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PubMed1998

Heart rate variability index in congestive heart failure: relation to clinical variables and prognosis.

AIM: To evaluate the clinical and prognostic value of the heart rate variability index in patients with congestive heart failure. METHODS: Sixty-four patients with chronic congestive heart failure and sinus rhythm underwent clinical assessment, 24-h ambulatory electrocardiography and echocardiography. Patients were followed for 6 to 30 months. Cardiac death or heart transplantation constituted the primary end-point of the study. RESULTS: The heart rate variability index was related to left ventricular ejection fraction (r=0.29, P=0.02) and New York Heart Association class (P=0.01). Patients with a restrictive left ventricular filling pattern had a lower heart rate variability index compared to patients with a non-restrictive pattern (26+/-11 vs 33+/-9 units, P=0.01). Patients who died (n=11) or underwent heart transplantation (n=4) had a lower heart rate variability index compared to survivors (21+/-10 vs 33+/-9 units, P<0.0001). In multivariate survival analysis, a reduced heart rate variability index was related to survival independent of parameters of left ventricular function. CONCLUSION: The heart rate variability index provides independent information on clinical status and prognosis in patients with chronic congestive heart failure.

Aged↗

PubMed1989

[Effect of vasodilator agents on the effectiveness of the complex treatment of patients with ischemic heart disease and congestive heart failure].

A total of 153 coronary patients with congestive heart failure, stage IIA and IIB, were investigated. Thirty patients underwent a three-week course of treatment with cardiac glycosides, plus diuretics and potassium preparations where necessary. In addition to conventional treatment, 123 patients were treated with vasodilating agents (2% nitroglycerin ointment, nitrosorbide or molsidomin) with the doses adjusted individually on the basis of acute drug testing. Those patients with congestive heart failure who received combined treatment with cardiac glycosides and vasodilators demonstrated a more obvious improvement of clinical parameters and instrumental findings as compared to the patients, treated with cardiac glycosides alone.

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PubMed1999

Angiotensin-converting enzyme inhibition restores hepatocyte growth factor production in patients with congestive heart failure.

Endothelium-dependent vasodilation is impaired in patients with congestive heart failure. For vascular endothelium, hepatocyte growth factor (HGF) is one of the most potent and specific growth factors, which acts protectively against endothelial dysfunction. HGF production is downregulated by angiotensin II (Ang II) in vitro. We hypothesized that HGF production is impaired as the result of increased Ang II in patients with congestive heart failure, and that if so, the impaired production should be restored with angiotensin-converting enzyme inhibitors (ACE-I). We studied 16 patients with congestive heart failure caused by previous anterior myocardial infarction in whom left ventricular ejection fraction was 35+/-8% (mean+/-SD). Before and approximately 4 weeks after the treatment with ACE-I, blood samples were collected to measure the levels of HGF, Ang II, and brain natriuretic peptide as a biochemical marker for severity of heart failure. We also studied 5 control subjects, in whom heparin increased HGF production to 48+/-5-fold. However, in patients with heart failure, HGF response to heparin was significantly attenuated (24+/-5-fold, P<0.05 vs control). Therapy with ACE-I decreased the levels of Ang II and brain natriuretic peptide and restored HGF production in response to heparin by 43+/-7-fold, comparable to the control response. In conclusion, impaired HGF production was restored after the treatment with ACE-I probably by the mechanism of Ang II suppression. This novel effect of ACE-I may contribute to the clinical improvement in patients with heart failure and thereby may have an important therapeutic implication.

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PubMed1982

Long-term captopril therapy in severe refractory congestive heart failure.

1 The favourable haemodynamic effects of captopril in patients with congestive heart failure have been reported. 2 We have treated 25 patients with severe chronic congestive heart failure with captopril in doses of 75-450 mg daily. Before entering the study all patients remained in New York Heart Association functional class IV despite high-dose diuretic and vasodilator therapy. 3 Mean cardiothoracic ratio was 60%, and all patients had a shortening fraction of 18% or less on echocardiography (normal 25 to 40%). 4 Five patients died within one month of captopril and five between four and seven months, three of whom had improved to class IIM and one to IIS before death. 5 Of the 15 survivors one was referred for a heart transplant when he had improved to class IIM. The remaining 14 patients were followed for 8-16 months. Ten improved to New York Heart Association class I or IIS and four to class IIM or III. Diuretic requirements were decreased considerably in all 14. Side effects were common but captopril did not have to be withdrawn. Captopril is a highly effective drug in the treatment of patients with congestive heart failure refractory to currently accepted therapy.

