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Biomedical subjects

A Zalewski

Publications and source records attributed to A Zalewski.

At least 19 recordsLinked to original sources
PubMed1992

Selective dopamine-1 receptor agonist augments regional myocardial blood flow: comparison of fenoldopam and dopamine.

A new class of vasodilators exhibiting selective dopamine-1 receptor agonist activity is being introduced into clinical practice. Inasmuch as various vasodilators either augment or decrease myocardial blood flow ("coronary steal") depending on their pharmacologic action, the goal of this study was to assess the effects of fenoldopam (selective dopamine-1 receptor agonist) and dopamine (nonselective dopamine-1 receptor agonist) on regional myocardial blood flow in the presence of coronary occlusion. Accordingly, in 16 dogs anesthetized with pentobarbital, the left anterior descending coronary artery was occluded. Cardiovascular and renal hemodynamic effects were measured before and after intravenous infusion of renal equipotent doses of either fenoldopam (n = 9, 0.1 micrograms/kg/min) or dopamine (n = 7, 1 micrograms/kg/min). Both fenoldopam and dopamine caused a significant and comparable increase in renal blood flow. Fenoldopam but not dopamine significantly decreased the calculated peripheral vascular resistance and subsequently increased cardiac output. Dopamine had no effect on regional myocardial blood flow. In contrast, fenoldopam augmented transmural myocardial blood flow in normal (from 114 +/- 10 to 188 +/- 27 ml/100 gm/min, p less than 0.02) and ischemic border myocardium (from 45 +/- 5 to 68 +/- 11 ml/100 gm/min, p less than 0.03 and p less than 0.02 vs dopamine). There was a significant increase in blood flow to both the endocardial and epicardial layers of normal and ischemic border myocardium. These changes were accompanied by a significant reduction in coronary vascular resistance in the normal myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1992

Fibrinolytic activity after vessel wall injury.

The goal of this study was to assess fibrinolytic activity after vessel wall injury and to correlate changes in fibrinolytic activity with angiographic and histologic findings. Accordingly, in 18 atherosclerotic rabbits, vessel wall injury was produced by means of iliac artery balloon angioplasty (the injury group), whereas 8 atherosclerotic rabbits served as a control group. In all rabbits from the injury group, deep vessel wall injury was documented by either angiography or histologic study. Plasminogen activator inhibitor-1 activity in plasma increased significantly, from 21.79 +/- 1.29 arbitrary units/ml (AU/ml) at baseline study to 32.05 +/- 1.47 AU/ml at 6 h after vessel wall injury (p less than 0.01), whereas activity remained unchanged throughout the 24-h period in the control group. Plasma levels of tissue plasminogen activator activity were similar in both groups. Intravascular thrombus was found in five of six additional rabbits 6 h after vessel wall injury, that is, at the time of impaired fibrinolytic activity, whereas no thrombus was found in the control group (p less than 0.05). It is concluded that deep vessel wall injury is associated with reduced fibrinolytic activity. In addition to other procoagulant factors, elevated plasminogen activator inhibitor-1 activity may lead to intravascular thrombosis and impaired resolution of thrombus.

Angioplasty, Balloon↗
PubMed1991

Clinical and angiographic determinants of primary coronary angioplasty success. M-HEART Investigators.

Clinical and anatomic determinants of the initial success of percutaneous transluminal coronary angioplasty were prospectively evaluated in 826 patients enrolled in the Multi-Hospital Eastern Atlantic Restenosis Trial (M-HEART). The 639 men and 187 women ranged in age from 31 to 85 years. Successful angioplasty (residual stenosis less than 50% and no major complications) was achieved in 886 (88.6%) of 1,000 lesions. Success rates were uniform among the eight individual centers. Outcome was not influenced by gender, age or other clinical features, including severity and duration of angina, prior myocardial infarction, rest pain, transient ST segment elevation, history of smoking or diabetes. In contrast, procedural outcome was significantly associated with lesion-specific angiographic factors. Stenoses 60% to 74%, 75% to 89%, 90% to 99% and 100% were associated with success rates of 96%, 90%, 84% and 69%, respectively (p less than 0.001). Angioplasty was less successful in calcified than in noncalcified lesions (82% versus 90%, p less than 0.01), in thrombotic than in nonthrombotic lesions (82% versus 90%, p less than 0.05) and in lesions in the right coronary artery than in other vessels (84% versus 90%, p less than 0.01). Outcome was not related to other anatomic variables, including lesion location (proximal versus distal), vessel size, eccentricity, stenosis length or translesional gradient. By multivariate logistic regression, preangioplasty percent stenosis, right coronary artery location and lesion calcification were demonstrated to be significant independent predictors of angioplasty success. Alternative clinical and angiographic variables did not contribute to this regression model.(ABSTRACT TRUNCATED AT 250 WORDS)

