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At least 253 records · Page 14Linked to original sources
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↗
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↗
PubMed1988

Hemodynamic comparison of dopexamine hydrochloride and dopamine in ischemic left ventricular dysfunction.

The hemodynamic dose-response effects of intravenous dopexamine hydrochloride (0.5 to 2.0 micrograms/kg/min) have been compared with dopamine (2.5 to 10 micrograms/kg/min) in 12 patients with ischemic left ventricular dysfunction in an open randomized crossover study. Both drugs increased cardiac output and decreased systemic vascular resistance. Dopexamine hydrochloride appeared to increase heart rate more than dopamine although this did not reach statistical significance. Dopexamine hydrochloride produced small increases in systolic and decreases in diastolic blood pressure, whereas dopamine had a biphasic effect resulting in a decrease in mean blood pressure at low doses and an increase at the highest dose studied. With increasing dosage, there was a trend toward more vasodilator activity with dopexamine hydrochloride than with dopamine. Dopexamine hydrochloride produced fewer adverse effects than dopamine.

Adult↗
PubMed1995

Systolic ventricular dysfunction and heart failure due to coronary microangiopathy in hypertensive heart disease.

Left ventricular hypertrophy in arterial hypertension is characterized by myocyte hypertrophy, myocardial fibrosis, and structural changes of the intramural coronary arteries. Hypertensives with or without left ventricular hypertrophy have a reduced coronary vasodilator reserve due to alterations of the coronary microcirculation. The impairment in coronary vasodilator reserve is likely to initiate a process of malperfusion and malnutrition concomitant with increased metabolic demands. Further, malperfusion is supported by an increase in diastolic filling pressure, which will enhance the extravascular component of coronary resistance. The sum of interactions of these structural alterations of myocardium, interstitium, and coronary vasculature are likely to initiate and maintain a process of myocardial malperfusion and malnutrition, which can provoke functional depression of the myocardial performance, a loss of contractile proteins, an increase in interstitial fibrosis, and, not least, an overall decrease in contractile function in long-standing cardiac hypertrophy. Finally, the reversal of these processes by adequate antihypertensive treatment may contribute to renormalization of cardiac function and to prevention of late cardiac failure in hypertensive heart disease.

Antihypertensive Agents↗
PubMed1984

Vasodilator therapy in children: acute and chronic effects in children with left ventricular dysfunction or mitral regurgitation.

To determine the acute and chronic effects of vasodilator therapy in children, vasodilator therapy was evaluated in 13 children (aged 0.2 to 14.5 years) with severe left ventricular dysfunction or mitral regurgitation. In seven children, nitroprusside increased cardiac index by an average of 33% (P less than .01) and increased stroke index by 29% (P less than .01). In eight children, hydralazine caused a 31% increase in cardiac index (P less than .01) and a 27% increase in stroke index (P less than .02). Ten children received chronic oral vasodilator therapy and were followed for 5.7 +/- 1.4 (SEM) months. Early clinical improvement was observed in every child. Symptoms of heart failure diminished in all, and five children became entirely asymptomatic. A significant (P less than .05) improvement was noted in growth velocity, respiratory rate, heart size, and incidence of gallop rhythm after 1 month of therapy. The duration of the beneficial response to vasodilator therapy varied considerably, however, and significant improvement for the group was not found after 1 month. Four children had sustained clinical improvement for 6 months or longer, but the others experienced recurrent heart failure within 1 to 4 months.

Adolescent↗
PubMed1992

Effect of diltiazem on norepinephrine-induced acute left ventricular dysfunction.

