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PubMed1990

Cardiovascular and neurohormonal effects of atrial natriuretic peptide in conscious dogs with and without chronic left ventricular dysfunction.

Atrial natriuretic peptide (hANP 4-28) was infused for 1 h (0.3 microgram/kg/min) in 11 normal awake dogs and seven awake dogs with chronic left ventricular dysfunction, induced 16 weeks earlier by repetitive DC shock. The responses were similar in the two groups and included decreases in arterial pressure (107-99 mm Hg), heart rate (83-72 beats/min), and cardiac output (3.6-2.8 L/min), without changes in right or left ventricular filling pressures. Systemic vascular resistance (SVR) tended to rise during the infusion and was significantly increased (2,847-3,442 dyn s cm-5, p less than .05) during the postinfusion recovery period. Regional blood flows (microspheres) during infusion revealed a decrease in skin and splanchnic flow. Despite the apparent vasoconstrictor effect, plasma norepinephrine (PNE), renin activity (PRA), and arginine vasopressin (AVP) levels all fell during ANP infusion. These data suggest that ANP exerts a cardioinhibitory effect, possibly similar to that of arginine vasopressin (AVP), and that the net systemic vasoconstrictor effect of ANP in these dogs is mediated by a complex interrelationship between direct vascular effects, neurohormonal inhibition, and central reflex activation.

Animals↗
PubMed1990

Effect of indecainide in patients with left ventricular dysfunction.

Indecainide, a new antiarrhythmic agent classified as type Ic was evaluated in 11 patients with heart disease who had greater than or equal to 30 ventricular premature complexes/hour, moderate-to-marked left ventricular dysfunction, and mean ejection fraction 34% +/- 8%. Patients received indecainide, 50 mg by mouth, every 6 hours and the dose was increased until greater than or equal to 80% suppression was noted, adverse effects occurred, or a maximum dose of 100 mg indecainide was given every 6 hours. Ventricular premature complexes were suppressed greater than or equal to 80% in nine patients (p less than 0.05) and ventricular tachycardia episodes were completely suppressed in five of eight patients. The effective or maximal mean daily indecainide dose was 191 +/- 32 mg; half of the responders achieved achieved efficacy at serum drug concentration greater than or equal to 600 ng/ml. Serum drug concentration was directly related to gender (r = 0.78, p less than 0.04) and inversely related to creatinine clearance (r = 0.74, p less than 0.05) and ejection fraction (r = 0.71, p less than 0.02). Indecainide prolonged mean PR and QRS intervals (p less than 0.05) but not QT or QTc. There was a linear relation between percent change in PR (r = 0.80, p less than 0.001) and QRS (r = 0.66, p less than 0.001) intervals and serum drug concentration. After starting or increasing the dose, careful observation of patients with decreased renal function or reduced ejection fraction should be exercised because they attain higher drug concentration than normal subjects.

Adult↗
PubMed1995

"Escape" of aldosterone production in patients with left ventricular dysfunction treated with an angiotensin converting enzyme inhibitor: implications for therapy.

Despite the findings in randomized trials of a significant effect of angiotensin-converting enzyme (ACE) inhibitors in reducing morbidity and mortality of patients with symptomatic left ventricular dysfunction, the morbidity and mortality of these patients remains relatively high. One potential strategy to further improve morbidity and mortality in these patients is blockade of a aldosterone. Many clinicians have assumed that ACE inhibitors would block both angiotensin II and aldosterone. However, there are data to suggest that aldosterone production may "escape" despite the use of an ACE inhibitor. An escape of aldosterone production has several important consequences, including: sodium retention, potassium and magnesium loss, myocardial collagen production, ventricular hypertrophy, myocardial norepinephrine release, endothelial dysfunction, and a decrease in serum high density lipoprotein cholesterol. Due to the potential importance of these mechanisms, the finding that there is a significant correlation between aldosterone production and mortality in patients with heart failure, as well as evidence that an aldosterone antagonist, spironolactone, when administered to patients with heart failure treated with conventional therapy including an ACE inhibitor results in increased diuresis and symptomatic improvement, an international prospective multicenter study has been organized, the Randomized Aldactone Evaluation Study (RALES Pilot Study), to evaluate the safety of blocking the effects of aldosterone in patients with heart failure treated with an ACE inhibitor.

