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PubMed1989

Left ventricular dysfunction in obstructive lung disease: an echocardiographic and angiographic study of cor pulmonale patients with decreased mitral E-F slope.

Twenty-nine patients with cor pulmonale were investigated by echocardiography and cardiac catheterisation in order to assess the significance of a reduced mitral E-F slope. Seven patients had coronary arterial disease and were therefore excluded from further analysis. Of the remaining 22 patients, 15 had a reduced mitral E-F slope but an otherwise normal mitral valve on echocardiography. They were found to have an increased left ventricular end-diastolic pressure measured at cardiac catheterisation when compared to the other seven patients with cor pulmonale and a normal E-F slope. The patients with a reduced E-F slope had an increased mean right ventricular internal dimension and interventricular septal thickness measured echocardiographically when compared to the patients with a normal E-F slope. Right ventricular dysfunction was suggested in these patients by an increased right ventricular end-diastolic pressure measured at cardiac catheterisation. We discuss possible mechanisms of left ventricular dysfunction and of intracardiac pressure transmission in cor pulmonale, and the implications of these mechanisms for effective management.

Aged↗
PubMed1986

Atrial natriuretic peptide in chronic heart failure in the rat: a correlation with ventricular dysfunction.

To assess the relation between atrial natriuretic peptide and ventricular dysfunction, we simultaneously measured both atrial and plasma immunoreactive atrial natriuretic peptide concentrations in rats 4 weeks after myocardial infarction induced by left coronary artery ligation. When compared to controls (n = 39), rats with infarction (n = 16) had markedly elevated plasma immunoreactive atrial natriuretic peptide concentrations (1205.8 +/- 180.9 vs. 126.7 +/- 8.9 pg/ml, p less than 0.001) and reduced immunoreactive atrial natriuretic peptide concentrations in right and left atria (31.4 +/- 4.6 vs. 61.2 +/- 3.2 ng/mg, p less than 0.001; 14.9 +/- 2.2 vs. 32.7 +/- 2.4 ng/mg, p less than 0.001, respectively). Right ventricular weight increased in proportion to infarct size, and both were correlated with plasma immunoreactive atrial natriuretic peptide levels (r = 0.825, p less than 0.001 and r = 0.816, p less than 0.001, respectively). Right atrial immunoreactive atrial natriuretic peptide content was significantly higher than left in both controls and rats with infarction. Both right and left atrial immunoreactive atrial natriuretic peptide concentrations were negatively correlated with both right ventricular weight as well as plasma immunoreactive atrial natriuretic peptide concentrations (right atrium: r = -0.816, p less than 0.001, r = -0.708, p less than 0.01; left atrium: r = -0.687, p less than 0.01, r = -0.644, p less than 0.01, respectively). These results suggest that chronic stimulation of atrial natriuretic peptide release from both atria is associated with increased turnover and depleted stores of atrial natriuretic peptide in atria in proportion to the severity of heart failure. It also suggests that plasma atrial natriuretic peptide levels may be used as a reliable index of cardiac decompensation in chronic heart failure.

Animals↗
PubMed1990

Improvement of left ventricular contractility and relaxation with the beta 1-adrenergic receptor partial agonist xamoterol at rest and during exercise in patients with postinfarction left ventricular dysfunction. A placebo-controlled randomized trial.

A new cardioselective beta 1-adrenergic receptor agonist xamoterol (Corwin) has been developed for the treatment of heart failure. To study the acute hemodynamic effects of xamoterol, 24 patients, 39-70 years old, with mild-to-moderate postinfarction left ventricular dysfunction entered a double-blind, between-patient comparison of a single 5-minute intravenous infusion of xamoterol (0.2 mg/kg) and placebo. The acute hemodynamic effects of xamoterol were measured at rest and during two multistaged symptom-limited supine bicycle exercise tests (Ex-T), a control Ex-T followed by an Ex-T with either xamoterol or placebo. Compared with placebo, xamoterol significantly increased left ventricular contractility (Vmax and positive [+] dP/dt) and enhanced relaxation (dP/dt- and time constant relaxation) at rest and at the 25% and 50% levels of maximum exercise. The heart rate, the frequency and time to onset of anginal symptoms, the magnitude of exercise-induced ST segment depression, the left ventricular end-diastolic and peak systolic pressures, the mean pulmonary artery pressures, the cardiac index, the left ventricular stroke-work index, and the epinephrine and norepinephrine plasma levels at rest and during exercise did not differ significantly between placebo xamoterol groups. Thus, xamoterol can be a useful addition for the treatment of left ventricular dysfunction because of long-term ischemic heart disease.

