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Biomedical subjects

S G Ray

Publications and source records attributed to S G Ray.

At least 37 records · Page 2Linked to original sources
PubMed1996

Trends in pacemaker mode prescription 1984-1994: a single centre study of 3710 patients.

OBJECTIVE: To evaluate trends in pacemaker mode prescription from 1984 to 1994 with particular reference to the changes in pacemaker mode prescription for patients aged 80 years and older at implant. DESIGN: Prospective evaluation of indications for pacing and pacemaker mode prescription in all patients undergoing new pacemaker implantation from 1992 to 1994. Comparison with retrospectively obtained data for patients paced from 1984 to 1991. SETTING: Tertiary referral cardiothoracic centre. PATIENTS: Group 1: 2622 patients paced at one centre and entered into the national pacing database from 1984 to 1991. Group 2: 1088 consecutive patients paced from 1992 to 1994. RESULTS: Use of atrial (AAI) and dual chamber (DDD) pacemakers increased progressively in patients of all ages from 1984 to 1994. There was an increase in the proportion of patients aged 80 years and older from 25.4% (group 1) to 40.5% (group 2). Patients of all ages in group 2 were more likely to receive DDD units for atrioventricular block (odds ratio (95% confidence interval) (CI) 9.0 (7.0 to 11.5)) and AAI or DDD units for sinus node disease (odds ratio (95% CI) 11.0 (7.7 to 15.8)) than those in group 1. Elderly patients (age > or = 80 at implant) with atrioventricular block or sinus node disease and a suitable atrial rhythm were less likely to receive DDD or AAI pacemakers than younger patients in both groups. CONCLUSIONS: Use of atrial and dual chamber pacing modes has increased substantially in patients of all ages over the last decade. Although elderly patients represent an increasing proportion of the paced population, they remain less likely to receive atrial or dual chamber pacemakers than younger patients.

Age Factors↗
PubMed1995

Do radionuclide and echocardiographic techniques give a universal cut off value for left ventricular ejection fraction that can be used to select patients for treatment with ACE inhibitors after myocardial infarction?

OBJECTIVE: To determine whether echocardiography and radionuclide angiography give comparable results when the left ventricular ejection fraction is measured early after myocardial infarction and thus whether, irrespective of the method used, a single value for the ejection fraction could be used as a guide for starting treatment with an angiotensin converting enzyme inhibitor. DESIGN: Prospective comparison of measurement of left ventricular ejection fraction by echocardiography and radionuclide angiography. SETTING: Coronary care units of two university teaching hospitals in Glasgow. PATIENTS: 99 patients studied within 36 hours of acute myocardial infarction. OUTCOME MEASURES: Left ventricular ejection fraction assessed by echocardiography and radionuclide angiography. RESULTS: 70 (77%) of the 99 patients had ejection fraction measured by both echocardiographic and radionuclide techniques, 30 in centre 1 and 40 in centre 2. In centre 1 the mean difference (SD) in ejection fraction (radionuclide angiography--echocardiography) was -8 (10%); 95% CI -12 to -4%. In centre 2 the mean difference was -14 (11%); 95% CI -17 to -11%. If patients had been treated with an ACE inhibitor on the basis of a radionuclide ejection fraction of < 40% then 93% in centre 1 (28 of 30) and 98% in centre 2 (39 of 40) would have been treated. This compares with 63% (19 of 30) and 50% (20 of 40), respectively if echocardiography had been used as a guide. CONCLUSION: Measurement of ejection fraction is highly dependent on the method used and it is therefore impossible to quote a universally applicable figure for left ventricular ejection fraction below which an ACE inhibitor should be used after myocardial infarction.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Early complications of permanent pacemaker implantation: no difference between dual and single chamber systems.

