Low-dose dipyridamole infusion acutely increases exercise capacity in angina pectoris: a double-blind, placebo controlled crossover stress echocardiographic study.

OBJECTIVES: The aim of this study was to assess whether endogenous accumulation of adenosine, induced by low-dose dipyridamole infusion, protects from exercise-induced ischemia. BACKGROUND: Adenosine is a recognized mediator of ischemic preconditioning in experimental settings. METHODS: Ten patients (all men: mean age 63.4 +/- 7.3 years) with chronic stable angina, angiographically assessed coronary artery disease (n = 7) or previous myocardial infarction (n = 3) and exercise-induced ischemia underwent on different days two exercise-stress echo tests after premedication with placebo or dipyridamole (15 mg in 30 min, stopped 5 min before testing) in a double-blind, placebo controlled, randomized crossover design. RESULTS: In comparison with placebo, dipyridamole less frequently induced chest pain (20% vs. 100%, p = 0.001) and >0.1 mV ST segment depression (50% vs. 100%, p < 0.05). Wall motion abnormalities during exercise-stress test were less frequent (placebo = 100% vs. dipyridamole = 70%, p = ns) and significantly less severe (wall motion score index at peak stress: placebo = 1.55 +/- 0.17 vs. dipyridamole = 1.27 +/- 0.2, p < 0.01) following dipyridamole, which also determined an increase in exercise time up to echocardiographic positivity (placebo = 385.9 +/- 51.4 vs. dipyridamole = 594.4 +/- 156.9 s, p < 0.01). CONCLUSIONS: Low-dose dipyridamole infusion increases exercise tolerance in chronic stable angina, possibly by endogenous adenosine accumulation acting on high affinity A1 myocardial receptors involved in preconditioning or positively modulating coronary flow through collaterals.

Similarities and differences in the antihypertensive effect of two calcium antagonist drugs, verapamil and nifedipine.

The short- and long-term effects of two calcium channel blocking drugs, verapamil and nifedipine, on blood pressure, heart rate, plasma catecholamines, plasma renin activity, plasma volume and cardiac performance (echocardiography) were studied in essential hypertensive patients and in normal subjects. Verapamil, 160 mg orally, reduced blood pressure within 60 minutes in 22 hypertensive patients, but not in 12 normotensive subjects. Nifedipine, 10 mg sublingually, reduced blood pressure within 15 minutes in 19 hypertensive patients, but not in 7 normotensive subjects. Plasma noradrenaline was significantly increased both in normal subjects and in hypertensive patients only after nifedipine was administered. Verapamil (80 mg three times a day) first, and nifedipine (10 mg three times a day) thereafter, or vice versa, were given to 12 hospitalized hypertensive patients on a fixed sodium and potassium intake; the drugs produced similar blood pressure reductions, but heart rate and plasma catecholamines were increased only after nifedipine (p less than 0.05). Neither drug affected plasma volume, aldosterone or plasma renin activity. Long-term ambulatory treatment with verapamil (80 or 160 mg three times a day for 2 to 4 months) or nifedipine (10 mg three times a day for 2 months) produced changes in all variables that were similar to those observed in the hospital (controlled) study. Shortening fraction was significantly increased after nifedipine (p less than 0.05) but no change was observed after verapamil. In conclusion, blood pressure is effectively reduced by both verapamil and nifedipine; an appreciable adrenergic stimulation may be caused by nifedipine, but usually not by verapamil, and fluid retention, renin release or myocardial depression is not observed during verapamil or nifedipine treatment.

Low-dose captopril therapy in mild and moderate hypertension. Randomized comparison of twice daily vs three times daily doses.

