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Biomedical subjects

W Ganz

Publications and source records attributed to W Ganz.

At least 55 records · Page 3Linked to original sources

Intravenous streptokinase in evolving acute myocardial infarction.

Eighty-one consecutive patients presenting within 3 hours of the onset of acute myocardial infarction (AMI) and without contraindications to thrombolytic or anticoagulant therapy received a 15- to 30-minute intravenous infusion of 750,000 or 1.5 million units of streptokinase (STK) followed by anticoagulation. Treatment was instituted 130 +/- 41 minutes after the onset of symptoms and reperfusion was achieved 36 +/- 26 minutes later. Reperfusion of the "infarct artery" was recognized by indirect clinical criteria in 78 patients (96%). In all 66 patients who underwent coronary angiography 3 to 7 days later, there was complete concordance between indirect and angiographic evidence of reperfusion. In 6 patients there was early reocclusion within 24 hours of treatment; in 4 of these patients, the artery was reopened with an additional dose of STK. Two elderly patients suffered an intracranial hemorrhage and there were 8 other major hemorrhagic complications, of which 7 were related to procedural trauma. Five patients (6.2%) died in the hospital. The results of intravenous STK thrombolytic therapy are compared with those of our previous study using intracoronary STK.

Aged

ST elevations in leads V1 to V5 may be caused by right coronary artery occlusion and acute right ventricular infarction.

In 5 of 69 patients (7%) undergoing intracoronary or intravenous streptokinase treatment, the ST-segment elevations in leads V1 to V5 were caused by occlusion of the right rather than the left anterior descending coronary artery and by myocardial infarction (MI) of the right ventricular (RV) wall rather than the anterior left ventricular (LV) wall or the ventricular septum. RV involvement was documented by technetium pyrophosphate uptake, hypokinesia, dilatation and depressed RV ejection fraction. The left anterior descending artery was patent and the anterior LV wall had normal thallium-201 uptake, no technetium uptake and normal wall motion. ST-segment elevation was highest in lead V1 or V2 and decreased toward lead V5; in patients with anterior LV MI, the ST-segment elevations are usually lowest in lead V1 and increase toward the V5 lead. In contrast to anterior LV infarcts, the R waves in leads V1 to V5 did not decrease and Q waves did not evolve with progression of the MI. The ST-segment elevations in leads V1 to V5 in our patients were associated with small or absent ST-segment elevations in leads, II, III and aVF, suggesting that in other cases of RV infarction, the appearance of ST-segment elevations in leads V1 to V5 is blocked by the dominant electrical forces of the LV inferior MI. This suggestion was confirmed in a canine model. Recognition of the presence of RV infarction may be therapeutically important.

Adult

Improvement in regional and global left ventricular function after intracoronary thrombolysis: assessment with two-dimensional echocardiography.

After acute myocardial infarction, 23 patients undergoing intracoronary thrombolysis and 10 patients receiving conventional medical treatment were studied by 2-dimensional echocardiography to determine changes in regional and global left ventricular (LV) performance. Both quantitative and qualitative analysis of echocardiographic studies showed improvement in regional and global LV function in 18 patients with successful reperfusion immediately after thrombolysis to 10 days later (p less than 0.0005). Eleven patients who were studied before thrombolysis demonstrated no change in regional or global LV function immediately after thrombolysis. LV function did not improve in the conventionally treated group. These data indicate that in patients with acute coronary artery occlusion successfully reperfused by intracoronary thrombolysis, regional and global LV function improved by day 10 but not immediately after reperfusion.

Adult

Effects of late coronary artery reperfusion after myocardial necrosis is complete.

Early reperfusion salvages reversibly injured ischemic myocardium. Late reperfusion, after necrosis is complete, could be beneficial by accelerating healing, or the hemorrhage and contraction-band necrosis associated with reperfusion could impair healing. In closed-chest anesthetized dogs the left anterior descending coronary artery was occluded with a balloon-tipped catheter for either 1 day followed by reperfusion for 6 days (n = 9) or for 7 days without reperfusion (n = 9). All dogs were killed after 7 days. Pathologic changes were studied in transverse whole-mount ventricular histologic sections. When the two groups were compared, no differences were found in: (1) infarct size, 15.7 +/- 9.9% vs 10.2 +/- 8.6 (mean +/- SD); (2) number of transmural infarcts, 5 of 9 vs 6 of 9; (3) ratio of infarcted/normal wall thickness, 0.93 +/- 0.09 vs 0.95 +/- 0.13; (4) thickness of zone of collagen deposition at periphery of infarct, 1.69 +/- 1.16 mm vs 1.67 +/- 0.56; and (5) amount of hemorrhage, calcification, and inflammation. Thus, in this model, reperfusion after necrosis is complete did not improve or impair healing.

Animals

Clinical failure of streptokinase due to an unsuspected high titer of antistreptokinase antibody.

Neutralization of streptokinase by an unsuspected high titer of antistreptokinase antibody prevented activation of the fibrinolytic system and induction of a lytic state in a 62 year old man with an acute inferior myocardial infarction. There was no decrease in serum fibrinogen, minimal decrease in serum plasminogen and only a small increase in serum fibrin degradation products after intravenous administration of 1.5 million units of streptokinase. A high titer of antistreptokinase antibody, sufficient to neutralize 1.5 million units of streptokinase, was demonstrated by semiquantitative counterelectrophoresis . There was no clinical evidence of coronary artery reperfusion, and coronary angiography confirmed complete occlusion of the left circumflex artery.

