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Query: UMLS:C0010200 (
cough
)
23,843
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Angiotensin-converting enzyme
inhibitors (ACE inhibitors) have been shown to be effective in improving symptoms and survival in patients with systolic left ventricular dysfunction. Despite their proven benefits the use of ACE inhibitors is still limited in many parts of the western world. In part, the underutilization of ACE inhibitors is due to the occurrence of side effects such as
cough
, renal dysfunction and first dose hypotension. These side effects are in part due to ACE inhibitor-induced bradykinin formation. Blockade of the effects of angiotensin II can however also be achieved with an angiotensin II type I receptor blocking agent such as losartan. To determine the relative safety and effectiveness of ACE inhibitors compared to an angiotensin II type I receptor blocking agent the evaluation of losartan and the elderly trial (Elite) is comparing the ACE inhibitor captopril to the angiotensin II type I receptor blocking agent losartan in elderly patients. When used ACE inhibitors are often given in doses lower than those shown to be effective in reducing mortality in the major randomized trials. Several trials are currently under way comparing low to high doses of ACE inhibitors which should provide information on the need to achieve the doses used in the major mortality studies.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Importance of angiotensin-converting enzyme inhibitors in myocardial infarction and congestive heart failure: implications for clinical practice. 761 6
Angiotensin-converting enzyme
inhibitors (ACE-I) have become the mainstem of antihypertensive therapy and first-choice agents for vasodilatation in congestive heart failure (CHF). A typical dry
cough
is the main cause for discontinuation of ACE-I therapy. Data about the incidence, course, and clinical significance of this side effect are conflicting. This study determined the incidence of
cough
in ACE-I treated patients with hypertension and with CHF and to appreciate its clinical significance; 268 ACE-I treated patients, 164 with hypertension and 104 with CHF were prospectively followed for at least 1 year and specifically questioned about
cough
and other side effects. In those in whom
cough
developed, a second and then a third ACE-I were tried.
Cough
developed in 50 (18.6%) of the 268 patients; 23 patients with hypertension (14%) had coughs 24.7 +/- 17.1 (SD) weeks after initiation of therapy; 27 patients with CHF (26%) had coughs 12.3 +/- 12 (SD) weeks after the start of ACE-I therapy (P = 0.005). All but three patients had coughs also on the second and third ACE-I. The time from the beginning of therapy to the onset of
cough
was significantly shorter with the second than the first drug. ACE-I agents had to be discontinued in 50% of the patients in whom coughs developed, most of them in the CHF group. In the others,
cough
was well tolerated or disappeared during subsequent months. The incidence of
cough
, which necessitated discontinuation of ACE-I treatment, was 4% among patients with hypertension and 18% among patients with CHF (P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Angiotensin-converting enzyme inhibitors and cough: a prospective evaluation in hypertension and in congestive heart failure. 787 4
Angiotensin-converting enzyme
(
ACE
) inhibitors are an effective, well-tolerated option for management of mild-to-moderate hypertension. An increase of nearly 250% in prescriptions between 1986 and 1990 testifies to the growing importance of this drug class. With the development of newer
ACE
inhibitors, the debate on pharmacokinetic and pharmacodynamic differences and the clinical relevance of such differences has also been growing in importance. It is in this context that the clinical data on fosinopril will be reviewed. Fosinopril has several intriguing features, among them a unique chemical structure and elimination profile. In addition, preliminary data on cardiac effects and on risk for
cough
are provocative and support further study. The antihypertensive efficacy of fosinopril is comparable to other
ACE
inhibitors. Thus, fosinopril represents an interesting and useful addition to this antihypertensive class.
...
