ABSTRACT
The effectiveness of long-term administration of tolvaptan in heart failure (HF) patients with chronic kidney disease (CKD) has not been fully studied. Hence, in this study, we investigated the effects of chronic administration of tolvaptan on patients with HF and CKD. We consecutively enrolled 31 patients with acute HF syndrome (AHFS) who were administrated tolvaptan as a long-term medication (TLV group). All patients had a history of prior HF admission and CKD. We also consecutively enrolled 27 patients with AHFS, a prior history of HF and CKD (conventional group). We compared renal function and outcomes between the two groups at discharge for AHFS and after 6 months of follow-up. The estimate glomerular filtration rate (eGFR) was maintained at approximately the same level in the TLV group exhibited approximately the same eGFR (-1.1 ± 8.3 mL/min/1.73 m2) but decreased in the conventional group (-7.4 ± 10.4 mL/min/1.73 m2). There was a significant difference in the changes observed in eGFR between the conventional and TLV groups (p = 0.01). There were no significant differences in the frequencies of rehospitalization and death. Long-term administration of tolvaptan may prevent increased renal dysfunction in HF patients with CKD. This conclusion should be confirmed in a large-scale prospective study.
Subject(s)
Antidiuretic Hormone Receptor Antagonists/therapeutic use , Glomerular Filtration Rate , Heart Failure/drug therapy , Renal Insufficiency, Chronic/metabolism , Tolvaptan/therapeutic use , Aged , Aged, 80 and over , Case-Control Studies , Disease Progression , Female , Follow-Up Studies , Heart Failure/complications , Humans , Male , Middle Aged , Mortality , Patient Readmission , Renal Insufficiency, Chronic/complications , Treatment OutcomeSubject(s)
Adrenal Cortex Hormones/administration & dosage , Aortic Aneurysm, Thoracic/surgery , Takayasu Arteritis/diagnosis , Takayasu Arteritis/drug therapy , Vascular Surgical Procedures/methods , Adult , Angiography , Aortic Aneurysm, Thoracic/complications , Aortic Aneurysm, Thoracic/diagnostic imaging , Aortic Aneurysm, Thoracic/drug therapy , Dose-Response Relationship, Drug , Drug Administration Schedule , Female , Follow-Up Studies , Humans , Reoperation/methods , Risk Assessment , Severity of Illness Index , Takayasu Arteritis/complications , Thoracotomy/methods , Tomography, X-Ray Computed , Treatment OutcomeABSTRACT
Restenosis after coronary artery stent implantation is attributed chiefly to intimal hyperplasia, which is prevented experimentally by angiotensin-converting enzyme (ACE) inhibitors. Therefore, the present study investigated whether the effect of quinapril, a tissue-specific ACE inhibitor, on the prevention of coronary restenosis differs according to ACE polymorphism. One hundred consecutive patients with successful stent implantation were randomly assigned to quinapril and control groups. Both follow-up angiography and ACE polymorphism analysis were obtained from 92 patients (control, 46; quinapril treatment, 46). The prevalence of risk factors did not differ statistically according to quinapril treatment or ACE genotypes. There was no statistically significant difference in the occurrence of restenosis 6 months after stenting between the groups. Quantitative coronary angiography revealed that quinapril treatment resulted in significantly higher minimal lumen diameter and significantly lower percent diameter stenosis (22.9 +/- 22.6 vs 37.1 +/- 19.7% in the control group, p < 0.05) in patients with the D allele although there was no difference in those with the II genotype. In addition, intravascular ultrasound revealed that quinapril treatment significantly prevented the loss of minimal lumen cross-sectional area and the increase in percent area stenosis (34.5 +/- 14.0 vs 53.3 +/- 16.4% in the control group, p < 0.05) in patients with the D allele compared to those with the II genotype. These results suggest that the administration of ACE inhibitors for the attenuation of lumen loss after coronary stent implantation is best for subjects with the D allele of the ACE genotype.