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AIMS: The increasing prevalence of cardiovascular diseases has led to widespread use of cardiovascular drugs that can adversely impact glucose metabolism. This review focuses on the latest evidence on the potential of cardiovascular drugs to induce adverse glycemic effects but also the underlying mechanisms, prevention, and management strategies. MATERIALS AND METHODS: A comprehensive literature search was conducted across scientific databases until May 25th, 2024. RESULTS: Certain cardiovascular drugs can induce hyperglycemia through multiple mechanisms including altered the secretion and sensitivity of insulin through direct cytotoxic effects towards pancreatic beta cells, and increased glucose secretion. Notably, diuretics, beta-blockers, calcium channel blockers, and statins have been associated with significant glycemic disturbances. The risk of hyperglycemia varies based on individual factors, drug dosages, and concurrent medications. These drug-induced hyperglycemic effects may sometimes reverse upon discontinuation of related medication. Effective management should include lifestyle modifications, the use of glucose-lowering medications, and opting for lower-risk cardiovascular drugs. Monitoring for hyperglycemia involves educating affected individuals and conducting regular blood glucose tests. Identifying at-risk individuals and implementing preventive measures are crucial for improving both cardiovascular and metabolic outcomes. CONCLUSIONS: Certain cardiovascular drugs significantly contribute to hyperglycemia and diabetes mellitus through various mechanisms. Effective management includes identifying at-risk individuals, choosing lower-risk medications, and implementing monitoring and preventive strategies. Further research is needed to fully understand these mechanisms and develop targeted interventions to prevent and manage cardiovascular drug-induced hyperglycemia, thereby improving clinical outcomes.
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Background: Permanent hemodialysis access comes with a myriad of problems on top of the well-known benefits; flow disturbances, risk of infection and revision being among them. All of these could eventually lead to impaired cardiac function. Even so, the relationship between impaired cardiac function due to arteriovenous access in patients undergoing hemodialysis has not been clearly described. This study aimed to analyze the relationship of flow in an artificial arteriovenous access with left and right ventricular function in patients with chronic kidney disease (CKD) undergoing hemodialysis at a referral hospital in Indonesia. Material and methods: This was a cross sectional study with consecutive sampling technique. Samples were patients with CKD undergoing hemodialysis at Dr. Soetomo General Hospital from December 2021to January 2022. A total of 47 patients who met the inclusion criteria underwent Doppler ultrasound to assess arteriovenous access flow and transthoracic echocardiography to assess left and right ventricle function. Results: From 47 patients, 26 (55.3%) had high arteriovenous access flow. The clinical characteristics of the patients between the high and low arteriovenous access flow groups were not significantly different. We found that the value of left ventricular ejection fraction in the non-high-flow access group was significantly higher than the high-flow access group (p < 0.05). Other than that, the median right ventricle fractional area changes in the non-high-flow access group was also higher than the high-flow access group (p < 0.05). Conclusion: Arteriovenous access flow as measured by Doppler ultrasonography has a significant relationship with impaired left and right ventricular functions based on systolic function parameters from echocardiography.
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BACKGROUND: The cases of Rifampicin-Resistant Tuberculosis (RR-TB) in our country have increased every year and RR-TB deaths are thought to be caused by prolongation of the QTc interval due to side effects of anti-tuberculosis drugs. Thus, cytokines are needed to be used as early markers of prolongation of the QTc interval in RR-TB patients. OBJECTIVE: This study aims to analyze the correlation of inflammatory cytokines on QTc interval in RR-TB patients who received shorter regimens. METHODS: This study uses a case-control study with a time series conducted in the period September 2019 to February 2020 in one of the referral hospitals for Tuberculosis in Indonesia. Cytokines levels from blood samples were measured using the ELISA method, while QTc intervals were automatically recorded using an electrocardiography machine. The statistical analysis used was the Chi-square test, Man Whitney test, Independence t-test, and Spearman-rank test with p < 0.05. RESULTS: There was no significant correlation between inflammatory cytokines and QTc prolongation in intensive phase which TNF-α value (6.8 pg/ml; r = 0.207; p = 0.281), IL-1ß (20.13 pg/ml; r = 0.128; p = 0.509), and IL-6 (43.17 pg/ml; r = -0.028; p = 0.886). Meanwhile, in the continuation phase, the values for TNF-α (4.79 pg/ml; r = 0.046; p = 0.865), IL-1ß (7.42 pg/ml; r = -0.223; p = 0.406), and IL- 6 (40.61 pg/ml; r = -0.147; p = 0.586). CONCLUSION: inflammatory cytokines (TNF-α, IL-1ß, and IL-6) cannot be used to identify QTc interval prolongation in RR-TB patients who received shorter regimens.
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BACKGROUND: long-term use of anti-tuberculosis drugs (ATD) increases the risk of QTc prolongation, while C-reactive protein (CRP) can be used as an inflammatory marker of Mycobacterium tuberculosis infection.Objective: correlation of CRP on the QTc interval in Rifampicin-resistant tuberculosis (RR-TB) patients with the short regimen. METHODS: An observational study was conducted in Rifampicin-resistant tuberculosis (RR-TB) patients from 2 groups, patients on intensive phase and patients on continuation phase. CRP levels were measured from blood samples and measured automatically using the immunoturbidimetric assay. QTc interval was calculated using electrocardiography. Levels of CRP levels and QTc interval between the 2 groups were analyzed. The statistical analysis used includes the independent t-test, Mann Whitney test, and Rank Spearman test with p = 0.05. RESULTS: Forty-five eligible RR-TB patients were included in this study. CRP levels and QTc intervals between 2 groups (intensive and continuation phase) showed significant difference with p < 0.001 but found no significant correlation of CRP levels and QTc interval in both intensive and continuation phase with p = 0.226 and 0.805, respectively. A higher level of CRP strongly indicated the inflammation caused by RR-TB infection at the early phase of the disease, but not correlated with QTc interval in RR-TB patients. CONCLUSION: Levels of CRP and QTc interval do not correlate in RR-TB patients and can not be used to be the marker of QTc prolongation in RR-TB Patients.