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At least 19 recordsLinked to original sources

PubMed1985

[Effect of aortocoronary bypass surgery on left ventricular function and coronary sinus blood flow in patients with severe left ventricular dysfunction].

Left ventricular function and coronary sinus blood flow were evaluated in 7 patients with severe left ventricular dysfunction at rest before and after aortocoronary bypass surgery, and during exercise after surgery. Same evaluations were performed in 8 normal subject (G-C). Cardiac index (CI) at rest (2.09 +/- 0.55 l/min/m2) significantly increased after operation (2.94 +/- 0.59 l/min/m2) (p less than 0.02). There was no difference between CI during exercise after operation (5.94 +/- 1.51 l/min/m2) and that in G-C. Left ventricular end-diastolic pressure (LVEDP) at rest before operation (16 +/- 8 mmHg) was significantly higher than that in G-C (p less than 0.05). This difference disappeared after operation. LVEDP during exercise after operation (25 +/- 10 mmHg) was significantly higher than that in G-C (p less than 0.01). Coronary sinus blood flow (CSF) at rest (73 +/- 15 ml/min) significantly increased after operation (123 +/- 44 ml/min) (p less than 0.02). There was no difference between CSF during exercise after operation (282 +/- 99 ml/min) and that in G-C. These data indicated that the aortocoronary bypass surgery was effective on left ventricular function and coronary sinus blood flow in patients with severe left ventricular dysfunction.

Adult↗

PubMed1990

Circulatory support in infants with post-cardiopulmonary bypass left ventricular dysfunction using a left ventricular assist device.

Extracorporeal membrane oxygenation has been advocated as the most appropriate mode of circulatory support in the paediatric age group for post-cardiopulmonary bypass ventricular dysfunction. The results in infants who have predominantly left ventricular failure, or who require such support in order to be weaned off bypass, have been disappointing. Three infants with severe left ventricular dysfunction following cardiopulmonary bypass for correction of congenital heart defects have been managed with a left ventricular assist device. Two required this form of circulatory support in order to be weaned from full bypass while in the third infant it was instituted for progressive left ventricular dysfunction postoperatively. All three were less than 10 kg in weight. Left atrial appendage to aortic bypass was effected using a closed loop circuit with a constrained vortex pump (Biomedicus). Duration of support ranged between 40 and 146 h. One infant made a complete recovery and was able to be discharged home 20 days postoperatively. Another made a circulatory recovery such that both mechanical and inotropic support could be discontinued but had sustained massive neurological damage. The third died of progressive left ventricular dysfunction. This experience with a left ventricular assist device demonstrates that it is technically feasible in small infants, and can be performed to good effect in infants with predominant left ventricular dysfunction following cardiac surgery. It may well be more appropriate than extracorporeal membrane oxygenation in this group of patients.

Cardiac Output, Low↗

PubMed1993

Activation of neurohumoral systems in postinfarction left ventricular dysfunction.

OBJECTIVES: This study was conducted to evaluate the degree of neurohumoral activation around the time of hospital discharge after myocardial infarction. BACKGROUND: Because pharmacologic interventions that block the effects of neurohumoral activation improve the prognosis after infarction, we hypothesized that widespread neurohumoral activation persists in some patients until at least the time of hospital discharge and that the determinants of activation vary from one system to another. METHODS: Five hundred nineteen patients in the Survival and Ventricular Enlargement Study (SAVE) had plasma neurohormones measured before randomization at a mean of 12 days after infarction. All patients had left ventricular dysfunction (left ventricular ejection fraction < or = 40%) but no overt heart failure. RESULTS: Although all neurohormones except epinephrine were increased compared with values in age-matched control subjects, plasma norepinephrine (301 +/- 193 vs. 222 +/- 87 pg/ml, p < 0.001), renin activity (3.0 +/- 3.7 vs. 1.2 +/- 1.2 ng/ml per h, p < 0.001), arginine vasopressin (1.9 +/- 6.9 vs. 0.7 +/- 0.3 pg/ml, p < 0.001) and atrial natriuretic peptide (75 +/- 75 vs. 21 +/- 9 pg/ml, p < 0.001) values ranged from normal to very high, indicating a wide spectrum of neurohumoral activation. Activation of one system did not correlate with activation of another. The clinical and laboratory variables most closely associated with neurohumoral activation were Killip class, left ventricular ejection fraction, age and use of diuretic drugs. The association between neurohumoral activation and clinical and laboratory variables varied from one neurohormone to another. CONCLUSIONS: Neurohumoral activation occurs in a significant proportion of patients at the time of hospital discharge after infarction. Which neurohormone is activated and which clinical and laboratory variables determine this activation vary from one neurohormone to another.

