% vs. 9.78%). Eccentric stenosis(15.7% vs, 11,1%) and diffuse irregular lesion(25.5% vs. 16.7%) tended to be more frequent in the morning hour group. There were no differences in sex, age, incidence of hypertension, cigarette smoking, diabetes, degree of alcohol ingestion, ejection fraction, maximal CK value, preinfarction angina duration, past history of MI, and in incidence of arrhythmia. CONCLUSIONS: There were more ulcerative coronary atherosclerotic lesions, but fewer calcified coronary lesions in the morning group than in afternoon and night group. These findings indicate that morphology of coronary artery lesions may play a role in causing circardian variation in AMI.
Angina, Unstable ; Arrhythmias, Cardiac ; Aspirin ; Blood Platelets ; Constriction, Pathologic ; Coronary Vessels* ; Eating ; Female ; Humans ; Hypertension ; Incidence ; Myocardial Infarction* ; Oxygen ; Periodicity ; Plasma ; Smoking ; Thorax ; Thrombosis ; Ulcer

The proliferation and migration of vascular smooth muscle cells (VSMCs) are key contributors to the development of atherosclerosis and restenosis. We investigated the impact of rosuvastatin (RSV) on platelet-derived growth factor (PDGF)-BB-induced proliferation and migration of VSMCs, with a focus on the Akt/mTORautophagy signaling pathways. The cytotoxicity of RSV was assessed using MTT and annexin V staining, while the proliferation and migration capabilities of PDGF-BBinduced VSMCs were evaluated using MTT and cell migration assays. Confocal microscopy was employed to examine autophagic cell images, and protein expressions were analyzed via Western blotting. Our key findings revealed that RSV inhibited PDGF-BB-induced proliferation and migration of VSMCs, significantly reducing the expression of proliferating cell nuclear antigen and matrix metalloproteinase-2, which are crucial for these processes. RSV also enhanced autophagy in PDGF-BBstimulated cells by inducing the maturation of microtubule-associated protein light chain 3 and increasing the expression of Beclin-1, autophagy related (Atg)3, Atg5, and Atg7. The regulatory effects of RSV on PDGF-BB-induced autophagy, proliferation, and migration were associated with the suppression of the Akt/mTOR signaling pathway. These findings suggest that RSV may have potential therapeutic benefits in preventing and treating vascular diseases by targeting the Akt/mTOR pathway and inducing autophagy.

The proliferation and migration of vascular smooth muscle cells (VSMCs) are key contributors to the development of atherosclerosis and restenosis. We investigated the impact of rosuvastatin (RSV) on platelet-derived growth factor (PDGF)-BB-induced proliferation and migration of VSMCs, with a focus on the Akt/mTORautophagy signaling pathways. The cytotoxicity of RSV was assessed using MTT and annexin V staining, while the proliferation and migration capabilities of PDGF-BBinduced VSMCs were evaluated using MTT and cell migration assays. Confocal microscopy was employed to examine autophagic cell images, and protein expressions were analyzed via Western blotting. Our key findings revealed that RSV inhibited PDGF-BB-induced proliferation and migration of VSMCs, significantly reducing the expression of proliferating cell nuclear antigen and matrix metalloproteinase-2, which are crucial for these processes. RSV also enhanced autophagy in PDGF-BBstimulated cells by inducing the maturation of microtubule-associated protein light chain 3 and increasing the expression of Beclin-1, autophagy related (Atg)3, Atg5, and Atg7. The regulatory effects of RSV on PDGF-BB-induced autophagy, proliferation, and migration were associated with the suppression of the Akt/mTOR signaling pathway. These findings suggest that RSV may have potential therapeutic benefits in preventing and treating vascular diseases by targeting the Akt/mTOR pathway and inducing autophagy.

The proliferation and migration of vascular smooth muscle cells (VSMCs) are key contributors to the development of atherosclerosis and restenosis. We investigated the impact of rosuvastatin (RSV) on platelet-derived growth factor (PDGF)-BB-induced proliferation and migration of VSMCs, with a focus on the Akt/mTORautophagy signaling pathways. The cytotoxicity of RSV was assessed using MTT and annexin V staining, while the proliferation and migration capabilities of PDGF-BBinduced VSMCs were evaluated using MTT and cell migration assays. Confocal microscopy was employed to examine autophagic cell images, and protein expressions were analyzed via Western blotting. Our key findings revealed that RSV inhibited PDGF-BB-induced proliferation and migration of VSMCs, significantly reducing the expression of proliferating cell nuclear antigen and matrix metalloproteinase-2, which are crucial for these processes. RSV also enhanced autophagy in PDGF-BBstimulated cells by inducing the maturation of microtubule-associated protein light chain 3 and increasing the expression of Beclin-1, autophagy related (Atg)3, Atg5, and Atg7. The regulatory effects of RSV on PDGF-BB-induced autophagy, proliferation, and migration were associated with the suppression of the Akt/mTOR signaling pathway. These findings suggest that RSV may have potential therapeutic benefits in preventing and treating vascular diseases by targeting the Akt/mTOR pathway and inducing autophagy.

