Multiple neurological complications have been associated with the coronavirus disease-19 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus 2. This is a narrative review to gather information on all aspects of COVID-19 in elderly patients with cognitive impairment. First, the following three mechanisms have been proposed to underlie the neurological complications associated with COVID-19: 1) direct invasion, 2) immune and inflammatory reaction, and 3) hypoxic brain damage by COVID-19. Next, because the elderly dementia patient population is particularly vulnerable to COVID-19, we discussed risk factors and difficulties associated with cognitive disorders in this vulnerable population. We also reviewed the effects of the patient living environment in COVID-19 cases that required intensive care unit (ICU) care. Furthermore, we analyzed the impact of stringent social restrictions and COVID-19 pandemic-mediated policies on dementia patients and care providers. Finally, we provided the following strategies for working with elderly dementia patients: general preventive methods; dementia care at home and nursing facilities according to the activities of daily living and dementia characteristics; ICU care after COVID-19 infection; and public health care system and government response. We propose that longitudinal follow-up studies are needed to fully examine COVID-19 associated neurological complications, such as dementia, and the efficacy of telemedicine/telehealth care programs.

BACKGROUND: While inositol phospholipid-specific phospholipase C (PLC) plays a central role in signal transduction pathways, little is known about its role in the vascular response to injury. Recent studies have shown that phospholipase C-gamma1 (PLC-gamma1) is required for PDGF-induced DNA synthesis and angiotensin II signaling. This study was undertaken to determine the potential involvement of PLC-gamma1 in the in vivo response to vascular injury. METHODS: Vascular injury was achieved in the left common carotid artery of six-month-old male Wistar rats. The expression of PLC-gamma1 was evaluated at serial time points by immunohistochemistry and Western blot analysis following balloon de-endothelialization of the rat carotid artery. RESULTS: In the denuded carotid artery at 1 week, the neointima became thicker in a symmetrical manner with respect to the long axis. A strong expression of PLC-gamma1 at one week after injury was seen primarily in the thin layers of neointima. This increased immunoreactivity of PLC-gamma1 persisted at 2-3 weeks after injury, coinciding with the time when neointima gains of its mass. At 4 weeks after injury, staining intensity slightly declined but levels remained elevated. As determined by Western blot analysis, the amount of PLC-gamma1 was about 3-fold higher at 3 weeks after injury compared to uninjured vessels (p<0.01). CONCLUSION: These results suggest that the amplification of traffic within signal transduction pathways involving PLC-gamma1 occurs and may play a significant role in neointima formation following arterial injury.
Angiotensin II ; Animals ; Axis, Cervical Vertebra ; Blotting, Western ; Carotid Arteries* ; Carotid Artery, Common ; DNA ; Humans ; Immunohistochemistry ; Inositol ; Male ; Neointima ; Phospholipases* ; Rats* ; Rats, Wistar ; Signal Transduction ; Type C Phospholipases ; Vascular System Injuries

It has been generally accepted that high density lipoprotein cholesterol (HDL-C) level decreases with menopause in women. However, recent reports show different results. There is very little data concerning perimenopausal women. To verify these findings, lipids and lipoprotein(a) +AFs-Lp(a)+AF0- levels were compared among pre-, peri- and postmenopausal women of similar mean ages. Postmenopausal women had higher HDL-C levels than premenopausal women (p+ADw-0.001) and there was no difference between peri- and postmenopausal women. LDL-C level in perimenopausal women was lower than in postmenopausal women (p+ADw-0.001) and higher than in premenopausal women with borderline significance (p+AD0-.051). Total cholesterol levels showed stepwise elevation from premenopause to postmenopause. Perimenopausal women had lower Lp(a) levels than postmenopausal women (p+ADw-0.0005) and similar levels to premenopausal women. Lp(a) levels between 0.1 to 10.0 mg/dL were the most prevalent in pre- and perimenopausal women, and those between 10.1 to 20.0 mg/dL in postmenopausal women. In conclusion, menopause itself is associated with the elevation of HDL-C level, and the postmenopausal increase of coronary artery disease is not related to postmenopausal change of HDL-C level. Perimenopausal status, although transient, may favor Lp(a) and lipid profiles for delaying atherosclerosis.
Apolipoproteins A/blood ; Arteriosclerosis/epidemiology ; Biological Markers ; Cholesterol/blood ; Comparative Study ; Cross-Sectional Studies ; FSH/blood ; Female ; Human ; Lipids/blood+ACo- ; Lipoprotein(a)/blood ; Lipoproteins, HDL Cholesterol/blood+ACo- ; Menopause/blood+ACo- ; Middle Age ; Postmenopause/blood ; Premenopause/blood ; Risk Factors