Angioplasty, Balloon, Coronary↗
PubMed1991

Evidence for reduced fibrinolytic activity in unstable angina at rest. Clinical, biochemical, and angiographic correlates.

BACKGROUND: The goal of this study was to evaluate the role of the fibrinolytic system in patients with unstable angina at rest associated with transient electrocardiographic changes. METHODS AND RESULTS: Tissue plasminogen activator activity in plasma was comparable among patients with unstable angina (n = 17), patients with stable exertional angina (n = 10), and control patients with normal coronary arteriograms (n = 8). In contrast, plasminogen activator inhibitor-1 (PAI-1) activity in plasma was elevated in the unstable angina group (21.67 +/- 9.52 AU/ml) as compared with either the stable angina group (12.01 +/- 7.06 AU/ml, p less than 0.02) or the controls (12.49 +/- 8.54 AU/ml, p less than 0.02). Coronary angiography performed within 24 hours after the last anginal episode showed a similar extent of coronary artery disease in the unstable and stable angina groups. However, intracoronary thrombi were observed in eight patients in the unstable angina group while no thrombus was noted in the stable angina group (chi 2 = 7.22, p less than 0.01). CONCLUSIONS: We conclude that patients with unstable angina at rest have a reduced fibrinolytic activity and an increased incidence of intracoronary thrombi. It is postulated that elevated PAI-1 activity in the presence of coronary arterial wall injury may be an important factor leading to the development of acute coronary syndromes.

Angina Pectoris↗
PubMed1990

Does antiplatelet therapy enhance myocardial salvage after coronary reperfusion?

The aim of this study was to test the hypothesis that either the cyclooxygenase inhibitor aspirin or the thromboxane A2 receptor antagonist sulotroban exerts a direct myocardial effect that enhances myocardial salvage afforded by reperfusion. Accordingly, 21 anesthetized dogs underwent suture occlusion of the left anterior descending coronary artery. At 2.5 h after occlusion, all dogs received intravenous streptokinase (20,000 U/kg body weight over 30 min) and were randomized to the following groups: group I (n = 7) received no additional treatment, group II (n = 7) received aspirin (5 mg/kg intravenously) and group III (n = 7) received sulotroban (10 mg/kg followed by 10 mg/kg per h intravenously). At 3 h after occlusion, the dogs underwent coronary reperfusion for the next 3 h. Myocardial infarct size as a percent of the hypoperfused zone was similar among dogs in group I (42 +/- 8%), group II (41 +/- 10%) and group III (45 +/- 11%). The incidence and the extent of myocardial hemorrhage were similar in all three study groups. Infarct size as a percent of the hypoperfused zone was significantly smaller in dogs without hemorrhage irrespective of treatment (35 +/- 9% versus 63 +/- 5%, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Myocardial protection with autoperfusion during prolonged coronary artery occlusion.

Passive transcatheter coronary arterial perfusion, i.e., autoperfusion, has been introduced for clinical use to ameliorate short episodes of myocardial ischemia during percutaneous transluminal coronary angioplasty. The primary goal of this study was to evaluate the cardioprotective effect of autoperfusion after prolonged coronary artery occlusion. Accordingly, in 24 anesthetized dogs, either the left anterior descending or left circumflex coronary artery was occluded for 6 hours. The dogs were randomized to a control group subjected to coronary artery occlusion alone (n = 13) or to a group treated with transcatheter autoperfusion (n = 11). The hypoperfused zone, i.e., risk area and infarct size, were measured by autoradiography and triphenyltetrazolium chloride staining, respectively. The hypoperfused zone was 30 +/- 2% and 29 +/- 2% in the control and treated (NS) groups, respectively. When infarct size was expressed as a percent of the hypoperfused zone, it was 84 +/- 5% in the control group and 25 +/- 9% in the group treated with transcatheter autoperfusion (p less than 0.001), showing a reduction of 70%. In addition, an in vitro study showed pressure-dependent flow during autoperfusion as reflected by close linear relationship between perfusion pressure and flow (Flow = 0.54 X Pressure + 16.16, r = 0.99, n = 16). These data suggest that although passive coronary arterial perfusion for 6 hours after coronary occlusion does not prevent myocardial necrosis, it markedly reduces myocardial infarction in the canine model.