Aldosterone↗
PubMed1990

Acute haemodynamic effects of the beta 1-adrenoceptor partial agonist xamoterol at rest and during supine exercise in patients with left ventricular dysfunction due to ischaemic heart disease: a double-blind randomized trial.

The effects of xamoterol 0.2 mg kg-1 i.v. and placebo on left ventricular function at rest and on exercise were compared in patients with left ventricular dysfunction due to ischaemic heart disease. Improvements were seen in systolic and diastolic function at rest, and at up to 50% of maximal exercise, without evidence of worsening myocardial ischaemia.

Adrenergic beta-Agonists↗
PubMed1984

Left ventricular dysfunction after acute myocardial infarction: results of a prospective multicenter study.

In a multicenter prospective study of 866 patients who survived the coronary care unit phase of an acute myocardial infarction, variables reflecting left ventricular function were examined to assess their impact on 2 year survival. Single variables that reflected left ventricular dysfunction before infarction and in the acute and recovery phases were, respectively, history of prior myocardial infarction, rales in the coronary care unit dichotomized at greater than bibasilar and predischarge radionuclide ejection fraction dichotomized at less than 0.40. When combined in a stepwise fashion, patients lacking these three risk characteristics had a 2 year 4.2% mortality rate, whereas patients possessing all three characteristics had a 45% mortality rate. Rales in the coronary care unit and predischarge ejection fraction act independently, and each contributes to mortality. Fifty-two patients with advanced rales but an ejection fraction of 0.40 or greater had a 21% mortality rate. Similarly, 208 patients with few rales but an ejection fraction of less than 0.40 had a 15% mortality rate. These data suggest that the mortality risk imposed by those factors that assess permanent left ventricular damage is independent of and additive to the mortality risk contributed by dynamic, acute phase dysfunction. These data fit the hypothesis that acute phase dysfunction is, in part, due to transient ischemia that, on reversal, can restore function toward normal. The results suggest 1) that assessment of left ventricular function during the acute and recovery phases of myocardial infarction is necessary to define prognostic characteristics of an individual patient, and 2) that of particular importance is the identification of patients whose postinfarction course is consistent with reversible ischemia.

Cardiac Output↗
PubMed1993

Comparative neurohormonal responses in patients with preserved and impaired left ventricular ejection fraction: results of the Studies of Left Ventricular Dysfunction (SOLVD) Registry. The SOLVD Investigators.

OBJECTIVES: The aim of this study was to determine the differences in neurohumoral responses between patients with pulmonary congestion with and without impaired left ventricular ejection fraction. BACKGROUND: Previous studies have established the presence of neurohumoral activation in patients with congestive heart failure. It is not known whether the activation of these neurohumoral mechanisms is related to the impairment in systolic contractility. METHODS: The 898 patients recruited into the Studies of Left Ventricular Dysfunction (SOLVD) Registry substudy were examined to identify those patients with pulmonary congestion on chest X-ray film who had either impaired (< or = 45%, group I) or preserved (> 45%, group II) left ventricular ejection fraction. Plasma norepinephrine, plasma renin activity, arginine vasopressin and atrial natriuretic peptide levels were measured in these two groups of patients and compared with values in matched control subjects. RESULTS: Distribution of the New York Heart Association symptom classification was the same in the two groups of patients. Compared with control subjects, patients in group II with pulmonary congestion and preserved ejection fraction had no activation of the neurohumoral mechanisms, except for a small but statistically significant increase in arginine vasopressin and plasma renin activity. Compared with patients in group II, those in group I with pulmonary congestion and impaired ejection fraction had significant increases in plasma norepinephrine (p < 0.002), plasma renin activity (p < 0.02) and atrial natriuretic peptide levels (p < 0.0007). When we controlled for baseline differences between groups I and II, the between-group differences in plasma norepinephrine (p < 0.02) and atrial natriuretic peptide (p < 0.002) remained significant. However, plasma renin activity was not significantly different between groups I and II. When the effects of diuretic agents and angiotensin-converting enzyme inhibitors were adjusted, patients with lower ejection fraction were found to have significantly higher plasma norepinephrine and atrial natriuretic peptide levels. CONCLUSIONS: The results point to the importance of the decrease in left ventricular ejection fraction as one of the mechanisms for activation of neurohormones in patients with heart failure.

