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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↗
PubMed1980

Effects of amrinone on myocardial energy metabolism and hemodynamics in patients with severe congestive heart failure due to coronary artery disease.

Amrinone has been shown to exhibit a potent inotropic effect in patients with heart failure secondary to congestive cardiomyopathy, but its effects on myocardial oxygen consumption (MVO2) and coronary blood flow (CBF) are unknown. Accordingly, the hemodynamic, myocardial metabolic and ECG responses to amrinone (2.5 mg/kg i.v. over 1 hour) were measured in nine patients with congestive heart failure secondary to coronary artery disease. Increases were observed in cardiac index (1.3 +/- 0.4 to 2.2 +/- 0.7 l/min/m2) and left ventricular stroke work (10.6 +/- 3.0 to 19.2 +/- 6.3 g-m/m2), and decreases in mean pulmonary wedge (31 +/- 5 to 26 +/- 4 mm Hg), mean pulmonary artery (44 +/- 8 to 36 +/- 7 mm Hg) and mean right atrial pressures (18 +/- 4 to 10 +/- 4 mm Hg), myocardial arteriovenous oxygen difference (129 +/- 19 to 109 +/- 17 ml/l), CBF (215 +/- 117 to 178 +/- 84 ml/min) and MVO2 (27 +/- 14 to 19 +/- 9 ml/min). All changes were significant (p less than 0.01). No significant changes occurred in aortic mean pressure, heart rate, myocardial lactate extraction or ECG, and no patient developed angina. In explaining the decline in MVO2, it is possible that the increase in contractility was more than offset by the reductions in preload and afterload. The amrinone-induced hemodynamic improvement in patients with congestive heart failure secondary to coronary artery disease was associated with reductions in MVO2 and CBF and no evidence of myocardial ischemia.

Aged↗
PubMed1997

Pacing mode and long-term survival in elderly patients with congestive heart failure: 1980-1985.

Dual-chamber pacing may improve short-term hemodynamics and functional class in some patients with congestive heart failure, even in the absence of conventional indications for pacemaker implantation. However, the impact of different pacing modes on survival of patients with congestive heart failure is controversial. In this retrospective study we analyzed survival data from 546 elderly patients, aged 70 years and older, who underwent implantation of a permanent dual-chamber (DDD, n = 62, DVI, n = 102) or single-chamber (VVI) pacemaker (n = 382) between 1980 and 1985. Survival was further analyzed according to the presence of absence of congestive heart failure, and pacemaker mode (DDD vs. DVI vs. VVI). Overall, dual-chamber pacing (DDD and DVI) was associated with a more favorable long-term outcome when compared with single-chamber ventricular pacing, although differences were only significant for DDD pacing (P = 0.002). When patients with and without preexisting congestive heart failure were analyzed separately, survival following dual-chamber pacing (DDD and DVI) was significantly better than survival following single-chamber pacing in patients without congestive heart failure (P = 0.03), but not in patients with preexisting heart failure (P = 0.139). When patients were analyzed according to the electrophysiological indication for pacemaker implantation, overall survival of patients with AV block (P = 0.0025) but not sinus node dysfunction (P = 0.346) was improved with dual-chamber pacing. This survival advantage in patients with AV block following dual-chamber pacing was lost in the presence of heart failure (P = 0.11). These findings suggest that dual-chamber pacing, in particular DDD pacing, improves the survival in elderly patients without preexisting congestive heart failure. In contrast to the short-term hemodynamic improvement observed in selected patients with congestive heart failure, dual-chamber pacing in elderly patients with congestive heart failure, paced for conventional indications, is not associated with improved survival when compared with single-chamber ventricular pacing.

Aged↗
PubMed2004

[Use of antihypertensive drug therapy and risk of development of congestive heart failure].

