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Biomedical subjects

P Grande

Publications and source records attributed to P Grande.

At least 55 records · Page 3Linked to original sources

Impact of infarct artery patency on the relationship between electrocardiographic and ventriculographic evidence of acute myocardial ischaemia.

Routine invasive evaluations are being abandoned, and thus simple non-invasive methods for estimating the extent of jeopardized myocardium during evolving myocardial infarction are needed for risk stratification to guide the appropriate therapeutic intervention. With this in mind the aim of the paper was to evaluate the association between ischaemic changes in the standard electrocardiogram and the function of acutely infarcted myocardium in relation to infarct artery patency status. Forty consecutive patients with a first acute myocardial infarction, admitted within 6 h of symptom onset and without bundle branch or fascicular block were included. Summated ST segment elevation in 11 electrocardiographic leads (aVR excluded) was measured to the nearest 0.05 mV and compared to regional wall motion, estimated by the centreline method (SD/chord) and global left ventricular ejection fraction (% LVEF) after thrombolytic therapy. Acute angiographic and ST segment measurements were performed at a median 254 min (range 70-485) after the onset of symptoms. Patients were grouped according to infarct artery patency status after intravenous thrombolysis. Of the 40 patients, 27 had a patent (Thrombolysis In Acute Myocardial Infarction trial (TIMI) grade 2-3 flow) and 13 had persistently occluded (TIMI 0-1 flow) infarct arteries. Anterior myocardial infarction was present in 13 and seven patients in the two groups. In the TIMI 2-3 group, the summated ST elevation did not correlate with % LVEF or SD/chord (rs = -0.08; and rs = -0.17, respectively). In the TIMI0-1 group the summated ST elevation correlated inversely with both % LVEF and SD/chord (rs = -0.70; and rs = -0.56, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiocardiography↗

Effects of atenolol and diltiazem on exercise tolerance and ambulatory ischaemia.

Twenty-five normotensive patients with stable angina, angiographically documented coronary disease and normal left ventricular function were randomized to a crossover study comparing atenolol 100 mg x 1, sustained-release diltiazem 120 mg x 2, and their combination. A maximal symptom limited bicycle exercise test and a 24-h ambulatory electrocardiographic (ECG) monitoring were performed at the end of each treatment period. Exercise duration was increased equally in the different treatment groups. Time to onset of 1-mm ST-segment depression was longer with atenolol (P < 0.02) and combination therapy (P < 0.01) than with diltiazem. The maximal ST-segment depression was decreased with atenolol (P < 0.05) and combination therapy (P < 0.02), whereas, time to onset of angina was prolonged only with combination therapy (P < 0.03). The number of ischaemic episodes during ambulatory monitoring was lower with atenolol and combination therapy than with diltiazem (P < 0.01). The difference between atenolol and diltiazem was mainly due to lower ischaemic activity with atenolol between 06:00 h and 12:00 h (P < 0.05). Anginal frequency (P < 0.01) and nitroglycerin consumption (P < 0.05) were lower with combination therapy than with monotherapy. Thus, while comparable effects were achieved on clinical variables, atenolol appeared to be more effective than diltiazem, reducing myocardial ischaemia during exercise and ambulatory monitoring. With combination therapy, both clinical and electrocardiograph signs of ischaemia were improved.

Adult↗

Patency and morphology of fibrous polyurethane vascular prostheses implanted in the femoral artery of dogs after seeding with subcultivated endothelial cells.