Adrenergic beta-Agonists↗
PubMed1987

[Mid-term outcome of acute right ventricular dysfunction in biventricular myocardial infarction. Hemodynamic and cineangiographic studies].

This study was designed to evaluate the mid-term outcome of the right ventricular (RV) dysfunction which characterizes infarction of both ventricles in the acute phase. Thirteen patients hospitalized for inaugural posterior or infero-posterior infarction extending to the right ventricle (haemodynamic and cineangiographic diagnosis) were explored in the acute phase and 4 months later by right heart catheterization and selective cineangiography of the right ventricle in a 30 degrees RAO projection. The results were compared with those obtained in a control group. Haemodynamically, the RV filling pressures (p less than 0.001) and the indices of RV dysfunction--i.e. RV end-diastolic pressure/RV systolic pressure ratio (p less than 0.001) and right atrial pressure/pulmonary wedge pressure ratio (p less than 0.02)--were significantly decreased between the acute and chronic phases, but they remained pathological compared with those measured in the control group. Angiographically, the right ventricular dysfunction in the acute phase was reflected in an increase of the RV end-systolic volume (p less than 0.02) and a decrease of the RV ejection fraction (p less than 0.01), whereas diastolic cavitary dilatation was inconstant, with mean values of RV end-diastolic volume close to those found in the control group. The systolic dysfunction persisted, unchanged, during the chronic phase. Segmental kinetics of the inferior wall was much reduced in the acute phase (p less than 0.001), this hypokinesia partially regressing in the chronic phase; but in fact there were wide individual variations, and some patients even recovered an almost normal contractility. Tricuspid valve regurgitation was frequent (6/13 cases) in the acute phase and regressed in 2 out of 3 cases in the chronic phase; its presence introduced a degree of bias in the measurement of RV end-systolic volume and RV ejection fraction, with a tendency to underestimate the severity of diastolic dysfunction. To summarize, right ventricular dysfunction was constant but often modest in the acute phase and remained relatively stable at mid-term, whereas segmental kinetics of the inferior wall improved, sometimes dramatically.

Adult↗
PubMed1991

[Relaxation and diastolic filling precisely evaluated in patients with left ventricular dysfunction].

To assess left ventricular (LV) diastolic function in patients with LV dysfunction, LV pressures (manometer tip) and biplane angiograms were analyzed for 27 patients with LV systolic dysfunction (EF < or = 0.45) (dilated cardiomyopathy or coronary artery disease) and 18 normal controls. LV volumes were obtained from frame-by-frame analyses of angiograms. LV relaxation was assessed by the time constant (T) of LV pressure decay. LV relaxation was impaired in patients with LV dysfunction, however, early diastolic filling assessed by the peak filling rate (PFR) and mean filling rate (MFR) during the rapid filling phase was maintained. Compared to the control group, early diastolic filling was significantly decreased in patients with LV dysfunction without mitral regurgitation (MR), but not in those with LV dysfunction with MR. In conclusion, although diastolic filling may be modified by MR, LV relaxation and early diastolic filling are essentially impaired in patients with LV dysfunction.

Adolescent↗
PubMed1991

Does ventricular dysfunction occur during liver transplantation?

In conclusion, we believe that ventricular dysfunction occurs infrequently during liver transplantation, except for the very short period of "cardioplegia" of the heart on reperfusion in some patients. There is no evidence that prolonged cardiac dysfunction is a common problem during liver transplantation. Understanding the physiologic changes that occur during liver transplantation should allow the anesthesiologist to correct many factors that might otherwise cause hemodynamic instability.

Heart Diseases↗
PubMed1989

[Successful repair of tetralogy of Fallot with severe right ventricular dysfunction using veno-arterial bypass in an adult].