Chloroma (granulocytic sarcoma) indicates an extramedullary leukemic cell collection. It often develops in the course of, or as a presenting sign of leukemia. Cardiac chloroma is uncommon and rarely detected as a mass. We report the first case of cardiac chloroma in a patient with acute lymphocytic leukemia in Korea. A 73-year-old man was admitted because of exertional dyspnea, orthopnea and generalized weakness. Thrombocytopenia and immature leukocytes were detected in the peripheral blood. An X-ray film of the chest showed mild cardiome-galy and bilateral pleural effusion. Transthoracic and transesophageal echocardiography showed a low echogenic mass at the lateral wall of the right ventricle. The size of the mass was about 6x4 cm. MRI of the chest showed right ventricular mass with slightly increased inhomogeneous signal intensity. Bone marrow aspiration and biopsy confirmed that he had a L3 FAB subtype of acute lymphocytic leukemia. Induction chemotherapy with vincristine, prednisolone, daunorubicin resulted in hematologic complete remission. At 6 weeks after the induction chemotherapy, transesophageal echocardiography demonstrated disappearance of the right ventricular mass which suggested that it was a cardiac chloroma complicating acute lymphocytic leukemia.
Aged ; Biopsy ; Bone Marrow ; Daunorubicin ; Dyspnea ; Echocardiography, Transesophageal ; Heart Ventricles ; Humans ; Induction Chemotherapy ; Korea ; Leukemia ; Leukocytes ; Magnetic Resonance Imaging ; Pleural Effusion ; Precursor Cell Lymphoblastic Leukemia-Lymphoma* ; Prednisolone ; Sarcoma, Myeloid* ; Thorax ; Thrombocytopenia ; Vincristine ; X-Ray Film

BACKGROUND AND OBJECTIVES: The octapeptide hormone of the renin-angiotensin system, angiotensin ii, regulates a wide variety of physiological responses including salt and water balance, blood pressure, and vascular tone. Contradictory results have been reported regarding the effects of angiotensin ii on vascular smooth mu-scle cell (VSMC) proliferation. The aim of the present study was to investigate the direct effect of angiotensin ii on the growth of VSMC. MATERIALS AND METHOD: Rat aortic smooth muscle cells were obtained by the combined collagenase and elastase methods. Cells between the 4th and 8th passages were used for the experiments. Cultures were treated daily for 3 days with either angiotensin ii alone or angiotensin ii with equimolar concentrations of saralasin. Incorporated radioactivity of [3H]thymidine and [14C]phenylalanine was measured by liquid scintillation spectrometry. RESULTS: Angiotensin ii increased [14C]phenyalanine incor-poration about 20-30%, and saralasin completely blocked the stimulation by angiotensin ii. However, there was no significant increase in [3H]thymidine incorporation by angiotensin ii stimulation in this study. CONCLUSION: These results suggest that angiotensin ii alone induces cellular hypertrophy but has no detectable mitogenic activity in cultured rat aortic VSMC.
Angiotensin II* ; Angiotensins* ; Animals ; Blood Pressure ; Collagenases ; Hypertrophy ; Muscle, Smooth, Vascular* ; Myocytes, Smooth Muscle ; Pancreatic Elastase ; Radioactivity ; Rats ; Renin-Angiotensin System ; Saralasin ; Spectrum Analysis