A cell culture line was established from enzymatically-derived canine jugular endothelial cells and further cultured. Whenever sufficient cells were present, fibrous polyurethane vascular prostheses, impregnated with gelatin and coated with fibronectin, were seeded with 4.8 x 10(5)/cm2 cells, sufficient to establish a confluent monolayer, and implanted in the femoral arteries of 16 dogs. A non-seeded prosthesis on the contralateral side served as control. Eight dogs received antiplatelet aggregation medication: 250 mg aspirin together with 25 mg dipyridamole, orally three times daily, starting 2 weeks prior to the implantation operation and continued for the duration of the experiment. Results show that in the non-medicated dogs all control prostheses become occluded within 3 weeks after implantation, whereas five out of eight seeded prostheses remained patent. In the medicated group, two out of eight control prostheses occluded and all seeded prostheses remained patent. Scanning and light microscopy revealed that seeded prostheses were completely lined with endothelial cells (Factor VIII positive stain) week 3 (n = 3) and 12 (n = 3) after implantation, while endothelialisation in control prostheses had advanced only 5 mm into the prostheses in 12 weeks. Two dogs of each group were included in long-term patency studies. We conclude that prostheses seeded with a confluent monolayer of endothelial cells result in superior patency rates for both medicated and non-medicated dogs. No immunological reaction against the (allogeneic) seeded endothelial cells were noted.

Anastomosis, Surgical↗

Importance of early and complete reperfusion to achieve myocardial salvage after thrombolysis in acute myocardial infarction.

The importance of the timing and completeness of coronary artery reperfusion for limitation of acute myocardial infarction (AMI) size after intravenous thrombolytic therapy was studied in 39 patients. All had electrocardiographic epicardial injury and acute coronary angiography performed < 8 hours after symptom onset. Acutely jeopardized myocardium was estimated at baseline, and before and after angiography by quantitative ST-segment analysis. The AMI size was estimated on the final electrocardiogram by the Selvester QRS score. Left ventricular ejection fraction was measured at the time of acute angiography and before discharge in 31 of these patients. In the 21 patients with normal flow (Thrombolysis in Myocardial Infarction [TIMI] trial grade 3) in the infarct-related artery, the amount of jeopardized myocardium decreased from baseline to that before and after angiography (17 to 11 and 11%, respectively; p < 0.00005), and the median final AMI size was reduced (17 to 9%; p = 0.0004). In 6 patients with suboptimal flow (TIMI grade 2), the median amount of jeopardized myocardium decreased slightly from baseline to that before to after angiography (15 to 12%); however, the median final AMI size was not reduced (17%). In 12 patients with no reperfusion (TIMI 0 to 1) flow, the median amount of jeopardized myocardium remained unchanged from baseline to that before angiography (21%), and the final AMI size was not significantly reduced. There was a significant inverse correlation between the change in global left ventricular function and the difference between electrocardiographic estimated jeopardized and final AMI size (rs = -0.53; p = 0.008).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Thrombocyte aggregation and serum thromboxane B2 in patients with unstable angina pectoris treated with diltiazem or verapamil].

Patients with unstable angina pectoris have increased thrombocyte aggregation and disturbances in serum prostaglandin balance. As a pilot project, we conducted a single-blind investigation of 24 patients with unstable angina pectoris treated with dilthiazem (n = 12, 240-360 mg) or verapamil (n = 12, 240-360 mg) for ten days. At the commencement of the investigation, both patient groups had hyperaggregating thrombocytes and increased serum-thromboxan-B2 (TXB2) as compared to healthy individuals (p < 0.01). In the patient group treated with dilthiazem, the aggregation threshold rose (p < 0.01), and the serum TXB2 values fell to approximately normal (p < 0.05). In the patient group treated with verapamil, no significant changes were observed in the measurements registered. The difference between the two groups remained significant during the entire therapeutic period (p < 0.01). Thus, dilthiazem appears to counteract thrombocyte aggregation in patients with unstable angina pectoris.

Angina, Unstable↗

[Serum creatine kinase isoenzyme MB and myoglobin in patients with acute myocardial infarction and coronary reperfusion].

Thrombolytic therapy in patients with acute myocardial infarction (AMI) changes the time-concentration curve of serum creatine kinase isoenzyme MB (CK-MB) and serum myoglobin. In this study, 60 AMI patients received thrombolytic therapy and acute coronary arteriography, or conservative treatment. Group one (n = 32) demonstrated a patent infarct-related artery after intravenous thrombolytic therapy; group two (n = 17) had an initially occluded coronary artery which became patent during catheterisation; group three (n = 11) did not receive thrombolytic therapy. Frequent serum CK-MB and myoglobin measurements showed that patients with acute coronary reperfusion had a rapid increase, an earlier peak value and less total release of both CK-MB and myoglobin to blood compared to AMI patients treated conservatively. The changes in serum myoglobin compared to CK-MB demonstrated an even more rapid, more uniform, and relatively greater increase. Measurements of serum myoglobin may be a useful non-invasive method for evaluation of thrombolytic therapy in AMI patients.

