Left ventricular diastolic dysfunction in chronic renal failure patients on chronic hemodialysis in Dr. Cipto-Mangunkusumo Hospital : the association with left ventricular mass.

Fourty three patients with chronic renal failure undergoing chronic hemodialysis in Division of Nephrology and Hypertension, Faculty of Medicine, University of Indonesia/Cipto-Mangunkusumo Hospital, Jakarta, since October 2003 until February 2004, were examined for echocardiography (2-D, M-mode, Doppler imaging).Diastolic dysfunction was found in 58.1 % of chronic renal failure patients on hemodialysis. There was no significant difference between left ventricular mass in the group with or without left ventricular diastolic dysfunction.

Left ventricular diastolic dysfunction in type 2 diabetes mellitus patient without cardiovascular disease: the association with microalbuminuria.

Twenty-eight cases of type 2 diabetes mellitus (DM) without any cardiovascular disease were recruited from the Department of Metabolic-Endocrine, Faculty of Medicine, University of Indonesia / Dr. Cipto Mangunkusumo General Hospital, Jakarta. Recruitment of the study began in October 2001 and was completed by December 2001. Participants were examined for echocardiography and microalbuminuria urinary examination. Diastolic dysfunction was found in 73.7% of type 2 diabetic patients without microalbuminuria and 66.7% in type 2 diabetic patients with microalbuminuria. Neither type 2 diabetic groups with nor without microalbuminuria indicated any significant association to the occurrence of diastolic dysfunction.

Correlation of neuropathy with corneal sensitivity and lacrimal gland secretion in type 2 diabetes mellitus patient.

AIM: To evaluate correlation between blood glucose control, corneal sensitivity and lacrimal secretion in type 2 DM with peripheral neuropathy. METHODS: A cross sectional study has been conducted in 20 type DM with peripheral neuropathy and 20 without peripheral neuropathy at the Department of Internal Medicine and Ophthalmology, Ciptomangunkusumo Hospital, Faculty of Medicine University of Indonesia, from August through November 2002. All subject underwent a comprehensive medical examination, including esthesiometer Semmes-Weinstein 10 g, HbA1c, Schirmer test, and corneal sensitivity measurements. RESULTS: The mean corneal sensitivity was significantly lower in diabetic patients with neuropathy (p=0.000). HbA1(c) was related to corneal sensitivity (p=0.016). CONCLUSION: In type 2 DM with peripheral neuropathy, corneal sensitivity was demonstrated to be significantly decrease, all of which seems to be due to the status of blood glucose control.

The correlation between high sensitivity C-Reactive Protein level and the Extent of Coronary Lesion and Cardiac Systolic Function in Coronary Heart Disease.

To determine the mean value of high sensitivity C-Reactive Protein (hs-CRP), association between plasma level of hs-CRP with extent of disease and systolic function. A cross sectional study had been conducted to 106 coronary artery disease patients (90 stable angina pectoris, 11 unstable angina pectoris and 5 acute myocardial infarction). Plasma quantitative level of hs-CRP with cor angiography to determine extent of disease and ejection fraction were measured. The mean of hs-CRP levels in patients with SVD were 5,5 ± 7,6 mg/L, DVD were 6,6 ± 21,7 mg/L and TVD were 5,5 ± 8,0 mg/L and p=0,056, respectively. There were no significant association between hs- CRP levels with extent of disease. Systolic function had negative correlation with levels of hs-CRP (p=0,015, r=-0,235). This study showed that plasma level of hs-CRP cannot reflect the extent of disease, and it had negative correlation with systolic function.

The level of C.pneumoniae, Cytomegalovirus, and H.pylori antibody in a patient with coronary heart disease.

Atherosclerosis is still the chief cause of morbidity and mortality in developed nations. Even though in developed nations the modification of risk factors is able to reduce the prevalence rate of atherosclerosis, such reduction is starting to slow down. Such condition has stimulated researchers to identify environmental exposure, including infection, that can influence the process of atherosclerosis. This cross sectional study was conducted from March to August 1998, on 122 patients that clinically demonstrate coronary heart disease and have underwent cardiac catheterization, 92 males and 30 females with an average age of 55 years. Patients undergo clinical and laboratory evaluation (blood glucose, cholesterol, triglyceride, and antibody for C.pneumoniae. Cytomegalovirus, and H.pylori). We found a significant difference in cholesterol, triglyceride, and HDL levels in those with coronary stenosis and those without. However, we did not find a significant difference in the levels of C.pneumoniae, Cytomegalovirus, and H.pylori antibodies. This study is unable to conclude the influence of these antibodies on atherosclerosis, since in the non-stenosis group, we cannot eliminate the possibility of atherosclerosis, since the average age of study subject is 55 years. Studies on the interaction between infection and traditional risk factors as well as gender and nutrition is needed to find a clear answer of the influence of infection in atherosclerosis.

Anti-thrombin III, Protein C, and Protein S deficiency in acute coronary syndrome.

The final most common pathway for the majority of coronary artery disease is occlusion of a coronary vessel. Under normal conditions, antithrombin III (AT III), protein C, and protein S as an active protein C cofactor, are natural anticoagulants (hemostatic control) that balances procoagulant activity (thrombin antithrombin complex balance) to prevent thrombosis. If the condition becomes unbalanced, natural anticoagulants and the procoagulants can lead to thrombosis. Thirty subjects with acute coronary syndrome (ACS) were studied for the incidence of antithrombin III (AT III), protein C, and protein S deficiencies, and the result were compare to the control group. Among patients with ACS, the frequency of distribution of AT-III with activity < 75% were 23,3% (7 of 30), and only 6,7% ( 2 of 30 ) in control subject. No one of the 30 control subject have protein C activity deficient, in ACS with activity < 70% were 13,3% (4 of 30). Fifteen out of the 30 (50%) control subjects had protein S activity deficiency, while protein S deficiency activity < 70% was found 73.3.% (22 out of 30). On linear regression, the deterministic coefficient of AT-III activity deficiency to the development ACS was 13,25 %, and the deterministic coefficient of protein C activity deficient to the development of ACS was 9,06 %. The cut-off point for AT-III without protein S deficiency expected to contribute to the development of vessel disease was 45%. On discriminant analysis, protein C activity deficiency posed a risk for ACS of 4,5 greater than non deficient subjects, and AT-III activity deficiency posed a risk for ACS of 3,5 times greater than non deficient subjects. On binary logistic regression, protein S activity acted only as a reinforcing factor of AT-III activity deficiency in the development of ACS. Protein C and AT III deficiency can trigger ACS, with determinant coefficients of 9,06% and 13,25% respectively. Low levels of protein C posed a greater risk of ACS than low levels of AT III. Protein S deficiency was a reinforcing factor on AT-III deficient to development of ACS. The cut-off point of AT-III without protein S deficiency expected to give single vessel disease was 45%, and 9,5% for the development of triple vessel disease.