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Contribution of kinin system to the antihypertensive action of angiotensin converting enzyme inhibitors

Sharma JN

Adv Exp Med Biol, 1989;247A:197-205.
PMID: 2690588
Matched MeSH terms: Angiotensin-Converting Enzyme Inhibitors/pharmacology*; Angiotensin-Converting Enzyme Inhibitors/therapeutic use
Efficacy and quality of life in 30 hypertensive patients treated with low dose captopril

Choy YW, Cheong I

Family Physician, 1989;1:19-22.

This study was carried out on 30 patients to: i) determine the efficacy of low dose captopril as monotherapy (with or without a diuretic) in the treatment of various grades of hypertension. ii) assess the quality of life of these patients 12 weeks after commencement of therapy. Our results showed that there was a sustained and significant fall in both mean systolic and diastolic blood pressure from 171.9 Â± 24 to 150.5 Â± 25 mm Hg and 109.0 Â± 14 to 93.6 Â± 15mmHg respectively (p<0.001). Improvement in quality of life was however not statistically significant (p<0.05). We concluded that low dose captopril used alone or in combination with a diuretic can be considered for the initial therapy of mild to moderate hypertension. The optimal dosage and the longterm benefits on quality of life need further evaluation in a larger series.

Matched MeSH terms: Angiotensin-Converting Enzyme Inhibitors
Does kinin mediate the hypotensive action of angiotensin converting enzyme (ACE) inhibitors?

Sharma JN

Gen. Pharmacol., 1990;21(4):451-7.
PMID: 2199299

The lack of kinin formation in systemic circulation and in the renal system may lead to the pathogenesis of high blood pressure (hypertension). Angiotensin converting enzyme inhibitors are able to protect the kinin inactivation by kininase II, therefore, causing an accumulation of kinin. Although the concentrations of kinin in plasma after oral administration of ACE inhibitors are conflicting this is mainly due to methodological difficulties. Kinin receptor antagonists are becoming most reliable pharmacological probes for defining the molecular actions of kinin in several physiopathological states, and in the mechanism of actions of drugs which are dependent on the kinin system. The blood pressure lowering effect of ACE inhibitors can be antagonized by the pretreatment with kinin receptor antagonists. I have therefore proposed that the hypotensive action of ACE inhibitors may reflect the activation of kinin receptor. It is suggested that the development of compounds having protective properties on the kallikrein-kinin system might be therapeutically applicable as anti-hypertensive drugs.

Matched MeSH terms: Angiotensin-Converting Enzyme Inhibitors/pharmacology*
Tolerability with special reference to cough, of captopril in patients with congestive cardiac failure

Quek DKL, Alfred E, Ong SBL

Family Physician, 1991;3:34-38.

Cough associated with angiotensin converting-enzyme (ACE) inhibitor therapy has been reported in Western communities, where its incidence is disputed. We, therefore, reviewed our patients who were treated with captopril primarily for congestive cardiac failure. 19 of 61 patients (31.1%) receiving an ACE inhibitor had volunteered cough as an important adverse effect, compared with only one of 59 patients who recieved other treatment. In 3 patients, the cough was intolerably severe to require discontinuation of treatment. Another 7 patients were withdrawn from ACE inhibitor treatment because of other adverse effects including deteriorating renal function, insomnia, dizzy spells, ageusia and proteinuria, and skin rash. We suggest that although ACE inhibitors are very beneficial in improving the clinical status of congestive heart failure, intolerable adverse effects are not uncommon and might mandate withdrawal in a sizeable minority (16.4%).