Antibodies, Bacterial

Intracoronary thrombolysis in acute myocardial infarction.

Forty-seven patients with acute myocardial infarction (MI) underwent intracoronary infusion of Thrombolysin or streptokinase. In 41, a completely reoccluded artery was reopened. Patency was associated with appearance of arrhythmias, relief of pain, gradual return of the ST-segment to the baseline and appearance of abnormal Q waves. Creatine kinase (CK) and MB-CK enzyme levels peaked earlier. Serial thallium scintigrams showed reduction in defect size after reperfusion, and the ejection fraction was higher compared with control. Eighteen patients were recommended for coronary bypass surgery for recurrent pain or severe multivessel disease.

Arrhythmias, Cardiac

Hemodynamic measurements in clinical practice: a decade in review.

Hemodynamic measurement is now an important and feasible adjunct to clinical practice. Its successful application to alleviate illness in human beings is evident in its contribution to an understanding of the pathophysiology of disease and the efficacy of various interventions to alter the course of a variety of diseases. Its application is widespread in the high risk patient undergoing surgery and the critically ill medically treated patient. Hemodynamic measurement permits accurate determination of the state and, if necessary, of the continuously changing function of the heart as related to disease process and guides treatment and interventions on a rational physiologic basis.

Anesthesia

Nonsurgical reperfusion in evolving myocardial infarction.

Nonsurgical recanalization of the occluded coronary artery has been performed in patients with evolving myocardial infarction since the late 1970s by intracoronary administration of thrombolytic agents at the ostium of the occluded artery or directly to the site of occlusion. The authors review the basic concepts underlying intracoronary thrombolysis, the method applied at their institution and the clinical results. Reperfusion of totally occluded arteries or termination of the ischemic state in subtotally occluded arteries was achieved in 71 (87.7%) of 81 patients. Reocclusion occurred in four patients, in three of these at a time when anticoagulation became temporarily ineffective, emphasizing the need for uninterrupted anticoagulation with a partial thromboplastin time longer than 80 seconds. Thallium scintigraphic studies before and after reperfusion showed a decrease in defect, indicating myocardial salvage, in the successful cases but not in failures or untreated control subjects. A decrease in thallium-201 defect was followed by improvement of regional wall motion and usually also left ventricular ejection fraction. Three of the patients with an unsuccessful result and one patient with a successful result died. Bypass surgery was performed electively in 18 patients because of multiple vessel involvement. Intracoronary thrombolysis appears to be a relatively safe and promising procedure. A large controlled study will be needed for definitive assessment of its role in the management of acute myocardial infarction.

Adult

Divergent effects of inotropic stimulation on the ischemic and severely depressed reperfused myocardium.

Mechanical function remains depressed for hours and days after even brief periods of ischemia. To determine whether the depressed function of the reperfused myocardium could be improved y inotropic stimulation, we studied segmental function during ischemia and after reperfusion using mercury-in-Silastic length gauges in 15 dogs. During coronary artery occlusion, segmental function could not be improved by inotropic stimulation with dopamine. Release of occlusion after 30 minutes of ischemia resulted in only slight improvement in segmental function (systolic shortening at 20% of control). After reperfusion, segmental function could be markedly enhanced by inotropic stimulation. The response to inotropic stimulation was similar after reperfusion after 3 hours of ischemia if the myocardium remained viable (nine dogs). When the myocardium was necrotic (five dogs), there was no improvement after reperfusion, either spontaneously or in response to inotropic stimulation. If applicable to humans, these results suggest that intractable pump failure caused by extensive but reversible ischemia could be effectively treated by reperfusion and inotropic stimulation.

Animals

Intermittent brief periods of ischemia have a cumulative effect and may cause myocardial necrosis.

We investigated the effects of brief intermittent periods of ischemia on myocardial viability. Brief periodic coronary occlusions were produced up to 18 times by inflating and deflating the balloon of an intracoronary No. 2F catheter for periods of 15, 10 or 5 minutes, followed by 15-minute periods of reperfusion. Creatine kinase (CK) release, triphenyl tetrazolium chloride staining, and light and electron microscopy were used to detect the presence of myocardial necrosis. For the study of CK release, blood was taken from the great cardiac vein and the aorta before and at 5-minute intervals during each left anterior descending coronary occlusion, as well as during and 1, 5, 10 and 15 minutes after balloon deflation. In seven of 24 dogs with 15-minute occlusions, in five of 21 dogs with 10-minute occlusions, and in three of 32 dogs with 5-minute occlusions, small but distinct areas of subendocardial necrosis were present. In all dogs with morphologic proof of necrosis, there was periodic release of CK into the great cardiac vein, which peaked immediately after reperfusion, reflecting CK washout. Thus, brief periods of ischemia, which when single do not cause necrosis, have a cumulative effect and may cause myocardial necrosis. This mechanism of necrosis may be relevant clinically in patients with frequent anginal episodes. Since many dogs of this study did not have any myocardial necrosis, the findings also suggest that intermittent reperfusion has a beneficial effect and may prevent necrosis, even when total occlusion time exceeds 200 minutes.

Animals