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Biomedical subjects

M Been

Publications and source records attributed to M Been.

35 records · Page 2Linked to original sources
PubMed1988

Serial changes in the T1 magnetic relaxation parameter after myocardial infarction in man.

A low field resistive nuclear magnetic resonance imaging system (0.08 Tesla) was used to study the in vivo changes in the relaxation parameter T1 of the left ventricular myocardium from the first day to six months after acute myocardial infarction in 41 consecutive patients admitted to a coronary care unit. T1 maps were constructed from transverse and coronal images at various times after infarction. Thrombolytic treatment had been successful in 28 patients. Thirty three of the 34 patients studied within two weeks of infarction had a significantly increased T1 value but this developed only after the third day in four. At day 1-3 the mean (1 SD) maximum T1 was 413 (29) ms (n = 23) compared with 430 (41) ms (n = 22) at day 4-7, 433 (35) ms (n = 24) at day 8-14, 420 (34) at one month (n = 22), 388 (39) (n = 20) at three months, and 361 (24) (n = 14) at six months. The number of regions of interest with an increased T1 followed a similar time course. Although the increase in T1 measured at three months correlated with the initial maximum creatine kinase and with the left ventricular ejection fraction measured at one month, the number of regions with abnormal T1 from day 4 through to one month correlated best with left ventricular ejection fraction. There was no significant difference in T1 between patients with or without reperfusion. The rise in T1 over the first few days together with the prolonged time course of T1 increase suggests that the increase in T1 may reflect cellular infiltration as much or more than tissue oedema.

Adult↗
PubMed1988

Congenital left atrial wall aneurysm in a patient with neurofibromatosis.

A congenital intrapericardial aneurysmal dilatation of the left atrial wall was found in a 28 year old man who presented with atrial fibrillation after a syncopal event. The patient had cutaneous manifestations of neurofibromatosis. The diagnosis was made by cross sectional echocardiography and confirmed by angiocardiography. Surgical excision of the aneurysm resolved the symptoms.

Adult↗
PubMed1987

Left ventricular function after anisoylated plasminogen streptokinase activator complex.

Limitation of the reduction in left ventricular function after acute myocardial infarction is an important indicator of benefit following thrombolytic therapy. Therefore, left ventricular function was studied by radionuclide ventriculography in 91 patients entering 3 separate studies of anisoylated plasminogen streptokinase activator complex (APSAC) administered within 4 hours of acute myocardial infarction. Global left ventricular ejection fraction was measured at 10 days and at 6 months to assess early and late effects of therapy, with particular emphasis on the timing of treatment and the site of infarction. Successful therapy with APSAC in anterior infarction resulted in preservation of left ventricular function at 10 days. The magnitude of benefit declined with increasing symptom duration before treatment, and was maintained at 6 months in those patients without reocclusion. The benefit of successful therapy was less marked in the inferior infarct group at 10 days. By 6 months, no significant benefit was detected because of an increase in ejection fraction in the placebo and occlusion or reocclusion group with inferior infarction. Early therapy results in greater preservation of left ventricular function, and recovery of function may be more rapid than with later treatment. More emphasis on early administration of thrombolytic therapy is indicated.

Anistreplase↗
PubMed1986

Clinical effects and kinetic properties of intravenous APSAC--anisoylated plasminogen-streptokinase activator complex (BRL 26921) in acute myocardial infarction.

Fifty patients with a first myocardial infarction presenting within 4 hours of the onset of symptoms were treated with intravenous anisoylated plasminogen-streptokinase activator complex (APSAC-BRL 26921). Vessel patency with good flow was documented in 88%. The left ventricular ejection fraction declined with the duration of symptoms before treatment (r = -0.53, P less than 0.001). The correlation persisted for the group with anterior infarction (r = -0.46, P less than 0.05) where the mean left ventricular ejection fraction prior to discharge from hospital was 36 +/- 9% compared to 49 +/- 7% for the group with inferior infarction. Reinfarction developed in 12% and mortality at 6 months for the whole group was 6%. A degree of systemic fibrinolysis did occur with a fall in mean plasma fibrinogen from 3.20 g/l to 1.08 g/l. A pharmacokinetic study was performed in six patients demonstrating a clearance half-life of fibrinolytic activity of 87.5 +/- 5.0 min. APSAC is an effective intravenous thrombolytic agent with a relatively long half-life of fibrinolytic activity.

Adult↗
PubMed1986

Effect of the specific thromboxane receptor blocking drug AH23848 in patients with angina pectoris.

