Diuretics for hypertension.
Explore the source record for details and available documents.
Antihypertensive Agents↗
Biomedical subjects
B D Nunez
Publications and source records attributed to B D Nunez.
Comparison of immediate and long-term outcome of coronary angioplasty performed for unstable angina and rest pain in men and women.
OBJECTIVE: To determine whether a sex-related difference in outcome is present among patients who undergo percutaneous transluminal coronary angioplasty (PTCA) for unstable angina. DESIGN: We retrospectively analyzed the results after PTCA was performed between January 1981 and June 1993 in a series of 2,073 men and 941 women with unstable angina and rest pain. RESULTS: The success rates of PTCA were similar for women and men (87.9% and 87.2%, respectively), as were the in-hospital mortality rates (4.1% and 3.2%, respectively) and the need for emergency coronary artery bypass operation (3.1% and 3.5%, respectively). Fewer women than men had Q-wave myocardial infarction (0.5% versus 1.6%; P = 0.02). During the follow-up period (mean, 4 years), no significant differences were noted between women and men in overall survival (81% and 85% at 6 years, respectively) or survival free of Q-wave myocardial infarction (81% and 83% at 6 years, respectively) with use of the Kaplan-Meier method. Women were less likely than men to have had coronary artery bypass grafting (19% versus 22% at 6 years; P = 0.02), and the occurrence of severe angina was higher in women than in men (52% versus 44% at 6 years; P = 0.001). A subgroup analysis of patients who had myocardial infarction within 7 days preceding PTCA showed a similar pattern of results. CONCLUSION: After PTCA performed for unstable angina and rest pain, survival rates were excellent in both women and men, and no difference was observed in subsequent myocardial infarction rates. During follow-up, however, women were more likely to have severe angina and were less likely to have had coronary artery bypass grafting. Concerns about possible sex-related complications should not dissuade physicians from performing PTCA when clinically indicated for unstable angina and rest pain.
Aged↗
Management of balloon rupture during rigid stent deployment.
Balloon rupture may occur during stent placement and will only become apparent when the stent has been maneuvered across the target stenosis and deployment is attempted. Withdrawal may be complicated by displacement of the stent off the balloon. We describe two cases in which a power injector was used to momentarily inflate the balloon and partially expand the stent in place. The punctured balloon could then be withdrawn and the stent fully deployed, using a new balloon.
Aged↗
Cocaine and the porcine coronary microcirculation: effects of chronic cocaine exposure and hypercholesterolemia.
OBJECTIVE: To examine the acute effect of cocaine on the coronary microcirculation and whether chronic cocaine administration with or without a concomitant high-cholesterol diet affects beta-adrenoceptor and endothelial functions in the coronary microcirculation. DESIGN: Prospective experimental study. SETTING: Laboratory and animal research facility. PARTICIPANTS: Yorkshire pigs. INTERVENTIONS: Pigs were fed a high (2%)-cholesterol diet or a regular diet for 3 months. Animals in both groups received cocaine chronically (7 mg/kg/day, IM). Control animals were fed a regular diet. MEASUREMENTS AND MAIN RESULTS: Responses of the porcine coronary arterioles (90 to 190 microns in diameter) were examined in vitro in a pressurized (40 mmHg) no-flow state using a video-imaging apparatus. Acute application of cocaine caused a significant contraction with a mean maximal diameter decrease of 14% +/- 5%, which was markedly reduced by muscarinic blockade but not significantly affected by alpha 1-adrenergic blockade. Lidocaine or procainamide had no vasoconstrictor effect. Chronic exposure of animals to cocaine diminished contractile responses to cocaine and reduced relaxation responses to the nonselective beta-adrenergic receptor agonist isoproterenol. Phenylephrine caused a minimal (< 4%) contraction of vessels in all groups. Chronic cocaine administration with concomitant high-cholesterol feeding attenuated endothelium-dependent relaxations to serotonin, whereas endothelium-dependent relaxations to bradykinin were unaffected. Endothelium-independent relaxations to sodium nitroprusside were similar in all groups. CONCLUSIONS: These results suggest that cocaine can exert a direct vasoconstrictor effect on the porcine coronary microcirculation via a muscarinic mechanism. Chronic exposure to cocaine significantly decreases beta-adrenoceptor-mediated relaxation and blunts endothelium-dependent relaxation to a small degree.
