[Limitation of the size of the myocardial infarct by using intracoronary streptokinase administration].
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Biomedical subjects
Publications and source records attributed to H Blanke.
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A multicenter study evaluated the early management and subsequent hospital course of 204 patients with acute myocardial infarction who were receiving intracoronary infusions of streptokinase (STK). The in-hospital mortality in 37 patients with thrombotic occlusion of the infarct-related vessel, in whom recanalization could not be achieved, was 24%. However, the cardiac mortality in 129 patients who were successfully treated by percutaneous transluminal coronary recanalization (PTCR) was only 5.4%. Cardiac deaths (5 patients) and nonfatal reinfarctions (20 patients) occurred in the early period in the cardiac care unit (CCU) in 21% of the latter group and, despite anticoagulation measures, could not be consistently prevented. Hemorrhagic complications, necessitating blood transfusion, occurred in 15 (7.4%) of the total 204 patients in the group, usually in the acute CCU stage, and were positively related to decline of fibrinogen serum concentrations below 100 mg/dl and to use of the Judkins technique. The later course of most of the patients on the general ward was uneventful until hospital discharge. Thus there were only 2 more cardiac deaths, and of 64 successfully treated STK-PTCR patients who left the CCU without clinical indications of reinfarction and agreed to repeat coronary angiography before hospital discharge, the infarct-related vessel was patent in 59 patients and reoccluded in only 5 (7.8%).
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The advantages of a new low osmolality contrast medium (sodium meglumine ioxaglate) in clinical coronary angiography are demonstrated at two groups of patients in comparison to sodium meglumine diatrizoate. One group included patients undergoing diagnostic angiography in chronic state of CHD, the other during diagnosis and therapy (intracoronary lysis) in state of acute myocardial infarction. Injection of the low osmolality contrast material was followed in both groups by significant reduction of pressure drop and cardiac slowing. In both groups there was also a reduction of changes in ECG compared to side effects of the conventional contrast material.
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Percutaneous transluminal coronary recanalization, a new therapeutic procedure used in acute myocardial infarction, offers significant reduction in mortality, as well as more effective limitation of the zone of infarction than has been possible with other pharmacologic treatment employed in the past. The risk of coronary angiography during acute myocardial infarction was surprisingly low, as was the risk of hemorrhagic complications following the intracoronary administration of relatively low doses of thrombolytic substances such as streptokinase. Mechanical recanalization was possible in about one fifth of patients and successful in approximately half of all such attempts, but complications occurred in a small percentage of attempts at this step. Coronary artery spasm was excluded as a possible cause of occlusion in almost all cases. Selective intracoronary infusion of streptokinase produced the highest degree of myocardial reperfusion, and best results were achieved when therapy was initiated shortly after thrombotic occlusion occurred. Residual stenosis of more than 75% luminal diameter narrowing was present in approximately three fourths of cases after complete thrombolysis, and the majority of patients remained appropriate candidates for coronary bypass surgery or for percutaneous transluminal coronary angioplasty (Grüntzig procedure). Although complete analysis of the efficacy of selective recanalization was difficult because it was not possible to establish a suitable control group for purposes of comparison, the mortality of less than 1% in the present group of 232 patients within the first 6 hours following myocardial reperfusion provides an encouraging result.
A multicenter study evaluated the early management and subsequent hospital course of 204 patients with acute myocardial infarction who were receiving intracoronary infusions of streptokinase (STK). The in-hospital mortality in 37 patients with thrombotic occlusion of the infarct-related vessel, in whom recanalization could not be achieved, was 24%. However the cardiac mortality in 129 patients who were successfully treated by percutaneous transluminal coronary recanalization (PTCR) was only 5.4%. Cardiac deaths (five patients) and nonfatal reinfarctions (20 patients) occurred in the early period in the cardiac care unit (CCU) in 21% of the latter group and, despite anticoagulation measures, could not be consistently prevented. Hemorrhagic complications, necessitating blood transfusion, occurred in 15 (7.4%) of the total 204 patients in the group, usually in the acute CCU stage, and were positively related to decline of fibrinogen serum concentrations below 100 mg/dl and to use of the Judkins technique. The later course of most of the patients on the general ward was uneventful until hospital discharge. Thus there were only two more cardiac deaths, and of 64 successfully treated STK-PTCR patients who left the CCU without clinical indications of reinfarction and agreed to repeat coronary angiography before hospital discharge, the infarct-related vessel was patient in 59 patients and reoccluded in only five (7.8%).