The present study has examined the role of diltiazem as a protective agent in a canine model of norepinephrine cardiotoxicity. Effects of diltiazem, 20 micrograms/kg/min x 5 min pretreatment followed by 10 micrograms/kg/min x 90 min, or saline infusion were examined at baseline and 1 h after infusion of norepinephrine, 4 micrograms/kg/min for 90 min, in closed-chest anesthetized dogs. Left ventricular function was assessed by equilibrium radionuclide angiogram and two-dimensional echocardiogram. In 7 saline experiments, hypotension and increased heart rate were observed at 1 h post infusion. In the diltiazem-treated group (n = 7), mean arterial pressure and heart rate were unchanged. In the saline group, left ventricular ejection fraction fell from 0.50 +/- 0.04 to 0.28 +/- 0.04. Left ventricular ejection fraction was unchanged in the diltiazem-treated group: 0.52 +/- 0.03 to 0.55 +/- 0.07. Left ventricular end-diastolic volume was increased at 1 h post infusion in saline controls but not in the diltiazem-treated group. Measurement of fractional shortening from two-dimensional echocardiograms also indicated left ventricular dysfunction in the saline but not diltiazem-treated groups. Left ventricular end-systolic wall stress following norepinephrine infusion was significantly increased in the saline but not diltiazem-treated groups: 122.7 +/- 18.7 vs 67.6 +/- 19.7 g/cm2, respectively. In dogs receiving saline without norepinephrine infusion, no significant changes occurred over the course of the experiment. Histologic examination showed mild contraction band necrosis in saline controls but not in sham saline dogs. Diltiazem showed intermediate histologic evidence of injury, which was not further quantified. This study suggests that effects of norepinephrine on left ventricular function in the canine model of norepinephrine cardiotoxicity may be largely due to increased wall stress following a prolonged increase in afterload. Diltiazem pretreatment afforded significant protection of left ventricular function.

Animals↗
PubMed1987

Conventional and high frequency controlled mechanical ventilation in patients with left ventricular dysfunction and pulmonary edema.

The cardiopulmonary effects of conventional controlled mechanical ventilation (CMV), high frequency controlled mechanical ventilation (HFV), and intermittent mandatory ventilation (IMV) were compared in nine patients with ischemic left ventricular dysfunction and pulmonary edema. Ventilatory support during IMV and CMV was adjusted by changing the ventilator rate while tidal volume was maintained at 12 ml/kg. HFV was produced at a frequency of 100 cycles/min and an I/E ratio of 1:2. End-expiratory airway pressure and inspired oxygen concentration were maintained constant. The three ventilatory modes produced similar mean airway, transpulmonary, and intra-thoracic pressures. Mechanical control of respiration required hyperventilation during both CMV and HFV. Arterial blood oxygenation, heart rate, vascular pressures, cardiac output, and myocardial ischemia were unaffected by the changes in ventilation. Decreased arteriovenous oxygen content difference (p less than 0.05) and increased mixed venous oxygen content (p less than 0.05) suggested improved systemic blood flow during IMV. Controlled ventilation by conventional means or with a high frequency technique had no detectable advantage over partial ventilatory support with IMV during cardiopulmonary failure stabilized with vasoactive therapy and continuous positive airway pressure.

Aged↗
PubMed1991

Electrophysiologic mechanisms for ventricular arrhythmias in left ventricular dysfunction: electrolytes, catecholamines and drugs.

Cardiac arrhythmias are generated as the result of disorders of automaticity or of impulse conduction. Regardless of the mechanism, calcium is likely to be involved, although calcium antagonists are rarely useful antiarrhythmics in ventricular arrhythmias. Myocardial cells that do not ordinarily initiate action potentials may do so when they are partially depolarized, giving rise to an ectopic focus. Early afterdepolarizations (EADs) are also induced in cardiac cells by partial depolarization, whereas delayed afterdepolarizations (DADs) are induced by Ca++ overloading. EADs may be the initiating mechanism of torsade de pointes, a complication of QT prolongation associated with quinidine therapy. Both in the animal model and in humans, treatment with magnesium, isoproterenol, or pacing, all of which suppress EADs, will also suppress torsade de pointes. Ventricular tachycardia is a manifestation of ordered re-entry, and may be exacerbated by antiarrhythmics, especially class 1c drugs. In the individual patient, prediction of proarrhythmia is not possible. The risk of proarrhythmia is increased in patients with episodes of sustained ventricular tachycardia or with significant left ventricular dysfunction.

Anti-Arrhythmia Agents↗
PubMed1992

Reversible and irreversible left ventricular dysfunction after acute myocardial infarction.