We have investigated the antihypertensive activity of relatively low daily doses of captopril in patients with mild and moderate arterial hypertension. In a first trial, at the end of a 2-week placebo washout period, 18 patients with essential hypertension WHO Stage I or II were treated with captopril, 25 mg three times daily (t.i.d.), 25 mg twice daily (b.i.d.), 50 mg t.i.d., and 50 mg b.i.d., according to a randomized within-patient open design, with each regimen lasting for a 2-week period. In a second trial, 12 hypertensive patients not adequately controlled by chlorthalidone 25 mg daily as monotherapy (supine diastolic blood pressure at rest greater than 95 mm Hg), continued the diuretic treatment in combination with captopril, 25 mg t.i.d. and 25 mg b.i.d. according to a randomized within-patient open design. Analysis of variance did not reveal differences between the four captopril dosing schedules (1st trial), or between the two captopril dosing schedules (2nd trial). Both the patients on captopril monotherapy (1st trial) and those cotreated with chlorthalidone (2nd trial) showed lower systolic and diastolic blood pressure values on each captopril regimen compared to prerandomization values (all p less than 0.01). No relevant unwanted effects were noted. We conclude that in patients with mild or moderate essential hypertension, either untreated or resistant to chlorthalidone, captopril is effective in reducing blood pressure even at daily doses not exceeding 150 mg, without differences between a t.i.d. and a b.i.d. dosing schedule.

Echocardiographic left ventricular hypertrophy as related to arterial pressure and plasma norepinephrine concentration in arterial hypertension. Reversal by atenolol treatment.

We tried to assess relationships between echocardiographic left ventricular hypertrophy (LVH), arterial pressure levels, and plasma norepinephrine concentration (NE) in 20 previously untreated stable hypertensive patients with LVH, and in 11 healthy normotensive control subjects. Interventricular septal (IVS) thickness, posterior wall (PW) thickness, and left ventricular mass index (LVMI) were related to arterial pressure levels and to NE by univariate and multivariate regression analyses. In addition, after 18 months of monotherapy with atenolol (carried out in nine of 20 patients), the relationship between echocardiographic changes and degree of pressure reduction was tested. Before treatment, PW thickness weakly correlated with systolic (r = 0.55; p less than 0.01) and mean (r = 0.50; p less than 0.05) arterial pressure. IVS thickness weakly correlated with NE (r = 0.53; p less than 0.05). On this relatively small sample, multivariate regression analysis showed an association of both IVS thickness (R = 0.57; p less than 0.05) and PW thickness (R = 0.58; p less than 0.05) with mean arterial pressure (MAP) and NE. After atenolol, there was a reduction in IVS thickness (1.15 to 1.02 cm; p less than 0.01), PW thickness (1.08 to 0.99 cm; p less than 0.01), and LVMI (136.3 to 113.8 g/m2; p less than 0.01), besides a significant reduction in blood pressure and heart rate. The degree of pressure reduction induced by treatment did not correlate the change in IVS or PW thickness. In contrast, the change in diastolic and mean arterial pressure positively correlated the change in LVMI (r = 0.72 and r = 0.75, respectively; both p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Noninvasive assessment of chronotropic and inotropic response to preferential beta-1 and beta-2 adrenoceptor stimulation.

The relative chronotropic and inotropic activity of preferential beta 1- and beta 2-adrenoceptor stimulation was investigated in seven healthy male subjects in a randomized within-subject, single-blind study. Two doses of beta 1-selective agonist prenalterol (1 mg/hr or 2 mg/hr) and of beta 2-selective agonist salbutamol (300 micrograms/hr or 600 micrograms/hr) were infused intravenously in four separate sessions, with intervals of at least 48 hr between sessions. At each session cuff blood pressure and heart rate (HR) were measured and some hemodynamic information on the inotropic state were derived by echocardiography. Both prenalterol and salbutamol induced increases in HR, but tachycardia was greater after salbutamol, whereas the positive inotropic response to beta-stimulation was greater after prenalterol. At comparable HR rises (prenalterol, from 66.0 +/- 5.5 to 72.2 +/- 4 bpm; salbutamol, from 64.6 +/- 6 to 70.0 +/- 7 bpm), inotropic response seemed to be greater after prenalterol than after salbutamol (systolic blood pressure [SBP]: 133.5 +/- 8 and 120.7 +/- 8 mm Hg; mean velocity of circumferential fiber shortening [Vcf]: 1.54 +/- 0.13 and 1.31 +/- 0.12 c/s; ejection fraction [EF]: 72.4% +/- 5% and 69.5% +/- 4%; stroke index: 47.4 +/- 4 and 41.7 +/- 3 ml/m2). In presence of a chronotropic effect (HR from 64.6 +/- 6 to 70.0 +/- 7 bpm), the low salbutamol dose did not induce any changes in the indices of inotropism (SBP: from 119.2 +/- 6 to 120.7 +/- 8 mm Hg; mean Vcf: from 1.28 +/- 0.11 to 1.31 +/- 0.12 c/s; EF: from 68.1% +/- 5% to 69.5% +/- 4%; stroke index: from 40.2 +/- 3 to 41.7 +/- 3 ml/m2.(ABSTRACT TRUNCATED AT 250 WORDS)

Valsartan, a new angiotensin II antagonist for the treatment of essential hypertension: a comparative study of the efficacy and safety against amlodipine.

