PubMed Health⌕ Search

Biomedical subjects

W Ganz

Publications and source records attributed to W Ganz.

At least 73 records · Page 4Linked to original sources
PubMed1981

Early phase acute myocardial infarct size quantification: validation of the triphenyl tetrazolium chloride tissue enzyme staining technique.

Gross histochemical delineation of myocardium which has lost dehydrogenase enzyme activity has been shown to facilitate macroscopic recognition of necrotic myocardium. The present study was undertaken to assess the accuracy of the triphenyl tetrazolium chloride (TTC) technique for quantitating myocardial infarct size very early after coronary occlusion. In 16 closed-chest dogs the left anterior descending coronary artery was occluded with an intra-arterial balloon. Twelve dogs were killed 6 hours after occlusion, their hearts excised, cut from apex to base into 1 cm thick slices, and incubated in TTC. Whole-mount histologic sections of each slice were prepared. Myocardial infarct size was measured by planimetry of photographs of each gross slice and histologic section using classical criteria of necrosis. Myocardial infarct size determined in 54 slices by the TTC technique and histologically was similar (25 +/- 16% vs 27 +/- 16% of the left ventricular mass, mean +/- SD) with close correlation between the two methods (r = 0.91). Four dogs were killed 3 hours after occlusion and TTC stained and unstained myocardium was studied by electron microscopy. When the TTC technique identified necrosis so did electron microscopy. Areas identified by the TTC technique as non-necrotic were either normal or only ischemic by electron microscopy. Thus, using TTC, necrosis can be quantitated reliably 6, and even 3 hours after coronary occlusion, before histologic changes are clearly diagnostic. This technique represents a reliable, practical means for quantitation of recent infarction and for studying the evolution of ischemic injury in its early phase.

Acute Disease↗
PubMed1981

Intracoronary thrombolysis in evolving myocardial infarction.

After experimental studies in dogs confirmed the feasibility and safety of rapid intracoronary thrombolysis by local infusion of Thrombolysin (streptokinase and plasmin), intracoronary thrombolysis was attempted in 20 patients with evolving myocardial infarction who were hospitalized within 3 hours from the onset of symptoms during the day and within 2 hours at night. Thrombolysin was infused in the immediate vicinity of the site of coronary occlusion using a 0.85 mm outer diameter catheter advanced through the lumen of the Judkins catheter. Reperfusion was achieved in four patients after an average of 43 minutes of Thrombolysin infusion at a rate of 2000 IU/min and in 15 patients after an average of 21 minutes of Thrombolysin infusion at a rate of 4000 IU/min. The failure to open the artery in one patient may have been caused by our inability to advance the infusion catheter close to the site of occlusion. Rethrombosis occurred in one patient 8 days after reperfusion and 2 days after discontinuation of anticoagulants because of a history of chronic alcoholism. Wall motion and perfusion studies showed improvement following reperfusion. Patency of the artery was achieved an average of 4 hours after the onset of symptoms. The need for earlier reperfusion is emphasized.

Adult↗
PubMed1981

Intracoronary thrombolysis in acute myocardial infarction: experimental background and clinical experience.

Occlusive intracoronary (IC) thrombosis was produced experimentally in dogs by placement of a copper coil. The thrombus was consistently lysed by application of Thrombolysin (streptokinase and plasminogen) at the site of occlusion, 1 to 6 hours after thrombosis. Thrombolysin has no toxic effect on the coronary artery wall or the myocardium. Reperfusion after 30 to 60 minutes of occlusion frequently resulted in ventricular fibrillation, but gradual reperfusion reduced the probability of ventricular fibrillation. Intramyocardial bleeding was noted after reperfusion in areas of advanced necrosis and was shown to be the consequence, rather than the cause, of necrosis. The reperfused myocardium remained hypocontractile, but in contrast to the occlusion period, its mechanical function could be enhanced by inotropic stimulation. After experimental studies confirmed the feasibility and safety of IC thrombolysis, the technique was applied within 3 hours of onset of pain in 29 patients with evolving acute myocardial infarction (AMI) and showing ST elevations without pathologic Q waves. Nitroglycerin (NTG), 0.1 mg, was injected into the occluded coronary artery to rule out spasm; NTG failed to open the occluded artery. A special, very flexible, radiopaque No. 2 French catheter was advanced through the angiography catheter to the site of occlusion. Thrombolysin was infused at a rate of 4000 to 6000 IU/min until patency was achieved, followed by 2000 IU/min for 60 minutes. Lysis of clot was achieved in 27 of 29 patients. The single death (unrelated to the procedure) occurred subsequently in a patient in whom the artery was not reopened. After successful thrombolysis, 12 patients underwent elective coronary bypass surgery because of multiple stenoses. The need for early reperfusion is emphasized for effective IC thrombolysis therapy in evolving AMI.

Animals↗
PubMed1981

Early appearance of MB-creatine kinase activity in nontransmural myocardial infarction detected by a sensitive assay for the isoenzyme.

The early release patterns of MB-creatine kinase (CK-MB) in myocardial ischemia and infarction are largely unknown. We utilized a sensitive column chromatographic assay of CK-MB activity (precision = 1.1 IU/liter) and sequential CK-MB samples were obtained during the first 6 hours of illness to define the early time course of enzyme release. The average CK-MB in 39 normal subjects was 2.4 +/- 0.93 (mean +/- standard deviation (SD)). Twenty-two patients with ischemic chest pain, in whom myocardial infarction did not develop, were characterized by normal CK-MB's (2.4 +/- 1.0). Of 39 patients in whom transmural myocardial infarction developed, 28 (72 percent) were found to have abnormal CK-MB either initially or over a 20-minute sampling period. In contrast, 100 percent of the patients considered to have sustained a nontransmural myocardial infarction had abnormal initial CK-MBs and subsequently demonstrated significant increases in CK-MB from 28 +/- 19 initially to 41 +/- 30 IU/liter (P less than 0.01, N = 16) over the 20-minute sampling period. Thus, CK-MB appears earlier in plasma following nontransmural myocardial infarction than transmural myocardial infarction, probably reflecting perfusion to ischemic myocardium.