OBJECTIVE: To evaluate the incidence of intraoperative and early postoperative complications (up to two months after implant) of endocardial permanent pacemaker insertion in all patients under-going a first implant at a referral centre. METHODS: Prospective evaluation of all endocardial pacemaker implantation procedures performed from April 1992 to January 1994 carried out by completion of standard audit form at implant. Patients' demographic data, medical history, details of pacemaker hardware used, and any complications were noted. Follow up information was also collected prospectively onto standard forms at pacemaker outpatient clinic. SETTING: United Kingdom tertiary referral cardiothoracic centre. PATIENTS: 1088 consecutive patients underwent implantation of their first endocardial permanent pacemaker from April 1992 to January 1994. Implant and follow up data were available for 1059 (97.3%) patients at analysis. The median (range) age was 77 years (16-99); 51.2 % were male. RESULTS: Dual chamber units were implanted in 54.1% of patients, single chamber atrial in 5.2%, and ventricular in 40.7%. A temporary pacing lead was present at implant in 22.9% of patients. Most (93.6%) implants were performed via the subclavian vein. Immediate complications were rare: eight (0.8%) patients developed pneumothorax requiring medical treatment and 11 (1.0%) an insignificant pneumothorax. There was no significant difference in the pneumothorax rate for dual chamber (DDD) compared with single chamber systems. Arterial puncture without sequelae was documented in 2.7% of attempts at subclavian vein cannulation. A total of 35 patients (3.3%) required reoperation; the reoperation rate for dual chamber (3.5%) was similar to that for single chamber (3.1%) systems. Electrode displacement (n = 15, 1.4%) was the most common reason for reoperation. Atrial lead displacement (n = 10, 1.6% of atrial leads) was significantly more common than ventricular lead displacement (n = 5, 0.5% of ventricular leads, P = 0.047). There was no difference in electrode displacement rates for dual (1.6%) compared with single (1.2%) chamber systems. Pacemaker pocket infection led to reoperation in 10 patients (six dual, four single chamber, P = not significant) and was significantly more common in patients who had a temporary pacing lead in place at implant (2.9%) than in those who did not (0.4%, P = 0.0014). Five patients (0.5%) required reoperation for generator erosion (two dual, three single chamber, P = not significant). and a further five for drainage of haematoma or a serous fluid collection (three dual, two single chamber, P = not significant). Complications that did not require reoperation were also rare. Undersensing occurred in 10 patients (0.9%). Atrial undersensing (n = 8) was significantly more common than ventricular undersensing (n = 2, P = 0.017). All patients were successfully treated by reprogramming of sensitivity. Superficial wound infection was treated successfully with antibiotics in nine patients (six dual, three single chamber, P = not significant). Three patients with DDD generators developed sustained atrial fibrillation: two required reprogramming to VVI mode and one required cardioversion. CONCLUSIONS: Permanent pacing in a large tertiary referral centre with experienced operators carries a low risk. Infection rates are low, < 1% overall but significantly higher in patients who undergo temporary pacing before implantation. Lead displacement and undersensing are more likely to occur with atrial than ventricular leads. The overall complication rate for dual chamber pacing, however, is no higher than for single chamber pacing.

Adolescent↗
PubMed1994

Cardiorespiratory and symptomatic variables during maximal and submaximal exercise in men with stable effort angina: a comparison of atenolol and celiprolol.

Celiprolol is a novel beta 1 selective adrenoreceptor blocker with partial beta 2 agonism and direct vasodilator activity. These ancillary properties may reduce symptomatic breathlessness and fatigue and modify respiration during exercise. To test this hypothesis 20 men with stable effort angina were enrolled in a double-blind crossover study to investigate the effects of atenolol 100 mg once daily (A) and celiprolol 400 mg once daily (C) on cardiorespiratory and symptomatic variables during maximal and submaximal exercise. Total exercise time on a modified Bruce protocol was similar on both treatments: C12.5 min, A 13.1 min. During steady state submaximal exercise at 60-75% (mean 68%) of maximum work capacity, minute ventilation (C33.81 min-1, A 33.51 min-1), oxygen uptake (C14.6 ml.kg-1.min-1, A15.1 ml.kg-1.min-1), respiratory exchange ratio (C 0.89, A 0.87), ratio of VE/VCO2 (C 33.6, A 33.4), ratio of VE/VO2 (C 2.34, A 2.72), Borg perceived exertion score (C 11.2, A 10.9) and visual analogue scores for breathlessness (C 29.5, A 25.9) and muscle fatigue (C 28.9, A 26.0) were all similar on both treatments. At maximal exercise capacity on the modified Bruce protocol, minute ventilation (C 58.31 min-1, A 60.41 min-1), oxygen uptake (C 21.3 ml.kg-1.min-1, A 21.7 ml.kg-1.min-1), respiratory exchange ratio (C 1.02, A.1.05), ratio VE/VCO2 (C 34.8, A 35.9), and ratio VE/VO2 (C 2.80, A 2.83) were also similar on both drugs. Over a 10 day period anginal attacks (C 10.1 +/- 10.4, A 5.4 +/- 5.9) and sublingual GTN use (C 5.9 +/- 10.3, A 4.4 +/- 9.8) were both more frequent on celiprolol).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