Left ventricular function after acute myocardial infarction depends on several mechanisms leading to left ventricular remodeling: (a) infarct size and healing and (b) adaptive changes involving both the dysfunctioning but viable myocardium (hibernating and stunned myocardium) and the nonischemic myocardium. The prognosis after acute myocardial infarction is strongly related to regional and global left ventricular function and the loss of dysfunctioning viable myocardium is a main factor in the worsening in left ventricular function in survivors of the acute phase. Thus, medical strategies should exert their beneficial effect on the "mechanical instability" of ventricular myocardium by saving the viable myocardium. beta-Blocker therapy has been shown to be effective in improving the prognosis via anti-ischemic and antiarrhythmic actions. The combination of metoprolol and nisoldipine seems to be able to preserve the contractile function of viable myocardium in the first 6 months after acute myocardial infarction.

Adrenergic beta-Antagonists↗
PubMed1991

Coronary sinus occlusion: effect on ischemic left ventricular dysfunction and reactive hyperemia.

Pressure-controlled intermittent coronary sinus occlusion (PICSO) has been shown to reduce experimental infarct size. To examine the role of PICSO in limiting the consequences of brief ischemia on left ventricular function, we studied the effect of PICSO in nine open-chest anesthetized dogs. PICSO was performed using a pump-inflated, balloon-tipped catheter in the coronary sinus until coronary sinus occlusion pressure reached a plateau (10 +/- 3 seconds). The balloon was then rapidly deflated (2 seconds) and the cycle was repeated. Regional left ventricular function in the ischemic zone was assessed by sonomicrometry. Coronary blood flow was measured with a flow probe around the left anterior descending artery (LAD) proximal to an occluding suture. Measurements were obtained at baseline, during a 3-minute LAD occlusion, and for 10 minutes of reperfusion. In an additional five dogs, this sequence was repeated during an infusion of adenosine at a dose that abolished reactive hyperemia following LAD occlusion. The addition of PICSO beginning 15 minutes prior to ischemia and continuing throughout LAD occlusion and reperfusion did not prevent, reduce, or shorten ischemic left ventricular dysfunction. PICSO uniformly blunted reactive hyperemia during reperfusion. However, PICSO also reduced coronary blood flow during maximal vasodilatation achieved by adenosine infusion prior to LAD occlusion. Therefore, it is likely that PICSO decreases reactive hyperemia due to mechanical factors arising from venous engorgement rather than by reducing the ischemic stimulus causing vasodilation.

Animals↗
PubMed1989

Nursing implication for pulmonary artery balloon counterpulsation: a treatment for right ventricular dysfunction after cardiac surgery.

PPRVD is a phenomenon frequently observed in the operating room. Its development can be attributed to a single or many factors associated with cardiac operation. Namely, its presence is precipated by injury to the RV myocardium or changes in the normal hemodynamic functions of the RV. While PPRVD occurs in isolation, it is usually seen with concomitant LV dysfunction. When conventional medical management of LV dysfunction does not improve yet unmasks RV dysfunction, some type of ventricular assist device to support RV dysfunction may be needed to wean patients from cardiopulmonary bypass such as PABC. PABC has been demonstrated to be useful in the management of mild to moderate PPRVD and weaning from CPB. Severe PPRVD has not been demonstrated to benefit from PABC. The major concern in managing PPRVD is the lack of quantifiable criteria for determining levels of RV injury. Research is continuing in this area. Likewise, investigations are under way to develop a transvenous PABC catheter. This catheter would allow for increased PABC use as it would not require surgical placement or removal. The present PABC model could potentially be used in any hospital that uses conventional intra-aortic balloon counterpulsation. The patient presented in this case was cared for in a 350-bed community hospital in the Northeast section of the United States. A PABC patient can present a unique nursing challenge. It is hoped that this article will assist nurses in the future management of these patients.

Aged↗
PubMed1989

Emergency coronary angioplasty in patients with severe left ventricular dysfunction or cardiogenic shock after acute myocardial infarction.