Chromatography, Ion Exchange↗
PubMed1980

The effect of mild-to-moderate mental stress on coronary hemodynamics in patients with coronary artery disease.

Eleven men with coronary artery disease were studied to determine whether they would manifest inappropriate coronary vasoconstriction in response to mental stress. Mental stress was induced by having the patient perform difficult mental arithmetic in time with a clicking metronome. Aortic blood pressure and thermodilution coronary sinus blood flow were recorded continuously before and during the mental arithmetic. For the group, heart rate rose from 70 to 82 beats/min, systolic blood pressure rose from 161 to 181 mm Hg and diastolic blood pressure rose from 71 to 78 mm Hg. Coronary resistance decreased by 16%. The index of myocardial oxygen consumption rose by 40%, and there was an equivalent rise in coronary sinus blood flow of 41%, with no changes in coronary arteriovenous oxygen difference. Because the increase in myocardial oxygen consumption was accompanied by a proportional increase in coronary sinus blood flow, a decrease in coronary resistance and no change in myocardial oxygen extraction, we conclude that the response of patients with coronary artery disease to at least moderately severe mental stress is not characterized by abnormal coronary vasoconstriction.

Adult↗
PubMed1980

The relationship of vascular injury and myocardial hemorrhage to necrosis after reperfusion.

Early reperfusion may salvage ischemic myocardium; late reperfusion often intensifies morphologic changes of necrosis and causes hemorrhage. To determine whether hemorrhage after reperfusion increases the extent of myocardial infarction, six closed-chest, anesthetized dogs underwent balloon occlusion of the left anterior descending coronary artery for 5.5 hours, followed by 30 minutes of reflow. Colloidal carbon was injected distal to the balloon before reperfusion to label injured vessels. After sacrifice, the area of myocardial necrosis was measured by planimetry of 1-cm-thick serial slices of left ventricle stained with triphenyl tetrazolium chloride. Areas of hemorrhage and vascular injury were also measured. In all hearts, the extent of hemorrhage and vascular injury was less than the extent of necrosis (10.2 +/- 4.6% vs 19.8 +/- 8.6% [mean +/- SD], p < 0.01). Further, hemorrhage was always within the area of necrosis, primarily in the subendocardial portion. Hemorrhage after reperfusion occurred only in necrotic tissue where carbon labeling indicated severe vascular injury before reperfusion, suggesting that the hemorrhage was the consequence of preexisting microvascular injury, not its cause.

Animals↗
PubMed1979

Nitroglycerin in acute myocardial infarction. X. Effect of small and large doses of nitroglycerin on sigma ST segment deviation -- experimental and clinical results.

The purpose of the present study was to investigate the effect of the dose of nitroglycerin (NTG) on myocardial ischemic injury. In 20 closed chest dogs the anterior descending branch of the left coronary artery was occluded by inflating a balloon in its lumen. Compared with the untreated control group the sigma ST elevation was significantly lower when NTG was applied at a rate of 0.02 mg/min, but significantly higher when NTG was administered at a rate of 0.10 mg/min. In 12 patients with acute myocardial infarction NTG was infused at a rate of 3 mg in the first hour (0.05 mg/min) and 6 mg in the second hour (0.1 mg/min). Sigma ST elevation and sigma ST depression decreased during the lower infusion rate (p less than 0.001). When the rate of NTG infusion was raised to 6 mg/hr, the improvement in ST segment deviation was partially reversed. This effect, particularly evident in patients not in heart failure, was associated with a significant rise in heart rate (p less than 0.05) and a fall in diastolic arterial pressure (p less than 0.025). Patients with left ventricular failure were less sensitive to higher doses of NTG than those without failure. Thus, the effect of NTG on myocardial ischemic injury depends on the NTG dose and on the functional state of the injured left ventricle.

Animals↗
PubMed1979

Haemodynamic and electrocardiographic accompaniments of resting postprandial angina.

The early postprandial changes in 10 patients with angiographically proven coronary artery disease and history of postprandial angina were studied by the continuous recording on magnetic tape of the electrocardiogram and haemodynamic variables. The significant changes 20 minutes after a meal not followed by angina included increases in cardiac index and stroke index, with a decrease in systemic vascular resistance. When angina developed after a meal, there were significant increases in mean systemic arterial blood pressure, heart rate, pulmonary capillary wedge pressure, and systemic vascular resistance with decreases in stroke index at the onset of pain rather than at the onset of ischaemic electrocardiographic abnormalities. The first haemodynamic variable to change was pulmonary capillery wedge pressure which tended to increase coincident in time with the electrocardiographic abnormalities. In all cases, postprandial angina occurred within 25 minutes after a meal. In every instance, there was little or no change in the product of heart rate and systolic arterial blood pressure at the onset of the ischaemic electrocardiographic abnormalities at a time when the pulmonary capillary wedge pressure had begun to rise. Postprandial angina, like many cases of rest angina, may rise on the basis of a primary decrease in myocardial perfusion, the nature of which is unclear but merits further investigation.

Aged↗