Relationship of renin, angiotensin II and atrial natriuretic factor to clinical status in the early post-infarct period in patients with left ventricular dysfunction.

The vasoconstrictor and cardiotoxic effects of angiotensin II may be particularly harmful in the early post-infarct period, but could be partially offset by the release of atrial natriuretic factor. We studied the relationship of renin, angiotensin II and atrial natriuretic factor to clinical status in the first 72 h after infarction in 36 patients not requiring treatment with diuretics on clinical grounds. Since these patients were treated with streptokinase, 16 non-thrombolysed patients were included to control for the acute effects of streptokinase on plasma hormones. Streptokinase caused transient fluctuations in plasma renin and atrial natriuretic factor but did not limit the subsequent development of supranormal hormone levels. Streptokinase-treated patients were divided on the basis of the highest recorded Killip class. Activation of the renin angiotensin system occurred only in those patients in Killip class 2 (n = 11), was maximal at 24-72 h and was proportional to the extent of left ventricular dysfunction. Plasma levels of atrial natriuretic factor were elevated on admission, even in patients in Killip class 1 (n = 25), but declined within an hour before rising again to supranormal levels at 24-72 h. Cumulative release of renin and angiotensin II, but not atrial natriuretic factor, were significantly greater in patients in Killip class 2. Heart rate was greater in Killip class 2 at 24 and 72 h but there was no difference in mean arterial pressures. We conclude that the renin angiotensin system is activated in the early post-infarction phase, but only in patients in Killip class 2, possibly as a result of increased sympathetic activity and reduced renal perfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Factor↗
PubMed1994

Stability of the DDD pacing mode in patients 80 years of age and older.

We reviewed the records of 119 consecutive patients aged 80 years or older (mean age 84 +/- 3.7 years) in whom a dual chamber pacemaker was implanted between 1984 and 1991. Follow-up data was available up to February 1993. Immediate postimplantation complications were rare. Nine patients were lost to follow-up, all within 6 months of implantation. An additional seven patients died within 6 months of implantation. Long-term follow up for at least 6 months from implantation was available for 103 of the 119 patients (87%). Of these 89 (86%) remained in functioning DDD mode for a mean of 22 +/- 15 months from implantation. Nine patients were reprogrammed to VVI mode, six due to atrial fibrillation and three due to failure of atrial sensing or pacing. One patient was programmed DVI for failure of atrial sensing; 94 of 112 patients (84%) whose status was definitely known in February 1993 remained in functioning DDD mode until death or last follow-up. Cumulative survival in DDD mode was 78% at 30 months. We conclude that DDD pacing is stable in the great majority of patients in their ninth and tenth decades who present with rhythms amenable to dual chamber pacing and who have no history of sustained atrial fibrillation.

Aged↗
PubMed1994

Impact of internal audit on pacemaker prescription and the immediate costs of pacing in the northern region: towards implementation of the recommendations of the British Pacing and Electrophysiology Group.