Adult↗

[Routine coronary arteriography in younger patients with acute myocardial infarction].

Coronary arteriography was performed in 50 patients aged 40 years of less all of whom had had acute myocardial infarction (AMI). Forty-seven patients had at least one risk factor for development of ischaemic cardiac disease. Smoking and familial predisposition were the commonest predisposing factors. Seventeen patients had stenosis in a single coronary artery only. Six patients had three-vessel disease and none had stenosis of the main stem of the left coronary artery. Eight patients had no stenoses. All patients with three-vessel disease had sign of ischaemia after infarction. The type of infarction was related to the number of stenosed vessels, so that patients with Q-wave infarction had a greater number of stenoses than patients with non-Q-wave infarcts. A congenital coronary in the form of abnormal origin of the left coronary artery from the pulmonary artery was the cause of AMI in an isolated case. On the basis of this retrospective investigation, the authors have assessed the value of routine coronary arteriography (CAG) in 50 relatively young patients who had recently sustained AMI. CAG does not appear to be indicated as a routine procedure in all of these patients but could have been performed primarily on the basis of symptoms or the findings from non-invasive investigations.

Adolescent↗

Use of the 12-lead ECG to detect myocardial reperfusion and salvage during acute myocardial infarction.

In this era of thrombolytic therapy, the standard 12-lead electrocardiogram (ECG) is easily available and noninvasive and could provide indicators of myocardial reperfusion and salvage. Previous reports have proposed that a decrease of total ST-segment elevation of > or = 20% from the pre- to the immediate posttreatment ECG is indicative of reperfusion, and that a > or = 20% decrease from the initial infarct size predicted by ST-segment deviation on the admission ECG to the final infarct size estimated by QRS score on the predischarge recording is indicative of myocardial salvage. This prospective study of 29 patients with myocardial infarction and angiographically documented reperfusion shows that the > or = 20% threshold for ST resolution achieved 79% sensitivity and 70% specificity in patients receiving intravenous therapy and 90% sensitivity in those receiving rescue intracoronary therapy. However, it should be noted that 21% of patients with successful intravenous therapy failed to achieve even this threshold of ST resolution. Regarding myocardial salvage, 63% of patients receiving intravenous and 90% of those receiving rescue intracoronary therapy achieved the threshold of > or = 20% decrease in infarct size.

Adult↗

Seeding of enzymatically derived and subcultivated canine endothelial cells on fibrous polyurethane vascular prostheses.

Fibrous polyurethane (FPU) prostheses with or without fibronectin coating and gelatin impregnation and FPU prostheses with or without fibronectin coating were seeded with 4.8 x 10(5) subcultivated dog endothelial cells per cm2 prosthesis. Expanded polytetrafluoroethylene (ePTFE) prostheses with and without fibronectin coating served as controls. The numbers of cells retained on uncoated polyurethane prostheses were minimal but increased with fibronectin coating and/or gelatin impregnation. Adhering cells were predominantly round in shape and few cells were seen stretched over the prosthetic fibres. Optimum numbers of cells were found in prostheses impregnated with gelatin and coated with fibronectin, where almost all the cells were stretched forming a confluent monolayer. In ePTFE prostheses only minimal numbers of cells were retained but in the fibronectin-coated prostheses a high cell count was noted. Gelatin-impregnated and fibronectin-coated FPU prostheses, as well as ePTFE prostheses coated with fibronectin, were additionally perfused in vitro after seeding under nearly physiological conditions for 1 h. Cells in the FPU prostheses were still present after perfusion, whereas all the cells in the ePTFE prostheses were lost from the inner surface. It is concluded that FPU prostheses impregnated with gelatin and coated with fibronectin are a suitable substrate for subcultivated endothelial cells to be seeded on. The cells remained at the surface even after 1 h in vitro perfusion with tissue culture medium under nearly physiological conditions. Further research including in vivo implantations is indicated.