Adrenergic alpha-Antagonists↗
Comparison of diastolic left ventricular filling and cardiac dysrhythmias in hypertensive patients with and without isolated septal hypertrophy.
Although many patients with hypertension develop isolated septal hypertrophy (ISH) rather than concentric or eccentric left ventricular (LV) hypertrophy, limited data are available on cardiac structure, function, and arrhythmias in hypertensive patients with ISH. Clinical features, hemodynamics, M-mode echocardiograms, and 24-hour electrocardiographic recordings were evaluated in 21 healthy normotensive subjects, 23 hypertensive patients without LV hypertrophy, 31 hypertensive patients with concentric LV hypertrophy, and 23 hypertensive patients with ISH to determine the prevalence and complexity of cardiac arrhythmias and diastolic LV filling abnormalities. Age, sex, race, obesity indexes, preload, ejection fraction, and LV contractility were similar in all 4 groups, and arterial pressure and afterload were statistically similar in the 3 hypertensive groups. Left atrial emptying index (p < 0.01) and peak LV filling rate (p < 0.01), 2 indexes of diastolic LV filling, were significantly reduced in the 3 hypertensive groups compared with the normotensive group. The duration of rapid LV filling, however, was significantly prolonged only in hypertensive patients with concentric LV hypertrophy and ISH (p < 0.05) but not in hypertensive patients without LV hypertrophy. The prevalence (p < 0.001) and complexity (p < 0.001) of ventricular ectopic activity was also significantly increased to a similar degree in hypertensive patients with concentric LV hypertrophy and in those with ISH compared with normotensive subjects or hypertensive patients without LV hypertrophy. The prevalence and complexity of atrial ectopic activity was only increased significantly (p < 0.001) in those with ISH.
Adult↗
Nitroglycerin ointment in the treatment of impotence.
Topical nitroglycerin ointment has been studied in the laboratory as a possible treatment for impotence of various etiologies. However, there is limited information on the topical administration of nitroglycerin in a natural environment allowing normal sexual function. We report 3 cases of impotence that were successfully treated with topical nitroglycerin ointment.
Administration, Cutaneous↗
Effect of cardiac catheterization on renal function.
Sensitive acute renal clearance methodology was used to investigate the incidence of radiocontrast-induced nephrotoxicity in patients undergoing cardiac catheterization. Patients at the University of Oklahoma Teaching Hospitals scheduled for elective cardiac catheterization had their creatinine clearance measured on the day preceding and the day following their procedure. All patients had a serum creatinine concentration lower than 175 mumol/l. The creatinine clearance was calculated from the mean of four consecutive 30-minute renal clearance periods obtained in the fasted state during water loading. The change in renal function following the catheterization was evaluated. There was no significant change in the creatinine clearance after the cardiac catheterization (Ccr 101.5 +/- 6.4 ml/min before and 111.6 +/- 7.4 ml/min after the procedure). A decrease in Ccr exceeding 25% occurred in 1 of 23 subjects (4.3%. Patient age, presence of diabetes, and volume of contrast agent were not adverse risk factors. The results suggest a low risk of nephrotoxicity in low-risk patients undergoing elective cardiac catheterization, even when very sensitive measures of glomerular filtration rate are utilized.
Acute Kidney Injury↗
Hypertension and sudden death. Disparate effects of calcium entry blocker and diuretic therapy on cardiac dysrhythmias.
This study was designed to evaluate the impact of antihypertensive therapy on cardiac dysrhythmias in 13 hypertensive patients who received calcium entry blockers and in 10 hypertensive patients who received hydrochlorothiazide. Mean arterial pressure fell to a similar extent in both treatment groups; however, left ventricular mass index decreased (from 102 +/- 4 to 95 +/- 2 g/m2) only in patients receiving calcium entry blockers, but not in those taking hydrochlorothiazide. The prevalence of premature ventricular contractions decreased 74% from 21 +/- 14/h to 5.7 +/- 6/h in the calcium entry blocker group, but did not change in the hydrochlorothiazide group (15 +/- 17/h to 16 +/- 13/h). Couplets, multiform contractions, ventricular tachycardia, and supraventricular tachycardia were completely abolished after calcium entry blocker therapy, whereas the prevalence of these arrhythmias remained unchanged during treatment with hydrochlorothiazide. We conclude that antihypertensive therapy with calcium entry blockers (but not with thiazide diuretics) reduces left ventricular mass and the prevalence and severity of ventricular dysrhythmias. Whether this reduction will improve the ominous prognosis of left ventricular hypertrophy and diminish the risk of sudden death remains unknown.