The proliferation and migration of vascular smooth muscle cells (VSMCs) are key contributors to the development of atherosclerosis and restenosis. We investigated the impact of rosuvastatin (RSV) on platelet-derived growth factor (PDGF)-BB-induced proliferation and migration of VSMCs, with a focus on the Akt/mTORautophagy signaling pathways. The cytotoxicity of RSV was assessed using MTT and annexin V staining, while the proliferation and migration capabilities of PDGF-BBinduced VSMCs were evaluated using MTT and cell migration assays. Confocal microscopy was employed to examine autophagic cell images, and protein expressions were analyzed via Western blotting. Our key findings revealed that RSV inhibited PDGF-BB-induced proliferation and migration of VSMCs, significantly reducing the expression of proliferating cell nuclear antigen and matrix metalloproteinase-2, which are crucial for these processes. RSV also enhanced autophagy in PDGF-BBstimulated cells by inducing the maturation of microtubule-associated protein light chain 3 and increasing the expression of Beclin-1, autophagy related (Atg)3, Atg5, and Atg7. The regulatory effects of RSV on PDGF-BB-induced autophagy, proliferation, and migration were associated with the suppression of the Akt/mTOR signaling pathway. These findings suggest that RSV may have potential therapeutic benefits in preventing and treating vascular diseases by targeting the Akt/mTOR pathway and inducing autophagy.

The proliferation and migration of vascular smooth muscle cells (VSMCs) are key contributors to the development of atherosclerosis and restenosis. We investigated the impact of rosuvastatin (RSV) on platelet-derived growth factor (PDGF)-BB-induced proliferation and migration of VSMCs, with a focus on the Akt/mTORautophagy signaling pathways. The cytotoxicity of RSV was assessed using MTT and annexin V staining, while the proliferation and migration capabilities of PDGF-BBinduced VSMCs were evaluated using MTT and cell migration assays. Confocal microscopy was employed to examine autophagic cell images, and protein expressions were analyzed via Western blotting. Our key findings revealed that RSV inhibited PDGF-BB-induced proliferation and migration of VSMCs, significantly reducing the expression of proliferating cell nuclear antigen and matrix metalloproteinase-2, which are crucial for these processes. RSV also enhanced autophagy in PDGF-BBstimulated cells by inducing the maturation of microtubule-associated protein light chain 3 and increasing the expression of Beclin-1, autophagy related (Atg)3, Atg5, and Atg7. The regulatory effects of RSV on PDGF-BB-induced autophagy, proliferation, and migration were associated with the suppression of the Akt/mTOR signaling pathway. These findings suggest that RSV may have potential therapeutic benefits in preventing and treating vascular diseases by targeting the Akt/mTOR pathway and inducing autophagy.

In the originally published version of this article, the last line of footnotes was omitted in Table 2.

PURPOSE: To evaluate the 1-year results of Descemet's membrane endothelial keratoplasty (DMEK) in Korea. METHODS: The medical records of 9 patients (10 eyes) with endothelial disease who underwent DMEK from January 2012 to December 2013, and were followed up for more than 12 months were reviewed retrospectively. RESULTS: In 8 eyes with successful results after surgery, best corrective visual acuity (BCVA) was significantly improved from 1.64 +/- 0.21 (log MAR, mean) to 0.35 +/- 0.22 at 1 month and was maintained at 12 months (p = 0.012, Wilcoxon signed ranks test). BCVA at postoperative 3, 6 and 12 months were gradually increased (0.25 +/- 0.23, 0.20 +/- 0.17 and 0.16 +/- 0.17 log MAR). Endothelial cell counts were 1,996 +/- 528/mm2, 1,564 +/- 174/mm2 and 1,463 +/- 541/mm2, 1,205 +/- 358/mm2 at 1, 3, 6, and 12 months after surgery, tended to decrease but showed no statistical significance. There was no statistical difference in astigmatism before and 3 months after the operation (3.32 +/- 2.36 diopter and 2.57+/- 1.44 diopter). Primary graft failure occurred in 2 eyes and 1 received reoperation. Total detachment was found in 1 eye. CONCLUSIONS: The 1-year results of DMEK showed fast visual recovery which was maintained for 12 months. DMEK may be a very efficient option for the surgical management of corneal endothelial disease.
Astigmatism ; Cornea ; Corneal Transplantation* ; Descemet Membrane* ; Endothelial Cells ; Humans ; Korea ; Medical Records ; Reoperation ; Retrospective Studies* ; Transplants ; Visual Acuity

BACKGROUND: Nevus of Ota (NO) is a relatively common pigmentary disorder in Asians. Tanino's classification is an old but tacit consensus to delineate the disease. Various treatment options have been presented. However, a few studies have been conducted on available laser options and current treatment strategies or the classification of NO. OBJECTIVE: To investigate current laser options and their effectiveness for the treatment of NO, contributing factors to clinical outcomes, and verification of classification. METHODS: A retrospective study of NO was conducted by reviewing medical charts and photographs of sixty-seven patients. Statistical analysis was used to compare excellent and poor outcomes and determine contributing factors. RESULTS: The median age of onset was below the age of 1 (interquartile range [IQR], 0~1). Tanino's and PUMCH classification systems failed to classify patients in 24 (35.8%) and 6 (9.0%) of patients, respectively. A 1,064 nm Q-switched Nd:YAG laser without additional lasers was used most frequently in 42 patients (62.7%). The frequency of treatment was 19.0 (IQR, 10.0~23.0) in the cured group defined as subjects showing 95% improvement or above, compared to 10.0 (IQR, 6.25~13.75) in the unattained group defined as subjects showing less than 95% improvement (p=0.001). CONCLUSION: A 1,064 nm Q-switched Nd:YAG laser is a reliable treatment armamentarium, functioning as a single infallible modality as well as a combination treatment modality for NO. Repetitive laser treatments without interruption seems to be the most suitable in clearing NO. The current classification systems of NO are defective. Thus, a new classification should be developed.
Age of Onset ; Asian Continental Ancestry Group ; Classification* ; Consensus ; Humans ; Laser Therapy ; Nevus of Ota* ; Nevus* ; Pigmentation ; Retrospective Studies