Emergency percutaneous transluminal coronary angioplasty (PTCA) was performed during an acute myocardial infarction (AMI) after either systemic or intracoronary thrombolytic therapy in six patients with severe ischaemic left ventricular dysfunction or cardiogenic shock, among 37 patients (17%) who were treated with PTCA during AMI over a 13-month period. Thrombolytic therapy with streptokinase (1.5 x 10 Units) was initiated after a mean (+/- SD) time delay of 5.5 +/- 1.3 h from the onset of symptoms. The infarct-related artery was found to be occluded (TIMI grade 0-1) in three patients and partially reperfused (TIMI grade 2) in the remaining patients at baseline coronary angiography. Intracoronary administration of urokinase (100-200,000 Units) was ineffective in those patients failing systemic thrombolysis and resulted in only a slight increase of residual lumen in three patients. The coronary artery could be opened by a guidewire mechanical technique in patients with persistent coronary artery occlusion and coronary dilation could be done in all patients. The mean percentage diameter stenosis of the infarct-related vessel was reduced from 98.8 +/- 2% to 27 +/- 11% (P less than 0.005). After the procedure, left ventricular ejection fraction increased from 27 +/- 8% to 41 +/- 7% (P less than 0.02), systemic blood pressure and cardiac index increased respectively from 86 +/- 10 to 126 +/- 14 mmHg (P less than 0.005) and from 2.2 +/- 0.6 to 3.3 +/- 0.6 (P less than 0.01). Left ventricular end-diastolic pressure decreased from 26 +/- 8 to 18 +/- 3 mmHg (P less than 0.05). Severe mitral regurgitation was relieved in one patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[Value of the handgrip apex cardiography test for detection of early diastolic ventricular dysfunction in patients with angina pectoris].

Left ventricular (LV) diastolic dysfunction is the earliest manifestation of myocardial ischemia. There are no simple stress tests for detecting ischemia by assessing abnormal changes of early (relaxation) and late (end-diastolic compliance) LV diastolic function. This study attempts to establish the diagnostic accuracy of the handgrip-apexcardiographic test (HAT) for detecting exercise-ischemia-induced diastolic dysfunction. Apex- and phonocardiogram were obtained during a 2-min handgrip (40% of maximal voluntary contraction using a balloon dynamometer). Indices of LV diastolic function were provided by relative A-wave to total height (A/H) of ACG, total apexcardiographic relaxation time (TART), TART corrected for heart rate (TARTI), and diastolic amplitude time index (DATI). HAT was performed in 63 patients with typical stable angina pectoris and 202 healthy volunteers. Positivity of HAT is defined by the presence of at least one of the following new criteria: 1) A/H during or after handgrip greater than 21% (= largest individual value in controls), 2) TART during greater than TART before handgrip greater than 143 ms or TARTI during handgrip less than 0.14 (= lowest individual value in controls), and 3) DATI during handgrip less than 0.27. According to this definition, all controls showed a negative HAT (specificity: 100%). By contrast, HAT was positive in 54 out of the 63 angina patients (sensitivity: 86%). These results demonstrate that HAT is a highly sensitive stress test for identifying patients with angina pectoris by assessing LV diastolic abnormalities. Thus, this quick and simple exercise method represents a new aspect in the clinical evaluation of angina patients for the practicing physician.

Adolescent↗
PubMed1981

Doxorubicin cardiotoxicity: assessment of late left ventricular dysfunction by radionuclide cineangiography.

Radionuclide cineangiography was used to evaluate 32 patients who sustained long-term remission of soft tissue sarcoma after adjuvant therapy with a cumulative doxorubicin dose from 480 to 550 mg/m body surface area. Left ventricular ejection fraction at rest was below normal (less than 45%) in eight of 32 patients. The abnormal response of ejection fraction to exercise identified an additional 12 patients with diminished left ventricular functional reserve. Ejection fraction determined at rest or during exercise did not differ 1 to 9 months) and those studied 30 months (range, 21 to 43 months) after completing doxorubicin treatment. Sequential studies in 13 patients, done 6 to 15 months after initial post-doxorubicin evaluation also showed persistent depression of average ejection fraction at rest and with exercise, with the continued deterioration of left ventricular function in six patients. Left ventricular dysfunction, evident in over half of asymptomatic patients even long after "acceptable" cumulative doses of doxorubicin, may persist for years.