Adult↗
Cardiac performance after reduction of myocardial hypertrophy.
PURPOSE: The current study was performed to assess the functional sequelae of reducing left ventricular hypertrophy in patients with essential hypertension. PATIENTS AND METHODS: To analyze left ventricular function and contractility in patients with essential hypertension after reduction of left ventricular hypertrophy, 14 patients with essential hypertension and left ventricular hypertrophy were studied prospectively by echocardiogram (1) before, (2) during, and (3) after left ventricular mass had been reduced by antihypertensive therapy of 19 +/- 3 months' duration. All drugs were discontinued four weeks before the first and the third study. RESULTS: At the time of the third study, arterial pressure had returned to pretreatment values, and mean, peak, and isovolumetric (but not end-systolic) wall stress increased, whereas left ventricular mass remained diminished. Despite the increased pressure load to the heart, myocardial contractility was maintained or improved after reduction of left ventricular hypertrophy, as indicated by the ratio of end-systolic wall stress to end-systolic volume index (p less than 0.02) and by the relation of fractional shortening to end-systolic wall stress (p less than 0.06). End-diastolic volume, an indicator of preload, remained reduced after therapy (p less than 0.05). As a result, pump function of the left ventricle improved as shown by an increase in the ejection fraction (p less than 0.05), fractional fiber shortening (p less than 0.05), and velocity of circumferential fiber shortening (p less than 0.01). CONCLUSION: Thus, in patients with essential hypertension, reduction of myocardial hypertrophy by antihypertensive therapy appears to be beneficial rather than detrimental to cardiac pump performance.
Adult↗
Sex differences in cardiac adaptation to essential hypertension.
Left ventricular functional and structural adaptations to mild essential hypertension were assessed by 2D-guided M-mode echocardiography in a population of premenopausal and postmenopausal women (n = 29) who were matched with the same number of men with regard to mean arterial pressure, age and race. Premenopausal women had a thinner posterial wall (P less than 0.05), a smaller left ventricular systolic and diastolic diameter, and a smaller left ventricular mass than men with the same level of arterial pressure. Left ventricular performance indices, ejection fraction, velocity of circumferential fibre shortening, and the ratio of the end-systolic wall stress to the end-systolic volume index (a load-insensitive contractility index) were higher in women than in men. These sex differences were most pronounced before the menopause and tended to disappear thereafter. We conclude that in the presence of the same level of arterial pressure, women have smaller left ventricular dimensions and enhanced ventricular performance compared with men. These differences in cardiac adaptations between the genders may account for the lower risk of cardiovascular morbidity and mortality in premenopausal women with essential hypertension.
Adaptation, Physiological↗
Hemodynamic, humoral and volume findings in systemic hypertension with isolated ventricular septal hypertrophy.
To analyze the hemodynamic, endocrine and volume characteristics of isolated septal hypertrophy (ISH) in established systemic hypertension, 22 patients with ISH were compared to 23 patients with symmetric hypertrophy and to 28 without left ventricular (LV) hypertrophy. Mean arterial pressure and 24-hour ambulatory pressure readings did not differ between the 2 groups. At the same level of arterial pressure, patients with ISH had a high cardiac index (p less than 0.02) and a faster heart rate (p less than 0.05); consequently, total peripheral resistance was decreased (p less than 0.05). Although there was no change in intravascular volume, central blood volume was expanded (p less than 0.02), and the ratio of central to peripheral blood volume was increased (p less than 0.02), thereby indicating peripheral venoconstriction. Patients with isolated ISH had greater responses of diastolic pressure and heart rate (p less than 0.05) to isometric stress than the other 2 groups. A hyperdynamic circulatory state is a hemodynamic hallmark of ISH in early essential hypertension that might be produced by increased sympathetic activity.
Adult↗
Immediate and short-term cardiovascular effects of a new converting enzyme inhibitor (lisinopril) in essential hypertension.
