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Biomedical subjects

P A Crean

Publications and source records attributed to P A Crean.

At least 19 recordsLinked to original sources

Bypass surgery versus stenting for the treatment of multivessel disease in patients with unstable angina compared with stable angina.

BACKGROUND: Earlier reports have shown that the outcome of balloon angioplasty or bypass surgery in unstable angina is less favorable than in stable angina. Recent improvements in percutaneous treatment (stent implantation) and bypass surgery (arterial grafts) warrant reevaluation of the relative merits of either technique in treatment of unstable angina. Methods and Results- Seven hundred fifty-five patients with stable angina were randomly assigned to coronary stenting (374) or bypass surgery (381), and 450 patients with unstable angina were randomly assigned to coronary stenting (226) or bypass surgery (224). All patients had multivessel disease considered to be equally treatable by either technique. Freedom from major adverse events, including death, myocardial infarction, and cerebrovascular events, at 1 year was not different in unstable patients (91.2% versus 88.9%) and stable patients (90.4% versus 92.6%) treated, respectively, with coronary stenting or bypass surgery. Freedom from repeat revascularization at 1 year was similar in unstable and stable angina treated with stenting (79.2% versus 78.9%) or bypass surgery (96.3% versus 96%) but was significantly higher in both unstable and stable patients treated with stenting (16.8% versus 16.9%) compared with bypass surgery (3.6% versus 3.5%). Neither the difference in costs between stented or bypassed stable or unstable angina ($2594 versus $3627) nor the cost-effectiveness was significantly different at 1 year. CONCLUSIONS: There was no difference in rates of death, myocardial infarction, and cerebrovascular event at 1 year in patients with unstable angina and multivessel disease treated with either stented angioplasty or bypass surgery compared with patients with stable angina. The rate of repeat revascularization of both unstable and stable angina was significantly higher in patients with stents.

Acute Disease↗

Relationship between intracoronary and peripheral expression of soluble cell adhesion molecules.

BACKGROUND: Elevated levels of soluble cell adhesion molecules (sCAMs) have been reported in various coronary artery disease processes. The principle stimulus for expression of sCAMs is believed to be an inflamed atherosclerotic plaque within the coronary vessel. The relationship between levels of sCAMs in the coronary circulation and the peripheral circulation has not been defined. The primary aim of this study was to define the relationship between levels of sCAMs sampled from the systemic circulation and from the coronary circulation. We also set out to document the acute expression of soluble CAMs following coronary angioplasty with or without stent implantation. METHODS: The coronary sinus was cannulated in patients undergoing LAD angioplasty. Samples were drawn from left coronary ostium (LCO) and coronary sinus (CS) and femoral vein simultaneously before, immediately after and 4 h after the PTCA procedure. Levels of sICAM-1, sVCAM-1, sE-selectin and sP-selectin were measured using ELISA technique. RESULTS: 10 patients (7 male/3 female, 61+/-11 y) entered the study. There was no significant difference in the levels of sICAM-1, sVCAM-1, sE-selectin and sPselectin whether sampled from left coronary ostium, coronary sinus or femoral vein at all time points. There was no significant change in the acute expression of sICAM-1, sVCAM-1 and sE-selectin following coronary angioplasty. Levels of sP-selectin fell significantly during the PTCA procedure (142+/-7 ng/ml to 64+/-6 ng/ml, P<0.001) but then rose again after 4 h and returned toward baseline levels at 24 h. CONCLUSION: Levels of soluble CAMs sampled in the systemic circulation directly reflect levels in the coronary circulation. Coronary angioplasty results in rapid fall in levels of sP-selectin which returns to normal within 24 h following the procedure.

Aged↗

Enhanced endothelial activation in diabetic patients with unstable angina and non-Q-wave myocardial infarction.

