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Biomedical subjects

W Ganz

Publications and source records attributed to W Ganz.

At least 73 records · Page 4Linked to original sources
PubMed1982

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↗
PubMed1982

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↗
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↗