Aged↗

PubMed1991

Experimental model of chronic global left ventricular dysfunction secondary to left coronary microembolization.

A model of chronic left ventricular dysfunction characterized by left ventricular dilation, elevated filling pressures and histologic changes has been lacking. In this study the use of coronary microsphere embolization-induced ischemia was explored as a method of producing chronic left ventricular dysfunction. Acute ischemic left ventricular dysfunction was induced in 13 mongrel dogs with 50 microns plastic microspheres until the peak positive first derivative of left ventricular pressure (dP/dt) decreased by 25% and the left ventricular end-diastolic pressure increased to greater than or equal to 12 mm Hg. After 8 weeks of observation, hemodynamic and echocardiographic variables were measured in each dog. Acute left ventricular dysfunction resulted in a dilated left ventricle with systolic dysfunction (area ejection fraction 24 +/- 6% vs. 57 +/- 9% initially, p less than 0.01) and elevated left ventricular filling pressures. Isovolumetric relaxation was prolonged and the peak rapid filling/atrial filling velocity and integral ratios were reduced. Eight weeks after embolization, there was an increased left ventricular size (end-diastolic area 15.1 +/- 2.1 cm2 at 8 weeks vs. 13.5 +/- 1.4 cm2 early after microsphere injection, p less than 0.05), unchanged end-systolic area, improved area ejection fraction and increased left ventricular mass. Left ventricular end-diastolic pressure increased and, despite continued abnormal relaxation, the peak rapid filling/atrial filling velocity and integral ratios increased to above baseline values, demonstrating a "restrictive" pattern. Gross and histologic examination revealed diffuse, patchy scarring associated with perivascular fibrosis. Thus, coronary microsphere embolization resulted in a model of chronic moderate left ventricular systolic dysfunction and abnormal diastolic function characterized by a "restrictive" filling pattern.

Animals↗

PubMed1992

Characteristics of peak aerobic capacity in symptomatic and asymptomatic subjects with left ventricular dysfunction. The Studies of Left Ventricular Dysfunction (SOLVD) Investigators.

Expired gas analysis was used to determine the aerobic exercise performance of subjects with depressed left ventricular (LV) systolic function and congestive heart failure (CHF). To determine whether subjects with no or minimal CHF have better aerobic exercise performance than do those with overt CHF, oxygen consumption (VO2) at anaerobic threshold (AT) and peak exercise was measured in 184 subjects with LV ejection fraction less than or equal to 0.35 who participated in the Studies of Left Ventricular Dysfunction. Subjects were divided into those with overt CHF needing treatment (treatment trial; n = 20) and those who had neither overt CHF nor treatment for CHF (prevention trial; n = 164). Treatment trial subjects had a lower LV ejection fraction (0.25 +/- 0.07) than did prevention trial ones (0.29 +/- 0.05; p = 0.001), but there were no differences in age, gender, body weight, resting heart rate and blood pressure. Treadmill exercise testing was performed after 2 to 3 weeks of placebo (no angiotensin-converting enzyme inhibitor) treatment. Treatment trial subjects exercised for a shorter time (493 +/- 160 seconds) and attained a lower peak VO2 (13 +/- 4 ml/kg/min) and VO2 at AT (11 +/- 4 ml/kg/min) than did prevention trial ones (842 +/- 277 seconds, and 20 +/- 6 and 16 +/- 5 ml/kg/min, respectively). Analysis of covariance showed that the differences in peak VO2 and VO2 at AT were statistically significant between the 2 trials after adjusting for age, gender, LV ejection fraction and New York Heart Association functional class.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1995

Neurohumoral variability in left ventricular dysfunction. SOLVD Investigators. Studies of Left Ventricular Dysfunction.