PMID:Fosinopril: an overview. 828 78
Angiotensin-converting enzyme
inhibitors (ACE-I) have been proven to be effective in reducing morbidity and mortality in patients with heart failure or post-myocardial infarction left ventricular dysfunction. Despite evidence from several large-scale randomized trials, the use of ACE-I in patients with heart failure remains relatively low. In part, the failure to achieve more widespread use of ACE-I in patients with heart failure may be due to physician's perceptions of the side effects associated with ACE-I, such as angioedema, renal dysfunction,
cough
, and hypotension. Many of these side effects are thought to be due to ACE-I-induced bradykinin accumulation. It is possible to inhibit the effect of angiotensin II without increasing bradykinin levels using an angiotensin II type I blocking agent such as losartan. How effective losartan is compared with an ACE-I is uncertain, however. Some of the beneficial effects of ACE-I have been attributed to bradykinin accumulation, and therefore ACE-I might have an advantage compared with an angiotensin II type I receptor antagonist such as losartan. On the other hand, angiotensin II may be produced by non-ACE-I-dependent mechanisms, which would suggest that an angiotensin II type I receptor blocking agent would be advantageous. To determine the relative safety and efficacy of an ACE-I, which results in bradykinin accumulation and inhibitors of angiotensin II, versus an angiotensin II type I receptor blocking agent, which does not result in bradykinin accumulation, we have begun the Evaluation of Losartan In The Elderly (ELITE) trial, which will compare the safety and efficacy of captopril and losartan in elderly patients with heart failure.
...
PMID:Angiotensin II receptor antagonists in heart failure: rationale and design of the evaluation of losartan in the elderly (ELITE) trial. 857 52
One hundred and thirty five non-smoking hypertensive patients with ACE inhibitor
cough
confirmed by lisinopril rechallenge and placebo dechallenge were recruited into a double-blind random parallel-group comparison of losartan 50 mg, lisinopril 20 mg and hydrochlorothiazide 25 mg each given once daily for a maximum of 8 weeks. The aim of the study was to compare the incidence of
cough
with the angiotensin II antagonist losartan, the ACE inhibitor lisinopril and the hydrochlorothiazide in hypertensive patients with previous ACE inhibitor
cough
.
Cough
detected by self-administered questionnaire was the primary end-point, and
cough
frequency by visual analogue scale a secondary end-point. The incidence of
cough
with losartan (29%) was lower than that for lisinopril (72%, P < 0.01) and similar to that for hydrochlorothiazide (34%).
Cough
frequency by visual analogue scale was lower for losartan than lisinopril (P < 0.01) and similar to that for hydrochlorothiazide. The specific selective AT1 angiotensin II receptor antagonist losartan is significantly less likely than lisinopril to cause
cough
in patients who previously have had ACE inhibitor
cough
. ACE inhibitor
cough
is likely to be related to non-specific
kininase II
inhibition.
...
PMID:ACE inhibitors, angiotensin II antagonists and cough. The Losartan Cough Study Group. 858 82
Pharmacologic agents that attenuate the influence of the renin-angiotensin-aldosterone system are known to reduce systemic arterial blood pressure through vasodilatory action and enhanced renal clearance of sodium and water.
Angiotensin-converting enzyme
inhibitors are known to antagonize the renin-angiotensin-aldosterone system through their ability to inhibit conversion of angiotensin I to angiotensin II. A new class of antihypertensive agents, angiotensin-II receptor antagonists, has recently been developed. These agents specifically block the receptor for angiotensin II, thereby limiting angiotensin II-mediated vasoconstriction and reducing aldosterone secretion. These effects result in a reduction in systemic arterial blood pressure through reduced vascular tone and enhanced sodium and water clearance. Clinical trials have demonstrated the efficacy of these agents in reducing blood pressure. These new antihypertensive agents also have uricosuric actions and are well tolerated, with a low incidence of
cough
and angioedema, side effects that are seen with angiotensin-converting enzyme inhibitors. Clinical trials are underway to see if these drugs will be useful in the treatment of diseases other than hypertension, such as congestive heart failure and chronic renal disease.
...
PMID:Angiotensin-II receptor antagonists: a new class of antihypertensive agents. 862 40
Angiotensin-converting enzyme
inhibitors (ACEI) cause
cough
in some patients, but the mechanism of this side effect is not clear. Five patients (group I) who had developed chronic cough induced by ACEI were evaluated to determine the bronchial hyperreactivity (BHR) by challenge with methacholine inhalation using a reservoir method at Respiratory Unit, Chulalongkorn Hospital University. Five patients (group II) who did not experience
coughing
associated with ACEI were also challenged as controls. The results revealed that two patients (40%) in group I demonstrated BHR with the mean PC20 at 15 mg/ml of methacholine solution. On the other hand, none of the patients in group II disclosed BHR. We concluded that
coughing
during ACEI therapy may be due to an increased inflammatory state in the airway in some susceptible subjects.
...