Left ventricular (LV) contrast cineventriculograms were obrained in 174 patients with evolving acute myocardial infarction (AMI) treated by intracoronary streptokinase (SK) infusion. Ejection fraction (EF) increased slightly, from 52% +/- 13% before admission SK intervention to 58% +/- 13% immediately after early recanalization of the completely obstructed coronary vessel (p less than 0.0005, n = 68), while local wall motion usually improved. Immediately improved LV function appears to be the result of early reperfusion and/or decreased LV afterload. In 55 chronic (long-term follow-up) post-AMI (2 to 4 weeks after successful early SK reperfusion) patients, repeat angiography revealed late reocclusion of the infarct vessel in nine patients. Chronic EF was not significantly different from pre-SK intervention EF in these nine patients with late reocclusion, whereas in the remaining 46 patients with persistent patency, EF increased mildly from 52% +/- 13% (before SK intervention) to 56% +/- 16% (in long-term recanalization) (p less than 0.025). Ventricular loading conditions were not different at pre-SK intervention angiography and chronic angiography. EF rose modestly from 51% +/- 14% to 57% +/- 18% in the 23 patients recanalized on follow-up, in whom pre-SK intervention angiography revealed collaterals to the infarcting area (p less than 0.025), whereas there was no EF change in the 23 chronically recanalized patients without pre-SK collaterals. In the eight patients recanalized at late follow-up, who had preadmission chest pain for less than 3 hours and successful SK reperfusion within 4 hours of symptom onset (group A), EF increased significantly from 51% +/- 12% to 65% +/- 6% (p less than 0.025). In the 25 chronically recanalized patients admitted 3 to 6 hours after onset of chest pain, in whom SK reperfusion was successful (group B), EF was unchanged at late study. In the 13 chronically recanalized patients with preadmission chest pain lasting longer than 6 hours, in whom SK reperfusion was successful (group C), EF increased from 52% +/- 13% before SK intervention to 56% +/- 16% at late study (p less than 0.025). Pre-SK intervention angiography revealed collateral vessels to the infarct area in 69% of group C patients but in only 42% of patients in groups A and B. These findings suggest that the critical interval for myocardial salvage, as well as for early and long-term improvement of LV function by SK reperfusion at admission, is 4 hours after onset of chest pain in the majority of AMI patients. This time interval may be longer in patients with well-developed collateral supply to the region of the acute infarct.
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40 patients with acute myocardial infarction had serial determinations of CK, CKMB and an addition of serum myoglobin (SMb) by radioimmunoassay. In 10 patients with normal values on admission SMb rose earlier than CK and CKMB. In another 20 patients SMb was pathologically increased while CK and CKMB were normal and in 10 patients all parameters were elevated on admission. In all 40 patients SMb was significantly elevated in between 10 hrs after beginning of angina, and peak myoglobin occurred 10 hrs before CK and CKMB. In 10 patients peak SMb correlated with infarct size as determined by angiocardiography in the chronic stage (r = 0.863; p less than 0.01). Peak SMb also correlated with infarct size as estimated by CK release (r = 0.73; p less than 0.001). Thus determination of SMb is a sensitive method in diagnosing early myocardial infarction, and peak serum myoglobin allows early prediction of infarct size.
In 19 patients with coronary heart disease, biplane cineventriculography of the left (LV) and right ventricle (RV) at rest (r) and under exercise induced angina pectoris (e) was performed. The RV enddiastolic volume index (EDVI) increased from 107.4 +/- 27.5 ml/m2 at r to 125.2 +/- 41.5 ml/m2 under e (p less than 0,001), the LVEDVI from 117 +/- 46.2 to 140.3 +/- 54.5 ml/m2 (p less than 0,001). The LV endsystolic volume index (ESVI) increased from 50.3 +/- 36.7 to 62.4 +/- 46.9 ml/m2 (p less than 0,005), RVESVI did not change significantly under e. Ejection fraction (EF) increased significantly under e in the RV from 57.5 +/- 10.8 to 61.8 +/- 12.5%; LVEF did not change significantly under e. There was a significant correlation between RV and LV enddiastolic pressure (EDP) under e: RVEDP = 0.31 LVEDP + 3.9, r = 0.72, p less than 0.001. EDVI as well as ESVI of RV and LV correlated significantly at r and under e: r: RVEDVI = 0.28 LVEDVI + 76.1, r = 0.47, p less than 0.05, e: RVEDVI = 0.41 LVEDVI + 67.2, r = 0.544, p less than 0.05; r: RVESVI = 0.26 LVESVI + 32.6, r = 0.565, p less than 0.05, e: RVESVI = 0.33 LVESVI + 27.4, r = 0.58, p less than 0.01. There was a significant correlation of mean circumferential fiber shortening of the RV (VD) and LV (VCF) under e: VD = 0.53 VCF + 0.56, r = 0.779, p less than 0.001. RVEF and LVEF showed no significant correlation at r and under e. The data suggest that the degree of coronary heart disease is a major factor in determining RV performance under stress.
