PubMed Health⌕ Search

Biomedical subjects

B Silke

Publications and source records attributed to B Silke.

At least 91 records · Page 5Linked to original sources
PubMed1989

Nitrate therapy for left ventricular failure complicating acute myocardial infarction: a haemodynamic comparison of intravenous, buccal, and transdermal delivery systems.

The haemodynamic effects of three different methods of nitrate administration [intravenous (i.v.) isosorbide dinitrate (ISDN) and buccal and transdermal nitroglycerin (NTG)] were evaluated in 36 patients with acute left ventricular failure due to a recent myocardial infarction. Similar reductions in pulmonary artery occluded pressure (p less than 0.01) followed all three regimens without change in heart rate and cardiac and stroke volume indices. Significant reductions in systemic arterial pressure and vascular resistance followed both ISDN and buccal NTG but not transdermal NTG. A disadvantage of the buccal NTG delivery was an abrupt and, on occasion, inappropriate reduction in blood pressure. The more gradual and controlled reduction of systemic blood pressure with substantial falls in pulmonary artery occluded pressure following ISDN infusion suggest that in the context of myocardial infarction this method of nitrate delivery may have safety advantages; however, when invasive haemodynamic monitoring facilities are not available, transdermal delivery may offer a practical alternative.

Administration, Buccal↗
PubMed1989

Comparative effects of atenolol and cicloprolol on cardiac performance in coronary heart disease.

Cicloprolol is a new cardioselective beta-blocking agent with partial agonist activity (intrinsic sympathomimetic activity, ISA). Its haemodynamic profile was compared with that of atenolol (cardioselective; no ISA) in a comparative dose-response study of 24 ischaemic patients with diminished cardiac reserve. Following a stable control period, equivalent intravenous (i.v.) beta-blocking boluses of atenolol (1, 1, 2, and 4 mg) or cicloprolol (0.025, 0.025, 0.05, and 0.1 mg/kg) were randomly administered and haemodynamics and left ventricular ejection fraction were determined at rest and during bicycle exercise. At rest, atenolol reduced heart rate (HR) and cardiac index; diastolic blood pressure (DBP), systemic vascular resistance index (SVRI), and pulmonary artery occluded pressure (PAOP) increased without change in mean arterial pressure (MAP). Cicloprolol increased left ventricular ejection fraction, reduced its end-diastolic volume, and tended to reduce filling pressure without change in other variables. During exercise, atenolol reduced ejection fraction and increased SVRI; in contrast, cicloprolol did not significantly alter these parameters. Attenuation of exercise tachycardia and cardiac index increase was similar after each agent. Thus, the cardiac performance assessed from left ventricular stroke index or ejection fraction/filling pressure relationships was less depressed after cicloprolol as compared with atenolol. The relevance of such haemodynamic differences to exercise ability or quality of life during sustained therapy warrants examination.

Adrenergic beta-Antagonists↗
PubMed1989

Haemodynamic comparison of different routes of nitrate administration in postmyocardial infarction left ventricular failure.

An open randomised parallel group comparison of the haemodynamic effectiveness of three different routes of nitrate administration was undertaken in 36 male patients aged 40-69 years who had developed acute left ventricular failure within 18 h of the onset of myocardial infarction. All patients had electrocardiographic and serum cardiac enzyme changes compatible with transmural myocardial infarction and all had both radiographic and haemodynamic evidence of left ventricular failure. None were hypotensive, all were in sinus rhythm and none were receiving other cardioactive drugs. Control haemodynamic measurements were made over a period of one h, following which patients were randomised to receive either intravenous isosorbide dinitrate (mean dose 12.9 mg; range 7.7-14.9), buccal nitroglycerine (5 mg) or transdermal nitroglycerin (nitro TTS 10). The raised left heart filling pressure was reduced by all nitrate preparations but none significantly changed the heart rate or cardiac output. Systemic arterial pressure and vascular resistance were reduced by i.v. ISDN and buccal NTG but not by a transdermal NTG. The only adverse circulatory reaction was hypotension in the three patients following buccal NTG. Nitroglycerin by the transdermal route appears to be equally effective in reducing the raised left heart filling pressure in patients with postinfarction heart failure without the practical disadvantages of monitoring its intravenous administration or the potential hazard of hypotension with buccal NTG.

Administration, Buccal↗
PubMed1988

Is the measurement of cardiac output useful in clinical practice?