BACKGROUND AND OBJECTIVE: It has been suggested that the use of some antihypertensive agents may favour the development of congestive heart failure. The aim of the present study was to evaluate such a possible association in patients who had a new diagnosis of congestive heart failure. PATIENTS AND METHOD: This was a retrospective case-control study of 81 patients who had a first hospital admission with a new diagnosis of congestive heart failure (cases) and 162 patients admitted for other hypertensive complications (controls). Previous antihypertensive drug use was registered and the possible association with congestive heart failure was evaluated. RESULTS: The presence of congestive heart failure was not associated with the use of any antihypertensive drug class. When treatments were grouped in classic (diuretics and betablockers) or modern (calcium channel blockers, angiotensin-converting-enzyme inhibitors, alphablockers or angiotensin receptor blockers), a negative association was observed with the latter group, which was observed in 48.1% of cases and 63.6% of controls (odds ratio: 0.532; 95% confidence interval, 0.310-0.913). This association was lost after adjustment for other cardiovascular risk factors or previous hypertensive complications. CONCLUSIONS: The development of congestive heart failure was not associated with the use of any specific antihypertensive drug class. From the present evidence, it is not possible to recommend a specific antihypertensive agent in patients at risk of developing congestive heart failure but without evidence of such disease.

Aged↗
PubMed1993

Beneficial effect of ACE inhibitor in congestive heart failure.

The effects of captopril, an angiotensin-converting enzyme inhibitor, on congestive heart failure (CHF) were investigated in animal and clinical studies. Congestive heart failure was induced in rats by a combination of pressure and volume overload. Cardiac pressure overload was induced by constricting one renal artery (Goldblatt rat) and volume overload was induced by aorto-caval fistula. Captopril (100 mg/kg/day) was then administered for 14 weeks. Isometric contraction was assessed using isolated left ventricular papillary muscles. The maximum developed tension and the maximum rate of increase in tension (dT/dtmax) were decreased in untreated rats with CHF and improved in captopril-treated rats. The left ventricular myosin isoenzyme pattern was shifted towards V3 in untreated rats with CHF, and was shifted back towards V1 in the captopril-treated rats. In the clinical study, captopril (37.5-75 mg/day) was administered to patients with cardiomyopathy for 12 months. There was no effect on left ventricular mass in hypertrophic cardiomyopathy, although systolic anterior motion of the mitral valve disappeared in one patient. In dilated cardiomyopathy, however, left ventricular mass tended to decrease. These results indicate that captopril has a beneficial effect in congestive heart failure.

Animals↗
PubMed2001

Effects of ambient air pollution on daily mortality in a cohort of patients with congestive heart failure.

This study was planned to test the hypothesis that patients with congestive heart failure are more susceptible to the harmful effects of ambient air pollution than the general population. We used both general additive Poisson regression and the case-crossover approach to test the hypothesis. The effect of air pollution on daily mortality of patients with congestive heart failure among residents of Seoul, South Korea, during the period 1994--1998 was compared with that of the general population in the same area and the same period. The odds ratios and 95% confidence intervals (95% CIs) estimated from general additive models in the general population for an interquartile range increase of particulate matter less than 10 microm in diameter (42.1 microg/m(3)), carbon monoxide (0.59 ppm), nitrogen dioxide (14.6 ppb), sulfur dioxide (9.9 ppb), and ozone (20.5 ppb) were 1.014 (95% CI = 1.006- 1.022), 1.022 (95% CI = 1.017- 1.029), 1.021 (95% CI = 1.014- 1.029), 1.020 (95% CI = 1.012--1.028), and 1.010 (95% CI = 1.002--1.017), respectively. The estimated effects appeared larger among the congestive heart failure patients than among the general population (2.5 approximately 4.1 times higher depending on the pollutants). The results from the case-crossover analysis were similar. The finding of a stronger association in the patients with congestive heart failure reinforces the evidence that a harmful effect of air pollution is mediated by cardiovascular mechanisms.

Adult↗
PubMed2000

[Electrolyte abnormalities and metabolic acidosis in two Duchenne muscular dystrophy patients with advanced congestive heart failure].