The immediate and longer term variability of selected vasoactive- and volume-regulating neurohormones were measured in patients entering a substudy of the Studies of Left Ventricular Dysfunction--a randomized clinical trial in patients with left ventricular ejection fraction < or = 35%. The variability of these hormones has not been determined in a large cohort of patients. Immediate (short-term) variability was assessed by systematically comparing levels after 15 and 30 minutes of supine rest at the initial visit, and longer term variability was assessed by comparing 30-minute supine rest values at the initial visit with corresponding values taken at 30 minutes after 16 to 24 days of stable therapy. Initial values obtained at the first visit after 30-minute supine rest for all 209 patients were (mean +/- SEM) 512 +/- 21 pg/ml pg/ml for plasma norepinephrine, 1.9 +/- 0.2 ng/ml/hr for plasma renin activity, 3.0 +/- 0.1 pg/ml for plasma arginine vasopressin, and 129 +/- 5.3 pg/ml for plasma atrial natriuretic peptide. All variables were moderately increased relative to established normal values. There was a small but significant decrease from 15- to 30-minute supine posture in all neurohormones, except arginine vasopressin. In the presence of stable background therapy, no significant differences were found between measurements obtained after 30 minutes supine rest at the initial visit and 16 to 24 days later. Spearman correlation coefficients corresponding to immediate and longer term variability were high (range 0.55 to 0.79) (p < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1988

Effects of left ventricular dysfunction on left atrial performance in previous myocardial infarction and during pacing-induced myocardial ischemia in angina pectoris.

This study aimed to evaluate acute and chronic response of left atrial function to left ventricular dysfunction in patients with coronary artery disease. We studied simultaneous measurements of left atrial volume by biplane cineangiography and left ventricular pressure at rest and after pacing in 59 patients with coronary artery disease and 11 normal subjects. At rest, 35 patients with previous myocardial infarction (MI group) had low left ventricular filling rate of the first third in diastolic time, large left atrial volume before contraction (LA pre-ACV) and large left atrial ejection volume (LAEV), compared with control group. Left atrial ejection fraction (LAEF), the ratio of LAEV to LA pre-ACV, was similar between both groups. LAEF was maintained within a wide range of values in accordance with left ventricular peak A pressure, except for 3 patients who had high values of left ventricular peak A pressure and low values of LAEF. After a right atrial pacing stress test, time constant was prolonged and mean emptying rate of left atrial volume during early diastole decreased in 11 patients with angina pectoris who had an increase greater than 5 mmHg in left ventricular end-diastolic pressure after pacing. In these group, LA pre-ACV increased, LAEF decreased and LAEV was unchanged. These results suggest that left atrial performance responds differently to acute and chronic left ventricular dysfunction in patients with coronary artery disease.

Angina Pectoris↗

PubMed1994

The ever expanding spectrum of ischemic left ventricular dysfunction.

Ischemic left ventricular (LV) dysfunction includes a number of discrete entities, such as acute LV failure in angina, acute myocardial infarction, and ischemic cardiomyopathy. Recently, new entities have arisen to expand the spectrum of ischemic LV function. These include postinfarct diastolic dysfunction, stunning, hibernation, and preconditioning. The tantalizing possibility exists that several of these states can coexist. There are widely differing underlying pathophysiologic states. Hence it is not easy to be dogmatic about whether a given group of therapeutic agents, such as the calcium antagonists, may be beneficial in ischemic LV dysfunction. Nonetheless, there is experimental evidence that calcium antagonists may benefit the specific entity of stunning and clinical evidence that they benefit postinfarct ischemic LV diastolic dysfunction. These agents, as a group, should be evaluated in reperfusion and postinfarct dysfunctional syndromes.

