9 research outputs found
1128-130 The blood pressure response to the valsalva maneuver: An independent predictor of mortality in elderly cardiac patients
Effect of sitagliptin on cardiovascular outcomes in type 2 diabetes
BACKGROUND: Data are lacking on the long-term effect on cardiovascular events of adding sitagliptin, a dipeptidyl peptidase 4 inhibitor, to usual care in patients with type 2 diabetes and cardiovascular disease. METHODS: In this randomized, double-blind study, we assigned 14,671 patients to add either sitagliptin or placebo to their existing therapy. Open-label use of antihyperglycemic therapy was encouraged as required, aimed at reaching individually appropriate glycemic targets in all patients. To determine whether sitagliptin was noninferior to placebo, we used a relative risk of 1.3 as the marginal upper boundary. The primary cardiovascular outcome was a composite of cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for unstable angina. RESULTS: During a median follow-up of 3.0 years, there was a small difference in glycated hemoglobin levels (least-squares mean difference for sitagliptin vs. placebo, -0.29 percentage points; 95% confidence interval [CI], -0.32 to -0.27). Overall, the primary outcome occurred in 839 patients in the sitagliptin group (11.4%; 4.06 per 100 person-years) and 851 patients in the placebo group (11.6%; 4.17 per 100 person-years). Sitagliptin was noninferior to placebo for the primary composite cardiovascular outcome (hazard ratio, 0.98; 95% CI, 0.88 to 1.09; P<0.001). Rates of hospitalization for heart failure did not differ between the two groups (hazard ratio, 1.00; 95% CI, 0.83 to 1.20; P = 0.98). There were no significant between-group differences in rates of acute pancreatitis (P = 0.07) or pancreatic cancer (P = 0.32). CONCLUSIONS: Among patients with type 2 diabetes and established cardiovascular disease, adding sitagliptin to usual care did not appear to increase the risk of major adverse cardiovascular events, hospitalization for heart failure, or other adverse events
1128-130 The blood pressure response to the valsalva maneuver: An independent predictor of mortality in elderly cardiac patients
Detection of elevated pulmonary capillary wedge pressure in elderly patients with various cardiac disorders by the Valsalva manoeuvre.
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49614.pdf (publisher's version ) (Closed access)In the present study, we assessed whether elevated (> or =15 mmHg) PCWP (pulmonary capillary wedge pressure) can be detected using the blood pressure response to the Valsalva manoeuvre in a group of elderly patients with various cardiac disorders, including atrial fibrillation and valvular heart disease, and healthy elderly controls. The Valsalva manoeuvre was performed in 93 patients (71+/-4 years) and 28 healthy controls (70+/-4 years) undergoing right-sided cardiac catheterization. Blood pressure was measured non-invasively with Finapres. PPR (pulse pressure ratio), the ratio of minimum pulse pressure during phase 2 and maximum pulse pressure during phase 1 of the Valsalva manoeuvre, was correlated with PCWP (r=0.63, P<0.001). The area under the receiver operator characteristic curve of PPR with elevated PCWP was 0.85 (P<0.001). For PPR=0.62, sensitivity for elevated PCWP was 80%, specificity was 79%, positive predictive value was 76% and negative predictive value was 83%. Correlation of PPR with PCWP and the ability of PPR to detect elevated PCWP was present in atrial fibrillation, heart failure and valvular heart disease. In conclusion, PPR is a sensitive and specific instrument to diagnose elevated PCWP non-invasively in a large group of elderly patients with various cardiac disorders. This makes the Valsalva manoeuvre a useful non-invasive tool for diagnosing heart failure, applicable in elderly patients with common cardiac disorders, such as atrial fibrillation and valvular heart disease
Finapres arterial pulse wave analysis with Modelflow® is not a reliable non-invasive method for assessment of cardiac output
Finapres arterial pulse wave analysis with Modelflow is not a reliable non-invasive method for assessment of cardiac output
Normal values of pulmonary capillary wedge pressure and the blood pressure response to the Valsalva manoeuvre in healthy elderly subjects
Effect of sitagliptin on cardiovascular outcomes in type 2 diabetes
BACKGROUND
Data are lacking on the long-term effect on cardiovascular events of adding sitagliptin,
a dipeptidyl peptidase 4 inhibitor, to usual care in patients with type 2
diabetes and cardiovascular disease.
METHODS
In this randomized, double-blind study, we assigned 14,671 patients to add either
sitagliptin or placebo to their existing therapy. Open-label use of antihyperglycemic
therapy was encouraged as required, aimed at reaching individually appropriate
glycemic targets in all patients. To determine whether sitagliptin was noninferior
to placebo, we used a relative risk of 1.3 as the marginal upper boundary. The
primary cardiovascular outcome was a composite of cardiovascular death, nonfatal
myocardial infarction, nonfatal stroke, or hospitalization for unstable angina.
RESULTS
During a median follow-up of 3.0 years, there was a small difference in glycated
hemoglobin levels (least-squares mean difference for sitagliptin vs. placebo,
120.29 percentage points; 95% confidence interval [CI], 120.32 to 120.27). Overall,
the primary outcome occurred in 839 patients in the sitagliptin group (11.4%;
4.06 per 100 person-years) and 851 patients in the placebo group (11.6%; 4.17 per
100 person-years). Sitagliptin was noninferior to placebo for the primary composite
cardiovascular outcome (hazard ratio, 0.98; 95% CI, 0.88 to 1.09; P<0.001).
Rates of hospitalization for heart failure did not differ between the two groups
(hazard ratio, 1.00; 95% CI, 0.83 to 1.20; P=0.98). There were no significant
between-group differences in rates of acute pancreatitis (P=0.07) or pancreatic
cancer (P=0.32).
CONCLUSIONS
Among patients with type 2 diabetes and established cardiovascular disease, adding
sitagliptin to usual care did not appear to increase the risk of major adverse cardiovascular
events, hospitalization for heart failure, or other adverse events.
(Funded by Merck Sharp & Dohme; TECOS ClinicalTrials.gov number, NCT00790205.