We experienced two Duchenne muscular dystrophy patients with advanced congestive heart failure, who showed abrupt severe hyponatremia, hyperkalemia and metabolic acidosis. Two patients received respiratory management, parenteral nutrition, and drugs including angiotensin converting enzyme inhibitors (ACEI). The patient 1 who was 19 years old showed abdominal pain, hematuria, diarrhea and disorientation. Laboratory findings were as follows; Na 120 mEq/L, K 7.3 mEq/L, BUN > 140 mg/dl (scale over), ACTH 20.2 pg/ml, cortisol 25 micrograms/dl, renin 40.7 ng/ml/hr and aldosterone 203 ng/dl. Arterial blood gas analysis (ABG) showed metabolic acidosis (pH 7.232). Combination therapy with hydrocortisone, glucose-insulin therapy (GIT) and NaHCO3 successfully rescued this patient. The patient 2 (28 years of age) was admitted to our hospital because of congestive heart failure. Laboratory findings were as follows; Na 129 mEq/L, K 5.5 mEq/L, BUN 60 mg/dl, cortisol 21 micrograms/dl, renin 36 ng/ml/hr and aldosterone 47 ng/dl. He complained abdominal discomforts from the next day of admission. Ten days after the admission Na, K and BUN were 111 mEq/L, 6.2 mEq/L and 154 mg/dl, respectively. ABG showed compensated metabolic acidosis. He fell into shock during GIT therapy. Laboratory findings at that time were as follows; Na 108 mEq/L, K 3.2 mEq/L, ACTH 77.6 pg/ml, cortisol 24 micrograms/dl, renin 58 ng/ml/hr and aldosterone 24 ng/dl. Although hydrocortisone was introduced, he could not recover and died. There are some reports about life-threatening electrolyte abnormalities and metabolic acidosis in the patients receiving ACEI. These phenomena were more frequent in patients with renal dysfunction and/or congestive heart failure. Hyponatremia, hypovolemia, combination therapy with nonsteroidal anti-inflammatory drugs (NSAID) and/or potassium sparing diuretics were reported as risk factors. We could not prove the correlation between the acute changes in our cases and ACEI. However ACEI is suspicious, because many of these risk factors were observed in our cases. Aldosterone was extremely elevated in the patient 1 when potassium was severely elevated. On the other hand, the patient 2 showed lower aldosterone level after correction of potassium than that on admission. Potassium is regarded as a major secretion factor of aldosterone for patients receiving ACEI. The fact the patient 2 fell into shock during GIT, tells us that we should use steroid simultaneously when we try to correct potassium quickly in severe cases, because acute reduction of potassium may decrease aldosterone. Today, ACEI is a common drug for CHF, so we should pay attentions that ACEI could cause such acute changes. To prevent such acute changes, excessive restriction of water and sodium intake should be avoided. If possible, NSAID and potassium sparing diuretics also should be avoided. Steroid therapy must be introduced rapidly when needed.

Acidosis↗
PubMed1999

Renal effects of brain natriuretic peptide in patients with congestive heart failure.

The effect of a continuous infusion of human brain natriuretic peptide, 2 pmol.min-1.kg-1, during 60 min was studied in nine patients with congestive heart failure and in 10 healthy control subjects. Brain natriuretic peptide increased from 1.6 to 101 pmol/l in control subjects and from 25 to 173 pmol/l in congestive heart failure during infusion. Urinary sodium excretion increased significantly in both congestive heart failure (60%) and control subjects (71%), but the absolute increase was significantly lower in congestive heart failure (27 micromol/min) than in control subjects (190 micromol/min). Urinary flow rate did not change. The lithium clearance technique was used to evaluate the segmental tubular function; the distal fractional reabsorption of sodium decreased significantly less in congestive heart failure (DFRNa: -0.8%) than in control subjects (DFRNa: -3.7%). Baseline values for glomerular filtration rate and renal plasma flow were reduced in congestive heart failure, but brain natriuretic peptide induced no significant changes between congestive heart failure and control subjects. Brain natriuretic peptide induced the same absolute increase in secondary messenger cGMP in plasma and urine in both patients and healthy subjects. It is concluded that the natriuretic response to brain natriuretic peptide infusion was impaired in patients with congestive heart failure compared with healthy subjects, and it is likely that the impaired natriuretic response was caused by a reduced responsiveness in the distal part of the nephron.

Adult↗
PubMed1997

Left ventricular dilatation and the risk of congestive heart failure in people without myocardial infarction.