Acute Disease↗

PubMed1993

Effect of angiotensin-converting enzyme inhibitors in left ventricular dysfunction: results of the studies of left ventricular dysfunction in the context of other similar trials.

Over 13,000 patients have been randomized in 35 long-term trials of the use of angiotensin-converting enzyme (ACE) inhibitors in patients with heart failure or left ventricular dysfunction. Overall, there is a clear reduction in mortality and hospitalizations for heart failure and myocardial infarction with a trend toward fewer sudden deaths. Furthermore, there is a significant reduction in myocardial infarction in three of the larger trials. These benefits have been demonstrated with several different agents and are consistently seen in various subgroups of patients defined by symptomatic status, etiology of left ventricular dysfunction, age, and gender. However, benefits were greatest among patients with the lowest ejection fraction. In conclusion, ACE inhibitors are of established value in patients with heart failure and/or left ventricular dysfunction.

Angina, Unstable↗

PubMed1984

Reversal of left ventricular dysfunction after aortic valve replacement for chronic aortic regurgitation: influence of duration of preoperative left ventricular dysfunction.

Preoperative left ventricular systolic function is an important predictor of postoperative prognosis in patients with aortic regurgitation. Although left ventricular dysfunction is reversible after aortic valve replacement to a greater extent in patients with good preoperative exercise capacity compared with patients with impaired exercise capacity, not all patients with preserved exercise capacity demonstrate improved left ventricular function after aortic valve replacement. To determine the influence of duration of preoperative left ventricular dysfunction on postoperative reversal of left ventricular dysfunction, we studied 37 patients with aortic regurgitation who preoperatively had left ventricular dysfunction, defined as subnormal echocardiographic fractional shortening (less than 29%), and good preoperative exercise capacity, defined as completion of stage I of the NIH treadmill protocol without limiting symptoms. Eight patients were asymptomatic. In 11 patients left ventricular dysfunction was documented 18 to 57 months preoperatively (prolonged); in 10 patients left ventricular dysfunction developed in an interval of 14 months or less preoperatively (brief); in 16 patients duration of left ventricular dysfunction was unknown. Patients with brief vs those with prolonged left ventricular dysfunction did not differ with respect to severity of preoperative symptoms or exercise tolerance, echocardiographically determined left ventricular dimensions or fractional shortening (25 +/- 3% [SD] vs 25 +/- 3%), or radionuclide angiographic ejection fraction (42 +/- 5% vs 42 +/- 5%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Quality of life among 5,025 patients with left ventricular dysfunction randomized between placebo and enalapril: the Studies of Left Ventricular Dysfunction. The SOLVD Investigators.

OBJECTIVES: This study was performed to assess the quality of life of patients with left ventricular dysfunction for up to 2 years after randomization to enalapril or placebo. BACKGROUND: Previous reports have documented that survival of patients with congestive heart failure can be extended by the angiotensin-converting enzyme inhibitor enalapril. However, it is unknown whether enalapril has a long-term favorable impact on the quality of life in patients with heart failure. METHODS: A brief quality of life questionnaire assessing the quality of life was administered at baseline and at 6 weeks, 1 year and 2 years of follow-up to patients randomized to placebo or enalapril in the Studies of Left Ventricular Dysfunction (SOLVD). Participants had an ejection fraction < or = 0.35, no other serious illnesses and either symptomatic heart failure (treatment trial, n = 2,465) or asymptomatic left ventricular dysfunction (prevention trial, n = 2,560). RESULTS: Among the 14 scales of quality of life, better scores at one or more follow-up intervals were noted in 6 scales in the treatment trial and in 1 scale in the prevention trial among patients assigned to enalapril. Consistent superiority with enalapril at two consecutive follow-up intervals was noted in the treatment trial for social functioning and dyspnea but for no scale in the prevention trial. However, an average of 40% of quality of life responses were missing at 2 years of follow-up because of death or failure to complete the questionnaire. In the treatment trial, survivors with more severe heart failure were less likely to complete the questionnaire. CONCLUSIONS: Modest benefits in quality of life for > or = 1 year occurred when patients with left ventricular dysfunction and symptomatic heart failure were treated with enalapril. No apparent beneficial or adverse effect on quality of life was observed with enalapril in asymptomatic patients with left ventricular dysfunction.