Adolescent↗

PubMed2005

Ultrafiltration versus usual care for hospitalized patients with heart failure: the Relief for Acutely Fluid-Overloaded Patients With Decompensated Congestive Heart Failure (RAPID-CHF) trial.

OBJECTIVES: The purpose of this research was to assess the safety and efficacy of ultrafiltration (UF) in patients admitted with decompensated congestive heart failure (CHF). BACKGROUND: Ultrafiltration for CHF is usually reserved for patients with renal failure or those unresponsive to pharmacologic management. We performed a randomized trial of UF versus usual medical care using a simple UF device that does not require special monitoring or central intravenous access. METHODS: Patients admitted for CHF with evidence of volume overload were randomized to a single, 8 h UF session in addition to usual care or usual care alone. The primary end point was weight loss 24 h after the time of enrollment. RESULTS: Forty patients were enrolled (20 UF, 20 usual care). Ultrafiltration was successful in 18 of the 20 patients in the UF group. Fluid removal after 24 h was 4,650 ml and 2,838 ml in the UF and usual care groups, respectively (p = 0.001). Weight loss after 24 h, the primary end point, was 2.5 kg and 1.86 kg in the UF and usual care groups, respectively (p = 0.240). Patients tolerated UF well. CONCLUSIONS: The early application of UF for patients with CHF was feasible, well-tolerated, and resulted in significant weight loss and fluid removal. A larger trial is underway to determine the relative efficacy of UF versus standard care in acute decompensated heart failure.

Adrenergic beta-Antagonists↗

PubMed1999

Doxorubicin-induced congestive heart failure in elderly patients with metastatic breast cancer, with long-term follow-up: the M.D. Anderson experience.

PURPOSE: Correlation between aging and doxorubicin-induced congestive heart failure in patients with metastatic breast cancer was studied to determine whether doxorubicin-induced congestive heart failure in elderly patients with metastatic breast cancer is a clinically significant issue. METHODS: This was a retrospective study with a median follow-up of 16.8 years. The setting was a comprehensive cancer center in a large city. A group of 682 consecutive patients with metastatic breast cancer presented to The University of Texas M.D. Anderson Cancer Center between 1973 and 1980. All patients received doxorubicin by bolus infusion. Patients in group 1 (n = 538) were aged 50 to 64 years; patients in group 2 (n = 144) were aged 65 years and older. Medical records of all patients were reviewed. Patients who had congestive heart failure were identified and analyzed. The diagnosis of doxorubicin-induced congestive heart failure was made and confirmed by a cardiologist at the time of its development. The main outcome measure was the cumulative probability of developing doxorubicin-induced congestive heart failure in elderly patients with metastatic breast cancer compared to a younger age group. RESULTS: In group 1, 33 patients, and in group 2, 13 patients developed doxorubicin-related congestive heart failure. The cumulative doses of doxorubicin administered to patients with congestive heart failure were 410 mg/m2 (range 150-550 mg/m2) and 400 (range 100-570 mg/m2), respectively. The time interval from the last date of doxorubicin treatment to the development of congestive heart failure was, respectively, 5 months (range < 1-65 months) and 9 months (range < 1-28 months). There was no statistically significant difference between the two congestive heart failure subgroups, nor were we able to identify risk factors that could have increased the risk of congestive heart failure among these patients. CONCLUSION: Older patients with metastatic breast cancer and no significant comorbidity can be treated with doxorubicin-based chemotherapy with no added risk of developing congestive heart failure beyond that in the younger age group.

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PubMed1986

Diuretic therapy in congestive heart failure for the elderly patient.