Angioplasty, Balloon, Coronary↗
PubMed1990

The M-Heart percutaneous balloon mitral Valvuloplasty Registry: initial results and early follow-up. The M-Heart Group.

The initial results, complications and early follow-up of 74 patients undergoing percutaneous balloon mitral valvuloplasty in seven hospitals participating in a multicenter registry are reported. Seventy-four patients with a mean age of 53 years had 75 valvuloplasty procedures performed over a 2.5 year period. Eighty-nine percent of the attempted procedures were completed and resulted in an increase in mean mitral valve area from 1.0 +/- 0.04 to 2.0 +/- 0.1 cm2 (p less than 0.0001); the valve area increased greater than or equal to 50% of the baseline valve area in 73% of the patients. Major complications included procedure-related death (2.7%), cardiac tamponade (6.7%), systemic embolism (2.7%) and emergency surgery (6.7%). At a mean follow-up period of 14.6 months, the condition of the majority of patients had improved, and 89% of 55 patients treated only with valvuloplasty were in New York Heart Association functional class I or II. Thus, hemodynamic and clinical improvement can be obtained in the majority of patients with mitral stenosis treated with balloon valvuloplasty in multiple centers. However, suboptimal results and major complications occurred in a significant number of patients and may limit this procedure to use by experienced operators in hospitals with facilities for cardiac surgery.

Adolescent↗
PubMed1989

Surface electrocardiogram in the detection of transmural myocardial ischemia during coronary artery occlusion.

To examine whether coronary occlusion causing transmural ischemia was accurately reflected by ST-segment elevation on routine electrocardiograms, intracoronary and surface electrocardiograms were simultaneously recorded during percutaneous transluminal coronary angioplasty (PTCA). The study group consisted of 54 patients who had intracoronary ST-segment elevation during transient coronary occlusion (left anterior descending [LAD]: 25 patients, left circumflex [LC]: 19 patients, right coronary artery: 12 patients). Elevation of the ST segment on the surface electrocardiogram (greater than or equal to 0.1 mV) was recorded in 84% of patients during LAD dilatation, in 32% of patients during LC dilatation (p less than 0.01 vs LAD and right), and in 92% of patients during right coronary dilatation (not significant vs LAD). The magnitude of intracoronary ST elevation was 1.10 +/- 0.8, 1.68 +/- 1.2 and 0.8 +/- 0.6 mV for the LAD, LC and right occlusions, respectively (not significant). Thus, despite the comparable magnitude of intracoronary ST elevation, LC occlusion resulted in ST-segment elevation on the surface electrocardiogram in significantly fewer patients than did LAD or right occlusion. During LC occlusion, 9 patients had no electrocardiographic changes and 4 had only precordial ST depression. Thus, in patients with transmural ischemia during right or LAD occlusions, concordant ST elevation on the surface electrocardiogram is common. In contrast, ST-segment elevation is an insensitive marker of LC occlusion. In patients with ongoing ischemic symptoms and isolated precordial ST depression or no repolarization abnormalities, LC occlusion should be considered in the differential diagnosis.

Adult↗
PubMed1989

Myocardial salvage after regional beta-adrenergic blockade.