A 35-year-old male with tetralogy of Fallot, who had undergone left Blalock-Taussig shunt at ten year old, developed severe dysfunction of right ventricle with decreased right ventricular ejection fraction of 25% and frequent premature ventricular contractions of right ventricular origin. Following intracardiac procedure, the venoarterial assist circulation was successfully employed for 9 hours, until his hemodynamic conditions were improved. This experience reemphasized the importance of right ventricular protection and mechanical circulatory assist in the surgical treatment of Fallot's tetralogy in older children and adults who developed severe right ventricular dysfunction as a natural history of this disease.

Adult↗
PubMed1992

Chronic coronary artery constriction leads to moderate myocyte loss and left ventricular dysfunction and failure in rats.

Coronary artery narrowing, ranging from 19% to 61%, was induced in rats and ventricular performance, myocardial damage, and myocyte hypertrophy were examined 1 mo later. Animals were separated into two groups, exhibiting ventricular dysfunction and failure, respectively. Dysfunction consisted of a 2.4-fold increase in left ventricular end diastolic pressure (LVEDP), 15% decrease in left ventricular peak systolic pressure (LVPSP), 24% reduction in developed pressure (DP), and a 16% depression in-dP/dt. Failure was defined on the basis of a 4.7-fold elevation in LVEDP, and a 26%, 47%, 45%, and 41% decrease in LVPSP, DP, +dP/dt, and -dP/dt. Moreover, in this group, right ventricular end diastolic and systolic pressures increased 5.5- and 1.2-fold. Left and right ventricular weights expanded 23% and 51% with dysfunction and 30% and 56% with failure. Left ventricular hypertrophy was characterized by ventricular dilation and wall thinning which were more severe in the failing animals. Foci of damage were found in both groups but tissue injury was more prominent in the endomyocardium and in failing rats. Finally, myocyte loss in the ventricle was 10% and 20% with dysfunction and failure whereas the corresponding enlargements of the unaffected myocytes were 34% and 53%. Thus, coronary narrowing led to abnormalities in cardiac dynamics with an increase in diastolic wall stress and extensive ventricular remodeling in spite of a moderate loss of myocytes and compensatory reactive hypertrophy of the viable cells.

Animals↗
PubMed1990

Hemodynamic profile of amiodarone during acute and long-term administration in patients with ventricular dysfunction.

One of the potential adverse effects of anti-arrhythmic agents is an impairment of cardiac function as a result of their intrinsic negative inotropic properties. Amiodarone, in animals, also induces dose-related negative inotropic effects, in addition to coronary and systemic vasodilatation and slowing of the heart. Likewise, in most human studies, intravenous amiodarone gives rise to early systemic and coronary vasodilatation, followed by a reduction in contractility. Depending on the relative impact of these opposing effects on the left ventricle, the changes in heart rate, cardiac output and left ventricular filling pressure are variable. Particularly in patients with pre-existing ventricular dysfunction, cardiac pump function is impaired further when relatively high dosages of amiodarone are used without its solvent Tween 80. In contrast, fast bolus administrations, eg. 5 mg/kg amiodarone in 5 minutes, result in an improvement of cardiac output, albeit at the expense of an increase in left ventricular filling pressure. The latter observation suggests that intravenous amiodarone should be given with caution in patients with heart failure and elevated left ventricular filling pressures. When given by mouth, amiodarone does not have significant hemodynamic effects, other than a moderate reduction in heart rate and, occasionally, in diastolic blood pressure. Cardiac pump function is not affected, even in patients with ventricular dysfunction or heart failure, in whom chronic oral administration of the drug is well tolerated.

Amiodarone↗
PubMed1991

Early prevention of left ventricular dysfunction after myocardial infarction with angiotensin-converting-enzyme inhibition.