Activities of Daily Living↗

PubMed1995

[Surgical results of aortic stenosis with or without left ventricular dysfunction--postoperative change of left ventricular function].

Between January 1980 and December 1992, 82 patients with aortic stenosis underwent isolated aortic valve replacement at our institution. Age of the patients ranged from 26 to 72 (58 +/- 6.4) years, and 58 were men and 24 were women. The patients were divided into two groups according to preoperative left ventricular ejection fraction (LVEF): 23 patients (LVEF < 50%, mean 39.7%; Group D) and 59 patients (LVEF > or = 50%, mean 62.6%; Group N). By means of echocardiography, LV function were evaluated before and at one month after operation in terms of left ventricular fractional shortening (LVFS), left ventricular systolic internal diameter (LVIDs), left ventricular mass index (LVMI), and left ventricular end systolic wall stress (ESWS). Postoperative early mortality including hospital death was 8.7% in group D (2 cases; myocardial infarction 1, cerebral complication 1) and 3.3% in group N (2 cases; myocardial infarction 1, low output syndrome 1), and this difference was not significant (NS) between two groups. The 5- and 12-year actuarial survival rate were 87.8% and 87.8% in group D, 91.5% and 87.6% in group N, respectively (NS). LVFS (pre/post) was 0.25 %/- 0/08/0.24 +/- 0.10 in group D, 0.38 +/- 0.10/0.32 +/- 0.10 in group N. The difference were significant before (p < 0.0005) and after (p < 0.005) operation between two groups. LVIDs (mm; pre/post) were 39.0 +/- 7.9/35.0 +/- 9.6 in group D, 28.7 +/- 7.3/229.3 +/- 7.6 in group N. The difference were significant before (p < 0.0005) and after (p < 0.01) operation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

Ventricular arrhythmias in hypertensive left ventricular hypertrophy. Relationship to coronary artery disease, left ventricular dysfunction, and myocardial fibrosis.

Ventricular arrhythmias occur with increased frequency in hypertensive patients with left ventricular hypertrophy (LVH). The relationships, however, between ventricular arrhythmias and coexistent coronary artery disease, left ventricular dysfunction and left ventricular fibrosis have not been examined in hypertensive LVH. We carried out coronary arteriography on fifteen hypertensive patients with LVH and nonsustained ventricular tachycardia (greater than or equal to 3 consecutive ventricular complexes) of whom nine (60%) were free of significant (greater than 50% stenosis) coronary disease. To identify other possible correlates of left ventricular arrhythmias, 28 patients with LVH, comprising 17 with ventricular tachycardia and 11 without ventricular arrhythmias, underwent quantitative assessment of left ventricular function (angiographic ejection fraction), left ventricular mass (echocardiography), and left ventricular fibrosis (endomyocardial biopsy). Ejection fraction was not significantly different between the two groups (53 +/- 8% v 62 +/- 2%, P = NS). However, left ventricular mass was significantly greater (442 +/- 28 g v 339 +/- 34 g, P less than .05) and percentage fibrosis significantly higher (19 +/- 4% v 3 +/- 1%, P less than .001) in those patients with ventricular tachycardia. Thus ventricular arrhythmias in hypertensive patients with LVH cannot be entirely attributed to coexistent coronary disease, nor to left ventricular dysfunction, but are related to the degree of cardiac hypertrophy and subendocardial fibrosis.

Biopsy↗

PubMed1990

Cardiac tamponade in left ventricular dysfunction.