The derivation of the "cardiac output" in man is fraught with difficulties whatever principle of measurement is used. The theories underlying the principles involved are sound; the problem arises in their application to the measurement in man. Of equal moment are the immense practical difficulties in applying the techniques available. Together these difficulties frequently give rise to unacceptable errors in the derivation of the "cardiac output". There is no "gold standard" of measurement; all methods have inherent difficulties in their application to man. If intense attention is paid to the practice of any one of the techniques available, then it is possible to reduce the variability of the measurement to acceptable proportions, but the conditions necessary to obtain such narrow ranges of variability in the human subject rarely obtain in routine clinical practice. These realizations apply to the techniques available at present, and it is difficult to imagine that there will be further development of the invasive methods available which would negate these. In contrast, it is possible that refinement of some of the non-invasive techniques now being introduced will allow reasonably reliable measurement of the cardiac output with greater facility than is possible at present. Finally, this brings into question the whole objective of the utility of measurement of cardiac output in practice. Frequently it is measured without due deference to its usefulness. Doubtless there are situations in which the measurement of cardiac output may be of scientific, if not of individual clinical benefit, for example the influence of drugs in hypertension and heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Output↗
PubMed1988

Sympathetic (alpha-beta) or calcium channel blockade for hypertensive myocardial infarction? A haemodynamic comparison of labetalol and nifedipine.

The haemodynamic impact of alpha- and beta-adrenoceptor blockade (labetalol) was compared with that of slow-calcium channel blockade (nifedipine) in 32 patients with sustained elevation of systemic arterial pressure (systolic blood pressure greater than 160; diastolic blood pressure greater than 95 mmHg) following a recent myocardial infarction (6-22 h). Patients with normal (pulmonary artery occluded pressure; (PAOP less than 18 mmHg; n = 16) or impaired (PAOP greater than 18 mmHg; n = 16) left ventricular function were randomized to labetalol (1 mg/kg i.v. 15 min) or nifedipine (20 mg sublingually) and haemodynamic profile was measured over 2 h. Both drugs equally reduced mean systemic arterial pressure (P less than 0.01 versus pretreatment control), and presumably left ventricular afterload; however, the heart rate (P less than 0.01) and cardiac index (P less than 0.01) increased after nifedipine, contrasting with reductions in both variables following labetalol (P less than 0.01). The elevated left ventricular filling pressure was reduced by both labetalol (P less than 0.05) and nifedipine (P less than 0.01) but the reduction was greater following nifedipine (-2 mmHg versus -5 mmHg, P less than 0.05). Thus both compounds were equally effective hypotensive agents. Labetalol consistently reduced cardiac stroke work and double product, important determinants of myocardial oxygen requirements; however, nifedipine afforded some improvement in cardiac performance in patients with left ventricular dysfunction.

Adrenergic alpha-Antagonists↗
PubMed1988

Circulatory effects of intravenous and oral atenolol in acute myocardial infarction.

The hemodynamic dose-response effects of intravenous (0.05 and 0.10 mg/kg) and oral (50 and 100 mg) atenolol were compared in a randomized between-group study of 24 men within seventeen hours of an acute uncomplicated myocardial infarction; 6 subjects were evaluated in each of the four groups. Hemodynamic variables were determined over a one-hour control period, following which the randomized dose of atenolol was administered and measurements repeated at 15 (intravenous therapy only), 30, 60, 90, 120, 180, 240, 300, and 360 minutes. The peak hemodynamic effect was similar and independent of either the dosage or route of administration. In all groups atenolol reduced heart rate and cardiac and stroke volume indices. The pulmonary artery occluded pressure and systemic vascular resistance index were transiently increased. Mean arterial pressure was significantly reduced only in the oral group with the highest pretreatment pressure. Maximum changes developed between fifteen and thirty minutes after intravenous dosing and between two and three hours after oral dosing. However, substantial reductions in cardiac index (-0.6 L/min/m2; p less than 0.05) were already achieved at sixty minutes following oral dosing. The duration of pharmacodynamic activity was for two to three hours following intravenous and for the study duration (four to six hours) after oral dosing. These data confirm the hemodynamic safety of atenolol after acute myocardial infarction.

Administration, Oral↗
PubMed1988

Haemodynamic dose-response effects of a transdermal nitrate delivery system in acute myocardial infarction with and without left heart failure.