BACKGROUND: In September 1990 a working party of the British Pacing and Electrophysiology Group recommended the routine use of physiological pacing systems in patients with bradycardia. An audit of the impact of these recommendations on pacemaker prescription in the Freeman Hospital between March 1990 and August 1991 has previously been reported. This paper considers the effect of that internal audit on subsequent pacemaker prescription from September 1991 to February 1993. PATIENTS AND METHODS: The records of 1228 patients who underwent first pacemaker implantation at the Freeman Hospital between March 1990 and February 1993 were audited retrospectively. The patient's age, indication for pacing, pacing mode, and cost of the generator and leads were recorded. The indications for pacing were sinus node dysfunction (24.9%) (including patients with coexistent sinus node dysfunction and atrioventricular block), atrioventricular block (57.2%), atrioventricular block and atrial fibrillation (12.2%), and carotid sinus syndrome (5.7%). There was an increase in carotid sinus syndrome (2.7% to 8.1%) between the two study periods but no other differences in the distribution of case mix or characteristics of patients. The cost of the working party's recommended optimal pacing mode was calculated from multiplication of the mean cost of the recommended unit over the second half of the study period by the number of patients who would have received that unit. RESULTS: Between March 1990 and August 1991 atrial pacing for sinus node dysfunction (AAI, AAIR, DDD, or DDDR) increased by 138% (from 25.0% to 59.6%), mainly because of increased use of AAI mode. Physiological pacing for atrioventricular block (DDD or VVIR) increased by 41% (from 17.0% to 24.0%), and VVIR pacing for atrioventricular block with atrial fibrillation increased by 111% (from 10.5% to 22.2%). After the internal audit (that is, between September 1991 and February 1993), physiological pacing for atrioventricular block increased by a further 126% (from 24.0% to 54.2%). Sixty three per cent of this increase was in the first six months after the internal audit. Pacemaker prescriptions in sinus node dysfunction and atrioventricular block with atrial fibrillation were unchanged (59.6% physiological pacing for sinus node dysfunction and 22.2% v 27.3% VVIR pacing for atrioventricular block with atrial fibrillation). These changes in practice were accompanied by an increase in the age of patients receiving physiological units. Costs of pacemaker hardware for the final six months of the audit (excluding carotid sinus syndrome) increased by 38% over the costs that would have accrued had pacing policy remained the same as for the initial six month period before the circulation of the recommendations of the working party. Adoption of the guidelines of the working party in full would lead to a further 66% increase in the costs of hardware. CONCLUSIONS: The principal effect of the recommendations of the working party alone was increased use of AAI pacing for sinus node dysfunction, with little change in the costs of hardware. The internal audit was followed by an increase in physiological pacing for atrioventricular block, and this has had important financial consequences. Internal audit was followed by closer adherence to the recommendations of the working party.

Aged↗
PubMed1993

Neuroendocrine activation and markers of early reperfusion in the acute phase of myocardial infarction.

Potentially harmful stimulation of the neuroendocrine axis occurs in the early hours of myocardial infarction. It has been suggested that this acute neuroendocrine response might be attenuated by early therapeutic reperfusion. To test this hypothesis we measured plasma concentrations of atrial natriuretic factor (ANF), renin, adrenaline (ADR) and noradrenaline (NADR) on admission and at 1 h and 4 h in 32 patients undergoing streptokinase treatment within 6 h of myocardial infarction. Fractional changes (FC) in hormone levels were calculated: e.g. ANFO-ANF4/ANFO. Resolution of ST segment elevation at 4 h was the primary measure of reperfusion. Sixteen patients showed ST segment resolution. There was no difference in hormone levels at baseline between reperfused and non-reperfused patients. Fractional changes in ANF, renin and ADR were similar in both groups. NADR fell from admission to 4 h in reperfused patients but rose in non-reperfused (FC 0.28 vs -0.10; P = 0.054). There was no difference in the changes in pulse rate or blood pressure from admission to 4 h between the two groups. Thus there is no evidence that early reperfusion acutely alters the release of ANF, renin or ADR to myocardial infarction. Although plasma NADR tended to fall acutely in reperfused patients this was not accompanied by other markers of sympathetic withdrawal.

Atrial Natriuretic Factor↗
PubMed1993

Early treatment with captopril after acute myocardial infarction.

