Diabetes Is Not Associated With Increased Mortality In Adults With Advanced Heart Failure
HFSA ePoster Library. Dunlay S. 09/10/21; 343360; 137
Dr. Shannon Dunlay
REGULAR CONTENT
Login now to access Regular content available to all registered users.
Abstract
Discussion Forum (0)
Background: Systemic autoimmune rheumatic diseases (SARDs), including systemic sclerosis (SSc), systemic lupus erythematosus (SLE), and rheumatoid arthritis (RA), are associated with an increased independent risk of heart failure (HF). Hypothesis: We hypothesize that cardiovascular (CV) drugs prescribed at time of SARD diagnosis may be associated with delayed onset of incident HF.
Methods: We reviewed electronic health records from a large multispecialty institution of adult patients with SARDs from 2000-2020. Demographic data, SARD diagnosis, HF and comorbidity status, and cardiovascular medication use data were extracted retrospectively. CV drugs included were angiotensin converting enzyme inhibitors (ACE-i), angiotensin receptor blockers (ARBs), beta blockers (BBs), calcium channel blockers (CCBs), and thiazide diuretics. Baseline was defined as time of SARD diagnosis. Inclusion criteria were SSc, SLE, or RA diagnosis. Patients with HF at baseline were excluded. Cox proportional hazards regression was performed to investigate the association between CV drugs exposure at baseline and time to incident HF, adjusting for traditional risk factors (age, sex, hypertension, diabetes, coronary artery disease, myocardial infarction, and chronic kidney disease).
Results: In our study cohort, we identified 3,714 patients with SSc (5.7%), 15,940 patients with SLE (24.7%), and 44,966 patients with RA (69.6%), among which 14.4% of SSc, 12.2% of SLE, and 10.5% of RA patients developed incident HF during follow-up. In our study cohort (n = 64,620), ARB (aHR: 1.1 [1.0-1.2]; p = 0.005) and thiazide (aHR: 1.2 [1.1-1.2]; p <0.001) use were significantly associated with decreased time to incident HF, while BB (aHR: 0.68 [0.61-0.75]; p <0.001) use was associated with increased time to HF. In SSc patients (compared with no CV drugs), ACE-i (aHR: 1.5; 95% CI [1.14-1.9]; p = 0.004), ARB (aHR: 1.4 [1.06-1.9]; p = 0.018), and thiazide (aHR: 1.5 [1.15-1.9]; p =0.003) use were significantly associated with decreased time to incident HF. Baseline BB use had near significant association with increased time to incident HF in SSc (aHR: 0.73 [0.51-1.0]; p = 0.079). In SLE patients (compared with no CV drugs), baseline thiazide use was associated with decreased time to incident HF (aHR: 1.2 [1.0-1.4]; p = 0.01), and BB use was associated with increased time to incident HF (aHR: 0.71 [0.57-0.89]; p = 0.003). In RA patients, baseline ARB (aHR: 1.1 [1.0-1.2]; p = 0.026) and thiazide (aHR: 1.1 [1.0-1.2]; p = 0.003) were associated with decreased time to incident HF and BB use was associated with increased time to incident HF (aHR: 0.68 [0.61-0.76]; p <0.001).
Conclusion: In our single-center experience, the use of beta-blockers at the time of SARD diagnosis was associated with delayed onset of HF. Further investigations into the potential cardioprotective effects of beta-blockers in patients with SARDs are warranted.
Methods: We reviewed electronic health records from a large multispecialty institution of adult patients with SARDs from 2000-2020. Demographic data, SARD diagnosis, HF and comorbidity status, and cardiovascular medication use data were extracted retrospectively. CV drugs included were angiotensin converting enzyme inhibitors (ACE-i), angiotensin receptor blockers (ARBs), beta blockers (BBs), calcium channel blockers (CCBs), and thiazide diuretics. Baseline was defined as time of SARD diagnosis. Inclusion criteria were SSc, SLE, or RA diagnosis. Patients with HF at baseline were excluded. Cox proportional hazards regression was performed to investigate the association between CV drugs exposure at baseline and time to incident HF, adjusting for traditional risk factors (age, sex, hypertension, diabetes, coronary artery disease, myocardial infarction, and chronic kidney disease).