Left ventricular dysfunction can be improved with angiotensin-converting-enzyme inhibition started 1 week after myocardial infarction or later. To see whether earlier intervention may confer greater benefit, a double-blind study was carried out in which 100 patients with Q wave myocardial infarction, but without clinical heart failure, were randomly allocated treatment with captopril 50 mg twice daily or placebo starting 24-48 h after onset of symptoms. Left ventricular volumes were measured regularly during 3 months of treatment and after a 48 h withdrawal period by means of two-dimensional echocardiography. The placebo group showed significant increases in left ventricular end-diastolic (LVEDVI) and end-systolic (LVESVI) volume indices, with the ejection fraction unchanged. By contrast, the captopril group showed a slight but not significant rise in LVEDVI and a significant reduction in LVESVI with ejection fraction increased significantly. At 3 months there was a 4.6% difference in the change in ejection fraction from baseline between the groups (p less than 0.0001). Most of the treatment benefit was evident at 1 month and there were no changes in left ventricular volumes after 48 h withdrawal of treatment at 3 months. Heart failure requiring treatment with frusemide developed in 7 patients in each group during the study period; 3 of these (1 captopril-treated, 2 placebo-treated) had to be withdrawn from the trial with severe heart failure requiring open treatment. Thus early treatment with captopril is effective in preventing the ventricular dilatation that can occur after Q wave myocardial infarction.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1988

Beta-blocker therapy in patients with ventricular tachyarrhythmias in the setting of left ventricular dysfunction.

Although several studies suggest beta blockers (BB) are effective in suppressing ventricular arrhythmias, less is known about their role in the treatment of patients with ventricular tachyarrhythmias associated with impaired left ventricular function. To assess the tolerance and efficacy of these agents, 32 patients presenting with either ventricular fibrillation (18) or sustained ventricular tachycardia (14) were studied during BB therapy. Left ventricular dysfunction (mean ejection fraction 29%) was present as a consequence of coronary artery disease (26) or cardiomyopathy (6). Baseline arrhythmia assessment revealed recurrent ventricular tachycardia in all patients. Antiarrhythmic drug therapy including BB was guided by programmed stimulation (10), exercise testing (8), ambulatory monitoring (12), or was given empirically (2). Beta blockers were well tolerated, as measured by exercise duration, which improved significantly, and by long-term maintenance, which continued in 23 of 32 (72%) patients. Over a mean follow-up of 668 days, patients treated with BB had a relatively low incidence of both sudden (3%) and nonsudden (9%) death. Thus, BB can be effective and well tolerated adjunct therapy in patients with a history of ventricular tachyarrhythmias in the setting of impaired left ventricular function.

Adrenergic beta-Antagonists↗
PubMed1991

Cardiovascular profile of 5 novel nitrate-esters: a comparative study with nitroglycerin in pigs with and without left ventricular dysfunction.

1. Four cumulative 10 min intravenous infusions of 0.05, 0.2, 0.5 and 2.0 mg min-1 were used to compare the cardiovascular profile of 5 novel nitrate-esters dissolved in Intralipid 10% to that of nitroglycerin (GTN) in conscious pigs. 2. Infusion of Intralipid 10% alone had no effect on any of the systemic haemodynamic parameters. GTN infusions decreased mean arterial blood pressure dose-dependently from 94 +/- 2 mmHg to 79 +/- 3 mmHg (P less than 0.05) and raised cardiac output from 2.74 +/- 0.09 l min-1 to 3.40 +/- 0.18 l min-1 (P less than 0.05) due to an increase in heart rate (by up to 43 +/- 3%), as stroke volume decreased slightly. Systemic vascular resistance decreased (by 32 +/- 3%) and left ventricular end-diastolic pressure fell from 5.2 +/- 0.4 mmHg to 2.2 +/- 0.5 mmHg (both P less than 0.05). 3. The novel compounds CEDO 8811, CEDO 8834 and CEDO 8901 increased cardiac output only at the highest dose (7%, 8% and 9%, respectively). There was no change in mean arterial blood pressure as the increase in cardiac output was counterbalanced by arterial vasodilatation. All three compounds reduced left ventricular end-diastolic pressure slightly. 4. CEDO 8816 was a more potent arterial and venodilator than the aforementioned CEDO compounds, as the decreases in systemic vascular resistance and left ventricular end-diastolic pressure were already significant at lower doses. The fall in stroke volume was fully compensated by the increase in heart rate and as a result cardiac output increased by 11 +/- 3% (P less than 0.05) at the highest dose. 5. CEDO 8956 was the most potent vasodilator of the novel compounds and exhibited a cardiovascular profile similar to that of GTN. Left ventricular end-diastolic pressure decreased significantly during infusion of 0.2mgmin-'. Mean arterial blood pressure decreased by 11 +/- 2% (P < 0.05) in spite of an increase in cardiac output by up to 20 +/- 2% (P < 0.05), due to a decrease (by 27 +/- 1%, P <0.05) in systemic vascular resistance. The increases in heart rate (20 +/- 5%, P < 0.05) and LVdP/dtmax (38 +/- 4%, P < 0.05) were, however, considerably less after CEDO 8956 than after GTN. 6. The potential of CEDO 8956 in the treatment of chronic left ventricular dysfunction was evaluated during administration to conscious pigs (21-23 kg), in which the left circumflex coronary artery was ligated 4 weeks earlier. In these animals, baseline values for cardiac output and LVdP/dtx were lower and those of systemic vascular resistance and left ventricular end-diastolic pressure were higher than in the first group of experiments. 7. Both GTN and CEDO 8956 in doses of 0.05 to 2.0 mg inm increased cardiac output dosedependently (by up to 34% and 19%, respectively). The decrease in systemic vascular resistance was larger with GTN (35%) than with CEDO 8956 (17%), which resulted in a 13% decrease in mean arterial pressure during infusion of GTN, whereas there was no change in mean arterial pressure during infusion of CEDO 8956. Both compounds increased LVdP/dt,,,,X (by 48% and 30%, respectively) and lowered left ventricular end-diastolic pressure to normal levels. 8. At a dose of 1.0Omg min- 1, both GTN and CEDO 8956 increased left ventricular blood flow parallel to the increase in myocardial oxygen demand. At this dose, GTN also caused vasodilatation in the vascular beds of the brain, kidneys and adrenals. With CEDO 8956 no significant changes were achieved. 9. We conclude that the cardiovascular profile of CEDO 8956 in both normal animals and in animals with chronic left ventricular dysfunction warrants further study on its usefulness in the treatment of a number of cardiovascular disorders.