Cardiodepressive side effects of angiocardiography can be reduced by using non-ionic metrizamide (Amipaque) or adding calcium to diatrizoate (Urografin 76%). In 15 patients with coronary artery disease undergoing heart catheterization, we compared cardiac side effects of coronary angiography and left ventricular angiography using metrizamide and diatrizoate with and without additional calcium (11.3 mmol/l) as contrast media under randomized conditions. In selective intracoronary injection with diatrizoate alone, peak left ventricular pressure and contractility (dP/dtmax) showed a fall of 30 +/- 11% and 31 +/- 15% (n = 33 injections). Using diatrizoate with added calcium (11.3 mmol/l), the fall was only 23 +/- 12% and 20 +/- 10% respectively (n = 31 injections). With metrizamide (n = 32 injections) cardiac side effects are even less and the decrease in pressure and contractility only 13 +/- 10% and 7 +/- 7% respectively, which its highly significant (p less than 0.0001) compared with the effect of diatrizoate. The heartrate slowing, not essentially altered by calcium addition, was minimal using non-ionic metrizamide. In left ventricular angiography, the pressure fall in the late phase after injection of diatrizoate, caused by decrease peripheral vascular resistance (vasodilation), was lacking when injecting metrizamide (p less than 0.001). Metrizamide has even less cardiodepressive side effects than diatrizoate with additional calcium when used in angiocardiography and seems to be suitable particularly for the evaluation of high risk patients.
Streptokinase, 1000-2000 U/h, was administered into the coronary artery via catheter over 15-60 minutes to 12 patients. Six of them had an infarct in the early stage (A), two a fresh re-infarction (B) and four nonstable angina (C). Nitroglycerine had been injected at a dose of 0.1-0.45 mg into the coronary artery before infusion of streptokinase. Nitroglycerine induced angiographic demonstrably better filling of the infarcted vessel in two patients of group A. After intracoronary injection of streptokinase the occluded artery re-opened or, if there had been subtotal stenosis, significantly widened in all patients of group A. But there was no complete disappearance of the narrowing. In the patients of group B and C there was no angiographic evidence of change, neither after nitroglycerine nor after streptokinase. There was no marked change in systemic clotting function. The findings indicate that after acute, first-time infarction a fresh coronary thrombus forms on the basis of atheromatous narrowing. The thrombus can be quickly removed by selective lysis via coronary catheter. Fresh thrombotic deposition is less likely on re-infarction or in nonstable angina. These results must be confirmed by observation on a larger group of patients.
Coronary angiography was performed in the acute stage of myocardial infarction in 65 patients. The infarct-related vessel was occluded in 50 patients; it was narrowed greater than 90% in the remaining 15 patients. Control angiography was performed 55 +/- 46 d after acute myocardial infarction in 18 patients. In the chronic stage, five of thirteen previously occluded vessels showed antegrade filling of the distal segment. The narrowing at the site of previous obstruction was 80--95%. In two of five patients with a subtotal stenosis, the lumen of the infarct-related vessel was clearly larger in the chronic stage. The end-diastolic volume index increased significantly from 86 +/- 23 ml/m2 in the acute stage to 110 +/- 35 ml/m2 in the chronic stage (p less than 0.001). The increase in the end-systolic volume index from 42 +/- 15 ml/m2 to 63 +/- 31 ml/m2 was also statistically significant (p less than 0.005). Stroke volume index, ejection fraction, and the length of the akinetic segment (AKS) did not change significantly. There was a weak correlation between the end-systolic volume index and the length of the AKS in the acute stage (r = 0.489, p less than 0.05) and a better correlation in the chronic stage (r = 0.602, p less than 0.01). The ejection fraction and the length of the AKS correlated in the chronic stage only (r = 0.795, p less than 0.001).
The cardiotoxicity of commonly used contrast media such as sodium methylglucamine diatrizoate is related to nonphysiologic concentrations of ions and high osmolality. Following injection there is an excessive decrease in ambient calcium which disturbs the extracellular Na+/Ca2+ ratio and results in myocardial depression. In animal studies (anesthetized, intact mongrel dogs) this cardiodepressive effect could be fully compensated by adding 22.5 mEq/1 of ionic calcium to the contrast medium. In 16 patients studied for coronary artery disease (CAD) 72 injections of sodium methylglucamine diatrizoate, mainly in the left coronary artery, were thoroughly investigated. There was marked depression of left ventricular pressure (-22%) and (dP/dt)max (-27%), and marked heart rate slowing (-29%). Added calcium in the concentration cited reduced significantly (p < 0.001) the myocardial depression to -15% and -13%, respectively, but did not completely compensate it. The heart rate slowing was not altered significantly. It was concluded that the addition of calcium may be helpful when studying high-risk patients and using high injection volumes.
To verify the predictive value of thallium exercise scintigraphy, 20 normal individuals and 60 patients with coronary artery disease (CAD) were examined, using a quantitative standard technique and receiver operating characteristic analysis. The sensitivity of thallium scintigraphy for the presence of CAD was 97% for patients with previous infarction and 85% for those without infarction. The sensitivity for the extent of CAD was 93% for vessels perfusing infarcted areas and only 67% for vessels without infarction. In patients without myocardial infarction, sensitivity for the number of diseased vessels decreased with increasing extent of CAD. An underestimation of hemodynamically significant stenoses was proven by a comparison with the results of exercise ventriculography. The predictive value of a normal scintigram at a high prevalence of CAD is as low as the predictive value of an abnormal scintigram at a low prevalence level (screening). Thallium scintigraphy is indicated in patients with a medium prevalence of CAD, e.g., in patients with atypical angina and in asymptomatic patients with pathologic ECG.