AIMS: Diabetes mellitus (DM) is associated with chronic endothelial dysfunction. Diabetic patients presenting with acute coronary syndromes have a worse prognosis than non-diabetics. An acute inflammatory reaction at the site of coronary plaque rupture and increased expression of surface and soluble cellular adhesion molecules (CAMs) are pathological features of acute coronary syndromes. We set out to characterize the expression of soluble CAMs in patients with and without diabetes presenting with unstable angina (UA) and non Q-wave myocardial infarction (NQMI). METHODS: Patients presenting with UA and NQMI had serum samples taken on presentation, after 72 h and then 3, 6 and 12 months after discharge. Levels of soluble intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin and P-selectin were measured using an ELISA technique. RESULTS: We studied 15 diabetic patients and 15 age- and sex-matched non-diabetic patients presenting with either UA or NQMI. Levels of soluble E-selectin were elevated in the diabetic patients in comparison with the non-diabetic patients at all measured time points: 74 +/- 10 ng/ml vs. 47 +/- 3 ng/ml, P < 0.03 at t = 0 h, 55 +/- 5 ng/ml vs. 38 +/- 2 ng/ml, P < 0.02 at t = 72 h. However, levels of soluble P-selectin were lower in the diabetic cohort during follow-up: 134 +/- 15 ng/ml vs. 225 +/- 32 ng/ml, P < 0.02 at t = 3/12 and 112 +/- 8 ng/ml vs. 197 +/- 23 ng/ml, P < 0.02 at t = 6/12. There was no significant difference in levels of soluble ICAM-1 and VCAM-1 between diabetic and non-diabetic patients. CONCLUSIONS: Levels of soluble E-selectin are significantly elevated in diabetic patients presenting with UA and NQMI in comparison with non-diabetics. This finding may reflect enhanced endothelial activation which may contribute to the adverse prognosis of diabetic patients with acute coronary syndromes.

Aged↗

Risk stratification in unstable angina and non-Q wave myocardial infarction using soluble cell adhesion molecules.

OBJECTIVE: To assess prospectively the prognostic value of soluble cellular adhesion molecules (CAMs) in patients with unstable angina and non-Q wave myocardial infarction and to compare their prognostic accuracy with that of C reactive protein (CRP). DESIGN AND SETTING: Prospective observational study of patients presenting acutely with unstable angina and non-Q wave myocardial infarction to a single south Dublin hospital. METHODS: Patients with Braunwald IIIA unstable angina and non-Q wave myocardial infarction had serum samples taken at presentation before initiation of antithrombotic treatment and were followed for six months. The primary end point was the occurrence of major adverse cardiovascular events (recurrent unstable angina, non-fatal myocardial infarction, and cardiovascular death) at six months. Concentrations of soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble endothelial selectin, and soluble platelet selectin were measured using an enzyme linked immunosorbent assay technique. CRP was measured with an immunophelometric assay. RESULTS: 91 patients (73 men and 18 women, mean (SD) age 61 (11) years) were studied; 27 patients (30%) had major adverse cardiac events during the six months of follow up. Concentration of CRP were significantly raised in patients who had an ischaemic event (mean (SEM) 11.5 (6.4) mg/l v 5.4 (2.5) mg/l, p < 0.001). Concentrations of sVCAM-1 were also significantly raised in the ischaemic event group (979 (30) ng/ml v 729 (22) ng/ml, p < 0.001). Both sVCAM-1 and CRP concentrations correlated strongly with the occurrence of an adverse event. The sensitivity of CRP > 3 mg/l and sVCAM-1 > 780 ng/ml for predicting future events was > 90%. There was no difference in concentrations of sICAM-1, soluble endothelin selectin, or soluble platelet selectin between event and non-event groups. CONCLUSION: Raised concentrations of sVCAM-1 and CRP are predictive of an increased risk of major adverse cardiovascular events six months after presentation with unstable angina and non-Q wave myocardial infarction. These findings suggest that the intensity of the vascular inflammatory process at the time of presentation is a determinant of clinical outcome in unstable coronary artery disease.

Aged↗

Intra-coronary stents--extending the role of angioplasty in angina--initial experience.

Percutaneous transluminal coronary angioplasty (PTCA) is a widely successful revascularisation procedure. The restenosis rate has not significantly improved, despite the addition of many therapeutic agents. We describe the role of intra-coronary stents in the management of recurrent occlusion, restenosis and intracoronary dissection. We describe and discuss the problems associated with placement of the stent. The intracoronary stent has a successful adjuvant role to play with angioplasty in reducing both the elective and emergency requirements for coronary artery bypass grafting.

Adult↗

Lipids and fatty acids and their relationship to restenosis.