UNLABELLED: The aim of the study was to determine whether regional beta-adrenergic blockade via the coronary sinus limited myocardial damage after coronary artery occlusion in the canine model. Accordingly, open-chest anesthetized dogs were randomly allocated to one of three groups: a control group and groups treated with propranolol (in doses of 0.02, 0.2, and 2.0 mg/kg) given either intravenously or via the coronary sinus. The hypoperfused zone (i.e., risk area) and the extent of myocardial damage were assessed by autoradiography and triphenyltetrazolium chloride staining, respectively. Myocardial damage expressed as a percent of the hypoperfused zone was 84 +/- 5% in the control group (n = 9) and 78 +/- 7% (0.02 mg/kg, n = 7, NS), 63 +/- 6% (0.2 mg/kg, n = 7, p less than 0.05), and 62 +/- 7% (2.0 mg/kg, n = 9, p less than 0.02) in the groups receiving intravenous propranolol and 73 +/- 6% (0.02 mg/kg, n = 7, NS), 58 +/- 7% (0.2 mg/kg, n = 7, p less than 0.01), and 44 +/- 9% (2.0 mg/kg, n = 9, p less than 0.001) in groups receiving propranolol via the cardiac veins. There was a significant enhancement of myocardial salvage with increasing doses of propranolol delivered via the cardiac veins (linear regression trend, p less than 0.05). In contrast, myocardial damage expressed as a percent of the hypoperfused zone remained comparable with propranolol doses of 0.2 and 2.0 mg/kg administered intravenously (linear regression trend, NS). IN CONCLUSION: (1) regional beta-adrenergic blockade via the cardiac veins afforded significant myocardial salvage and (2) the regional administration of propranolol resulted in significant reduction of myocardial damage in a dose-dependent fashion.

Administration, Topical↗
PubMed1989

Interventional therapy in acute myocardial infarction.

Large multicenter trials have shown an improvement in both survival and left ventricular function in patients undergoing reperfusion therapy in acute myocardial infarction. The most practical approach in treatment of patients with acute myocardial infarction involves intravenous administration of effective thrombolytic agents as soon as possible in the course of myocardial infarction. This approach using r-tPA results in reperfusion in approximately two-thirds of patients. In patients with contraindications to thrombolytic therapy and extensive injury current or hemodynamic compromise, emergent cardiac catheterization should be performed followed by immediate PTCA or bypass surgery. In patients who have already been treated with thrombolytic agents, controversy exists as to the optimal timing of cardiac catheterization to define coronary anatomy and the need for additional revascularization. We suggest that the most beneficial therapeutic strategy for the majority of patients is rapid administration of an effective intravenous thrombolytic agent combined with aspirin and heparin. Cardiac catheterization and PTCA or coronary artery bypass graft surgery may be deferred in stable patients. This approach is supported by evidence showing a lack of additional improvement in mortality and left ventricular function in patients treated with urgent PTCA. The advent of new therapeutic modalities in acute myocardial infarction, such as thrombolysis, has created a new subset of patients who either will have an improved prognosis if coronary artery reperfusion is completed or will have an increased risk for recurrent myocardial ischemia if definite revascularization is delayed.

Fibrinolytic Agents↗
PubMed1988

Protection of the ischemic myocardium during percutaneous transluminal coronary angioplasty.

Therapeutic balloon coronary angioplasty provides a useful model for studying the effects of epicardial coronary artery occlusion in conscious humans. In addition, it is a potent model in which the effectiveness of interventions designed to ameliorate ischemia can be evaluated. Whereas intravenous beta-adrenergic blocking drugs and nitrates appear to have a limited protective effect, the regional (i.e., intracoronary) use of beta-adrenergic blocking drugs and calcium antagonists seem more potent. Currently, coronary venous retroperfusion with arterial blood does not appear practical, and the intraaortic balloon is a useful adjunctive measure in relatively few patients undergoing percutaneous transluminal coronary angioplasty. In contrast, the direct anterograde delivery of oxygen-rich blood or fluorocarbons holds promise as a reliable means of providing local myocardial protection. If ischemia could be markedly reduced, percutaneous transluminal coronary angioplasty might be applied safely in more high-risk clinical settings. In addition, if prolonged balloon inflation could be performed, there might be an increase in primary success rate and possibly a reduction in restenosis rate.

Adrenergic beta-Antagonists↗
PubMed1988

Recurrent ischemia in the zone of prior myocardial infarction: results of coronary angioplasty of the infarct-related artery.