Matched MeSH terms: Angiotensin-Converting Enzyme Inhibitors
Suppression of hypotensive responses of captopril and enalapril by the kallikrein inhibitor aprotinin in spontaneously hypertensive rats

Sharma JN, Amrah SS, Noor AR

Pharmacology, 1995 Jun;50(6):363-9.
PMID: 7568335

The present investigation evaluated the effects of aprotinin, an inhibitor of kallikrein, on blood pressure responses, heart rate, and duration of hypotension induced by acute administration of captopril and enalapril (angiotensin-converting enzyme inhibitors) in anaesthetized spontaneously hypertensive rats. Captopril (20 mg/kg) and enalapril (20 mg/kg) administered intravenously caused a significant (p < 0.001) fall in systolic and diastolic blood pressures in the absence of aprotinin. In contrast, captopril (20 mg/kg) and enalapril (20 mg/kg) failed (p > 0.05) to cause a fall in systolic and diastolic blood pressures in the presence of aprotinin (2 mg/kg). Captopril and enalapril were able to significantly reduce the heart rate (p < 0.05 and p < 0.001) in the presence as well as in the absence of aprotinin. The duration of hypotension produced by captopril and enalapril was abolished significantly (p < 0.001) in the presence of aprotinin. These findings may suggest that captopril and enalapril caused hypotension via the kallikrein pathway, since the kallikrein inhibitor aprotinin can antagonize the hypotensive responses of these agents. Thus, kallikrein may be an independent mediator in the regulation of blood pressure.

Matched MeSH terms: Angiotensin-Converting Enzyme Inhibitors/pharmacology
The effect of enalapril on tyramine induced changes in renal function in man

Rahman AR, Lang CC, Struthers AD

Int J Clin Pharmacol Ther, 1995 Jul;33(7):404-9.
PMID: 7582398

Increasing animal evidence support an important facilitatory interaction between angiotensin II and norepinephrine within the kidney. This angiotensin II/norepinephrine interaction was investigated in man by examining the effect of enalapril pretreatment (5 mg for 5 days) on the renal response to a low non-pressor dose of intravenous tyramine 4 micrograms/kg/min for 120 min in 8 healthy subjects undergoing water diuresis. Tyramine is an indirect sympathomimetic agent which causes neuronal release of norepinephrine. Enalapril and tyramine, alone and in combination, had no effect on glomerular filtration, effective renal plasma flow or sodium excretion. Tyramine caused a significant increase in urinary flow rate (p < 0.05) but this was not influenced by enalapril pretreatment. The lack of effect of enalapril on the renal response to tyramine contrasts with a previous study which examined the effect of enalapril on the renal response to circulating norepinephrine. This may suggest that enalapril affect renal function only when there is renal vasoconstriction (as with norepinephrine) and not when renal blood flow is unchanged (as with tyramine).

Matched MeSH terms: Angiotensin-Converting Enzyme Inhibitors/pharmacology*
Blood pressure regulation by the kallikrein-kinin system

Sharma JN, Uma K, Noor AR, Rahman AR

Gen. Pharmacol., 1996 Jan;27(1):55-63.
PMID: 8742494

1. The kallikrein-kinin system has a significant role in regulating arterial blood pressure. 2. Reduced formation of the kinin compontents may cause hypertensive diseases. This is because of the fact that this system is responsible for vasodilatation, reduction in total peripheral resistance, natriuresis, diuresis, increasing renal blood flow and releasing various vasodilator agents. 3. Reduced kinin-kallikrein generation in hypertensive subjects may also be associated with genetic and environmental defects. 4. The kallikrein-kinin system when administered to hypertensive patients can lower their raised blood pressure to normotensive levels. 5. The mode of action of angiotensin-converting enzyme inhibitors principally may be dependent on the kinin system protection.

Matched MeSH terms: Angiotensin-Converting Enzyme Inhibitors/pharmacology; Angiotensin-Converting Enzyme Inhibitors/therapeutic use
Fulltext Pilot study of formestane in postmenopausal women with breast cancer

Joseph JK, Lim AKH

Med J Malaysia, 1998 Mar;53(1):37-41.
PMID: 10968135

A pilot study of Formestane or 4-Hydroxyandrostenedione (Lentaron), a new endocrine agent, was conducted on 18 postmenopausal patients with locally advanced and metastatic breast cancer. 16 patients were evaluable for response and objective responses were seen in 4 patients (25%). Stabilisation of disease was seen in 5 patients (32%). Out of 17 patients evaluable for toxicity, 3 (18%) reported adverse effects including hot flushes, lethargy and myalgia. Adverse effects were mild, transient and no patient required discontinuation of drug. Our study confirms that Formestane is a well tolerated endocrine agent with low toxicity and reasonable efficacy in postmenopausal patients with locally advanced and metastatic breast cancer.