The immediate and short-term effects of lisinopril, a new converting enzyme inhibitor, on systemic and regional hemodynamics, cardiac structure and function and humoral indexes were evaluated in 10 patients with mild to moderate essential hypertension. A single oral dose of 5 mg lisinopril reduced mean arterial pressure from 118 to 104 mm Hg (p less than 0.01) and significantly increased (p less than 0.05) all load-dependent indexes of ventricular function (i.e., ejection fraction, velocity of circumferential fiber shortening and fractional fiber shortening rate). After 10 to 12 weeks of once-daily administration of lisinopril, mean arterial pressure remained reduced over a full 24-hour period (p less than 0.01), and was mediated through arteriolar dilation as expressed by the close correlation (r = 0.93, p less than 0.01) between changes in mean arterial pressure and changes in total peripheral resistance. Cardiac index decreased from 3.06 to 2.68 liters/min/m2 (p less than 0.01) without correlation to the decrease in arterial pressure (r = 0.06). Despite this reduction in cardiac index, renal blood flow increased from 861 to 1,053 ml/min (p less than 0.05) and renal vascular resistance decreased from 14 to 9 units (p less than 0.01). Left ventricular mass index decreased from 124 to 109 g/m2 (p less than 0.05), and left ventricular function remained unchanged. Thus, the decrease in arterial pressure produced by lisinopril was associated with improved renal hemodynamics and reduced left ventricular mass.
Adult↗
Myocardial contractility and left ventricular function in obese patients with essential hypertension.
Although the risk of developing congestive heart failure increases in parallel with the degree of obesity, load-dependent indexes of left ventricular function are found to be reduced in patients with morbid obesity only. We used the ratio of end-systolic wall stress to end-systolic volume index, which is load-independent, to assess myocardial contractility in 23 nonobese, 28 mildly obese and 26 moderately obese patients with mild to moderate essential hypertension. Although load-dependent indexes (i.e., ejection fraction, fractional fiber shortening and velocity of circumferential fiber shortening) were similar in the 3 groups, end-systolic wall stress to end-systolic volume index was lower in the moderately obese group (2.63 +/- 0.4, p less than 0.002) and even in the mildly obese group (2.88 +/- 0.8, p less than 0.05) than in the nonobese group (3.27 +/- 0.7). Further, there was a significant inverse relation between end-systolic wall stress to end-systolic volume index and body mass index (r = -0.34, p less than 0.005), diastolic diameter (r = -0.56, p less than 0.001) and left ventricular mass index (r = -0.55, p less than 0.001). Some obese patients have depressed myocardial contractility when compared with lean patients despite well-preserved pump function.
Adult↗
Angiotensin converting enzyme inhibitors. Disparities in the mechanism of their antihypertensive effect.
Systemic and renal hemodynamics were studied by invasive and noninvasive techniques in 30 patients with mild to moderate essential hypertension before and after antihypertensive therapy with captopril (12 patients), enalapril (8 patients), and lisinopril (10 patients). All three angiotensin-converting enzyme (ACE) inhibitors reduced arterial pressure to about the same extent: captopril by 14%, enalapril by 18%, and lisinopril by 13%. However, lisinopril produced a significant fall (14%, P less than 0.001) in cardiac output that was not seen with captopril or enalapril therapy. Moreover, lisinopril elicited an increase in renal blood flow (22%, P less than 0.05) that was more marked than that with enalapril (12%) or captopril (4%). Although left ventricular mass was reduced (P less than 0.05) with all three agents, enalapril induced a twofold greater reduction (29%) than captopril (14%) or lisinopril (12%). These findings suggest that systemic and renal hemodynamic effects may be drug specific and not uniform for all ACE inhibitors.
Adult↗
Sodium intake modulates left ventricular hypertrophy in essential hypertension.
In order to assess the impact of dietary sodium intake on the degree of left ventricular hypertrophy, we determined posterior wall thickness, relative wall thickness and left ventricular mass by two-dimensionally guided M-mode echocardiography, and related these parameters to sodium excretion over 24 h. There was no restriction on sodium intake. The first cohort comprised 43 subjects (residents of New Orleans) with mild to moderate essential hypertension who had not been treated for at least 4 weeks; in this cohort sodium excretion correlated with posterior wall thickness (r = 0.64, P less than 0.001), relative wall thickness (r = 0.67, P less than 0.001) and left ventricular mass (r = 0.37, P less than 0.02). A stepwise multiple regression analysis confirmed that sodium excretion was a determinant of posterior wall thickness (P less than 0.02) and relative wall thickness (P less than 0.05) independently of age, arterial pressure and body weight. The second cohort comprised 60 white male patients (residents of Bonn) with mild essential hypertension who had never been treated in the past; in this cohort sodium excretion correlated with diastolic diameter (r = 0.36, P less than 0.001) and with left ventricular mass (r = 0.35, P less than 0.001). Sodium excretion and systolic pressure emerged as independent variables (P less than 0.02) for left ventricular mass as evaluated by multiple regression analysis. These results identify dietary sodium intake as an independent powerful determinant of left ventricular hypertrophy in two disparate patient cohorts. Thus, for a similar haemodynamic load, sodium intake might accelerate, and conversely salt restriction mitigate, cardiac structural adaptation in patients with essential hypertension.
