Clinical implications of increased plasma angiotensin II despite ACE inhibitor therapy in patients with congestive heart failure

Roig, Eulàlia; Pérez‐Villa, Félix; Morales, María Gabriela; Jiménez, Wladimiro; Orús, Josefina; Heras, Magda; Sanz, Ginés

doi:10.1053/euhj.1999.1740

Cited by 221 publications

(167 citation statements)

References 23 publications

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“…Systemic and tissue Ang II levels are increased in CHF patients (Roig et al 2000) and in CHF rabbits . Ang II enhances CB chemoreceptor activity via the AT 1 receptor (AT 1 R) in the CB (Allen, 1998).…”

Section: Role Of Ang II On Cb Function In Chfmentioning

confidence: 99%

Carotid body function in heart failure

Schultz

2007

Respiratory Physiology & Neurobiology

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In this review, we summarize the present state of knowledge of the functional characteristics of the carotid body (CB) chemoreflex with respect to control of sympathetic nerve activity (SNA) in chronic heart failure (CHF). Evidence from both CHF patients and animal models of CHF has clearly established that the CB chemoreflex is enhanced in CHF and contributes to the tonic elevation in SNA. This adaptive change derives from altered function at the level of both the afferent and central nervous system (CNS) pathways of the reflex arc. At the level of the CB, an elevation in basal afferent discharge occurs under normoxic conditions in CHF rabbits, and the discharge responsiveness to hypoxia is enhanced. Outward voltage-gated K + currents (I K ) are suppressed in CB glomus cells from CHF rabbits, and their sensitivity to hypoxic inhibition is enhanced. These changes in I K derive partly from downregulation of nitric oxide synthase (NOS) / NO signaling and upregulation of angiotensin II (Ang II) / Ang II receptor (AT 1 R) signaling in glomus cells. At the level of the CNS, interactions of the enhanced input from CB chemoreceptors with altered input from baroreceptor and cardiac afferent pathways and from central Ang II further enhance sympathetic drive. In addition, impaired function of NO in the paraventricular nucleus of the hypothalamus participates in the increased SNA response to CB chemoreceptor activation. These results underscore the principle that multiple mechanisms involving Ang II and NO at the level of both the CB and CNS represent complementary and perhaps redundant adaptive mechanisms to enhance CB chemoreflex function in CHF.

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Section: Role Of Ang II On Cb Function In Chfmentioning

confidence: 99%

Carotid body function in heart failure

Schultz

2007

Respiratory Physiology & Neurobiology

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“…Angiotensinogen can be converted to angiotensin II by non-renin enzymes, including tissue plasminogen activator (t-PA), cathepsin G, elastase, and chymostatin, while angiotensin I can be converted to angiotensin II by non-ACE enzymes such as chymostatin-sensitive angiotensin II-generating enzyme, chymase, and cathepsin G. 23 Studies have in fact demonstrated "angiotensin II escape," with return of angiotensin II to pretreatment levels, during chronic ACE inhibitor therapy. 15,[29][30][31] Rebound of angiotensin II levels during ACE inhibitor therapy has been correlated with excess mortality in patients with HF. 15 In addition, ACE inhibition is associated with persistent cough in up to 20% of patients, and angioedema in 0.1 to 0.2% of patients.…”

Section: Rationale For Angiotensin II Receptor Blockers In the Managementioning

confidence: 99%

“…15,[29][30][31] Rebound of angiotensin II levels during ACE inhibitor therapy has been correlated with excess mortality in patients with HF. 15 In addition, ACE inhibition is associated with persistent cough in up to 20% of patients, and angioedema in 0.1 to 0.2% of patients. 14 In the Omapatrilat Cardiovascular Treatment vs. Enalapril (OCTAVE) trial, the frequency of angioedema with enalapril was 0.68% (86 of 12,557 patients with hypertension), and was 1.62% in black patients.…”

Section: Rationale For Angiotensin II Receptor Blockers In the Managementioning

confidence: 99%

“…4, 13 The utilization of ACE inhibitors in clinical practice, however, may be limited by associated adverse effects, particularly cough, and incomplete long-term blockade of the RAS due to the formation of angiotensin II by non-ACE enzymatic pathways. 14,15 In fact, prognosis of HF remains poor despite utilization of ACE inhibitors and beta blockers. [1][2][3] Angiotensin II receptor blockers (ARBs) also inhibit the RAS and are generally better tolerated than ACE inhibitors.…”

Section: Introductionmentioning

confidence: 99%

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Rationale for the use of angiotensin ii receptor blockers in patients with left ventricular dysfunction (part I of II)

Levine

2005

Clin Cardiol

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Summary: Almost 5 million individuals in the United States are diagnosed with chronic heart failure (HF), and the prevalence is increasing. Angiotensin-converting enzyme (ACE) inhibitors and beta blockers, neurohormonal antagonists that block the renin-angiotensin system (RAS) and the sympathetic nervous system, respectively, have been shown in clinical trials to reduce morbidity and mortality in patients with HF, and these therapies are now integral components of standard HF treatment. Yet, morbidity and mortality rates in HF remain unacceptably high, and the limitations of current standard therapies are becoming increasingly apparent. About 10% of patients with HF are unable to tolerate ACE inhibitors, often because of cough. In addition, ACE inhibition may not completely block the RAS because angiotensin II, the main end product of the RAS, can be generated via non-ACE enzymatic pathways. Angiotensin II receptor blockers (ARBs) may exert more complete RAS blockade than ACE inhibitors by interfering with the binding of angiotensin II at the receptor level, regardless of the enzymatic pathway of production. They are also better tolerated than ACE inhibitors and have been shown to improve symptoms and function in clinical trials in patients with HF. These factors provide a strong rationale for the study of the clinical effects of ARBs in patients with HF.

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“…Second, other mediators, such as natriuretic peptides, adrenomedullin and cytokines, induce opposite responses and cause vasodilation and diuretic effects, reduce cellular proliferation and induce apoptosis. High plasma concentrations of some of these mediators, such as norepinephrine and angiotensin, directly contribute to increasing mortality in heart failure, whereas it is believed that other hormones are only indirect markers of greater severity [65,66].…”

Section: Neurohormonal Markersmentioning

confidence: 99%

The Recent Advances in the Serological Detection of Acute Myocardial Infarction

Gh¹,

Ac²

2016

Clin Med Biochemistry

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Acute Myocardial Infarction (AMI) is one of the leading causes of morbidity and mortality worldwide. The greatest risk of fatality occurs within the first hours of initiation of AMI. Thus, the early diagnosis of cardiac ischemia is fundamental for the effective management of AMI patients. Inadequate diagnosis of patients with chest pain often leads to inadequate admission of patients without AMI and vice versa. In addition to the clinical history, physical examination, accurate electrocardiogram findings, and evaluation of cardiac biomarkers play an important role in the early diagnosis of acute ischemia. The present review discusses in detail the various cardiac biomarkers released during the event of an AMI.

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Clinical implications of increased plasma angiotensin II despite ACE inhibitor therapy in patients with congestive heart failure

Abstract: Fifty per cent of patients with heart failure, ha increased plasma angiotension II despite chronic ACE inhibitor therapy. These patients had higher neurohormonal activation and poor prognosis.

Cited by 221 publications

References 23 publications

Carotid body function in heart failure

Carotid body function in heart failure

Rationale for the use of angiotensin ii receptor blockers in patients with left ventricular dysfunction (part I of II)

The Recent Advances in the Serological Detection of Acute Myocardial Infarction

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