Matched MeSH terms: Enzyme Inhibitors/therapeutic use*
Comparative efficacy of perindopril and enalapril once daily using 24-hour ambulatory blood pressure monitoring

Yusoff K, Razak TA, Yusof N, Rafee NM

Int J Clin Pract, 1999 Jun;53(4):277-80.
PMID: 10563072

ACE inhibitors are important therapeutic agents in controlling hypertension, correcting some of its pathophysiological derangement and improving its prognosis. While there are many such agents, there may be some important differences between them. This placebo run-in, double blind, crossover study, using 24-hour ambulatory blood pressure monitoring, compares the efficacy of perindopril 4-8 mg and enalapril 10-20 mg as once daily antihypertensive agents on 32 patients. For diastolic blood pressure (DBP), perindopril had a placebo-corrected peak (P) reduction of blood pressure (BP) of -6.4 +/- 1.3 mmHg vs its placebo-corrected trough (T) of -5.2 +/- 1.7 mmHg. Enalapril had a reduction in DBP of -8.5 +/- 1.3 mmHg (P) and -5.7 +/- 1.7 mmHg (T). For systolic blood pressure (SBP), perindopril had a reduction of -7.5 +/- 1.6 mmHg (P) vs -7.3 +/- 2.2 mmHg (T) compared to enalapril with -10.8 +/- 1.6 mmHg (P) vs -8.3 +/- 2.3 mmHg (T). Placebo-corrected trough-to-peak ratio (SBP/DBP) for perindopril was 0.97/0.81 vs 0.77/0.67 for enalapril. There was no difference noted in 24-hour mean BP, area under the curve or post-dose casual BP measurements. Both perindopril and enalapril were well tolerated and the two treatment groups had similar safety profiles. Perindopril thus had a predictable and sustained blood pressure effect giving a 24-hour cover for the patient without excessive peak effect or poor trough effect.

Matched MeSH terms: Angiotensin-Converting Enzyme Inhibitors/therapeutic use*
Short- and long-term effects of glycyrrhizic acid in repetitive stress

Ainsah O, Nabishah BM, Osman CB, Khalid BA

Clin Exp Pharmacol Physiol, 1999 7 1;26(5-6):444-8.
PMID: 10386236

1. This study was carried out to determine the effect of short-term and long-term ingestion of glycyrrhizic acid on the response to 2 h of restraint stress by measuring locomotor activity and plasma corticosterone levels. 2. Male Sprague-Dawley rats were randomly assigned into four groups, each group having eight rats. Group 1 (control) was given ordinary tap water, while groups 2 (short term), 3 and 4 (both long term) were given tap water containing 1 mg/mL glycyrrhizic acid to drink for 10 days, 4 weeks and 9 weeks, respectively. All the rats were subjected to 2 h of restraint stress and the locomotor activity assessed using an activity test in an open field arena followed by blood sampling to determine the plasma corticosterone level. These procedures were repeated daily for 14 days. 3. The basal locomotor activity scores for rats given glycyrrhizic acid for 10 days or 4 weeks were similar to those of controls; however, that of the rats treated long term with glycyrrhizic acid was significantly lower (21.0 +/- 3.0 squares crossed; P < 0.0005). Following the first period of restraint stress there was a highly significant decrease in locomotor activity, which remained significantly lower until the seventh and subsequent periods, indicating an adaptation to the repeated stress had occurred. Although the decrease in locomotor activity was partially blocked and adaptation to repetitive stress was enhanced in the rats given glycyrrhizic acid for 10 days, this was not seen in rats treated with glycyrrhizic acid for 4 or 9 weeks. The corticosterone levels in control rats were significantly elevated for 4-5 days following the exposure to repetitive stress but decreased gradually from day 7 onwards. However, both short- and long-term glycyrrhizic acid-treated rats had higher plasma corticosterone levels than the controls (P < 0.05). 4. In conclusion, repetitive restraint stress caused decreased locomotor activity associated with increased plasma corticosterone levels, both of which, in normal rats, decreased with adaptation to stress. The stress response was partially blocked and adaptation enhanced in rats given glycyrrhizic acid for 10 days, but not in rats given glycyrrhizic acid for 4 and 9 weeks. Glycyrrhizic acid ingestion caused high plasma corticosterone.