Adult↗
PubMed1991

Comparative hemodynamic effects of mexiletine and quinidine in patients with severe left ventricular dysfunction.

Mexiletine and quinidine are often administered to patients with severe congestive heart failure, but their hemodynamic effects have not been adequately studied in these individuals. In a randomized, crossover study, the hemodynamic responses to single oral doses of quinidine (600 mg) and mexiletine (400 mg) were compared in 20 patients with marked left ventricular dysfunction. Quinidine predominantly caused vasodilation, with mean arterial, left ventricular filling, and right atrial pressures all decreasing (-7 +/- 2, -2.3 +/- 1.0, and -1.1 +/- 0.5 mm Hg, respectively) and the systemic vascular resistance also declining (-308 +/- 84 dynes.sec.cm5). In contrast, the systemic vascular resistance increased (314 +/- 84 dynes.sec.cm-5) and the mean arterial, left ventricular filling, and right atrial pressures also increased (+2 +/- 2, +6.1 +/- 1.8, and +1.8 +/- 0.6 mm Hg, respectively) after mexiletine. Cardiac performance declined with mexiletine (cardiac and stroke work indexes decreasing -0.3 +/- 0.1 L/min/m2 and -5 +/- 1 gm.m/m2, respectively), but there was no significant change in cardiac or stroke work indexes with quinidine (+0.1 L/min/m2 and -0.3 +/- 0.9 gm.m/m2, respectively). The response to the two agents significantly differed for all parameters measured (p less than 0.005). These hemodynamic changes were accompanied by clinical effects. Mexiletine induced increased dyspnea in five patients and quinidine led to symptomatic hypotension in two patients. Plasma concentrations of mexiletine and serum concentrations of quinidine were within or below the therapeutic range in all patients. In conclusion, mexiletine and quinidine exert different hemodynamic effects when given to patients with severe congestive heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1995

Detection of regional left ventricular dysfunction in early pacing-induced heart failure using ultrasonic integrated backscatter.

BACKGROUND: It has been demonstrated that cyclic variation of ultrasonic integrated backscatter (CVIBS) may be useful in detecting altered physical conditions in the heart. However, no previous study has examined serial changes of CVIBS in the myocardium during the development of left ventricular dysfunction. METHODS AND RESULTS: We examined alterations of CVIBS in pacing-induced cardiac dysfunction. Eight pigs (36 +/- 2 kg) were studied before and sequentially during sustained rapid ventricular pacing (225 +/- 9 beats per minute). CVIBS was measured in the IVS and left ventricular PLW before pacing and daily for 4 days after onset of pacing. Five additional pigs (35 +/- 10 kg) were examined after 14 days of pacing. Regional function and CVIBS were assessed with pacemakers inactivated. A quantitative integrated backscatter imaging system (two-dimensional format) was used. Over 4 days of pacing, the magnitude of CVIBS progressively decreased in the PLW but was unchanged in the IVS, findings that persisted at 14 days. Percent wall thickening in the PLW progressively decreased to a greater degree than percent wall thickening in the IVS. A linear relation between the magnitude of CVIBS and percent wall thickening was found. At 14 days, blood flow to the two regions was similar but regional differences in CVIBS persisted. CONCLUSIONS: Rapid left ventricular pacing produces abnormalities of regional myocardial function within 48 hours of pacing. Regional myocardial dysfunction is accompanied by a reduction in CVIBS in the same region.

Animals↗
PubMed1990

Acute hemodynamic and arrhythmogenic effects of high-dose intravenous salbutamol in patients with chronic left ventricular dysfunction.