Echocardiographic and hemodynamic data were measured in closed-chest dogs during graded cardiac tamponade (pericardial pressure 5, 10, and 15 mm Hg) before and after production of diffuse ischemic left ventricular dysfunction. Left ventricular dysfunction was produced by intracoronary injection of nonradioactive microspheres (54 +/- 3.9 mm diameter). Changes in left atrial pressure with cardiac tamponade were influenced by coexisting left ventricular dysfunction. Left atrial pressure increased with tamponade and was equal to pericardial pressure before left ventricular dysfunction was produced. However, after left ventricular dysfunction was produced, left atrial pressure was significantly higher than pericardial pressure before tamponade, but it fell toward pericardial pressure when tamponade was produced. Pulsus paradoxus (greater than 10 mm Hg) was present in all animals with cardiac tamponade before left ventricular dysfunction but in only one animal afterward. During each level of tamponade, the inspiratory fall of aortic systolic pressure was greater before than with left ventricular dysfunction. The slope of the linear regression between pericardial pressure and millimeters of mercury of inspiratory fall in aortic systolic pressure was significantly greater before than with left ventricular dysfunction (0.74 +/- 0.12 versus 0.32 +/- 0.12, p less than 0.05). Left ventricular dysfunction caused a leftward and upward shift of the pericardial pressure-volume relation. As a result, right atrial and ventricular collapse occurred with significantly smaller volumes of pericardial fluid after than before left ventricular dysfunction. We conclude that pulsus paradoxus may be absent in cardiac tamponade with coexisting left ventricular dysfunction and unequal filling pressures. Echocardiographic signs of cardiac tamponade may occur with small effusions in the presence of left ventricular dysfunction.

Animals↗

PubMed1994

Tolerability of enalapril initiation by patients with left ventricular dysfunction: results of the medication challenge phase of the Studies of Left Ventricular Dysfunction.

Although converting-enzyme inhibitors are useful for the treatment of congestive heart failure (CHF), there are concerns about adverse reactions especially on initiation of therapy. In the Studies of Left Ventricular Dysfunction, enalapril, 2.5 mg twice per day was given on an open-label outpatient basis for 7 days (mean 6.1, range 2 to 7, and median 7) as a prerandomization drug challenge to 7487 patients with left ventricular dysfunction (ejection fraction < or = 0.35). Four hundred forty-four (5.93%) patients reported side effects, including symptoms attributed to hypotension (in 166 patients [2.2%]). The majority (346 [77.9%] of 444 and 129 [77.7%] of 166 with symptoms attributed to hypotension) of patients who reported side effects were willing to participate in the study and to continue receiving enalapril. Thus only 98 (1.3%) of 7487 patients (0.5% because of symptoms attributed to hypotension) were not willing to continue because of side effects. Women and patients of CHF class III or IV were more likely to report side effects. In conclusion, enalapril is well tolerated by patients with left ventricular dysfunction; treatment can be initiated on an outpatient basis in the majority of patients.

Enalapril↗

PubMed1990

Comparison of neuroendocrine activation in patients with left ventricular dysfunction with and without congestive heart failure. A substudy of the Studies of Left Ventricular Dysfunction (SOLVD).

Neuroendocrine activation is known to occur in patients with congestive heart failure, but there is uncertainty as to whether this occurs before or after the presence of overt symptoms. In the Studies of Left Ventricular Dysfunction (SOLVD), a multicenter study of patients with ejection fractions of 35% or less, we compared baseline plasma norepinephrine, plasma renin activity, plasma atrial natriuretic factor, and plasma arginine vasopressin in 56 control subjects, 151 patients with left ventricular dysfunction (no overt heart failure), and 81 patients with overt heart failure before randomization. Median values for plasma norepinephrine (p = 0.0001), plasma atrial natriuretic factor (p less than 0.0001), plasma arginine vasopressin (p = 0.006), and plasma renin activity (p = 0.03) were significantly higher in patients with left ventricular dysfunction than in normal control subjects. Neuroendocrine values were highest in patients with overt heart failure. Plasma renin activity was normal in patients with left ventricular dysfunction without heart failure who were not receiving diuretics and was significantly increased (p less than 0.05) in patients on diuretic therapy. We conclude that neuroendocrine activation occurs in patients with left ventricular dysfunction and no heart failure. Neuroendocrine activation is further increased as overt heart failure ensues and diuretics are added to therapy.