Matched MeSH terms: Enzyme Inhibitors/pharmacology; Enzyme Inhibitors/therapeutic use
Effects of naloxone, glycyrrhizic acid, dexamethasone and deoxycorticosterone in repetitive stress

Ainsah O, Nabishah BM, Osman CB, Khalid BA

Clin Exp Pharmacol Physiol, 1999 7 1;26(5-6):433-7.
PMID: 10386234

1. The present study examined the effect of naloxone (NAL), glycyrrhizic acid (GCA), deoxycorticosterone (DOC) and dexamethasone (DEX) on daily repeated 2 h chronic restrained stress (RS) on the locomotor activity (LA) of rats tested in the open field arena to elucidate the possible roles of opioids, glucocorticoids and mineralocorticoids in response to stress. 2. Intact and adrenalectomized (ADX) rats were either injected with 0.1 mL of NAL (0.32 microgram/100 g BW), 2.4 mg/kg DOC or 120 micrograms/kg DEX or had 1.0 mg/mL GCA dissolved in their drinking water or normal saline (for the ADX group) dissolved in their drinking water. 3. In intact groups, treatment with NAL completely blocked the stress response and treatment with GCA, DOC and DEX partially prevented the stress response. Adaptation occurred on either days 4, 5, 6 or 7 for intact rats treated with DEX, DOC, GCA or control rats, respectively. All ADX control rats died following the first 2 h RS. Adrenalectomized rats treated with DEX or DOC adapted later compared with intact rats, while rats given either GCA or NAL were unable to block or adapt to chronic RS. 4. These findings demonstrate that the stress response is primarily mediated by endogenous opioids, in that it is blocked by NAL. Both mineralocorticoids and glucocorticoids, which can act centrally to inhibit endorphins, partially blocked the stress response. The effect of GCA in intact rats was similar to that of both DEX and DOC in intact rats. Adrenalectomized rats treated with GCA (despite their lack of endogenous corticosterone) showed a stress response that was significantly different from the other ADX groups, implying that GCA had effects independent of endogenous corticosterone.

Matched MeSH terms: Enzyme Inhibitors/pharmacology; Enzyme Inhibitors/therapeutic use
Fulltext COX-2 inhibitors: a potential target for drug therapy in the management of colorectal cancer

Ryan ARA, Rosita ARA, Kamarul AK, Qureshi A

Med J Malaysia, 1999 Sep;54(3):293-5.
PMID: 11045053

Colorectal cancer is currently the third most common cancer in Malaysia. Elevated expression of COX-2, an induced cyclooxygenase isoenzyme, has been seen in colonic adenomas and colorectal carcinoma. There is evidence that inhibition of this COX-2 can decrease the risk of colorectal cancer. Selective COX-2 inhibitors may have a role in reducing the risk of colorectal cancer in high-risk individuals.