The short-term hemodynamic and possible arrhythmogenic effects of intravenous salbutamol at a dose of 30 or 60 micrograms/min were evaluated in 14 patients with severe chronic left ventricular dysfunction using equilibrium radionuclide angiocardiography and electrocardiographic monitoring. Salbutamol infusions at a dose of 30 micrograms/min did not cause significant hemodynamic changes; however, at a dose of 60 micrograms/min there was a significant increase in stroke volume, cardiac output, and left ventricular ejection fraction. Heart rate increased significantly while systemic peripheral resistance decreased significantly. Two patients developed ventricular premature beats and another two supraventricular tachycardia, but none were associated with adverse consequences. Thus, high-dose intravenous salbutamol is effective and safe, and may be used in the acute management of patients with poor left ventricular function.

Adult↗
PubMed1984

Intravascular and extravascular pulmonary fluid volumes during chronic experimental left ventricular dysfunction.

To assess the effects of chronic left ventricular (LV) dysfunction on intravascular pulmonary blood volume (PBV) and extravascular lung water (EVLW) lung fluid volumes, 56 dogs were evaluated by means of double-indicator dilution techniques. PBV and EVLW were measured in seven control dogs, in eight dogs 4 hours after the production of left heart dysfunction, and then in three additional groups of dogs (n = seven in each group) 7, 14, and 30 days after the production of LV dysfunction. Twenty dogs were excluded because we were unable to produce elevations in LV end-diastolic volume greater than 25 mm Hg. EVLW was measured using heat as the diffusible indicator, and electric shock was used to create heart block and myocardial scarring in order to produce LV dysfunction. Plasma volume was calculated prior to death by means of radioiodinated albumin. In the remaining animals, electric shock acutely and chronically elevated LV end-diastolic pressure (control 2.3 +/- 1.0 mm Hg; postshock pressures greater than 25 mm Hg). PBV increased initially after cardiac failure and remained so as time progressed, although it represented a smaller fraction of the plasma volume as time passed (11.2 +/- 2.1% control, 15.9 +/- 3.4% at 4 hours after failure, and 12.6 +/- 2.0% at 7 days; the former p less than 0.005 vs control, the latter p less than 0.01 vs control). EVLW increased as time progressed, in consort with small but progressive increases in left atrial pressure. Thus, we conclude that the effects of acute and chronic LV dysfunction on pulmonary circulation are significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Effects of oral hydralazine on rest and exercise hemodynamics in patients with aortic or mitral regurgitation and left ventricular dysfunction.

The hemodynamic effects of afterload reduction were studied at rest and during two levels of upright exercise in patients with aortic or mitral regurgitation and left ventricular dysfunction. Eleven patients underwent invasive hemodynamic monitoring before and after 50-70 mg of oral hydralazine was given ever 6 h for 48 h. At rest, heart rate and mean arterial pressure after hydralazine were unchanged from control. During exercise, there was no significant change in heart rate, but mean arterial pressure fell significantly during the first level of exercise. Systemic vascular resistance was elevated before hydralazine and was significantly reduced after treatment at both exercise levels. After hydralazine, the resting oxygen consumption was significantly elevated at rest but was unchanged during exercise, the arteriovenous oxygen difference was significantly narrowed at both rest and exercise, and the pulmonary capillary wedge pressure was also significantly lower at both rest and exercise. In this select group of patients who are not candidates for surgical valve replacement, chronic afterload reduction with oral hydralazine may result in increased cardiac performance, decreased pulmonary congestion, reduced myocardial oxygen demands, and improvement in resting and/or exertional symptoms.

Administration, Oral↗
PubMed1991

Short-term haemodynamic evolution and late follow-up of post-infarct patients with left ventricular dysfunction undergoing a physical training programme.

The aims of this study were to investigate the short-term haemodynamic changes occurring in post-infarct patients with left ventricular dysfunction undergoing a physical training programme and the prognostic implications of such changes. Ninety-five male patients with no evidence of congestive heart failure, consecutively admitted for exercise testing with haemodynamic monitoring in the supine position, in whom exercise pulmonary artery diastolic pressure (PAdP) exceeded 20 mmHg were enrolled in an in-hospital one-month physical training programme. After training all patients' exercise capacity increased by 24% (P less than 0.001) with no change of PAdP. At matched work load, heart rate decreased (126 +/- 21 vs 120 +/- 19 bt min-1, P less than 0.05) as did PAdP (27 +/- 5 vs 25 +/- 6 mmHg, P less than 0.05) and A-VO2 difference increased (9.5 +/- 1.7 vs 10 +/- 1.6 ml%, P less than 0.01). Similar results were observed in a subset of patients with exercise PAdP greater than 30 mmHg (30 patients). In 11 patients with inadequate cardiac output neither heart rate nor PAdP decreased after training and a disproportionate increase in blood pressure was noted. Clinical follow-up ranged from 1 to 8 years (62 +/- 32 months). Seven deaths, 12 reinfarctions and 14 coronary artery bypass graftings occurred. The modifications, after training in work capacity, heart rate and PAdP, were not predictive of events.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Long-term treatment of ventricular tachycardia with amiodarone in presence of severe left ventricular dysfunction.

