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Matthew R Weir - One of the best experts on this subject based on the ideXlab platform.

  • effect of patiromer on reducing serum potassium and preventing recurrent hyperkalaemia in patients with heart failure and chronic kidney disease on raas inhibitors
    European Journal of Heart Failure, 2015
    Co-Authors: Bertram Pitt, David A Bushinsky, Dahlia Garza, Lance Berman, George L Bakris, Martha Mayo, Yuri Stasiv, Heidi Christschmidt, Matthew R Weir
    Abstract:

    Aims We evaluated the effects of patiromer, a potassium (K+)-binding polymer, in a pre-specified analysis of hyperkalaemic patients with heart failure (HF) in the OPAL-HK trial. Methods and results Chronic kidney disease (CKD) patients on renin–angiotensin–aldosterone system inhibitors (RAASi) with serum K+ levels ≥5.1 mEq/L to <6.5 mEq/L (n = 243) received patiromer (4.2 g or 8.4 g BID initially) for 4 weeks (initial treatment phase); the primary efficacy endpoint was mean change in serum K+ from baseline to week 4. Eligible patients (those with baseline K+ ≥5.5 mEq/L to <6.5 mEq/L and levels ≥3.8 mEq/L to <5.1 mEq/L at the end of week 4) entered an 8-week randomized withdrawal phase and were randomly assigned to continue patiromer or switch to placebo; the primary efficacy endpoint was the between-group difference in median change in the serum K+ over the first 4 weeks of that phase. One hundred and two patients (42%) had heart failure (HF). The mean [± standard error (SE)] change in serum K+ from baseline to week 4 was −1.06 ± 0.05 mEq/L [95% confidence interval (CI), −1.16,−0.95; P < 0.001]; 76% (95% CI, 69,84) achieved serum K+, 3.8 mEq/L to <5.1 mEq/L. In the randomized withdrawal phase, the median increase in serum K+ from baseline of that phase was greater with placebo (n = 22) than patiromer (n = 27) (P < 0.001); recurrent hyperkalaemia (serum K+, ≥5.5 mEq/L) occurred in 52% on placebo and 8% on patiromer (P < 0.001). Mild-to-moderate constipation was the most common adverse event (11%); hypokalaemia occurred in 3%. Conclusion In patients with CKD and HF who were hyperkalaemic on RAASi, patiromer was well tolerated, decreased serum K+, and, compared with placebo, reduced recurrent hyperkalaemia.

  • efficacy of candesartan cilexetil as add on therapy in hypertensive patients uncontrolled on background therapy a clinical experience trial
    American Journal of Hypertension, 2000
    Co-Authors: Matthew R Weir, Eric L. Michelson, Jennifer Vendetti, Joel M Neutel, Michael A Weber, Rebecca Wang
    Abstract:

    Abstract A large-scale, 8-week, open-label, clinical experience trial evaluated the efficacy of the angiotensin II receptor (AT 1 subtype) blocker candesartan cilexetil (16 to 32 mg once daily) either alone or as add-on therapy in 6465 hypertensive patients. The study population was 52% female and 16% African American with a mean age of 58 years. It included 5446 patients who had essential hypertension (HBP) and 1014 patients who had isolated systolic hypertension (ISH). These patients had either untreated or uncontrolled hypertension (systolic blood pressure [SBP] 140 to 179 mm Hg or diastolic blood pressure [DBP] 90 to 109 mm Hg inclusive at baseline) despite a variety of antihypertensive medications including diuretics, calcium antagonists, angiotensin converting enzyme (ACE) inhibitors, and α- or β-blockers, either singly or in combination. The mean baseline blood pressure for the HBP group was 156/97 mm Hg. Candesartan cilexetil as monotherapy (in 51% of HBP patients) reduced mean SBP/DBP by 18.7/13.1 mm Hg. As add-on therapy (in 49% of HBP patients) to various background therapies, candesartan cilexetil consistently reduced mean SBP/DBP further, irrespective of the background therapy: diuretics (17.8/11.3 mm Hg), calcium antagonists (16.6/11.2 mm Hg), β-blockers (16.5/10.4 mm Hg), ACE inhibitors (15.3/10.0 mm Hg), α-blockers (16.4/10.4 mm Hg). The mean baseline blood pressure for the ISH group was 158/81 mm Hg. Candesartan cilexetil, as monotherapy (in 34% of ISH patients), reduced SBP/DBP by 17.0/4.4 mm Hg. As add-on therapy (in 66% of ISH patients) to various background therapies, candesartan cilexetil consistently reduced mean SBP/DBP further, irrespective of the background therapy: diuretics (17.4/5.1 mm Hg), calcium antagonists (15.6/3.6 mm Hg), β-blockers (14.0/4.8 mm Hg), ACE inhibitors (13.4/4.3 mm Hg), and α-blockers (11.6/4.5 mm Hg). The further blood pressure lowering effects of candesartan cilexetil as add-on therapy were seen regardless of age, sex, and race. Overall, 6.8% of the 6465 patients withdrew because of adverse events, most commonly headache (6.3%) and dizziness (5.0%). Orthostatic hypotension was infrequent; 0.2% with candesartan cilexetil alone, and 0.8% with candesartan cilexetil as add-on therapy. Thus, candesartan cilexetil either alone or as add-on therapy was highly effective for the control of systolic or diastolic hypertension regardless of demographic background when used in typical clinical practice settings.

Thomas Kahan - One of the best experts on this subject based on the ideXlab platform.

  • soluble cell adhesion molecules in hypertensive concentric left ventricular hypertrophy
    Journal of Hypertension, 2002
    Co-Authors: Karin Malmqvist, Hakan Wallen, Claes Held, Thomas Kahan
    Abstract:

    OBJECTIVE Concentric left ventricular (LV) hypertrophy is an important cardiovascular risk factor. We investigated whether concentric LV hypertrophy is associated with activation of the vascular endothelium, as assessed by measurements of soluble cell adhesion molecules. DESIGN E-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular adhesion molecule-1 (VCAM-1) were measured in serum from hypertensive patients with LV hypertrophy (64 with concentric and 47 with eccentric hypertrophy) and from two matched control groups consisting of 38 hypertensive patients without LV hypertrophy and 38 normotensive subjects. Carotid artery intima-media thickness (IMT) was examined by ultrasonography and LV mass by echocardiography. Neurohormone activities of the renin-angiotensin-aldosterone system were also measured. RESULTS E-selectin levels were higher in hypertensive than in normotensive subjects (56 +/- 19 versus 49 +/- 11 ng/ml, P = 0.031). Patients with concentric LV hypertrophy had higher levels of E-selectin (61 +/- 21 versus 49 +/- 15 ng/ml, P < 0.001), ICAM-1 (273 +/- 49 versus 254 +/- 49 ng/ml, P = 0.043), VCAM-1 (591 +/- 131 versus 544 +/- 78 ng/ml, P = 0.038) and greater carotid artery IMT (0.99 +/- 0.26 versus 0.83 +/- 0.15 mm, P = 0.018) than eccentric LV hypertrophy patients. E-selectin and VCAM-1 correlated positively to LV relative wall thickness (P = 0.040 and 0.037, respectively), with a similar trend for ICAM-1 (P = 0.083). E-selectin correlated with serum aldosterone (P < 0.001), and E-selectin and ICAM-1 with plasma angiotensin converting enzyme activity (P = 0.003 and 0.036, respectively). CONCLUSION Increased levels of soluble cell adhesion molecules and an increased carotid artery IMT characterize concentric LV hypertrophy. This indicates perturbations at the vascular level, involving activation of the vascular endothelium in hypertensive patients with concentric LV hypertrophy.

Bertram Pitt - One of the best experts on this subject based on the ideXlab platform.