One hundred consecutive patients had fasting lipids and percutaneous fat biopsy performed at the time of percutaneous transluminal coronary angioplasty to determine if there was an association between restenosis and lipids or fatty acids. Angiographic follow-up and complete lipid and fatty acid results were available in 82 patients. Restenosis occurred in 37/82 (45%). Total cholesterol, triglyceride, high density lipoprotein, low density lipoprotein, and apolipoproteins A1 and B were not associated with restenosis. There was a significantly lower level of the monounsaturated fat palmitoleic acid (p less than 0.02), a trend towards a lower level of the monounsaturated fat oleic acid (p less than 0.09), and a trend towards a higher level of the saturated fat palmitic acid (p less than 0.08) in the restenosis group. The polyunsaturated fatty acids were not associated with restenosis. We conclude that lipids are not significantly associated with restenosis, and that lower levels of monounsaturated fatty acids may increase the risk of restenosis.

Angina Pectoris↗

Cardiac catheterisation with 5 French catheters.

From the beginning of November 1987 to the end of January 1989, 526 coronary arteriograms and left ventricular angiograms were performed with 5 French coronary catheters. In 448 (85%) patients diagnostic pictures were obtained with three standard types of 5 French catheters (No 4 Judkins): that is, left coronary, right coronary, and pigtail catheters. In 60 patients (11.4%) various other 5 French catheters were required to complete the study. In nine patients (1.7%), a 7 or 8 French catheter was used. Major complications causing cardiac arrest or requiring urgent operation developed in five patients. Sixty two patients (11.77%) had minor complications that required sublingual nitrates or a single bolus of atropine, or developed a haematoma that did not need intervention or had a mild reaction to the contrast material. Complications of moderate severity developed in 17 patients (3.2%): severe chest pain, arrhythmia requiring a temporary pacemaker, contrast reaction associated with hypotension, haematoma requiring blood transfusion, or a transient ischaemic episode. There were no deaths. 5 French catheters were used for routine coronary angiography and left ventriculography in 98.3% of patients. There were no major complications related to femoral artery puncture. The routine use of 5 French coronary catheters should increase the feasibility of safe coronary angiography in outpatients and should reduce the cost of this investigation.

Angina Pectoris↗

The variable effects of angiotensin converting enzyme inhibition on myocardial ischaemia in chronic stable angina.

The effect of angiotensin converting enzyme inhibition on myocardial ischaemia was studied in 12 normotensive patients with chronic stable angina and exercise induced ST segment depression. The study was randomised, double blind, placebo controlled, and crossover with treatment periods of two weeks. Enalapril was used to inhibit angiotensin converting enzyme. Assessment was by angina diaries and maximum symptom limited treadmill exercise tests. The results for the whole group showed a significant reduction in systolic blood pressure at rest and at peak exercise. Mean total exercise duration was 466 s (95% confidence interval 406 to 525) when the patients were taking placebo and 509 s (436 to 583) when they were taking enalapril. Four patients prolonged their total exercise time (mean 450 to mean 591 s) by more than 20%. Two patients, however, developed ischaemia earlier on exercise and reduced their total exercise duration (mean 490 to mean 390 s). Although angiotensin converting enzyme inhibition tended to reduce myocardial ischaemia in the group as a whole, some patients improved while others deteriorated. Thus the effects of enalapril are variable and this may have important implications when enalapril is used to treat heart failure in patients with underlying severe ischaemic heart disease.

Aged↗

Sequence and magnitude of ventricular volume changes in painful and painless myocardial ischemia.

Stimulation of left ventricular stretch receptors has been proposed as a possible mechanism for the occurrence of cardiac pain. Changes in left ventricular volume were continuously assessed in 12 patients during 11 spontaneous (two painful) and 12 ergometrine-induced (nine painful) ischemic attacks with a precordial scintillation probe and blood pool labeling with technetium-99m. In all ischemic episodes, spontaneous or induced, painful or painless, severe dilatation of the left ventricle was consistently observed. These changes always preceded the onset of ST segment shifts and occurred long before pain, when present. The maximum increase in end-diastolic volume was slightly greater in painful than in painless episodes, 38 +/- 8.0% versus 28 +/- 12.4%, but no significant difference was observed in the rate of volume change or in the maximum increase of end-systolic volume (133 +/- 50% and 110 +/- 27.3%), stroke volume (-28 +/- 15% and -25 +/- 12.4%), or ejection fraction (-32 +/- 8.7% and -26 +/- 6.0%). Although the maximum end-diastolic volume achieved is greater in painful episodes, this effect cannot be separated from that of duration, and, furthermore, there was no significant difference in end-diastolic volume at the moment chest pain began. Thus, in patients with angina at rest, transient asymptomatic ST segment shifts are consistently associated with large changes in left ventricular volume, similar to those observed during painful episodes. The rate and extent of acute left ventricular dilatation do not appear to be factors directly causing anginal pain.