Matched MeSH terms: Enzyme Inhibitors/therapeutic use*
First-dose response to angiotensin-converting enzyme inhibition in congestive cardiac failure: a Malaysian experience

Navookarasu NT, Rahman AR, Abdullah I

Int J Clin Pract, 1999 Jan-Feb;53(1):25-30.
PMID: 10344062

Despite their proven value in reducing morbidity and mortality in different grades of heart failure, angiotensin converting enzyme (ACE) inhibitors continue to be underused. One reason for this is clinicians' apprehension of first-dose hypotension. We conducted a double-blind, randomised, placebo-controlled parallel group study to investigate the effect of various ACE inhibitors on first-dose hypotension. Eighty unselected patients were randomised into five treatment groups: placebo, captopril 6.25 mg, enalapril 2.5 mg, perindopril 2 mg and lisinopril 2.5 mg. Blood pressure was measured at baseline, half hourly for two hours and hourly for three hours after drug treatment. The maximum drops in mean arterial pressure (in mmHg +/- SD) were placebo 5.89 +/- 2.65, perindopril 5.29 +/- 2.49, enalapril 13.28 +/- 3.31, lisinopril 15.04 +/- 5.74 and captopril 16.76 +/- 5.74 (all p < 0.05 vs placebo except for perindopril). Perindopril, unlike the other ACE inhibitors studied, did not produce first-dose hypotension following its initiation in patients with congestive heart failure.

Matched MeSH terms: Angiotensin-Converting Enzyme Inhibitors/therapeutic use*
Fulltext Angioedema secondary to angiotensin converting enzyme inhibitors

Thiruventhiran T, Ho BK

JUMMEC, 1999;4(2):113-114.

Angioedema due to whatever cause is potelltially life threatening, especially if it involves the head and neck region. Patients at risk need to be identified and precautionary measures are necessary. The use of Angiotensin Converting Enzyme Inhibitors (ACEIs) has been associated with angioedenia of the face and tongue. Its widespread use has resulted in an increased awareness of this rare but important camplication. We report liere a case of angioedenla secondary to ACEls developing a few months after initiation of therapy and discuss its clinical importance. KEYWORDS: Angioedema, Angiotensin Converting Enzyme Inhibitor.

Matched MeSH terms: Angiotensin-Converting Enzyme Inhibitors; Enzyme Inhibitors
ß-blockers in congestive heart failure

Teh BT, Wan Azman WA, Thuraisingham S, Choy AM, Tan KH, Jesudason P, et al.

JUMMEC, 1999;4:26-33.

Activation of the synlpathetic nervous system (SNS) and renin-angiotensin system (RAS) plays a pivotal role in the pathophysiology and progression of the disease in chronic heart failure (CHF). Blocking the activation of the RAS with angiotensin converting enzyme inhibitors not only improves sylnptonls but also prolongs life in symptomatic CHF. Does a similar analogy hold true for the use of ß-blockers in CHF? Evidence from a number of small trials and several recent large prospective trials show that b-blockers may improve ventricular function and symptoms in CHF. In a combination of trials investigating the use of carvedilol (an α, and ß-blocker) in congestive heart failure a mortality benefit appears to be evident. There are still a number of key questions that relnaill unanswered regarding the tolerability, patient type and stage of CHF in which ß-blockers should be advocated. Several large scale trials are in progress to answer some of these questions and also to add further information regarding its efficacy and impact on survival. KEYWORDS: Beta-adrenoreceptor antagonist, congestive heart failure.

Matched MeSH terms: Enzyme Inhibitors
Nitric oxide production by murine spleen cells stimulated with Porphyromonas gingivalis-derived lipopolysaccharide