PMID:Methacholine inhalation challenge in patients with chronic cough induced by angiotensin-converting enzyme inhibitors. 870 98
A dry, tickly and often bothersome
cough
is the most common adverse effect of ACE inhibitors. Recent studies indicate that
cough
may develop in around 10% of the patients treated with ACE inhibitors. In half of these patients, the ACE inhibitor has to be discontinued.
Cough
has emerged as a class effect occurring with all ACE inhibitors with no clear difference between the single substances. While ACE inhibition is safe in the vast majority of patients with obstructive airways disease, asthmatic symptoms or exacerbation of asthma as well as a rise in bronchial reactivity have been occasionally reported. ACE inhibition increases the
cough
reflex. The mechanisms underlying ACE inhibitor-induced
cough
are probably linked to suppression of
kininase II
activity, which may be followed by an accumulation of kinins, substance P and prostaglandins. Physicians should be aware that a dry
cough
is the most common adverse effect of ACE inhibitors and that this symptom may occur not necessarily shortly after institution of therapy but months or even a year later. Replacement by another ACE inhibitor should not be tried, since the
cough
will almost always recur on rechallenge with the same or another ACE inhibitor. After withdrawal of the ACE inhibitor, which is the treatment of choice,
cough
will resolve usually within a few days.
...
PMID:ACE inhibitor-induced cough and bronchospasm. Incidence, mechanisms and management. 906 25
The human
cough
reflex is still poorly understood, although it is known to occur independently of bronchoconstriction. Sensitization of the
cough
reflex is a unifying hypothesis for chronic dry
cough
in several conditions, including gastroesophageal acid reflux, angiotensin-converting enzyme inhibitor
cough
, and
cough
-variant asthma. The most common cause of chronic dry
cough
is a group of related conditions of chronic rhinitis, sinusitis, and postnasal drip. In these cases the
cough
reflex may be sensitized through an action of inflammatory mediators from the nasal mucosa on the airways or a reflex sensitization of airway sensory nerves. The association of
cough
with gastroesophageal reflux may occur through a local esophageal-tracheobronchial reflex.
Angiotensin-converting enzyme
inhibitor
cough
is a side effect of treatment in about 10% of patients; it probably results from inhibition of the degradation of kinins, particularly bradykinin, in the airway. Why some patients with asthma have
cough
as the principal feature of their disease is unclear. Tachykinins are probably involved in the mechanism of sensitization of the
cough
reflex, and the development of neuropeptide antagonists may open new research opportunities. A study that used ambulatory recording of
cough
in a group of subjects with asthma confirmed the presence of significant
cough
, the frequency of which did not correlate with lung function or diurnal variation in peak flow. This finding highlights the problem of
cough
in patients with asthma, a problem that probably has been underestimated in the past.
...
PMID:Pathophysiology and clinical presentations of cough. 893 82
Angiotensin-converting enzyme
inhibitors reduce proteinuria in both normotensive and hypertensive patients with proteinuric renal disease. However, the mechanism of the antiproteinuric effect has not been clarified. We performed a prospective, double-blind, placebo-controlled, randomized crossover trial to test the hypothesis that the antiproteinuric effect of ramipril was due to an improvement in glomerular permselectivity independent of blood pressure and glomerular filtration rate. The effect of low-dose (1.25 mg/d) and high-dose (5 mg/d) ramipril was assessed in 15 normotensive nondiabetic patients with proteinuria (> 150 mg/d). The study was divided into four 12-week periods: placebo, high- or low-dose ramipril, crossover to low- or high-dose ramipril, and placebo. Blood pressure, glomerular filtration rate, renal plasma flow rate, urinary protein excretion rate, and plasma angiotensin II levels were measured at the end of each period. Mean arterial pressure, urine protein to creatinine ratio, and albumin excretion rate decreased significantly during low- and high-dose ramipril. Glomerular filtration rate and renal plasma flow rate were not changed significantly. Plasma angiotensin II levels decreased with both low- and high-dose ramipril. There were no episodes of hypotension and only one subject developed
cough
during ramipril that did not require discontinuation of the study drug. In conclusion, administration of ramipril in both low and high doses lowered blood pressure and reduced proteinuria in this cohort of normotensive patients with a variety of proteinuric renal diseases. The antiproteinuric effect of ramipril is probably mediated by a reduction in glomerular capillary pressure.
...
PMID:Effect of ramipril on blood pressure and protein excretion rate in normotensive nondiabetic patients with proteinuria. 895 34
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