BACKGROUND: Left ventricular dilatation is a well-recognized precursor of ventricular dysfunction and congestive heart failure after myocardial infarction. The effect of left ventricular dilatation on the risk of heart failure in people initially free of myocardial infarction is not known. METHODS: We examined the relation of the left ventricular end-diastolic and end-systolic internal dimensions, as measured by M-mode echocardiography, to the risk of congestive heart failure in 4744 subjects (2083 men and 2661 women) who had not sustained a myocardial infarction and who were free of congestive heart failure. We used sex-stratified proportional-hazards regression to assess the association between base-line left ventricular internal dimensions and the subsequent risk of congestive heart failure, after adjusting for age, blood pressure, hypertension treatment, body-mass index, diabetes, valve disease, and interim myocardial infarction. RESULTS: Over an 11-year follow-up period, congestive heart failure developed in 74 subjects (38 men and 36 women). The risk-factor-adjusted hazard ratio for congestive heart failure was 1.47 (95 percent confidence interval, 1.25 to 1.73) for an increment of 1 SD in the left ventricular end-diastolic dimension, indexed for height. We obtained similar results using the left ventricular end-systolic dimension (hazard ratio, 1.43; 95 percent confidence interval, 1.24 to 1.65). CONCLUSIONS: An increase in left ventricular internal dimension is a risk factor for congestive heart failure in men and women who have not had a myocardial infarction. Knowledge of the left ventricular dimension improves predictions of the risk of congestive heart failure made on the basis of traditional risk factors, perhaps by aiding in the identification of subjects with subclinical left ventricular dysfunction.

Female↗
PubMed1997

Haemodynamic, neuroendocrine and metabolic correlates of circulating cytokine concentrations in congestive heart failure.

OBJECTIVES: Increased activity of pro-inflammatory cytokines in the circulation has been observed in many, though not all, patients with congestive heart failure. To identify the predictors of cytokine activation in congestive heart failure, we assessed the relationship of peripheral and hepatic venous cytokines to central haemodynamics, neuroendocrine status and intermediary metabolism in patients with moderate or severe congestive heart failure. PATIENTS AND METHODS: Concentrations of tumour necrosis factor-alpha, soluble tumour necrosis factor-receptor II and interleukin 6 were measured from peripheral and hepatic venous plasma in 58 adult cardiac patients, of whom 44 had congestive heart failure, undergoing heart catheterization, echocardiography and assessment of selected neuroendocrine and metabolic characteristics. RESULTS: Peripheral venous soluble tumour necrosis factor-receptor II was directly related to NYHA class (rs = 0.46, P < 0.001) and inversely to 6-min walking distance (rs = -0.46, P < 0.001). Peripheral venous tumour necrosis factor-alpha was related to 6-min walking distance (rs = -0.37, P < 0.01), but like soluble tumour necrosis factor-receptor II, was unrelated to other haemodynamic and neuroendocrine measurements. Peripheral venous interleukin 6 correlated with NYHA class (rs = 0.66, P < 0.001) and 6-min walking distance (rs = -0.52, P < 0.001). In addition, interleukin 6 was related to right atrial pressure (rs = 0.55, P < 0.001), pulmonary artery wedge pressure (rs = 0.50, P < 0.001) and left ventricular ejection fraction (rs = -0.39, P < 0.01); in multivariate analysis, only right atrial pressure was an independent predictor of interleukin 6 concentration (P < 0.001). Comparisons between patients with and without congestive heart failure showed significantly higher hepatic venous tumour necrosis factor-alpha, soluble tumour necrosis factor-receptor II and interleukin 6 in the heart failure group; the differences in peripheral venous cytokines were less consistent. CONCLUSIONS: In cardiac patients, increased plasma tumour necrosis factor-alpha and soluble tumour necrosis factor-receptor II are associated with symptoms of heart failure and poor exercise capacity, while the most important predictor of increased interleukin 6 is elevated systemic venous pressure. Different but still unknown mechanisms may be responsible for the increased release of cytokines in congestive heart failure.

