Relaxin for Treatment of Acute Heart Failure: Making the Case for Treating Targeted Patient Profiles

Hernández-Montfort, Jaime; Arora, Sonali; Slawsky, Mara

doi:10.1007/s11897-013-0148-6

Cited by 7 publications

(5 citation statements)

References 32 publications

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“…Hernandez-Montfort studied patients with ischemic heart disease and reduced ejection fraction. Their patients were normotensive or hypertensive and had moderate renal impairment [23].…”

Section: Discussionmentioning

confidence: 99%

Relaxin Does Not Improve Angiotensin II-Induced Target-Organ Damage

et al. 2014

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Relaxin is a corpus-luteum produced protein hormone with vasodilatatory, anti-fibrotic, and angiogenic properties that are opposite to angiotensin (Ang) II. We investigated whether or not relaxin ameliorates Ang II-induced target-organ damage. We used double transgenic rats harboring both human renin and angiotensinogen genes (dTGR) that develop severe hypertension, target-organ damage, and die untreated within 7–8 weeks. Recombinant relaxin at a low (26 μg/kg/d) and a high dose (240 μg/kg/d) was given to 4 week-old dTGR and age-matched Sprague-Dawley rats (SD). Systolic blood pressure increased progressively in untreated dTGRs from 162±3 mmHg at week 5 to 225±5 mmHg at week 7. Relaxin had no effect on blood pressure whereas SD rats were normotensive (106±1 mmHg). Untreated and relaxin-treated dTGR had similarly severe cardiac hypertrophy indices. Relaxin did not ameliorate albuminuria and did not prevent matrix-protein deposition in the heart and kidney in dTGR. Finally, relaxin treatment did not reduce mortality. These data suggest that pharmacological doses of relaxin do not reverse severe effects of Ang II.

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“…Hernandez-Montfort studied patients with ischemic heart disease and reduced ejection fraction. Their patients were normotensive or hypertensive and had moderate renal impairment [23].…”

Section: Discussionmentioning

confidence: 99%

Relaxin Does Not Improve Angiotensin II-Induced Target-Organ Damage

et al. 2014

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“…By binding to the LGR7 and LGR8 receptors, it activates and enhances the vascular endothelin B receptor and vascular endothelial growth factor (VEGF) and leads to the production of nitric oxide [102]. Its influence on the inhibition of angiotensin II and endothelin was also proven [103]. Serelaxin reduces systemic vascular resistance, increases cardiac output, increases renal blood flow and increases glomerular filtration rate [102,104].…”

Section: Serelaxinmentioning

confidence: 99%

Clinical Review of Hypertensive Acute Heart Failure

Lasica,

Djukanovic,

Vukmirovic

et al. 2024

Medicina

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Although acute heart failure (AHF) is a common disease associated with significant symptoms, morbidity and mortality, the diagnosis, risk stratification and treatment of patients with hypertensive acute heart failure (H-AHF) still remain a challenge in modern medicine. Despite great progress in diagnostic and therapeutic modalities, this disease is still accompanied by a high rate of both in-hospital (from 3.8% to 11%) and one-year (from 20% to 36%) mortality. Considering the high rate of rehospitalization (22% to 30% in the first three months), the treatment of this disease represents a major financial blow to the health system of each country. This disease is characterized by heterogeneity in precipitating factors, clinical presentation, therapeutic modalities and prognosis. Since heart decompensation usually occurs quickly (within a few hours) in patients with H-AHF, establishing a rapid diagnosis is of vital importance. In addition to establishing the diagnosis of heart failure itself, it is necessary to see the underlying cause that led to it, especially if it is de novo heart failure. Given that hypertension is a precipitating factor of AHF and in up to 11% of AHF patients, strict control of arterial blood pressure is necessary until target values are reached in order to prevent the occurrence of H-AHF, which is still accompanied by a high rate of both early and long-term mortality.

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“…By binding to the LGR7 and LGR8 receptors, it activates and enhances the vascular endothelin B receptor, vascular endothelial growth factor (VEGF) and leads to the production of nitric oxide [108]. Its influence on the inhibition of angiotensin II and endothelin has also been proven [109]. Serelaxin reduces systemic vascular resistance, increases cardiac output, increases renal blood flow, and increases glomerular filtration rate [108,110].…”

Section: Serelaxinmentioning

confidence: 99%

Clinical Review of Hypertensive Acute Heart Failure

Lasica,

Djukanovic,

Vukmirovic

et al. 2023

Preprint

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Although acute heart failure (AHF) is a common disease associated with significant symptoms, morbidity and mortality, the diagnosis, risk stratification and treatment of patients with hypertensive acute heart failure (H-AHF) still remain a challenge in modern medicine. Despite great progress in diagnostic and therapeutic modalities, this disease is still accompanied by a high rate of both in-hospital (from 3.8% to 11%) and one-year mortality (from 20% to 36%). Considering the high rate of re-hospitalization (22% to 30% in the first three months), the treatment of this disease represents a major financial blow to the health system of each country. This disease is characterized by heterogeneity in precipitating factors, clinical presentation, therapeutic modalities and prognosis. Since heart decompensation usually occurs quickly (within a few hours) in patients with H-AHF, establishing a rapid diagnosis is of vital importance. In addition to establishing the diagnosis of heart failure itself, it is necessary to see the underlying cause that led to it, especially if it is de novo heart failure. Given that hypertension is a precipitating factor of AHF and in up to 11% of AHF patients, strict control of arterial blood pressure is necessary until target values are reached in order to prevent the occurrence of H-AHF, which is still accompanied by a high rate of both early and long-term mortality.

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Relaxin for Treatment of Acute Heart Failure: Making the Case for Treating Targeted Patient Profiles

Cited by 7 publications

References 32 publications

Relaxin Does Not Improve Angiotensin II-Induced Target-Organ Damage

Relaxin Does Not Improve Angiotensin II-Induced Target-Organ Damage

Clinical Review of Hypertensive Acute Heart Failure

Clinical Review of Hypertensive Acute Heart Failure

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