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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
PubMed1985

Factors that determine the direction and magnitude of precordial ST-segment deviations during inferior wall acute myocardial infarction.

Sixty-one patients with inferior acute myocardial infarction (AMI) and no evidence of prior AMI were studied to determine which factors influence the magnitude of precordial ST-segment depression. In the total study group, there was a significant but weak correlation between the magnitude of precordial ST-segment depression and the magnitude of inferior ST-segment elevation (r = -0.46, p less than 0.001). In the 29 patients with evidence of concomitant right ventricular (RV) involvement, precordial ST-segment depression was significantly smaller both in absolute terms (-1.3 +/- 1.8 vs -2.8 +/- 1.9 mm, p less than 0.01) and relative to the magnitude of inferior ST-segment elevation (ratio of -0.2 +/- 1.0 vs -1.1 +/- 0.5, p less than 0.01), whereas in the 15 patients with lateral ST-segment elevation (greater than or equal to 1 mm in lead V6), precordial ST-segment depression was significantly greater both in absolute terms (-3.5 +/- 2.3 vs -1.6 +/- 1.7 mm, p less than 0.01) and relative to the magnitude of inferior ST-segment elevation (ratio of -1.1 +/- 0.8 vs -0.5 +/- 0.9, p less than 0.02). Consistent with these findings, the correlation between the magnitudes of precordial and inferior ST-segment deviations was considerably improved when only the 24 patients with neither evidence of RV involvement nor lateral ST-segment elevation were analyzed (r = 0.89, p less than 0.001, n = 24). These data suggest that in patients with inferior AMI, there is a reciprocal relation between precordial and inferior ST-segment deviations, which is distorted by concomitant RV involvement and by concomitant lateral left ventricular wall involvement.

Aged↗
PubMed1985

Spontaneous ventricular tachycardia associated with isolated right ventricular infarction, one day after right coronary artery occlusion in the dog: studies on the site of origin and mechanism.

The electrophysiologic and arrhythmic properties of isolated infarcted right ventricle (RV) were studied in 17 dogs during the first 24 hours after complete occlusion of the right coronary artery (RCA). During the 16-to-20-hour post occlusion period, spontaneously occurring sustained monomorphic ventricular tachycardia (VT) was present in all 17 dogs. Overdrive ventricular pacing (cycle lengths 200 to 250 msec) caused significant suppression of the VT when the rate of the VT was slower than 150 bpm (range 120 to 145 bpm) (n = 9), but had negligible effect when VT rate was higher than 150 bpm (range 160 to 245 bpm (n = 8). Overdrive pacing could not terminate either the slow or the fast type of VT. Bipolar intramural electrograms have showed electrical activity in the infarcted RV zone to precede Q wave of the VT by 15.4 +/- 5.8 msec regardless of VT rate. Microelectrode studies on isolated RV endocardial infarcted tissues 24 hours after RCA occlusions have shown the presence of spontaneous repetitive activity at a rate of 87 +/- 47 bpm, which was overdrive suppressed in dogs with slow VT, and spontaneous activity at a rate of 115.2 +/- 36 bpm (p less than 0.05) which was not overdrive suppressed in dogs with fast VT. Maximum diastolic potential, action potential amplitude, and Vmax of surviving subendocardial Purkinje fibers (SEPF) in the infarct zone were slightly but significantly depressed (p less than 0.05), and they manifested enhanced phase 4 depolarization, giving rise to automatic impulse initiation. Although action potential duration of these fibers was somewhat prolonged (p less than 0.05), no conduction delay occurred. Histopathologic examinations have shown necrosis of the basal two thirds of the RV, with no left ventricular involvement. Electron microscopy revealed lipid accumulation in the surviving SEPF as the sole abnormality. We conclude (1) that occlusion of the RCA in the dog is associated with high survival rate despite extensive necrosis involving exclusively the RV and (2) that VT seen during the 20 to 24 hours after occlusion arise in the infarcted zone of the RV, by an enhanced automatic mechanism in the surviving SEPF, possibly caused by cytoplasmic lipid accumulation. This model, by virtue of its high survival rate and frequency of late VTs, should be useful in providing clues to determine factors involved in the genesis of early VT/VF and for the evaluation of new pharmacologic agents during the 20- to 24-hour VT period.

Animals↗
PubMed1985

Precordial ST segment depression during acute inferior myocardial infarction: early thallium-201 scintigraphic evidence of adjacent posterolateral or inferoseptal involvement.

To investigate the myocardial perfusion correlates of precordial ST segment depression during acute inferior myocardial infarction, a rest thallium-201 scintigram and a closely timed 12 lead electrocardiogram were obtained within 6 hours of the onset of infarction in 44 patients admitted with their first acute inferior myocardial infarction. Thirty-six patients demonstrated precordial ST segment depression (group 1) and eight did not (group 2). A perfusion defect involving the inferior wall was present in all 44 patients. Additional perfusion defects of the adjacent posterolateral wall (n = 20), the ventricular septum (n = 9) or both (n = 6) were present in 35 of 36 patients from group 1 compared with only 1 of 8 patients from group 2 (p less than 0.001). There was no significant difference in the frequency of multivessel coronary artery disease or disease of the left anterior descending artery between group 1 and group 2 or between patients with and those without a thallium-201 perfusion defect involving the ventricular septum. Thus, precordial ST segment depression during an acute inferior myocardial infarction is associated with thallium-201 scintigraphic evidence of more extensive involvement of the adjacent posterolateral or inferoseptal myocardial segments, which probably reflects the extent and pattern of distribution of the artery of infarction, rather than the presence of coexistent multivessel coronary artery disease or disease of the left anterior descending artery.