OBJECTIVES: To determine the effects of early treatment with captopril on haemodynamic function, neuroendocrine biochemistry, left ventricular structure, clinical outcome, and exercise capacity over one year from acute myocardial infarction. DESIGN: Randomised, double blind, placebo controlled comparison of captopril and placebo. SETTING: Coronary care units and cardiology departments of two university teaching hospitals in Glasgow. PATIENTS: 99 haemodynamically stable patients with acute myocardial infarction, selected on clinical grounds as being at risk of late ventricular dilatation. INTERVENTION: Captopril or identical placebo started between six and 24 hours after start of symptoms and continued for 12 months. Target maintenance dose was 25 mg three times a day. MAIN OUTCOME MEASURES: (a) Acute haemodynamic effects of treatment; (b) neuroendocrine biochemistry from admission to two months; and (c) change in echocardiographic measures of left ventricular size, clinical outcome, and exercise capacity after 12 months of treatment with a separate analysis of the effects of one month of treatment withdrawal on left ventricular volumes. RESULTS: Captopril caused acute reductions in mean (SEM) pulmonary artery pressure (2.48 (0.69) mm Hg) and systemic vascular resistance (260 (103)) dyn.s.cm-5). Over the first 10 hours captopril reduced mean arterial pressure by 12.1 (2.4) mm Hg compared with 3.8 (1.9) mm Hg in the placebo group. No patient had to be withdrawn from the captopril group because of hypotension. From day 1 onwards systolic and diastolic arterial pressures in the captopril treated group were slightly but not significantly lower than on placebo. There was no difference in the incidence of ventricular or supraventricular arrhythmia with treatment. Captopril prevented the day 3 peak in angiotensin II that occurred in the placebo group (peak concentration (interquartile range): 10.1 (4.8-19.4) pg/ml v 16.8 (4.3-46.3) pg/ml)) but had no effect on atrial natriuretic factor, arginine vasopressin, or catecholamines. Plasma atrial natriuretic factor remained above normal in both groups at two months after infarction. After one year left ventricular volume indices had increased less on captopril than on placebo: left ventricular end systolic volume index 5.4 ml/m2 v 14.7 ml/m2 (95% confidence interval (95% CI) of difference -14.6 to -3.9; p = 0.0011); left ventricular end diastolic volume index 8.4 ml/m2 v 19.0 ml/m2 (95% CI of difference, -17.0 to -4.2; p = 0.0016). Withdrawal of captopril for one month did not affect ventricular volumes. There was no difference in exercise capacity. CONCLUSIONS: Captopril started between six and 24 hours after acute myocardial infarction is not associated with significant hypotension. It suppresses activation of the renin angiotensin system but has no effect on plasma concentrations of other neurohormones. Atrial natriuretic factor remains raised at two months after myocardial infarction. Captopril significantly decreases left ventricular dilatation. This effect is not lost after one month of treatment withdrawal and is thus due to an alteration of left ventricular structure and not to a short lived haemodynamic action of captopril. Long-term treatment with captopril does not result in improved aerobic exercise capacity after acute myocardial infarction.

Adult↗
PubMed1992

Circulating endothelin in acute ischaemic syndromes.

BACKGROUND: Endothelin is an extremely potent vasoconstrictor that may have a role in the pathogenesis of acute myocardial ischaemia. Atrial natriuretic factor is an endogenous antagonist of endothelin. To find the pattern and possible importance of circulating endothelin in ischaemic heart disease, concentrations in normal controls and those in patients with stable and unstable angina, acute myocardial infarction, and chronic cardiac failure were compared. The relation between circulating concentrations of endothelin and atrial natriuretic factor in the aftermath of myocardial infarction was also examined. METHODS: Eighteen patients with acute myocardial infarction, 10 with unstable angina, 10 with stable angina, 12 with chronic cardiac failure, and 10 normal controls were studied. Endothelin concentration was measured in venous plasma by radioimmunoassay. In patients with acute myocardial infarction simultaneous concentrations of endothelin and atrial natriuretic factor were measured on admission and at one, four, and 24 hours. RESULTS: Mean concentrations (SEM) of endothelin were 5.72 (0.19) fmol/ml in controls, 6.56 (0.48) fmol/ml in stable angina, 6.41 (0.48) fmol/ml in unstable angina, and 13.83 (0.95) fmol/ml in chronic cardiac failure. In acute myocardial infarction concentrations were 8.81 (0.69) fmol/ml on admission, 11.85 (1.02) fmol/ml at one hour, 11.88 (1.10) fmol/ml at four hours, and 7.30 (0.49) fmol/ml at 24 hours. Concentrations of atrial natriuretic factor at the same times were 68.1 (13.1) pg/ml, 8.4 (1.5) pg/ml, 24.4 (4.1) pg/ml, and 42.0 (6.9) pg/ml. CONCLUSIONS: Plasma endothelin is raised in chronic heart failure and in the aftermath of acute myocardial infarction but not in stable or unstable angina. After myocardial infarction endothelin concentrations are raised whereas concentrations of atrial natriuretic factor are relatively low. The role of endothelin in the pathogenesis of acute myocardial infarction and its interactions with other humoral factors require further investigation.