Adult↗
PubMed2005

Impact of specialist follow-up in outpatients with congestive heart failure.

BACKGROUND: There is uncertainty about whether physician specialty influences the outcomes of outpatients with congestive heart failure after adjustment for differences in case mix. Our objective was to determine the impact of physician specialty on outcomes in outpatients with new-onset congestive heart failure. METHODS: The study was a population-based retrospective cohort study involving patients with new-onset congestive heart failure discharged from 128 acute care hospitals in Alberta between Apr. 1, 1998, and July 1, 2000. Outcomes were resource utilization (clinic visits, emergency department visits and hospital admissions) and survival at 30 days and 1 year. RESULTS: A total of 3136 patients were discharged from hospital with a new diagnosis of congestive heart failure (median age 76 years, 50% men). Of these, 1062 (34%) received no follow-up visits for cardiovascular care, 738 (24%) were seen by a family physician (FP) alone, 29 (1%) by a specialist (cardiologist or general internist) alone and 1307 (42%) by both a specialist and an FP. Compared with patients who received no follow-up cardiovascular care, patients who received regular cardiovascular follow-up visits with a physician had fewer visits to the emergency department (38% v. 80%), fewer were admitted to hospital (13% v. 94%), and the adjusted 1-year mortality was lower (22% v. 37%) (all p < 0.001). Compared with patients who received combined specialist and FP care, patients cared for exclusively by FPs had fewer outpatient visits (median 9 v. 17 in the first year), fewer of these patients presented to the emergency department (24% v. 45% in the first year), and fewer were readmitted for cardiovascular care (7% v. 16%) (all p < 0.001). However, the adjusted mortality at 1 year was lower among patients treated with combined care (17% v. 28%, p < 0.001) despite a higher burden of comorbidities. In a multivariate model adjusting for comorbidities (with no cardiovascular follow-up visits as the reference category), the mortality was lower among patients followed on an outpatient basis by an FP alone (odds ratio [OR] 0.66, 95% confidence interval [CI] 0.53-0.82) or by an FP and a specialist (OR 0.34, 95% CI 0.28-0.42). In a proportional hazards model with time-dependent covariates (with adjustment for frequency of follow-up visits), the risk of all-cause mortality was reduced significantly (hazard ratio 0.98, 95% CI 0.97- 0.99) with each specialist visit compared with FP care alone. INTERPRETATION: Patients with congestive heart failure followed by both specialists and FPs had significantly better survival than those followed by FPs alone (or those who received no specific cardiovascular follow-up care). Methods to improve timely and appropriate access to specialists and to improve collaborative care structures are needed.

Aged↗
PubMed1986

The effects of two new inotropic agents on microsomal liver function in patients with congestive heart failure.

The aminopyrine breath test (APBT) was used to study patients with chronic congestive heart failure before and after treatment with two chemically similar inotropic agents, amrinone (AR) and milrinone (MR), to determine their effects on hepatic microsomal function. Liver chemistries and cardiac indices were measured and correlated with the 2-hour APBT score in 11 patients with chronic congestive heart failure (5 treated with AR, 6 with MR) and five healthy control subjects. Despite normal or near-normal liver chemistries, patients with chronic congestive heart failure demonstrated overall depressed hepatic microsomal oxidative function. Patients with severe congestive heart failure had a lower mean pretreatment APBT score (AR = 3.05 +/- 1.02, MR = 5.38 +/- 3.09) when compared with healthy controls (10.02 +/- 1.02). However, the APBT score for each individual could not be predicted from the cardiac index. Although the mean cardiac index increased significantly in both the AR and the MR treated patients by 26.14% +/- 15.28 (p less than 0.01) and 40.0% +/- 42.27 (p less than 0.025), respectively, compared with pretreatment values, the mean APBT score fell by 62.02% +/- 22.5 (p less than 0.005) in the former and increased by 38.35% +/- 25.69 (p less than 0.01) in the patients receiving MR. This discordance between the effects of AR and MR suggests possible differences in the effects of the two drugs on hepatic microsomal function.

Adult↗
PubMed2005

Right heart failure after left ventricular assist device implantation in patients with chronic congestive heart failure.