BACKGROUND: In Korea, cerebrovascular accident (CVA) is the most significant cause of death among older people, and the incidence of cerebral hemorrhage is much higher than that of developed countries. There have been many investigations about the risk factors for CVA in both Korea as well as developed countries. A few papers reported various risk factors for cerebral hemorrhage in developed countries:however, well-designed studies of risk factors for the various causes of CVA were rare in Korea. Therefore, the purpose of this study was to compare the risk factors for the various causes of CVA and to evaluate the risk factors compared with age- and sex-matched control groups. In addition, duplex sonographic findings of the carotid artery were evaluated in patients with cerebral infarction. METHODS: One hundred and sixty-four patients admitted to the hospital in 1996 were enrolled. The four groups were divided based on the following states: cerebral infarction (n-63), cerebral hemorrhage (n-64), cerebral infarction with atrial fibrillation (n-19), and lacunar infarction (n-18). Major risk factors were compared with age- and sex-matched control groups and among CVA groups. Duplex sonography of the carotid artery was done in 14 patients with cerebral infarction. RESULTS: In multiple logistic regression analysis, patients with cerebral infarction had higher prevalence of diabetes mellitus and lower high density lipoprotein-cholesterol level than the control group, and hypertension showed borderline significance. Patients with cerebral hemorrhage had higher prevalence of hypertension, higher high density lipoprotein-cholesterol level, and more frequent prevalence of smoking compared with the control group. Patients with cerebral infarction showed lower high density lipoprotein-cholesterol, higher low density lipoprotein-cholesterol levels, more frequent diabetes mellitus, lower prevalence of hypertension and older age than patients with cerebral hemorrhage. Patients with cerebral infarction and atrial fibrillation showed only older age than patients with cerebral infarction only. There were no differences in risk factors between patients with cerebral infarction and lacuna infarction. Atheromatous plaque was found in 71% of patients with cerebral infarction. CONCLUSION: Metabolic abnormalities played more important role in the development of cerebral infarction and hemodynamic abnormalities in cerebral infarction. Sonographic examination of the carotid artery may be useful for predicting the occurrence of cerebrovascular accident in high risk patients.
Atrial Fibrillation ; Carotid Arteries* ; Cause of Death ; Cerebral Hemorrhage ; Cerebral Infarction* ; Developed Countries ; Diabetes Mellitus ; Hemodynamics ; Humans ; Hypertension ; Incidence ; Infarction ; Korea ; Logistic Models ; Prevalence ; Risk Factors* ; Smoke ; Smoking ; Stroke ; Stroke, Lacunar ; Ultrasonography*

Background and objectives: Carvedilol is a cardiovascular drug, beta- and alpha1-adrenoceptor antagonist, currently approved for the treatment of hypertension, angina, congestive heart failure by FDA. Carvedilol has been shown to attenuate oxygen free radical-initiated lipid peroxidation and to inhibit neointimal formation of aorta following vascular injury by balloon angioplasty. We have investigated the effect of carvedilol on DNA synthesis of vascular smooth muscle cells (VSMC) stimulated by platelet-derived growth factor (PDGF)-BB. MATERIALS AND METHOD: Rat aortic smooth muscle cells were obtained by the combined collagenase and elastase methods. Cells between the 4th and 8th passages were used for the experiments. Incorporated radioactivity of [3H]-thymidine was measured by liquid scintillation spectrometry. RESULTS: PDGF-BB (1 nM) increased [3H]-thymidine incorporation about 70-100% over basal value in cultured VSMC. PDGF-stimulated increase in DNA synthesis was significantly suppressed by simultaneous administration of carvedilol. In contrast, propranolol did not significantly affect 3[H]-thymidine uptake in rat aortic VSMC. CONCLUSION: The present study demonstrate that carvedilol significantly inhibits the proliferation of vascular smooth muscle cell in our condition. These results indicate that carvedilol may be effective in the treatment of cardiovascular diseases principally associated with abnormal vascular smooth muscle growth.
Angioplasty, Balloon ; Animals ; Aorta ; Cardiovascular Diseases ; Cell Proliferation ; Collagenases ; DNA ; Heart Failure ; Hypertension ; Lipid Peroxidation ; Muscle, Smooth, Vascular* ; Myocytes, Smooth Muscle ; Oxygen ; Pancreatic Elastase ; Platelet-Derived Growth Factor ; Propranolol ; Radioactivity ; Rats ; Spectrum Analysis ; Vascular System Injuries

BACKGROUND: Atherosclerosis is a diffuse disease process that produce thickening of the vascular wall because of intimal deposition of lipid, fibrous tissue, and calcific material. Nowadays it is possible to evaluate atherosclerotic changes of carotid arteries accurately by developed noninvasive techniques such as ultrasonography. Left ventricular hypertrophy (LVH) is known to be an important risk factor for cardiovascular events in hypertension. The purpose of this study was to establish whether the carotid intimal - medial thickness (IMT) correlates with the severity of LVH. METHOD: We measured intimal-medial thickness (IMT) for 12 sites in carotid arteries (near and far walls in common carotid, bifurcation, and internal carotid arteries of both sides) by B-mode ultrasonography in both 38 normotensive and 72 hypertensive patients. Left ventricular measurements were made according to the recommendations of the American Society of Echocardiography. Left ventricular mass was derived from the formula described by Devereux et al. and each left ventricular mass value was indexed to body surface area. And then we have investigated whether hypertensive patients have significant changes of carotid IMT and IMT correlates with left ventricular mass index (LVMI). RESULTS: (1) Most hypertensive patients had diffuse thickening of the carotid artery and some had focal or multiple plaques. (2) In general, mean IMT was widest in the carotid bifurcation. (3) The mean IMT of all 12 segments increased about 40% in hypertensive patients compared with normal control group. (4) LVMI significantly correlates with IMT of carotid artery, especially bifurcation site and mean all 12 segments. CONCLUSION: The mean IMT may serve as a useful marker of the severity of atherosclerosis in hypertensive patients. The significant association between carotid IMT and LVMI suggests a simultaneous correlation of carotid atherosclerosis with left ventricular hypertrophy in hypertension.
Atherosclerosis ; Body Surface Area ; Carotid Arteries* ; Carotid Artery Diseases ; Carotid Artery, Internal ; Echocardiography ; Humans ; Hypertension ; Hypertrophy, Left Ventricular* ; Risk Factors ; Ultrasonography