Results: In our study cohort, we identified 3,714 patients with SSc (5.7%), 15,940 patients with SLE (24.7%), and 44,966 patients with RA (69.6%), among which 14.4% of SSc, 12.2% of SLE, and 10.5% of RA patients developed incident HF during follow-up. In our study cohort (n = 64,620), ARB (aHR: 1.1 [1.0-1.2]; p = 0.005) and thiazide (aHR: 1.2 [1.1-1.2]; p <0.001) use were significantly associated with decreased time to incident HF, while BB (aHR: 0.68 [0.61-0.75]; p <0.001) use was associated with increased time to HF. In SSc patients (compared with no CV drugs), ACE-i (aHR: 1.5; 95% CI [1.14-1.9]; p = 0.004), ARB (aHR: 1.4 [1.06-1.9]; p = 0.018), and thiazide (aHR: 1.5 [1.15-1.9]; p =0.003) use were significantly associated with decreased time to incident HF. Baseline BB use had near significant association with increased time to incident HF in SSc (aHR: 0.73 [0.51-1.0]; p = 0.079). In SLE patients (compared with no CV drugs), baseline thiazide use was associated with decreased time to incident HF (aHR: 1.2 [1.0-1.4]; p = 0.01), and BB use was associated with increased time to incident HF (aHR: 0.71 [0.57-0.89]; p = 0.003). In RA patients, baseline ARB (aHR: 1.1 [1.0-1.2]; p = 0.026) and thiazide (aHR: 1.1 [1.0-1.2]; p = 0.003) were associated with decreased time to incident HF and BB use was associated with increased time to incident HF (aHR: 0.68 [0.61-0.76]; p <0.001).
Conclusion: In our single-center experience, the use of beta-blockers at the time of SARD diagnosis was associated with delayed onset of HF. Further investigations into the potential cardioprotective effects of beta-blockers in patients with SARDs are warranted.
Background: Systemic autoimmune rheumatic diseases (SARDs), including systemic sclerosis (SSc), systemic lupus erythematosus (SLE), and rheumatoid arthritis (RA), are associated with an increased independent risk of heart failure (HF). Hypothesis: We hypothesize that cardiovascular (CV) drugs prescribed at time of SARD diagnosis may be associated with delayed onset of incident HF.
Methods: We reviewed electronic health records from a large multispecialty institution of adult patients with SARDs from 2000-2020. Demographic data, SARD diagnosis, HF and comorbidity status, and cardiovascular medication use data were extracted retrospectively. CV drugs included were angiotensin converting enzyme inhibitors (ACE-i), angiotensin receptor blockers (ARBs), beta blockers (BBs), calcium channel blockers (CCBs), and thiazide diuretics. Baseline was defined as time of SARD diagnosis. Inclusion criteria were SSc, SLE, or RA diagnosis. Patients with HF at baseline were excluded. Cox proportional hazards regression was performed to investigate the association between CV drugs exposure at baseline and time to incident HF, adjusting for traditional risk factors (age, sex, hypertension, diabetes, coronary artery disease, myocardial infarction, and chronic kidney disease).