BACKGROUND: Right heart failure (RHF) is not an infrequent complication of left ventricular assist device (LVAD) implantation. Few studies have examined outcomes for LVAD patients who subsequently develop RHF. This study details one center's experience with RHF in chronic congestive heart failure (CHF) patients. METHODS: One hundred eight patients with chronic CHF (>or=6 months) who underwent HeartMate LVAD implantation were identified during June 1996 to July 2004. Acute heart failure patients requiring LVADs were excluded to eliminate the impact of confounding non-cardiac factors. RHF was defined as the need for a subsequent right ventricular assist device (RVAD), >or=14 days of intravenous inotropes/pulmonary vasodilators, or both. Forty-two (38.9%) RHF patients were identified. Fourteen of these required RVAD insertion. Outcome parameters included early (<or=30-day) mortality, intensive care unit (ICU) length of stay (LOS), incidence of re-operation for bleeding and acute renal failure, and stroke, bridge-to-transplantation rate and post-transplantation survival rate. RESULTS: More female patients developed RHF than not (73.3% vs 26.7%, p = 0.003). RHF patients had a higher early mortality rate, greater ICU LOS, higher rates of re-operation for bleeding and renal failure, and lower bridge-to-transplantation rate than non-RHF patients (19.0% vs 6.2%, p = 0.039; 23.8 +/- 23.7 vs 9.6 +/- 7.1 days, p < 0.001; 38.9% vs 18.3%, p = 0.026; 61.0% vs 22.6%, p < 0.001; 65.0% vs 89.9%, p = 0.003; respectively). Fourteen (33.3%) RHF patients required RVAD insertion. Elevated intra-operative central venous pressure (CVP) was found to be an independent predictor of post-LVAD RHF. Overall bridge-to-transplantation rate for the entire study cohort was 73.1%. CONCLUSIONS: The development of RHF after LVAD insertion confers significant morbidity and mortality. Judicious application of inotropes and pulmonary vasodilators and timely RVAD insertion, if necessary, should be maintained. Further investigations evaluating pre- and intra-operative risk factors for the development of RHF are warranted.

Adult↗
PubMed1990

Low sodium content formula for infants with congestive heart failure.

Twenty-two infants of isolated ventricular septal defect with congestive heart failure were fed with lower-sodium content formula-Lonalac (Mead-Johnson) to study the clinical response of treatment for congestive heart failure. There were no significant changes of intake, urinary output, serum sodium, potassium and osmolality before, 2 days and 6 days after Lonalac feeding. The low sodium content formula may feed the infants with congestive heart failure in addition to the traditional anticongestive therapy.

Diet, Sodium-Restricted↗
PubMed1987

Cardiac and plasma atrial natriuretic factor in experimental congestive heart failure.

The cardiac and plasma levels of immunoreactive (IR-) atrial natriuretic factor (ANF) in cardiomyopathic hamsters with moderate and severe congestive heart failure were measured, compared with those of controls, and correlated by HPLC analysis of IR-ANF in atria, ventricles, and plasma and with the ultrastructure of atrial and ventricular cells. Congestive heart failure in the hamster produced a significant increase in plasma IR-ANF, a significant decrease in atrial IR-ANF, and a marked increase in ventricular IR-ANF. The HPLC pattern of IR-ANF was of the high mol wt type in atria and ventricles of control and cardiomyopathic animals. High mol wt forms of ANF appeared in the plasma of animals with severe congestive heart failure, but not in controls. Severe congestive heart failure produced a tremendous increase in the size of the Golgi complex, with a decrease in the number and size of secretory granules in atrial cardiocytes. Ventricular cardiocytes also showed a less marked increase in the size of the Golgi complex. Secretory-like granules indistinguishable from lysosomes were present in about 1% of ventricular cardiocytes of control hamsters; in hamsters with severe congestive heart failure, secretory granules, identical to those of atrial cardiocytes, were present in greater number in about 20% of ventricular cardiocytes. Immunocytochemistry (immunogold technique) revealed that secretory granules containing IR-ANF are not present in control ventricular cardiocytes but are localized in relatively large number in about 20% of ventricular cardiocytes in hamsters with severe congestive heart failure. These results suggest that the increased IR-ANF levels (including the high mol wt forms) in animals with congestive heart failure may come from hypersecretion of both atrial and ventricular cardiocytes.