OBJECTIVES: Hormone replacement therapy(HRT) in postmenopausal women decreases lipoprotein(a) [Lp(a)]. The influences of progesterone on Lp(a) and lipids, administered with estrogen, are controversial. However, previous studies had variable duration of therapy, and there was no report evaluating the effect of the duration of medication. METHODS: A total 246 postmenopausal women were divided into 4 groups: group A; 0.625mg conjugated equine estrogen(CEE)(n=90), group B; 0.625mg CEE plus 5mg medroxyprogesterone acetate(MPA)(n=35), group C; 0.625mg CEE plus 10mg MPA(n=43), and group D; 2mg estradiol valerate(E2) plus 0.5mg norgestrel(N)(n=76). Lp(a) and lipids levels were measured before, 2, 6 and 12 months after HRT. RESULTS: In total subjects, Lp(a) was decreased with medication for 2 months by 20.7%(p<0,0001). Compared with levels at 2 months after medication, levels at 6 and 12 months revealed further reduction(p<0.001) by 5.3% and 9.0% respectively. Medication for 2 months increased HDL-C in group A, not changed in group B and C, and decreased in group D. After 12 months, HDL-C levels were increased in Group A, B, and C, and not changed in group D, In total subjects, low density lipoprotein-cholesterol(LDL-C) was decreased by 12.2% after 2 months(p<0.001). Compared with levels at 2 months after medication, LDL-C level was decreased by 3.4% after 6 months(p<0.001) and there was no further reduction after 12 months. CONCLUSION: The effect of hormone replacement therapy on Lp(a) and lipids were dependent upon the duration of medication. Inconsistent results in previous studies can be partially explained by the difference in this parameter.
Estradiol ; Estrogens ; Female ; Hormone Replacement Therapy ; Humans ; Lipoprotein(a)* ; Lipoproteins ; Medroxyprogesterone ; Progesterone

OBJECTIVES: Echocardiographically determined left ventricular hypertrophy is associated with increased risk for sudden cardiae death and for complex ventricular arrhythmias in 24-hour ambulatory electrocardiographic monitoring. In subjects with left ventricular hypertrophy, the presence of asymptomatic complex ventricular arrhythmias is associated with higher incidence of sudden cardiac death and higher cardiovascular mortality. However, their accurate relationship and prognostic significances have been remained to be established. The purpose of this study was to evaluate the relationship between complex ventricular arrhythmias, left ventricular hypertrophy, and sudden cardiac death in Korean patients. METHODS: Twenty four hour ambulatory electrocardiographic monitoring, echocardiographic data and medical records were reviewed in 360 subjects from 1991 to 1994. We evaluated the relationship between complex ventricular arrhythmias and left ventricular mass index, and the prognostic values of them. Of the 360 subjects, 187 could be followed up for one to four years. The mean follow-up period was 2.8 years. RESULTS: The incidence of complex ventricular arrhythmias was significantly correlated with left ventricular mass index and ejection fraction in all subjects. During the follow-up periods, seven of 187 subjects died from sudden cardiac death. Six of them had complex ventricular arrhythmias with left ventricular hypertrophy. CONCLUSION: The incidence of complex ventricular arrhythmias was significantly correlated with echocardiographically determined left ventricular hypertrophy and it is suggested that subjects with complex ventricular arrhythmias combined with left ventricular hypertrophy have higher risk for sudden cardiac death.
Arrhythmias, Cardiac* ; Cardia ; Death, Sudden, Cardiac ; Echocardiography ; Electrocardiography, Ambulatory ; Follow-Up Studies ; Humans ; Hypertrophy, Left Ventricular* ; Incidence ; Medical Records ; Mortality ; Prognosis