Animals↗
PubMed1991

[CABG in 2 patients with severe left ventricular dysfunction].

Coronary artery bypass grafting was performed in two patients with left ventricular dysfunction (EF 16%). In both cases they had chest pain at rest and ischemic myocardium were detected by the SPECT. We considered them candidate for the operation regardless of LV dysfunction. They were eventful in the postoperative course. One case was discharged and is free from chest pain now, but another unfortunately died for multiple organ failure.

Coronary Artery Bypass↗
PubMed1990

Studies of left ventricular dysfunction (SOLVD)--rationale, design and methods: two trials that evaluate the effect of enalapril in patients with reduced ejection fraction.

The Studies of Left Ventricular Dysfunction (SOLVD) is an extensive program of research that has 3 components. (1) Two large double-blind randomized trials evaluate the effects of enalapril on mortality, morbidity and quality of life of patients with left ventricular (LV) dysfunction with overt congestive heart failure (CHF) (Treatment Trial in 2,500 patients) and without overt CHF (Prevention Trial in 4,600 patients). (2) Seven detailed sub-studies evaluate the effect of enalapril on a number of intermediate outcomes such as right and LV function and hemodynamics, LV mass and wall stress, hormones, arrhythmias, exercise capacity and quality of life in subsets of patients in the 2 large trials. (3) Finally, a registry of 6,336 patients with congestive heart failure or LV dysfunction is designed to describe the clinical course of an unselected group of patients. The rationale and design of a tiered approach to clinical trials that are large enough to provide reliable information on mortality and morbidity, yet provide relevant information on other endpoints, are described.

Adult↗
PubMed1989

Effect of the second-generation calcium channel blocking drug nisoldipine on diastolic left ventricular dysfunction in heart failure.