OBJECTIVE: To compare the antihypertensive efficacy of a new angiotensin II antagonist, valsartan, with a reference therapy, amlodipine. METHODS: One hundred sixty-eight adult outpatients with mild to moderate hypertension were randomly allocated in double-blind fashion and equal number to receive 80 mg valsartan or 5 mg amlodipine for 12 weeks. After 8 weeks of therapy, in patients whose blood pressure remained uncontrolled, 5 mg amlodipine was added to the initial therapy. Patients were assessed at 4, 8, and 12 weeks. The primary efficacy variable was change from baseline in mean sitting diastolic blood pressure at 8 weeks. Secondary variables included change in sitting systolic blood pressure and responder rates. RESULTS: Both valsartan and amlodipine were effective at lowering blood pressure at 4, 8, and 12 weeks. Similar decreases were observed in both groups, with no statistically significant differences between the groups for any variable analyzed. For the primary variable the difference was 0.5 mm Hg in favor of valsartan (p = 0.68; 95% confidence interval, -2.7 to 1.7). Responder rates at 8 weeks were 66.7% for valsartan and 60.2% for amlodipine (p = 0.39). Both treatments were well tolerated. The incidence of drug-related dependent edema was somewhat higher in the amlodipine group, particularly at a dose of 10 mg per day (2.4% for 80 mg valsartan; 3.6% for 5 mg amlodipine; 0% for valsartan plus 5 mg amlodipine; 14.3% for 10 mg amlodipine). CONCLUSIONS: The data show that valsartan is at least as effective as amlodipine in the treatment of mild to moderate hypertension. The results also show valsartan to be well tolerated and suggest that it is not associated with side effects characteristic of this comparator class, dihydropyridine calcium antagonists.

Plasma norepinephrine and left ventricular hypertrophy in systemic hypertension.

The relations between some pressure and humoral factors, and some echocardiographic indexes of left ventricular (LV) hypertrophy were studied in 64 patients with essential hypertension. Fifty-seven percent of these patients showed echocardiographic evidence of LV hypertrophy (LV mass greater than 215 g). Multivariate stepwise regression analysis showed that only mean blood pressure (BP) and circulating norepinephrine (NE) levels were significantly related to LV mass index in the group of patients with LV hypertrophy. However, mean BP was the only factor related to LV mass index in the subgroup of patients with LV hypertrophy and plasma NE within the normal laboratory range, whereas NE was the sole factor related to LV mass index in the subgroup with LV hypertrophy and abnormally elevated NE levels (greater than mean + 2 standard deviations of the normal laboratory range). Correlation of LV mass index vs NE was -0.35 (not significant) in the former group of patients and 0.89 (p less than 0.01) in the latter group. NE showed no relation with the echocardiographic variables in the hypertensive patients without LV hypertrophy; in this group, diastolic BP was the only factor related to LV mass index. Circulating NE levels were slightly higher in patients with LV hypertrophy (213 +/- 68 ng/liter) than in those without LV hypertrophy (187 +/- 46 ng/liter), but differences were not significant when adjusting NE for age. Plasma renin activity was not dissimilar in the absence or presence of hypertrophy. In conclusion, our findings suggest that NE might be associated with pressure factors in regulating LV hypertrophy development only in a subgroup of hypertensive patients characterized by echocardiographic LV hypertrophy and abnormally elevated circulating NE levels.

Usefulness of the severity and extent of wall motion abnormalities as prognostic markers of an adverse outcome after a first myocardial infarction treated with thrombolytic therapy.

