Acute regional circulatory and renal hemodynamic effects of converting-enzyme inhibition in patients with congestive heart failure.

Creager, Mark A.; Halperin, JL; Bernard, David B.; Faxon, David P.; Melidossian, Caroline D.; Gavras, Haralambos; Ryan, Thomas J.

doi:10.1161/01.cir.64.3.483

Cited by 170 publications

(23 citation statements)

References 36 publications

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“…First line therapy to improve RBF consists of ACE inhibitors and ARBs [33,34]. In addition to improved renal perfusion, this will also lead to Fig.…”

Section: Clinical Implications For Therapymentioning

confidence: 99%

Decreased cardiac output, venous congestion and the association with renal impairment in patients with cardiac dysfunction

Damman

Navis

Smilde

et al. 2007

European J of Heart Fail

422

291

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Background: Renal failure in heart failure is related to decreased cardiac output. However, little is known about its association with venous congestion. Aims: To investigate the relationship between venous congestion and glomerular filtration rate (GFR) in patients with cardiac dysfunction. Methods and results: Right atrial pressure (RAP) and cardiac index (CI) were determined by right heart catheterisation in 51 patients with cardiac dysfunction, secondary to pulmonary hypertension. GFR and renal blood flow (RBF) were measured as 125 I-Iothalamate and 131 IHippuran clearances, respectively. Mean age was 40 ± 11 years and 69% of patients were female. GFR was 73 ± 19 ml/min/1.73 m 2 with a CI of 2.1 ± 0.7 l/min/m 2 . In multivariate analysis, RBF (r = 0.664, p b 0.001) and RAP (r = − 0.367, p = 0.020) were independently associated with GFR. In patients in the lower ranges of RBF, venous congestion was an important determinant of renal function. Conclusion: RBF is the main factor determining GFR in patients with cardiac dysfunction. Venous congestion, characterised by an increased RAP, adjusted for RBF is also related to GFR. Treatment to preserve GFR should not only focus on improvement of renal perfusion, but also on decreasing venous congestion.

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“…First line therapy to improve RBF consists of ACE inhibitors and ARBs [33,34]. In addition to improved renal perfusion, this will also lead to Fig.…”

Section: Clinical Implications For Therapymentioning

confidence: 99%

Decreased cardiac output, venous congestion and the association with renal impairment in patients with cardiac dysfunction

Damman

Navis

Smilde

et al. 2007

European J of Heart Fail

422

291

View full text Add to dashboard Cite

show abstract

“…Some studies found an increase in GFR, 22 others found a decrease, and others did not find any significant effect. 23,24 The net effect of renin-angiotensin system inhibitors on renal function in CHF patients remains to be elucidated. However, to the best of our knowledge, no available data suggest that renin-angiotensin system blockade could alter the relationship between true renal function and equation-derived estimates of renal function.…”

Section: Limitationsmentioning

confidence: 99%

Drawbacks and Prognostic Value of Formulas Estimating Renal Function in Patients With Chronic Heart Failure and Systolic Dysfunction

et al. 2006

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Background-Renal function is an important risk marker for morbidity and mortality in chronic heart failure (CHF) and is often estimated with the use of creatinine-based formulas. However, these formulas have never been validated in a wide range of CHF patients. We validated 3 commonly used formulas estimating glomerular filtration rate (GFR) with true GFR in CHF patients. Furthermore, we compared the prognostic value of these formulas for cardiovascular outcome with that of true GFR during 12 months of follow-up. Methods and Results-In 110 CHF patients (age, 57Ϯ11.7 years; left ventricular ejection fraction, 0.27Ϯ0.09; NYHA class, 2.5Ϯ0.9), we measured 125 I-iothalamate clearance. Cockcroft-Gault (GFR cg ), Modification of Diet in Renal Disease (MDRD), and simplified MDRD (sMDRD) equations were used as creatinine-based renal function estimations. Furthermore, 24-hour creatinine clearance (CrCl) was determined. CrCl and GFR cg were the most accurate. MDRD was most precise formula, although it was also highly biased. All formulas overestimated in the lower ranges and underestimated in the upper ranges of the GFR corrected for body surface area. The predictive performance of the formulas was best in severe CHF (NYHA classes III and IV). The prognostic value of CrCl and MDRD for cardiovascular outcome was comparable to that of GFR, the sMDRD was slightly less, and the GFR cg had a significantly worse prognostic value. Conclusions-In the more severe ranges of CHF, creatinine-based formulas and CrCl corrected for body surface area appeared to be more precise and accurate in estimating true GFR corrected for body surface area. The MDRD formula is the most precise and has a good prognostic value, whereas the sMDRD is slightly less accurate but uses fewer parameters, which makes this formula a practical alternative in clinical practice.

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“…The rise in Ca2+ may affect the release of bradykinin and the activity of NO synthase. Thirdly, activation of a1-adrenoceptors produce a more than 40-fold increase in the rate of kallikrein secretion, and the kinin output in the venous effluent from the submandibular gland increases 700-fold (13), suggesting that a 1-adrenoceptor stimulation, which occurs during myocar- …”

Section: Effects Of Ace Inhibitorsmentioning

confidence: 99%

Cellular Mechanisms of Cardioprotection Afforded by Inhibitors of Angiotensin Converting Enzyme in Ischemic Hearts: Role of Bradykinin and Nitric Oxide.

et al. 2000

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Angiotensin converting enzyme (ACE) inhibitors inhibit the degradation of bradykinin and contribute to accumulation of bradykinin and NO, both of which may be beneficial for diseased hearts. To test this idea, we administered imidaprilat and cilazaprilat, respectively to the canine ischemic myocardium. In the open chest dogs with low constant coronary perfusion pressure (CPP, from 104 ± 3 to 42 ± 3 mmHg), coronary blood flow (CBF, 91 ± 1 to 32 ± 2 mI/100 g/min), fractional shortening (FS), and lactate extraction ratio (LER) decreased. Either imidaprilat or cilazaprilat increased CBF, FS, and LER with increases in cardiac bradykinin and NO levels. The beneficial effects of ACE inhibitors were blunted by either L-NAME (an inhibitor of NO synthase) and HOE140 (an inhibitor of bradykinin receptors), respectively. ACE inhibitors, on the other hand, are reported to attenuate the severity of myocardial stunning, which effect is partially attributable to bradykinin-and NO-dependent mechanisms.Further, ACE inhibitors limited infarct size following coronary occlusion and reperfusion. This infarct size-limitation was blunted by either L-NAME and IBTX (the antagonist of KCa channels). Bradykinin is also reported to close Kca channels. Thus, we concluded that ACE inhibitors attenuate both reversible and irreversible myocardial cellular injury via bradykinin/NOdependent mechanisms. In experimental and clinical settings, the cardioprotective effects of ACE inhibitors on the diseased heart may be attributable to these mechanisms. (Hypertens Res 2000; 23: 253-259)

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Acute regional circulatory and renal hemodynamic effects of converting-enzyme inhibition in patients with congestive heart failure.

Cited by 170 publications

References 36 publications

Decreased cardiac output, venous congestion and the association with renal impairment in patients with cardiac dysfunction

Decreased cardiac output, venous congestion and the association with renal impairment in patients with cardiac dysfunction

Drawbacks and Prognostic Value of Formulas Estimating Renal Function in Patients With Chronic Heart Failure and Systolic Dysfunction

Cellular Mechanisms of Cardioprotection Afforded by Inhibitors of Angiotensin Converting Enzyme in Ischemic Hearts: Role of Bradykinin and Nitric Oxide.

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