The effect of intravenous nisoldipine (0.12 microgram/kg/min) on diastolic left ventricular (LV) dysfunction was studied from simultaneous hemodynamic and radionuclide measurements in 12 patients with New York Heart Association class II to IV cardiac failure. The initial LV filling fraction was low, the peak LV filling rate normalized for end-diastolic volume was decreased, and the pulmonary capillary wedge pressure (PCWP) was high and associated with clinical shortness of breath. Nisoldipine produced an increase in LV filling fraction from 36 +/- 17% to 43 +/- 20% (p = 0.003). The increase in filling took place in both early and late diastole: peak early filling rate (PFR) increased in 11 of the 12 patients (p = 0.02) and late diastolic filling rate (atrial [A] wave in eight of them (NS). When the determinants of these changes, were examined further, it was found that in the control state PFR was inversely related to LV end-systolic volume (r = 0.77), whereas the A wave was related in exponential fashion to PCWP (preload) (r = 0.79). Nisoldipine did not change the slope of these relationships, and it did not alter the end-diastolic pressure-volume relationship, implying that inherent myocardial relaxation and distensibility were unaltered by the drug. In summary, nisoldipine improved measurements of diastolic LV dysfunction in patients with cardiac failure. This study illustrates the importance of considering ventricular loading conditions when analyzing and interpreting measurements of diastolic ventricular dysfunction. The measured changes in diastolic LV function during infusion of nisoldipine appear to be due to alterations in ventricular loading conditions rather than to a direct myocardial effect of the drug.

Aged↗
PubMed1989

Hemodynamic effects of dilevalol in patients with systemic hypertension and left ventricular dysfunction.

Hemodynamic and left ventricular function parameters were measured in patients with mild to moderate hypertension and compromised left ventricular function who were given dilevalol, an antihypertensive agent with selective beta 2-agonism and nonselective beta-antagonist activity. After a 2- to 3-week placebo washout period, 9 patients were given dilevalol titrated upward from 100 to 600 mg twice daily over a 7-week period to achieve a supine diastolic blood pressure of less than 90 mm Hg with a decrease of greater than or equal to 10 mm Hg from baseline. Multigated radionuclide ventriculography and systolic and diastolic time intervals were performed after the pretreatment placebo washout, at the end of 2 weeks' maintenance dosing, and after a 7- to 10-day post-treatment discontinuation and placebo washout period. At an average daily dose of dilevalol, 444 mg, heart rate at rest decreased significantly (p less than 0.01) during treatment and increased during post-treatment placebo. Systolic and diastolic blood pressures at rest decreased significantly (p less than 0.01) during treatment and increased during post-treatment placebo. At maximal exercise, changes in blood pressure and heart rate were significantly blunted (p less than 0.05) during treatment. Ejection fraction at rest increased significantly (p less than 0.01) during treatment, with no significant change occurring during exercise, and decreased during post-treatment placebo. Preejection period decreased significantly during treatment (p less than 0.005) and increased during post-treatment placebo.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Is the morphology of ventricular premature beats a marker for left ventricular dysfunction?

The morphology of ventricular premature beats has been described as a marker for the presence or absence of myocardial disease. Furthermore, the premature beat has been reported to be a potential marker for a dilated and hypokinetic left ventricle. To verify this previously tested hypothesis, 37 healthy patients with ventricular premature beats on an electrocardiogram (ECG), Holter monitor ECG, or a stress test ECG were classified according to the ventricular premature beat morphology. Group 1 had ventricular premature beat QRS complexes with a smooth contour or with narrow (less than 40 msec) notching. Group 2 had ventricular premature beats with broad (greater than 40 msec) notching or shelves. All of these patients had normal or borderline normal ECGs and normal multiple-gated acquisition (MUGA) scans. Nine patients had type 1 ventricular premature beats, 20 patients had type II ventricular premature beats, and eight patients had both type I and type II ventricular premature beats. We conclude that the presence of group 2 ventricular premature beats is so frequent in patients with normal left ventricular ejection fractions that the use of this marker in identifying abnormal left ventricular function is suspect.

Adult↗
PubMed1990

[Pulmo cardialis: effect of inhaled bronchodilators on airway resistance of acute left ventricular dysfunction].

Disturbance of left ventricular function leads to an impairment of ventilation: airway resistance increases, while pulmonary compliance is reduced. We therefore studied the effect of inhalable bronchodilators (Fenoterol, Ipratropium bromide) on oscillatory airway resistance in 16 patients with an acute left heart failure. The results show that the resistance can be significantly reduced to normal values by the bronchodilators. Fenoterol has the greatest spasmolytic potency, but Ipratropium bromide is also effective. Recompensation of left heart function alone does not lead to comparable acute effects on airway resistance. The possibility of immediate improvement of ventilation through the use of inhalable bronchodilators should therefore be considered in the treatment of acute left heart failure.

Airway Resistance↗