The prognostic value of wall motion score index (WMSI), assessed at predischarge after a first acute myocardial infarction (AMI) in the thrombolytic era, is still not well known. One-hundred forty-four consecutive patients with a first AMI treated with thrombolytic therapy underwent exercise testing and echocardiography at rest before discharge and were followed-up for a mean period of 18 months. During follow-up, there were 32 cardiac events (12 patients had cardiac deaths, 8 had unstable angina pectoris, 1 had nonfatal reinfarction, and 11 patients had congestive heart failure). The patients who experienced any cardiac event had a higher WMSI (1.67+/-0.15 vs. 1.30+/-0.16, p<0.0001), a higher end-systolic volume (75.1+/-34 vs. 59.5+/-22 ml, p<0.01), and a lower ejection fraction (47+/-16% vs. 55+/-10%, p<0.001) at predischarge than patients without events. The incidence of a positive predischarge exercise testing did not differ between patients with and without cardiac events (22% vs. 24%, p = NS). Multivariate Cox regression analysis, including clinical, exercise results, and echocardiographic parameters, showed that the most powerful predictor of a subsequent event was a resting WMSI > or =1.50 before discharge (chi-square 17.8, p<0.0001). Thus, in patients with a first AMI who underwent thrombolysis, the severity and extent of echocardiographically detected wall motion abnormalities are important independent predictors of cardiac events.

C-reactive protein as a marker for cardiac ischemic events in the year after a first, uncomplicated myocardial infarction.

The prognostic role of C-reactive protein levels in patients with a first acute myocardial infarction, an uncomplicated in-hospital course, and the absence of residual ischemia on a predischarge ergometer test and with an echocardiographic ejection fraction > or = 50% has not been described. C-reactive protein was determined during hospitalization in 64 patients (55 men, mean age 64.6 +/- 10.4 years). The patients were followed up for 13 +/- 4 months and the following cardiac events were recorded: cardiac death, new-onset angina pectoris, and recurrent myocardial infarction. Patients who developed cardiac events during the follow-up period had significantly higher C-reactive protein values than patients without events (3.61 +/- 2.83 vs 1.48 +/- 2.07 mg/dl, p <0.001). The probability of cumulative end points was: 6%, 12%, 31%, and 56% (p = 0.006; RR 3.55; confidence interval 1.56 to 8.04), respectively, in patients stratified by quartiles of C-reactive protein (< 0.45, 0.45 to 0.93, 0.93 to 2.55 and > 2.55 mg/dl). In the Cox regression model, only increased C-reactive protein levels were independently related to the incidence of subsequent cardiac events (chi-square 9.8, p = 0.001). Thus, increased C-reactive protein levels are associated with a worse outcome among patients with a first acute myocardial infarction, an uncomplicated in-hospital course without residual ischemia on the ergometer test, and with normal left ventricular function.

Prognostic value of left ventricular hypertrophy and geometry in patients with a first, uncomplicated myocardial infarction.

BACKGROUND: The prognostic impact of left ventricular (LV) geometry on cardiovascular risk for patients with a first, uncomplicated acute myocardial infarction (AMI), and echocardiographic ejection fraction > or =50% has not been well described. METHODS AND RESULTS: Accordingly, 111 AMI consecutive patients (mean age 59.3+/-10 years) performed echocardiographic examination at predischarge. LV mass was calculated by means of Devereux's formula and subsequently indexed by body surface area. Fifty-three patients had LV hypertrophy and 58 patients had normal LV mass. The two groups were homogeneous for demographic, clinical and angiographic variables as well as for the incidence of residual ischemia on predischarge stress testing. During follow-up period there were 24 cardiac events (cardiac death, unstable angina and non-fatal reinfarction) in the 53 patients with LV hypertrophy and only four events in the remaining 58 patients without LV hypertrophy (RR=2.45; CI=1.76-3.41; P<0.0001). The patients with concentric LV hypertrophy showed a higher incidence of events (64%) than patients with eccentric LV hypertrophy (32%, P<0. 05) and patients with normal geometry and mass (6%, P<0.0001). Multivariate Cox regression model identified concentric geometry as the most powerful predictor of combined end-points (chi(2)=32.7, P<0. 0001). CONCLUSIONS: An increased LV mass and concentric geometry resulted important independent markers of an adverse outcome in patients with a first, uncomplicated myocardial infarction and good LV function.

Leucocyte rheology in controlled coronary ischaemia.