The effect of the specific thromboxane receptor blocking drug AH23848 was investigated in two double blind placebo controlled studies in male patients with exercise induced angina pectoris and angiographically verified coronary lesions. In the first study cardiac pacing was performed in twenty patients after coronary angiography. Patients were then randomised into two groups and received either AH23848 (70 mg orally) or placebo. One hour later cardiac pacing was repeated. Neither treatment had any significant effect upon time to angina or the rate-pressure product at the onset of chest pain in these patients. In the second study twenty male patients were randomised to seven days' treatment with AH23848 (70 mg three times a day) or placebo followed by a crossover to the other treatment for a further seven days. Clinical assessment was performed before treatment and at the end of each treatment period. There was no significant difference between the placebo and AH23848 treatment periods in exercise tolerance, the rate-pressure product at angina after exercise testing, the number of ischaemic attacks as determined from 24 hour ambulatory electrocardiograms, the number of attacks of pain, or the number of glyceryl trinitrate tablets consumed. This lack of a clinical effect with AH23848 was seen despite a profound inhibition of ex vivo platelet aggregation stimulated by the thromboxane A2-mimetic U-46619. Because in experimental animals in vivo AH23848 blocks vascular thromboxane receptors as well as platelet thromboxane receptors the lack of effect of AH23848 in cardiac pacing and exercise induced angina is unlikely to be the result of inadequate blockade of thromboxane receptors. The lack of effect of the drug is more likely to indicate that thromboxane A2, is not a factor in the aetiology of the pain experienced by these patients during exercise or cardiac pacing.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1986

Intracoronary thrombolytic therapy performed within a coronary care unit: one year's experience.

Acute myocardial infarction is associated with a high incidence of occluding coronary arterial thrombi. Thrombolytic therapy has been advocated to restore coronary artery blood flow and to reduce myocardial damage. Coronary arteriography and intracoronary thrombolytic therapy was administered to 61 patients admitted to a Coronary Care Unit within eight hours of symptoms. Successful reperfusion was obtained in 38 of 46 single vessel occlusions associated with a first coronary attack. Failure of reperfusion occurred in patients with two vessel occlusions or with cardiogenic shock. This study demonstrates the feasibility of applying this technique within a Coronary Care Unit with low capital and running costs, and suggests that its widespread application is possible even within the setting of a District General Hospital.

Coronary Angiography↗
PubMed1985

Characterisation of acute myocardial infarction by gated magnetic resonance imaging.

In studies with gated nuclear magnetic resonance imaging, patients with recent transmural myocardial infarction showed significantly longer spin-lattice relaxation times (T1) in the infarct area than did healthy volunteers or patients with non-ischaemic or chronic ischaemic heart disease. 10 of the 13 patients had a T1 longer than that found in any healthy subject or in any patient with other heart disease. Changes in T1 should prove useful in the assessment of interventions designed to limit infarct size.

Adult↗
PubMed1985

Coronary thrombolysis with intravenous anisoylated plasminogen-streptokinase complex BRL 26921.

BRL 26921 is a protected plasminogen-streptokinase complex with selective affinity for thrombus. When given intravenously within three hours of the onset of a first acute myocardial infarction angiographic patency of the infarct related vessel was seen in all 16 patients receiving the active drug compared with only two of 16 receiving a placebo. There was relative sparing of left ventricular function in the active treatment group with anterior infarction (mean left ventricular ejection fraction 37% compared with 23% for placebo), but no significant difference in left ventricular function between the active and placebo groups was seen in patients with inferior infarction. Intravenous BRL 26921 is highly effective in causing coronary reperfusion and may help to preserve left ventricular function when given early in the course of anterior infarction.

Adult↗
PubMed1985

Preoperative prediction of prosthesis size using cross sectional echocardiography in patients requiring aortic valve replacement.

In 43 patients who underwent aortic valve replacement for aortic stenosis with or without regurgitation the accuracy of preoperative left ventricular angiography, parasternal long axis cross sectional echocardiography of left ventricular outflow tract and proximal ascending aorta, and M mode echocardiography of aortic root in predicting aortic root size and thereby prosthesis size was compared. Cross sectional echocardiographic measurements and angiographic measurements of aortic root correlated well with prosthesis size, with over two thirds of the indirect measurements being within 2 mm of prosthesis diameter. M mode echocardiography did not yield useful predictive information. Non-invasive preoperative evaluation of patients likely to require aortic valve replacement may be usefully extended to include aortic root dimensions measured by cross sectional echocardiography.

Adult↗
PubMed1985

Nuclear magnetic resonance in hypertrophic cardiomyopathy.