Cardiomegaly↗
Hypertensive concentric left ventricular hypertrophy: when is ventricular ectopic activity increased?
The Framingham Study has indicated that patients with left ventricular hypertrophy (LVH) have a greater risk of cardiovascular complications and sudden death than subjects with a normal heart. We have previously demonstrated that ventricular ectopy was more prevalent and complex in hypertensive patients with LVH by electrocardiographic (ECG) criteria than in those without ECG evidence of LVH. The present study was designed to detect and quantify ventricular dysrhythmias in hypertensive patients with early concentric LVH by echocardiography but without LVH by ECG criteria. Continuous ambulatory ECG tracings were recorded for 24 hours in 94 patients with essential hypertension: 37 without LVH, 26 with concentric LVH by echocardiographic but not ECG criteria, and 31 with LVH on both echocardiography and ECG. Patients with LVH by ECG criteria had significantly more premature ventricular contractions (P less than .001) and more complex (higher Lown's class) ventricular ectopy (P less than .001) than hypertensives without LVH or with LVH only by echocardiographic criteria. Prevalence and complexity of ventricular ectopic activity, however, was not affected by mild to moderate concentric cardiac hypertrophy detected echocardiographically. We conclude that unlike LVH shown by ECG, early hypertensive concentric LVH detected echocardiographically is not associated with increased electrical irritability of the myocardium.
Adult↗
Dietary salt intake. A determinant of cardiac involvement in essential hypertension.
Because a given increase in afterload does not consistently produce the same degree of left ventricular hypertrophy, we evaluated several clinical, hemodynamic, and endocrine factors that are prone to modify the adaptation of left ventricular structure in patients with mild essential hypertension (World Health Organization stages I or II). Dietary salt intake assessed by sodium excretion over 24 hours was a powerful determinant of posterior wall thickness (r = 0.64, p less than 0.001), relative wall thickness (r = 0.67, p less than 0.001), and left ventricular mass (r = 0.37, p less than 0.05). In contrast, diastolic pressure, body mass index, hematocrit, and epinephrine were found to be weaker determinants of left ventricular structure (r = 0.31-0.40, p less than 0.05). A stepwise multiple regression analysis revealed that sodium excretion was the strongest predictor for posterior wall thickness (p less than 0.02) and relative wall thickness (p less than 0.05) independent of the other examined variables. These results identify dietary salt intake as a strong determinant of cardiac structural adaptation to a persistent increase in arterial pressure. Consequently, a high salt intake might aggravate and, conversely, dietary salt restriction might prevent (or at least mitigate) the development of left ventricular hypertrophy in patients with essential hypertension.
Blood Pressure↗
Antihypertensive therapy and cardiovascular reactivity during isometric stress.
The cardiovascular reactivity to isometric stress test before and after antihypertensive therapy was evaluated by invasive haemodynamic techniques in 23 patients with mild to moderate essential hypertension. A beta-blocking agent (atenolol 50 to 100 mg daily) was given to 11 patients; 12 patients received calcium entry blockers (diltiazem 240 to 360 mg daily or verapamil 240 to 480 mg per day). The pressor response to isometric stress before therapy consisted of an increase in systolic, diastolic, and mean arterial pressure (all P less than 0.01) that was similar in both treatment groups. The rise in arterial pressure was mainly due to an increase in cardiac output (P less than 0.01), as total peripheral resistance did not change significantly. After treatment with the beta-blocker, the increase in total peripheral resistance during isometric stress was exaggerated (P less than 0.01), and, conversely, the increase in cardiac output was attenuated (P less than 0.01). In contrast, treatment with calcium entry blockers preserved the haemodynamic reactivity pattern of the untreated state: arterial pressure increased during isometric stress through an increase in cardiac output, while total peripheral resistance remained unchanged. Since the haemodynamic culprit of essential hypertension is an elevated peripheral resistance, a drug that numerically increases this culprit under conditions of resting and isometric stress becomes less attractive than one that lowers peripheral resistance and preserves the physiologic response pattern.
Adult↗