Since no studies have been carried out on the exact origin of the alterations in white blood cell rheology during the early stages of controlled ischaemia in coronary arterial disease, a model was set up using a cycle ergometer test (with a 25 watts increase every 2 minutes). Blood samples were taken (before and after exercise and again 8 minutes later at recovery) from 18 patients with stable angina pectoris and a group of 22 matched controls. The filterability (through 5 micrometer diameter pore filters) of the polymorphonuclear leucocyte sub-population (separated by density gradient), the monocyte and lymphocyte sub-fractions (separated by adhesion to Petri dishes) as well as leucocyte activation (observed under a light microscope) were monitored. Our results showed that the total leucocyte count in patients and controls rose after exercise and was accompanied by a differential shift from the polymorphonuclear to the lymphocyte cells. The polymorphonuclear filterability rate increased significantly in patients when compared to their basal values at rest, and to the controls after exercise (+ 19.58%; P less than 0.002 vs basal values at rest; + 18.72%; P less than 0.002 vs controls). This increase persisted throughout the recovery period (+ 19.86%; P less than 0.002 vs basal values; and + 23.52% P less than 0.001 vs controls), indicating that a reduced polymorphonuclear leucocyte filterability can be associated with the first signs of ischaemia.

Effects of hydrochlorothiazide combined with amiloride in atenolol-resistant hypertensive patients.

Twenty hypertensive outpatients WHO stage I or II, with supine diastolic blood pressure greater than or equal to 95 mmHg at the end of a 4-week treatment period with atenolol (Tenormin) 100 mg daily, continued atenolol in free association with half a tablet of Moduretic (i.e., hydrochlorothiazide 25 mg + amiloride 2.5 mg) for a further 4 weeks. Atenolol monotherapy induced a drop of systolic blood pressure from 175.0 +/- 11 (mean +/- s.d.) mmHg to 158.7 +/- 6 mmHg (p less than 0.01), and of diastolic blood pressure from 113.5 +/- 8 mmHg to 102.7 +/- 5 mmHg (p less than 0.01). After 4 weeks with atenolol in association with half a tablet of Moduretic, systolic blood pressure further decreased to 145.7 +/- 8 mmHg (p less than 0.01), and diastolic blood pressure to 90.2 +/- 10 mmHg (p less than 0.01). Seven out of 20 patients remained with diastolic blood pressure greater than or equal to 95 mmHg despite the above combination therapy. In these patients, the doubling of diuretic dose (hydrochlorothiazide 50 mg + amiloride 5 mg) in combination with atenolol resulted in a further drop in systolic pressure (to 142.1 +/- 9 mmHg) and diastolic (to 92.1 +/- 6 mmHg) (both p less than 0.01). Plasma potassium concentration showed a slight and non-significant increase during atenolol monotherapy (from 4.4 +/- 0.5 mEq/l to 4.6 +/- 0.7 mEq/l; n.s.).(ABSTRACT TRUNCATED AT 250 WORDS)

Isometric exercise before and after nadolol treatment in uncomplicated essential hypertension.

Systolic, diastolic and mean arterial pressure (SAP, DAP, MAP), heart rate (HR) and tension time index (TTI) were evaluated in 20 uncomplicated hypertensives and in 20 normotensives at rest and during isometric exercise, performed by handgrip (HG). In the hypertensive population the same parameters were evaluated also after two and six weeks of treatment with a beta-blocking agent, nadolol, given in a single daily dose. In all cases isometric exercise induced a significant increase of SAP, DAP, MAP, HR and TTI and this increase was more relevant in hypertensives than in controls. In the hypertensive population, nadolol was effective in lowering arterial pressure at rest, and significantly reduced the levels of SAP, DAP, MAP, HR and TTI reached at the end of the HG test. Moreover, the increments of the investigated parameters induced by isometric exercise were significantly reduced after nadolol. The results suggest that nadolol, unlike other beta-blocking agents, exerts a "protective" action against the hazardous increments of blood pressure which may occur in the daily life of hypertensive subjects during involuntary isometric exercises, and which could trigger dangerous cardiovascular complications.

Echocardiography in clinical pharmacology: developing new concepts on the pathophysiology of left ventricular hypertrophy in arterial hypertension.