Angina Pectoris↗
PubMed1992

Impact of the recommendations of the British Pacing and Electrophysiology Group on pacemaker prescription and on the immediate costs of pacing in the Northern Region.

BACKGROUND: The report from the Working Party of the British Pacing and Electrophysiology Group recommends the use of more sophisticated pacemakers in most patients. These proposals were initially circulated in September 1990 and are likely to have major cost implications. Their impact on pacing practice and the immediate costs of pacemaker hardware in the Northern Region were retrospectively audited. METHODS: The pacing records of 550 patients undergoing a first pacemaker insertion at the Freeman Hospital between March 1990 and August 1991 were reviewed. The patient's age, indication for pacing, pacing mode, and the cost of generator and lead(s) were recorded. The cost was compared with the costs of pacing with the optimal and alternative modes recommended by the Working Party. The costs were calculated from the actual mean cost of the recommended unit over the 18 month period of study multiplied by the number of patients who would have received that unit. RESULTS: 96% of patients were paced for sinus node dysfunction, atrioventricular block, or atrioventricular block and atrial fibrillation. The mean (SD) ages of patients in each diagnostic group were: sinus node dysfunction 69.4 (14), sinus node disease and atrioventricular block 67.2 (17.6), atrioventricular block 73.9 (12.5), atrial fibrillation and atrioventricular block 74.0 (13.9), and carotid sinus hypersensitivity 74.6 (11.6) years. Over the 18 month audit period there was an increase in physiological pacing. AAI pacing in patients with sinus node dysfunction increased by 100% and DDD pacing in atrioventricular block increased by atrioventricular block increased by 56%. Over the whole 18 month period the adoption of the British Pacing and Electrophysiology Groups optimal recommendations would have increased expenditure on pacemaker hardware in the Northern Region by 94% and the use of the alternative mode would have increased it by 61%. For the last six months alone the excess would be 78% and 48%. CONCLUSIONS: The adoption of the recommendations of the British Pacing and Electrophysiology group in the Northern Region would greatly increase the cost of pacing hardware. The greater part of this increase would be attributable to the routine use of dual chamber pacing in patients with atrioventricular block and the increased use of rate responsive units. The benefits of sophisticated pacing in a predominantly elderly population need to outweigh the disadvantages of the increased cost and complexity of follow up.

Aged↗
PubMed1992

Plasma endothelin in chronic heart failure.

BACKGROUND: Endothelins are recently characterized vasoconstrictor peptides. As chronic heart failure (CHF) is characterized by peripheral arteriolar and renal vasoconstriction, we have measured venous plasma endothelin-like immunoreactivity ("endothelin") in patients with this syndrome. METHODS AND RESULTS: Compared with age- and sex-matched healthy volunteers (mean +/- SEM plasma endothelin concentration 6.4 +/- 0.3 pmol/l, n = 16), patients with severe CHF had elevated peripheral venous endothelin concentrations (12.4 +/- 0.6 pmol/l, n = 47, p less than 0.01). Plasma endothelin did not increase with exercise in normal subjects or in patients. Plasma endothelin concentration (mean, 13.4 +/- 0.9 pmol/l) did not correlate with plasma atrial natriuretic factor concentration (mean, 88.9 +/- 11.9 pg/ml) in patients with CHF (n = 21). There was also no correlation between plasma endothelin and serum urea or between endothelin and serum creatinine in patients with CHF (n = 34). There was, however, significant renal extraction of endothelin (aorta, 11.1 +/- 0.8 pmol/l; renal vein, 8.8 +/- 0.6 pmol/ml; p = 0.02) in patients with CHF (n = 13). CONCLUSIONS: Evidence suggests that circulatory endothelin concentrations in the range 5-40 pmol/l are vasoactive. Consequently, the endothelin concentrations found in patients with CHF may be of pathophysiological significance.