Angina Pectoris↗

Comparative antianginal effects of nisoldipine and nifedipine in patients with chronic stable angina.

The acute antianginal effects of 5 mg and 20 mg nisoldipine were compared with 20 mg nifedipine and placebo. Maximal treadmill exercise testing was performed before and 3 hours after drug administration in 10 patients with chronic stable angina. Resting heart rate and systolic blood pressure were unchanged following low-dose nisoldipine, but 20 mg nisoldipine and 20 mg nifedipine increased heart rate and decreased systolic arterial pressure (p less than 0.05). Time (in seconds) to the onset of 0.1 mV ST segment depression was significantly prolonged after 5 mg nisoldipine (+60 +/- 53; p less than 0.05) and 20 mg nisoldipine (+100 +/- 78; p less than 0.01) but not after 20 mg nifedipine (+48 +/- 131; p = NS). Total exercise duration increased significantly following 5 mg and 20 mg nisoldipine (p less than 0.01 and p less than 0.001, respectively) but only slightly following nifedipine (p = NS). The maximal rate-pressure product was increased to a similar degree following doses of both nisoldipine and nifedipine (p less than 0.05). Nisoldipine is an effective antianginal agent which performs well in comparison to nifedipine.

Aged↗

Restenosis and its determinants in first and repeat coronary angioplasty.

Restenosis is the main problem limiting long-term success of percutaneous transluminal coronary angioplasty (PTCA) and is most accurately evaluated by follow-up angiography. We compared the primary and long-term results of angioplasty in 268 consecutive patients (293 segments) with first PTCA (PTCA 1, angiographic follow-up 98%) and in 66 patients (76 segments) with repeat PTCA after restenosis (PTCA 2, angiographic follow-up 92%). Forty clinical, angiographic and procedural factors were assessed in relation to outcome. Primary success rate was higher in PTCA 2 (91% vs 67.5%) and major complications were fewer (4.5% vs 16%). Higher inflation pressure (7.9 +/- 2.3 vs 6.8 +/- 1.8 atm, P less than 0.005) and larger balloons (3.5 +/- 0.5 vs 3.2 +/- 0.5 mm, P less than 0.005) were used for PTCA 2, resulting in lesser residual stenosis (33 +/- 16% vs 40 +/- 18%, P less than 0.05). Restenosis rate (greater than or equal to 70%) after PTCA 1 and after PTCA 2 (27% vs 36%, P = NS) and the mean time to recurrence (4.7 vs 5.3 months, P = NS) were similar. Procedural factors were the main determinants of long-term success in primary PTCA. The restenosis risk was independently related to residual stenosis greater than or equal to 45% (P less than 0.001), variant angina (P less than 0.05) and multivessel disease (P less than 0.05) after PTCA 1 and to male sex (P less than 0.001) and higher inflation pressure (P less than 0.05) after PTCA 2. Mild to moderate intimal tearing was associated with less restenosis after PTCA 1, but not after PTCA 2. Including 9 patients (10 segments) with a third PTCA, 70% of the 66 patients with repeat PTCA had a successful long-term outcome. Repeat angioplasty should therefore be considered as an integral part of PTCA therapy. Restenosis however remains a major concern. An optimal primary result with a minimal residual stenosis is decisive for first PTCA, whereas avoidance of a dissection by using lower inflation pressure on a restenosis might improve the long-term outcome of repeat PTCA.

Adult↗

Coronary sinus pH during percutaneous transluminal coronary angioplasty: early development of acidosis during myocardial ischaemia in man.