Sosroseno W

Asian Pac J Allergy Immunol, 2000 Dec;18(4):209-14.
PMID: 11316041

The aim of the present study was to determine whether Porphyromonas gingivalis-lipopolysaccharide (Pg-LPS) may stimulate nitric oxide (NO) production by murine spleen cells. Spleen cells derived from Balb/c mice were cultured in the presence of Pg-LPS or LPS from Salmonella Typhosa. The cell were also cultured in the presence of Pg-LPS with or without L-arginine, L-arginine plus NG-monomethyl-L-arginine (NMMA), or IFN-gamma. Furthermore, the plastic non-adherent spleen cells were stimulated with Pg-LPS and L-arginine. The results showed that Pg-LPS failed to stimulate splenic NO production by themselves. Exogenous L-arginine or IFN-gamma up-regulated the NO production of Pg-LPS-stimulated spleen cells, but the stimulatory effects of L-arginine were completely blocked by NMMA. It was also demonstrated that in the presence of Pg-LPS and L-arginine, splenic macrophages were the cellular source of NO. These results suggest, therefore, that P. gingivalis-LPS may induce murine splenic macrophages to produce NO in a L-arginine and an IFN-gamma-dependent mechanism.

Matched MeSH terms: Enzyme Inhibitors/pharmacology
Nitric oxide production by a murine macrophage cell line (RAW264.7) stimulated with lipopolysaccharide from Actinobacillus actinomycetemcomitans

Sosroseno W, Barid I, Herminajeng E, Susilowati H

Oral Microbiol. Immunol., 2002 Apr;17(2):72-8.
PMID: 11929552

The aim of this study was to determine whether Actinobacillus actinomycetemcomitans lipopolysaccharide (LPS-A. actinomycetemcomitans) could stimulate a murine macrophage cell line (RAW264.7 cells) to produce nitric oxide (NO). The cells were treated with LPS-A. actinomycetemcomitans or Escherichia coli LPS (LPS-Ec) for 24 h. The effects of N(G)-monomethyl-L-arginine (NMMA), polymyxin B and cytokines (IFN-gamma, TNF-alpha, IL-4 and IL-12) on the production of NO were also determined. The role of protein tyrosine kinase, protein kinase C and microtubulin organization on NO production were assessed by incubating RAW264.7 cells with genistein, bisindolylmaleide and colchicine prior to LPS-A. actinomycetemcomitans stimulation, respectively. NO levels from the culture supernatants were determined by the Griess reaction. The results showed that LPS-A. actinomycetemcomitans stimulated NO production by RAW264.7 cells in a dose-dependent manner, but was slightly less potent than LPS-Ec. NMMA and polymyxin B blocked the production of NO. IFN-gamma and IL-12 potentiated but IL-4 depressed NO production by LPS-A. actinomycetemcomitans-stimulated RAW264.7 cells. TNF-alpha had no effects on NO production. Genistein and bisindolylmalemaide, but not colchicine, reduced the production of NO in a dose-dependent mechanism. The results of the present study suggest that A. actinomycetemcomitans LPS, via the activation of protein tyrosine kinase and protein kinase C and the regulatory control of cytokines, stimulates NO production by murine macrophages.

Matched MeSH terms: Enzyme Inhibitors/pharmacology
Heart failure in a multiethnic population in Kuala Lumpur, Malaysia

Chong AY, Rajaratnam R, Hussein NR, Lip GY

Eur J Heart Fail, 2003 Aug;5(4):569-74.
PMID: 12921820

BACKGROUND: There are established differences in cardiovascular disease in different racial groups. Worldwide, the literature regarding the clinical epidemiology of congestive heart failure (CHF) in non-white populations is scarce.
OBJECTIVES: To document the prevalence of CHF in the multiracial population of Malaysia, and to describe the clinical features and management of these patients.
SETTING: Busy city centre general hospital in Kuala Lumpur, Malaysia.
RESULTS: Of 1435 acute medical admissions to Kuala Lumpur General Hospital over the 4-week study period, 97 patients (6.7%) were admitted with the primary diagnosis of CHF. Coronary artery disease was the main aetiology of CHF, accounting for almost half (49.5%) the patients, followed by hypertension (18.6%). However, there were variations in associated aetiological factors between ethnic groups, with diabetes mellitus affecting the majority of Indians-as well as underutilisation of standard drugs for CHF, such as the angiotensin converting enzyme (ACE) inhibitors, which were only used in 43.3%.
CONCLUSION: Amongst acute medical admissions to a single centre in Malaysia the prevalence of CHF was 6.7%. Coronary artery disease was the major aetiological factor in heart failure accounting for almost half the admissions. The under-prescription of ACE inhibitors was similar to other clinical surveys carried out amongst Caucasian populations in the West.