Animals↗
PubMed1995

The potential role of calcium antagonists in the management of congestive heart failure: initial experience with lacidipine.

First-generation calcium antagonists have been used in patients with congestive heart failure with rather disappointing results. Therefore, second-generation dihydropyridine calcium-channel blockers, such as felodipine and lacidipine, have been developed that may be beneficial in congestive heart failure owing to their high vasoselectivity and more favorable neurohumoral modulation. The effects of lacidipine in patients with congestive heart failure, who remain symptomatic despite receiving long-term therapy with angiotensin-converting enzyme inhibitors, digoxin, and diuretics, were investigated during a prospective, double-blind, randomized, placebo-controlled, parallel-group study. Twenty-five patients were randomized to receive either lacidipine (4 mg once daily; 12 patients) or placebo (once daily; 13 patients). After 8 weeks of treatment patients receiving lacidipine showed a significantly higher increase in cardiac output (p < 0.01), and a significantly greater reduction in vascular resistance (p < 0.02) than those patients in the placebo group. No significant changes were observed in filling pressures and heart rate. The arteriovenous oxygen content difference was significantly reduced in the lacidipine group (p < 0.01) without significant changes in arterial oxygenation, suggesting an increase in flow that was not a result of pulmonary shunting. Further peak oxygen consumption during cardiopulmonary exercise testing increased significantly in the lacidipine patients (p < 0.02). These beneficial effects were achieved without significant changes in neurohumoral parameters. Analysis of right and left ventricular ejection fractions revealed no cardiodepressant effects. Lacidipine was well tolerated during the course of the study, and adverse reactions were minor. These data suggest that lacidipine has a promising profile for the treatment of congestive heart failure patients, and that further investigation with second-generation dihydropyridines in the field of congestive heart failure appears warranted.

Aged↗
PubMed2006

Impact of the history of congestive heart failure on the utility of B-type natriuretic peptide in the emergency diagnosis of heart failure: results from the Breathing Not Properly Multinational Study.

PURPOSE: B-type natriuretic peptide is known to correlate with hemodynamic state, presence and severity of congestive heart failure, and prognosis. Although low-range B-type natriuretic peptide less than 100 pg/mL has a high negative predictive value (90%), and high-range B-type natriuretic peptide greater than 500 pg/mL has a high positive predictive value (87%), there remains some ambiguity in the interpretation of results in the medium range (100-500 pg/mL). We hypothesized that taking into account the history of congestive heart failure along with other clinical variables would be helpful in this range of B-type natriuretic peptide levels. METHOD: The Breathing Not Properly Multicenter Study was an international, 7-center, prospective study including 1475 patients with a mean age of 63 years (57% were male, and 54% were female); 35% of patients with a history of congestive heart failure were enrolled, and a final diagnosis of congestive heart failure was made in 46%. The index criteria was defined as positive if any 2 index findings (ie, history of coronary artery disease, lower extremity edema, pulmonary edema, cephalization of the pulmonary arteries, and cardiomegaly) were present. RESULTS: The interval likelihood ratios (LR) for low, medium, and high B-type natriuretic peptide ranges are 0.13, 1.85, and 8.1, respectively. For medium B-type natriuretic peptide levels a positive history of congestive heart failure makes the diagnosis of congestive heart failure more probable with a cumulative LR of 4.3. Also in this range a positive index criterion was strongly indicative of congestive heart failure even in the absence of a history of congestive heart failure (LR 3.3). Where there are both a positive history of congestive heart failure and a positive index criteria for the medium B-type natriuretic peptide group, the cumulative LR (10.2) is similar to that of a high B-type natriuretic peptide level (8.1). CONCLUSION: Even in the medium range (100-500 pg/mL), when using the history of congestive heart failure and index criteria, B-type natriuretic peptide can be a powerful diagnostic tool in the hands of clinicians in the emergency department.

Aged↗