Results: In our study cohort, we identified 3,714 patients with SSc (5.7%), 15,940 patients with SLE (24.7%), and 44,966 patients with RA (69.6%), among which 14.4% of SSc, 12.2% of SLE, and 10.5% of RA patients developed incident HF during follow-up. In our study cohort (n = 64,620), ARB (aHR: 1.1 [1.0-1.2]; p = 0.005) and thiazide (aHR: 1.2 [1.1-1.2]; p <0.001) use were significantly associated with decreased time to incident HF, while BB (aHR: 0.68 [0.61-0.75]; p <0.001) use was associated with increased time to HF. In SSc patients (compared with no CV drugs), ACE-i (aHR: 1.5; 95% CI [1.14-1.9]; p = 0.004), ARB (aHR: 1.4 [1.06-1.9]; p = 0.018), and thiazide (aHR: 1.5 [1.15-1.9]; p =0.003) use were significantly associated with decreased time to incident HF. Baseline BB use had near significant association with increased time to incident HF in SSc (aHR: 0.73 [0.51-1.0]; p = 0.079). In SLE patients (compared with no CV drugs), baseline thiazide use was associated with decreased time to incident HF (aHR: 1.2 [1.0-1.4]; p = 0.01), and BB use was associated with increased time to incident HF (aHR: 0.71 [0.57-0.89]; p = 0.003). In RA patients, baseline ARB (aHR: 1.1 [1.0-1.2]; p = 0.026) and thiazide (aHR: 1.1 [1.0-1.2]; p = 0.003) were associated with decreased time to incident HF and BB use was associated with increased time to incident HF (aHR: 0.68 [0.61-0.76]; p <0.001).
Conclusion: In our single-center experience, the use of beta-blockers at the time of SARD diagnosis was associated with delayed onset of HF. Further investigations into the potential cardioprotective effects of beta-blockers in patients with SARDs are warranted.
Methods: We reviewed electronic health records from a large multispecialty institution of adult patients with SARDs from 2000-2020. Demographic data, SARD diagnosis, HF and comorbidity status, and cardiovascular medication use data were extracted retrospectively. CV drugs included were angiotensin converting enzyme inhibitors (ACE-i), angiotensin receptor blockers (ARBs), beta blockers (BBs), calcium channel blockers (CCBs), and thiazide diuretics. Baseline was defined as time of SARD diagnosis. Inclusion criteria were SSc, SLE, or RA diagnosis. Patients with HF at baseline were excluded. Cox proportional hazards regression was performed to investigate the association between CV drugs exposure at baseline and time to incident HF, adjusting for traditional risk factors (age, sex, hypertension, diabetes, coronary artery disease, myocardial infarction, and chronic kidney disease).
Results: In our study cohort, we identified 3,714 patients with SSc (5.7%), 15,940 patients with SLE (24.7%), and 44,966 patients with RA (69.6%), among which 14.4% of SSc, 12.2% of SLE, and 10.5% of RA patients developed incident HF during follow-up. In our study cohort (n = 64,620), ARB (aHR: 1.1 [1.0-1.2]; p = 0.005) and thiazide (aHR: 1.2 [1.1-1.2]; p <0.001) use were significantly associated with decreased time to incident HF, while BB (aHR: 0.68 [0.61-0.75]; p <0.001) use was associated with increased time to HF. In SSc patients (compared with no CV drugs), ACE-i (aHR: 1.5; 95% CI [1.14-1.9]; p = 0.004), ARB (aHR: 1.4 [1.06-1.9]; p = 0.018), and thiazide (aHR: 1.5 [1.15-1.9]; p =0.003) use were significantly associated with decreased time to incident HF. Baseline BB use had near significant association with increased time to incident HF in SSc (aHR: 0.73 [0.51-1.0]; p = 0.079). In SLE patients (compared with no CV drugs), baseline thiazide use was associated with decreased time to incident HF (aHR: 1.2 [1.0-1.4]; p = 0.01), and BB use was associated with increased time to incident HF (aHR: 0.71 [0.57-0.89]; p = 0.003). In RA patients, baseline ARB (aHR: 1.1 [1.0-1.2]; p = 0.026) and thiazide (aHR: 1.1 [1.0-1.2]; p = 0.003) were associated with decreased time to incident HF and BB use was associated with increased time to incident HF (aHR: 0.68 [0.61-0.76]; p <0.001).
Conclusion: In our single-center experience, the use of beta-blockers at the time of SARD diagnosis was associated with delayed onset of HF. Further investigations into the potential cardioprotective effects of beta-blockers in patients with SARDs are warranted.
Code of conduct/disclaimer available in General Terms & Conditions
{{ help_message }}
{{filter}}