The haemodynamic effects of a transdermal nitroglycerin delivery system (NTG-TTS) were investigated in 67 patients with a recent myocardial infarction. The study objectives were to define the dose-response effects of NTG-TTS and to examine the influence of baseline haemodynamic status on subsequent response. Therefore, patients with normal cardiac function [pulmonary artery occluded pressure (PAOP) less than 18 mm Hg, n = 40] and those with acute heart failure (PAOP greater than 18 mm Hg, n = 27) were studied after one of three regimens (TTS-10, TTS-20, or TTS-40) with the intention of securing 10 evaluable patients in each group. In patients with acute heart failure, all three doses reduced the left ventricular filling pressure with a modest decrease in systemic arterial pressure; cardiac index and heart rate were unaltered. The systemic vascular resistance was significantly reduced from 120 min. In patients with normal left ventricular function, there were small but significant reductions in systemic arterial pressure and vascular resistance with limited increases in heart rate; the cardiac stroke work index was reduced. These results are compatible with actions of NTG-TTS mainly on capacitance vessels; PAOP fell with limited impact on systemic arterial pressure and vascular resistance index. This mode of nitrate delivery resulted in a low incidence of hypotension and side-effects; comparison with other delivery methods in myocardial infarction seems indicated.

Administration, Cutaneous↗
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↗
PubMed1987

Comparative hemodynamic dose-response effects of five slow calcium channel-blocking agents in coronary artery disease.

A prospective, randomized study compared the hemodynamic effects of equivalent doses of five slow calcium channel blockers (verapamil, diltiazem, nicardipine, nisoldipine, and amlodipine) in 50 patients with ischemia. After a stable control period, dose-response curves were constructed for each drug with hemodynamics measured 10 minutes after intravenous boluses. Each drug reduced mean systemic arterial pressure (P less than 0.01) and systemic vascular resistance index (P less than 0.01). The heart rate increased after nicardipine, nisoldipine, and amlodipine (P less than 0.01) but was unchanged after verapamil and reduced after diltiazem (P less than 0.01). The left ventricular filling pressure increased after amlodipine (P less than 0.05) and verapamil (P less than 0.01) but was unchanged with the other compounds. Cardiac index increased substantially after the dihydropyridines (P less than 0.01), with little change after verapamil or diltiazem. Cardiac double product fell only after verapamil and diltiazem. These studies provide quantitation of the comparative actions of acute intravenous calcium channel blockade in coronary disease.

Amlodipine↗
PubMed1987

Nifedipine following acute myocardial infarction--dependence of response on baseline haemodynamic status.

The haemodynamic effects of nifedipine (20 mg sublingually) were studied in 40 patients with acute myocardial infarction within 18 h of the onset of symptoms. To determine the influence of preload and afterload on the haemodynamic response to nifedipine, patients were prospectively stratified equally into four groups of 10 patients based on systemic blood pressure level (less than or greater than 160/100 mm Hg) and level of left ventricular filling pressure [pulmonary artery-occluded pressure (PAOP) less than or greater than 18 mm Hg]. In all groups, nifedipine reduced systemic arterial pressure (p less than 0.01) and vascular resistance index (p less than 0.01); heart rate (p less than 0.01) and cardiac index (p less than 0.01) were increased. PAOP was reduced by nifedipine only in those hypertensive patients in whom it was initially raised; in these patients cardiac stroke volume index also increased (p less than 0.01). In hypertensive patients with normal PAOP the cardiac stroke work index was reduced. In patients with normal systemic and pulmonary arterial pressures, nifedipine had no beneficial effects on cardiac function. These data suggested that haemodynamic criteria may allow selection of patients for nifedipine therapy following myocardial infarction; clear advantages were evident only in hypertensive patients in both the presence and the absence of left ventricular failure.

Adult↗
PubMed1987

First-line treatment of left ventricular failure complicating acute myocardial infarction: a randomised evaluation of immediate effects of diuretic, venodilator, arteriodilator, and positive inotropic drugs on left ventricular function.