The large differences in the spin lattice relaxation times (T1) of blood and myocardium (measured by nuclear magnetic resonance) allow the heart to be visualised without the use of contrast media. The findings using nuclear magnetic resonance in 11 unselected patients with hypertrophic cardiomyopathy were compared with those in equal numbers of normal subjects and patients with electrocardiographic features of left ventricular hypertrophy. In patients with hypertrophic cardiomyopathy characteristic septal hypertrophy was noted together with variable and sometimes pronounced hypertrophy of the left ventricular free wall, which is consistent with the heterogeneous nature of this disease. The mean (SD) ratio of septal to free wall thickness was 1.5(0.8) for patients with hypertrophic cardiomyopathy, 0.8(0.2) for those with left ventricular hypertrophy, and 0.9(0.2) for normal subjects. Although septal measurements by nuclear magnetic resonance were greater than those obtained by echocardiography there was a significant correlation between the two. Septal and free wall area were significantly smaller in normal subjects. There were no differences in septal or free wall T1 values between the three groups. Non-gated nuclear magnetic resonance can detect septal and free wall hypertrophy. With the addition of multiple slice acquisition, rapid estimation of myocardial mass will be possible allowing the potentially important assessment of progression or regression of myocardial hypertrophy.

Adult↗
PubMed1985

Electrophysiological effects of felodipine.

Oral felodipine (10mg) was given to 11 patients undergoing routine invasive electrophysiological studies. Systolic blood pressure fell by 31 mm Hg from 130 +/- 17.5 to 99 +/- 10 mm Hg (mean +/- SD, p less than 0.001) while diastolic pressure fell from 78 +/- 9 to 60 +/- 8mm Hg (p less than 0.001), thus confirming its vasodilator properties. Heart increased from 64 +/- 10 to 78 +/- 16 beats/min (p less than 0.001). The A-H interval was significantly prolonged from 97 +/- 14 to 110 +/- 24 msec (p less than 0.01) while there was no change in the H-V interval. Sinus node recovery time showed no change when corrected for heart rate. The effective refractory period of the atrioventricular node was shortened from 317 +/- 38 to 287 +/- 27 msec (p less than 0.01) as was the effective refractory period of the ventricular Purkinje fibres from 251 +/- 18 to 237 +/- 20 msec (p less than 0.005). These haemodynamic and electrophysiological changes suggest that this compound is an effective vasodilator and may have potential antiarrhythmic properties.

Adult↗
PubMed1985

Electrophysiological effects of felodipine in combination with metoprolol.

The combined use of some beta-adrenoceptor blocking agents with calcium channel blockers may cause adverse pharmacodynamic drug interactions: hypotension, heart block or even asystole may be precipitated. The electrophysiological effects of combined administration of intravenous metoprolol 10mg and the vasodilating calcium antagonist felodipine (0.1 mg/kg/bodyweight) were assessed in an open study by invasive methods. Following metoprolol, the heart rate was reduced from 69 +/- 24 to 60 +/- 16 beats/min (mean +/- SD, p less than 0.05) with a minor prolongation of the sinus node recovery time. The A-H interval was increased from 94 +/- 25 to 109 +/- 16 msec (p less than 0.005) and the H-V interval was unchanged. The effective refractory period of the atrioventricular node was prolonged from 327 +/- 54 to 361 +/- 62 msec (p less than 0.01) with a minor prolongation of the effective refractory period of the ventricular Purkinje fibres. Systolic and diastolic blood pressures showed a mean reduction of 11 (p less than 0.001) and 6mm Hg (p less than 0.05), respectively. Following felodipine, the changes in heart rate and effective refractory periods of the atrioventricular node and ventricular Purkinje fibres returned towards control values. No further prolongation of the A-H interval resulted and further blood pressure changes were minor. The absence of adverse haemodynamic or electrophysiological effects suggests that this combination of agents may be safely used.

Adult↗
PubMed1984

Effect of afterload reduction in patients with ventricular and physiological pacing.

The effect of afterload reduction was studied in a group of patients who remained breathless or tired after permanent ventricular pacing. Haemodynamic measurements were made before and after giving hydralazine 20 mg intravenously using a triple lumen thermodilution catheter and cuff blood pressure recordings during ventricular pacing at the standard rate of 71/min or an increased rate of 88/min and physiological pacing. Increasing the ventricular pacing rate had no effect on cardiac output as stroke volume fell. Hydralazine produced a greater rise in cardiac output than physiological pacing alone, although peak values were obtained by combining the two. Ventricular pacing produced intermittent large left and right atrial pressure peaks. Physiological pacing produced no such peaks, and mean right and left atrial pressures fell. Hydralazine did not significantly alter atrial pressures. These findings show that in these patients, most of whom had a low cardiac output, afterload reduction with ventricular pacing increased resting cardiac output more than physiological pacing alone. Nevertheless, persistence of high filling pressures despite afterload reduction may limit the potential therapeutic benefit. Care should be taken in extrapolating these data to other patient groups.

Adult↗