By using echocardiography it is possible to quantify accurately and repeatedly the degree of left ventricular hypertrophy (LVH) in patients with arterial hypertension. It therefore appears to be a valuable tool for investigating the mechanisms that may be involved in the pathogenesis of this condition in hypertensive patients. The role of increased afterload in LVH induction is well established, and results of several independent laboratories concord in indicating blood pressure as a major independent factor in the pathogenesis of LVH in hypertensive patients. The role of factors other than blood pressure has not yet been fully established, however, in this setting. Animal and human studies from different laboratories are providing conflicting results on the possible role of factors such as the catecholamines or the renin-angiotensin system as additional stimuli facilitating LVH development. Clinical pharmacology could be a useful tool in seeking to clarify this important question. Drugs that lower blood pressure without consistently affecting the humoral factors possibly responsible for LVH might be expected to induce a lesser degree of LVH reversal than drugs that lower blood pressure while at the same time reducing or inhibiting the factors responsible for LVH. This experimental approach raises several methodological and technical points which are crucial in the trial planning stages. The question whether borderline hypertensive patients should be considered separately from stable hypertensive patients in the search for relationships between LVH and possible pathogenic factors is also discussed.

[Multicenter clinical study of the antihypertensive activity of lisinopril]. / Studio clinico multicentrico sull'attività antiipertensiva del Lisinopril.

One-hundred patients suffering from slight-moderate hypertension (53 m, 47 f, aged between 18 and 78, average 49.08) have been studied in order to assess the effectiveness and tolerance of lisinopril ("Zestril", ICI-Pharma), a new ACE inhibitor in a single daily administration at doses of between 10 and 80 mg in relation to pressure values. Monotherapy with Lisinopril proved effective in 84 patients (88.4%), in 74 of whom (7.9%) pressure values were returned to normal. 11 patients (11.6%) did not respond to treatment. In most cases, the result was obtained with a dose of 20 mg in a single administration (32.6%). The incidence of side-effects was limited and in no case required the withdrawal of the drug.

[The Study Group of Quinapril in Arterial Hypertension. The Steering Committee]. / Gruppo di studio del quinapril nell'ipertensione arteriosa. Steering Committee.

The efficacy and safety of the treatment of arterial hypertension with the ACE-inhibitor quinapril, were evaluated in a multicentre study conducted in Italy. The study, lasting 14 weeks, after a preliminary wash-out period, allowed response-based titration of quinapril dose from 10 mg to 40 mg once a day, with provision to combine additional hydrochlorothiazide (12.5 to 25 mg), in case of persistently high diastolic pressure levels. The efficacy sample included 1267 patients: at therapy week 14, 78.6% of patients were treated with quinapril alone. Global response rate (intent-to-treat) was 83.3%, with a mean reduction of diastolic pressure of 15.8 mmHg (95% confidence interval from 15.5 to 16.2 mmHg). 91 patients reported 126 associated adverse events (7.0%); the most frequently reported event was cough (2.7%). First-dose hypotension was rarely reported (1.3%), even in elderly and diabetic patients.

[Multiple rhabdomyomas in a newborn infant. A clinical case report]. / Rabdomiomi multipli in età neonatale. Descrizione di un caso clinico.

Rhabdomyoma is a rare primary benign cardiac tumor usually diagnosed in newborn and infancy. The authors report a case of multiple and completely asymptomatic rhabdomyoma, diagnosed by echocardiography.

Antihypertensive efficacy and tolerability of captopril in the elderly: comparison with hydrochlorothiazide and placebo in a multicentre, double-blind study.

In this study we compared the antihypertensive efficacy and tolerability of captopril at 25 mg twice daily, hydrochlorothiazide (HCTZ), 12.5 mg twice daily and placebo in a multicentre, double-blind, randomized study that included 152 essential hypertensive patients (77 males, 75 females, 87 WHO stage I, 65 WHO stage II, aged 69 +/- 4 years, mean +/- s.d.). Supine and standing blood pressure were similarly reduced by captopril and HCTZ (P less than 0.01 for both compared with placebo). The heart rate did not change. Captopril (25-30 mg twice daily) and HCTZ (12.5 mg twice daily), alone or in combination, maintained their antihypertensive effect during a 24-week single-blind follow-up study. During the follow-up, diastolic blood pressure remained less than 100 mmHg in seven essential hypertensives on placebo, in 45 on captopril and in 25 on HCTZ. Side effects were observed in seven essential hypertensives during placebo (treatment withdrawn in two), in eight during HCTZ and in three during captopril. Serum potassium was reduced (P less than 0.05) and uric acid was increased (P less than 0.01) only during HCTZ. We conclude that captopril and HCTZ have similar antihypertensive efficacy in the elderly; however, captopril appears to be better tolerated.