The incidence of congestive heart failure (CHF) in the elderly increases with age as 80% of patients hospitalised with CHF are older than 60 years of age. In this age group CHF may result from several factors such as coronary artery disease, hypertension, valvular disease or intrinsic myocardiopathies. Important alterations of renal physiology have been observed in this condition: decreases in renal plasma flow and glomerular filtration rate, and increases in renal venous pressure. Natriuretic hormone inhibition occurs and renin-angiotensin-aldosterone system activation and antidiuretic hormone secretion increase, resulting in positive water and sodium balances that contribute to the manifestations of congestive heart failure. The treatment of CHF in the elderly is similar to that in younger patients; the difference in management is determined by the severity of the disease and the side effects of the drugs used. Diuretics increase water and sodium elimination by the kidney and increase the systolic volume of the left ventricle, probably by the reduction of preload and afterload. Diuretic therapy must be pursued carefully in patients receiving digitalis, especially in those elderly individuals who may be on restricted diets: the most common adverse effects of diuretics in this age group are hypovolaemia, hyponatraemia, hypokalaemia and hypomagnesaemia.

Aged↗

PubMed1995

Prognostic value of plasma catecholamines, plasma renin activity, and plasma atrial natriuretic peptide at rest and during exercise in congestive heart failure: comparison with clinical evaluation, ejection fraction, and exercise capacity.

Survival in congestive heart failure is related to plasma catecholamines and atrial natriuretic peptide at rest, but the prognostic importance of changes during exercise is unknown. The aim of this study was to evaluate the prognostic value of catecholamines and atrial natriuretic peptide at rest and during maximal exercise in congestive heart failure, and to compare it to clinical and exercise test variables and left ventricular ejection fraction. One hundred ninety consecutive patients (136 men and 54 women; median age, 66 years; range, 42-75 years) with clinically stable congestive heart failure were included. Sixteen patients were in New York Heart Association class I, 87 in class II, 83 in class III, and 4 in class IV. Left ventricular ejection fraction was 0.30 (range, 0.06-0.74). Total survival after 1 year was 79%, after 2 years, it was 68%. Prognostic variables at univariate analysis were: plasma noradrenaline at rest (P < .0001), plasma adrenaline at rest (P = .049), and atrial natriuretic peptide at rest (P = .016). During exercise, plasma catecholamines and plasma atrial natriuretic peptide increased significantly; the change, however, was not related to survival. Six variables carried significant, independent prognostic information in a multivariate analysis: left ventricular ejection fraction (P = .03), plasma noradrenaline at rest (P = .009), New York Heart Association class III + IV (P = .005), increase in heart rate during exercise < or = 35 min-1 (P < .0001), serum creatinine > 121 mumol/L (P = .004), and serum urea > 7.6 mmol/L (P = .007). Patients with congestive heart failure have a poor survival despite intensive medical treatment. Plasma catecholamines and plasma atrial natriuretic peptide are elevated at rest and rises further during exercise; the increase, however, is not related to mortality. Plasma noradrenaline at rest contributes with further prognostic information despite knowledge of clinical and exercise variables and was the only neurohormonal variable with independent, significant prognostic information on survival.

Adult↗

PubMed1988

High-dose furosemide in the treatment of refractory congestive heart failure.

Thirty-five patients with severe chronic congestive heart failure that was refractory to conventional therapy were given high dosages of furosemide (250 to 4000 mg/d) because of significantly reduced renal function (mean endogenous creatinine clearance, 0.53 mL/s/1.73 m2 [32 mL/min/1.73 m2]). Natriuresis, weight reduction (mean, 11 kg), and relief of symptoms were achieved in all patients. The mean survival after the start of the high-dose furosemide therapy was 11.3 months (range, 0.5 to 36 months) (n = 35). When this therapy eventually failed, long-term intermittent hemofiltration was performed in eight selected cases, further prolonging survival (mean, 3.0 months). High-dose furosemide therapy and hemofiltration improved the quality of life and prolonged survival. The use of diuretics in congestive heart failure should therefore include treatment with high-dose furosemide, which is effective and can be given over a long period without serious side effects.

Aged↗

PubMedDate not supplied

Standard electrocardiographic and signal-averaged electrocardiographic changes in congestive heart failure.

A 54-year-old man with congestive heart failure and peripheral edema was monitored during treatment with serial electrocardiograms (ECGs) and two signal-averaged ECGs. Weights and a host of ECG parameters were monitored. ECGs recorded in the 5 years before his index admission were also considered in the quantitative ECG analysis. Amelioration of his peripheral edema was associated with reduction of his weight and increase in the QRS and P-wave amplitudes, and duration in QRS complexes and QT intervals in the ECGs, but unchanged signal-averaged ECGs. This case report provides insight into the mechanism of the change in QRS duration in ECGs during changing edematous states resulting from clinical deterioration or improved compensation in patients with congestive heart failure.