Animals↗

Effect of thrombolytic therapy on exercise response during early recovery from acute myocardial infarction: a placebo controlled study.

Several studies have shown that infarct size is reduced following thrombolytic treatment in patients with acute myocardial infarction. Exercise test variables, such as an impaired heart rate response during exercise, are known to be related to left ventricular function and patient prognosis following acute myocardial infarction. The present study was performed to compare exercise test variables in acute myocardial infarction patients following either intravenous thrombolysis or placebo. Symptom-limited bicycle ergometer tests, carried out 1-2 weeks from the infarction, were performed in 85 patients randomized to intravenous streptokinase (N = 41) or placebo (N = 44) given within 12 h from onset of symptoms. At rest heart rate, systolic blood pressure and rate-pressure product were similar in the two groups. At maximum workload the streptokinase treated patients had a higher median maximal heart rate than controls (136 vs. 126 b.min-1, P less than 0.01) but only a trend towards higher systolic blood pressure was seen (175 vs. 163 mmHg, P = 0.09). Rate-pressure product at maximal exercise was 23,620 vs. 20,100 mmHg.b.min-1 respectively, (P less than 0.01). Total exercise time, ST-segment deviation, occurrence of angina pectoris and left ventricular ejection fraction were similar in the two groups. The trend towards an increased heart rate at maximum workload in streptokinase-treated patients was seen at all levels of left ventricular ejection fraction, and at all levels of exercise capacity.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗

Serum release of the creatine kinase tissue-specific isoforms MM3 and MB2 is simultaneous during myocardial reperfusion.

The release sequence of the creatine kinase MM and MB tissue-specific subforms after myocardial reperfusion was elucidated by computer-fitting serial enzyme data from 6 humans in whom coronary flow in the infarct-related artery was angiographically documented as initially zero, opening to normal after angioplasty. The model equation used demonstrated acceptable performance according to standard criteria including visual examination and statistical parameters. The model successfully described the sequential conversion of the MM3 and MB2 tissue isoforms to their respective MM2 and MM1, and MB1 isoforms. Release of MM3 and MB2 was simultaneous, differing in calculated release times by 0.2 to 10%, median 3%. Since MB2 release is not retarded after myocardial reperfusion compared to the more clinically established CK-MM3 isoform, assays for sensitive and rapid measurement of MB2 should be the focus for the non-invasive assessment of myocardial reperfusion due to its higher cardiospecificity.

Aged↗

Failure to obtain long-term patency after implantation of fibrous polyurethane prostheses in the carotid arteries of rabbits.

Fibrous polyurethane prostheses were implanted in the carotid arteries and aortae of New Zealand white (NZW) and Chinchilla (CHIN) rabbits. No immediate post-implantation patency was obtained after implantation in the carotid arteries in NZW rabbits. In CHIN rabbits patency up to 1 week was obtained after carotid implantation. Attempts to increase patency rates by administration of 20 mg/kg body weight/day of both dipyridamol (DIP) and acetyl-salicylic acid (ASA) p.o., starting the week before implantation, had an adverse effect; prostheses became occluded within a few hours after implantation. Coagulation tests (Lee and White, Am J Med Sci 145:495-503, 1913) carried out with blood drawn from CHIN rabbits revealed hypercoaguability after administration of either 10 or 20 mg/kg body weight/day of both DIP and ASA compared to pre-medication values. Prostheses implanted in the aortae of both strains remained patent without anti-platelet-aggregation therapy for a 3-month observation period. It is concluded that in the NZW rabbit carotid implantation was not successful due to severe spasmic reactions and that in CHIN rabbits only very short-term patency could be obtained both with and without administration of 10 or 20 mg/kg body weight/day medication DIP and ASA.

Animals↗