Adolescent↗
PubMed1980

Right myocardial infarction with predominant right ventricular dysfunction.

Two patients with right ventricular myocardial infarction are described. In both cases, the hemodynamic criteria established for this diagnosis were fulfilled, namely, right-side pressure values (central venous pressure and right atrial pressure) equal to or higher than left-side pressure values (pulmonary capillary wedge pressure and left ventricular end-diastolic pressure). ECG tracings showed acute diaphragmatic myocardial infarction. The lungs were clear both clinically and radiologically. The diagnosis of right ventricular myocardial infarction was confirmed in the first patient by hemodynamic studies and at autopsy, and in the second patient, by hemodynamic and echocardiographic studies. Only in the second care was the administration of massive quantities of fluids and dopamine followed by good results. The importance of establishing a precise diagnosis of right ventricular myocardial infarction is emphasized, since therapy for this condition is different than that for left ventricular myocardial infarction.

Aged↗
PubMed1980

Left ventricular dysfunction--bedside Valsalva manoeuvre.

Thirty-seven patients were evaluated before cardiac catheterisation by bedside physical examination, including Valsalva manoeuvre, to assess the value of the sphygmomanometrically determined arterial pressure responses during the Valsalva manoeuvre and to compare its sensitivity, specificity, and predictive accuracy in the detection of left ventricular dysfunction with that of the commonly used diagnostic signs including the chest x-ray. Patients not on beta-blockade treatment could be separated into three distinct arterial pressure responses detectable at the bedside which corresponded well to three statistically different groups with regard to left ventricular ejection fraction (0.29 +/0 0.11, 0.48 +/0 0.15, 0.69 +/0 0.11) and left ventricular end-diastolic pressure (38 +/- 5 mmHg, 24 +/- 10 mmHg, 14 +/- 5 mmHg) at subsequent cardiac catheterisation. In patients not on beta-blockade it was shown for the first time that (1) the height of the systolic arterial pressure overshoot was directly related to left ventricular ejection fraction and inversely related to left ventricular end-diastolic pressure, and that (2) the bedside sphygmomanometrically determined arterial pressure response during Valsalva manoeuvre provided a semiquantitative estimate of left ventricular function and was unsurpassed in its ability to do so by any of the standard diagnostic signs including the chest x-ray film.

Blood Pressure↗
PubMed1987

Sex differences in exercise induced left ventricular dysfunction in patients with syndrome X.

Clinical, electrocardiographic, and scintigraphic data were reviewed from 32 patients (18 men and 14 women) who had syndrome X (chest pain, evidence of ischaemia, and normal coronary arteries without coronary vasospasm). The mean (SD) resting left ventricular ejection fraction, determined by first pass radionuclide angiography was 62.6 (9.2)% and was greater than 50% in all subjects. There was no significant difference between men and women. On exercise, left ventricular ejection fraction decreased significantly to 57.4 (13.0)%. In 17 of 32 subjects there was a fall in left ventricular ejection fraction of greater than 5%, and regional wall motion abnormalities developed in 12 subjects. The fall in left ventricular ejection fraction on exercise was significant in women (from 61.9 (8.5)% at rest to 54.0 (9.8)% on exercise) but not in men (from 63.2 (9.8)% at rest to 60.0 (14.8)% on exercise). Exercise left ventricular ejection fraction fell by greater than 5% in 10 (71%) of 14 women and in seven (39%) of 18 men. Dyskinetic segments developed in eight (57%) of 14 women and only four (22%) of men. Exercise duration in women was significantly shorter than in men (4.1 (1.5) vs 6.6 (2.1) minutes) and was the only one of several clinical and scintigraphic variables that correlated with the change in left ventricular ejection fraction on exercise. In this selected group of subjects with chest pain and angiographically normal coronary arteries, exercise induced left ventricular dysfunction, as shown by a fall in ejection fraction or the development of regional abnormalities, is a common finding. These are more likely to occur in women than men and are associated with a lower exercise capacity. The data suggest that the sex of the patient is important in the interpretation of the non-invasive evaluation of subjects suspected of having syndrome X.

Adult↗