Body Weight↗

PubMedDate not supplied

Fixed-dose combination diuretics in congestive heart failure: an evaluation.

Thirty-two patients with congestive heart failure were studied for their clinical and biochemical responses to the administration of two combination diuretic products (hydrochlorothiazide/spironolactone and hydrochlorothiazide/triamterene) and the single entity diuretic furosemide. Data from these studies revealed the following: 1. Comparison of the patients on furosemide with those receiving the combination products showed no difference in serum potassium or 24-hour potassium excretion. 2. Significant changes in blood urea nitrogen, plasma renin activity, and urinary aldosterone excretion were noted with both fixed-combination medications but not with furosemide. 3. The combination diuretics offered no clinical benefits over the single agent furosemide. 4. Therapy is best served by the use of a single effective diuretic agent for the treatment of most patients with congestive heart failure.

Blood Urea Nitrogen↗

PubMed1988

Diagnostic heterogeneity in clinical trials for congestive heart failure.

There are no uniform diagnostic criteria for congestive heart failure. To determine the pattern of diagnostic criteria used, reports of 51 randomized, double-blind, placebo-controlled, clinical drug trials published between 1977 and 1985 were reviewed. Only 23 (45%) of the trials specified objective diagnostic criteria beyond treatment history, clinical diagnosis, or functional class. Of these, there were two trials each for digoxin, hydralazine, amrinone, and metoprolol; for each pair, only one study showed therapy beneficial. Of the amrinone pair, the positive study required a lower ejection fraction (less than 30% compared with less than 45%) and selected patients with more clinical severity. Conversely, for metoprolol, the positive study specified a higher ejection fraction (less than 49% compared with less than 35%) and selected patients with clinically milder disease, suggesting that conflicting results may relate to differences in study population. Many studies of congestive heart failure are done without explicit diagnostic criteria. Criteria lack uniformity, and such discrepancies may explain conflicting results.

Amrinone↗

PubMed2000

Cardiovascular drug therapy in patients with hepatic diseases and patients with congestive heart failure.

Hepatic impairment can alter the pharmacokinetic profiles of cardiovascular drugs, which can lead to unwanted toxicity. In the presence of cirrhosis, portosystemic shunting occurs and cytochrome P450 activity is reduced. Impaired oxygen uptake caused by changes in the liver's sinusoids, as proposed by the oxygen limitation theory, may also explain the alteration of drug metabolism seen in cirrhosis. With congestive heart failure, sinusoidal congestion and hypoperfusion of the liver are seen. Similar to cirrhosis, the common pathway for hepatic damage in congestive heart failure seems to be liver hypoxia, which may explain the disease's effect on drug metabolism. Since routine hepatic function tests do not always relate to the liver's ability to eliminate drugs, existing guidelines for dosing cardiovascular drugs in patients with hepatic impairment are limited. This article provides guidance for dosing cardiovascular drugs in cirrhotic and heart failure patients based on available research data. Altered drug metabolism, especially in congestive heart failure, tends to be overlooked or not realized in clinical practice. Therefore, further research is needed in congestive heart failure to better elucidate safe prescribing patterns.

Cardiovascular Agents↗

PubMed1986

Role of the kidney in congestive heart failure.

The changes in renal function observed in congestive heart failure include altered pressures and flows and increased reabsorption of sodium and water leading to expanded extracellular fluid volume. These renal effects are mediated by a variety of volume and pressure sensors that stimulate various effectors which act on the kidney. The role of these sensors and effectors, the relationship between left ventricular function (LVF) and urinary sodium excretion (UNaV) and the role of angiotensin II in mediating the renal hemodynamic changes are reviewed. Rats with experimentally induced myocardial infarction (MI) were studied 3 weeks after infarction. Although UNaV decreased as LVF worsened, the decrease in UNaV was evident even in rats with MI and minimal LVF impairment. Infusion of teprotide (an inhibitor of angiotensin I converting enzyme) returned the hemodynamic parameters to or toward values seen in rats without MI, thereby documenting an important role for angiotensin II in congestive heart failure.

Angiotensin II↗

PubMed1994

[Body fluid withdrawal with isolated ultrafiltration effects persistent improvement of functional capacity in patients with chronic congestive heart failure. Furosemide does not produce the same result].