A group of 34 consecutive patients with coronary artery disease (n = 29) or dilated cardiomyopathy (n = 5) (3 women, 31 men, age 38-80 yr) who had severely impaired left ventricular function (left ventricular ejection fraction less than or equal to 40%) and high-grade ventricular ectopic activity (sustained or nonsustained ventricular tachycardia or ventricular fibrillation) were treated with amiodarone (mean dose: 206 mg/d) and followed for 1-117 (mean: 49) months. In the total group, there were seven sudden deaths, five deaths due to pump failure, one non-cardiac death, and two successful heart transplantations during follow-up. Thus the annual cardiac mortality in these carefully selected and followed patients was 8, 6%, the annual cardiac event rate was 10, 1%. The cumulative cardiac survival-rate was 62% after 5 years and 41% after 10 years. In five patients, treatment was interrupted after 10 to 43 months, three of the patients were alive at follow-up and two suffered cardiac death, resulting in an annual cardiac death rate of 12% in this subgroup of treatment. Based on the results of this retrospective analysis we conclude that in patients with low left ventricular ejection fraction and nonsustained or sustained ventricular tachycardia treated with low dose amiodarone, mortality was unexpectedly low. Thus, it may be the antiarrhythmic treatment to be considered in patients with ventricular tachycardia and severe left ventricular dysfunction.

Adult↗
PubMed1987

Prognostic importance of the immediate hemodynamic response to nifedipine in patients with severe left ventricular dysfunction.

To determine the clinical significance of the occurrence of hemodynamic deterioration after the administration of calcium channel blocking drugs, nifedipine (20 mg orally) was administered to 29 patients with severe left ventricular dysfunction. Thirteen patients showed hemodynamic improvement with the drug (Group 1), as shown by a notable increase in cardiac index associated with a modest decrease in mean arterial pressure. The other 16 patients exhibited hemodynamic deterioration after nifedipine (Group 2), as reflected by a decline in right and left ventricular stroke work indexes accompanied by a marked hypotensive response. These differences were not related to differences in the peripheral vascular response to nifedipine, because both groups showed similar decreases in systemic and pulmonary vascular resistances. Groups 1 (hemodynamic improvement) and 2 (hemodynamic deterioration) were similar with respect to all demographic variables and pretreatment left ventricular performance (cardiac index, left ventricular filling pressure and systemic vascular resistance). Yet, the 1 year actuarial survival in patients in Group 1 was substantially better than that in patients in Group 2 (67 versus 23%, p = 0.009). Group 2, however, had higher values for plasma renin activity (17.7 +/- 6.0 versus 4.3 +/- 1.4 mg/ml per h, p less than 0.05), lower values for serum sodium concentration (134.6 +/- 1.2 versus 139.2 +/- 0.6 mEq/liter, p less than 0.05) and higher values for mean right atrial pressure (15.8 +/- 2.0 versus 7.9 +/- 1.4 mm Hg, p less than 0.01) than did patients in Group 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Haemodynamic dose-response actions of cicloprolol in left ventricular dysfunction due to ischaemic heart disease.