Matched MeSH terms: Angiotensin-Converting Enzyme Inhibitors/therapeutic use
Combination of drugs acting on the natriuretic system and the renin-angiotensin system in heart failure

Chee KH, Amudha K, Hussain NA, Haizal HK, Choy AM, Lang CC

J Renin Angiotensin Aldosterone Syst, 2003 Sep;4(3):140-8.
PMID: 14608517

Conventional diuretic agents are very effective agents in relieving volume overload and congestive symptoms in chronic heart failure (CHF). However, they are associated with activation of the renin-angiotensin system (RAS) and the sympathetic nervous system and a reduction in glomerular filtration rate, all of which have been associated with adverse outcomes in CHF. Therefore, there is an increasing interest in drugs that target the natriuretic system without neurohormonal activation and deterioration of renal function. In this review, we will discuss the underlying rationale and evidence behind currently pursued strategies that target the natriuretic system. This includes the administration of natriuretic peptides (NPs) and strategies that potentiate the NP system, such as neutral endopeptidase inhibition. We will also highlight some potentially important interactions of these strategies with drugs that target the RAS.

Matched MeSH terms: Angiotensin-Converting Enzyme Inhibitors/therapeutic use*
Admissions with atrial fibrillation in a multiracial population in Kuala Lumpur, Malaysia

Freestone B, Rajaratnam R, Hussain N, Lip GY

Int J Cardiol, 2003 Oct;91(2-3):233-8.
PMID: 14559136

BACKGROUND: There are established differences in cardiovascular disease in different racial groups. Worldwide, the literature regarding the clinical epidemiology of atrial fibrillation in non-white populations is scarce.
OBJECTIVES: To document the prevalence of atrial fibrillation (AF) in the multiracial population of Malaysia, and to describe the clinical features and management of these patients.
SETTING: Busy city centre general hospital in Kuala Lumpur, Malaysia, over a 1-month period.
SUBJECTS: One-thousand four hundred and thirty-five acute medical admissions, of whom 40 patients (2.8%) had AF.
RESULTS: Of 1435 acute medical admissions to Kuala Lumpur General Hospital over the 4-week study period, 40 had AF (21 male, 19 female; mean age 65 years). Of these, 18 were Malay, 16 Chinese and six Indian. Nineteen patients had previously known AF (seven with paroxysmal AF) and 21 were newly diagnosed cases. The principal associated medical conditions were ischaemic heart disease (42.5%), hypertension (40%) and heart failure (40%). Dyspnoea was the commonest presentation, whilst stroke was the cause of presentation in only two patients. Investigations were under-utilised, with chest X-ray and echocardiography in only 62.5% of patients and thyroid function checked in 15%. Only 16% of those with previously diagnosed AF were on warfarin, with a further three on aspirin. Anticoagulant therapy was started in 13.5% of patients previously not on warfarin, and aspirin in 8%. Records of contraindications to warfarin were unreliable, being identified in only 25%. For those with known AF, 58% were on digoxin. For new onset AF, digoxin was again the most common rate-limiting treatment, initiated in 38%, whilst five patients with new onset AF were commenced on amiodarone. DC cardioversion was not used in any of the patients with new onset AF.
CONCLUSION: Amongst acute medical admissions to a single centre in Malaysia the prevalence of AF was 2.8%. Consistent with previous similar surveys in mainly western (caucasian) populations, standard investigations in this Malaysian cohort were also inadequate and there was underuse of anticoagulation, medication for ventricular rate control and cardioversion to sinus rhythm.

Matched MeSH terms: Angiotensin-Converting Enzyme Inhibitors/therapeutic use

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