In moderate congestive heart failure pulmonary overhydration may be detected at chest X-ray even if therapy is optimized to keep the urinary output normal and to prevent weight gain and dependent edema formation. Removal of overhydration of the lung may help to define its significance. This study was aimed at investigating whether a subclinical accumulation of fluid in the lung interstitium in moderate congestive heart failure interferes with the patient's functional capacity, and whether furosemide is able to promote reabsorption of the excessive fluid. Patients whose digoxin, oral furosemide and ACE-inhibitor therapeutic regimen was kept constant, were randomly allocated to ultrafiltration (8 cases) or iv bolus (mean dose = 248 mg) of supplemental furosemide (8 cases). The amount of body fluid removed with each method approximated 1.600 ml. Functional performance was assessed with cardiopulmonary exercise tests. Soon after fluid withdrawal with either procedure the filling pressures of the two ventricles and body weight were reduced and plasma renin activity, norepinephrine and aldosterone were augmented. After furosemide hormones remained elevated in the subsequent 4 days, and, during this period, patients had positive water metabolism, recovery of the elevated ventricular filling pressures, recurrence of lung congestion without any improvement in functional capacity. In ultrafiltrated patients, renin, norepinephrine and aldosterone fell below control values within the first 48 hours and water metabolism was equilibrated at a new set point (less fluid intake and diuresis without weight gain). Functional capacity in these patients was improved through favorable circulatory and ventilatory adjustments consequent on reabsorption of lung water. This may also have restored the ability of the lung to clear norepinephrine, thus restraining its facilitation of renin release. Improvement persisted at 3 months after the procedure. In congestive heart failure the set point of fluid balance is altered despite oral furosemide; supplemental iv furosemide does not shift the set point, at least in the presence of ACE-inhibition; excessive, although silent, lung water limits the functional capacity of the patient.

Aged↗

PubMed1994

Short-term effects of naloxone on hemodynamics and baroreflex function in conscious dogs with pacing-induced congestive heart failure.

OBJECTIVES: The purpose of this study was to determine the effects of naloxone on systemic hemodynamics and reflex function in dogs with congestive heart failure induced by rapid pacing. BACKGROUND: We have shown previously that naloxone, an opiate receptor antagonist, improves cardiac output, aortic blood pressure, systolic performance and the baroreflex function in conscious dogs with chronic right-sided congestive heart failure. However, whether endogenous opioids also play a role n mediating the reduction of myocardial and baroreflex function in animals with left heart failure remains controversial. METHODS: We administered naloxone (1 mg/kg body weight) and normal saline solution to 15 dogs with pacing-induced congestive heart failure (225 beats/min for 8 weeks) and 11 control dogs. In addition to systemic hemodynamic measurements, the slope of pressure-area relation obtained from echocardiography with intravenous bolus injection of phenylephrine was taken as a load-independent index of myocardial contractility. Baroreflex function was estimated by the slope of the regression line relating systolic aortic pressure and RR interval. RESULTS: Plasma beta-endorphin levels were elevated in dogs with congestive heart failure. Naloxone administration increased heart rate, mean aortic pressure, first derivative of left ventricular pressure, cardiac output and myocardial contractility in pacing-induced congestive heart failure. These changes correlated significantly with basal plasma beta-endorphin levels and were accompanied by increases in plasma beta-endorphin and catecholamines after naloxone administration. However, unlike the hemodynamic and cardiac effects of naloxone, baroreflex function did not change after naloxone in dogs with congestive heart failure. CONCLUSIONS: The increase in basal plasma beta-endorphin suggests that the endogenous opiate system is activated in left-sided congestive heart failure. Because naloxone improves the systemic hemodynamics and myocardial contractile function under this condition, the endogenous opioids appear to play an important role in mediating the myocardial depression that occurs in heart failure. However, the endogenous opiate system has no apparent effect on the regulation of baroreflex control in heart failure induced by rapid pacing.

Animals↗

PubMed1998

Mesangiolytic glomerulopathy in severe congestive heart failure.