Cicloprolol is a cardioselective beta-1 partial agonist; its haemodynamic and radionuclide (nuclear stethoscope) effects were determined in 22 patients with impaired left ventricular function due to coronary artery disease. Following a 20 min stable control period, the effects of four doses of cicloprolol (0.025, 0.025, 0.05 and 0.1 mg/kg at 10 min intervals) were measured at rest 5-10 min after each intravenous injection. The effects of the cumulative 0.2 mg/kg dosage were assessed during supine bicycle exercise and compared with a control exercise period. At rest there were significant increases in systolic arterial without change in mean blood pressure. The heart rate and cardiac index were unchanged. There was a significant increase in left ventricular ejection fraction with a reduction in filling pressure and volume. Patients with resting heart rate below 75 beats/min and with ejection fraction greater than 35% showed the greatest improvement. During supine bicycle exercise, ejection fraction was increased compared to control (31 +/- 2 to 36 +/- 2; P less than 0.01), cardiac volume reduced and exercise tachycardia attenuated. These data suggest that cicloprolol may be of value where beta-blockade is considered in the presence of underlying left ventricular dysfunction due to ischaemic heart disease.

Adrenergic beta-Antagonists↗
PubMed1994

Exercise capacity in patients with left ventricular dysfunction following acute myocardial infarction: relation to systolic and diastolic function and intervention with captopril.

Patients with acute or chronic heart disease may have limited exercise capacity if they have reduced left ventricular function. Indexes of reduced left ventricular function during exercise are a predictor of subsequent survival although left ventricular ejection fraction is a poor predictor of physical endurance. We evaluated the effect of captopril on physical endurance in 48 males with left ventricular dysfunction following myocardial infarction. On the 7th day following myocardial infarction patients were randomized to either captopril 50 mg daily or corresponding placebo. Patients were followed up by means of serial echocardiography and exercise stress testing for a period of 180 days. Exercise capacity was significantly improved in the captopril group. Changes in exercise capacity were significantly correlated to changes in left ventricular (LV) volumes and compliance. The beneficial effect of captopril on exercise capacity was probably mediated via improvement in LV performance and compliance.

Captopril↗
PubMed1989

Hemodynamic effects of intravenous pimobendan in patients with left ventricular dysfunction.

Sequential hemodynamic effects of intravenous pimobendan (UD-CG 115 BS), a novel compound with positive inotropic and vasodilating properties, were investigated during left heart catheterization in nine patients with left ventricular dysfunction (ejection fraction less than or equal to 40%) and moderate congestive heart failure (NYHA classes II and III). Studies were carried out before (C) and for 60 min after intravenous administration of 5 mg of pimobendan over 1 min. Pimobendan immediately and progressively reduced systemic resistance [16 and 28% at 10 and 60 min postdrug, respectively (p less than 0.05 vs. C)] and left ventricular end diastolic pressure [from 24 +/- 3 (C) to 12 +/- 3 mm Hg at 60 min, p less than 0.001)]. Cardiac output gradually increased by 24%, but stroke volume did not, due to an equally progressive 14% rise in heart rate, whereas stroke work increased by 21% (all p less than 0.05 vs. C). Both contractility and relaxation, measured at fixed heart rates, significantly improved by 30 and 20%, respectively, at 50 min postdrug. Thus, pimobendan has immediate and prolonged arterial vasodilating effects, together with positive inotropic and lusitropic properties, resulting in an early but sustained improvement of left ventricular pump function and filling pressures.

Aged↗
PubMed1994

Patient perception of a long-term clinical trial: experience using a close-out questionnaire in the Studies of Left Ventricular Dysfunction (SOLVD) Trial. SOLVD Close-out Working Group.

A close-out questionnaire was distributed to the participants in a long-term heart failure trial, Studies of Left Ventricular Dysfunction (SOLVD). The respondents' primary motivation for enrollment, positive and negative experiences, and reported changes in habitual behavior was analyzed. Seventy-four percent (N = 3522) of the eligible patients responded to the survey. The most commonly cited reason for enrollment was recommendation by the primary physician. A wish "to contribute to medical science" and "to help others" was also a frequent incentive. A majority of the respondents were satisfied with participation and would be willing to participate in a future clinical trial. Most negative experiences included transportation to and from the clinic and frequent staff changes. A significant number of the patients reported changes in their smoking habits, alcohol intake, and diet despite the absence of behavioral interventions in the study protocol. There were minor differences between attitudes and perceptions of the male and female participants. No differences were found between patients who had previously participated in a clinical trial and those who had not.

Attitude↗