  • evaluation of an individualized dose titration regimen of patiromer to prevent hyperkalaemia in patients with heart failure and chronic kidney disease
    Esc Heart Failure, 2018
    Co-Authors: Bertram Pitt, David A Bushinsky, Dalane W Kitzman, Frank Ruschitzka, Marco Metra, Gerasimos Filippatos, Patrick Rossignol, Charles Du Mond, Dahlia Garza, Lance Berman
    Abstract:

    AIMS Hyperkalaemia risk precludes optimal renin-angiotensin-aldosterone system inhibitor use in patients with heart failure (HF), particularly those with chronic kidney disease (CKD). Patiromer is a sodium-free, non-absorbed potassium (K)-binding polymer approved for the treatment of hyperkalaemia. In PEARL-HF, patiromer 25.2 g (fixed dose) prevented hyperkalaemia in HF patients with or without CKD initiating spironolactone. The current study evaluated the effectiveness of a lower starting dose of patiromer (16.4 g/day) followed by individualized titration in preventing hyperkalaemia and hypokalaemia when initiating spironolactone. METHODS AND RESULTS This open-label 8-week study enrolled 63 patients with CKD, serum K4.3-5.1 mEq/L, and chronic HF, who, based on investigator opinion, should receive spironolactone. Eligible patients started spironolactone 25 mg/day and patiromer 16.8 g/day (divided into two doses), with patiromer titrated to maintain serum K4.0-5.1 mEq/L. Mean (standard deviation) serum Kwas 4.78 (0.51) mEq/L at baseline; weekly values were 4.48-4.70 mEq/L during treatment. Serum Kof 3.5-5.5 mEq/L at the end of study treatment (primary endpoint) was achieved by 57 (90.5%) patients; 53 (84.1%) had serum K4.0-5.1 mEq/L. One patient (1.6%) developed hypokalaemia, and two patients (3.2%) developed hypomagnesaemia. Spironolactone was increased to 50 mg/day in all patients; 43 (68%) patients required one or more patiromer dose titration. Adverse events (AEs) occurred in 36 (57.1%) patients, with a low rate of discontinuations [four (6.3%) patients]. The most common AE was mild to moderate abdominal discomfort [four (6.3%) patients]. CONCLUSIONS In this open-label study, patiromer 16.8 g/day followed by individualized titration maintained serum Kwithin the target range in the majority of patients with HF and CKD, all of whom were uptitrated to spironolactone 50 mg/day, patiromer was well tolerated, with a low incidence of hyperkalaemia, hypokalaemia, and hypomagnesaemia.

  • effect of patiromer on reducing serum potassium and preventing recurrent hyperkalaemia in patients with heart failure and chronic kidney disease on raas inhibitors
    European Journal of Heart Failure, 2015
    Co-Authors: Bertram Pitt, David A Bushinsky, Dahlia Garza, Lance Berman, George L Bakris, Martha Mayo, Yuri Stasiv, Heidi Christschmidt, Matthew R Weir
    Abstract:

    Aims We evaluated the effects of patiromer, a potassium (K+)-binding polymer, in a pre-specified analysis of hyperkalaemic patients with heart failure (HF) in the OPAL-HK trial. Methods and results Chronic kidney disease (CKD) patients on renin–angiotensin–aldosterone system inhibitors (RAASi) with serum K+ levels ≥5.1 mEq/L to <6.5 mEq/L (n = 243) received patiromer (4.2 g or 8.4 g BID initially) for 4 weeks (initial treatment phase); the primary efficacy endpoint was mean change in serum K+ from baseline to week 4. Eligible patients (those with baseline K+ ≥5.5 mEq/L to <6.5 mEq/L and levels ≥3.8 mEq/L to <5.1 mEq/L at the end of week 4) entered an 8-week randomized withdrawal phase and were randomly assigned to continue patiromer or switch to placebo; the primary efficacy endpoint was the between-group difference in median change in the serum K+ over the first 4 weeks of that phase. One hundred and two patients (42%) had heart failure (HF). The mean [± standard error (SE)] change in serum K+ from baseline to week 4 was −1.06 ± 0.05 mEq/L [95% confidence interval (CI), −1.16,−0.95; P < 0.001]; 76% (95% CI, 69,84) achieved serum K+, 3.8 mEq/L to <5.1 mEq/L. In the randomized withdrawal phase, the median increase in serum K+ from baseline of that phase was greater with placebo (n = 22) than patiromer (n = 27) (P < 0.001); recurrent hyperkalaemia (serum K+, ≥5.5 mEq/L) occurred in 52% on placebo and 8% on patiromer (P < 0.001). Mild-to-moderate constipation was the most common adverse event (11%); hypokalaemia occurred in 3%. Conclusion In patients with CKD and HF who were hyperkalaemic on RAASi, patiromer was well tolerated, decreased serum K+, and, compared with placebo, reduced recurrent hyperkalaemia.