Coronary sinus pH was measured continuously in eight patients undergoing angioplasty to the left anterior descending coronary artery. A catheter tip pH sensitive electrode with a response time of less than 300 ms and an output of greater than or equal to 57 mV/pH unit was placed high in the coronary sinus. Recordings were obtained during a total of 24 balloon occlusions of the left anterior descending coronary artery varying in duration from 5 to 45 s. Continuous 12 lead surface electrocardiograms were recorded. During or after balloon inflation of greater than or equal to 12 s (n = 4) there was no change in coronary sinus pH or the electrocardiogram. During balloon inflation of greater than or equal to 15 s (n = 20) coronary sinus pH was unaltered but between 4 and 6 s after balloon deflation coronary sinus pH fell transiently by between 0.010 and 0.120 pH units before returning to the control value within 65 s. Ischaemic changes were seen on the electrocardiogram during 15 balloon occlusions. In individual patients the peak fall in coronary sinus pH was related to the duration of occlusion of the left anterior descending coronary artery. A rise in coronary sinus pH (alkalosis) was never seen. In man acidosis occurs in the myocardium after short periods (greater than or equal to 12 s) of ischaemia. The fall of pH precedes ischaemic changes on the surface electrocardiogram and occurs concurrently with the earliest reported changes in contractile function.

Acidosis↗

Effect of intravenous and oral acebutolol in patients with bundle branch block.

We studied the effect of intravenous (1 mg/kg) and oral (400 mg) acebutolol on atrioventricular conduction in 22 patients with idiopathic bundle branch block and 1 to 1 atrioventricular conduction. Seven patients had previously symptomatic complete heart block (Group 1) and 15 were asymptomatic with bundle branch block only (Group 2). Following intravenous acebutolol heart rate decreased 82 +/- 16 to 63 +/- 16/min (P less than 0.01), A-H interval lengthened 98 +/- 22 to 121 +/- 30 msec (P less than 0.005) and H-V time was prolonged 60 +/- 13 to 70 +/- 17 msec (P less than 0.02) in those with previous heart block. The corresponding changes in the patients with no previous block were 74 +/- 14 to 61 +/- 8/min (P less than 0.01), 90 +/- 17 to 109 +/- 22 msec (P less than 0.05) and 48 +/- 15 to 56 +/- 14 msec (P less than 0.01). There was no difference between the basal or induced changes between these two groups. After intravenous acebutolol infusion 2 of 6 patients with previous spontaneous heart block and none of those without previous heart block developed atrioventricular block distal to His. The induced block was temporary (less than 10 min) and corresponded to the time of peak plasma acebutolol levels. Temporary atrioventricular block followed oral acebutolol administration in 4/7 patients with previous spontaneous heart block and 0/14 in those without block. In patients with bundle branch block intravenous acebutolol prolonged H-V conduction times in 19/20 patients and intravenous and oral acebutolol induced A-V block in 4/7 patients with previous spontaneous block.(ABSTRACT TRUNCATED AT 250 WORDS)

Acebutolol↗

An echocardiographic study of localized subaortic hypertrophy.

A prospective echocardiographic investigation was undertaken to determine the prevalence and significance of localized subaortic hypertrophy in 1000 consecutive patients presenting for a routine echocardiographic examination. Localized septal hypertrophy was diagnosed when the subaortic septum was hypertrophied (greater than 1.4 cm) and was 50% thicker than the mid-point of the septum. Patients with hypertrophic cardiomyopathy and fixed subvalvular aortic stenosis were excluded. Eight cases of localized subaortic hypertrophy were identified. In 7 the appearances of the left side of the interventricular septum were similar with an apparently sigmoid shape (reversed S on its side) and in 1 with associated mitral stenosis the septum was a tapered wedge. All patients with localized subaortic hypertrophy had left ventricular hypertrophy (left ventricular mass or posterior wall thickness greater than 2 SD from normal) with a normal size cavity due to aortic valve disease (2 patients were also hypertensive). Of the 180 patients with aortic valve disease, localized subaortic hypertrophy was found in 10% of those with left ventricular hypertrophy and 33% of those with asymmetrical septal hypertrophy (septum to posterior wall ratio of greater than 1.5:1). There was no evidence of subaortic stenosis by pulsed and continuous wave doppler echocardiography (8 cases) and cardiac catheterization (6 cases). The aetiology of this discrete localized muscular bulge is unclear but is presumably due to change in shape of the septum with left ventricular hypertrophy. However, this finding has important implications as a cause of asymmetrical septal hypertrophy and because of the possible false diagnosis of subvalvular stenosis and its effect on ultrasound measurements.

Adolescent↗