To study the glomerular morphological abnormalities in congestive heart failure (CHF), we analyzed 27 autopsy cases without other causes of renal disease. Their mean age was 59 years, and they showed mild prerenal azotemia. They had generally been treated with digitalis and diuretics, and a few of them with captopril or nifedipine. The abnormal glomerular findings of enlargement, hyperemia, and mesangial thickening were observed at high frequencies (61%, 64%, and 57%, respectively). They characteristically showed mesangiolysis (ML) by the findings of microaneurysms (81%) and mesangial degeneration (70%) such as loose reticular matrix and poor matrix area. In addition, glomerular infiltration of mononuclear leukocytes including macrophages was noted in 70% of the cases. Glomerular enlargement was not correlated with the grade of hyperemia, but it was correlated with the grade of ML index of % glomeruli with microaneurysms (F = 7.22, p < 0.004). There was an inverse relationship between the grades of mesangial thickening and of the ML index (P < 0.005). The number of glomerular leukocytes was positively correlated with mean glomerular size (P < 0.002) and with the ML index (P < 0.03). Notably, the glomerular macrophage-positive cases showed a prominently higher mean ML index than the negative cases (P < 0.005). There was an inverse correlation between the mean glomerular size and the partial oxygen pressure in arterial blood (PaO2; P < 0.01), and a positive correlation between the mean glomerular size and hematocrit (Hct) levels (P < 0.02). The cases positive for mesangiolytic mesangial degeneration showed significantly lower PaO2 values than the cases negative for this lesion (P < 0.04). In the analysis of the various causes of CHF, the patients with congenital cardiac anomalies showed mean levels of the lowest PaO2 (P < 0.02) and the highest Hct (P < 0.03) and histologically the largest mean glomerular size (P < 0.04). There was no difference in the ML index and the glomerular leukocyte number among the subgroups classified by the causes. These results indicate that ML associated with glomerular enlargement is the major glomerular abnormality characteristic in patients with severe CHF and suggest that glomerular infiltration of leukocytes, especially of macrophages, should play an important role in the progression of both ML and glomerulomegaly. The contributions of persistent hypoxia and up-regulated angiotensin II as the causative factors of these glomerular abnormalities in congestive heart failure are discussed.

Adult↗

PubMedDate not supplied

Pharmacokinetics and pharmacodynamics of enalapril in patients with congestive heart failure and patients with hypertension.

The clinical pharmacokinetics and pharmacodynamics of enalapril and its de-esterified active metabolite, MK 422, were determined in eight patients with congestive cardiomyopathy and five patients with hypertension. After administration of single doses of 2.5, 5, and 10 mg enalapril in the congestive heart failure patients and 20 or 40 mg in the hypertensive patients, serum levels and urine elimination of enalapril and MK 422 were determined. Standing and supine heart rate and blood pressure were measured as was ejection fraction in the congestive heart failure group and renin activity, aldosterone levels, and converting enzyme activity in the hypertensive group. Apparent oral clearance after administration of 5 and 10 mg enalapril was lower in the congestive heart failure patients (0.6 +/- 0.2 and 0.7 +/- 0.4 L/min) than after 20 and 40 mg given to hypertensive patients (2.5 +/- 1.3 and 2.7 +/- 2.7 L/min). The elimination of MK 422 was also slower in the congestive heart failure patients (7.8 +/- 5.0 and 6.8 +/- 2.5 h after 5 and 10 mg enalapril, respectively, vs. 4.6 +/- 2.0 and 5.3 +/- 1.1 h after 20 and 40 mg, respectively, in the hypertension group). The enalapril area under the concentration-time curve increased disproportionately to dose increments in both groups, but was more pronounced in congestive heart failure. Twenty and 40 mg enalapril lowered the blood pressure by 2 h after dosing in the hypertension group, and peak effects were seen 4-5 h after dosing. Peak effects correlated with peak serum MK 422 concentrations but not with enalapril (MK 421) levels. Supine heart rates were unchanged after 20 mg, but increased after 40 mg; standing heart rates were transiently increased after 20 and 40 mg enalapril. Blood pressure was not significantly changed in the congestive heart failure group, and cardiac ejection fraction was unchanged. In the hypertension group, renin stimulation and converting enzyme activity inhibition were seen at 4 h and persisted for at least 24 h after administration of 40 mg enalapril. In summary, the clearance of enalapril and elimination of MK 422 was slower in congestive heart failure patients versus hypertensive patients. Therefore, slower onset and longer duration of drug effect might be anticipated in patients with congestive heart failure versus patients with hypertension during enalapril administration.

Adult↗