Aged↗
PubMed1985

The effects of the rate of intravenous infusion of streptokinase and the duration of symptoms on the time interval to reperfusion in patients with acute myocardial infarction.

We studied the influence of the following variables on the time interval from initiation of an intravenous infusion of 750,000 U of streptokinase until reperfusion (reperfusion time) in 140 consecutive patients with an evolving acute myocardial infarction: (1) the rate of infusion of streptokinase, (2) the duration of chest pain before initiation of treatment, (3) patient age, (4) patient sex, (5) location of infarction, (6) history of previous myocardial infarction, and (7) pretreatment pathologic Q waves. The time of reperfusion was recognized by clinical criteria that were completely concordant with the anatomic findings in all 119 patients in whom patency or occlusion of the artery of infarction was established at delayed angiography (n = 116) or at postmortem examination (n = 3). The mean reperfusion time for the 129 patients for whom data were available was 49 +/- 36 min. The reperfusion time was inversely related to the rate of infusion of streptokinase (r = .41, p less than .001), but this effect of infusion rate appeared to plateau at rates of greater than 500 U/kg/min. In the 64 patients receiving infusions at rates of 500 U/kg/min or less, the mean reperfusion time was 60 +/- 40 min, whereas in the 58 patients receiving the drug at rates greater than 500 U/kg/min it was 35 +/- 22 min (p less than .001). The duration of chest pain before treatment was the only other studied variable found to influence the reperfusion time, but only at infusion rates of less than 250 U/kg/min (r = .6, p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1985

The hypotensive effect of intravenous streptokinase in patients with acute myocardial infarction.

We studied the hypotensive effect of a rapid intravenous infusion of high-dose streptokinase in 98 patients with an acute myocardial infarction. The systolic blood pressure fell from 132 +/- 20 (range 90 to 174) to 97 +/- 21 mm Hg (range 58 to 152) at 15 +/- 8 min (range 4 to 40) after the commencement of the streptokinase infusion (p less than .001). A fall in diastolic blood pressure from 80 +/- 16 (range 51 to 105) to 61 +/- 15 mm Hg (range 32 to 92) accompanied the fall in systolic pressure (p less than .001). The fall in blood pressure was associated with an increase in heart rate (73 +/- 14 to 78 +/- 17 beats/min, p less than .001), preceded the appearance of clinical signs of reperfusion by 37 +/- 38 min and was similar in magnitude and timing in patients with anterior and inferior infarction. There were direct relationships between the rate of infusion of streptokinase and both the magnitude (r = .49, p less than .001) and the rate of fall of systolic blood pressure (r = .67, p less than .001) as well as both the magnitude and rate of fall of diastolic blood pressure. In most patients, the fall in blood pressure was transient (9 +/- 6 min, range = 2 to 30) and easily managed by slowing or stopping the infusion, placing the patient in the Trendelenburg position, or by administering an infusion of low-dose norepinephrine or dopamine. However, in four patients with severe left ventricular dysfunction, severe hypotension persisted for more than 60 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

The effect of intravenous infusion of urokinase on coronary artery thrombolysis in the dog.

The effect of intravenous administration of urokinase on the rate and time of thrombolysis was investigated in 22 dogs with an occlusive coronary artery thrombus induced by placement of a copper coil in the left anterior descending artery. One hour after angiographic confirmation of complete coronary artery occlusion, an intravenous bolus of urokinase was administered in a dose of either 1.2 X 10(6) units (Group 1, n = 7); 0.6 X 10(6) units (Group 2, n = 9) or 0.3 X 10(6) units (Group 3, n = 6). Reperfusion occurred in all 7 (100%) Group 1 dogs, in 7 of 9 (78%) group 2 dogs and in 3 of 6 (50%) group 3 dogs (p = 0.07 for Group 1 vs Group 3). There was no residual intra-arterial thrombus in any group 1 (high dose) dog but 4 of the 10 reperfused Group 2 or Group 3 (intermediate or low dose) dogs had small thrombus in the distal left anterior descending artery (3.5 +/- 4.0 mg) and all 5 non-reperfused dogs had thrombus in the coil (26.1 +/- 6.2 mg). The frequency of residual thrombus was significantly less in Group 1 compared to Group 2 and 3 (p less than 0.01). We conclude that intravenous administration of urokinase has a dose dependent efficacy for lysing intracoronary thrombus in the canine model.

Animals↗
PubMed1985

Thrombolytic therapy with intracoronary or intravenous streptokinase during acute myocardial infarction.

This report compares the results of intracoronary (IC) and intravenous (IV) streptokinase in a sequential series of 200 patients (IC = 81 and IV = 119) admitted within 3 hours of the onset of an acute myocardial infarction. Reperfusion was achieved in 71 of 81 (88%) patients in the IC group and in 113 of 119 (95%) patients in the IV group (p = NS) 35 +/- 27 and 42 +/- 33 minutes after commencement of treatment respectively (p = NS). The interval from onset of symptoms to reperfusion was significantly longer in the IC than in the IV group, 235 +/- 62 versus 175 +/- 61 minutes (p less than 0.001). Mean values of peak creatine kinase-MB were 152 +/- 117 IU/L in the IC group and 117 +/- 79 IU/L in the IV group (p less than 0.05). Three patients in the IC group and 16 patients in the IV group suffered major hemorrhagic complications. In-hospital mortality was 7 of 81 (8.7%) in the IC group and 10 of 119 (8.4%) in the IV group (p = NS). We conclude that IV administration of streptokinase in patients with an acute myocardial infarction is at least as efficacious as IC administration.

Aged↗
PubMed1984

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↗
PubMed1984

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↗
PubMed1984

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↗
PubMed1984

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↗
PubMed1984

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↗
PubMed1983

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↗
PubMed1983

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↗
PubMed1983

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↗