A prospective randomised trial compared the immediate haemodynamic effects of intravenous diuretic (frusemide), venodilator (isosorbide dinitrate), arteriolar dilator (hydralazine), and positive inotropic stimulation (prenalterol) as first-line therapy for acute left ventricular (LV) failure following myocardial infarction. Forty-eight patients with transmural myocardial infarction and a pulmonary artery occluded pressure (PAOP) of greater than 20 mm Hg were studied within 18 h of admission to a coronary care unit. Both frusemide (-4 mm Hg; p less than 0.01) and isosorbide dinitrate (-6 mm Hg; p less than 0.01) reduced LV filling pressure without change in cardiac index and heart rate. Although both hydralazine and prenalterol increased cardiac index (p less than 0.01), the reduction in LV filling pressure (-2 mm Hg; p less than 0.05) was less than with frusemide and isosorbide dinitrate, and was associated with an increased heart rate (+8 and +13 beats min-1; p less than 0.01). These data suggest that in acute heart failure following myocardial infarction the four treatment modalities could be ranked in descending order of potential benefit as follows: venodilatation (isosorbide dinitrate)--decrease of LV pressure/work; diuretic therapy (frusemide)--decrease of LV pressure/work offset by a transient pressor effect; arteriolar dilatation (hydralazine)--decrease of LV pressure/work and of PAOP, but offset by tachycardia; and positive inotropic therapy (beta 1-agonist prenalterol)--tachycardia and augmented LV afterload. Combination of the former and latter agents, because of their differing modes of action, should offer haemodynamic advantages over monotherapy and deserves further evaluation.

Adult↗
PubMed1987

A haemodynamic and radionuclide assessment of diltiazem in coronary heart disease.

To obtain multiple dose-response haemodynamic and radionuclide data on i.v. diltiazem, 12 ischaemic patients were studied during routine catheterization. At rest, following a 20 min stable control period, the effects of four doses (0.0625, 0.0625, 0.125 and 0.25 mg kg-1 diltiazem at 5 min intervals) were measured in the 3-5 min following i.v. injection. The exercise effects of the cumulative 0.5 mg kg-1 dosage were assessed by comparing a control and post drug period of supine bicycle exercise. The increase in plasma diltiazem levels correlated linearly with the administered dose and achieved therapeutic levels. There were significant dose-related reductions in systemic arterial blood pressure and vascular resistance index; the heart rate fell and cardiac stroke index increased. The calculated double-product (heart rate X systolic blood pressure) was significantly reduced. The left ventricular filling pressures, ejection fraction and cardiac volumes were unaltered. During supine bicycle exercise, the systemic diastolic blood pressure, heart rate and calculated double-product were reduced without change in other parameters. Over the dose range 0.0625-0.5 mg kg-1, diltiazem acutely increased cardiac stroke index and reduced resting heart rate. These haemodynamic data, taken together with its described coronary vasodilator activity suggest that its role in acute vasospastic angina and during angiographic procedures ought to be explored further.

Aged↗
PubMed1987

Immediate effects of bumetanide on systemic haemodynamics and left ventricular volume in acute and chronic heart failure.

1 The haemodynamic and radionuclide effects of i.v. bumetanide (25 micrograms kg-1) were prospectively studied in 24 patients with angiographically documented coronary artery disease and either acute exercise-induced (Group I, n = 12) or chronic (Group II, n = 12) heart failure. 2 Bumetanide at rest increased systemic arterial blood pressure and vascular resistance index; cardiac index and pulmonary artery occluded pressure (PAOP) were reduced at an unchanged heart rate in all patients. The left ventricular ejection fraction fell in patients with normal resting left ventricular filling pressure without change in those with chronic heart failure. The cardiac volumes were unchanged in either group. 3 During constant-load supine bicycle exercise, there were similar effects on systemic arterial pressures, vascular resistance index and PAOP; however the cardiac index was maintained at a reduced left ventricular filling pressure and unchanged ejection fraction and volumes. 4 These data demonstrate immediate mild pressor and vasoconstrictor actions of bumetanide which appear independent of the state of cardiac function; they suggest that any immediate improvement in patient symptomatology following bumetanide may be consequent on the reduction in PAOP; short-term reductions in volume may not occur.

Acute Disease↗
PubMed1987

Comparative haemodynamic dose-response effects of dobutamine and amrinone in left ventricular failure complicating acute myocardial infarction.