Arginine Vasopressin↗

PubMed1987

Antiarrhythmic efficacy and hemodynamic effects of cibenzoline in patients with nonsustained ventricular tachycardia and left ventricular dysfunction.

This was a prospective single-blind, placebo-controlled study of cibenzoline in 21 patients with five or more runs of nonsustained ventricular tachycardia (VT) and left ventricular dysfunction (mean left ventricular ejection fraction 36 +/- 24%). Ambulatory electrocardiographic monitoring revealed a baseline of 616 +/- 431 runs of VT/day on placebo. Of the 18 patients tolerating the drug, 14 (77%) patients initially had a 75% or greater reduction in VT (177 +/- 164 runs of VT/day, p less than .05). A repeat ambulatory electrocardiogram documented long-term suppression of VT in 13 of 14 patients at 1 month (2.1 +/- 1.3 runs VT/day, p less than .01), in 10 of 14 patients at 3 months (2.5 +/- 1.9 runs VT/day, p less than .01), and in nine of 14 patients at 6 months (1.5 +/- 0.8 runs VT/day, p less than .01). Aggravation of arrhythmia or drug failure was seen in four of 18 (22%) patients (new onset of sudden cardiac death, two patients; sustained VT, two patients). Hemodynamic measurements were obtained with the use of right heart catheterization in patients at rest and exercising during the placebo phase and after 60 hr of oral cibenzoline. Group hemodynamic variables, both measured and derived, showed no detrimental effect of cibenzoline. However, in three of 21 patients (mean ejection fraction 21%), cibenzoline was discontinued due to severe depression of left ventricular function. Caution is recommended in the use of cibenzoline in patients with left ventricular ejection fractions of less than 25%.

Aged↗

PubMed1995

A functional role for endogenous atrial natriuretic peptide in a canine model of early left ventricular dysfunction.

Asymptomatic or early left ventricular dysfunction in humans is characterized by increases in circulating atrial natriuretic peptide (ANP) without activation of the renin-angiotensin-aldosterone system (RAAS). We previously reported a canine model of early left ventricular dysfunction (ELVD) produced by rapid ventricular pacing and characterized by an identical neurohumoral profile and maintenance of the natriuretic response to volume expansion (VE). To test the hypothesis that elevated endogenous ANP suppresses the RAAS and maintains sodium excretion in ELVD, we assessed the effects of antagonism of ANP on cardiorenal and neurohumoral function in ELVD. Chronic ANP suppression was produced by bilateral atrial appendectomies before the production of ELVD by rapid ventricular pacing (ELVD-APPX, n = 5). This group was compared with a separate group with ELVD and intact atrial appendages (ELVD-INTACT, n = 8). ELVD-APPX was characterized by lower circulating ANP (50 +/- 11 vs. 158 +/- 37 pg/ml, P < 0.05), activation of plasma renin activity (PRA) (9.4 +/- 2.4 vs. 0.6 +/- 0.4 ng/ml per h, P < 0.05) and aldosterone (36.4 +/- 12.5 vs. 2.5 +/- 0.0 ng/dl, P < 0.05) when compared to ELVD-INTACT. In comparison to the ELVD-INTACT group, sodium excretion was decreased before and during VE in the ELVD-APPX group. Acute ANP antagonism was produced by administration of the particulate guanylate cyclase coupled natriuretic peptide receptor antagonist, HS-142-1, to seven conscious dogs with ELVD and intact atrial appendages (ELVD-INTACT). HS-142-1 decreased plasma concentrations and renal generation of the ANP second messenger, cGMP, and was associated with activation of PRA and sodium retention with enhanced tubular sodium reabsorption. These data support a significant role for elevated endogenous ANP in the maintenance of sodium excretion and regulation of the RAAS in experimental ELVD.

Aldosterone↗