We studied the efficacy of coronary angioplasty (PTCA) of the infarct-related artery in 54 patients with recurrent myocardial ischemia in the zone of prior infarction. Our patients had recurrent ischemia 10 +/- 7 days after infarction, with 75% experiencing rest angina and 15% having evidence of reinfarction. Angiography of the infarct-related artery demonstrated a critical stenosis in 35 of 54, a subtotal occlusion in 5 of 54, and a total occlusion in 14 of 54. PTCA was successful in 94% of critical stenoses, 80% of subtotal occlusions, but in only 50% of total occlusions. Complications related to PTCA included a 3.7% rate of emergency surgery, but no deaths or infarctions. During the clinical follow-up period of 11 +/- 7 months, there was one reinfarction and no deaths. Although 27% of our 44 patients with a successful initial PTCA required a second revascularization procedure for recurrent angina, 40 patients (91%) remained symptomatically improved with angioplasty alone (including successful repeat PTCA in eight patients). We conclude that PTCA of the infarct-related artery is beneficial for selected patients with recurrent ischemia in the zone of prior infarction.

Adult↗
PubMed1988

The effects of phospholipase A2 inhibition on experimental infarct size, left ventricular hemodynamics and regional myocardial blood flow.

It has been reported that activation of phospholipase A2 and the subsequent degradation of membrane phospholipids are responsible for irreversible myocardial injury. Thus, we examined whether a phospholipase A2 inhibitor 1-(benzylmethyl-amino)-3-[(alpha, alpha, alpha-trifluoro-m-tolyl)oxy]-2- propanol hydrochloride, can reduce myocardial necrosis after coronary artery occlusion. In 14 anesthetized dogs, 1 minute after coronary occlusion, 99mTc-labeled albumin microspheres (8 mCi) were injected into the left atrium for future assessment of the hypoperfused zone. After 15 minutes, the dogs were randomized to a control group (n = 7) and a treated group (n = 7, 2 mg/kg i.v.). After 6 hours, infarct size and hypoperfused zones were measured using triphenyltetrazolium chloride staining and autoradiography, respectively. The hypoperfused zone, as a percentage of the left ventricle, was 26 +/- 3% and 23 +/- 1% in the control and the treated groups (NS), respectively. The percentage of the hypoperfused zone that evolved to necrosis was 98 +/- 4% in the control group and 45 +/- 10% in the treated group (P less than 0.001) showing a reduction of 54%. By weight, in the control group, necrosis involved 26 +/- 4 g of the left ventricle while in the treated group it was 9 +/- 2 g (P less than 0.005). In 6 additional dogs, left ventricular hemodynamics and regional myocardial blood flow were studied before and after treatment i.e., 15 and 30 minutes after coronary occlusion, respectively. Phospholipase A2 inhibitor did not acutely change heart rate, aortic pressure, left ventricular end-diastolic and systolic pressures, left ventricular dP/dt and regional myocardial blood flow. Thus, phospholipase A2 inhibitor salvaged the acutely ischemic myocardium, reducing necrosis by over 50% in the canine model. It is postulated that since this effect was not related to the studied hemodynamic parameters and regional myocardial blood flow, it may be related to the preservation of membrane integrity.

Animals↗
PubMed1987

The effects of cytochrome C on the extent of myocardial infarction and regional function of the ischemic myocardium.

The effects of cytochrome C, an electron carrier in the process of oxidative phosphorylation, on infarct size and regional left ventricular function after a coronary artery occlusion were investigated. Thus, in 30 dogs, 1 minute after left anterior descending coronary artery occlusion, 99mTc-labeled albumin microspheres (8 mCi) were injected into the left atrium for subsequent assessment of the hypoperfused zone, that is, the area at risk of infarction. Fifteen minutes after coronary artery occlusion, dogs were randomized into a control group (n = 15) and a cytochrome C-treated group (n = 15). The latter immediately received cytochrome C, 2.5 mg/kg intravenously. Six hours after coronary artery occlusion the dogs were sacrificed and their left ventricles were cut into 3 mm thick slices. Infarct size was determined by triphenyltetrazolium chloride staining and measured by planimetry. The same slices were then submitted to autoradiography and the hypoperfused zone was then measured by planimetry. The hypoperfused zone was 22 +/- 2% and 23 +/- 2% of the left ventricle in the control and treated groups, respectively (NS), indicating that the extent of myocardium at risk before treatment was similar. The extent of the hypoperfused zone which evolved to necrosis was 90 +/- 3% in the control group but only 50 +/- 7% in the treated group (p less than 0.001). Myocardial salvage in the treated group was paralleled by improvement in systolic wall thickness of the ischemic segment as measured by two-dimensional echocardiography. Thus, cytochrome C reduced the extent of myocardial necrosis by 44% and improved systolic function of the ischemic myocardium.

Animals↗