Aged↗
PubMed1992

Circulating endothelin is not extracted by the pulmonary circulation in man.

To determine whether endothelin is extracted from plasma during passage through the pulmonary circulation, we measured its concentration at several points, including the pulmonary artery and the left superior pulmonary vein in seven patients undergoing cardiac surgery. Endothelin concentrations were very similar at all sites sampled. In patients undergoing coronary artery bypass grafting, there is no net pulmonary clearance of endothelin.

Adult↗
PubMed1991

Effects of early captopril administration on infarct expansion, left ventricular remodeling and exercise capacity after acute myocardial infarction.

In a double-blind study, 99 patients (82 men, age range 40 to 75 years) with acute myocardial infarction (AMI) were randomly assigned to receive captopril or placebo. Treatment began within 24 hours of admission. Serial echocardiographic measurements of endocardial segment lengths and left ventricular (LV) volumes, and ejection fractions were obtained. The 2 groups were matched at baseline except for an excess of previous AMI in the placebo group (13 of 50 vs 2 of 49 patients, p = 0.002). The increase in anterior segment length, from baseline to 2 months, was significantly less in the captopril than in the placebo group (2.8 +/- 1.6 vs 10.4 +/- 2.4mm, 95% confidence interval [CI] -13.5 to -1.7, p = 0.01). The increase in posterior segment length was also less in the captopril group, but the difference was not significant (3.2 +/- 1.2 vs 7.0 +/- 1.8mm, 95% CI -8.0 to 0.5, p = 0.08). Fewer patients in the captopril group demonstrated increases in segment length greater than 2 standard deviations of the measurement error (14 of 70 [20%] vs 29 of 72 [40%] patients, p = 0.009). In patients with anterior AMI, the infarct-containing anterior segment length increased by 4.5 +/- 2.3 mm in the captopril versus 12.4 +/- 3.1 mm in the placebo group (95% CI -15.7 to -0.2, p = 0.046), and fewer patients in the captopril group demonstrated infarct expansion (6 of 20 [30%] vs 13 of 21 [62%] patients, p = 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Importance of RAA system and the treatment of patients with ACE inhibition after myocardial infarction.

There is activation of the renin angiotensin system after both complicated and uncomplicated myocardial infarction. Angiotensin II increases myocardial oxygen consumption whilst reducing coronary flow and is also directly toxic to the myocardium. Angiotensin converting enzyme inhibitors produce beneficial haemodynamic and neuroendocrine changes in patients with acute left ventricular failure, and may have a role in selected patients with cardiogenic shock. There is evidence to suggest that they might prevent the development of late cardiac failure by limiting the extent of post infarction ventricular dilation. Further research is necessary to define their role in the treatment of acute myocardial infarction.

Angiotensin II↗
PubMed1989

The effects of angiotensin-converting enzyme inhibition on coronary blood flow and infarct size limitation.

A number of theoretical and practical aspects of acute myocardial infarction suggest a potential role for ACE inhibition in enhancing coronary blood flow and limitation of infarct size. Indeed, the use of ACE inhibitors in acute myocardial infarction could be viewed as a logical intervention in the face of the neuroendocrine response which accompanies the acute phase. During the first 24 h post-infarction, very high plasma concentrations of arginine-vasopressin and catecholamines occur. This is followed by a sharp rise in the concentration of angiotensin II (ANG II) over the next few days. The neuroendocrine response is most marked in those patients with larger infarcts, who frequently develop left ventricular failure. The extent to which these factors influence coronary flow in acute myocardial infarction is unknown, although in chronic heart failure ACE inhibition does not reduce coronary blood flow despite a reduction in rate-pressure product, suggesting a coronary vasodilator effect. However, in the presence of fixed coronary stenoses, the fall in blood pressure and, therefore, of coronary perfusion pressure must be taken into account. Whether or not the use of ACE inhibitors can limit infarct size in man also remains to be determined, although it has been clearly demonstrated that concentrations of ANG II similar to those observed in the early phase of myocardial infarction can cause myocardial cell damage in experimental animals. Post-infarction ventricular enlargement can be reduced by ACE inhibitors. Additionally, ACE inhibitors, through their balanced vasodilator effect, maintain cardiac output whilst reducing filling pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