The comparative haemodynamic dose-response effects of intravenous (i.v.) amrinone and dobutamine were evaluated in 20 male patients with haemodynamic (pulmonary artery occluded pressure (PAOP) greater than 20 mm Hg) and radiographic left heart failure following a recent myocardial infarction. Following a 1-h control period, 10 patients were each randomised to amrinone (800, 1,600, or 3,200 micrograms/kg/h) or dobutamine (200, 400, or 800 micrograms/kg/h) sequentially infused for 30 min at each dose level; haemodynamic parameters were recorded at the end of each infusion period. Amrinone reduced systemic arterial blood pressure and vascular resistance index with a moderately increased heart rate; PAOP (-10 mm Hg; p less than 0.01) fell substantially without change in cardiac or stroke work indices. Dobutamine increased systemic arterial blood pressure, heart rate, and stroke work index at an unchanged PAOP; cardiac index (+0.7 L/min/m2; 25%; p less than 0.01) increased. Systemic vascular resistance index was significantly reduced by both drugs. Thus, dobutamine increased cardiac index at an unchanged PAOP; myocardial stroke work increased. Amrinone had lesser effect on cardiac pumping but reduced PAOP (preload) at an unchanged stroke work. The implications of these differential actions for the clinical therapy of myocardial infarction deserves further evaluation.

Adult↗
PubMed1986

Pharmacokinetic, haemodynamic and radionuclide studies with nicardipine in coronary artery disease.

Pharmacokinetic, haemodynamic and radionuclide studies explored the acute pharmacokinetic and pharmacodynamic actions of nicardipine in patients with coronary heart disease. Nicardipine infusion resulted in dose-related reductions in systolic and diastolic blood pressure and an increased heart rate. Pharmacodynamic activity was evident between 12 and 24 min following 5 and 10 mg i.v. nicardipine but by 3-6 min following the higher doses of 15 and 20 mg; hypotensive activity persisted for up to 2 h. Post-infusion nicardipine concentrations declined biexponentially; however the limited data precluded formal compartmental analysis. Plasma clearance ranged from 5-12 ml/min/kg, and appeared lower than previously reported volunteer data. The haemodynamic actions of nicardipine (10 mg infusion over 10 min) in 6 patients undergoing diagnostic catheterization were reductions in systolic, diastolic and mean systemic arterial pressure and systemic vascular resistance index. Heart rate and stroke volume index increased, and there was a small but statistically significant increase in pulmonary artery occluded pressure. Radionuclide parameters were measured in 20 patients with stable angina, at rest and during supine bicycle exercise, before and 3-5 min after nicardipine 10 mg intravenously. The left ventricular ejection fraction increased by 4% at rest but not during exercise. The left ventricular rest and exercise ejection and filling rates both increased with a concurrently reduced left ventricular ejection time. There was a highly significant inverse relationship between baseline exercise ejection fraction and the response to nicardipine; ejection fraction increased with low initial values but was either unchanged or fell with higher initial values.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Differences in haemodynamic response to beta-blocking drugs between stable coronary artery disease and acute myocardial infarction.

Theoretically the increased sympathoadrenal activity following acute myocardial infarction might augment the haemodynamic impact of beta-adrenoceptor blockade. To evaluate this question 32 haemodynamic studies were performed to compare the effects of equivalent beta-blocking doses of propranolol (8 mg i.v.) and pindolol (0.8 mg i.v.) in patients with a recent acute myocardial infarction (A.M.I.) or stable coronary artery disease (and a presumptive low sympathetic state). In stable coronary artery disease there were clear differences between the haemodynamic impact of propranolol and pindolol. Propranolol decreased both heart rate (delta HR -7 beat/min) and cardiac index (delta CI -0.4 l/min/m2), with an increased pulmonary artery occluded pressure (delta PAOP +4 mmHg) and systemic vascular resistance index (delta SVRI +358 dyn X s X cm-5 m2). However an equivalent beta-blocking dose of pindolol increased PAOP (delta PAOP +3 mmHg) leaving other variables unchanged. These differential actions of propranolol and pindolol have previously been ascribed to the intrinsic sympathomimetic activity (I.S.A.) of pindolol maintaining cardiac pumping function in a low sympathetic state. In contrast following myocardial infarction, both drugs reduced cardiac index to a significantly greater extent compared with stable coronary artery disease (delta CI propranolol -0.81/min/m2; pindolol -0.4 l/min/m2; p less than 0.05); propranolol also reduced the systemic arterial blood pressure (delta systolic -10 mmHg; delta mean -5 mmHg; p less than 0.05). The haemodynamic relevance of the I.S.A. of pindolol appeared attenuated following A.M.I. These data are compatible with experimental evidence of sympathetic nervous activation following coronary occlusion; the resulting hyperadrenergic state appears to condition an augmented haemodynamic response to beta-blocking drugs irrespective of their ancillary pharmacological properties.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