Lance Berman - One of the best experts on this subject based on the ideXlab platform.

  • evaluation of an individualized dose titration regimen of patiromer to prevent hyperkalaemia in patients with heart failure and chronic kidney disease
    Esc Heart Failure, 2018
    Co-Authors: Bertram Pitt, David A Bushinsky, Dalane W Kitzman, Frank Ruschitzka, Marco Metra, Gerasimos Filippatos, Patrick Rossignol, Charles Du Mond, Dahlia Garza, Lance Berman
    Abstract:

    AIMS Hyperkalaemia risk precludes optimal renin-angiotensin-aldosterone system inhibitor use in patients with heart failure (HF), particularly those with chronic kidney disease (CKD). Patiromer is a sodium-free, non-absorbed potassium (K)-binding polymer approved for the treatment of hyperkalaemia. In PEARL-HF, patiromer 25.2 g (fixed dose) prevented hyperkalaemia in HF patients with or without CKD initiating spironolactone. The current study evaluated the effectiveness of a lower starting dose of patiromer (16.4 g/day) followed by individualized titration in preventing hyperkalaemia and hypokalaemia when initiating spironolactone. METHODS AND RESULTS This open-label 8-week study enrolled 63 patients with CKD, serum K4.3-5.1 mEq/L, and chronic HF, who, based on investigator opinion, should receive spironolactone. Eligible patients started spironolactone 25 mg/day and patiromer 16.8 g/day (divided into two doses), with patiromer titrated to maintain serum K4.0-5.1 mEq/L. Mean (standard deviation) serum Kwas 4.78 (0.51) mEq/L at baseline; weekly values were 4.48-4.70 mEq/L during treatment. Serum Kof 3.5-5.5 mEq/L at the end of study treatment (primary endpoint) was achieved by 57 (90.5%) patients; 53 (84.1%) had serum K4.0-5.1 mEq/L. One patient (1.6%) developed hypokalaemia, and two patients (3.2%) developed hypomagnesaemia. Spironolactone was increased to 50 mg/day in all patients; 43 (68%) patients required one or more patiromer dose titration. Adverse events (AEs) occurred in 36 (57.1%) patients, with a low rate of discontinuations [four (6.3%) patients]. The most common AE was mild to moderate abdominal discomfort [four (6.3%) patients]. CONCLUSIONS In this open-label study, patiromer 16.8 g/day followed by individualized titration maintained serum Kwithin the target range in the majority of patients with HF and CKD, all of whom were uptitrated to spironolactone 50 mg/day, patiromer was well tolerated, with a low incidence of hyperkalaemia, hypokalaemia, and hypomagnesaemia.

  • effect of patiromer on reducing serum potassium and preventing recurrent hyperkalaemia in patients with heart failure and chronic kidney disease on raas inhibitors
    European Journal of Heart Failure, 2015
    Co-Authors: Bertram Pitt, David A Bushinsky, Dahlia Garza, Lance Berman, George L Bakris, Martha Mayo, Yuri Stasiv, Heidi Christschmidt, Matthew R Weir
    Abstract:

    Aims We evaluated the effects of patiromer, a potassium (K+)-binding polymer, in a pre-specified analysis of hyperkalaemic patients with heart failure (HF) in the OPAL-HK trial. Methods and results Chronic kidney disease (CKD) patients on renin–angiotensin–aldosterone system inhibitors (RAASi) with serum K+ levels ≥5.1 mEq/L to <6.5 mEq/L (n = 243) received patiromer (4.2 g or 8.4 g BID initially) for 4 weeks (initial treatment phase); the primary efficacy endpoint was mean change in serum K+ from baseline to week 4. Eligible patients (those with baseline K+ ≥5.5 mEq/L to <6.5 mEq/L and levels ≥3.8 mEq/L to <5.1 mEq/L at the end of week 4) entered an 8-week randomized withdrawal phase and were randomly assigned to continue patiromer or switch to placebo; the primary efficacy endpoint was the between-group difference in median change in the serum K+ over the first 4 weeks of that phase. One hundred and two patients (42%) had heart failure (HF). The mean [± standard error (SE)] change in serum K+ from baseline to week 4 was −1.06 ± 0.05 mEq/L [95% confidence interval (CI), −1.16,−0.95; P < 0.001]; 76% (95% CI, 69,84) achieved serum K+, 3.8 mEq/L to <5.1 mEq/L. In the randomized withdrawal phase, the median increase in serum K+ from baseline of that phase was greater with placebo (n = 22) than patiromer (n = 27) (P < 0.001); recurrent hyperkalaemia (serum K+, ≥5.5 mEq/L) occurred in 52% on placebo and 8% on patiromer (P < 0.001). Mild-to-moderate constipation was the most common adverse event (11%); hypokalaemia occurred in 3%. Conclusion In patients with CKD and HF who were hyperkalaemic on RAASi, patiromer was well tolerated, decreased serum K+, and, compared with placebo, reduced recurrent hyperkalaemia.

Karin Malmqvist - One of the best experts on this subject based on the ideXlab platform.

  • soluble cell adhesion molecules in hypertensive concentric left ventricular hypertrophy
    Journal of Hypertension, 2002
    Co-Authors: Karin Malmqvist, Hakan Wallen, Claes Held, Thomas Kahan
    Abstract:

    OBJECTIVE Concentric left ventricular (LV) hypertrophy is an important cardiovascular risk factor. We investigated whether concentric LV hypertrophy is associated with activation of the vascular endothelium, as assessed by measurements of soluble cell adhesion molecules. DESIGN E-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular adhesion molecule-1 (VCAM-1) were measured in serum from hypertensive patients with LV hypertrophy (64 with concentric and 47 with eccentric hypertrophy) and from two matched control groups consisting of 38 hypertensive patients without LV hypertrophy and 38 normotensive subjects. Carotid artery intima-media thickness (IMT) was examined by ultrasonography and LV mass by echocardiography. Neurohormone activities of the renin-angiotensin-aldosterone system were also measured. RESULTS E-selectin levels were higher in hypertensive than in normotensive subjects (56 +/- 19 versus 49 +/- 11 ng/ml, P = 0.031). Patients with concentric LV hypertrophy had higher levels of E-selectin (61 +/- 21 versus 49 +/- 15 ng/ml, P < 0.001), ICAM-1 (273 +/- 49 versus 254 +/- 49 ng/ml, P = 0.043), VCAM-1 (591 +/- 131 versus 544 +/- 78 ng/ml, P = 0.038) and greater carotid artery IMT (0.99 +/- 0.26 versus 0.83 +/- 0.15 mm, P = 0.018) than eccentric LV hypertrophy patients. E-selectin and VCAM-1 correlated positively to LV relative wall thickness (P = 0.040 and 0.037, respectively), with a similar trend for ICAM-1 (P = 0.083). E-selectin correlated with serum aldosterone (P < 0.001), and E-selectin and ICAM-1 with plasma angiotensin converting enzyme activity (P = 0.003 and 0.036, respectively). CONCLUSION Increased levels of soluble cell adhesion molecules and an increased carotid artery IMT characterize concentric LV hypertrophy. This indicates perturbations at the vascular level, involving activation of the vascular endothelium in hypertensive patients with concentric LV hypertrophy.